Postpartum myocardial infarction treated by balloon coronary angioplasty.

Acute myocardial infarction in pregnancy is a rare event that carries substantial morbidity and mortality. New technologies have been developed in cardiology to open obstructed vessels during the acute evolution of coronary thrombosis. We present a case of acute postpartum myocardial infarction in a woman with class F/R diabetes. She underwent successful balloon angioplasty but developed chest pain suspicious of angina pectoris 6 weeks after the procedure. A thallium scan demonstrated fixed defects in the inferoposterior and posterolateral segments and minimal apical redistribution. This represents the second case of angioplasty performed in pregnancy and the first for an acute myocardial infarction.

Pharmacotherapy of unstable angina.

All patients with unstable angina should be admitted to a coronary or an intensive care unit. There should be an attempt to classify the patient according to the proposed Braunwald nomenclature. If the patient has a secondary cause for unstable angina (e.g., tachyarrhythmia, heart failure, fever, thyrotoxicosis, severe hypertension, hypoxia, unusual emotional stress, or anemia), this condition should be treated initially with therapy specific for that etiology. If the patient does not have a secondary etiology, therapy should be initiated with nitrates, preferably intravenous nitroglycerin. Heparin should be concomitantly administered. If the patient cannot receive heparin, aspirin should be initiated. All patients should receive beta-blockers. If the patient cannot take a beta-blocker, a calcium antagonist (probably diltiazem) should be initiated. However, if the patient is refractory to beta-blockers, the dihydropyridine nifedipine should be added. Failure to all pharmacologic interventions necessitates a progressive invasive approach dictated by the potential surgical risk of the patient. Long-term aspirin and beta-blockers should be strongly considered.

A negative thallium (+/- dipyridamole) stress test excludes significant obstructive epicardial coronary artery disease in hypertensive patients.

The operating characteristics of thallium stress testing for detection of significant epicardial coronary artery disease (CAD) in hypertensive subjects with chest pain or electrocardiographic (ECG) ischemia have not been previously defined. This becomes important because of the high prevalence of both hypertensive heart disease and CAD. Ninety-two hypertensives with a history of typical or atypical chest pain or ECG myocardial ischemia underwent coronary arteriography, 2D-guided echocardiography, and thallium-201 stress testing, combined with intravenous dipyridamole if the rate-pressure product was less than 20,000. Patients with myocardial infarction, prior revascularization procedure, valvular heart disease, and chronic ethanol abuse were excluded. The mean age was 54.8 +/- 9.9 years with 55% blacks and 46% women. Eighteen patients (19.6%) had significant (greater than or equal to 50% luminal diameter narrowing) epicardial CAD at catheterization, of whom 17 had positive thallium scans. Overall, there were 17 true positives, 47 true negatives, 27 false positives, and one false negative resulting in 94.4 +/- 5.4% sensitivity (95% confidence limits [95% CL] 71 to 100%), 63.5 +/- 5.6% specificity (95% CL 51 to 74%), 38.6 +/- 7.3% positive predictive value (95% CL 25 to 54%), 97.9 +/- 2.1% negative predictive value (95% CL 88 to 100%), and 69.6 +/- 4.8% overall accuracy (95% CL 59 to 79%). For hypertensive patients with chest pain or ECG myocardial ischemia, the high sensitivity and negative predictive value and low false negative rate support the role of thallium stress testing +/- dipyridamole as an exclusion test for significant CAD.

Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia.

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Management of coronary heart disease in the elderly.

The prevalence of coronary heart disease (CHD) increases rapidly with advancing age and remains the major cause of death among elderly Americans. The number of elderly has doubled in the last 30 years and is projected to continue growing at more than twice the rate of the general population. The resources required in managing CHD in this population will reach astronomical levels during the next few decades and will severely tax our ability to provide adequate medical care to all citizens, unless cost effective diagnostic and therapeutic strategies are developed which do not severely compromise health care. Risk factors for CHD should be identified and modified as early in life as possible. Modification of risk factors begun at advanced age appears to confer benefit, however. Anti-ischemic drug therapy is the treatment of choice for patients with mild or moderate stable angina. Select elderly may be willing to accept the increased risks of coronary revascularization to achieve relief from debilitating angina or prolongation of life. Physicians must use care in planning diagnostic and therapeutic strategies. Quality of life and independence are often more important considerations than longevity in this age group.

Relationship of left ventricular mass to impairment of coronary vasodilator reserve in hypertensive heart disease.

