Common adverse effects include ventricular arrhythmias (including ventricular ectopy and nonsustained ventricular tachycardia), supraventricular arrhythmias, hypotension, and headache.
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Ventricular ectopy is when the heartbeat is an abnormal heartbeat where the QRS complex is significantly wider. When the origin of the ectopic heartbeat is in the anterior fascicule then there is right axis deviation.
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In people without underlying heart disease and who do not have any symptoms, bigeminy in itself does not require any treatment. If it does become symptomatic, beta- blockers can be used to try and suppress ventricular ectopy. Class I and III agents are generally avoided as they can provoke more serious arrhythmias.
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Current treatment options for Boxer cardiomyopathy are largely restricted to the use of oral anti- arrhythmic medications. The aim of therapy is to minimize ventricular ectopy, eliminate syncopal episodes, and prevent sudden cardiac death.Meurs KM, Spier AW, Wright NA, Atkins CE, DeFrancesco T, Gordon S, et al. Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J Am Vet Med Assoc 2002;221:522–7.
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The dose is 5–10 mg/kg and side effects are high blood pressure followed by low blood pressure and ventricular ectopy. Originally introduced in 1959 for the treatment of hypertension. Its use as an antiarrhythmic for ventricular fibrillation was discovered and patented by Marvin Bacaner in 1969 at the University of Minnesota. The American Heart Association removed bretylium from their 2000 ECC/ACC guidelines due to its unproven efficacy and ongoing supply problems.
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Congenital hypothyroidism (CH) occurs in 1:1300 to 1:4000 births worldwide. The differences in CH-incidence are more likely due to iodine deficiency thyroid disorders or to the type of screening method than to ethnic affiliation. CH is caused by an absent or defective thyroid gland classified into agenesis (22-42%), ectopy (35-42%) and gland in place defects (24-36%). It is also found to be of increased association with female sex and gestational age >40 weeks.
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Sudden death from epilepsy is not very common, with a rate of approximately 2 in a thousand. The present understanding about how sudden cardiac death can result from epilepsy is that the brain is stimulating an arrhythmia. Recordings during seizures report that the onset of tachycardia just prior to the seizure is common, with both atrial and ventricular ectopy. The sudden epileptic death may be a result of the sympathetic activation or autonomic imbalance of the nervous system as described earlier.
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In general, subjects in bed rest studies do not exhibit increases in ventricular ectopy, although numerous studies have shown decreases in left ventricular mass and/or volume. During bed rest, left ventricular mass has been shown to decrease by eight percent after 6 weeks, which was thought to be related to decreased physiological loading. Ground- based animal studies also have been used to determine the effects of microgravity on the cardiovascular system. Tachycardia has been observed in standing rats, after hindlimb-unloading for 28 days.
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It has been demonstrated that sotalol alone, or a combination of mexiletine and atenolol, results in a reduction in the frequency and complexity of ventricular ectopy. It is likely that these medications also reduce syncopal episodes, and it is hoped this extends to a reduced risk of sudden death.Meurs, K.M. Arrhythmogenic Right Ventricular Cardiomyopathy; Kirk's Current Veterinary Therapy XV 2014 Consequently, antiarrhythmic therapy is typically recommended by veterinary cardiologists for Boxer dogs with ARVC. Although relatively rare, oral antiarrhythmic medications may be proarrhythmic in some dogs; consequently, appropriate monitoring and follow-up is recommended.
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It is due to slowed intraventricular conduction. The epsilon wave may be seen on a surface EKG; however, it is more commonly seen on signal averaged EKGs. Ventricular ectopy seen on a surface EKG in the setting of ACM is typically of left bundle branch block (LBBB) morphology, with a QRS axis of −90 to +110 degrees. The origin of the ectopic beats is usually from one of the three regions of fatty degeneration (the "triangle of dysplasia"): the RV outflow tract, the RV inflow tract, and the RV apex.
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Mechanisms underlying early afterdepolarisations (EADs) and delayed afterdepolarisations (DADs) responsible for the arrhythmias seen in Andersen–Tawil syndrome The prolonged action potentials can lead to arrhythmias through several potential mechanisms. The frequent ventricular ectopy and bidirectional VT typical of Andersen–Tawil syndrome are initiated by a triggering beat in the form of an afterdepolarisation. Early afterdepolarisations, occurring before the cell has fully repolarised, arise due to reactivation of calcium and sodium channels that would normally be inactivated until the next heartbeat is due. Under the right conditions, reactivation of these currents can cause further depolarisation of the cell, facilitated by the sodium-calcium exchanger.
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The most challenging cases involve palpitations that are secondary to supraventricular or ventricular ectopy or associated with normal sinus rhythm. These conditions are thought to be benign, and the management involves reassurance of the patient that these arrhythmias are not life- threatening. In these situations when the symptoms are unbearable or incapacitating, treatment with beta-blocking medications could be considered, and may provide a protective effect for otherwise healthy individuals. People who present to the emergency department who are asymptomatic, with unremarkable physical exams, have non-diagnostic EKGs and normal laboratory studies, can safely be sent home and instructed to follow up with their primary care provider or cardiologist.
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Andersen–Tawil Syndrome classically comprises three groups of features: abnormal electrical function of the heart, hypokalemic periodic paralysis, and characteristic physical features, although some of those affected will not exhibit all aspects of the condition. Electrocardiogram showing bidirectional Ventricular Tachycardia in a 9-year-old female with Andersen–Tawil syndrome Andersen–Tawil syndrome affects the heart by prolonging the QT interval, a measure of how long it takes the heart to relax after each heart beat. This, as in other forms of long QT syndrome, can lead to abnormal heart rhythms such as ventricular ectopy or ventricular tachycardia causing palpitations. The ventricular tachycardia seen in Andersen–Tawil syndrome often takes a form known as bidirectional ventricular tachycardia.
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The differential diagnosis for a prolonged QT interval includes other forms of long QT syndrome such as Romano–Ward syndrome in which only the electrical activity of the heart is affected without involving any other organs; Jervell and Lange-Nielsen syndrome in which a prolonged QT interval is combined with congenital deafness; and Timothy syndrome in which a prolonged QT interval is combined with abnormalities in the structure of the heart, in addition to autism- spectrum disorder. The frequent ventricular ectopy and bidirectional ventricular tachycardia seen in Andersen–Tawil syndrome can also occur in catecholaminergic polymorphic ventricular tachycardia. The intermittent weakness seen in Andersen–Tawil syndrome also occurs in other forms of periodic paralysis – hypokalaemic periodic paralysis, hyperkalaemic periodic paralysis, and paramyotonia congenita.
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