Regression Of Left Ventricular Hypertrophy In Patients Research Articles

STRICTER AMBULATORY BLOOD PRESSURE CONTROL IS POSSIBLE IN PATIENTS AFTER KIDNEY TRANSPLANTATION AND IS ASSOCIATED WITH REGRESSION OF LEFT VENTRICULAR HYPERTROPHY: POST HOC ANALYSIS

Objective: The recently published analysis of the 4C-T study demonstrated an association of stricter cumulative office blood pressure (BP) control with lower left ventricular mass (LVM) in children after kidney transplantation. The aim of our study was to investigate whether stricter control of ambulatory BP is also associated with improved LVMI and regression of left ventricular hypertrophy (LVH) in pediatric kidney transplant recipients. Design and method: A post-hoc analysis of nineteen patients (median age at baseline 9.7 years, range 3.3–15.1, median time after transplantation 4.3 years, range 1.0-13.1) from our previous ESCORT trial who had echocardiography performed at baseline (T0), 1 (T1), 2 (T2) and 3 (T3) years was performed. Cumulative 24-hour mean arterial pressure (MAP) Z-scores (CMAPz) were calculated according to 4C-T study (Sugianto et al. 2023). Left ventricular hypertrophy (LVH) was defined as LVMi>40 g/m^2.7 in girls >9 yrs of age and LVMi>45 g/m^2.7 in boys >9 yrs of age; in children <=9 yrs the LVH was defined as LVMi >95th percentile (Khoury et al 2009). Results: The median CMAPz decreased from a median +0.27 (IQR=-0.09 to +0.38) in the 1st year down to -0.06 (IQR=-0.26 to +0.32) in the 2nd year (p=0.02) and to +0.05 (IQR=-0.32 to 0.27) in the 3rd year (p=0.04) of follow-up. The prevalence (number) of children with LVH was 26% (5/19) at T0, 16% (3/19) at T1, 23% (3/13) at T2 and 0% (0/11) at T3 (trend in proportions p=0.06). All 5 children with elevated LVMi>0.9 at T0 decreased / normalized their LVMi at T3 (p=0.07), on contrary children without LVH at baseline did not significantly change their LVMi during follow-up. Conclusions: This first prospective interventional study demonstrated an association between stricter cumulative ambulatory MAP and regression of LVH in patients after kidney transplantation. Our data suggest that aiming stricter ambulatory BP can improve the often unfavourable cardiac phenotype in these patients. However, randomized control trial is required to confirm our findings.

The effect of intensive blood pressure lowering on left ventricular hypertrophy in patients with hypertension: a systematic review and meta-analysis of randomized controlled trials

Background We conducted a comprehensive systematic review to examine the efficacy of intensive blood pressure lowering on the risk of left ventricular hypertrophy (LVH). Methods We searched PubMed, Scopus, Web of Science, Cochrane Central, and EMBASE for all relevant randomized controlled trials. The primary outcome was the incidence of left ventricular hypertrophy. We used the risk ratio (RR) and hazard ratio (HR) with a 95% confidence interval as our effect sizes. Results Four studies, comprising 20,747 patients, were included. Intensive blood pressure lowering was linked with a diminished LVH incidence (RR: 0.66, 95% CI [0.56–0.77]). We also found that intensive blood pressure lowering increased the risk of LVH regression in patients with baseline LVH (RR: 1.21, 95% CI [1.11–1.32]). Finally, intensive blood pressure lowering was linked with a reduced risk of cardiovascular disease (HR: 0.71, 95% CI [0.60–0.85]). No significant heterogeneity was seen in either outcome. Conclusion Our study suggests that intensive blood pressure lowering effectively reduces the risk of LVH and cardiovascular disease. An interactive version of our analysis can be accessed here: https://databoard.shinyapps.io/lvh_hypertophy/

Remodeling and regression of left ventricular hypertrophy in patients with arterial hypertension (literature review)

