M Shahi

Left Ventricular Hypertrophy and QT Dispersion in Hypertension

The interlead variation in QT length on a standard electrocardiograph reflects regional repolarization differences in the heart. To investigate the association between this interlead variation (QT dispersion) and left ventricular hypertrophy, we subjected 100 untreated subjects to 12-lead electrocardiography and echocardiography. Additionally, 24 previously untreated subjects underwent a 6-month treatment study with ramipril and felodipine. In the cross-sectional part of the study, QT dispersion corrected for heart rate (QTc dispersion) was significantly correlated with left ventricular mass index (r = .30, P < .01), systolic pressure (r = .30, P < .01), the ratio of peak flow velocity of the early filling wave to peak flow velocity of the atrial wave (E/A ratio) (r = -.22, P = .02), isovolumic relaxation time (r = .31, P < .01), and age (r = .21, P < .04). In the treatment part of the study, lead-adjusted QTc dispersion decreased from 24 to 19 milliseconds after treatment, and after a subsequent 2 weeks of drug washout remained at 19 milliseconds (P < .01). The changes in left ventricular mass index at these stages were 144, 121, and 124 g/m2 (P < .01). Systolic pressure decreased from 175 to 144 mm Hg and increased again to 164 mm Hg after drug washout (P < .01). The E/A ratio (0.97, 1.02, and 1.02; P = 69) and isovolumic relaxation time (111, 112, and 112; P = .97) remained unchanged through the three assessment points. In conclusion, QT dispersion is increased in association with an increased left ventricular mass index in hypertensive individuals. Antihypertensive therapy with ramipril and felodipine reduced both parameters. If an increased QT dispersion is a predictor of sudden death in this group of individuals, then the importance of its reduction is evident.

Racial differences in cardiac structure and function in essential hypertension

Abstract Objective: To assess racial differences in cardiac structure and function in patients presenting with previously untreated hypertension. Design - Untreated black patients with hypertension were compared with untreated white patients matched for age and sex. Both groups had similar body mass indices, blood pressures, and reported duration of hypertension. Setting: Cardiovascular risk factor clinic for outpatients. Subjects: 36 men and 22 women with untreated essential hypertension. Main outcome measures: Variables of heart structure and function on cross sectional and Doppler echocardiography. Results: The black patients had a significantly greater interventricular septal thickness (mean 1.23 (95% confidence interval 1.14 to 1.33) v 1.09 (1.02 to 1.16) cm; P=0.02) and posterior wall thickness (mean 1.14 (1.07 to 1.22) v 0.96 (0.88 to 1.03) cm; P=0.001) than the white patients although left ventricular internal diameter was not significantly different (mean 4.90 (4.68 to 5.12) v 4.82 (4.64 to 5.01) cm; P=0.59). This resulted in a significantly greater left ventricular mass index (mean 151 (137 to 164) v 120 (107 to 133) g/m2; P=0.001) and relative wall thickness (mean 0.47 (0.43 to 0.51) v 0.40 (0.37 to 0.42) cm; P=0.004) in the black patients. Comparison of Doppler measures of left ventricular diastolic function showed a significantly longer isovolumic relaxation time in black patients (mean 107 (98 to 116) v 92 (83 to 101) ms; P=0.02) compared with white patients, although peak early to atrial filling ratios were similar in both groups (mean 1.14 (0.95 to 1.32) v 1.04 (0.94 to 1.15); P=0.37). Conclusion: Among previously untreated hypertensive patients, black subjects compared with white subjects have significantly higher left ventricular mass index and relative wall thickness, as well as more impairment of left ventricular function during diastole.

Regression of hypertensive left ventricular hypertrophy and left ventricular diastolic function

The 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 initiation of treatment. Left ventricular mass index was 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.

