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Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease of unknown cause that is characterized by a hypertrophied, nondilated, hypercontractile left ventricle. Its etiology and pathogenesis remain undefined but the three principal factors implicated are a genetic predisposition, a hypersensitivity to catecholamines, and an abnormal calcium metabolism. The hypertrophy typically involves the intraventricular septum to varying degrees, but may also involve the apex or free wall and even be concentric. The disease occurs in either an obstructive or a nonobstructive form depending on whether an intraventricular pressure gradient can be demonstrated at rest or on provocation. The gradient and obstruction to outflow is usually seen in patients with asymmetric septal hypertrophy (ASH) and anterior motion of the mitral valve during systole (SAM). Abnormal left ventricular diastolic function characterized by inadequate filling and impaired relaxation has been shown to be very important in both the obstructive and nonobstructive forms of the disease. In addition, inadequate coronary vasodilator reserve as a result of small vessel disease, microvascular spasm, and/or low capillary density per unit myocardial mass has been implicated as an important cause of ischemia in patients without coronary artery disease. HCM is a disease of young adulthood with relatively slow progression; young patients are often asymptomatic, whereas older patients are more limited by dyspnea, angina, dizziness, or syncope. Supraventricular tachyarrhythmias occur in 30% of patients, and high-grade ventricular arrhythmias occur in over 75%. The annual mortality is 3-5%. The common mode of demise is sudden cardiac death. Therefore, the primary objectives of treatment are the amelioration of symptoms, the control of arrhythmias, and the prevention of sudden death. Beta-adrenoreceptor blocking agents decrease myocardial contractility and oxygen demands and increase ventricular volume; therefore, they are most useful in patients with the obstructive form of HCM. Calcium channel antagonists enhance left ventricular relaxation, relieve microvascular spasm, and improve coronary filling and therefore are the agents of choice in patients with diastolic dysfunction. The ability of the calcium channel antagonists to decrease contractility makes them valuable in patients with obstructive HCM. Arterial vasodilators, diuretics, nitrates, and inotropic agents should be avoided because they can increase the intraventricular gradient. Myomyectomy is reserved for those patients with the obstructive form of HCM whose symptoms are refractory to medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37

34 patients have been controlled after beta-blocking therapy, for a mean period of 5 years. Symptoms and evolution: syncope disappeared, angoy passed from 47% to 23%, dyspnea from 65% to 47%, dizziness from 70% to 54%, weakness from 30% to 37%. A systolic murmur was present in 75% of the cases. Two patients died by heart failure. Phonocardiogram: the systolic murmur was unchanged, like the carotid pulse. Paradoxical splitting of the 2 degrees sound was more frequent, atrial sound unimodified, isometric contraction shortened (60%) and the Q-1 degree sound interval prolonged (90%). Electrocardiogram: 1 degree A/V block appeared in 24% of the cases, complete A/V block in 9%, atrial fibrillation in 3%. Left atrial enlargement was more frequent; left ventricular hypertrophy unchanged. Heart catheterization (10 cases, after a mean period of 5.5 years): left ventricular pressure gradient passed from 80% to 90%; a low cardiac index from 20% to 30%; telediastolic pressure of left ventricle was unmmodified in 10% of cases, more elevated in 50%, less elevated in 40%. Chest X ray: cardiac size was unchanged in 65% of cases, enlarged in 32%; smaller in 3%. In conclusion, symptoms improved in most of the patients; no case of sudden death was observed. Some data however show that the evolution of the myocardiopathy goes on to congestive heart failure and arise doubts on the real usefullness of beta-blocking drugs in the disease.
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PMID:[beta-Blocking therapy in obstructive hypertrophic cardiomyopathy. Long term results (author's transl)]. 610 83

The pharmacokinetics, clinical efficacy, and adverse effects of three calcium-channel blocking agents--verapamil, nifedipine, and diltiazem--are reviewed. Verapamil, nifedipine, and diltiazem are absorbed well after oral dosing, but absolute bioavailability of each is reduced substantially by a first-pass effect. Each drug is metabolized extensively (verapamil and diltiazem to moderately active metabolites) by the liver. A substantial percentage of each drug is bound to plasma proteins, but the binding is of clinical importance only for nifedipine (92--98% protein bound). Intravenous verapamil has become the agent of first choice for treatment of acute paroxysmal supraventricular tachycardia (PSVT); use of chronic oral verapamil therapy for prophylaxis remains controversial. Verapamil and diltiazem have been evaluated with mixed results for atrial flutter and fibrillation. For treatment of myocardial ischemia, calcium-channel blockers may be of some value (possibly in combination with nitrates of B blockers). All three agents have been studied in patients with exertional angina with good results. Calcium-channel blockers appear to be equal with nitrates for treatment of variant angina. Patients with hypertropic cardiomyopathy have been treated with verapamil and nifedipine with promising results. Nifedipine has been effective for treatment of essential hypertension. Adverse effects of calcium-channel blockers have been relatively minor or infrequent. Diltiazem overall has the best side-effect profile, with adverse effects causing discontinuation of therapy in about 2--10% of patients; verapamil in intermediate (8--10%) and nifedipine the worst (17%) in this respect. The most common side effects generally are fatigue, headache, dizziness, skin rash, and peripheral edema. While they generally should be reserved for patients in whom more conventional therapy has failed (except those with PSVT), calcium-channel blockers appear to have a valid role as reserve agents for exertional and variant angina, cardiomyopathy, and hypertension.
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PMID:Update on calcium-channel blocking agents. 635 66

