Infarct-like lesions, also called silent strokes, are changes neurologists usually see on MRI scans that look like minor strokes.
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Before what her hospital records list as "a right temporoparietal infarct," Ma was blunt, unconventional and such a monument of self-confidence you could have sold tickets.
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The study Researchers reviewed six population-based studies and 13 clinic-based studies to see whether migraine sufferers had an increased risk of brain lesions, white matter abnormalities, infarct-like lesions or brain volume changes in both the gray and white matter regions of the brain.
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There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain that is affected, the underlying cause, and the prognosis. Later publications distinguish between "syndrome" and "infarct", based on evidence from imaging.
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The Infarct Combat Project (ICP) is an international nonprofit organization founded in 1998 which tries to decrease ischemic heart diseases through education and research.ICP, bmj.com; accessed 25 October 2015.Infarct Combat Project website ; accessed 26 October 2015.
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Compare to Anemic infarct. Hemorrhagic infarction is also associated with testicular torsion.
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Brain stroke in a region affecting auditory function such as a posterior circulation infarct has been associated with deafness.
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Abulia and cognitive impairment in two patients with capsular genu infarct. [Article]. Acta Neurologica Scandinavica, 104(3), 185-190.
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The tissue that surrounds the infarct (stroke damaged area) has reduced blood flow and is called the penumbra. Though the dendrites in the penumbra have been damaged due to the stroke, they can recover during the restoration of blood flow (reperfusion) if done within hours to a few days of the stroke due to time sensitivity. Due to reperfusion in the peri-infarct cortex (found next to the infarct), the neurons can help with active structural and functional remodelling after stroke. Initial stages of cortical development Cortical remapping is activity-dependent and competitive.
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A Zahn infarct is a pseudo-infarction of the liver, consisting of an area of congestion with parenchymal atrophy but no necrosis, and usually due to obstruction of a branch of the portal vein. Zahn infarcts are unique in that there is collateral congestion of liver sinusoids that do not include areas of anoxia seen in most infarcts. Fibrotic tissue may develop in the area of the infarct and it could be caused by an occlusive phlebitis in portal vein radicles. Non ischemic infarct of liver with lines of Zahn.
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Red softening is one of the three types of cerebral softening. As its name suggests, certain regions of cerebral softening result in a red color. This is due to a hemorrhagic infarct, in which blood flow is restored to an area of the brain that was previously restricted by an embolism. This is termed a "red infarct" or also known as red softening.
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At 36 months FU, the improvement on infarct size persisted, as well as the effect LV function. A progressive improvement of cardiac remodelling was noted.
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Papillary muscle rupture can be caused by a myocardial infarct, and dysfunction can be caused by ischemia. Both complications may lead to worsening of mitral regurgitation.
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Friedrich Wilhelm Zahn Friedrich Wilhelm Zahn (14 February 1845 – 1904) was a German-Swiss pathologist born in Germersheim. His eponyms include Zahn infarct and lines of Zahn.
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The PCAs arise directly from the OA and are end arteries which is to say no PCA or any of its branches anastomose with any other artery. Consequently, sudden occlusion of any PCA will produce an infarct in the region of the choroid supplied by that particular PCA. Occlusion of a short or long PCA will produce a smaller choroidal infarct, within the larger area supplied by the specific parent PCA.
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This is often to distinguish diseases from their chronic forms, such as chronic leukaemia, or to highlight the sudden onset of the disease, such as acute myocardial infarct.
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In vitro and in vivo results show that Neuroaid makes cells more resistant against glutamate aggression, increases neurite outgrowth and connectivity as well as reduces the infarct volume.
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The First International Study of Infarct Survival (ISIS-1) was a placebo-controlled trial of the beta-blocker atenolol. It recruited 16,027 patients and was completed in 1985.
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The Infarct Combat Project (ICP) is an international nonprofit organization founded in 1998 to fight ischemic heart diseases through education and research.Infarct Combat Project website; accessed October 26, 2015.
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Lancet Neurol. 2011 Jun;10(6):550-60. [PubMed] 16\. Nishida Y, Irioka T, Sekiguchi T, Mizusawa H. Pure sensory infarct in the territories of anterior cerebral artery. Neurology.
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Mov Disord. 1994 Nov. 9(6):610-5Hsieh CY, Sung PS, Hwang WJ. Transient blepharospasm, apraxia of eyelid opening, and hemidyskinesia following a right parietotemporal infarct. Parkinsonism Relat Disord.
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The Second International Study of Infarct Survival (ISIS-2) was a 2×2 factorial placebo- controlled trial of aspirin and the thrombolytic drug streptokinase. It recruited 17,187 patients and was completed in 1988.
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Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity, as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality.
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StAR was found to have an anti-apoptotic effect on the fibroblasts, which may allow them to survive the initial stress of the infarct, differentiate and function in tissue repair at the infarction site.
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TRO40303 is a new cardioprotective compound that was shown to inhibit the MPT pore and reduce infarct size after ischemia- reperfusion. It was developed by Trophos company and currently is in Phase I clinical trial.
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Multiple-infarct dementia patients may show slight improvement in executive functions and behaviour. No firm evidence supports usage in schizophrenia patients. Its efficacy is similar to donepezil and tacrine. Doses below 6 mg/d may be ineffective.
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It also has pathological involvement in heart attacks (increased expression around myocardial infarct zone) and decreased expression in leiomyoma and fibrosis. In invertebrate, dermatopontin homologue plays a role in hemagglutination, cell-cell aggregation, and expression during parasite infection.
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When used in vivo in a mouse model of ischaemic stroke, PFKFB3 inhibitor alleviates motor discoordination and brain infarct injury 50px Material was copied from this source, which is available under a Creative Commons Attribution 4.0 International License.
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Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries. These are corticobulbar fibers travelling in internal capsule.
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The Fourth International Study of Infarct Survival (ISIS-4) was a 2×2×2 factorial placebo-controlled trial of the angiotensin-converting enzyme inhibitor (ACE inhibitor) captopril, isosorbide mononitrate and magnesium sulphate. It recruited 58,050 patients and was completed in 1993.
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In contrast, injection of amniotic stem cell aggregates seems to improve the function of the tissue significantly by reducing the size of the infarct area and improving the function of the left ventricle. In addition, vasculature density has been shown to increase. Injection of cells immediately following the infarct is particularly beneficial as the cells protect the cardiac tissue from further damage. Moreover, other findings have brought the proof of concept that secretome of amniotic stem cell could act as an effective paracrine agent against Doxorubicin induced cardiotoxicity, confirming the potential importance of this cellular population in the field of cardiological research.
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This model creates a unilateral infarct in the hemisphere ipsilateral to the ligation, since the hypoxia alone is subthreshold for injury at this age. The area of injury is typically concentrated in periventricular regions of the brain, especially cortical and hippocampal areas.
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There are numerous diseases affecting the central nervous system which can cause cognitive impairment. Many of these are associated with aging. Some common examples include Alzheimer's disease and Multi-infarct dementia. Many diseases may be neurological or psychiatric and may primarily affect the brain.
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First in USSR journalistic is raised in newspaper a topic of hospice and deontology, and about medical care for incurable patients. Last two years he worked in newspaper "Rodnaya gazeta" (The Native Newspaper). Polyanovsky died 11 March 2006 after third infarct, in age 69.
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The recovering peri-infarct regions that have bad circuits are competing with healthy tissue for cortical map space. An in vivo study by Murphy was done using mice to help identify the sequence and kinetics of the peri-infarct cortical remapping after stroke. The study showed that eight weeks after a stroke had occurred in the forelimb sensory cortex of a mouse, the 'surviving' portion was able to promptly relay enhanced sensory signals to the motor cortex, which resulted in the remapping of sensory function. The mouse that experienced a stroke had remapped responses that lasted longer and spread farther from the motor cortex than those of the control.
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Fimastartan can also block TGF-β1 production (also AT1 dependent), which contributes to fibrosis and ventricular damage post-infarct. After ARB administration, mice showed improved prognosis after a myocardial infarction, though further studies still need to be done to assess fimasartan's specific effects on decreasing cardiovascular damage.
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Laurel edition. 1966 p 623 Fitzgerald died suddenly of a myocardial infarct in the apartment of Sheilah Graham, December 21, 1940, 5:15 pm, and Dr. Nelson signed the death certificate.Matthew J. Bruccoli, Scottie Fitzgerald Smith. Some Sort of Epic Grandeur: The Life of F. Scott Fitzgerald.
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The International Studies of Infarct Survival (ISIS) were four randomized controlled trials of several drugs for treating suspected acute myocardial infarction ("heart attack"). More than 134,000 patients from over 20 countries took part in four large simple trials between 1981 and 1993, coordinated from Oxford, England.
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Although not many studies have been conducted and little is known between microinfarcts and other vascular or epidemiological risk factors, these brain lesions are thought to be masked by other pathologies. However, the common macroscopic infarct is not exhibited in 45% of people tested for microinfarcts.
