Allen B. Weisse

Arrhythmias and the “Holiday Heart”: Alcoholassociated cardiac rhythm disorders

An association between excessive alcohol use and cardiac rhythm disorders is often difficult to establish in the absence of overt cardiomyopathy. We studied 32 separate hospital admissions for dysrhythmias in 24 patients (20 men, 4 women) with heavy recent alcohol ingestion and prolonged excessive alcohol use. None had evidence of overt heart disease after treatment of arrhythmia. Episodes usually followed heavy weekend or holiday sprees, resulting in hospitalization between Sunday and Tuesday or in proximity to the year-end holidays, a relationship not observed in other alcohol-associated illnesses. Atrial fibrillation was most common, but atrial flutter, atrial tachycardia, junctional tachycardia, multiple APCs, multiple PVCs and ventricular tachycardia were also observed. Transient hypokalemia was present in four of 30. The mean PEPLVET ratio after treatment was 0.412 ± 0.014 (normal 0.299 ± 0.008, P < 0.001). High-speed ECGs showed prolongation of PRc, QRS, and QTc. At cardiac catheterization, intracardiac pressures and volumes, coronary arteriograms and ventricular wall motion were normal at rest and mean cardiac index was slightly low, but the left ventricular response to angiotensin was abnormal. Cardiac arrhythmias presenting during weekend or holiday drinking episodes are associated with conduction delays and depressed cardiac performance indicative of early cardiomyopathy and suggest a “holiday heart” syndrome.

Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.

Relation of microcirculatory thrombosis to thrombus in the proximal coronary artery: effect of aspirin, dipyridamole, and thrombolysis.

Abstract A study was designed to determine the distribution of platelets in the microcirculation of the myocardium following experimental platelet thrombosis in a major coronary vessel. Determination was made by means of 51 Cr-labelled platelets and histologic examination. The results suggest that thrombosis in a major coronary artery is associated, at least in the first hours following its occurrence, with the presence of platelet thrombi in the microcirculation of the ischemic area. Pretreatment with aspirin or dipyridamole minimized significantly the extent of microcirculatory thrombosis without affecting the thrombus in the proximal coronary artery. A thrombolytic agent given after thrombus formation had a similar effect upon microcirculatory thrombosis remaining also independent of its effect upon proximal coronary artery thrombosis. There was a decrease in incidence of arrhythmias and mortality rate in the group of animals pretreated with aspirin and dipyridamole.

Hemodynamic effects of staged hematocrit reduction in patients with stable cor pulmonale and severely elevated hematocrit levels

Patients with cor pulmonale and high hematocrit levels are often subjected to phlebotomy in the belief that the adverse effects of high viscosity may outweigh the benefit of increased oxygen carrying capacity. To evaluate this, 12 patients with stable cor pulmonale and hematocrit values greater than 55 per cent were studied before and after a series of venesections. Right heart and aortic pressures, cardiac output and blood gases were measured at three mean hematocrit levels, 61 per cent (stage I), 50 per cent (stage II) and 44 per cent (stage III), with blood volume unchanged. From stages I to II, there were significant decreases in both man pulmonary artery pressure and total pulmonary resistance. Oxygen transport fell but not oxygen consumption. Right ventricular end-diastolic pressure and cardiac output did not change. Right ventricular work either fell or was maintained by increased output. Frank-Starling performance (supine exercise) improved. No significant changes occurred with further reduction in hematocrit to normal levels (stage III). The findings of this study support the concept of overcompensating erythrocytosis in cor pulmonale, and the effects of moderate hematocrit reduction should not be overlooked in these severely ill patients.

Left ventricular function during the early and late stages of scar formation following experimental myocardial infarction

Abstract To evaluate changes in left ventricular (LV) function after myocardial infarction (MI), anesthetized closed-chest dogs were studied following survival from acute nonmassive MI induced by thrombus formed on a catheter electrode in either branch of the left main coronary artery. Seven dogs were studied 3 to 4 weeks after MI (early scar formation) and 12 dogs 6 to 8 weeks after MI (late scar formation). Ten normal dogs with heart rates and aortic pressures similar to the MI groups served as controls. LV function was evaluated at rest and during afterloading with angiotensin. In both the early and late stages of scar formation, the infarcted ventricles had normal end-diastolic volumes and normal isovolumetric velocity-force length relationships but elevated resting end-diastolic pressures. LV ejection-rate functions (stroke power, mean rate of ejection, and mean rate of circumferential fiber shortening) were reduced after MI, the differences becoming statistically significant by 6 to 8 weeks. There were no significant differences found between the two infarct groups. With augmented afterloading, LV function after MI appeared depressed when stroke work was plotted against LV end-diastolic pressure but not when plotted against end-diastolic circumference. Thus, although its length-tension (Frank-Starling) characteristics and isovolumetric velocity-force-length (contractility) relationships were not altered, the healing infarcted ventricle exhibited reduced velocity of shortening during ejection and increased LV end-diastolic pressure which, in the absence of evidence of cardiac decompensation, probably reflects a reduced compliance.

