458
Regression of hypertensive left ventricular hypertrophy and left ventricular diastolic function
effect of antihypertensive therapy on regression of left ventricular hypertrophy and left ventricular diastolic function was investigated in 25 hypertensive patients for up to 18 months after
The
initiation of treatment. Left ventricular mass index calculated by two-dimensional echocardiography and left ventricular diastolic function assessed by transmitral pulsed doppler ultrasound. Significant reduction in left ventricular mass index was observed after 9 months of treatment. Only 13 patients had a reduction in mass greater than the intraobserver variability of the technique. There was no change in doppler indices of left ventricular diastolic function. In 7 patients who were studied for a further 9 months after regression had occurred there was still no appreciable difference in left ventricular diastolic function. These findings indicate that there is no direct relation between left ventricular mass and abnormal left ventricular diastolic function.
The aim of this study was to ascertain whether reduction in LV mass with antihypertensuve therapy, known to reduce mass and collagen in laboratory animals, has a beneficial effect on LV diastolic filling in hypertensive patients with diastolic dysfunction.
was
Introduction Abnormal left ventricular (LV) diastolic function in the presence of normal systolic function is one of the earliest cardiac manifestations of systemic hypertension.1 This abnormality has been observed not only in patients with LV hypertrophy but also in those with mild or borderline hypertension2 and suggests that changes in the cardiac matrix develop early in the course of disease. Several studies have shown a significant negative correlation between LV mass and indices of diastolic function.3.4 However, the correlations have been weak and it has therefore become apparent that other factors may be important. The collagen matrix of the heart is thought to maintain myocyte alignment throughout the cardiac cycle, permitting reversible interdigitation of contracting myocytes during systole and limiting the degree of slippage between myocytes during diastole. In laboratory animals with hypertension, collagen synthesis increases before a rise in blood pressure and continues to increase with the hypertrophic process.6 The ratio of collagen phenotypes is altered although the collagen content of the heart is normal, and these changes may be important in the abnormalities of diastolic function seen in hypertensive patients. In spontaneously hypertensive rats, Sen and co-workers8 have shown that angiotensin converting enzyme (ACE) inhibitors reduce both LV mass and collagenous elements. LV mass regresses in hypertensive patients treated with most classes of antihypertensive drugs other than direct acting vasodilators9 and diuretics10 but whether there is concomitant reduction in collagen in man is not known.
Methods Patients
patients with essential hypertension (BP > 160/90) who had previously received treatment (n = 12) or whose blood pressure was uncontrolled on existing antihypertensive therapy (n = 13) were recruited from the hypertension clinic at our institution from February, 1988, to December, 1988. All patients had normal haematological and biochemical indices and normal fractional shortening (systolic function) determined by two dimensional (2D) echocardiography (> 35%). No patient had evidence of valvular stenosis or regurgitation determined clinically or by doppler ultrasound and all had doppler indices of LV diastolic function that were below the normal age-related reference values.ll,12 25
not
Echocardiography Each patient underwent 2D and doppler echocardiography at baseline and every 3 months for a minimum of 9 months (range 9-18) with a phased array sector scanner (General Electric Pass 11, 3-5 MHz transducer). LV septal wall thickness, posterior wall thickness, and cavity size were measured from either the parasternal long axis view or the LV short axis view with 2D guided M-mode echocardiography. Special attention was paid to obtaining a precise cross-sectional "on axis" image of the LV at the papillary muscle tip level. The papillary muscles were then bisected by the M-mode beam and simultaneous 2D and M-mode images obtained. This method ensured that the same level of ventricle was measured at each examination. LV mass was determined with an area x length method that had been validated in man.13,14 For this calculation two echocardiographic views are required: a parastemal short axis view of the LV at the papillary muscle tip level to assess the area of the myocardium and an apical four chamber view that maximises the distance from the mitral valve annulus to the LV apex to determine the length of the ventricle. LV mass is then calculated from the algorithm LV mass =1-04 (% Ai x 1,--X A2 x 12), where A, and Az represent the epicardial and endocardial areas, respectively, measured by planimetry and 11 and 12 represent the length of the LV from mitral annulus to epicardial and endocardial borders, respectively. LV mass index was determined by dividing LV mass by body surface area.