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It was studied as a possible treatment for Alzheimer's disease and multi-infarct dementia. Propentofylline has also been studied, to a lesser extent, as a possible adjunct in the treatment of ischemic stroke, due to its vasodilating properties. Propentofylline is in use as a veterinary medicine in older dogs.
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The effect of thrombolysis on HRV (assessed by pNN50) was reported in 95 patients with acute MI. HRV was higher 90 minutes after thrombolysis in the patients with patency of the infarct-related artery. However, this difference was no longer evident when the entire 24 hours were analyzed.
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This produces coronary steal by areas where arteries are maximally dilated. Areas of infarct or ischemic tissue will remain "cold". Pre- and post-stress thallium may indicate areas that will benefit from myocardial revascularization. Redistribution indicates the existence of coronary steal and the presence of ischemic coronary artery disease.
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Splenic infarct seen on CT Healed splenic infarct Several factors may increase the tendency for clot formation, such as specific infections (such as infectious mononucleosis, cytomegalovirus infection, malaria, or babesiosis), inherited clotting disorders (thrombophilia, such as Factor V Leiden, antiphospholipid syndrome), malignancy (such as pancreatic cancer) or metastasis, or a combination of these factors. In some conditions, blood clots form in one part of the circulatory system and then dislodge and travel to another part of the body, which could include the spleen. These emboligenic disorders include atrial fibrillation, patent foramen ovale, endocarditis or cholesterol embolism. Splenic infarction is also more common in hematological disorders with associated splenomegaly, such as the myeloproliferative disorders.
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It is due to inflammation of the vasculature supplying the central nervous system, that results in ischemia. It typically occurs about 6–7 years after initial infection and it may affect those with early disease. It may present as stroke or spinal cord infarct. Signs and symptoms vary with vascular territory involved.
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This produces coronary steal from areas of ischemia where arteries are already maximally dilated. Areas of infarct or ischemic tissue will remain "cold". Pre- and post-stress thallium may indicate areas that will benefit from myocardial revascularization. Redistribution indicates the existence of coronary steal and the presence of ischemic coronary artery disease.
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The side effects encountered are anorexia, nausea, diarrhea, metallic taste, and weight loss. Its use is contraindicated in diabetic coma, ketoacidosis, severe infection, trauma, other conditions where buformin is unlikely to control the hyperglycemia, renal or hepatic impairment, heart failure, recent myocardial infarct, dehydration, alcoholism, and conditions likely to predispose to lactic acidosis.
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While a TIA must by definition be associated with symptoms, a stroke may be symptomatic or silent. In silent stroke, also known as silent cerebral infarct (SCI), there is permanent infarction present on imaging, but there are no immediately observable symptoms. An SCI often occurs before or after a TIA or major stroke.
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As an ACE inhibitor, moexipril causes a decrease in ACE. This blocks the conversion of angiotensin I to angiotensin II. Blockage of angiotensin II limits hypertension within the vasculature. Additionally, moexipril has been found to possess cardioprotective properties. Rats given moexipril one week prior to induction of myocardial infarction, displayed decreased infarct size.
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Leukocytosis and elevated lactate dehydrogenase (LDH) may be found in splenic infarction. However, these results lack specificity to splenic infarct. Radiographic testing is required to detect this rare illness. In the hyperacute phase of infarction, abdominal CT scan performed with intravenous contrast is the imaging modality of choice in suspected splenic infarction.
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A case study involving two patients who suffered from acute confusional state and abulia was conducted to see if these symptoms were the result of an infarct in the capsular genu. Using clinical neuropsychological and MRI evaluations at baseline and one year later showed that the cognitive impairment was still there one year after the stroke. Cognitive and behavioral alterations due to a genu infarct are most likely because the thalamo-cortical projection fibers that originate from the ventral-anterior and medial-dorsal nuclei traverse the internal capsule genu. These tracts are part of a complex system of cortical and subcortical frontal circuits through which the flow of information from the entire cortex takes place before reaching the basal ganglia.
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The neural regeneration capability of Muse cells has been demonstrated in several models. In a rat stroke model induced by ischemic- reperfusion of middle cerebral artery occlusion (MCAO), 3 x 104 human dermal- Muse cells topically injected into three sites in the infarct area (each site received 1 x 104 Muse cells) delivered statistically significant functional recovery compared to vehicle and non-Muse fibroblast cell-injected groups after ~2.5 months. The functional recovery was supported by the incorporation of human Muse cells into rat pyramidal and sensory tracts with normalized hind limb somatosensory evoked potentials. Similarly, topically injected human bone marrow-Muse cells integrate into infarct region and replenish new neuronal cells and oligodendrocytes in mouse permanent MCAO and mouse lacunar stroke models.
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Clinical research indicates that as the size of the myocardial scar increases, so does the likelihood of the patient to develop heart failure.Stone, G. W. et al. Relationship Between Infarct Size and Outcomes Following Primary PCI: Patient-Level Analysis From 10 Randomized Trials. Journal of the American College of Cardiology 67, 1674-1683, (2016).
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The Third International Study of Infarct Survival (ISIS-3) was a 3×2 factorial trial that compared the three thrombolytic drugs streptokinase, tissue plasminogen activator (tPA) and anistreplase to each other, and also compared the anticoagulant heparin to no heparin. All patients were also given aspirin. It recruited 41,299 patients and was completed in 1991.
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Abdominal pain remains the leading chief complaint in patients diagnosed with a splenic infarct. Evaluation of patients who present with abdominal pain requires a broad differential approach. Lab evaluation may help rule in other causes of abdominal pain. Elevated liver function tests, bilirubin or lipase, may suggest a hepatobiliary or pancreatic source for pain.
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Acute cardiac unloading decreases cardiac MVO2 and has been demonstrated to limit the amount of scar tissue that forms, thus preserving heart function after a heart attack.Kapur, N. K. et al. Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation 128, 328-336, Sun, X. et al.
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Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries. Unlike peripheral facial palsy, central facial palsy does not affect the forehead, because the forehead is served by nerves coming from both motor cortexes.
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Elschnig spots are commonly caused by acute hypertensive events of the choroidal vascular system, mostly in the young, because their system of vessels is not ready to handle the changes in blood pressure. These changes in blood pressure cause an infarct of the vessels leading to death of the RPE and photoreceptors they support creating this window defect.
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The marriage with the unknown Russian woman was possibly still in force, and this could be the reason why the couple lived for long together before marrying in 1890. After that they had two sons: Wilhelm in 1891 and Eric in 1895. Wahlforss suffered an infarct during cycling trip in midsummer 1896. He was taken home unconscious.
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Not only did he have difficulty dancing, but he was unable to tap his foot or snap his fingers along with the beat of the music. The major difference between beat deafness and auditory arrhythmia, however, is that beat deafness is most likely something you are born with, whereas the arrhythmia most likely comes from damage, which was the case in the research done on "Mathieu," the first known case of beat-deafness. In another case, a former musician known as H.J. suffered damage from a temporoparietal infarct, which is an area of dead tissue due to lack of adequate blood supply. The infarct was believed to have been caused by a problem during a coronary angiography, which is a test to show the insides of an individual's coronary arteries.
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In therapy immediately following an AMI, increased cGMP triggers an increase in protein kinase G (PKG) activity. PKG reduces intracellular Ca2+ in vascular smooth muscle to increase smooth muscle relaxation and promote blood flow. PKG also limits smooth muscle cell proliferation, reducing intima thickening following AMI injury, ultimately decreasing myocardial infarct size. In Alzheimer's disease the brain's hydrogen sulfide concentration is severely decreased.
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Symptoms of cerebral infarction are determined by the parts of the brain affected. If the infarct is located in primary motor cortex, contralateral hemiparesis is said to occur. With brainstem localization, brainstem syndromes are typical: Wallenberg's syndrome, Weber's syndrome, Millard–Gubler syndrome, Benedikt syndrome or others. Infarctions will result in weakness and loss of sensation on the opposite side of the body.
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Rotigaptide acts at connexins, preferentially to connexin 43 (Cx43).Hennan K, Swillo R, Morgan G, Keith J, Schaub R, Smith R, Feldman H, Haugan K, Kantrowitz J, Wang P, Abu-Qare A, Butera J, Larsen B, Crandall D (2006). Rotigaptide (ZP123) Prevents Spontaneous Ventricular Arrhythmias and Reduces Infarct Size During Myocardial Ischemia/Reperfusion Injury in Open-Chest Dogs. JPET. 317: 236– 243.
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The most common complication during this period is arrhythmias. Day 1-7 is marked by the inflammatory phase. Days 1-3 are marked by “acute inflammation”, in which neutrophils infiltrate the ischemic tissue. A major complication during this period is fibrinous pericarditis, particularly in transmural ventricular wall damage (an infarct that impacted all 3 layers of the heart, the epicardium, myocardium, and endocardium).
