Abstract
The mechanism causing symptoms and signs of heart failure (HF) in patients with preserved global left ventricular (LV) systolic function remains poorly defined. Conventionally, LV diastolic dysfunction is implicated as a major factor responsible for the clinical syndrome of HF in these patients, provided that valvular heart disease, cor pulmonale, volume overload conditions, and noncardiac causes of symptoms are excluded. 1 Early LV functional abnormalities can be detected using analysis of its longitudinal function 2,3 by M-mode echocardiography, magnetic resonance imaging, or tissue Doppler imaging. In the present study we investigated long-axis LV function in patients with symptoms of HF and preserved global LV systolic function using color tissue Doppler imaging. ••• From 220 consecutive attendees (14 women and 206 men, aged 68 12 years) referred to a HF clinic we identified 44 patients with signs and symptoms of compensated HF (New York Heart Association functional class II and III) and preserved global LV systolic function according to the criteria proposed by the European Study Group on Diastolic Heart Failure (LV ejection fraction 45% and LV end-diastolic diameter index 3.2 cm/m 2 or LV end-diastolic volume index 102 ml/m 2 ). 4 Twenty-five patients had ischemic heart disease (16 with previous myocardial infarction), 16 patients had a history of hypertension, and 3 patients were previously diagnosed with idiopathic dilated cardiomyopathy. All patients had been receiving diuretics and angiotensin-converting enzyme inhibitors or angiotensin II antagonists at optimal doses and had been stable for the preceding 3 months. We performed basic spirometry on all patients to exclude pulmonary disease. The control group was composed of 44 subjects (16 women and 28 men, aged 68 11 years) with no known cardiovascular disease. Each subject underwent full echocardiographic examination including color-coded tissue Doppler imaging using commercially available equipment (GE Vingmed Vivid Five scanner, Horten, Norway) equipped with a 2.5-MHz phased-array transducer. The parasternal long-axis view was used to derive left atrial dimension at end-systole. Measurements of LV end-diastolic volumes and end-systolic volumes were performed using the modified Simpson’ s rule and LV ejection fraction was calculated. Early filling (E) and atrial filling (A) peak velocities, E/A ratio, deceleration time of early filling, and isovolumic relaxation time were measured from transmitral flow, and systolic (S), diastolic (D), and atrial reversal peak velocities were derived from pulmonary venous flow using pulsed Doppler. In color tissue Doppler mode, images were obtained in 3 apical views (4-chamber, 2-chamber, and apical long-axis), and stored digitally on magnetic optical disks. The coded data were reviewed off-line with a software analysis system (Echopac 6.3, GE Vingmed). Mitral annular systolic velocities (S m), ignoring the
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