Degree Of Left Ventricular Hypertrophy Research Articles

Limited echocardiography for hypertensive left ventricular hypertrophy.

Echocardiographic assessment of left ventricular (LV) mass has provided the best noninvasive information to permit diagnostic, therapeutic, and prognostic assessment of hypertensive heart disease1 2 3 4 5 6 7 (Table 1⇓). Reversal of hypertension-induced LV hypertrophy (LVH) occurs with all pharmacological (and some nonpharmacological) antihypertensive treatment, although few data are yet available to demonstrate that such reversal is associated with a reduced risk of LVH. However, one recent report suggested that patients who had changes of reversal of LVH (by electrocardiography [ECG]) were at substantially reduced risk compared with those who did not demonstrate diminished LVH.9 However, the cost of echocardiography has limited its utility in patients with hypertension. A less time-consuming and less-expensive LVH screening echocardiogram would be of great value; such a procedure is referred to as a limited echocardiogram.10 View this table: Table 1. Summary of Epidemiological Studies Relating Echocardiographic Left Ventricular Mass With Long-term Prognosis Echocardiography has been used as a standard procedure for the calculation of LV muscle mass for more than 25 years.11 Primary measurements of LV dimensions are made according to American Society of Echocardiography standards using the leading edge method of interface recognition and by identifying end diastole and end systole at the QRS onset and nadir of posterior systolic motion of the interventricular septum.12 13 14 Adequate M-mode images for calculation of LV mass can be obtained in approximately 90% of patients in an experienced echo laboratory.15 16 17 Assessment of the degree of LVH should include measurements of the posterior wall and septal thickness and calculation of LV mass index. However, even in patients with good-quality studies, there is significant intrareader and interreader variability of LV mass.15 For instance, in the Treatment of Mild Hypertension Study, the variance between the two readers was 23.8% (49.2g), and …

Volume overload, atrial natriuretic peptide, and left ventricular hypertrophy.

The development of high blood pressure leads to an increased hemodynamic afterload to the heart, wich is compensated by an increase of cardiac mass in order to maintain the cardiac output. However,despite the casual link between high blood pressure and left ventricular hypertrophy (LVH) clinical studies do not show a close correlation between blood pressure level and the degree of LVH (1).KeywordsCardiac IndexAtrial Natriuretic PeptideLeft Ventricular MassSodium IntakeTotal Peripheral ResistanceThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

M-Mode Echocardiography in Aortic Stenosis: Clinical Correlates and Prognostic Significance after Valve Replacement

To relate preoperative findings at M-mode echocardiography to preoperative clinical and haemodynamic status and to identify possible echocardiographic risk factors for mortality after aortic valve replacement (AVR), 250 patients with AVR for aortic stenosis (AS) were studied. In follow-up averaging 3.2 years there were 22 early (<30 days) and 23 late deaths. Rising NYHA function class and cardiothoracic index, and left ventricular (LV) failure were related to rising LV end-diastolic and end-systolic diameter index (EDDI, ESDI), and to increasing LV muscle mass index and decreasing fractional shortening (FS). High peak-to-peak systolic aortic valve gradient and LV end-systolic pressure were related to small dimensions of LV with increased FS and posterior wall thickness (PWTh). EDDI ≤20 mm/m2 and increasing PWTh were independent risk factors for early mortality. Patients with EDDI ≤20mm/m2 had normal or supranormal FS. PWTh was the only independent risk factor in long-term survival: 5-year rates being 81 ± 6%, 94 ± 3% and 85 ± 7% for PWTh < 13, 14–17 and ≥18 mm, respectively (p = 0.03). Prevalence of concomitant coronary artery disease (CAD) rose with decreasing PWTh. Angina pectoris in non-CAD patients was related to very high PWTh. Subnormal EDDI was associated with poor surgical outcome, and dilated, poorly contracting LV with congestive heart failure prior to AVR. The degree of LV hypertrophy seemed to be the dominant risk factor, but confounders included myocardial ischaemia due to CAD in low-grade hypertrophy or to hypertrophy per se. A hypofhetically confounding factor is the reversibility potential of moderate or severe LV hypertrophy following AVR.

