Background and Purpose-Despite theories that link stroke to left ventricular mass, few large, population-based studies have examined the predictive value of echocardiographically derived left ventricular mass index (LVMI) to incident stroke in African Americans. Methods-Participants in the Jackson cohort of the Atherosclerotic Risk in Communities study have had extensive baseline evaluations, have undergone echocardiography during the third examination (1993)(1994)(1995), and have been followed up for incident cardiovascular disease including ischemic stroke. Results-The study population consisted of 1792 participants, of whom 639 (35.7%) were men and the meanϮSD age was 58.8Ϯ5.7 years. Compared with those without ischemic stroke, those with ischemic stroke had a higher frequency of hypertension (85.6% vs 58.7%) and diabetes (46.9% vs 21.0%). Left ventricular hypertrophy was more prevalent in those with stroke (62.2% vs 38.6%). During a median follow-up of 8.8 years, 98 incident strokes occurred (6.5 per 1000 person-years). LVMI was independently associated with stroke after adjusting for age, sex, hypertension, systolic blood pressure, smoking, diabetes, total to HDL cholesterol ratio, body mass index, and low left ventricular ejection fraction (adjusted hazard ratio per 10 g/m 2.7 increment of LVMIϭ1.15; 95% CI, 1.02 to 1.28). The relation remained statistically significant after adding left atrial size and mitral annular calcification to the multivariable model. Conclusions-In this large, population-based African American cohort, we found that echocardiographic LVMI was an independent predictor of incident ischemic stroke even after taking into account traditional clinical risk factors. (Stroke.
About one-third of patients presenting with a clinical syndrome of heart failure (HF) have normal left ventricular (LV) systolic function (EF ≥ 45%). This group is described as having diastolic dysfunction with diastolic HF. 1 In the evaluation of patients with suspected cardiogenic dyspnea, echocardiography provides information about both LV function (systolic and diastolic) and LV loading conditions. 2 Obtaining reliable, reproducible data relative to diastolic ventricular performance can be challenging. This review summarizes the echocardiographic assessment of diastolic function and LV filling pressures, as well as pitfalls in acquisition and interpretation of applicable data.Diastole is defined clinically as that period of the cardiac cycle beginning with aortic valve closure (AVC), and ending with mitral valve closure (MVC). 3 Exactly when ventricular relaxation begins is not clear. At the cellular level, diastole starts with actin-myosin crossbridge unlinking, allowing sarcomere relaxation in an energy-consuming process requiring ATP hydrolysis. Active relaxation does not begin simultaneously throughout the heart; the process of crossbridge unlinking begins in some areas of the myocardium while active contraction continues in others. When a sufficient number of myocardial cells enter the active relaxation phase, ventricular pressure begins to fall and the aortic valve closes. 4 There are four clinical phases of diastole (Fig. 1). 5,6 The first is isovolumic relaxation, beginning with AVC and ending with mitral valve opening (MVO). Rapid filling begins at MVO with continued active myocardial relaxation causing LV pressure to drop below left atrial (LA) pressure (resulting in diastolic "suction"). The third phase, diastasis, is characterized by passive LV filling. During this phase, LV and LA pressures are nearly equal and LV filling mostly occurs by pulmonary vein (PV) flow and fluid inertia. The LA acts as a passive conduit, allowing PV flow to directly enter the LV. The last phase is atrial systole, during which atrial contraction contributes about 15% of LV filling in normal patients. [6][7][8] Active relaxation occurs early in diastole, during the isovolumic relaxation and rapid filling phases. Active relaxation is normally complete by mid-diastole. Diastasis and atrial contraction constitute the passive parts of diastole, during which LV passive stiffness is the predominant factor determining compliance. Interventricular interaction (septal impingement into the LV cavity) and the pericardium (limiting chamber enlargement via extra-ventricular restriction) also have important roles in late diastole. 9
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