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Overweight, Barreto was feeling ill during all June 23, 1921. He took a taxi and, with the increase of the malaise, he asked the driver to stop the car and bring him a glass of water. However, before help could arrive, he died of a sudden myocardial infarct. The news about João do Rio's death quickly spread all over the city.
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On the other hand, talks with the BnF proved unsuccessful. Božidar Kantušer died on May 9, 1999 in a Paris hospital, after a cerebral infarct, at the age of 77 years. Kantušer is buried in Paris at the Père Lachaise cemetery, together with Grace Renzi (Kantuser) who died in 2011. The manuscripts of his works are kept at the Library of Congress.
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Infarct size was reduced by ≈52%, and the ejection fraction was increased by ≈38% compared with vehicle injection at 2 months, ≈2.5 and ≈2.1 times higher, respectively, than that induced by mesenchymal stem cells. Muse cell allografts and xenografts efficiently engrafted and recovered functions, and allografts remained in the tissue and sustained functional recovery for up to 6 months without immunosuppression.
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In general, these types of techniques are considered to be potentially significant but further investigations are required. Another area of interest is the use of these cells for improvement of cardiac tissue following a myocardial infarction. Several strategies have been tested in rats including the injection of dissociated amniotic stem cells into the infarct region, which yielded conflicting results from several research groups.
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Splenic infarct appears as a wedge-shaped area of splenic tissue with the apex pointed toward the helium and the base of the splenic capsule. As the infarction matures, the affected tissue may normalize, liquefy or become contracted or scarred. Abdominal ultrasound has also been used to detect splenic infarction. Ultrasound findings of the hypoechoic wedge-shaped region of splenic tissue indicate infarction.
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In 1910 he made one of the earliest diagnoses of coronary thrombosis, and before his death in 1932, he had documented 144 cases of this condition.Heart Dr Carey Coombs and his non- existent cardiac infarct. His best written work is "Rheumatic Heart Disease", a book that was published in 1924. He is also remembered for his work in the management and prevention of childhood heart disease.
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Ephrin-A3 (Efna3) is a gene that is involved in the inhibition of angiogenesis. Although it is known that Efna3 inhibits the formation of new blood vessels, its specific role is still unknown. MiRNA-210 suppresses Efna3 at the mRNA level, thereby allowing angiogenesis to occur in cardiac tissue post-infarct. The second target gene, protein tyrosine phosphatase-1B (Ptp1b) is involved in the induction of apoptosis.
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Ptp1b gene protein has been known to regulate apoptosis by regulating the phosphorylation status of apoptotic proteins such as caspase-3 and caspase-8. MiRNA-210 inhibits the effects of Ptp1b protein, which suppresses its pro-apoptotic functions. Therefore, suppression of these two particular genes may contribute to the improvement of cardiac tissue and function by up-regulating angiogenesis and inhibiting apoptosis of cardiomyocytes after myocardial infarct.
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Ischemic damage can range from mucosal infarction, which is limited only to the mucosa; mural infarction of the mucosa and underlying submucosa; to transmural infarction of the full thickness of the gastrointestinal wall. Mucosal and mural infarcts in and of themselves may not be fatal, however may progress further to a transmural infarct. This has the potential for perforation of the wall, leading to peritonitis.
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Preclinical trials involving injections of adenovirus which contained the Ccna2 gene into infarcted porcine (pig) hearts has shown to be protective of MI in pig hearts. Ccna2 mediated cardiac repair showed both a decrease in fibrosis in the peri-infarct tissue and a greater number of cardiomyocytes at the sites of injection. Delivery of Ccna2 into cardiac tissue invokes a regenerative response and markedly enhances cardiac function.
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One small study, with 12 subjects given pyritinol, showed an improvement in performance on tests of reaction time, but not on memory tests. Some studies have found large doses of Pyritinol can help to reduce hangovers. Showed improvement over placebo in those with senile dementia of the Alzheimer type (SDAT) and multi- infarct dementia (MID). In healthy adults it improved several measure of cognition treating in one placebo controlled study.
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Sobel BE, Collen D. Questions unresolved by the Third International Study of Infarct Survival. Am J Cardiol. 1992; 70: 385–9. To end this controversy, the GUSTO trial (Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries) was set up, a head- to-head comparison between rt-PA and streptokinase. In the GUSTO-trial 41,021 heart attack patients were treated in 1,081 hospitals in 15 countries.
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On 18 February 1546, Luther died at the age of 62 years. The reason for his death is assumed to be a cardiac infarct. The question of how Martin Luther died became essential to the fate of the Protestant Reformation. The Roman Catholic church preached that the manner of death attests the life and that the devil uses the last moments of life as his last chance to tempt the individual.
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It is unclear which drug and which mode of administration is the most effective. Bleeding into the brain and in other sites of the body is a major concern in the use of thrombolysis. American guidelines make no recommendation with regards to thrombolysis, stating that more research is needed. In those where a venous infarct or hemorrhage causes significant compression of surrounding brain structures, decompressive craniectomy is sometimes required.
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ST elevation is associated with infarction, and may be preceded by changes indicating ischemia, such as ST depression or inversion of the T waves. Abnormalities can help differentiate the location of an infarct, based on the leads that are affected by changes. Early STEMIs may be preceded by peaked T waves. Other ECG abnormalities relating to complications of acute myocardial infarctions may also be evident, such as atrial or ventricular fibrillation.
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The youngest victim was sixteen, the oldest sixty. When the massacre was over, the corpses were loaded on trucks and carried to the old Jewish cemetery in Orlová, where they were dumped in a common grave. The German authorities then entered "cardiac insufficiency" and "cardiac infarct" as the causes of death in the death register. The bodies were transferred from Orlová to Životice when the war was over.
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It provides 3D images that can be studied on computer, and also allows measurement of heart ventricle size. Infarct area and arterial calcium can also be observed (however those require a somewhat higher radiation exposure). That said, one advantage retained by Catheter angiography is the ability of the physician to perform procedure such as balloon angioplasty or insertion of a stent to improve blood flow to the artery.
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Helms's health remained poor after he retired from the Senate in 2003. In April 2006, news reports disclosed that Helms had multi-infarct dementia, which leads to failing memory and diminished cognitive function, as well as a number of physical difficulties. He was later moved into a convalescent center near his home. Helms died of vascular dementia during the early morning hours of July 4, 2008, at the age of 86.
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This seems to be related to the location of the hemorrhages for each individual patient. Particularly, whether the infarct is anterior or bilateral. Localization of function of the thalamus can be illustrated through vascular thalamic amnesia. The damage to the tuberothalmic territory appears to have the most extensive effects in relation to this form of amnesia by affecting functions of arousal and orientation, learning and memory, personality, and executive function.
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The wallet bursts into flames, and when it is extinguished, the card she picked is in it. Kutner tells Foreman that the tests show there was no cause for the heart failure. Foreman suggests running a lung MRI, but Flynn starts bleeding internally as soon as they start the MRI. He has had three units of AB positive blood transfusions, so Thirteen wonders if he has had an intestinal infarct.
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He became discontented with the changes in football culture in the mid-1960s – essentially the abolition of the maximum wage (through teammates Jimmy Hill and Johnny Haynes), which led to the concentration of power in the hands of the richer clubs – and retired to run a pub. He died in May 2005 at the age of 77, and had been ill with multi-infarct dementia for some time before his death.
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His son, Răzvan Lucescu, was also a footballer, and is currently managing Al-Hilal. On 15 July 2009, Lucescu suffered an attack of pre-infarct angina, and was operated in an emergency hospital in Donetsk.Mircea Lucescu a suferit un preinfarct la Donețk! Soția sa a plecat astăzi de urgență în Ucraina On 6 January 2012, he was involved in a road accident in Bucharest and was seriously hurt.
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2001 Jul;48(4):1111-23. both methods having some, but different methodological weaknesses. Both methods, however, will acquire the same data (measurements may differ somewhat, however, being method dependent), and also can be displayed by the same type of display. The point of deformation imaging, is that a passive segment in the myocardium for instance after an infarct, may move due to the action of an adjacent segment (tethering).
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In multiple randomized controlled trials, remote ischemic conditioning reduced infarct size in ST- elevation myocardial infarction (STEMI) patients when used in the ambulance or emergency department as an adjunct therapy to primary percutaneous coronary intervention (PCI), or when used with thrombolytic drugs. In seven trials comprising 2,372 STEMI patients, infarct size—a measure of damage to the heart—was reduced by 17–30% on average, and the reduction was greatest (~60%) in the largest infarcts. Further analysis of a Danish study (CONDI-1), in which patients were treated in the ambulance, showed that those who received RIC did not show a decline in myocardial salvage index (a measure of a healthy heart) when they experienced a delay in treatment, while the control group experienced a significant decline in salvage index. The RIC treatment therefore resulted, effectively, in an extension of the "golden hour", the period in which medical treatment for heart attacks is most effective.
