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PubMedDate not supplied

Effects of captopril on left ventricular structure and function in SHR with established hypertension.

While antihypertensive therapy is considered to be an important clinical intervention in hypertensive patients, its effects on cardiac structure and function have not been intensely evaluated. In this study we tested the hypotheses that lowering blood pressure (BP) with the angiotensin I-converting enzyme inhibitor captopril, would: 1) normalize left ventricular mass and increase the cardiocyte mitochondria/myofibrils volume (Vmito/Vmyo) ratio; and 2) not compromise peak ventricular performance. We treated 16-week-old SHR and WKY with captopril (40-80 mg/kg) and hydrochlorothiazide (500 mg/l) via their drinking water. After six weeks of treatment peak cardiac performance was measured during rapid volume overload. Tissue samples from the left ventricular wall were analyzed by electron microscopy and stereology. Captopril lowered BP in SHR and WKY but had no affect on the left ventricular/body weight ratio. The only intracellular change in treated SHR was an increase in sarcoplasmic volume density. Treated WKY exhibited decreased midmyocardial mitochondrial volume density. At peak cardiac output, acceleration of flow and cardiac index were not affected by treatment. Stroke work at peak cardiac output was decreased in the treated groups due to a decrease in mean arterial pressure. In addition, captopril treatment resulted in a shift of the cardiac output (CO)-left ventricular end diastolic pressure (LVEDP) curves, such that LVEDP at peak cardiac output was approximately 50% less in the treated groups compared to their respective control groups. Although captopril was efficacious in lowering BP, it is suggested that lowering BP with this agent does not, at least within six weeks, lead to a reversal of hypertrophy or to a significant alteration in the volume densities of myofibrils and mitochondria. However, an important effect of this antihypertensive drug which may be of clinical significance, is that it leads to a leftward shift of the CO-LVEDP curve in both hypertensive and normotensive rats.

Animals↗
PubMed1987

Myocardial structure and left ventricular function in hypertrophic and dilative cardiomyopathy and aortic valve disease.

Left ventricular biopsies from 126 patients with advanced (EF less than 50%, n = 45) and mild (EF 50-60%, n = 21) and latent cardiomyopathy (EF greater than 60%, n = 60) and 18 additional patients with aortic valve disease and 22 cases with hypertrophic cardiomyopathy were analyzed to define possible correlations between myocardial structure and function. Deterioration of ventricular function was combined with increasing muscle cell diameters (r = 0.47) and increasing nuclear size of the myocytes (r = 0.74) in latent and dilative cardiomyopathies and in patients with aortic valve disease (cell diameter, r = 0.6; nuclear size, r = 0.9). Patients with HCM showed a wide range of cell diameter and nuclear size. 24% of the latter patients had no bioptic evidence of myocardial hypertrophy. The mitochondrial volume of the myocytes was 23% in the normal and hypertrophied myocardium independent of the kind of disease and ventricular function. The volume fraction of the myofibrils continuously decreased with worsening of the left ventricular function in patients with latent and dilative cardiomyopathy (from 45 +/- 6.9 to 37.6 +/- 6.3%) and aortic valve disease (from 46.2 +/- 3.4 to 27.9 +/- 9.3%). Patients with hypertrophic cardiomyopathy presented with normal or slightly decreased values of myofibrils consistent with normal ventricular function (42.5 +/- 5.0). The data demonstrate that the degree of myocardial hypertrophy and certain ultrastructural findings are inversely correlated with left ventricular function.

Aortic Valve↗
PubMedDate not supplied

The limited utility of the plain chest film in the assessment of left ventricular structure and function.