A prospective study of arrhythmias was performed in 33 patients with hypertrophic cardiomyopathy with obstruction by Holter monitoring. The aim of the study was to assess the incidence of "occult" arrhythmias in this condition and to establish a "profile" of high risk patients from clinical, echocardiographic and haemodynamic data. The Holter monitoring demonstrated asymptomatic arrhythmias in 31 of the 33 patients (94%). A supraventricular arrhythmia was detected in 15 cases (45%), including 7 episodes of supraventricular tachycardia (21%). Ventricular arrhythmias were observed in 28 patients (85%), including 5 episodes of ventricular tachycardia (15%). Some patients presented several types of arrhythmia. A number of patients with arrhythmia including short bursts of ventricular tachycardia were asymptomatic during Holter monitoring; conversely, other patients complained of dizziness or syncope but had no arrhythmias. A retrospective study of clinical, echocardiographic and haemodynamic data showed no difference between patients with and patients without arrhythmias. Medium-dose betablocker therapy (propranolol, 110 mg/day) did not seem to protect patients with hypertrophic cardiomyopathy with obstruction from arrhythmias. We conclude that Holter monitoring should form part of the routine evaluation of patients with cardiomyopathy with obstruction, and that potentially dangerous arrhythmias should be treated by anti-arrhythmic agents other than betablockers. This attitude could reduce the incidence of syncope and eventually decrease the risk of sudden death in this condition.
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PMID:[Long-duration electrocardiographic recording in 33 patients with obstructive cardiomyopathy]. 643 35

There were 84 confirmed cases of congestive (or dilated) cardiomyopathy (CCM or DCM), 57 of hypertrophic nonobstructive cardiomyopathy (HNCM) and 52 of hypertrophic obstructive cardiomyopathy (HOCM) collected from 15 cardiology divisions of university or national hospitals in Japan. Out of the 193 patients with cardiomyopathy, 145 (75%) were male and 48 (25%) female (M/F ratio = 3:1). The mean age of the patients was 34.1 years. Patients with HNCM or HOCM were usually asymptomatic, but palpitation was the most common symptom, followed in frequency by chest oppression, dyspnoea, chest pain, arrhythmia and syncope in HNCM, and by dyspnoea, chest oppression, chest pain, dizziness and syncope in HOCM. ST-T abnormalities were most frequently observed, 90.3% in HNCM and 86.3% in HOCM. Left ventricular hypertrophy was observed in 76.4% of HNCM and in 79.1% of HOCM. Abnormal Q waves were observed equally in HNCM (32.4%) and in HOCM (35.3%). A fourth sound was more common (69.2% in HNCM; 75.8% in HOCM) than a third sound (39.7% in HNCM; 36.5 in HOCM). The heart size on conventional radiography was within normal limits or slightly enlarged; the mean cardiothoracic ratio was 0.52 in HNCM and 0.54 in HOCM. A cumulative survival rate in 149 patients with hypertrophic cardiomyopathy demonstrated that the 10-year survival rate after the time when the diagnosis was made was 34.2% for CCM, 81.7% for HNCM and 84.4% for HOCM. Autopsy studies in 11 patients with hypertrophic cardiomyopathy revealed that marked fibre disarray of the heart could be detected by the endomyocardial biopsy of the right ventricular septum in 40% at most of the patients with hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertrophic obstructive and non-obstructive cardiomyopathy in Japan. Diagnosis of the disease with special reference to endomyocardial catheter biopsy. 668 27