An impaired coronary vasodilator reserve has been demonstrated in all stages of hypertensive heart disease but is most likely in the setting of hypertrophy. The decrease in coronary flow reserve has, however, not been predictable previously. We postulated that flow reserve depression might be related to a left ventricular mass threshold. Seventy-two patients (82% with hypertension) with suspected ischemic heart disease who were found to be free of significant coronary artery disease at cardiac catheterization were evaluated utilizing the intracoronary Doppler catheter and two-dimensional directed M-mode echocardiography for determination of coronary flow reserve and left ventricular mass. For left ventricular mass indexed (LVMI) by body surface area (BSA) greater than or equal to 50% above normal using established gender-specific norms, American Society of Echocardiography (ASE) and PENN methods (correction of LV mass by regression equation agreeing with necropsy estimates of mass) predicted impairment of flow reserve (p = 0.005 and 0.009, respectively). Unindexed left ventricular mass and LVMI by height were not helpful in this regard. Using the ASE method for LV mass determination, coronary flow reserve was moderately depressed (2.4 +/- 1.0) for those with LVMI greater than or equal to 50% above normal; in comparison, flow reserve was normal (3.5 +/- 1.3) for those with LVMI less than 50% above normal. A rare patient was able to maintain a normal flow reserve when ASE- and Penn-indexed mass estimates were greater than or equal to 50% above normal, but only in the setting of a markedly elevated mean arterial pressure.

Current perspectives in hypertrophic cardiomyopathy: diagnosis, clinical management, and prevention of disability and sudden cardiac death.

Hypertrophic cardiomyopathy is a rare primary myocardial disease known for its dramatic morphologic and clinical manifestations. Sudden cardiac death and functional cardiac symptoms are common. However, differing pathologic mechanisms may be responsible for similar clinical symptoms and make a unified approach to therapy impossible. This review will discuss the genetics, criteria for diagnosis, relationship among pathophysiologic abnormalities and clinical symptoms, and management of hypertrophic cardiomyopathy.

Monoclonal antibody-based immunoassays for serum myoglobin quantification in acute myocardial infarction.

We have developed a monoclonal antibody-based enzyme immunoassay and a solid-phase radioimmunoassay for human myoglobin. Both assays are based on competition for the monoclonal antibody between the free myoglobin present in the standards or serum samples and the myoglobin coated to the wells of microtiter plates. Consequently, the absorbance at 630 nm and the radioactivity are inversely related to the concentrations of free myoglobin. The sensitivity of both assays was 10 micrograms/L with linearity up to 1,000 micrograms/L. There was no interference with other serum proteins, as judged from analysis of specimens with high concentrations of lactate dehydrogenase, creatine kinase, or hemoglobin. The average serum myoglobin concentration in 30 normal individuals was 67 micrograms/L. Five patients with cardiac arrhythmias had normal values (average, 63 micrograms/L) while four patients with myocardial infarction had abnormally high concentrations of myoglobin (300-1,000 + micrograms/L). In a typical case of myocardial infarction, serum myoglobin rose 21 hr earlier and peaked 12 hr earlier than creatine kinase and its cardiac isoenzyme. These rapid immunoassays appear to be useful for the early detection of increased serum myoglobin indicative of myocardial infarction.

Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease.

Invasive Doppler catheter-derived coronary flow reserve, echocardiographic measurements of left ventricular hypertrophy and intravenous dipyridamole-limited stress thallium-201 scintigraphy were compared in 48 patients (40 were hypertensive or diabetic) with clinical ischemic heart disease and no or minor coronary artery disease. Abnormal vasodilator reserve (ratio less than 3:1) occurred in 50% of the study group and markedly abnormal reserve (less than or equal to 2:1) occurred in 27%. Coronary vasodilator reserve was significantly lower (2.2 +/- 0.8 versus 3.5 +/- 1.3, p = 0.003) and indexed left ventricular mass significantly higher (152.6 +/- 42.2 versus 113.6 +/- 24.0 g, p = 0.0007) in patients with a positive (n = 11) versus a negative (n = 32) thallium perfusion scan. Coronary flow reserve was linearly related in coronary basal flow velocity as follows: y = -0.17x + 4.59; r = -0.57; p = 0.00002. The decrement in flow reserve was not linearly related to the degree of left ventricular hypertrophy. Abnormal vasodilator reserve subsets found in hypertensive patients were defined on the basis of basal flow velocity, indexed left ventricular mass and clinical factors. In this series, diabetes did not cause a detectable additional decrement in flow reserve above that found with hypertension alone. These findings demonstrate that thallium perfusion defects are associated with depressed coronary vasodilator reserve in hypertensive patients without obstructive coronary artery disease. Left ventricular hypertrophy by indexed mass criteria is predictive of which hypertensive patients are likely to have thallium defects.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial ischemia without atherosclerosis.