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However, increases in cardiac myostatin can increase its serum concentration, which may cause skeletal muscle atrophy. Pathological states that increase cardiac stress and promote heart failure can induce a rise in both cardiac myostatin mRNA and protein levels within the heart. In ischemic or dilated cardiomyopathy, increased levels of myostatin mRNA have been detected within the left ventricle. As a member of the TGF-β family, myostatin may play a role in post-infarct recovery.
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At last, Johnson was able to develop classes. Eventually, he self-published a book in 1975. In December 1976, Johnson, who also worked as a professional diver, was seriously injured in an underwater accident and sustained a near-fatal brain stem infarct causing stroke-like symptoms. Initially told he would never walk again, he once again defied odds and within a matter of months, was walking and looking as healthy as ever.
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Daniel Lawton also predeceased his father as a young adult. Lawton had a nearly-fatal myocardial infarct in 1977; after a difficult recovery, he resumed all of his professional activities. However, Lawton ultimately developed pancreatic carcinoma in late 1986; he was visited during his last illness by many state and national political figures who were among his friends and admirers. Dr. Lawton died on May 18, 1987, and he is buried in Marshfield, WI.
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Cardiogenic shock as a result of the heart being unable to adequately pump blood may develop, dependent on infarct size, and is most likely to occur within the days following an acute myocardial infarction. Cardiogenic shock is the largest cause of in-hospital mortality. Rupture of the ventricular dividing wall or left ventricular wall may occur within the initial weeks. Dressler's syndrome, a reaction following larger infarcts and a cause of pericarditis is also possible.
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Pure alexia almost always involves an infarct to the left posterior cerebral artery (which perfuses the splenium of the corpus callosum and left visual cortex, among other things). The resulting deficit will be pure alexia – i.e., the patient can write but cannot read (even what they have just written). However, because pure alexia affects visual input, not auditory input, patients with pure alexia can recognize words that are spelled out loud to them.
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Another common and under-recognized cause of hypertension is sleep apnea, which is often best treated with nocturnal nasal continuous positive airway pressure (CPAP), but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, septoplasty, or weight loss. Another cause is an exceptionally rare neurological disease called Binswanger's disease, causing dementia; it is a rare form of multi- infarct dementia, and is one of the neurological syndromes associated with hypertension.
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Neutrophils are the primary white blood cells that respond to a bacterial infection, so the most common cause of neutrophilia is a bacterial infection, especially pyogenic infections.Table 12-6 in: 8th edition. Neutrophils are also increased in any acute inflammation, so will be raised after a heart attack, other infarct or burns. Some drugs, such as prednisone, have the same effect as cortisol and adrenaline (epinephrine), causing marginated neutrophils to enter the blood stream.
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It is well documented that the caudate nucleus is involved in degenerative diseases of the central nervous system such as Huntington disease. In a case study of 32 acute caudate stroke patients, 48% were found to be experiencing abulia. Most of the cases where abulia was present were when the patients had a left caudate infarct that extended into the putamen as seen through a CT or MRI scan.Kumral, E., Evyapan, D., & Balkir, K. (1999).
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Long-chain L-3-hydroxyacyl-coenzyme A dehydrogenase deficiency is associated with some pregnancy-specific disorders, including preeclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), hyperemesis gravidarum, acute fatty liver of pregnancy, and maternal floor infarct of the placenta. Additionally, it has been correlated with Acute fatty liver of pregnancy (AFLP) disease. From a clinical perspective, HADHA might also be a useful marker to predict resistance to certain types of chemotherapy in patients with lung cancer.
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Neurological examination that confirms macular sparing can go far in representing the type of damage mediated by an infarct, in this case, indicating that the caudal visual cortex (which is the principal recipient of macular projections of the optic nerve) has been spared. Further, it indicates that cortical damage rostral to, and including, lateral geniculate nucleus is an unlikely outcome of the infarction, as too much of the lateral geniculate nucleus is, proportionally, devoted to macular- stream processing.
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Hemorrhagic infarcts are infarcts commonly caused by occlusion of veins, with red blood cells entering the area of the infarct, or an artery occlusion of an organ with collaterals or dual circulation. This is commonly seen in brain, lungs, and the GI tract, areas referred to as having "loose tissue," or dual circulation. Loose-textured tissue allows red blood cells released from damaged vessels to diffuse through the necrotic tissue. White infarcts can become hemorrhagic with reperfusion.
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Midline shift (arrow) is present in this brain after a stroke (infarct depicted in shaded area). Midline shift is a shift of the brain past its center line. The sign may be evident on neuroimaging such as CT scanning. The sign is considered ominous because it is commonly associated with a distortion of the brain stem that can cause serious dysfunction evidenced by abnormal posturing and failure of the pupils to constrict in response to light.
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Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as the pons. Most frequently caused by vascular disease or tumors involving the dorsal pons. Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus. There's involvement of the fifth to eighth cranial nerves, central sympathetic fibres (Horner syndrome) and horizontal gaze palsy.
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On the other hand, they often detach, move into blood circulation, and eventually block smaller downstream branches of arteries causing a thromboembolism. Generally, emboli travel as far outward as their size permits along the vascular branches of the brain. Using this hypothesis, microemboli are viewed as the cause of the infarct rather than secondary events. Nevertheless, secondary thrombi do form after infarcts, and therefore it has been difficult to distinguish between emboli and thrombi in watershed locations.
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"Gerstmann syndrome and similar posterior parietal symptom combinations (like acalculia) are usually the result of focal cerebrovascular disease in a posterior branch of the left middle cerebral artery or a broader zone infarct, usually involving the angular gyrus or subjacent white matter (Brodmann area 39). In rare cases, traumatic brain injury of an expanding neoplasm in this same region can cause all or elements (acalculia is one of four elements) of the symptoms of this syndrome".
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Other factors such as toxicants can adversely impact bone cells. Infections, chronic or acute, can affect blood flow by inducing platelet activation and aggregation, contributing to a localized state of excess coagulability (hypercoagulability) that may contribute to clot formation (thrombosis), a known cause of bone infarct and ischaemia. Exogenous estrogens, also called hormonal disruptors, have been linked with an increased tendency to clot (thrombophilia) and impaired bone healing. Heavy metals such as lead and cadmium have been implicated in osteoporosis.
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Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. Post-myocardial complications occur after a period of ischemia, these changes can be seen in gross tissue changes and microscopic changes.Muscle Tissue.
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Monocytes and macrophages play important roles in healing after myocardial infarction. With the absence of monocytes and macrophages, chances of LVT formation are very high. Failure to clear cellular debris from the infarct compromises the endothelial lining of the left ventricle and exposes the damaged tissue to the blood.Frantz, S., Hofmann, U., Fraccarollo, D., Schäfer, A., Kranepuhl, S., Hagedorn, I., Nieswandt, B., Nahrendorf, M., Wagner, H., Bayer, B., Pachel, C., Schon, M., Kneitz, S., Bobinger, T., Weidemann, F., Ertl, G., Bauersachs, J. (2012).
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This leads to an ischemic cascade of intracellular changes, necrosis and apoptosis of affected cells. Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage. Ischemia first affects this region, the subendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply. The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thickness transmural infarct.
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Neurologists have observed that olfactory dysfunction is a cardinal feature of several neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Most of these patients are unaware of an olfactory deficit until after testing where 85% to 90% of early- stage patients showed decrease activity in central odor processing structures. Other neurodegenerative diseases that affect olfactory dysfunction include Huntington's disease, multi-infarct dementia, amyotrophic lateral sclerosis, and schizophrenia. These diseases have more moderate effects on the olfactory system than Alzheimer's or Parkinson's diseases.
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Both studies found there is no statistical difference in outcome with cyclosporin administration. Research is ongoing. Reperfusion leads to biochemical imbalances within the cell that lead to cell death and increased infarct size. More specifically, calcium overload and excessive production of reactive oxygen species in the first few minutes after reperfusion set off a cascade of biochemical changes that result in the opening of the so-called mitochondrial permeability transition pore (MPT pore) in the mitochondrial membrane of cardiac cells.
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In test with rabbits, significant improvement in protection against arrhythmic effects and infarct size reduction was observed after administrating exogenously SRTX-c (in dosage of 0.24 nmol/kg, i.v.) prior the coronary occlusion accident. That was achieved thanks to ability of SRTX-c to activate selected ETB receptors. In rat thoracic aorta, the contractile activity is grouped as follows: ET-1 > SRTX-b > SRTX-a > SRTX-c at lower concentrations, but SRTX-b > ET-1 > SRTX-a > SRTX-c at higher concentrations.
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Brodmann area 8, or BA8, is part of the frontal cortex in the human brain. Situated just anterior to the premotor cortex (BA6), it includes the frontal eye fields (so-named because they are believed to play an important role in the control of eye movements). Damage to this area, by stroke, trauma or infection, causes tonic deviation of the eyes towards the side of the injury. This finding occurs during the first few hours of an acute event such as cerebrovascular infarct (stroke) or hemorrhage (bleeding).
