Viral myocarditis mimicking acute myocardial infarction.

Anecdotal reports have shown that myocarditis can mimic acute myocardial infarction with chest pain, electrocardiographic (ECG) abnormalities, serum creatine kinase elevation and hemodynamic instability. Thirty-four patients with clinical signs and symptoms consistent with acute myocardial infarction underwent right ventricular endomyocardial biopsy during a 6.5-year period after angiographic identification of normal coronary anatomy. Myocarditis was found on histologic study in 11 of these 34 patients. Cardiogenic shock requiring intraaortic balloon support developed within 6 h of admission in three (27%) of the patients with myocarditis. The mean age of the group with myocarditis was 42 +/- 5 years. A preceding viral illness had been present in six patients (54%). The ECG abnormalities were varied and included ST segment elevation (n = 6), T wave inversions (n = 3), ST segment depression (n = 2) and pathologic Q waves (n = 2). The ECG abnormalities were typically seen in the anterior precordial leads but were diffusely evident in three patients. Left ventricular function was normal in six patients and globally decreased in the remaining five patients, whose ejection fraction ranged from 14% to 45%. Lymphocytic myocarditis was diagnosed in 10 patients, and giant cell myocarditis was detected in the remaining patient. Four patients with impaired left ventricular function received immunosuppressive therapy with prednisone and either azathioprine (n = 2) or cyclosporine (n = 2). All six patients whose left ventricular function was normal on admission remain alive in functional class I. Of the five patients with impaired systolic function, ejection fraction normalized in three of the four patients who received immunosuppressive therapy within 3 months of treatment and in the one patient who received only supportive therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Underestimation of prosthetic mitral valve areas: role of transseptal catheterization in avoiding unnecessary repeat mitral valve surgery.

In patients with symptoms of heart failure after mitral valve replacement, identification of a stenosed prosthesis may be difficult. Twelve such patients were evaluated, presenting at a mean of 8.4 years after mitral valve replacement (four mechanical, eight porcine). Transvalvular pressure gradients were obtained using both indirect (pulmonary capillary wedge) and direct (transseptal catheterization) measurements of left atrial pressure. In all 12 patients, the diastolic gradient across the prosthetic valve was overestimated when pulmonary wedge rather than transseptal measurements were used. Calculated mitral valve prosthetic area was underestimated by the pulmonary wedge determinations. These findings may be caused by either the phase delay of the pulmonary wedge V wave relative to the transseptal V wave, resulting in a higher diastolic mean left atrial pressure, or the faulty wedge determinations in the setting of pulmonary hypertension, or both. In patients being considered for repeat mitral valve replacement because of prosthetic valve stenosis, transseptal catheterization allows for more accurate determination of prosthetic valve area and more accurately defines the need for repeat mitral valve surgery.

Continuous monitoring of left ventricular function by an ambulatory radionuclide detector in patients with coronary artery disease.

Global left ventricular function and a modified V5 electrocardiographic (ECG) lead were continuously monitored by a radionuclide recorder in 12 normal subjects and 39 patients with coronary artery disease while the subjects were performing various daily activities. The ambulatory studies revealed that walking on a level surface caused 11 of 12 normal subjects and 18 of 32 patients to increase their left ventricular ejection fraction by greater than 6% units. A transient decrease in left ventricular ejection fraction (6 to 18%) lasting greater than or equal to 1 min was observed on 36 occasions in 16 patients with coronary artery disease; 12 episodes were accompanied by chest pain or shortness of breath and 24 were asymptomatic. Electrocardiographic ST segment depression suggestive of ischemia was recorded in 6 of the 12 symptomatic and 5 of the 24 asymptomatic episodes. In 10 of the 12 symptomatic episodes, left ventricular ejection fraction began to decrease 30 to 90 s before the onset of symptoms. These studies suggest that continuous monitoring of both left ventricular function and the ECG may permit stratification of episodes of ST depression suggesting ischemia by the degree of left ventricular dysfunction they produce.

Early discharge following acute myocardial infarction. Long-term follow-up of randomized patients.