The determination of radiographic cardiac size as an estimation of the state of cardiac function is one of the more common correlations made. Despite the widespread use of these measurements, the correlation between cardiac function and radiographic appearance, and the validity of clinical judgments based on this correlation, has not been fully determined. Similarly, the increment in left ventricular chamber size necessary to produce a change in the plain film appearance of the left ventricle has not been defined. The results of a two observer, blind, retrospective analysis of plain film radiographs of the chest, and related quantitative left ventricular angiograms, and left ventricular pressure studies performed on 256 patients is presented. The sensitivity, speficity, predictive value and accuracy of six previously described plain film measurements of left ventricular size together with determinations of the extent of left ventricular volume change necessary to produce a perceptible change in the plain film radiographic appearance of the left ventricle are reported. The performance of each of these measurements proved to be disappointing. A sensitivity of 75% was not possible using any of the methods unless the left ventricular chamber volume was more than 66% above the upper limit of normal.

Cardiac Volume↗
PubMedDate not supplied

[Changes in left ventricular function and structure in hypertensive patients treated with methyldopa and urapidil].

In a randomized cross-over and double-blind trial twenty mild-to-moderate hypertensives (11 males, 9 females, mean age 48.4 +/- 7.6 years) were receiving methyldopa (250 mg b.i.d.) or urapidil (30 mg b.i.d.) for 7 weeks and then treated with alternative drug for additional 7 weeks, separated by one week of wash-out period. Both antihypertensives induced significant reduction (P less than 0.01) in systolic and diastolic arterial pressure, while no significant changes (P greater than 0.20) in the body weight and the heart rate were observed. The echocardiographic features of left ventricular hypertrophy (LVH) did not decrease significantly (P greater than 0.05) on either drug, except for the left ventricular posterior wall thickness (LVPWd), which decreased on methyldopa from 10.4 +/- 1.3 to 9.8 +/- 1.4 mm (P less than 0.05). The drugs under study did not change significantly the echocardiographic indices of left ventricular function. Echocardiography resulted to be more sensitive in detecting LVH than electrocardiography. It is concluded that methyldopa might successfully reduce LVH, while direct and indirect vasodilators (such as urapidil) are less effective.

Adult↗
PubMed1992

Comparison of the effects of isradipine and lisinopril on left ventricular structure and function in essential hypertension.

The effects on cardiac structure and function of antihypertensive regimens with different effects on the renin-angiotensin system were compared. In a 1-year study, 32 patients with essential hypertension were randomized to treatment with either the converting enzyme inhibitor lisinopril or the calcium antagonist isradipine; hydrochlorothiazide could be added. Blood pressure (BP) decreased significantly (p less than 0.001) and similarly in the 2 treatment groups. Left ventricular (LV) mass was already significantly reduced after 16 weeks of treatment (p less than 0.001) and remained decreased thereafter, with no difference in the response to the 2 treatment regimens. The change in LV mass was related to the decrease in systolic BP for the total study group (p less than 0.001) and for each treatment group separately. During the 3-week run-out period on placebo, BP and LV mass increased again (p less than 0.01). Afterload decreased during active treatment (p less than 0.001), and fractional shortening of the LV internal diameter was significantly increased (p less than 0.01) to a similar extent in both groups. The ratio of peak mitral flow velocities during atrial contraction and early filling was reduced after 1 year of active treatment in the total study group (p less than 0.01); this change was similar in both groups. The data suggest that the regression of LV mass during antihypertensive therapy is mainly related to the decrease in systolic BP.

Adult↗
PubMed1998

Left ventricular structure and function in children infected with human immunodeficiency virus: the prospective P2C2 HIV Multicenter Study. Pediatric Pulmonary and Cardiac Complications of Vertically Transmitted HIV Infection (P2C2 HIV) Study Group.

