Roman W. DeSanctis

Myocardial Changes Associated with Cardiogenic Shock

Abstract The amount of left ventricular myocardium destroyed by recent and old infarcts in patients with acute myocardial infarction with and without cardiogenic shock was compared in hearts obtained at autopsy. All 20 patients with, and only one of 14 without, shock had lost 40 per cent or more of the left ventricle. The remainder lost 35 per cent or less. These results indicate that cardiogenic shock is associated with extensive loss of left ventricular myocardium due to new and frequently old infarcts as well. In five cases the new infarct was small as compared to the total amount of myocardial destruction. Patients with cardiogenic shock consistently showed marginal extension of the recent infarct (unlike those not in shock) and focal areas of necrosis throughout both left and right ventricles. Similar focal lesions were encountered in a third series of 20 patients with shock from other causes. A sharp reduction in coronary perfusion pressure could explain this combination of findings, which indicate ...

Cocaine-Related Aortic Dissection in Perspective

Cardiovascular complications of cocaine use have been ever more widely recognized and include the acceleration of atherosclerosis, coronary artery spasm, acute myocardial infarction, myocarditis, dilated cardiomyopathies, and cardiac arrhythmias. Less well known is the potentially lethal complication of aortic dissection. In the present issue of Circulation , Hsue and colleagues1 report on their 20-year experience with acute aortic dissection at an inner-city hospital. Remarkably, their findings indicate that 14 (37%) of 38 patients treated for acute dissection reported having used cocaine in the minutes or hours preceding their presentation. Cocaine, particularly crack cocaine, seemed to have played a significant role in precipitating aortic dissection among this cohort of young (age 41±8.8 years), predominantly black (11 of 14; 79%), and hypertensive (11 of 14; 79%) individuals. This study represents the largest cohort of cocaine-related dissection ever reported. Its findings provoke a number of questions for those of us who study or manage this rare but highly lethal condition. See p 1592 How common is cocaine-related aortic dissection? Previous reports predominantly have been descriptions of a single patient2 or a summary of individual case reports.3 The presumption has been that cocaine is a very rare cause of a very rare condition. The report by Hsue et al1 would seem to challenge that logic, but the authors freely admit that the inner-city population served by their hospital likely is responsible for this. In fact, because they accumulated only 14 patients over 20 years at their hospital, a cocaine-related dissection was encountered less than once per year. The International Registry for Aortic Dissection (IRAD) represents a unique effort by 17 aortic centers around the world to characterize the current status of acute aortic dissection, including its predisposing conditions.4,5⇓ We were able to work with IRAD’s coordinating center to …

Clinical Spectrum of the Sick Sinus Syndrome

The clinical spectrum of the sick sinus syndrome (SSS) is described in a series of 56 patients who demonstrated either persistent unexplained sinus bradycardia (group I: eight patients); sinus arrest (group II: 15 patients); or bradycardia with episodic supraventricular tachyarrhythmias (group III: 33 patients). Coronary disease was the most common form of heart disease where etiology could be determined, but in 25 patients no clear etiologic diagnoses could be established. Thirty-three patients showed associated electrocardiographic conduction disturbances. Symptoms were common and were produced by both bradycardia and tachycardia. Eight patients in the bradycardia-tachycardia group experienced cerebral embolization. Despite bother-some symptoms, only six of the 56 patients died over an average follow-up of 7 years, and only one of these deaths appeared related to an arrhythmia. Drug therapy of bradycardia was generally ineffective, but digitalis was frequently helpful in patients with tachycardia. Electrical pacing was uniformly successful in treating symptoms of bradycardia but was disappointing in preventing tachyarrhythmias.

Unstable angina pectoris: National cooperative study group to compare surgical and medical therapy: II. In-Hospital experience and initial follow-up results in patients with one, two and three vessel disease

Abstract A prospective randomized study comparing intensive medical therapy with urgent coronary bypass surgery for the acute management of patients with unstable angina pectoris was carried out by nine cooperating medical centers under the auspices of the National Heart, Lung, and Blood Institute. Between 1972 and 1976, a total of 288 patients were entered into the study. All patients had transient S-T or T wave changes, or both, in the electrocardiogram during pain; 90 percent had pain at rest in the hospital, and 76 percent had multivessel coronary disease. The medically and surgically treated patients were comparable with respect to clinical, electrocardiographic and angiographic characteristics and left ventricular function. During the total study period, the hospital mortality rate was 5 percent in the surgical group and 3 percent in the medical group (difference not significant). The rate of in-hospital myocardial infarction was 17 and 8 percent in the respective groups (P In the 1st year after hospital discharge class III or IV angina (New York Heart Association criteria) was more common in medically than in surgically treated patients with one vessel disease (22 percent versus 3 percent, P The results indicate that patients with unstable angina pectoris can be managed acutely with intensive medical therapy, including the administration of propranolol and long-acting nitrates in pharmacologic doses, with adequate control of pain in most patients and no increase in early mortality or myocardial infarction rates. Later, elective surgery can be performed with a low risk and good clinical results if the patients angina fails to respond to intensive medical therapy.