Myocardial ischemia in the presence of normal epicardial coronary arteries can be caused by an abnormality in the microcirculation or myocardial cell or by hypertrophy resulting in depressed coronary vasodilator reserve. Newly developed methods of assessing coronary blood flow and velocity make definitive diagnosis possible. Treatment, which may be difficult, includes therapy for the underlying cause, a calcium blocker, and nitrates.

Significance of positive or negative thallium-201 scintigraphy in hypertrophic cardiomyopathy.

Myocardial ischemia, fibrosis and infarction may occur in patients with hypertrophic cardiomyopathy (HC) in the absence of epicardial coronary artery disease. To determine their prevalence and relation with common characteristics, stress thallium-201 scintigraphy was performed in 28 patients. Eleven (39%) had positive scans despite normal epicardial coronary arteries (7 patients) or a pretest risk of coronary disease less than or equal to 5% (4 patients). There was no relation between thallium defects and age, sex, chest pain or outflow tract gradients at rest. However, the mean left ventricular ejection fraction was significantly lower in those with perfusion abnormalities compared with those without (64 +/- 15 vs 75 +/- 11%, respectively, p less than 0.05). Also, the mean ventricular septal thickness was greater in patients with positive scans (27 +/- 7 vs 21 +/- 6 mm, p less than 0.05), and there was a nonparametric relation between increasing septal thickness and the frequency of positive scans (p less than 0.025). Seven of 11 patients with positive scans had ventricular tachycardia compared with none among those who had negative scans (p less than 0.001), and 5 of these 11 patients had conduction system disease requiring permanent pacemaker insertion compared with 1 of 17 with negative scans (p less than 0.025). It is concluded that thallium perfusion abnormalities are common in patients with HC in the absence of epicardial coronary disease, and are strongly associated with potentially lethal arrhythmias. Thallium scintigraphy appears to identify a subset of patients with HC at increased risk for sudden death, who therefore require closer follow-up.

Presyncope and syncope. How to find the cause and avoid staggering costs.

Presyncope and syncope are relatively common in the primary care population, but episodes may signal serious metabolic, neurologic, or cardiovascular disease. Accurate diagnosis is important, because treatment must be directed to the underlying cause. The cost of a full evaluation can be staggering; therefore, a goal-oriented approach to diagnosis is most productive and cost-effective.

Pathophysiology and management of unstable angina.

Significant progress has been made in recent years in unraveling the dynamic mechanisms involved in the production of unstable angina. This knowledge, and advances in medical and interventional therapy allow the formulation of treatment strategies aimed at specific pathogenic mechanisms and promise to reduce mortality and morbidity. This review covers the diagnosis, pathogenesis, risk stratification, and therapy of unstable angina.

Mitral valve prolapse and stroke: echocardiographic evidence for a missing causative link.

There is general acceptance of a causal connection between mitral valve prolapse and systemic embolic events. The precise mechanism, however, remains controversial, with current hypotheses favoring the embolization of thrombotic deposits from the abnormal mitral valve. It might be surmised that echocardiography could easily document the presence of such thrombi, but actually, this has never been reported previously. Described herein is a patient with a severe cerebrovascular accident in whom echocardiography clearly demonstrated a mass of high embolic potential attached directly to the prolapsing mitral valve leaflet.

How can we diagnose coronary heart disease in hypertensive patients?

Chest pain is a common complaint among hypertensive patients. Hypertension and coronary heart disease each may present with symptoms and signs that are clinically indistinguishable. Noninvasive testing by routine exercise stress testing and stress radionuclide angiography are not reliably predictive of ischemia resulting from obstructive epicardial coronary artery disease and should be abandoned for that diagnostic purpose. Noninvasive thallium-201 myocardial perfusion imaging for this purpose may prove to be a valuable tool, avoiding the risk and expense of coronary arteriography. However, carefully performed prospective studies are not available. Because of the high prevalence of both diseases, a high priority must be given to obtaining these data and evaluating other noninvasive methods (especially positron emission tomography) if they appear promising.