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At least 19 recordsLinked to original sources

PubMed1989

A case of atrial septal defect combined with hypertension and left ventricular hypertrophy. Left ventricular failure induced by balloon occlusion and the effect of nifedipine.

A 46 year old woman with hypertension and left ventricular hypertrophy accompanied by an atrial septal defect is reported. Hemodynamic changes induced by balloon occlusion and concomitant nifedipine were studied. Left ventricular failure appeared after balloon closure of the defect. Nifedipine decreased the increment in left ventricular end-diastolic pressure induced by balloon occlusion. After the reduction of systemic vascular resistance, the ratio of intracardiac shunt flow was still larger. Surgical closure of the defect was performed and the postoperative course was good with the use of vasodilators.

Blood Pressure↗

PubMed1990

[Ventricular arrhythmia in patients with hypertension and left ventricular hypertrophy].

Left ventricular hypertrophy is a problem in itself in patients with hypertension. Hypertensives with left ventricular hypertrophy have a higher incidence of ventricular arrhythmias and sudden death. This article reviews the epidemiological evidence in favour of this association. Although the mechanism of ventricular arrhythmias in patients with left ventricular hypertrophy in unclear, several hypotheses have been suggested including cellular electrophysiological changes, alterations of the myocardial tissue and silent myocardial ischemia. The management of ventricular arrhythmias in hypertensive patients implies an effort to prevent left ventricular hypertrophy by early and aggressive treatment and a judicious choice of antihypertensive agents capable of reducing left ventricular hypertrophy. It is also important to avoid hypokalemia and other electrolytic disorders. Antiarrhythmic drugs should be reserved for symptomatic patients who do not respond to other preventive measures.

Arrhythmias, Cardiac↗

PubMed1991

Circadian blood pressure pattern in patients with treated hypertension and left ventricular hypertrophy.

Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P less than 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.

Antihypertensive Agents↗

PubMed1992

Reversibility of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a powerful independent risk factor for coronary artery disease. This overview of 104 studies examines the ability of various types of antihypertensive therapies to reverse LVH as assessed by echocardiography. Combination therapy, angiotensin converting enzyme (ACE) inhibitors, and methyldopa were the most effective in reversing LV mass; vasodilators such as minoxidil and hydralazine had no effect on LVH. These differences were independent of the degree of fall in blood pressure and duration of therapy. beta-blockers were as effective as ACE inhibitors in decreasing LV wall thickness. Possible reasons for drug differences in reversing LVH are discussed. Preliminary evidence suggests that reversing LVH by antihypertensive drug therapy is associated with a reduction in cardiovascular complications.

Antihypertensive Agents↗

PubMed1992

Effect of diuretic therapy on hypertensive left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) has been identified as a major independent risk factor for cardiovascular morbidity in patients with essential hypertension. It is also established that antihypertensive drug therapy is associated with regression of LVH in many patients. However, it is unclear whether all antihypertensive agents are equally effective in regressing LVH and whether this process is drug-specific or primarily related to blood pressure control. There is no universal agreement on the influence of diuretics on LVH in hypertension. Several major trials have shown consistent reversal of electrocardiographic manifestations of LVH during diuretic-based therapy. The results of studies employing echocardiographic measurements have been more variable; however, most echocardiographic studies have been flawed by lack of controls or blinding, short duration of follow-up, small sample size, inclusion of patients without LVH, and lack of consideration of previous or concomitant therapy. This review provides a critical examination of the available data on both sides of the question.

Diuretics↗

PubMed1992

ACE inhibitors and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a common condition and a powerful independent risk factor for coronary heart disease, congestive heart failure, and other cardiac morbidity. It is associated with the male sex and advancing age. Its most common cause is hypertension, and many antihypertensive agents induce regression of LVH. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reverse LVH by a mechanism as yet unknown. Reduction in afterload and other hemodynamic abnormalities by reduction of blood pressure is clearly a factor, but ACE inhibitors also block adrenergic action and other sympathetic nervous system influences, and the reduction in angiotensin II produces many effects. By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Angiotensin II promotes protein synthesis in myocardial myocytes, and blocking this action may arrest the hypertrophic process. To determine the effect of angiotensin II on LVH and normalization of LV function, a study is now underway evaluating the effects of lisinopril, a new lysine analog of enalapril, and a diuretic agent in the treatment of hypertension LVH.