BACKGROUND: The frequency of, course of, and factors associated with cardiovascular abnormalities in pediatric HIV are incompletely understood. METHODS AND RESULTS: A baseline echocardiogram (median age, 2.1 years) and 2 years of follow-up every 4 months were obtained as part of a prospective study on 196 vertically HIV-infected children. Age- or body surface area-adjusted z scores were calculated by use of data from normal control subjects. Although 88% had symptomatic HIV infection, only 2 had CHF at enrollment, with a 2-year cumulative incidence of 4.7% (95% CI, 1.5% to 7.9%). All mean cardiac measurements were abnormal at baseline (decreased left ventricular fractional shortening [LV FS] and contractility and increased heart rate and LV dimension, mass, and wall stresses). Most of the abnormal baseline cardiac measurements correlated with depressed CD4 cell count z scores and the presence of HIV encephalopathy. Heart rate and LV mass showed significantly progressive abnormalities, whereas FS and contractility tended to decline. No association was seen between longitudinal changes in FS and CD4 cell count z score. Children who developed encephalopathy during follow-up had depressed initial FS, and FS continued to decline during follow-up. CONCLUSIONS: Subclinical cardiac abnormalities in HIV-infected children are common, persistent, and often progressive. Dilated cardiomyopathy (depressed contractility and dilatation) and inappropriate LV hypertrophy (elevated LV mass in the setting of decreased height and weight) were noted. Depressed LV function correlated with immune dysfunction at baseline but not longitudinally, suggesting that the CD4 cell count may not be a useful surrogate marker of HIV-associated LV dysfunction. However, the development of encephalopathy may signal a decline in FS.

AIDS Dementia Complex↗
PubMed1986

Left ventricular structure and function in normotensive adolescents with a genetic predisposition to hypertension.

It has been suggested that the heart plays an active role in the pathogenesis of arterial hypertension. If this is true, there must be early cardiac involvement in young normotensive subjects who develop hypertension later in life and differences in cardiac morphology or function may exist between young normotensive subjects with different risks of developing hypertension. M-mode echocardiography was performed in 51 normotensive male adolescents with at least one hypertensive parent (SHT). These subjects were compared with 55 normotensive sons of normotensive parents (SNT) and with 25 adolescents with borderline hypertension (BH). Control groups were matched for sex and age. The following morphologic parameters were significantly greater in the SHT group than in the SNT group: interventricular septum (0.54 +/- 0.08 vs 0.49 +/- 0.09 cm/m2; p less than 0.01) and posterior wall (0.54 +/- 0.11 vs 0.50 +/- 0.08 cm/m2; p less than 0.05) thickness, left ventricular mass (125.0 +/- 29.1 vs 109.2 +/- 25.4 gm/m2; p less than 0.005), and cross-sectional area (9.9 +/- 1.8 vs 8.9 +/- 1.6 cm2/m2; p less than 0.005). No significant differences between SHT and BH subjects were observed. Excursion of left ventricular posterior wall was significantly higher in the BH group. No differences were observed between SHT and SNT subjects. These data show that the same kinds of changes in cardiac morphology are present in normotensive subjects with a family history of hypertension and in subjects with borderline hypertension, suggesting that cardiac involvement may precede elevation of blood pressure.

Adolescent↗
PubMed1989

Assessment of left ventricular structure and function by cross sectional echocardiography.

Cross sectional echocardiography can be used to give semiquantitative estimates of ventricular volumes and ejection fraction which are very valuable in detecting the severe abnormalities seen clinically. The technique has also been widely used to study regional abnormalities of wall motion. However, with a frame rate of 30 s-1 and lateral resolution of 3-4 mm critical analysis of disturbances of timing is not possible, so the method should be used in conjunction with M-mode and Doppler techniques. In spite of physical limitations, based on the underlying mechanisms of image generation, its advantages of real time application and noninvasive nature, its ability to demonstrate myocardial thickness as well as echo intensity, and its relative cheapness have made cross sectional echocardiography a major tool in documenting abnormalities of left ventricular function occurring in disease.

Cardiac Volume↗
PubMed1998

Relation of left ventricular midwall function to cardiovascular risk factors and arterial structure and function.