Long-term follow-up was obtained on 138 patients who participated in a prospective, randomized study comparing two weeks with three weeks of hospitalization following uncomplicated acute myocardial infarction. Follow-up information was available on 123 (89%) of all randomized patients. The mean follow-up period was 35 months for those patients who died and 99 months for those who survived. No differences were found between the two groups with respect to survival, cardiac-related deaths, frequency or severity of angina pectoris, subsequent myocardial infarction, incidence of congestive heart failure, number of ventricular aneurysms, or subsequent medical therapy. A significantly greater number of survivors in both groups stopped smoking and had a normal initial heart size than those who died. This long-term follow-up study further supports the conclusions of earlier short-term studies that two weeks of hospitalization is safe in patients with uncomplicated acute myocardial infarction.

Chest pain with angiographically insignificant coronary arterial obstruction. Clinical presentation and long-term follow-up.

Among 3,242 coronary angiograms performed from November 1972 through October 1975 at the Massachusetts General Hospital, 175 patients had normal coronary arteries or luminal narrowings of less than 30 per cent. All patients were studied for chest pain, and none had experienced prior myocardial infarction. Subsequent information was available in 159 patients over a mean follow-up period of 42.7 months. There were no deaths, and only one myocardial infarction occurred during this period. However, among the patients followed, continued chest pain with episodes occurring at least once monthly was present in 54 per cent. In addition, 17 per cent of all patients required subsequent hospitalization and 44 per cent continued to receive antianginal medication. Nearly half of the group (46 per cent) suffered some limitation of activity, and 22 per cent stated that they had either changed jobs or stopped work because of chest pain. Continuing chest pain was significantly more common in women and in patients who had experienced chest pain for more than one year before angiography. However, typicality of chest pain for angina or the occurrence of electrocardiographic changes of ischemia prior to angiography did not predict continued chest pain during the follow-up period. Thus, although mortality and morbidity are low in this group of patients, the syndrome of chest pain with angiographically insignificant coronary artery obstruction has an important impact on the lives of a majority of those affected.

Atrial tachyarrhythmias in acute myocardial infarction.

Causative factors, clinical consequences and treatment of atrial tachyarrhythmias were reviewed in 917 monitored patients with definite acute myocardial infarction. Significant atrial tachyarrhythmias were found in 104 (11 per cent) of them and included atrial fibrillation in 67, atrial flutter in 29 and paroxysmal atrial tachycardia in 33. These episodes were single in 79 patients and multiple in 25, and began within the first four days of acute myocardial infarction in 90 per cent of the patients. Fifty per cent of these atrial tachyarrhythmias were heralded by premature atrial contractions. The incidence of atrial tachyarrhythmia was not related to the location of the acute myocardial infarction or to the presence or degree of power failure; however, atrial tachyarrhythmias were significantly more frequent in patients with pericarditis. Atrial tachyarrhythmias were well tolerated in almost one fifth of the patients, caused marginal compromise in almost two thirds and led to severe clinical deterioration in one fifth. Paroxysmal atrial tachycardia rarely required specific treatment, atrial fibrillation was best managed with intravenous administration of digoxin except when associated with severe clinical compromise, and atrial flutter generally required cardioversion or rapid intravenous therapy and usually caused severe clinical deterioration. Over-all, atrial tachyarrhythmia was not associated with a significantly increased mortality, and in those who died, death was not related specifically to the atrial tachyarrhythmia but rather to the severity of the underlying acute myocardial infarction. However, persisting atrial tachyarrhythmias, particularly atrial flutter which tends to be refractory to both heart rate control and cardioversion, may contribute indirectly to morbidity and mortality.

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.

Prognostic utility of predischarge dipyridamole-thallium imaging compared to predischarge submaximal exercise electrocardiography and maximal exercise thallium imaging after uncomplicated acute myocardial infarction.

