Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension (original) (raw)
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Change in Diastolic Left Ventricular Filling After One Year of Antihypertensive Treatment
Circulation, 2002
Background — It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. Methods and Results — Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all P <0.001). Directionally opposite changes in isovolumic relaxation time (IVRT) and deceleration time indicate improvement in active LV relaxation and passive chamber stiffness during early diastole. Prevalences of normal LV filling increased, abnormal relaxation and pseudonormalization decreased, and ...
Echocardiographic studies of regression of left ventricular hypertrophy in hypertension
Hypertension, 1987
The availability of echocardiography has allowed direct determinations of left ventricular wall thickness and calculation of left ventricular mass. As a result, the past decade has witnessed a remarkable evolution in our understanding of structural changes in the heart. Moreover, cardiac hypertrophy was found to be reversible by some forms of therapy. In general, reduction of left ventricular mass became evident after 8 to 12 weeks of antihypertensive therapy. Sympatholytics (including methyldopa and reserpine), converting enzyme inhibitors (captopril and enalapril), and calcium entry blockers led to significant regression of left ventricular hypertrophy. On the other hand, arteriolar vasodilators (hydralazine, trimazosin, and minoxidil) were not associated with regression of hypertrophy despite adequate blood pressure control. Finally, data regarding diuretics and beta-blockers are controversial. These differences in results among various antihypertensive drugs reflect the multipli...
Determinants of left ventricular hypertrophy and function in hypertension
The American Journal of Cardiology, 1982
Ventricular mass and 02 supply of the myocardium were evaluated in patients with left ventricular hypertrophy due to stenosis or insufficiency of the aortic valve and in control patients without cardiac disease. Calculation of left ventricular mass from the angiogram was verified by autopsy data in seven patients. Total mass, 03 consumption, and coronary blood flow, each was related quantitatively to left ventricular total load (force) in all patients. Left ventricular equatorial tension, however, was greater in proportion to HYPERTROPHY OF THE LEFT VENTRICLE, which involves both contractile and mitochondrial elements,' presumably is a result of the increase in ventricular wall force (total load) and metabolic rate. The degree of the hypertrophy as assessed by left ventricular wall thickness has been found to be related quantitatively to the increase in left ventricular systolic blood pressure.2 Left ventricular wall force per unit cross-sectional area (i.e., stress)3 and 02 consumption per gram4`6 have been reported to be nearly normal in chronically hypertrophied hearts. These observations suggest that the extent of hypertrophy may be regulated to keep wall force and 02 consumption per unit of myocardium within normal limits, a finding consistent with the theory that myocardial growth is regulated by the steady-state level of adenosine nucleotide phosphorylation.7 The objectives of the present investigation were to delineate more precisely the mechanical determinants of left ventricular hypertrophy and to evaluate the adequacy of the compensatory increase in coronary blood flow in meeting the augmented myocardial 02 requirements of the hypertrophied heart. We calculated equatorial tension and total force3 (load) of the left ventricular wall and determined the quantitative relationship between these mechanical expressions and left ventricular mass, 02 consumption, and coronary blood flow. The studies were performed in patients whose left ventricular hypertrophy was in response to one of two different types of chronic hemodynamic burden: isolated aortic stenosis or insufficiency. Methods Subjects We studied 24 patients with aortic valve disease: 15 had nearly pure aortic stenosis (AS) and nine nearly pure aortic
Circulation, 2002
Background-It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. Methods and Results-Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all PϽ0.001).