Coronary artery dimensions in primary and secondary left ventricular hypertrophy

Background. Coronary artery enlargment has been previously described in left ventricular hypertrophy.Objectives. We sought to assess coronary artery dimensions and their relation to left ventricular muscle mass in primary and secondary hyperthropy.Methods. Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease). As a measure of left ventricular hypertrophy, angiographic left ventricular mass and equatorial cross-sectional muscle area were determined.Results. Cross-sectional area of both the left and right coronary arteries is increased in left ventricular hypertrophy (p < 0.05 vs. values in control subjects). There is a curvilinear relation between left coronary artery size and left ventricular muscle mass (r = 0.76) or cross-sectional muscle area (r = 0.75). However, normalization of coronary cross-sectional area for left ventricular muscle mass or muscle area shows insufficient enlargement of the coronary arteries in both primary and secondary hypertrophy.Conclusions. 1) Coronary artery size increases as left ventricular mass increases in both primary and secondary hypertrophy. 2) The enlargement of left coronary cross-sectional area is independent of the cause of the increase in left ventricular mass. 3) The size of the coronary arteries is inappropriate with regard to left ventricular hypertrophy. Thus, the stimulus for growth of the coronary arteries is not influenced by the underlying disease but appears to depend on the degree of left ventricular hypertrophy.

GENETIC VARIANTS OF PROTEINS FROM THE RENIN ANGIOTENSIN SYSTEM ARE ASSOCIATED WITH PRESSURE LOAD CARDIAC HYPERTROPHY

1. The relationship between the angiotensinogen (AGT) T174M, angiotensin converting enzyme (ACE) insertion/deletion (I/D) and the angiotensin II type 1 receptor (AT1) genetic markers and left ventricular hypertrophy was examined in normal subjects and those with aortic stenosis. 2. Subjects with aortic stenosis had higher left ventricular systolic pressure and relative wall thickness (RWT) compared with normal. However, within aortic stenosis subjects, left ventricular RWT did not correlate with left ventricular systolic pressure or with aortic valve area. 3. In subjects with aortic stenosis, left ventricular RWT was higher in those with ACE DD (P < 0.05) or AGT T174M (P < 0.06) compared with those with the ACE II or ID genotype or AGT TT174 genotype. No relationship was observed with any of the AT1 alleles. The ACE and AGT genetic markers independently predicted left ventricular RWT in aortic stenosis. No association was observed between these genotypes and left ventricular RWT in normal subjects. 4. The data suggest that the AGT T174M and ACE I/D genotypes may act together to influence the degree of hypertrophy in subjects with aortic stenosis. 5. In patients with aortic stenosis, genetic variants of proteins from the renin angiotensin system may be at least as important as left ventricular systolic pressure in determining the degree of left ventricular hypertrophy and could therefore explain the clinical variation observed in the progression to cardiac dysfunction.

Characterization of myocardial tissue in patients undergoing maintenance hemodialysis by quantitative echocardiography

The uremic state affects myocardial structure, bringing about, among other things, interstitial calcium deposition. Abnormalities of myocardial structure can be assessed quantitatively and noninvasively during life by the analysis of the gray-level distribution of conventional two-dimensional echocardiograms. The aim of this study was to evaluate the role of quantitative echocardiography in providing information on myocardial structure in patients under maintenance hemodialysis and to relate the ultrasonic findings with abnormalities in calcium-phosphate metabolism. Forty patients undergoing dialysis without abnormalities in left ventricular regional and global function and 17 hypertensive patients with comparable left ventricular hypertrophy were studied. The distribution of the gray levels within a region of interest in the interventricular septum was analyzed off-line by an array processor-based computer. Compared with hypertensive patients, patients undergoing dialysis showed a greater myocardial echogenicity (mean 92 ± 20 versus 72 ± 15; p = 0.004) and a reduced homogeneity of distribution of gray levels (entropy 4.5 ± 0.2 versus 4.2 ± 0.2, p < 0.01; uniformity 0.010 ± 0.003 versus 0.020 ± 0.004, p < 0.005). In the same patients, a significant negative linear relation was found between entropy and calcium-phosphate product ( r = −0.66; p = 0.001). Quantitative analysis of conventional two-dimensional echocardiograms allows the detection of a pathologic myocardial structure in patients under maintenance hemodialysis with normal left ventricular function. These abnormalities are related to disorders of calcium-phosphate metabolism and bear no relationship to the degree of left ventricular hypertrophy.

Coronary vascular ATP-sensitive potassium channels are activated to a greater extent in spontaneously hypertensive rats than in Wistar-Kyoto rats.

