Biomedical subjects
Publications and source records attributed to R O Bonow.
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We demonstrate that patients with left ventricular mural apical thrombi can safely undergo dobutamine stress echocardiography. These patients also have more severe wall motion abnormalities at rest compared with a group of patients with left ventricular dysfunction without evidence of apical thrombus.
Chronic heart failure (HF) is a leading cause of morbidity and mortality in the United States, affecting >4 million people. The increasing prevalence of HF has placed an enormous burden on the US healthcare system. For many patients with cardiovascular disease, HF is the final common pathway. Treatment strategies for HF are aimed at preventing and delaying progression of the disease and ultimately improving survival. This article reviews recent clinical drug trials for HF, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists, vasodilators, beta-adrenergic blockers, positive inotropic agents, calcium antagonists, and antiarrhythmics. The benefits and shortcomings of these agents and the study designs are discussed. For patients with left ventricular (LV) systolic dysfunction, ACE inhibitors are the only agents that consistently improved survival and decreased the rate of HF progression. It is likely that beta-adrenergic blockers have the same effect. The syndrome of HF is complex with both peripheral and cardiac factors contributing to disease progression. The addition of a diuretic and/or digoxin is often needed to prevent worsening heart failure. Although an angiotensin II antagonist may also be beneficial in the treatment of HF, further studies are needed to clarify their precise role in the management of this condition. Calcium anatagonists, antiarrhythmics excluding amiodarone, and positive inotropes other than digoxin do not appear to prevent progression of HF nor improve survival. The most common cause of HF in the United States is related to coronary artery disease. Reduction of cardiac risk factors, such as smoking cessation, lowering serum cholesterol with diet and a lipid lowering agent, and blood pressure control, is likely to prevent the development or progression of HF.
OBJECTIVE: To determine the prognostic significance of creatine kinase (CK) elevation following elective percutaneous transluminal coronary angioplasty (PTCA). DESIGN: Retrospective cohort study. SETTING: Tertiary care referral center. SUBJECTS: A total of 253 consecutive patients with total CK and CK-MB fraction (CK-MB) elevation (case patients) and 120 patients without CK elevation (controls). Control patients had undergone interventions during the same month and year using the same devices. MAIN OUTCOME MEASURES: In-hospital and late cardiac mortality, subsequent myocardial infarction, and the combined end point of cardiac mortality or myocardial infarction. RESULTS: Patient groups were similar with respect to age, sex, extent of coronary artery disease, left ventricular function, number of lesions treated by PTCA, and mean duration of follow-up (>3.5 years). Cardiac mortality was significantly greater (P=.02) for patients with CK elevation after PTCA. When patients were categorized according to peak CK elevation, cardiac mortality differed significantly among patient groups (P=.007), with increased cardiac mortality observed for patients with high (>3.0 times normal) and intermediate (1.5 to 3.0 times normal) CK elevations. In multivariate analyses, higher peak CK and lower ejection fraction were the most important predictors of increased cardiac mortality (both, P<.001); the relative risk for cardiac mortality was 1.05 (95% confidence interval, 1.03-1.08) per 100-U/L increment increase in CK. CONCLUSIONS: Creatine kinase elevation following elective PTCA is associated with increased late cardiac mortality. This increase in cardiac mortality is independent of clinical variables, severity of heart disease, coronary artery lesion characteristics, interventional devices, and procedural outcomes. Even patients with lesser degrees of CK elevation are at significantly increased risk for late cardiac death.
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BACKGROUND: Hypertrophic cardiomyopathy (HCM) has different clinical and prognostic aspects in young than in adult patients. This study was undertaken to determine whether these reported differences are reflected by changes in ultrasonic backscatter parameters and whether oral treatment with verapamil modifies backscatter variables in children with HCM. METHODS AND RESULTS: Sixty-eight subjects underwent backscatter analysis to assess the ultrasonic myocardial reflectivity and the amplitude of the cardiac cycle-dependent variation of the backscatter power curve. Subjects were divided into four groups: 10 HCM and 23 normal subjects < 10 years old and 17 HCM and 18 normal adults. Myocardial reflectivity and amplitude of the cyclic variation were assessed in the septum and in the posterior wall of all subjects. The children with HCM were restudied after long-term oral administration of verapamil. Both children and adult patients, compared with the normal control groups, showed a significant reduction in the amplitude of the cyclic variation both in the septum and in the posterior wall. In contrast, myocardial reflectivity, although significantly increased in adult HCM patients, was unchanged in the young HCM group. Verapamil administration did not significantly alter the results in the children with HCM. CONCLUSIONS: These data demonstrate that in young HCM patients, the ultrasonic myocardial reflectivity is normal, in contrast to the significant increase observed in adult patients affected by the same disease. This observation is in accord with the different clinical manifestations reported in young HCM patients and indicates an age-dependent difference in the echogenic structure of the hypertrophied myocardium in HCM.
In patients with coronary artery disease (CAD), left ventricular (LV) function, the number of diseased vessels, and the severity of myocardial ischemia are important determinants of survival. These factors can be used to identify subsets of high-risk patients who are candidates for aggressive intervention. Among patients with LV dysfunction, those with left main CAD, three-vessel disease, and one- or two-vessel disease with inducible ischemia are at highest risk. High-risk subsets among those with preserved LV function include patients with left main CAD and those with inducible ischemia and either three-vessel disease or two-vessel disease with involvement of the proximal left anterior descending coronary artery. Thus, exercise testing, assessment of ventricular function and, in selected patients, coronary angiography to determine coronary anatomy are valuable tools in risk stratification. In the primary-care setting, patient characteristics such as gender, race, age, and concomitant medical conditions may also be most useful in identifying high-risk patients. Although women in general have some primary protection against premature CAD, especially prior to the menopause, coronary risk in women who have experienced a cardiovascular event is similar to that in men. Coronary mortality is increased in minority populations, and the presence of other risk factors, such as diabetes and hyperlipidemia, can further increase this risk. Up to 80% of diabetic patients die of cardiovascular disease, 75% of which is CAD. The risk in this population is exacerbated by the abnormalities in lipid metabolism associated with the diabetic state. CAD mortality increases with aging, but it is recommended that elderly patients with CAD also receive risk factor intervention, such as cholesterol-lowering therapy. Consideration of the impact of such therapy on quality of life is especially important in initiating such interventions in the older population.
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A significant subset of patients with chronic heart failure have preserved systolic function and their symptoms are attributable to left ventricular diastolic abnormalities. In the setting of diastolic heart failure, the cardiac chambers are nondilated and have normal contractility, but left ventricular filling is impaired. This impairment in diastolic filling is related to both abnormalities of the passive elastic properties of the ventricle and impaired active relaxation as a result of any of the following: myocardial ischemia, hypertrophy, reduced beta-adrenergic tone, or increases in myocardial connective tissue. Therapy of diastolic heart failure is aimed at preventing and reducing left ventricular hypertrophy, treating elevated blood pressure, and reducing left ventricular filling pressure without reducing cardiac output. This may be achieved by maintaining sinus rhythm, slowing heart rate, and treating ischemia. Although calcium-channel blockers, beta-blockers, angiotensin-converting enzyme inhibitors, diuretics, and nitrates may improve symptoms in patients with diastolic heart failure, there are few data to indicate that these agents have an important effect on prognosis. Further studies of patients with diastolic heart failure are needed to assess its prevalence, clinical characteristics, prognosis, and response to therapy.
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