Left ventricular (LV) midwall shortening (MWS) is subnormal in relation to LV circumferential end-systolic stress (ESS) (ESS-corrected MWS) in many hypertensive patients with normal LV chamber function and predicts subsequent morbidity and mortality. However, little is known of the relations of LV midwall function to demographic and metabolic variables or to arterial geometry. Asymptomatic, unmedicated normotensive (n=366) or hypertensive (n=282) adults were assessed with echocardiography and carotid ultrasound. In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P<.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03). Among hypertensive patients, lower values for both midwall function indices were associated independently with higher peripheral resistance (P<.00001), heart rate (P<.00005), body mass index (P<.01), and arterial RWT (P=.04), as well as male gender (P<.0002). In the entire population, lower LV MWS was independently related to higher peripheral resistance, heart rate (both P<.00001), body mass index (P=.0006) and arterial RWT (P=.009); male gender (P<.00001); and lower age (P=.004), diastolic pressure (P=.042), and systolic carotid artery expansion (P=.032). Lower ESS-corrected MWS in the entire population was independently associated with higher peripheral resistance and heart rate (both P<.00001), body mass index (P=.0006), arterial RWT (P=.004); male gender; and lower diastolic pressure (both P<.00001), age (P<.00005), arterial expansion in systole (P=.006), and serum HDL cholesterol levels (P=.04). Among a subset (n=60), ESS-corrected MWS was positively related to apolipoprotein A1 (P=.004) and negatively to hemoglobin A1c (P<.01). Thus, higher LV midwall function is associated with female gender and more favorable profiles of hemodynamics, metabolic pattern, and arterial structure and function.

Apolipoproteins↗
PubMed1985

Chronic exercise and left ventricular structure and function in healthy human subjects.

Twelve healthy well-trained participants in a supervised exercise program (mean age, 41.3 yr) were compared with 12 sedentary control subjects (mean age, 38.9 yr) with physical characteristics similar to the exercised group (EG) before training. Resting echocardiograms revealed significantly lower heart rates (HR) in the EG compared with control group (CG) but no evidence for cardiac structural differences between groups. Radionuclide angiograms performed at rest and during two levels of supine cycling (HR targets: 120 and 140 beats X min-1) resulted in increases in background-corrected end-diastolic counts [EDC(bc)] and confirmed use of the Frank-Starling mechanism in the majority of subjects. Mean values (+/- SD) for ejection fraction (EF) and normalized peak systolic ejection rate (PSER) (P greater than 0.05 between groups) were the following. (Formula: see text) The results suggested that fitness training does not induce significant cardiac enlargement as apparent from measurements at rest or important changes in contractile state during exercise. Increases in exercise stroke volume with such training may be the result of an increased end-diastolic volume.

Adult↗
PubMed1990

Premature ventricular complex morphology. A marker for left ventricular structure and function.

The shape of a premature ventricular complex (PVC) might reflect the presence or absence of myocardial disease. To test this, 100 patients with a PVC on a 12-lead electrocardiogram at cardiac catheterization or nuclear angiography were classified according to PVC morphology. Group 1 (n = 50) had PVC QRS complexes with either smooth and uninterrupted contour or with narrow (less than 40 msec) notching. Group 2 (n = 50) demonstrated PVC with broad (greater than or equal to 40 msec) notching or shelves. Clinical, electrocardiographic and angiographic variables were assessed to define group differences. All patients had one or more etiological forms of heart disease none of which distinguished either group. Groups 1 and 2 differed with respect to a history of congestive heart failure (12% vs. 66%, p = 0.0004), dilated cardiomyopathy (2% vs. 38%, p = 0.0005), and the presence of mitral regurgitation (13% vs. 58%, p = 0.001), respectively. In group 1, 45 of 50 (90%) patients with a PVC had no notching. Patients in group 2 had greater PVC QRS duration as compared with patients in group 1 (181 +/- 6 vs. 134 +/- 3 msec, p = 0.0001). End-diastolic volume index (EDVI) (78 +/- 3 vs. 139 +/- 11 ml/m2, p = 0.0000) and ejection fraction (EF) (0.59 +/- 0.02 vs. 0.34 +/- 0.03, p = 0.0000) significantly discriminated between group 1 and 2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults.