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The initial "wave" of infarction can take place over 3–4 hours. These changes are seen on gross pathology and cannot be predicted by the presence or absence of Q waves on an ECG. The position, size and extent of an infarct depends on the affected artery, totality of the blockage, duration of the blockage, the presence of collateral blood vessels, oxygen demand, and success of interventional procedures. Tissue death and myocardial scarring alter the normal conduction pathways of the heart, and weaken affected areas.
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Research done in animals has shown that subjects recovering in an enriched environment 15 days after having a stroke had significantly improved neurobehavioral function. In addition these same subjects showed greater capability of learning and larger infarct post-intervention than those who were not in an enriched environment. It was thus concluded that environmental enrichment had a considerable beneficial effect on the learning and sensorimotor functions on animals post-stroke. A 2013 study also found that environmental enrichment socially benefits patients recovering from stroke.
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Indian Journal of Psychiatry, 45(4), 255–256. They discovered that hyperglutamatergic states, which are caused by both strokes and stress, share a relationship with dissociative symptoms, suggesting a possible organic pathology that can predispose individuals to the syndrome. Wirtz and colleagues (2008) described a patient with Ganser syndrome after a left-hemispheric middle cerebral artery infarct. A neuropsychological examination revealed atypical lateralisation of cognitive functions, leading to the conclusion that the giving of approximate answers might be related to frontal-executive cerebral dysfunction.
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From that point on, her memory gradually worsened until she was officially diagnosed in 1985 with multi-infarct dementia, although some descriptions of her life assume she had been diagnosed with Alzheimer's disease. However, at that time such a conclusion could only be confirmed by an autopsy after death. Stephen cared for Joyce at home until 1992, when she was moved into the Fairlawn Nursing Home in Lexington, Massachusetts. She died there from cardiac arrest on August 23, 1994 at the age of 76.
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A coronal section of the brain confirmed an infarct, tissue death due to lack of oxygen, in the left superior frontal gyrus with the main lesion in the subcortical white matter. Fiber bundles are also present in the subcortical white matter connecting the prefrontal area with the nucleus of the thalamus. The researchers believed that utilization behavior could also be a result of the disordering of these fibers. The researchers established that a network exists between the frontal cortical and some subcortical lesions, especially the thalamus, and a white matter lesion may disconnect this network.
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Neurological imaging has shown that TMoA is typically caused by an infarct of the anterior superior frontal lobe in the perisylvian area of the left, or language-dominant, hemisphere. The anterior superior frontal lobe is known as the prefrontal cortex which is responsible for the initiation and ideation of verbal speech. The damage leaves the major language networks, Broca's and Wernicke’s areas and the arcuate fasiculus, unaffected. Brain injury can result from a stroke caused by left anterior cerebral artery (ACA) occlusion, brain tumors, traumatic brain injury (TBI), or progressive neurological disorders.
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The first documented case of peduncular hallucinosis was by French neurologist and neuropsychiatrist Jean Lhermitte, which described a 72-year-old woman’s visual hallucinations. The hallucinations occurred during normal conscious state and the patient’s neurological signs were associated with those characteristic of an infarct to the midbrain and pons. Von Bogaert, Lhermitte’s colleague, named this type of hallucination “peduncular,” in reference to the cerebral peduncles, as well as to the midbrain and its surroundings. In 1925, Von Bogaert was the first to describe the pathophysiology of peduncular hallucinosis through an autopsy of a patient.
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Erythropoietin and its receptor have an essential role in neurogenesis, specifically in post- stroke neurogenesis and in the migration of neuroblasts to areas of neural injury. Severe embryonic neurogenesis defects in animals that were null for Epo or EpoR genes are found. In EpoR knock-down animals, deletion of EpoR genes specific to the brain lead to a reduction in cell growth in the subventricular zone and impaired neurogenesis after stroke. This post-stroke neurogenesis was characterized by an impaired migration of neuroblasts in the peri-infarct cortex.
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Arrhythmia in the auditory modality is defined as a disturbance of rhythmic sense; and includes deficits such as the inability to rhythmically perform music, the inability to keep time to music and the inability to discriminate between or reproduce rhythmic patterns. A study investigating the elements of rhythmic function examined Patient H.J., who acquired arrhythmia after sustaining a right temporoparietal infarct. Damage to this region impaired H.J.'s central timing system which is essentially the basis of his global rhythmic impairment. H.J. was unable to generate steady pulses in a tapping task.
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This artery supplies blood to the anterior portion of the inferior cerebellum, the middle cerebellar peduncle, and to the facial (CN VII) and vestibulocochlear nerves (CN VIII). Obstruction of the AICA can cause paresis, paralysis, and loss of sensation in the face; it can also cause hearing impairment. Moreover, it could cause an infarct of the cerebellopontine angle. This could lead to hyperacusia (dysfunction of the stapedius muscle, innervated by CN VII) and vertigo (wrong interpretation from the vestibular semi-circular canal's endolymph acceleration caused by alteration of CN VIII).
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Anemic infarcts (also called white infarcts or pale infarcts) are white or pale infarcts caused by arterial occlusions, and are usually seen in the heart, kidney and spleen. These are referred to as "white" because of the lack of hemorrhaging and limited red blood cells accumulation, (compare to Hemorrhagic infarct). The tissues most likely to be affected are solid organs which limit the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds. The organs typically include single blood supply (no dual arterial blood supply or anastomoses).
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He was chair of The Joint Committee of the Nordic Medical Research Councils (NOS-M) 2010-2012 and member of the European Medical Research Councils Core Group 2009-2012. He is now chairing the Scientific Review Group for the Biomedical Sciences in European Science Foundation and has been a member of the board of Division for Science at The Research Council of Norway. He has also been member of the board of SINTEF and The Cancer Registry of Norway. Slørdahl has led the work to establish The Norwegian Myocardial Infarct Registry.
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Similarly, sarcKATP regulates vascular smooth muscle tone, and deletion of the kir6.2 or sur2 genes leads to coronary artery vasospasm and death. Upon further exploration of sarcKATP’s role in cardiac rhythm regulation, it was discovered that mutant forms of the channel, particularly mutations in the SUR2 subunit, were responsible for dilated cardiomyopathy, especially after ischemia/reperfusion. It is still unclear as to whether opening of KATP channels has completely pro- or antiarrhythmic effects. Increased potassium conductance should stabilize membrane potential during ischemic insults, reducing the extent infarct and ectopic pacemaker activity.
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Infarct size is a predictor of future cardiovascular events as well as mortality, and researchers doing long-term follow-up on STEMI patients treated with RIC found that the reduction in heart damage at the time of the heart attack resulted in clinical improvement four years later: MACCE (major adverse cardiovascular and cerebrovascular event) rates were reduced by 47% (13.5% vs. 25.6%, p=0.018). This improvement resulted in mean cumulative cardiovascular medical care costs that were €2,763 lower in the RIC-treated group than in the control group (€12,065 vs. €14,828)—savings of approximately 20%.
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Fogging phenomenon in computerized tomography (CT) scanning of the head is vanishing signs of an infarct on the serial CT imaging in a patient with a recent stroke. It is a reversal of the hypodensity on the CT after an acute ischemic stroke. This happens as a result of re-nourishment of the infarcted area in subacute phase about one to three weeks after the stroke. In fact, resolution of the edema, which was caused by the accident, leads to increased attenuation of infarcted area that may regain near-normal density and mask the stroke.
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Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.
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Bert elucidated the overall genetic transcriptional pathway of steroid and intracellular hormone action, discovered nuclear receptor(NR) coactivators (CoAs), discovered the functional 3-D structures CoA-NR complexes on DNA, and the critical roles for coactivators in physiology and diseases. He has published over 700 papers and holds 29 patents in the fields of gene regulation, molecular endocrinology and steroid receptors and transcriptional coactivators. His work on molecular mechanisms of steroid receptor coactivators has great relevance to genetic and reproductive diseases, disorders of metabolism and diabetes, myocardial infarct induced heart failure, and especially, cancers.
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Examining 37 patients who underwent intercoronary thrombolysis within six hours of MI, Fujita found that 2 of 19 patients without preinfarct angina had collaterals and 9 of 18 patients with angina had them. No other variables pertaining to collateral development distinguished the groups. Fujita therefore suggests that the absence of symptomatic angina may not always portend favorable developments, and infarct prevention must surely be targeted to those with coronary disease who are without symptoms, as they may be without the protective effects of collateral development provoked by the presence of angina.
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This thin, weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue. As a result, there is dilatation of the chamber arising from the infarct region. The initial remodeling phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may, to some extent, be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output. Over time, however, as the heart undergoes ongoing remodeling, it becomes less elliptical and more spherical.