Adult↗

PubMed1990

Improvement in left ventricular hypertrophy and left ventricular diastolic function following verapamil therapy in mild to moderate hypertension.

We evaluated the effect of verapamil therapy on left ventricular hypertrophy and left ventricular diastolic function in 13 patients with mild to moderate hypertension. Left ventricular hypertrophy was determined by M-mode echocardiographic measurements of interventricular septal thickness (IVST), posterior wall thickness (PWT) and left ventricular mass index (LVMI) both before (T0) and after 3 months (T3) of verapamil therapy. Left ventricular diastolic transmitral flow was measured by pulsed Doppler indices of early (E) and atrial (A) velocity, E/A ratio, total area (Ta), A area (Aa), Aa/Ta ratio, E-pressure half-time (E-PHT). A-pressure half-time (A-PHT) and E-PHT/A-PHT ratio both before and after 3 months of verapamil therapy. No significant changes occurred in mean heart rate, systolic function or body weight. We conclude that 3 months' therapy with verapamil resulted in an improvement in left ventricular hypertrophy and left ventricular diastolic function and a normalization of blood pressure, without a corresponding deterioration in left ventricular systolic function.

Adult↗

PubMedDate not supplied

Transmural distribution of myocardial blood flow and of coronary reserve in canine left ventricular hypertrophy.

Left ventricular hypertrophy was induced by banding of the ascending aorta in pupies at the age of 6 weeks. At the age of one year left ventricular weight per body weight was increased by 87% compared to control litter mates. While myocardial perfusion and myocardial oxygen consumption per 100 g were identical in the hypertrophy and control group, there was a significantly diminshed ratio of subendocardial/subepicardial flow in the hypertrophy group during moderate exercise. With maximal coronary dilation subendocardial diastolic resistance (mm Hg/ml-min-1 per 100 g) was 0.16 +/- 0.03 in the control group and 0.26 +/- 0.03 in the hypertrophy group. This diminished coronary reserve indicates an insufficient growth of the vascular bed in these hypertrophied hearts.

Animals↗

PubMed1986

Nuclear magnetic resonance spectroscopy of rat ventricles following supravalvar aortic banding. A model of left ventricular hypertrophy.

Left ventricular hypertrophy produced by supravalvar aortic banding in infant rats was studied by proton magnetic resonance spectroscopy. Weight gain at 11 weeks of age in the 11 male Sprague-Dawley rats with aortic bands placed at three weeks was similar to that of the 14 controls. The left ventricle of banded rats hypertrophied, increasing the ratio of left ventricle plus septum to body weight (LV + S/BW) by more than 50% (P less than .00001). Right ventricular weight (RV/BW) increased slightly (P less than .03). T1 and T2 relaxation times of LV + S, RV, and thigh muscle (Th) from the banded and control rats were compared. The T2 value distinguished hypertrophied from control LV + S (P less than .003), but not between RV or Th from the two groups. For banded rats only, the T2 value distinguished each muscle type: LV + S from RV, LV + S from Th, and RV from Th (P less than .00001 for each). For control rats, cardiac muscle was distinguished from Th (P less than .00001), but LV + S and RV were similar. The T1 value did not distinguish either the banded from the control group or any of the muscle types. Percent water content was similar for all tissues. Any correlation between water content and T1 or T2 was inconsistent or weak.

