To assess the systolic and diastolic dysfunction of the left ventricle (LV) in relation to age and the severity of impairment in Duchenne muscular dystrophy (DMD), we performed M-mode, two-dimensional and pulsed-wave Doppler echocardiography in 45 male subjects with DMD aged 8 to 25 years and in 40 age-matched healthy controls. Systolic dysfunction started in the first decade of life, with some patients showing severe systolic dysfunction in their early teens. This dysfunction, however, did not always depend on the severity of the skeletal muscle disease. No patients with DMD showed an increase in peak atrial velocity and time-velocity integrals of the atrial contraction velocity curve, findings frequently reported to precede the abnormalities in many cardiac diseases; it was thought therefore that these patients had no increase in left atrial compensation. Diastolic dysfunction may not routinely precede or accompany the systolic dysfunction in DMD, in contrast with what is reported in patients with ischaemic or hypertensive heart disease. DMD patients usually show a predominant systolic dysfunction.
To estimate the effects of diltiazem on the left ventricular diastolic abnormalities in patients with hypertrophic cardiomyopathy, transmitral flow velocity during diastole was studied before and immediately after dynamic leg exercise with the pulsed Doppler technique combined with two-dimensional echocardiography. Seventeen patients with hypertrophic cardiomyopathy and 24 apparently healthy men performed bicycle ergometer exercise in the supine position with the target heart rate set at 120 beats/min. The patients with cardiomyopathy were directed to perform the exercise at the same intensity after receiving 30 to 60 mg of diltiazem, three times daily, for 1 or 2 weeks. The pattern of transmitral flow velocity in diastole had two components, one corresponding to the rapid filling phase in early diastole and the other to the atrial contraction phase in late diastole. To assess left ventricular diastolic behavior, the following variables were analyzed: peak velocity in the rapid filling and atrial contraction phases, the ratio of peak velocity in the atrial contraction phase to that in the rapid filling phase, and pressure half-time. The changes in peak velocity in the atrial contraction phase, pressure half-time and the ratio of peak velocity in the atrial contraction phase to that in the rapid filling phase with exercise differed significantly between patients with hypertrophic cardiomyopathy with no medication and control subjects. After diltiazem, the response of these variables to exercise was almost identical in the two groups. These results suggest that diltiazem can lessen the left ventricular diastolic abnormality in patients with hypertrophic cardiomyopathy on dynamic exercise of mild intensity.
1. The structures, including stereochemistry, of the two major metabolites of pravastatin sodium in an isolated rat hepatocyte system, i.e. the 4'a alpha-glutathione conjugate (CM-1) and the 3',5'-dihydrodiol (CM-2), were determined by one- and two-dimensional n.m.r. spectroscopy. 2. The structures of two synthetic pravastatin epoxides, possible precursors of the metabolites, were also established. 3. One of the synthetic epoxides, 4'a beta, 5' beta-epoxide was converted to the pravastatin metabolite, 4'a alpha-glutathione conjugate (CM-1) by a rat liver cytosol system and is proposed as the common metabolic intermediate between pravastatin sodium and the metabolites, CM-1 and CM-2.
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