Ethnic Differences in the Hypertensive Heart and 24-Hour Blood Pressure Profile

Black hypertensive persons have been observed to have a greater degree of left ventricular hypertrophy than white hypertensives. However, previous studies have matched groups for blood pressure (BP) measured in the clinic, and it has been demonstrated that black hypertensives have an attenuated nocturnal BP dip. Clinic BPs may thus underestimate mean 24-hour BP in this group. To investigate whether the differences in left ventricular hypertrophy can be accounted for by the greater mean 24-hour BP in black hypertensives, 92 previously untreated hypertensives were studied with 24-hour ambulatory BP monitoring and echocardiography. The 46 black hypertensives (24 men and 22 women) were matched with the 46 white hypertensives for age, gender, and mean 24-hour BP. Despite similar mean 24-hour BPs (blacks, 142/93 mm Hg; whites, 145/92 mm Hg; P=.53/.66), the black group had a smaller mean nocturnal dip than the white group (blacks, 8/8 mm Hg; whites, 16/13 mm Hg; P<.01). In addition, mean left ventricular mass index (LVMI) was greater (blacks, 130 g/m2; whites, 107 g/m2; P<.001). Mean 24-hour systolic BP was significantly related to LVMI in both groups (blacks, r=.45, P<.01; whites, r=.56, P<.01). However, systolic BP dip correlated inversely with LVMI only in the black group (blacks, r=-.30, P<.04; whites, r=.05, P=.76). In a multiple regression model, LVMI was independently related to both mean daytime BP and mean nocturnal BP dip in black subjects but only to mean daytime BP in white subjects. In conclusion, the increased left ventricular hypertrophy observed in black hypertensives compared with white hypertensives is not accounted for by differences in mean 24-hour BP. However, LVMI in black hypertensives appears to be more dependent on nocturnal BP than that in white hypertensives; this, coupled with the attenuated BP dip in black hypertensives, suggests that the BP profile rather than 24-hour BP may be important in determining the differences in left ventricular hypertrophy.

Absence of sympathetic overactivity in Afro-Caribbean hypertensive subjects studied by heart rate variability.

Black hypertensives present a greater prevalence of left ventricular hypertrophy and an increased mortality compared to white hypertensives. Differences in sympathetic activity might contribute to explain these racial differences in hypertension. Nevertheless, previous laboratory studies did not show any increase of sympathetic activity direct to the heart in black subjects. The aim of the present study was to investigate the cardiac sympatho-vagal balance in black and white hypertensives analysing heart rate variability, during the entire 24u2009h. We analysed Holter recordings of 52 essential hypertensive patients, who had never received antihypertensive treatment, 26 of whom were black and 26 were white. Consecutive series of 300 beats, with 150 beats overlapped (approximately 600 series/day), were considered for the analysis in time and frequency domain. The mean 24-h value of the power of the low frequency spectral component (0.04–0.15u2009Hz), expressed in normalised units, ie a marker of sympathetic modulation, was significantly lower in the group of black patients compared to whites (respectively 40.0u2009±u20092.1 vs 53.6u2009±u20093.6u2009nu, Pu2009<u20090.01). similar results were observed for the lf/hf ratio, an index of the sympatho-vagal balance (respectively 4.11u2009±u20090.58 vs5.98u2009±u20090.79; Pu2009<u20090.05). in a multiple linear regression analysis, considering diastolic blood pressure, left ventricular mass index, race and age as independent variables, only race (Pu2009<u20090.002) and age (Pu2009<u20090.01) could independently predict the normalised low frequency power or the lf/hf ratio, as dependent variables. the results of this study suggest some blunting of the cardiac sympathetic neural modulation in black hypertensives compared to white hypertensives, during the entire 24u2009h.

Midwall myocardial shortening in athletic left ventricular hypertrophy

BACKGROUNDnPatients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown.nnnMETHODSnForty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects.nnnRESULTSnLeft ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2).nnnCONCLUSIONnSubjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.

The effects on cardiac arrhythmias of antihypertensive therapy causing regression of left ventricular hypertrophy

To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensive subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with baseline, left ventricular mass index (LVMI) was significantly reduced both at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure control; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8* g/m2, *P < .01 compared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 months of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained after 6 months of further treatment, either before (78 +/- 50) or after drug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraventricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of treatment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between improvement or worsening of a defect with changes in ventricular ectopic total. In conclusion, antihypertensive therapy with ramipril and felodipine, although causing regression of left ventricular hypertrophy did not lead to a sustained reduction in ventricular ectopic total.

Left ventricular geometry in presenting untreated hypertension

In order to investigate the spectrum of geometry in our patient population, 63 untreated hypertensives underwent two-dimensional echocardiography. Left ventricular (LV) mass index and relative wall thickness, a measure of wall thickness in relation to cavity size, were calculated from the M-mode strip. In addition, to assess the sphericity of the left ventricle the ratio of LV minor to major hemiaxis was calculated. The subjects comprised 41 men (17 Caucasian, 22 Afro–Carribean and two Oriental), and 21 women (five Caucasian, 12 Afro–Carribean and two Oriental). Concentric hypertrophy was present in 46% of subjects, concentric remodelling in 32% of subjects, eccentric hypertrophy in only 6% of subjects and a normal left ventricular shape in 16% of subjects. The degree of sphericity of the left ventricle was similar among the four groups, suggesting that it does not change in uncomplicated hypertension. In contrast to the previously published combined series from Sassari and New York we had a low proportion of patients with either eccentric hypertrophy or normal left ventricular geometry. This is probably due to the high proportion of Afro–Carribean subjecs in our clinic population who are more likely to have left ventricular hypertrophy.