OBJECTIVES: The present study sought to determine whether conduit artery structure and function vary according to the pattern of left ventricular adaptation to hypertension. BACKGROUND: Although left ventricular geometric pattern has been shown to predict cardiovascular events in hypertension, the arterial status in patients with the different patterns is unknown. METHODS: We evaluated arterial structure and function by carotid ultrasound and applanation tonometry in 271 unmedicated hypertensive patients classified by echocardiography as having normal ventricular geometry (n = 176), concentric remodeling (n = 54), concentric hypertrophy (n = 16) or eccentric hypertrophy (n = 25). RESULTS: All groups were similar in age, gender distribution and body size. Patients with concentric and eccentric hypertrophy had similar blood pressures (mean 173/100 and 171/99 mm Hg, respectively) and left ventricular mass, but compared with patients with normal left ventricular geometry and concentric remodeling, only those with concentric hypertrophy had increased arterial wall thickness (0.96 +/- 0.20 vs. 0.80 +/- 0.18 mm, p < 0.05), end-diastolic diameter (6.38 +/- 0.97 vs. 5.76 +/- 0.87 mm, p < 0.05), cross-sectional area (22.1 +/- 5.71 vs. 16.6 +/- 5.4 mm(1)2 p < 0.05) and elastic modulus (713 +/- 265 vs. 471 +/- 241 dynes/cm2 x 10(-5), p < 0.05). Patients with concentric remodeling and eccentric hypertrophy had similar values for these measures (0.85 +/- 0.22 and 0.89 +/- 0.21 mm, 5.67 +/- 0.77 and 6.04 +/- 0.44 mm, 17.2 +/- 5.4 and 19.7 +/- 5.9 mm2, 558 +/- 263 and 614 +/- 257 dynes/cm2 x 10(-6), respectively), despite lower systolic blood pressures in the former group (156/94 mm Hg, p < 0.001). The prevalence of plaque was comparable in patients with concentric (56%) and eccentric (42%) hypertrophy and significantly greater than that in patients [corrected] with normal geometry (21%). CONCLUSIONS: Among patients with generally mild, uncomplicated systemic hypertension, arterial structure and function are most abnormal when concentric left ventricular hypertrophy is present and may contribute to the more adverse outcome associated with this geometric pattern.

Adaptation, Physiological↗
PubMed1984

Left ventricular function and myocardial structure in aortic valve disease before and after surgery.

47 patients with aortic valve disease were studied by left ventricular micromanometry and cineangiography before and 18 months after successful valve replacement. There were 27 patients (17 with aortic stenosis, ten with aortic insufficiency) with moderate hypertrophy (angiographic mass less than 180 g/m2) and 20 patients (ten with aortic stenosis, ten with aortic insufficiency) with severe hypertrophy (angiographic mass greater than or equal to 180 g/m2). In the patients with moderate hypertrophy ejection fraction was slightly although not significantly smaller than in 14 controls. Peak systolic circumferential wall stress was, however, significantly increased. In the patients with severe hypertrophy ejection fraction was significantly decreased although afterload was similar to that in the patients with moderate hypertrophy. This indicated a depressed contractile state in the patients with mass exceeding 180 g/m2. After surgery peak systolic wall stress returned to normal levels in both groups. Among the patients with severe preoperative hypertrophy only the patients with aortic stenosis showed a normal ejection fraction after surgery, whereas in the patients with aortic insufficiency ejection fraction improved but remained depressed compared to the controls. In a second study, comparison of left ventricular function with myocardial structure (endomyocardial biopsies) was carried out in 30 patients with aortic valve disease (group 1: 18 with aortic stenosis, group 2: twelve with aortic insufficiency). Both groups were restudied 18.8 and 17.4 months, respectively, following successful aortic valve replacement. Preoperative biplane ejection fraction (60 and 57%), angiographic mass (183 and 186 g/m2), muscle fibre diameter (31.1 and 30.8 mu), interstitial fibrosis (17.1 and 17.4%) and left ventricular fibrous content (31.0 and 32.2 g/m2) were similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Stenosis, Subvalvular↗