To determine whether opening of coronary vascular adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels is involved in the maintenance of resting coronary flow in hypertrophied hearts. We examined the effects of glibenclamide, a selective inhibitor of KATP channels, on basal coronary vascular tone in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Using a Langendorff system, the hearts from WKY rats and SHRs were isolated and perfused with oxygenated Krebs-Henseleit solution at a constant perfusion pressure of 60 and 100 mmHg respectively. Basal coronary flow and myocardial oxygen consumption (MV02) were similar in SHRs and WKY rats. The percentage decreases in coronary flow with glibenclamide at graded doses were greater (P < 0.01) in SHRs than in WKY rats (n = 8), whereas the percentage decreases in MV02 with glibenclamide were similar in the two groups. The decreases in coronary flow caused by U46619 (a thromboxane A2-mimetic agent) were similar in SHRs and WKY rats (n = 4). The increase in coronary flow caused by pinacidil (a KATP opener) was greater in SHRs than in WKY rats; glibenclamide prevented the pinacidil-induced increase in coronary flow in both SHRs and WKY rats. There was a significant positive correlation between the glibenclamide-induced decrease in coronary flow and the degree of left ventricular hypertrophy (r = 0.54, P < 0.05). Our results suggest that the basal opening state of coronary vascular KATP channels is activated to a greater extent in SHRs than WKY rats, which may contribute to the maintenance of basal myocardial perfusion in hypertrophied hearts.

Gender-specific cardiovascular adaptation due to circadian blood pressure variations in essential hypertension

To determine the effects of circadian variation in arterial pressure on early hypertensive target organ disease, we examined systemic hemodynamics (cardiac output by indocyanine green dye dilution), renal hemodynamics (renal plasma flow by iodine-131 para-aminohippuric acid clearance), left ventricular structure and function (2D-guided M-mode echocardiogram), and 24-h ambulatory blood pressure in 20 women and 46 men with untreated essential hypertension. Both gender groups were subdivided into "dippers" and "nondippers" according to the physiologic nocturnal decrease in mean arterial pressure by 10% of daytime values. Systemic and renal hemodynamics, neurohumoral findings (norepinephrine, epinephrine, dopamine, plasma renin activity), causal blood pressure values, duration of hypertension, and body weight did not differ between the two groups. In contrast, left ventricular mass and mass index was higher in female nondippers than dippers (255 +/- 68 v 184 +/- 81 g, and 137 +/- 30 v 102 +/- 39 g/m2, P < .05, respectively), while in men no significant differences were found (234 +/- 48 v 240 +/- 54 g, and 119 +/- 27 v 121 +/- 13 g/m2, P = NS, respectively). Relative wall thickness (0.45 +/- 0.06 v 0.39 +/- 0.06, P < .05) and posterior wall thickness (1.1 +/- 0.1 v 0.89 +/- 0.2 mm, P < .05) were also found to be greater in female nondippers than in dippers, whereas no significant differences were obtained in men. Thus, the degree of left ventricular hypertrophy correlated with the circadian blood pressure variations in women only, which indicates that left ventricular structure may be more load-dependent in women than in men with essential hypertension.

Functional explanation for increased atrial natriuretic peptide in systemic sclerosis.

We related atrial natriuretic peptide (ANP) among 30 consecutive patients with systemic sclerosis (SScl) and 48 gender- and age-matched controls to the measurements of left ventricular (LV) function as evaluated by echocardiography and external pulse curves to determine possible causative factors for an increased level of plasma ANP. The patients had a markedly elevated plasma ANP level (239.4 +/- 59 vs. 178.2 +/- 36 pmol/l, p < 0.0005), which was not related to LV systolic function, heart rate, or blood pressure. Patients had LV hypertrophy and plasma ANP correlated directly to interventricular septal thickness (r = 0.41, p < 0.005), LV posterior wall thickness (r = 0.32, p < 0.01), and wall thickness to cavity dimension (r = 0.44, p < 0.0005), LV mass index (r = 0.40, p < 0.005). LV early filling properties were impaired, with reduction of atrial emptying index (p < 0.0005) and increased contribution of atrial contraction to LV filling. Plasma ANP correlated to atrial emptying index (r = 0.41, p < 0.0005) and to apex-cardiographic a wave (r = 0.28, p < 0.05). Plasma ANP was also related to left atrial dimension index (r = 0.27, p < 0.05), and was still related to atrial emptying index, but not to left atrial dimension, when considering the degree of LV hypertrophy in multivariate analysis. We conclude that ANP is elevated in patients with SScl. Reduced LV compliance, probably due to increased fibrosis, may cause changes in atrial pressure sufficient to stimulate ANP production without systolic dysfunction as a prerequisite.