Animals↗

PubMed1990

Effects of indapamide on left ventricular mass and function in systemic hypertension with left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is frequently associated with hypertension and constitutes a major cardiovascular risk factor, the reduction of which should be considered when initiating antihypertensive therapy. To assess the effects of indapamide on LVH, 18 hypertensive patients were included in the study (11 men and 7 women, age 53.6 +/- 2.9 years, mean +/- standard deviation) whose supine diastolic blood pressure was greater than 95 mm Hg without (n = 11) or with (n = 7:6 beta blockers, 1 calcium antagonist) antihypertensive therapy. All presented with LVH, echocardiographically defined by a left ventricular mass index greater than 110 g/m2. After a 2-week preinclusion period, all patients received indapamide, 2.5 mg/day, for a period of 6 months. Physical examination including blood pressure measurement was performed on selection (M-1/2), before (M0), and after 1 (M1), 3 (M3) and 6 (M6) months of indapamide treatment, and echocardiography was performed at M0 and M6. Quality of life was evaluated by means of questionnaires completed by the patient and the physician, and a visual analog scale was completed by the patient at M-1/2, M0 and M6. All clinical parameters remained stable during the 2-week preinclusion period. Indapamide administration induced a highly significant reduction in both supine systolic and diastolic blood pressures from 173.9 +/- 2.9/100.5 +/- 1.2 mm Hg at M0 to 150.9 +/- 1.9/90.5 +/- 1.3 mm Hg at M1 (p less than 0.001), and 145.0 +/- 1.7/86.0 +/- 1.5 mm Hg at M6 (p less than 0.001). Similar favorable effects were observed in the upright position.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effects of calcium entry blockade on hypertension-induced left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart and is a response to increased hemodynamic and metabolic demands, which are most commonly caused by systemic hypertension. LVH induced by hypertension is associated with reduced myocardial compliance, structural alterations, and changes in coronary perfusion. Calcium entry blockers have caused LVH regression both in experimental studies and in clinical trials. Although their efficacy as antihypertensive agents is primarily due to their vasodilating properties, the mechanisms by which calcium entry blockers accomplish LVH regression are complex and include various hemodynamic and neurohumoral factors. Calcium entry blockade has decreased LVH with no apparent deterioration of left ventricular function. Because LVH is a major risk factor for sudden cardiac death and other cardiac morbidities, it is possible that the regression of LVH can improve the prognosis in hypertensive patients.

Animals↗

PubMed1991

Left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) may be physiological or pathological. Only pathological LVH has been shown to be a risk factor for cardiovascular events. LVH may not be homogeneous. It seems to progress from muscle hypertrophy to eventual cell death and myocardial fibrosis. Potential for reversal of LVH may therefore depend on the stage at which it has been attempted. An interaction between LVH and serum potassium levels could have important therapeutic implications, particularly with regard to the use of thiazide diuretics as long-term treatment for hypertension.

Animals↗

PubMed1990

[Dynamic left ventricular obstruction increased by nitroglycerin in elderly patients with hypertension and concentric left ventricular hypertrophy].

Left ventricular outflow tract (LVOT) obstruction has been observed in elderly patients with concentric hypertrophic hypertensive cardiomyopathy (HHCM) and no significant valvular disease or regional wall motion abnormalities. In order to determine whether nitroglycerin (NTG) can increase the intraventricular obstruction, we performed echocardiographic (echo) and doppler studies, before and during administration of sublingual NTG (0.8 mg). Twenty patients (n = 20) with long-standing hypertension (19 women and 1 man, mean age 78 +/- 8 yr, mean duration of hypertension 13 +/- 10 yrs were examined. The clinical findings in 17 patients were: angina 5 (29%), dyspnea 9 (53%), syncope or malaise 4 (23%). Electrocardiographic criteria of left ventricular hypertrophy was present in 4 patients and an increased cardio-thoracic ratio (greater than 0.5) in 9 cases. The following echo parameters were determined using M-mode echocardiograms: LV end-diastolic (LVID) and systolic diameter (LVIS), fractional shortening (FS), ventricular septum thickness (IVST), posterior wall thickness (PWT) and the ratio ISVT/PWT (less than 1.3 in all patients). LVM could be calculated in 15 patients and was corrected for body surface area (LVMI). Pulsed and continuous wave Doppler study showed a characteristic late-peaking velocity waveform. We localized the elevated velocities in the LVOT and determined before and during administration of NTG: LVOT peak velocities (V) and peak intraventricular gradients (G) using simplified Bernoulli equation. Results were as follows: [table: see text] Mild mitral regurgitation was observed in 14 patients (70%) and mitral annular calcifications in 11 (55%). Systolic function, as assessed by FS, was normal in all patients. NTG induced a significant acceleration of the LVOT velocities in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Population implications of electrocardiographic left ventricular hypertrophy.

Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.

Adult↗

PubMed1990

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.

Adult↗

PubMed1991

[Correlations between blood pressure, left ventricular hypertrophy, and left ventricular diastolic function in hypertensive patients].

We examined the relationship of hypertension to left ventricular hypertrophy (LVH) and left ventricular diastolic function by ambulatory blood pressure monitoring device and echocardiography. We studied 36 untreated hypertensive non-diabetic patients (16 males and 20 females) whose casual systolic blood pressure (CSBP) and/or diastolic blood pressure (CDBP) were higher than 140 mmHg and 90 mmHg, respectively. All patients were less than 65 years of age without organic heart disease. Resting systolic and diastolic blood pressures (RSBP, RDBP) were measured after lying in a supine position for 30 min by the auscultatory method. Ambulatory blood pressure was measured every 30 or 60 min for 24 hours by Colin ABPM 630, and the mean 24-hour ambulatory systolic and diastolic blood pressures (ASBP, ADBP) and the systolic and diastolic hyperbaric indices (SHI, DHI) were obtained. The left ventricular mass index (LVMI) was obtained as an indicator of LVH by M-mode echocardiography. The ratio of peak velocity of mitral inflow caused by atrial contraction to that of rapid inflow (A/R) was obtained as an indicator of the LV diastolic function by Doppler echocardiography. The coefficients of correlation between BP and the LVMI, and the A/R were determined. There were significant positive correlations between the LVMI and ASBP (r = 0.51, p < 0.005), the SHI (r = 0.49, p < 0.005), CSBP (r = 0.47, p < 0.01) and RSBP (r = 0.41, p < 0.05), however, there were no significant correlations between the LVMI and ADBP, the DHI, CDBP, RDBP and age. There were significant positive correlations between the A/R and ADBP (r = 0.44, p < 0.01), age (r = 0.40, p < 0.02), CSBP (r = 0.38, p < 0.05) and RDBP (r = 0.38, p < 0.05), however, no significant correlations between the A/R and ASBP, the SHI, DHI, RSBP and CDBP. Only a weak correlation was observed in all subjects between the LVMI and A/R, which was slightly improved by use of > 90 mmHg CSBP readings (r = 0.32). It was concluded that LVH is related mainly to continuous systolic hypertension, and that LV diastolic dysfunction is related mainly to continuous diastolic hypertension. Therefore, it was suggested that LVH and LV diastolic dysfunction in hypertensive patients are caused by different mechanisms.

Adult↗

PubMed1978

Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.

Adult↗

PubMed1990

Relation of obesity, high sodium intake, and eccentric left ventricular hypertrophy to left ventricular exercise dysfunction in essential hypertension.

PURPOSE: To elucidate determinants of abnormal left ventricular functional responses to exercise in hypertensive patients. PATIENTS AND METHODS: One hundred twenty-seven patients with uncomplicated essential hypertension were studied by rest and exercise radionuclide angiography and by echocardiography at rest. RESULTS: The 24 patients with subnormal left ventricular ejection fraction at peak exercise (less than 54%) were similar in age and rest and exercise blood pressures to the 103 with normal exercise ejection fraction, but were more obese (p less than 0.005) and had greater left ventricular mass (p less than 0.03) and internal dimensions (p less than 0.001). The parallel increase in left ventricular chamber size and mass (eccentric hypertrophy) in the group of patients with exercise dysfunction was associated with higher resting end-systolic wall stress (p less than 0.001) and abnormal increases of end-systolic left ventricular volume from rest to peak exercise (p less than 0.001). Multivariate analysis revealed that exercise left ventricular dysfunction was independently associated with higher left ventricular mass (p less than 0.0005), end-systolic wall stress (p less than 0.001), dietary sodium intake (p less than 0.01), and body mass index (p less than 0.03). CONCLUSION: Among patients with uncomplicated essential hypertension, abnormal functional responses to exercise are strongly associated with eccentric ventricular hypertrophy, obesity, and high sodium intake.

Cardiomegaly↗