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Investigations of various exogenous circulating ligands such as the delta active opiates and opioids simulate the phenomenon of IPC thus protecting the downstream tissues without the IPC intermittent ligating procedure. Methods to either mimic or elicit IPC have been attempted in clinical practice, in the area of coronary heart disease in an attempt to limit the injury caused to the heart via ischemia and reperfusion injury. Such injury would occur when a patient has an acute myocardial infarct followed by reperfusion by either percutaneous coronary intervention or thrombolysis.
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Eventually, however, it was agreed that the age limit was artificial, and that Alzheimer's disease was the appropriate term for persons with that particular brain pathology, regardless of age. After 1952, mental illnesses including schizophrenia were removed from the category of organic brain syndromes, and thus (by definition) removed from possible causes of "dementing illnesses" (dementias). At the same, however, the traditional cause of senile dementia – "hardening of the arteries" – now returned as a set of dementias of vascular cause (small strokes). These were now termed multi-infarct dementias or vascular dementias.
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Leaving in May 1924 for London due to illness, he died from pneumonia due to infarct of the lung at a London nursing home at the night of 27 August. The funeral took place on 2 September at the Kensal Green Cemetery. HSBC's principal offices, including the HSBC Main Building in Hong Kong, the former office in Shanghai, and the current global headquarters in London, all feature a pair of bronze lions. The first of these, in Shanghai, were commissioned by Stephen and inspired by his visit to the Venetian Arsenal.
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Thomas Whitman is a 75-year-old former musician who has lapsed into a coma after years of suffering from multi-infarct dementia. As he is clinging to his life while his estranged daughter Gem ponders on signing a do not resuscitate order, Thomas' mind enters a fantasy world where he relives his life as a ten- year-old orphan. After meeting a girl named Ann at the orphanage and acquiring a snow globe containing a dancing figurine named "Arabesque", young Thomas befriends a snowman named "Mr. White", who takes him on a flight to the skies.
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Hypertension is also associated with impaired cognition in an aging population. Hypertension- related cognitive impairment and dementia may be a consequence of a single infarct due to occlusion of a "strategic" larger vessel or multiple lacunar infarcts due to occlusive small vessel disease resulting in subcortical white matter ischemia. Several clinical trials suggest that antihypertensive therapy has a beneficial effect on cognitive function, although this remains an active area of investigation. Cerebral blood flow remains unchanged over a wide range of arterial pressures (mean arterial pressure of 50–150 mmHg) through a process termed autoregulation of blood flow.
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Some cases presented with episodic liver dysfunction during otherwise mild illnesses or cardiomyopathy, along with chronic neurologic dysfunction. Brain findings were notable for generalized edema with diffuse ventricular compression, acute left tonsillar herniation, and diffuse multifocal acute damage in the hippocampus. In addition, some abnormalities consistent with nonacute changes were seen, including a subacute right cerebellar hemispheric infarct and reduction in the number of neurons in several areas. In one patient, whose clinical manifestations of hypotonia, cardiomyopathy, and lactic acidosis, a vigorous treatment with riboflavin allowed the individual to have normal psychomotor development and no cognitive impairment at 5 years of age.
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Cytori’s APOLLO study was designed to evaluate the use of ADRCs in the treatment of patients who have undergone myocardial infarctions. In March 2009, the study’s Steering Committee and the data safety and monitoring board (DSMB) deemed that the safety and feasibility goals of the study had been met after the enrollment of 14 patients. Primary outcomes for the study will be assessed at the six month follow up. The ADRC therapy resulted in a reduction in infarct size by 60%, and significant improvement of LV perfusion (MIBI SPECT) and an improvement of left ventricular function by 6% at 6 month followup.
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The infarct generally results grossly in a wedge shaped area of necrosis with the apex closest to the occlusion and the base at the periphery of the organ. The margins will become better defined with time with a narrow rim of congestion attributable to inflammation at the edge of the lesion.Robbins Basic Pathology Relatively few extravasated red cells are lysed so the resulting hemosiderosis is limited and results in a progressively more pale area of infarction with time. Ischemic coagulative necrosis results and fibrosis of the affected area develops from the reparative response beginning at the preserved margins and working its way inwards.
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Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the thrombolytic is used within two hours of the onset of symptoms. Failure rates of thrombolytics can be as high as 50%. In cases of failure of the thrombolytic agent to open the infarct-related coronary artery, the person is then either treated conservatively with anticoagulants and allowed to "complete the infarction" or percutaneous coronary intervention (and coronary angioplasty) is then performed.
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The neurological complications per central nervous system lesions are increasingly reported. The neurological complications found are meningoencephalitis, subdural effusion, cerebral hypoperfusion, cerebral ischemia and infarct, cerebellar infarction, manifesting with seizures, chorea, hemiplegia, mental confusion, lethargy and coma, or even a cerebral infarction with no neurological manifestations. Other neurological complications from cranial nerve involvement are reported as ataxia, facial palsy, and sensorineural hearing loss. Behavioral changes are thought to be caused by localised cerebral hypoperfusion, can include attention deficits, learning deficits, emotional disorders (emotional lability, fear of night, and night terrors), and internalization problems (anxious, depressive or aggressive behavior).
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Mn3O4@nanoerythrocyte-T7 (MNET) nanosponges can regulate oxygen and scavenge free radicals in the event of an ischemic stroke, which is a global leading cause of death and disability. These engineered nanosponges can help attenuate hypoxia after a stroke by mimicking red blood cells and increasing the amount of oxygen in the infarct area. This allows for the extension of the survival time of neurocytes, a crucial part of treating an ischemic stroke because their normal functions must be maintained. MNET works because it contains hemoglobin, which allows for there to be an oxygen sponge effect.
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Complications may occur immediately following the myocardial infarction or may take time to develop. Disturbances of heart rhythms, including atrial fibrillation, ventricular tachycardia and fibrillation and heart block can arise as a result of ischemia, cardiac scarring, and infarct location. Stroke is also a risk, either as a result of clots transmitted from the heart during PCI, as a result of bleeding following anticoagulation or as a result of disturbances in the heart's ability to pump effectively as a result of the infarction. Regurgitation of blood through the mitral valve is possible, particularly if the infarction causes dysfunction of the papillary muscle.
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Posterior cord syndrome (PCS), also known as posterior spinal artery syndrome (PSA), is a type of incomplete spinal cord injury. PCS is the least commonly occurring of the six clinical spinal cord injury syndromes, with an incidence rate of less than 1%. PCS originates from an infarct in the posterior spinal artery and is caused by lesions on the posterior portion of the spinal cord, specifically the posterior column, posterior horn, and posterolateral region of the lateral column. These lesions can be caused by trauma to the neck, occlusion of the spinal artery, tumors, disc compression, vitamin B12 deficiency, syphilis, or multiple sclerosis.
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In a study that is currently underway (February 2012), however, more positive results were being reported: In the SCIPIO trial, patients treated with autologous cardiac stem cells post MI have been reported to be showing statistically significant increases in LVEF and reduction in infarct size over the control group at four months after implant. Positive results at the one-year mark are even more pronounced. Yet the SCIPIO trial "was recently called into question". Harvard University is "now investigating the integrity of some of the data". The Lancet recently published a non-specific ‘Expression of concern’ about the paper.
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They may either rupture, producing an intracerebral hemorrhage that is initially centered in the region they supply, or they become occluded, producing a lacunar infarct in the tissue they supply. The lenticulostriate arteries are "end arteries", meaning that the regions they supply do not have significant collateral blood supply. Occlusion of these vessels therefore leads to stereotyped stroke syndromes. In the case of the lenticulostriate vessels, hemorrhage may remain localized to the putamen and caudate nucleus, may involve neighboring structures such as the internal capsule and other more distant white matter of the hemisphere, or may even rupture into the ventricular system.
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Clin Sci (Lond). 2007 Sep;113(6):287-96Eek C, Grenne B, Brunvand H, Aakhus S, Endresen K, Hol PK, Smith HJ, Smiseth OA, Edvardsen T, Skulstad H.Strain echocardiography and wall motion score index predicts final infarct size in patients with non-ST-segment-elevation myocardial infarction. Circ Cardiovasc Imaging. 2010 Mar;3(2):187-94 However, the incremental diagnostic and prognostic value of measuring LV shortening was already shown for the absolute measure Willenheimer R, Cline C, Erhardt L, Israelsson B. Left ventricular atrioventricular plane displacement: an echocardiographic technique for rapid assessment of prognosis in heart failure.
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Similarly, short (8-nt) oligonucleotides designed to inhibit miR-21 could not inhibit cardiac hypertrophy or fibrosis. In another study with a mouse model of acute myocardial infarction, miR-21 expression was found to be significantly lower in infarcted areas and overexpression of miR-21 in those mice via adenovirus- mediated gene transfer decreased myocardial infarct size. miR-21 has been hypothesized to be an intermediary in the effects of air pollution that lead to endothelial dysfunction and eventually to cardiac disease. Expression of miR-21 is negatively associated with exposure to PM10 air pollution and may mediate its effect on small blood vessels.