Stroke Following Coronary-Artery Bypass Surgery

Abstract The causes of stroke following coronary-artery bypass surgery are largely unknown. To determine whether carotid bruits increase the risk of these events, we compared 54 patients with postoperative stroke or transient ischemic attacks with 54 randomly selected control patients. Both groups were drawn from 5915 consecutive patients who had coronary bypass surgery at our hospital from 1970 to 1984. Carotid bruits were noted preoperatively in 13 patients with postoperative stroke and in 4 control patients. case-control analysis showed that the presence of carotid bruits increased the risk of stroke or transient ischemic attacks by 3.9-fold (95 percent confidence interval, 1.2 to 12.8; P<0.05). This increased risk remained essentially unchanged after adjustment for potentially confounding variables in a multiple logistic regression analysis. Other factors associated with a significantly increased risk (P<0.05) of these neurologic deficits were a history of stroke or transient ischemic attack (odds rat...

Aspirin prophylaxis of venous thromboembolism after total hip replacement.

Abstract We assessed aspirin prophylaxis against venous thromboembolism in a prospective, controlled, double-blind study of patients over 40 years of age, who had undergone total hip replacement. Radiographic phlebography was the diagnostic end point. Thromboembolism developed in 11 of 44 patients receiving aspirin, as compared to 23 of 51 receiving the placebo (P<0.03). Unexpectedly, this protection was limited to men. In four of 23 men on aspirin thrombi developed, as compared to 14 of 25 receiving placebo (P<0.01). Corresponding figures for women were seven of 21 versus nine of 26. Review of a similar group of patients receiving aspirin revealed significantly greater protection (P<0.03) in men (three of 15) than in women (15 of 27). These data establish statistically significant prophylaxis in men over the age of 40 by 600 mg of aspirin given twice daily. The absence of a protective effect in women remains unexplained. (N Engl J Med 297:1246–1249, 1977)

Right ventricular infarction: Clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction

Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside findings of jugular venous distension, clear lungs on auscultation, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.

The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up.

SUMMARY To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients.Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P < 0.001). In the absence of pulmonary edema or shock, patients with Type lI second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P < 0.005), with nearly all the deaths due to abrupt development of AV block.Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.

Nontransmural myocardial infarction: A comparison of hospital and late clinical course of patients with that of matched patients with transmural anterior and transmural inferior myocardial infarction

The hospital and long-term course of 67 patients with nontransmural myocardial infarction was compared with that of 66 patients with transmural anterior and 63 patients with transmural inferior infarction matched for age, sex, previous infarction and prior congestive heart failure. During their hospital stay, patients with nontransmural infarction had significantly less congestive heart failure and fewer intraventricular conduction defects than did patients with transmural anterior infarction; fewer atrial tachyarrhythmias and less sinus bradycardia and atrioventricular block than did patients with transmural inferior infarction; and an incidence of hypotension, pericarditis and ventricular irritability similar to that of patients in the other two groups. Patients with nontransmural infarction had a significantly lower coronary care unit mortality rate (9 percent) than that of patients with transmural anterior or transmural inferior infarction (20 and 19 percent, respectively). By 3 months, the mortality rate had risen to 14 percent in patients with nontransmural infarction, but was significantly higher (29 and 27 percent, respectively) in patients with transmural anterior or transmural inferior infarction. Angina was common in all three groups, occurring in more than 50 percent of patients during a mean follow-up period of 28.6 months after hospital discharge. In contrast, the incidence of subsequent myocardial infarction was significantly greater in patients with nontransmural myocardial infarction, occurring in 21 percent at 9 months compared with only 3 percent of patients with transmural anterior (p less than 0.01) and 2 percent of patients with transmural inferior (p less than 0.05) infarction. By 54 months, 57 percent of patients with nontransmural infarction had sustained a new infarction contrasted with only 12 percent of patients with transmural anterior (p less than 0.001) and 22 percent of patients with transmural inferior (p less than 0.01) infarction. Late mortality increased in patients with nontransmural myocardial infarction and, although this group had a significantly better survival rate at 3 months, the overall late mortality of the three groups was comparable. The study suggests that nontransmural myocardial infarction is an unstable ischemic event associated with a great risk of later myocardial infarction and high late mortality rate. A more aggressive diagnostic and therapeutic approach may be warranted in patients with nontransmural myocardial infarction.

Antiarrhythmic Prophylaxis with Procainamide in Acute Myocardial Infarction

Abstract The effectiveness of prophylactic therapy with procainamide in preventing active ventricular arrhythmias after acute myocardial infarction was determined in a double-blind study using electrocardiographic monitoring of 70 patients with acute infarctions uncomplicated by shock, heart block or severe heart failure. After a loading dose, 250, 375 or 500 mg of procainamide or placebo were administered every three hours according to patient weight. Procainamide afforded highly significant protection against all types of active ventricular arrhythmias, markedly reduced the need for acute therapy of arrhythmias, and prevented death from active arrhythmias. Adverse effects of procainamide therapy occurred only in patients with excessive plasma concentrations. The effective plasma procainamide concentration for suppressing active ventricular arrhythmias after acute myocardial infarction is 4 to 6 mg per liter. Lower plasma levels protect incompletely whereas concentrations above 7 mg per liter can produce...