Left ventricular chamber dilatation in hypertrophic cardiomyopathy: related variables and prognosis in patients with medical and surgical therapy.

To determine the incidence and prognosis of left ventricular dilatation and systolic dysfunction in 139 patients with hypertrophic cardiomyopathy during long term follow up. Left ventricular chamber dilatation and systolic dysfunction (both together referred to as left ventricular chamber dilatation) were determined echocardiographically. Chamber dilatation was defined as an increase in the left ventricular end diastolic diameter of > 2% per year combined with a decrease in midventricular systolic fractional shortening of > 2% per year of follow up [10.3 (SD 6) years]. The predictive value for left ventricular chamber dilatation of clinical, invasive, and echocardiographic variables and its prognosis were assessed. In 119 of 139 individuals (86%), left ventricular chamber size and systolic function remained stable (group 1), and in 20/139 patients (14%) left ventricular chamber dilatation occurred during follow up (group 2). At baseline examination, symptoms such as dyspnoea and syncope occurred less often in group 1 than in group 2; New York Heart Association classification was lower in group 1 than in group 2 (P = 0.001). Left ventricular mass index relative to sex specific normal values was increased by 18% in group 1 and by 41% in group 2 (P = 0.04). Cumulative survival rates were slightly although not significantly higher in group 1 than in group 2. Event-free survival was significantly higher in group 1 than in group 2 (P < 0.05). (1) The development of left ventricular chamber dilatation and systolic dysfunction in hypertrophic cardiomyopathy occurs in approximately 1.5% of the patients per year. (2) Factors associated with left ventricular dilatation are dyspnoea, syncope, a higher functional classification, and a higher degree of left ventricular hypertrophy. (3) Patients with chamber dilatation have a worse prognosis than those without, particularly regarding quality of life.

Effects of hypertrophy and heart failure on [Na +] i in pressure-overloaded guinea pig heart

Intracellular free sodium levels ([Na+]i) were assessed with 23Na nuclear magnetic resonance (NMR) spectroscopy in isolated, Langendorff-perfused normal, compensated hypertrophied, and hypertrophied failing guinea pig hearts under several conditions. Baseline [Na+]i measured with a shift reagent was significantly greater than normal in the compensated hypertrophied hearts (12.8 +/- 1.2 mmol/L v 6.4 +/- 0.7 mmol/L, means +/- SEM, P < .01), but not in the hypertrophied failing hearts (8.7 +/- 1.9 mmol/L, P = N.S.). Moreover, the highest levels of [Na+]i were seen just 3 to 4 weeks after aortic constriction. [Na+]i was inversely related to both time after aortic constriction (R = -0.71, P < .03) and to the degree of left ventricular hypertrophy (R = -0.79, P < .01), suggesting that the hypertrophied failing heart is capable of maintaining relatively normal [Na+]i. In addition, triple quantum filtered NMR measurements were made to assess changes in [Na+]i subsequent to altered perfusion or loading conditions. In hypertrophied failing hearts, but not normal hearts, low coronary perfusion pressure (60 cm H2O) was associated with relatively higher [Na+]i (ANOVA, P < .05), suggesting greater sensitivity of hypertrophied failing hearts to hypoperfusion. On the other hand, when all hearts were perfused at 90 cm H2O and intraventricular balloon volume was increased from 100 microL to 300 microL, [Na+]i increased significantly only in the normal guinea pig hearts (12.3 +/- 1.8%, P < .01). These findings suggest complex changes in the expression or modulation of proteins involved in Na+ regulation. Interpretation regarding the physiological significance of these changes depends on the specific mechanism(s) proposed. Previous work in this and other models of hypertrophy suggest that changes in the number or activity of both Na(+)-K(+)-ATPase and Na(+)-Ca2+ exchange proteins are involved.

Structural cardiovascular alterations and blood pressure variability in human hypertension.