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Persons with ONJ may have either necrotic bone or bone marrow that has been slowly strangulated or nutrient-starved. Bone with chronically poor blood flow develops either a fibrous marrow since fibres can more easily live in nutrient starved areas, a greasy, dead fatty marrow (wet rot), a very dry, sometimes leathery marrow (dry rot), or a completely hollow marrow space (osteocavitation), also typical of ONJ. The blood flow impairment occurs following a bone infarct, a blood clot forming inside the smaller blood vessels of cancellous bone tissue. Under ischaemic conditions numerous pathological changes in the bone marrow and trabeculae of oral cancellous bone have been documented.
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Following an ischemic stroke, DWI is highly sensitive to the changes occurring in the lesion. It is speculated that increases in restriction (barriers) to water diffusion, as a result of cytotoxic edema (cellular swelling), is responsible for the increase in signal on a DWI scan. The DWI enhancement appears within 5–10 minutes of the onset of stroke symptoms (as compared to computed tomography, which often does not detect changes of acute infarct for up to 4–6 hours) and remains for up to two weeks. Coupled with imaging of cerebral perfusion, researchers can highlight regions of "perfusion/diffusion mismatch" that may indicate regions capable of salvage by reperfusion therapy.
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There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as secondary prevention after an initial myocardial infarct. Recommendations include stopping smoking, a gradual return to exercise, eating a healthy diet, low in saturated fat and low in cholesterol, and drinking alcohol within recommended limits, exercising, and trying to achieve a healthy weight. Exercise is both safe and effective even if people have had stents or heart failure, and is recommended to start gradually after 1–2 weeks. Counselling should be provided relating to medications used, and for warning signs of depression.
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At the beginning of Hachinski's career, the prevailing view was that most dementias were caused by hardened brain arteries (mental deterioration via cerebral atherosclerosis). Still a junior neurologist at the time, Hachinski showed in 1974 that, in fact, only a small minority of dementias were so-caused, and that most were “multi-infarct dementias” — dementias caused by multiple, small, often imperceptible strokes. The terms “vascular dementia” and “vascular cognitive impairment” would later be widely adopted to describe all cognitive impairments in order to distinguish them from primary degenerative dementia (i.e., Alzheimer disease and senile dementia) and to emphasize that they are preventable and treatable, insofar as their vascular causes (i.e.
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Cerebral ischemia is a frequently disputed possible cause, at least for some segment of the TGA population, and until the 1990s it was generally thought that TGA was a variant of transient ischemic attack (TIA) secondary to some form of cerebrovascular disease. Those who argue against a vascular cause point to evidence that those experiencing TGA are no more likely than the general population to have subsequent cerebral vascular disease. In fact, "in comparison with TIA patients, TGA patients had a significantly lower risk of combined stroke, myocardial infarct, and death." Other vascular origins remain a possibility, however, according to research of jugular vein valve insufficiency in patients with TGA.
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Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischaemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as suffering from lacunar stroke syndrome (LACS). Much of the current knowledge of lacunar strokes comes from C. Miller Fisher's cadaver dissections of post-mortem stroke patients. He observed "lacunae" (empty spaces) in the deep brain structures after occlusion of 200–800 μm penetrating arteries and connected them with five classic syndromes.
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Affected individuals generally exhibit motor control problems or other developmental delays, and they often develop cerebral palsy or epilepsy later in life. This pathology of the brain was described under various names ("encephalodystrophy", "ischemic necrosis", "periventricular infarction", "coagulation necrosis", "leukomalacia," "softening of the brain", "infarct periventricular white matter", "necrosis of white matter", "diffuse symmetrical periventricular leukoencephalopathy"), and more often by German scientists, but the worldwide dissemination was the term periventricular leukomalacia, introduced in 1962 B. A. Banker and J. C. Larroche. The term can be misleading, as there is no softening of the tissue in PVL. V. V. Vlasyuk and V. P. TumanovVlasjuk VV, Tumanov VP Pathology periventricular leukomalacia.
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Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming. Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.
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Within approximately six months following the infarct, visual acuity improves by three or more lines of vision on the Snellen Chart (the chart with smaller letters on each lower line) in 42.7% of patients, while in 12.4% of patients, vision worsens by three lines. Opposite eye involvement occurs in approximately 15% to 20% of patients with NAION within 5 years.IONDT(The Ischemic Optic Neuropathy Decompression Trial) Study It is not always devastating as visual acuity may remain only moderately impaired. Furthermore, most cases of NAION involve the loss of a hemifield (either the upper or lower half of the visual field, but not both).
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In: "Coronary thrombolysis in perspective", Eds. BE Sobel and D Collen, Marcel Dekker Inc, New York, N.Y. 1993, p. 303-316. After the GUSTO studies, rt-PA became the thrombolytic drug of choice for most of the cardiologists in the Western world and would save the lives of many tens of thousands of heart attack patients. Nowadays, cardiologists agree that timely performed percutaneous coronary intervention (PCI), also known as 'angioplasty’ and ‘stenting', is the preferred strategy to treat acute myocardial infarction instead of thrombolysis. PCI is associated with less mortality on the short term (7% versus 9% for thrombolysis), a lower risk of a recurrent infarct (3% versus 7%) and a lower frequency of cerebral hemorrhage (1% versus 2%).
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The exogenous regulation of calpain activity is therefore of interest for the development of therapeutics in a wide array of pathological states. As a few of the many examples supporting the therapeutic potential of calpain inhibition in ischemia, calpain inhibitor AK275 protected against focal ischemic brain damage in rats when administered after ischemia, and MDL28170 significantly reduced the size of damaged infarct tissue in a rat focal ischemia model. Also, calpain inhibitors are known to have neuroprotective effects: PD150606, SJA6017, ABT-705253, and SNJ-1945. Calpain may be released in the brain for up to a month after a head injury, and may be responsible for a shrinkage of the brain sometimes found after such injuries.
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He has been a member of the steering committees of important clinical trials, including the International Studies of Infarct Survival, ISIS2, ISIS3, ISIS4, and the EU funded trials of the European Secondary Prevention Study Group and, furthermore, a national co-ordinator of HOPE and GUARDIAN. He has extensive experience in clinical research. In recent years his main scientific interest has been pharmacotherapy and pharmacoepidemiology of cardiovascular diseases, particularly management of myocardial infarction. He is the author or co- author of 250 scientific papers and has published in reputable journals, including Nature, the Lancet, BMJ, Heart, Journal of Internal Medicine, European Heart Journal, European Journal of Clinical Pharmacology, and British Journal of Clinical Pharmacology.
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This finding was validated by multiple independent studies occurring shortly thereafter, and has since been observed in multiple animal models and human tissue, as well as in studies employing transgenesis and PKCε activators/inhibitors. Mitochondrial targets of PKCε involved in cardioprotection have been actively pursued, since the translocation of PKCε to mitochondria following protective stimuli is one of the most well-accepted cardioprotective paradigms. PKCε has been shown to target and phosphorylate alcohol dehydrogenase 2 (ALDH2) following preconditioning stimuli, which increased the activity of ALDH2 and reduced infarct size. Moreover, PKCε interacts with cytochrome c oxidase subunit IV (COIV), and preconditioning stimuli evoked phosphorylation of COIV and stabilization of COIV protein and activity.
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Ischemic preconditioning (IPC) is an experimental technique for producing resistance to the loss of blood supply, and thus oxygen, to tissues of many types. In the heart, IPC is an intrinsic process whereby repeated short episodes of ischaemia protect the myocardium against a subsequent ischaemic insult. It was first identified in 1986 by Murry et al. This group exposed anesthetised open-chest dogs to four periods of 5 minute coronary artery occlusions followed by a 5-minute period of reperfusion before the onset of a 40-minute sustained occlusion of the coronary artery. The control animals had no such period of “ischaemic preconditioning” and had much larger infarct sizes compared with the dogs that did.
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In non-bisphosphonate cases of ONJ, it is mainly the cancellous portion of the bone and its marrow content that are involved in the disease process. The first stage is an oedema of the bone marrow initiated by a bone infarct, which is itself modulated by numerous causes, leading to myelofibrosis as a result of hypoxia and gradual loss of bone density characteristic of ischaemic osteoporosis. Further deterioration can be triggered by additional bone infarcts leading to anoxia and localized areas of osteonecrosis within the osteoporotic cancellous bone. Secondary events such as dental infection, injection of local anaesthetics with vasoconstrictors, such as epinephrine, and trauma can add further complications to the disease process and chronic non-pus forming bone infection osteomyelitis can also be associated with ONJ.