The article contains literature information concerning the pathogenesis of hypertrophy and remodeling of the left ventricle (LV) of the heart in patients with arterial hypertension (AH), regression of left ventricular hypertrophy (LVH) under the influence of anti-hypertensive treatment. Remodeling of the heart is its structural geometrical changes occurring under the influence of pathological factors: increasing the number of sarcomeres, length and thickness of cardiomyocytes, increasing or decreasing the wall thickness, and enlargement of the ventricular cavity. The renin-angiotensin-aldosterone system (RAAS) plays a central role in the pathogenesis of hypertrophy and remodeling of the myocardium with AH and heart failure. LVH is one of the most significant predictors of cardiovascular events, including myocardial infarction, stroke, life-threatening ventricular arrhythmias, mortality from cardiovascular diseases, and general mortality. Treatment with angiotensin-converting enzyme inhibitors (ACEI), dihydropyridine calcium channel blockers (CCB), АТ ІІ receptor blockers (ARB) promotes reverse development of LVH and regression of the processes of the heart muscle remodeling. ACEIs are found to be more effective in achieving regression of LVH in patients with AH compared to CCB and beta-blockers. An early beginning of anti-hypertensive therapy and attention to metabolic aspects are critically important to avoid irreversible LVH. The ESH/ESC recommendations (2018) indicate that ACEI and ARB are effective for the prevention or regression of LVH in patients with AH, and beta-blockers are less effective than RAAS blockers and CCB.Objective: to systematize literature data about the pathogenesis of the left ventricle remodeling in patients with arterial hypertension, and the role of anti-hypertensive therapy in the regression of left ventricular hypertrophy. Conclusion. Today, the concept about the role of the renin-angiotensin-aldosterone system in the pathogenesis of hypertrophy and remodeling of the left ventricle in patients with arterial hypertension has been formulated. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are the most effective in the prevention or regression of left ventricular hypertrophy in patients with arterial hypertension.

PS 14-14 24-HOUR URINARY SODIUM PREDICTS LEFT VENTRICULAR HYPERTROPHY REGRESSION TO SPIRONOLACTONE IN PATIENTS WITH RESISTANT HYPERTENSION

Objective: Patients with resistant hypertension (RHTN) commonly have primary aldosteronism (PA), which is associated with left ventricular hypertrophy (LVH). Aldosterone activates mineralocorticoid receptors (MR) and induces hypertrophy. Experimental studies indicate a paradoxical activation of the MR in sodium-loaded rats despite adequate suppression of aldosterone. MR antagonists slow down cardiac hypertrophy. We hypothesized that the MR antagonist spironolactone (SPL) would cause greater LVH reduction in patients on high sodium (Na) diet independent of aldosterone. Design and Method: Overall 34 patients with RHTN, defined as BP ≥ 140/90 mmHg despite ≥3 different medications, including a diuretic, were treated with SPL. Cardiac magnetic resonance imaging and biochemical evaluation was performed at baseline, 3 and 6 months in patients with PA and non-PA. PA was defined as renin activity (PRA) <1 ng/ml/h and urinary aldosterone ≥12 ug /24h. We dichotomized patients according to UNa level (UNa ≥200 mEq/24h: high Na diet) and PA status. LVH reduction was indexed by left ventricular mass (LVM) and interventricular septum thickness (IVS) regression. Results: LVM and IVS regression after treatment with SPL at 3 and 6 months was greater in patients with PA on a normal sodium diet and less pronounced in patients on a high sodium diet suggesting that Na blunts the effects of cardiac MR when treated with SPL. However, in patients with non-PA high Na intake did not blunt the effects of SPL. Conclusions: Contrary to our hypothesis, high dietary Na blunted LVH regression in patients with PA treated with SPL. Further studies are needed to elucidate mechanisms for sodium dependent MR activation in patients with PA and non-PA.

High dietary sodium blunts effects of mineralocorticoid receptor antagonism on left ventricular hypertrophy regression in patients with resistant hypertension

Purpose of Study: Patients with resistant hypertension (RHTN) commonly have primary aldosteronism (PA), which is associated with left ventricular hypertrophy (LVH). Aldosterone activates mineralocorticoid receptors (MR) and induces hypertrophy. Experimental studies indicate a paradoxical activation of the MR in sodium-loaded rats despite adequate suppression of aldosterone. MR antagonists slow down cardiac hypertrophy. We hypothesized that the MR anatagonist spironolactone (SPL) would cause greater LVH reduction in patients on high sodium (Na) diet independent of aldosterone. Methods Used: Overall 34 patients with RHTN, defined as BP 140/90 mmHg despite 3 different medications, including a diuretic, were treated with SPL. Cardiac magnetic resonance imaging and biochemical evaluation was performed at baseline, 3 and 6 months in patients with PA and non-PA. PA was defined as renin activity (PRA)<1 ng/ml/h and urinary aldosterone 12 ug /24h. We dichotomized patients according to UNa level (UNa 200 mEq/24h: high Na diet) and PA status. LVH reduction was indexed by left ventricular mass (LVM) and interventricular septum thickness (IVS) regression. Summary of Results: LVM and IVS regression after treatment with SPL at 3 and 6 months was greater in patients with PA on a normal sodium diet and less pronounced in patients on a high sodium diet suggesting that Na blunts the effects of cardiac MR when treated with SPL. However, in patients with non-PA high Na intake did not blunt the effects of SPL. Conclusions: Contrary to our hypothesis, high dietary Na blunted LVH regression in patients with PA treated with SPL. Further studies are needed to elucidate mechanisms for sodium dependent MR activation in patients with PA and non-PA.