To evaluate the cardiovascular risk of hypertensive patients in relation to left ventricular hypertrophy, arteriolar hypertrophy and blood pressure variability, and the effects of antihypertensive treatment. In hypertensive subjects with marked left ventricular hypertrophy, cardiovascular problems are about three times more frequent than in hypertensives who do not have left ventricular hypertrophy. The evidence suggests, however, that a moderate degree of left ventricular hypertrophy may be compensatory and that regression of mild hypertrophy should not necessarily be pursued. An increased wall to lumen ratio leads to an increase in vascular resistance and thus promotes hypertension. Regression of this alteration with antihypertensive treatment appears to be both beneficial and achievable, although it is not clear whether all antihypertensive agents have the same effect. Moreover, there are methodological problems in determining whether a regression has actually been achieved. There is evidence to suggest that end-organ damage is more frequent and more marked in hypertensives with greater 24 h blood pressure variability. It appears that antihypertensive treatment does not easily reduce this variability, although the intermittent measurements taken by automatic monitoring devices do not fully reflect patterns of blood pressure variation. It may be that hypertensives with a greater degree of blood pressure variability can obtain a reduction in the magnitude of this variability with antihypertensive treatment.

Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM.

The determinants of left ventricular mass in normal control subjects and subjects with non-insulin-dependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects. Measurements of erythrocyte sodium-lithium counter-transport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26%) and 15 diabetic subjects (44%) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n = 21) had an elevated mean rate of sodium-lithium countertransport (0.40 +/- 0.13 vs 0.31 +/- 0.09 mmol.l-1.h-1; p < 0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57%) had elevated rates of sodium-lithium counter-transport compared to only seven (19%) of those without (p < 0.05). There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r = 0.35; F1.55 = 7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk.

Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM

The determinants of left ventricular mass in normal control subjects and subjects with non-insulindependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects. Measurements of erythrocyte sodium-lithium countertransport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26%) and 15 diabetic subjects (44%) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n=21) had an elevated mean rate of sodium-lithium countertransport (0.40±0.13 vs 0.31±0.09 mmol·l−1 ·h−1; p<0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57%) had elevated rates of sodium-lithium counter-transport compared to only seven (19%) of those without (p<0.05). There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r=0.35; F 1.55=7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk.

1030-10 The Severity of Left Ventricular Hypertrophy is Greater in Patients with Hypertrophic Cardiomyopathy Due to Malignant Mutations

Genotype-phenotype correlation studies have shown that β myosin heavy chain ( β MHC) mutations are determinants of frognosis in patients with hypertrophic cardiomyopathy (HCM). While Arg 719 Trp mutation is associated with a high incidence of sudden cardiac death (SCD) and an average life expectancy of 38 years, the Val 606 Met mutation is associated with a near normal life expectancy in the families studied here. However, it is unknown whether the prognostic significance of HCM mutations correlates with the degree of left ventricular hypertrophy (LVH) associated with each mutation. Accordingly, we determined the left ventricular mass index (LVMI) and the extent of LVH in 12 patients with the Arg 719 Trp mutation and five patients with the Val 606 Met mutation. Left ventricular mass was derived by the arealength method using 2-D echocardiograms and indexed for body surface area (BSA). Extent of LVH was determined using a semi-quantitative point score method that takes into account the extent of involvement of the septum, apex, and lateral wall of the left ventricle. The mean LVMI was 147.0 ± 36 g/m 2 in patients with the Arg 719 Trp mutation and 111.7 ± 19 g/m 2 in patients with the Val606 Met mutation (p = 0.020). Similarly the extent of hypertrophywas greater in patients with the Arg 719 Trp mutation than in those with the Val 606 Met mutation (5.92 ± 2.3 vs. 3.2 ± 1.5, respectively, p = 0.015). The mean septal thickness was also greater in patients with the Arg 719 Trp mutation than in those with the Val60 Met mutation, however, this was not statistically significant (2.03 ± 0.7 vs. 1.62 ± 0.26, p = 0.095). There was no difference in the mean BSA, age, or gender among the two groups of patients. In conclusion, HCM patients, due to a malignant mutation such as the Arg 719 Trp, have greater LVH than patients with a benign mutation such as the VaI 606 Met. These results indicate the grave prognosis of HCM mutations are associated with expression of greater hypertrophy. This provides an easily detectable clinical parameter to further stratify patients at risk of sudden death that are candidates for invasive interventions such as implantation of cardiac defibrillators.

Intracoronary angiotensin-converting enzyme inhibition improves diastolic function in patients with hypertensive left ventricular hypertrophy.