Acute myocardial infarction in toxic cardiomyopathy without coronary obstruction.

Confluent left ventricular scar without significant coronary obstruction has been found in alcoholic subjects at autopsy. To evaluate the pathogenesis, 12 patients with chronic alcoholism and severe precordial pain persisting 4-24 hours were observed clinically. Cardiac isoenzymes of lactic dehydrogenase rose in serum. ST segment was elevated in anterior or posterior ECG leads, and abnormal Q waves appeared. Hypertnesion and hypercholesterolemia were present in two (group B) but not in the ten (group A). The latter exhibited no significant obstructive disease, based on coronary angiography in seven survivors and postmortem examination of the remaining three. Clinical evidence, as well as the quantitative assessment of platelets, made arterial thromboembolism an unlikely cause for the symptoms. Neither hemotologic or systemic disease affecting myocardium was present. The morphology of the left ventricle in three autopsies was compared with that of patients with alcoholism who had no cardiac disease, cardiomyopathy, or an asymptomatic scar. All had accumulation of Alcian positive glycoprotein in the interstitium. The patients with cardiac disease also had interstitial fibrosis which was characterized, particularly in the acute infarction group, by concentric periarterial fibrosis. Restriction of coronary vasodilation by this process during periods of high blood flow requirements was postulated as a basis for infarction.

The fate of experimentally induced coronary artery thrombosis

Abstract The evolution of a thrombus in a coronary artery is uncertain. To evaluate this process, coronary artery thrombosis was induced in intact anesthetized dogs by passage of current through an electrode catheter in the circumflex or anterior descending branch of the left coronary artery. Twenty-five animals survived the immediate period after arterial occlusion, which was established angiographically. Survivors were placed in one of two groups depending upon the interval between thrombosis and spontaneous death or sacrifice: group I (1 to 17 days; 15 dogs) and group II (30 to 70 days; 10 dogs). Gross examination of the coronary arteries was performed post mortem in all dogs, with additional premortem angiographic studies in group II. At the time of death all dogs but 1 in group I showed continued evidence of significant obstructive thrombosis. In group II angiography and postmortem examination of the involved arteries indicated that within the second month after clot production sufficient changes occur within the thrombus to re-establish varying degrees of blood flow.

Effect of nitrate infusions on the systemic and coronary circulations following acute experimental myocardial infarction in the intact dog.

Abstract To determine the systemic and the coronary effects of nitrates in acute myocardial infarction, 3 groups of anesthetized closed chest dogs were studied. In a group of normal dogs an hour-long intravenous infusion of isosorbide dinitrate was administered. In a second group a small infarct of the myocardium was produced by catheter wedging in a small coronary side branch. In the third group occlusion of a branch of the main left coronary artery was produced by a thrombus-forming catheter electrode. Isosorbide dinitrate infusion in normal dogs caused reductions in aortic pressure, left ventricular end-diastolic pressure and cardiac output and work. Coronary resistance was reduced only at 5 minutes of infusion. Systemic effects of isosorbide dinitrate were similar in the 2 groups with infarction. Mild hypotension (average 10 mm Hg) did not provoke ventricular arrhythmias. Unlike the cardiac output in normal dogs, this value tended to rise rather than fall and left ventricular work was unchanged. The dogs with catheter wedging showed a significant increase in coronary collateral flow and a decrease in resistance. Narrowing of the coronary arteriovenous oxygen difference occurred in the dogs with wedging and thrombus formation. In the absence of cardiogenic shock nitrates may be safely administered to dogs with acute experimental myocardial infarction and may result in enhanced collateral coronary flow and reduction in oxygen requirements of the heart.

Ethyl alcohol as a cardiac risk factor.

Abstract The widespread use of ethyl alcohol suggests its potential importance in clinical medicine. There is no proved therapeutic effect in cardiac patients, and its role as an etiologic factor in heart disease has been disputed over the years and attributed to coexistent malnutrition. The latter factor, however, has been dissociated from ethanol use in many patients with cardiomyopathic form of heart failure. Major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period has been obtained in various species of animals, including the subhuman primate. Abnormalities include depression of ventricular function and metabolic and morphologic changes that parallel the changes in humans with preclinical malfunction of the heart. Although the mechanism of progression to heart failure or arrhythmias is not known, several factors may be associated. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, simultaneous exposure to trace metals in excess and occasional specific nutritional deficiency or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the infrequency of heart disease in patients with cirrhosis or neuropathy support the view that the cardiac abnormality is not commonly dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenetic process may continue unabated in some patients who become abstinent.

The Question of Cardiomyopathy in Diabetes Mellitus

Excerpt Controversy during the past decade on the influence of hypoglycemic agents on mortality in diabetes mellitus has served to focus attention on the diabetic patients cardiovascular system. A...