Doppler studies Pulsed doppler examination of transmitral flow for assessment of LV diastolic function was done with reference to the 2D
Departments of Cardiology and Clinical Pharmacology, St Mary’s Hospital, London W2 1NY, UK (M Shahi, MRCP, S. Thom, MRCP, N. Poulter, MRCP, P. S Sever, FRCP, R A. Foale, MRCP) Correspondence to Dr M Shahi
ADDRESSES
459
EARLY FILLING WAVE
TABLE I-EFFECTS OF TREATMENT ON BLOOD PRESSURE AND LEFT VENTRICULAR MASS INDEX OVER TIME (MONTHS)
’-p< 0-05, LVMI
=
t= p
Regression of hypertensive left ventricular hypertrophy and left ventricular diastolic function
effect of antihypertensive therapy on regression of left ventricular hypertrophy and left ventricular diastolic function was investigated in 25 hypertensive patients for up to 18 months after
The
initiation of treatment. Left ventricular mass index calculated by two-dimensional echocardiography and left ventricular diastolic function assessed by transmitral pulsed doppler ultrasound. Significant reduction in left ventricular mass index was observed after 9 months of treatment. Only 13 patients had a reduction in mass greater than the intraobserver variability of the technique. There was no change in doppler indices of left ventricular diastolic function. In 7 patients who were studied for a further 9 months after regression had occurred there was still no appreciable difference in left ventricular diastolic function. These findings indicate that there is no direct relation between left ventricular mass and abnormal left ventricular diastolic function.
The aim of this study was to ascertain whether reduction in LV mass with antihypertensuve therapy, known to reduce mass and collagen in laboratory animals, has a beneficial effect on LV diastolic filling in hypertensive patients with diastolic dysfunction.
was
Introduction Abnormal left ventricular (LV) diastolic function in the presence of normal systolic function is one of the earliest cardiac manifestations of systemic hypertension.1 This abnormality has been observed not only in patients with LV hypertrophy but also in those with mild or borderline hypertension2 and suggests that changes in the cardiac matrix develop early in the course of disease. Several studies have shown a significant negative correlation between LV mass and indices of diastolic function.3.4 However, the correlations have been weak and it has therefore become apparent that other factors may be important. The collagen matrix of the heart is thought to maintain myocyte alignment throughout the cardiac cycle, permitting reversible interdigitation of contracting myocytes during systole and limiting the degree of slippage between myocytes during diastole. In laboratory animals with hypertension, collagen synthesis increases before a rise in blood pressure and continues to increase with the hypertrophic process.6 The ratio of collagen phenotypes is altered although the collagen content of the heart is normal, and these changes may be important in the abnormalities of diastolic function seen in hypertensive patients. In spontaneously hypertensive rats, Sen and co-workers8 have shown that angiotensin converting enzyme (ACE) inhibitors reduce both LV mass and collagenous elements. LV mass regresses in hypertensive patients treated with most classes of antihypertensive drugs other than direct acting vasodilators9 and diuretics10 but whether there is concomitant reduction in collagen in man is not known.
Methods Patients
patients with essential hypertension (BP > 160/90) who had previously received treatment (n = 12) or whose blood pressure was uncontrolled on existing antihypertensive therapy (n = 13) were recruited from the hypertension clinic at our institution from February, 1988, to December, 1988. All patients had normal haematological and biochemical indices and normal fractional shortening (systolic function) determined by two dimensional (2D) echocardiography (> 35%). No patient had evidence of valvular stenosis or regurgitation determined clinically or by doppler ultrasound and all had doppler indices of LV diastolic function that were below the normal age-related reference values.ll,12 25
not
Echocardiography Each patient underwent 2D and doppler echocardiography at baseline and every 3 months for a minimum of 9 months (range 9-18) with a phased array sector scanner (General Electric Pass 11, 3-5 MHz transducer). LV septal wall thickness, posterior wall thickness, and cavity size were measured from either the parasternal long axis view or the LV short axis view with 2D guided M-mode echocardiography. Special attention was paid to obtaining a precise cross-sectional "on axis" image of the LV at the papillary muscle tip level. The papillary muscles were then bisected by the M-mode beam and simultaneous 2D and M-mode images obtained. This method ensured that the same level of ventricle was measured at each examination. LV mass was determined with an area x length method that had been validated in man.13,14 For this calculation two echocardiographic views are required: a parastemal short axis view of the LV at the papillary muscle tip level to assess the area of the myocardium and an apical four chamber view that maximises the distance from the mitral valve annulus to the LV apex to determine the length of the ventricle. LV mass is then calculated from the algorithm LV mass =1-04 (% Ai x 1,--X A2 x 12), where A, and Az represent the epicardial and endocardial areas, respectively, measured by planimetry and 11 and 12 represent the length of the LV from mitral annulus to epicardial and endocardial borders, respectively. LV mass index was determined by dividing LV mass by body surface area.
Doppler studies Pulsed doppler examination of transmitral flow for assessment of LV diastolic function was done with reference to the 2D
Departments of Cardiology and Clinical Pharmacology, St Mary’s Hospital, London W2 1NY, UK (M Shahi, MRCP, S. Thom, MRCP, N. Poulter, MRCP, P. S Sever, FRCP, R A. Foale, MRCP) Correspondence to Dr M Shahi
ADDRESSES
459
EARLY FILLING WAVE
TABLE I-EFFECTS OF TREATMENT ON BLOOD PRESSURE AND LEFT VENTRICULAR MASS INDEX OVER TIME (MONTHS)
’-p< 0-05, LVMI
=
t= p