There is increasing recognition of myocardial angiotensin-converting enzyme, which is induced with the development of left ventricular hypertrophy (LVH). The potential physiological significance of subsequent increased angiotensin I to II conversion in the presence of LVH is unclear but has been postulated to cause abnormal Ca2+ handling and secondary diastolic dysfunction. Accordingly, we hypothesized that acute angiotensin-converting enzyme inhibition would result in decreased production of angiotensin II and improved active (Ca(2+)-dependent) relaxation in patients with hypertensive LVH. Intracoronary (IC) enalaprilat was administered to 25 patients with and without LVH secondary to essential hypertension. Indexes of diastolic and systolic LV function were determined from pressure (micromanometer)-volume (conductance) analysis at steady state and with occlusion of the inferior vena cava. Patients were divided into those receiving high- (5.0 mg, n = 15) and low-dose (1.5 mg, n = 10) IC enalaprilat during a 30-minute infusion at 1 mL/min. The high-dose patients were further divided along the median normalized LV wall thickness of 0.671 cm/m2. The time constant of isovolumic relaxation (TauL) was prolonged at baseline in patients receiving high-dose enalaprilat with wall thickness > 0.671 cm/m2 (TauL, 56 +/- 2 versus 44 +/- 2 and 45 +/- 2 milliseconds, respectively, P < .01 by ANOVA) and shortened only in this patient group (TauL, 49 +/- 3 versus 46 +/- 2 and 43 +/- 2 milliseconds, respectively, P < .01 versus baseline and other groups by ANOVA). The improvement in TauL was directly proportional to the degree of LVH (r = .92, P < .001). Although there was a decrease in LV end-diastolic pressure (23 +/- 2 to 15 +/- 1 mm Hg, P < .01) and volume (86 +/- 8 to 67 +/- 9 mL/m2, P < .05) in those patients with a reduction in TauL, this is due to movement down a similar diastolic pressure-volume relation with no change in chamber elastic stiffness (0.023 +/- 0.002 to 0.025 +/- 0.004 mL-1, P = NS). Intracoronary enalaprilat resulted in an improvement in active (Ca(2+)-dependent) relaxation in those patients with more severe hypertensive LVH. The improvement in active relaxation was directly proportional to the severity of LVH. These results support the hypothesis that the cardiac renin-angiotensin system is an important determinant of active diastolic function in hypertensive LVH.

Racial differences in myocardial ischemia and coronary flow reserve in hypertension

Objectives. Using invasive measurements of endothelium-independent coronary flow reserve and stress thallium testing with or without dipyridamole, this study investigated racial differences in ischemia and coronary reserve in hypertensive left ventricular hypertrophy.Background. African Americans compared with Caucasian Americans appear to have a higher case fatality from coronary heart disease but lesser amounts of atherosclerotic coronary artery disease. This paradox may be explainable by intrinsic or acquired racial differences in coronary arteriolar autoregulation and vasoreactivity.Methods. The study enrolled 91 African and 81 Caucasian Americans referred for cardiac catheterization because of suspected myocardial ischemia but found to have no significant coronary stenosis. Patients were stratified by degree of left ventricular hypertrophy for comparison purposes after calculation of indexed left ventricular mass by means of echocardiographic M-mode measurements. Coronary flow reserve measurements were made using the intracoronary Doppler catheter and hyperemic doses of intravenous dipyridamole in 100 patients and intracoronary papaverine and adenosine in 72 patients. Seventyseven percent of patients underwent adequate stress thallium testing with or without dipyridamole.Results. In African Americans, mean (±SD) coronary flow reserve decreased from 4.4 ± 2.3 for 38 without mass hypertrophy to 3.2 ± 1.3 for 53 with hypertrophy (p = 0.005) to 2.7 ± 1.1 for 12 with severe hypertrophy (p = 0.02). Thallium testing was abnormal in 31% of those without mass hypertrophy and 59% of those with hypertrophy. In Caucasian Americans, coronary flow reserve decreased from 4.1 ± 2 for 58 without hypertrophy to 3.6 ± 1.5 for 23 with hypertrophy (p = NS) to 3 ± 1.5 for 6 with severe hypertrophy (p = NS). Thallium testing was abnormal in 36% without mass hypertrophy and in 39% with hypertrophy.Conclusions. This study establishes that development of left ventricular hypertrophy in hypertension carries greater physiologic morbidity for African compared with Caucasian Americans, typified by marked reduction in endothelium-independent coronary flow reserve and increased frequency of abnormal thallium tests.