To elucidate electrophysiologic mechanism of exercise-induced ventricular tachycardia (VT), electrophysiologic studies were performed in 12 patients in whom sustained VT had developed during treadmill exercise testing. Six patients had arteriosclerotic coronary heart disease, 3 had cardiomyopathy, and 3 had no clinical evidence of organic heart disease. All patients had had documented episodes of sustained VT related to exertion and had experienced dizziness, syncope, or both. In addition, 3 patients had had nonfatal cardiac arrest. Electrophysiologic studies provoked paroxysms of sustained VT identical to those observed during treadmill exercise testing in 10 patients and provoked ventricular flutter/fibrillation in 1. Seven patients had VT suggestive of a reentrant mechanism, as the VT could be readily initiated with programmed ventricular extrastimulation or terminated by ventricular overdrive pacing, or both. Three patients had VT suggestive of catecholamine-sensitive automaticity. The VT could not be initiated with programmed electrical stimulation, but it could be provoked by intravenous isoproterenol infusion; furthermore, the VT could not be terminated with ventricular overdrive pacing, but it could be abolished by discontinuing isoproterenol infusion. Reproduction of VT in these 10 patients allowed serial pharmacologic testing in selecting an effective antiarrhythmic regimen. Thus (1) exercise-induced VT can be caused by either reentry or catecholamine-sensitive automaticity, and (2) electrophysiologic studies are of use in defining the underlying mechanism of exercise-induced sustained VT.
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PMID:Electrophysiologic mechanism of exercise-induced sustained ventricular tachycardia. 682 68

In a 52-year-old patient with beginning dilatative cardiomyopathy dizziness and syncopes could be observed due to a ventricular bigeminy at rest and under exercise conditions. The patient also showed a marked reduction of exercise capacity and was handicapped in his profession as electrician and unable to work for more than 10 months. Antiarrhythmic drug therapy including the subsequent use of all available antiarrhythmic agents failed in suppressing this arrhythmia. In an electrophysiological study the arrhythmogenic focus could be localized in the right ventricular outflow tract. Application of radiofrequency current resulted in instantaneous termination of the extrasystoly; this result could be documented in repeat Holter monitorings over 12 weeks to present. This case report shows that radiofrequency catheter ablation can in special cases be applied for therapy of extrasystolic phenomena when clinical symptoms necessitate treatment and antiarrhythmic drug therapy fails.
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PMID:[Ventricular bigeminy with fixed with fixed coupling at rest and during exercise as the cause of recurrent dizziness and syncope--successful anti-arrhythmic therapy by high frequency current catheter ablation of a right ventricular arrhythmogenic focus. A case report]. 757 78

Interferon alpha is a biologic agent with demonstrated anti-tumor activity in a variety of hematologic and solid malignancies. Many patients treated with interferon experience acute toxicity manifested as a flu-like syndrome of fever, chills, myalgias, and malaise. However, fatigue, anorexia, bone marrow suppression, nausea, vomiting, dizziness, and confusion may also occur. Cardiotoxicity is a rare complication of interferon therapy that most frequently presents as transient episodes of hypotension and tachycardia, with few significant life-threatening cardiovascular effects reported. A small number of cases of suspected interferon-induced cardiomyopathy, all of which improved after discontinuing interferon, have recently been documented. We report a patient with multiple myeloma who developed severe congestive cardiomyopathy while receiving interferon alpha that did not reverse subsequent to discontinuation of interferon therapy. Although the patient had previously received doxorubicin, the presence on endomyocardial biopsy of a prominent intracellular lipid accumulation within myocytes and only grade 2 anthracycline cardiotoxicity suggested that other or additional factor(s) contributed to the severity of this patient's cardiomyopathy. Etiologies of cardiac dysfunction other than interferon and doxorubicin were excluded. While a direct cause-effect relationship between interferon alpha and irreversible congestive cardiomyopathy cannot be firmly established in this case report, patients who either concurrently or sequentially receive interferon and anthracyclines should be carefully monitored for evidence of cardiac toxicity.
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PMID:Irreversible, severe congestive cardiomyopathy occurring in association with interferon alpha therapy. 771 76

The use of radiofrequency energy for the treatment of supraventricular tachycardia in pediatric patients has gained widespread acceptance, especially for tachyarrhythmias associated with palpitations, dizziness, presyncope or syncope, cardiomyopathy, and cardiac arrest. Ablation of the substrate supporting atrioventricular reentry, atrioventricular node reentry, and automatic atrial tachycardia yields a 90%-98% success rate with low incidence (< 1%) of complications and adverse side-effects. Ablation of intra-atrial reentry, including atrial flutter and fibrillation, appears to be promising and would be a significant advance in the management of patients following extensive atrial surgery for congenital heart disease. Radiofrequency energy is also used to treat various forms of idiopathic ventricular tachycardia. Finally, radiofrequency energy has been extended to control the ventricular rate associated with malignant atrial tachycardia by either modification or ablation of the atrioventricular node, and subsequent pacemaker implant. Long-term outcome of radiofrequency ablation is unknown, but the short-to-intermediate (1-5 yrs) outcome is excellent, with low recurrence rate of the tachycardia, no proarrhythmic effect, and excellent clinical state.
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PMID:The use of radiofrequency energy in pediatric cardiology. 1015 20

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.
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PMID:Atrial fibrillation. 1197 40


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