Circulation
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Little information is available regarding the effects of myocardial infarction on the characteristics of ventricular fibrillation (VF). Epicardial activation during VF can be characterized by the cycle length and by the characteristics of activation wave fronts. ⋯ During VF, in animals with subacute or chronic healing MI, (1) the size of activation wave fronts is larger, (2) the cycle length of VF is longer, (3) the conduction velocities are slower, and (4) the degree of organization is greater than in control animals. Thus, the characteristics of VF throughout the heart are altered by the presence of regional myocardial infarction. The implications of these findings for the initiation and maintenance of VF in the presence of different underlying myocardial substrates require further study.
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The objective of this study was to describe the distribution of echo left ventricular (LV) mass and its association with demographic and cardiovascular risk factors in a large race- and sex-balanced cohort of young adults. Recent epidemiological data have suggested that M-mode echocardiographically determined LV hypertrophy is an independent predictor of mortality and morbidity from coronary heart disease (CHD) in older adults. Echocardiographic LV mass has been associated in middle-aged and older adults with multiple factors including age, arterial blood pressure, body mass, and sex. However, there are few data describing the distribution of echo LV mass among black and white young adult men and women and relating LV mass to cardiovascular disease risk factors within race-sex subgroups. ⋯ In the healthy young adults of the CARDIA cohort, LV mass was highly correlated with body weight, subscapular skinfold thickness, height, and systolic blood pressure across race and sex subgroups. Furthermore, after adjustment for anthropometric, blood pressure, and other covariates, LV mass remained higher in men than in women and in blacks than in whites. Longitudinal studies are necessary to delineate the possible roles of these factors in the genesis of LV hypertrophy.
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Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. ⋯ In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.
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Although autonomic imbalance is known to be characteristics of patients with clinically overt symptomatic congestive heart failure, it is currently unknown whether this autonomic response arises early in the course of left ventricular dysfunction or is restricted to the later stages of circulatory failure. ⋯ The results indicate that autonomic imbalance as reflected in an abnormal pattern of heart rate variability evolves early in the course of ventricular systolic dysfunction consisting of both a significant increase in sympathetically influenced low-frequency heart rate variability and a significant reduction of parasympathetically mediated high-frequency variability. The early appearance of these autonomic abnormalities suggests that autonomic imbalance plays a significant role in promoting the progression of circulatory failure.