Left ventricular mass regression in the LIFE study: effect of previous antihypertensive treatment
2003
Background: Whether to include only those patients who have not had prior hypertension treatment in clinical trials of left ventricular (LV) mass reduction is controversial. Accordingly, our aim was to study the relationship between prior treatment and both baseline and 1-year echocardiographic LV mass in subjects enrolled in the Losartan Intervention For Endpoint reduction (LIFE) study. Methods: We studied clinical and baseline echocardiographic data on 960 patients with electrocardiographically confirmed left ventricular hypertrophy enrolled in the electrocardiographic substudy of the LIFE study, 847 of whom had LV mass remeasured after 1 year of blinded treatment. The majority (75%) of these patients had prior medical treatment for hypertension. Results: In multivariable regression analysis, controlling for age, sex, blood pressure (BP), body mass index, and indices of pump and myocardial function, prior antihypertensive treatment was not associated with either greater LV mass or relative wall thickness on the baseline study. Moreover, there was no significant difference between the 637 subjects who were previously treated and the 210 who were not treated with regard to the mean reduction in systolic or diastolic pressures (Ϫ25 Ϯ 17 v Ϫ24 Ϯ Ϫ16 and Ϫ13 Ϯ 9 mm Hg v Ϫ12 Ϯ 9 mm Hg), LV mass (Ϫ27 Ϯ 38 v Ϫ29 Ϯ 34 g), or LV mass/body surface area (Ϫ14 Ϯ 20 v Ϫ15 Ϯ 18 g/m 2), all P Ͼ .05. Conclusions: Prior treatment is not associated with either greater LV mass or greater relative wall thickness when age, body mass index, sex, systolic BP, heart rate, or indices of LV volume load and systolic function are taken into account. In addition, prior treatment is not associated with lesser degrees of LV mass reduction. For design of future clinical trials, restriction of inclusion criteria to only previously untreated patients does not appear to be necessary when the selection criterion is electrocardiographically determined left ventricular hypertrophy.
American journal of hypertension, 1997
Doppler-derived indices of diastolic filling are widely used in the routine evaluation of essential hypertensives. However, these indices are affected by loading conditions and systolic performance. This study aimed at monitoring the transmitral flow pattern and indices of left ventricular systolic function during acute nonpharmacological isolated reduction of preload in essential hypertensives with left ventricular hypertrophy. Nine essential hypertensive patients with left ventricular hypertrophy and nine age- and sex-matched normotensive controls underwent echocardiographic and Doppler evaluation of both systolic function and diastolic filling indices at baseline and during lower body suction at -40 mm Hg. Lower body suction caused a similar decrease in end-diastolic volume index, stroke volume index, and midwall fractional shortening in the normotensives and hypertensives. Circumferential end-systolic stress was unaffected in both groups. Acceleration time of early diastolic fil...
The American Journal of Cardiology, 2000
Abnormal left ventricular (LV) filling may exist in early stages of hypertension. Whether this finding is related to LV hypertrophy is currently controversial. This study was undertaken to assess relations between abnormal diastolic LV filling and LV geometry in a large series of hypertensive patients with electrocardiographic LV hypertrophy. M-mode, 2-dimensional, and pulsed Doppler echocardiographic recordings of mitral inflow velocity and isovolumetric relaxation time (IVRT) were obtained in 750 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiography (sexadjusted Cornell voltage duration criteria or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. The patients' mean age was 67 ؎ 7 years and 44% were women. One hundred forty patients (19%) had normal LV geometric pattern, 79 (11%) had concentric remodeling, 342 (45%) had eccentric LV hypertrophy, and 189 (25%) had concentric LV hypertrophy. A normal LV filling pattern was found in 116 patients (16%), abnormal relaxation in 519 (69%), "pseudonormal" filling was found in 83 (11%), and a restrictive filling pattern in 32 (4%). Prolonged IVRT was associated with LV hypertrophy (p <0.01) as well as elevated relative wall thickness (p <0.05). A stronger difference (p <0.01) in IVRT was found between groups with and without LV hypertrophy. Multiple regression analysis revealed that increased LV mass correlated with prolonged IVRT, whereas LV mass and geometry were not associated with peak early LV filling velocity (E), peak atrial filling velocity (A) ratio or mitral valve E-peak deceleration time, although IVRT was found to be an independent correlate of E/A ratio and deceleration time. Thus, abnormal IVRT was highly prevalent in all LV geometric subgroups among hypertensive patients with electrocardiographic LV hypertrophy, even in those with normal LV geometry determined by echocardiography. We found that IVRT differed significantly among patient groups with different LV geometric patterns, primarily because of the association of IVRT to LV mass. ᮊ2000