The prognostic value of predischarge dipyridamole-thallium scanning after uncomplicated myocardial infarction was determined by comparison with submaximal exercise electrocardiography and 6-week maximal exercise thallium imaging and by correlation with clinical events. Two endpoints were defined: cardiac events and severe ischemic potential. Of the 40 patients studied, 8 had cardiac events within 6 months (1 died, 3 had myocardial infarction and 4 had unstable angina requiring hospitalization). The finding of any redistribution on dipyridamole-thallium scanning was common (77%) in these patients and had poor specificity (29%). Redistribution outside of the infarct zone, however, had equivalent sensitivity (63%) and better specificity (75%) for events (p less than 0.05). Both predischarge dipyridamole-thallium and submaximal exercise electrocardiography identified 5 of the 8 events (p = 0.04 and 0.07, respectively). The negative predictive accuracy for events for both dipyridamole-thallium and submaximal exercise electrocardiography was 88%. In addition to the 8 patients with events, 16 other patients had severe ischemic potential (6 had coronary bypass surgery, 1 had inoperable 3-vessel disease and 9 had markedly abnormal 6-week maximal exercise tests). Predischarge dipyridamole-thallium and submaximal exercise testing also identified 8 and 7 of these 16 patients with severe ischemic potential, respectively. Six of the 8 cardiac events occurred before 6-week follow-up. A maximal exercise thallium test at 6 weeks identified 1 of the 2 additional events within 6 months correctly. Thallium redistribution after dipyridamole in coronary territories outside the infarct zone is a sensitive and specific predictor of subsequent cardiac events and identifies patients with severe ischemic potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Predicting cardiac morbidity based on risk factors and coronary angiographic findings.

A cohort of 189 men was followed up for 1 year after performance of coronary angiography and determination of risk factors to ascertain which risk factors or clinical and laboratory findings could aid in predicting the patients who would have a substantial cardiac morbid event. Data on clinical signs and symptoms, psychosocial assessments, angiographic findings and presence of standard risk factors for coronary artery disease were collected in each case. Twenty-five percent of the men experienced a substantial cardiac morbid event (hospitalization, myocardial infarction, resuscitation or death). With or without inclusion of the patients who underwent surgery, discriminant analysis equations were successful in predicting morbidity on the basis of risk factor data. For the whole sample such analysis was significant at p < 0.00005 and accurately predicting the fate of 78 percent of the subjects. With exclusion of the surgically treated patients, the discriminant analysis accurately predicted future morbidity 83 percent of the time (p < 0.0001). The following risk factors for increased morbidity were common to both analyses: severity of angina, history of myocardial infarction, family history of heart disease, fatigue and absence of type A behavior.

Plasma heparin neutralizing activity in coronary artery disease.

Platelets contain heparin neutralizing activity that is released into plasma after platelet aggregation. Increased amounts of plasma heparin neutralizing activity were found in patients with acute myocardial infarction, unstable angina pectoris and stable arteriographically confirmed coronary artery disease. Plasma heparin neutralizing activity levels provide additional evidence for a role of platelet aggregation in coronary artery disease.

Type A personality and extent of coronary atherosclerosis.

The relation between type A personality and the extent of coronary artery disease was studied in 109 patients who underwent selective coronary angiography. Type A personality as measured with the Jenkins Activity Survey was not correlated with the extent of coronary artery disease as assessed from the number of vessels with 50 percent or greater narrowing of diameter.

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.

Variant angina pectoris: Clinical and anatomic spectrum and results of coronary bypass surgery.

Twenty patients are described with the variant angina syndrome (recurrent angina at rest with S-T segment elevations occurring only during pain and no evolution of infarction). In contrast to patients previously reported on, all but one had progressive unstable angina before hospitalization. Angina was frequently associated with arrhythmias, including ventricular fibrillation (2 instances), ventricular tachycardia (4), frequent ventricular premature beats (5), atrioventricular block (4), sinus bradycardia (2), sinoatrial exit block (1) and supraventricular tachycardia (1). Seventeen patients had significant proximal stenosis of one or more coronary arteries with good distal vessels. Bypass surgery in 15 of these patients resulted in one noncardiac postoperative death, one perioperative infarction and relief of pain in all 14 survivors. After a 17 month mean follow-up period (range 4 to 38 months), all survivors are pain-free. Three patients had no significant coronary disease; one of these became asymptomatic with medical therapy, one continues to have angina and one died suddenly. Patients with normal coronary arteries could not be distinguished clinically or by electrocardiogram from those with severe obstructive lesions. This experience suggests that all patients with the variant angina syndrome should be studied by coronary angiography, and that most patients with significant fixed coronary lesions will do well after coronary bypass surgery.

Variant angina. Clinical spectrum and results of medical and surgical therapy.