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The phenomenon of ischemic preconditioning (IPC) was discovered in 1986 by C. E. Murry and colleagues, who observed that repeated, temporary cross-clamping of the left anterior descending artery (LAD) in dogs protected the LAD territory of the heart against a subsequent prolonged ischemic event, reducing infarct size by 75%. This was thought to be a local effect and was termed local ischemic preconditioning. The phenomenon was confirmed by other researchers in dogs, pigs, mice, and rats. In 1993, Karin Przyklenk and colleagues began using the term "remote" when they observed that cross- clamping on the right side of the heart (right circumflex artery) protected the left side of the heart (LAD territory) from ischemia: that is, the protective trigger was remote from the observed effect.
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Both CIMT and modified CIMT may be applicable to up to 20–25 percent of stroke patients, and the amount of improvement produced by either regimen appears to diminish as the initial motor ability of the patient decreases. Both CIMT and modified CI therapy has been shown to be an effective means of stroke rehabilitation regardless of the level of initial motor ability, amount of chronicity, amount of prior therapy, side of hemiparesis, or infarct location. This suggests that plasticity may work irrespective of the pathways in the damaged motor network. Although, due to the duration of this treatment, patients who have suffered profound upper extremity paralysis from their condition are normally not eligible for constraint-induced upper extremity training.
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As indicated elsewhere on this page, EETs inhibit inflammation, inhibit blood clot formation, inhibit platelet activation, dilate blood vessels including the coronary arteries, reduce certain types of hypertension, stimulate the survival of vascular endothelial and cardiac muscle cells by inhibiting apoptosis, promote blood vessel growth (i.e. angiogenesis), and stimulate smooth muscle cell migration; these activities may protect the heart. Indeed, studies on in vivo animal and in vitro animal and human cell model systems indicate that the ETEs reduce infarct (i.e. injured tissue) size, reduce cardiac arrhythmias, and improve the strength of left ventricle contraction immediately after blockade of coronary artery blood flow in animal models of ischemia-reperfusion injury; EETs also reduce the size of heart enlargement that occurs long after these experiment-induced injuries.
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Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE. While PE may present with syncope, less than 1% of syncope cases are due to PE. On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct).
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Kumar et al. (1996) suggests that lesions to the subcortical regions of the cortex such as the thalamus, basal ganglia, internal capsule, and paraventricular white matter can also cause speech and language deficits. This is due to the fact that the subcortical regions are closely associated with the language centers in the brain. Kumar et al. state that while lesions to the subcortical regions could cause certain types of aphasia, a lesion to these regions would rarely cause global aphasia. In a study performed by Ferro (1992), it was found that five different brain lesion locations were linked to aphasia. These locations include: "fronto-temporo-parietal lesions", "anterior, suprasylvian, frontal lesions", "large subcortical infarcts", "posterior, suprasylvian, parietal infarcts", and "a double lesion composed of a frontal and a temporal infarct".
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The anterior spinal artery arises bilaterally as two small branches near the termination of the vertebral arteries which descend anterior to the medulla and unite at the level of the foramen magnum. The infarction (which arises in the paramedian branches of the anterior spinal artery and/or the vertebral arteries) leads to death of the ipsilateral medullary pyramid, the medial lemniscus, and the hypoglossal nerve fibers that pass through the medulla. The spinothalamic tract is spared because it is located more laterally in the brainstem and is not supplied by the anterior spinal artery, but rather by the vertebral and posterior inferior cerebellar arteries. The trigeminal nucleus is also spared, since most of it is higher up in the pons, and the spinal part of it found in the medulla is lateral to the infarct.
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The vertebral artery supplies the part of the brain that lies in the posterior fossa of the skull, and this type of stroke is therefore called a posterior circulation infarct. Problems may include difficulty speaking or swallowing (lateral medullary syndrome); this occurs in less than a fifth of cases and occurs due to dysfunction of the brainstem. Others may experience unsteadiness or lack of coordination due to involvement of the cerebellum, and still others may develop visual loss (on one side of the visual field) due to involvement of the visual cortex in the occipital lobe. In the event of involvement of the sympathetic tracts in the brainstem, a partial Horner's syndrome may develop; this is the combination of a drooping eyelid, constricted pupil, and an apparently sunken eye on one side of the face.
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A possible mechanism of ASIC1a channel-mediated cell death is due to the activation of other channels, leading to elevated Ca2+ which creates signaling pathways for apoptosis and necrosis in the cell. Gene knockout studies as well as ASIC blockades have shown to reduce brain infarct volume by as much as 60%, suggesting ASIC channels play a major role in the development of the pathological states resulting from acidosis and ischemia induced neuronal injury. The effects of both ASIC and NMDA blockades have been studied to determine the roles of both channels in Ca2+ toxicity and assess their respective contributions. The use of blockade for both channels provides greater neuroprotection than using a blockade for just one channel, and the ASIC blockade creates prolonged effectiveness of the NMDA blockade.
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The favored explanation for why the center visual field is preserved after large hemispheric lesions is that the macular regions of the cortex have a double vascular supply from the middle cerebral artery (MCA) and the posterior cerebral artery (PCA). If there is damage to one vascular pathway, like in the case of a MCA or PCA stroke, there is still another blood supply that the macular portions of the visual cortex can rely on. Vision in the center of the visual field is then preserved whereas vision in peripheral areas is lost due to the resulting infarct. Another possible reason is that the maculae project to both hemispheres, so in the event of a lesion in one hemisphere, the other intact hemisphere will still receive and process visual information from the maculae in both eyes.
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Deleting the GSNOR gene from both yeast and mice increased the cellular levels of GSNO and nitrosylated proteins, and the yeast cells showed increased susceptibility to nitrosative stress. Null mice show increased levels of S-nitrosated proteins, increased beta adrenergic receptor numbers in lung and heart, diminished tachyphylaxis to β2-adrenergic receptor agonists, hyporesponsiveness to methacholine and allergen challenge and reduced infarct size after occlusion of the coronary artery. In addition, null mice show increased tissue damage and mortality following challenge with bacteria or endotoxin and are hypotensive under anesthesia yet normotensive in the conscious state. More related to its alcohol dehydrogenase activity, GSNOR null mice show a 30% reduction in the LD50 for formaldehyde and a decreased capacity to metabolize retinol, although it is clear from these studies that other pathways exist for the metabolism of these compounds.
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In addition to its well-known immunosuppressive capabilities, the one-time administration of cyclosporin at the time of percutaneous coronary intervention (PCI) has been found to deliver a 40 percent reduction in infarct size in a small group proof of concept study of human patients with reperfusion injury published in The New England Journal of Medicine in 2008. Cyclosporin has been confirmed in studies to inhibit the actions of cyclophilin D, a protein which is induced by excessive intracellular calcium flow to interact with other pore components and help open the MPT pore. Inhibiting cyclophilin D has been shown to prevent the opening of the MPT pore and protect the mitochondria and cellular energy production from excessive calcium inflows. However, the studies CIRCUS and CYCLE (published in September 2015 and February 2016 respectively) looked at the use of cyclosporin as a one time IV dose given right before perfusion therapy (PCI).
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In later years, Global strain by speckle tracking has achieved popularity as the global functional measure. It has an advantage over Ejection fraction (EF), it shows reduced cardiac function also in hypertrophic hearts with small ventricles and normal ejection fraction (HFNEF), which is often seen in Hypertensive heart disease, Hypertrophic cardiomyopathy and Aortic stenosis. The EF is not a pure functional measure, as it is also dependent on wall thicknessMaciver DH. A new method for quantification of left ventricular systolic function using a corrected ejection fraction.Eur J Echocardiogr. 2011 Mar;12(3):228-34 It has also been shown to be more sensitive than EF.Gjesdal O, Hopp E, Vartdal T, Lunde K, Helle-Valle T, Aakhus S, Smith HJ, Ihlen H, Edvardsen T. Global longitudinal strain measured by two-dimensional speckle tracking echocardiography is closely related to myocardial infarct size in chronic ischaemic heart disease.
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Animal model studies indicate that TP receptor activation contracts vascular smooth muscle cells and acts on cardiac tissues to increase heart rate, trigger Cardiac arrhythmias, and produce myocardial ischemia. These effects may underlie, at least in part, the protective effects of TP gene knockout in mice. TP(-/-) mice are: a) resistant to the cardiogenic shock caused by infusion of the TP agonist, U46619, or the prostaglandin and thromboxane A2 precursor, arachidonic acid; b) partially protected from the cardiac damage caused by hypertension in IP-receptor deficient mice feed a high salt diet; c) prevented from developing angiotensin II-induced and N-Nitroarginine methyl ester-induced hypertension along with associated cardiac hypertrophy; d) resistant to the vascular damage caused by balloon catheter-induced injury of the external carotid artery; e) less likely to develop severe hepatic microcirculation dysfunction caused by TNFα as well as kidney damage caused by TNFα or bacteria-derived endotoxin; and f) slow in developing vascular atherosclerosis in ApoE gene knockout mice. In addition, TP receptor antagonists lessen myocardial infarct size in various animal models of this disease and block the cardiac dysfunction caused by extensive tissue ischemia in animal models of remote ischemic preconditioning.
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