Hypertension in blacks.

In the United States, blacks have higher blood pressure levels than whites at all ages, a finding that cannot be explained solely by differences in body habitus. A European population survey reported similar differences. Several physiologic mechanisms have been evaluated, including sodium sensitivity and insulin resistance. Although it is often stated that blacks show a greater blood pressure reactivity than whites, recent data are conflicting, and such differences may be attributable to family history of hypertension. The physiologic mechanisms underlying any reactivity differences could be structural changes in the resistance vessels. Blacks tend to show smaller falls of nocturnal blood pressure than whites, and this could be related to the observation of a greater degree of left ventricular hypertrophy seen in blacks for a given level of clinic blood pressure. Severe left ventricular hypertrophy may be associated with functional myocardial ischemia, even in the absence of epicardial coronary artery disease. Renal damage is also more pronounced in blacks than in whites.

Evaluation of left atrial contribution to left ventricular filling in aortic stenosis by velocity-encoded cine MRI

Velocity-encoded cine MRI (VEC-MRI) can measure volume flow at specified sites in the heart. This study used VEC-MRI to measure flow across the mitral valve to compare the contribution of atrial systole to left atrial filling in normal subjects and patients with left ventricular hypertrophy. The study population consisted of 12 normal subjects (mean age 34.5 years) and nine patients with various degrees of left ventricular hypertrophy resulting from aortic stenosis (mean age 70 years). VEC-MRI was performed in double-oblique planes through the heart to measure both the mitral inflow velocity pattern (E/A ratio) and the volumetric flow across the mitral valve. The left atrial contribution to left ventricular filling (AC%) was calculated. The results were compared with Doppler echocardiographic parameters. The VEC-MRI-derived mitral EA ratios showed a significant linear correlation with EA ratios calculated from Doppler echocardiography ( r = 0.94), and the VEC-MRI-derived E/A ratios (2.1 ± 0.5 vs 1.0 ± 0.4) and AC% values (24.9 ± 7.2 vs 45.7 ± 16.4) were significantly different between normal subjects and patients with aortic stenosis ( p < 0.01 in both groups). The same differences were seen in the Doppler echocardiographic parameters. The VEC-MRI-derived E/A ratio and AC% showed significant hyperbolic and linear correlations with left ventricular mass indexes ( r = 0.95 and 0.86). In addition, the VEC-MRI-determined E/A ratio and the volumetric AC% displayed a highly significant hyperbolic correlation ( r = 0.95). Thus VEC-MRI can be used to evaluate left ventricular diastolic filling characteristics in normal subjects and patients with abnormalities of diastolic filling.

Autonomic function in hypertrophic cardiomyopathy.

Autonomic dysfunction has been found to be a powerful predictor of arrhythmic events and sudden death after myocardial infarction. Hypertrophic cardiomyopathy carries a risk of sudden death and this risk is increased by the occurrence of syncope. To determine if autonomic dysfunction occurs in patients with hypertrophic cardiomyopathy and if it is associated with the occurrence of syncope. Autonomic function was measured in 30 patients with hypertrophic cardiomyopathy, 15 with and 15 without a history of syncope, and in 28 healthy volunteers. Tests of parasympathetic activity showed that the mean (SD) variation in heart rate during deep breathing was reduced in patients compared with controls, 17 (9) v 22 (9) beats/min, p = 0.03, the Valsalva ratio was also reduced in patients, 1.52 (0.33) v 1.70 (0.36), p = 0.05 but the immediate heart rate response to standing, the 30:15 ratio, was similar in both groups. Tests of sympathetic activity--namely the diastolic blood pressure response to sustained handgrip and the change in systolic blood pressure on standing--did not differ between patients and controls. There was no significant difference in autonomic function between patients with and without a history of syncope. A secondary predetermined analysis showed that the degree of impairment in variation of heart rate with breathing was correlated with the severity of left ventricular hypertrophy, r = 0.39, p = 0.03. Patients with hypertrophic cardiomyopathy have a selective impairment of variability of heart rate with deep breathing and the Valsalva manoeuvre indicating decreased cardiac parasympathetic activity. The data suggest that the afferent limb of these reflexes is impaired and that the severity of impairment is related to the degree of left ventricular hypertrophy.