Fifty-four patients with variant angina are described. They are divided into patients without hemodynamically (less than 50%) important coronary artery lesions (Group 1), patients with intermediate (greater than or equal to 50% and less than 90%) fixed obstruction (Group 2A), and patients with high grade (greater than or equal to 90%) fixed obstruction (Group 2B). Inferior ischemia occurred significantly more often in Group 1 (90% versus 33%. p less than 0.001), and exertional angina was more frequent in Group 2 (70% versus 36%, p less than 0.05). Maximum medical therapy with propranolol and nitrates failed to control angina in 55% of Group 1, 69% of Group 2A, and 63% of Group 2B. Twelve patients underwent intra-aortic balloon pumping (IABP), and in 10 there was complete control of variant angina. A total of 35 Group I patients underwent coronary artery bypass grafting (CABG), with a 2.9% mortality rate in patients without preoperative cardiogenic shock. Of these patients, 55% in Group 2A and 73% in Group 2B experienced marked improvement in their angina status. Therefore, we currently recommend bypass grafting for medically intractable variant angina in those patients with severely stenotic, fixed atherosclerotic lesions.

Cardiovascular radiology. Cardiac alterations during intravenous urography.

Electrocardiographic monitoring of 406 patients undergoing intravenous urography was performed before, during, and after the examination. Major cardiac arrhythmias and ischemia were encountered frequently (18%) in those with cardiac disease but also occurred (5%) in the healthy individual with no history of heart disease. Rapid higher dose (28-g iodine) bolus injections result in more cardiac alterations than the slower but larger (42-g iodine) infusion method, whereas the smaller (14-g iodine) bolus injections have the least cardiac effect. Ectopic ventricular beats, the most common abnormality, are usually transient but remain the most potentially lethal of the effects of intravenous contrast media on the heart.

Cardiac conduction abnormalities preceding transoesophageal echocardiographic evidence of perivalvar extension of infection in a case of Salmonella prosthetic valve endocarditis.

A 59 year old African-American man developed complete heart block in association with Salmonella enteritidis prosthetic valve endocarditis. Severe cardiac conduction abnormalities signalled the presence of perivalvar extension of infection before development of evidence of abscess by transoesophageal echocardiography. Cardiac conduction temporarily returned after debridement and aortic homograft placement. This case emphasises the value of electrocardiographic monitoring in the detection of perivalvar extension of infection complicating infective endocarditis, even in the era of sophisticated imaging modalities.

The association of clinical, psychosocial, and angiographic variables with work status in patients with coronary artery disease.

The bearing of clinical history, epidemiological risk factors, psychosocial factors, angiographic findings, and treatment characteristics was studied in relationship to the work status of 182 men who underwent coronary angiography because of presumptive coronary artery disease. Follow-up at one year found 42% of the cohort persistently unemployed or working at a lower level, 40% at the same job, and 19% at a more demanding job. Multiple regression analysis was used to derive the most important variables predictive of work status. Neither number of vessels diseased nor Coronary Artery Bypass Graft surgery entered the multiple regression analysis. Instead, the most important variables, listed in decreasing order of importance, are: age, subsequent cardiac morbid events, past myocardial infarction, and mood during the follow-up year. Together, they account for 24% of the variance in work status outcome (p less than 0.001).

Chest pain: how to distinguish between cardiac and noncardiac causes. Interview by Eric R. Leibovitch.

Classic coronary pain--or angina--involves a substernal pressure that commonly begins with exertion and is relieved by rest. However, some patients experience angina in the absence of physical exertion or emotional stress, and not all chest pain that begins after exertion is angina. Atypical chest pain must be differentiated from other types of chest pain, including chest wall pain, pleurisy, gallbladder pain, hiatal hernia, and chest pain associated with anxiety disorders. Careful examination of the chest wall is essential, and abnormal heart sounds can tell you a great deal. Further testing is individualized. An exercise ECG is important in identifying the presence of ischemic heart disease and the amount of myocardium at risk. If the ECG is abnormal at rest, the patient should undergo a thallium stress test or exercise echocardiography. A coronary angiogram is indicated if the exercise test or an ECG during pain show that a lot of live heart muscle is at risk.