Clinical importance of detecting exaggerated blood pressure response to exercise on antihypertensive therapy

ObjectiveIn patients with hypertension, regression of left ventricular hypertrophy (LVH) is associated with improved prognosis. Impact of exaggerated blood pressure response to exercise (Ex-BP) seen in patients with hypertension undergoing...

Impact of chronic use of cibenzoline on left ventricular pressure gradient and left ventricular remodeling in patients with hypertrophic obstructive cardiomyopathy

BackgroundCibenzoline, a class Ia antiarrhythmic drug, is useful for reducing the left ventricular pressure gradient (LVPG) in patients with hypertrophic obstructive cardiomyopathy (HOCM). However, chronic effects of cibenzoline on LVPG and left ventricular (LV) remodeling are unknown. MethodsForty-one patients with HOCM participated in this study. Echocardiographic, electrocardiographic, and brain natriuretic peptide (BNP) data collected before and after cibenzoline treatment were compared. From the relation between LVPG and plasma concentration of cibenzoline, an efficacious plasma concentration of cibenzoline was estimated. ResultsThe mean follow-up period was 74.2±47.1 months. The LVPG decreased from 104.8±62.6mmHg to 27.6±30.5mmHg (p<0.0001). The LV end-diastolic dimension increased from 42.8±5.8mm to 46.2±5.4mm (p<0.0001), but neither LV end-systolic dimension nor LV fractional shortening changed significantly. The left atrial dimension decreased from 40.0±4.7mm to 36.2±5.1mm (p<0.0001). The E-wave velocity/A-wave velocity ratio increased, early diastolic annular velocity (Ea) increased, and E/Ea ratio decreased. The interventricular septal wall thickness, LV posterior wall thickness, the Sokolow-Lyon index, and the depth of negative T wave decreased. The heart rate-corrected QT interval was shortened. Plasma BNP level decreased from 418.8±423.7pg/ml to 213.7±154.1pg/ml (p<0.02). The safe and efficacious plasma concentration of cibenzoline was between 300ng/mL and 1500ng/mL. ConclusionsLong-term treatment with cibenzoline attenuated LVPG, improved LV diastolic dysfunction, and induced LV hypertrophy regression in patients with HOCM without causing serious complications.

Allopurinol Reduces Left Ventricular Mass in Patients With Type 2 Diabetes and Left Ventricular Hypertrophy

This study sought to ascertain whether high-dose allopurinol causes regression of left ventricular mass (LVM) in patients with type 2 diabetes mellitus (T2DM). Left ventricular hypertrophy (LVH) is common in T2DM and contributes to patients' high cardiovascular (CV) event rate. Oxidative stress (OS) has been implicated in LVH development, and allopurinol has been previously shown to reduce vascular OS. We therefore investigated whether allopurinol causes regression of LVH in patients with T2DM. We conducted a randomized, double-blind, placebo-controlled study of 66 optimally-treated T2DM patients with echocardiographic evidence of LVH. Allopurinol, 600 mg/day, or placebo was given over the study period of 9 months. The primary outcome was reduction in LVM as calculated by cardiac magnetic resonance imaging at baseline and at 9 months' follow-up. Secondary endpoints were change in flow-mediated dilation and augmentation index. Allopurinol significantly reduced absolute LVM (-2.65 ± 5.91 g vs. placebo group+1.21 ± 5.10 g [p= 0.012]) and LVM indexed to body surface area (-1.32 ± 2.84 g/m(2) vs. placebo group+0.65 ± 3.07 g/m(2) [p= 0.017]). No significant changes were seen in either flow-mediated dilation or augmentation index. Allopurinol causes regression of LVM in patients with T2DM and LVH. Regression of LVH has been shown previously to improve CV mortality and morbidity. Therefore, allopurinol therapy may become useful to reduce CV events in T2DM patients with LVH. (Allopurinol in Patients with Diabetes and LVH; UKCRN 8766).

Factors influencing left ventricular mass regression in patients with primary aldosteronism post adrenalectomy

Primary aldosteronism (PA) is a type of secondary hypertension with prominent left ventricular hypertrophy (LVH). Unilateral aldosterone-producing adenoma (APA) is the most common subtype that can be cured by adrenalectomy. To investigate left ventricular structural change after surgery and the factors associated with the degree of LVH regression in patients with PA. We performed a retrospective analysis in the Taiwan Primary Aldosteronism Investigation (TAIPAI) database, including demography, biochemical data, echocardiography and medication. From July 1994 to January 2007, 20 patients (8 men) with APA receiving adrenalectomy and having pre- and postoperative echocardiography were selected. After 21 ± 19 months post operation, the left ventricular wall thickness and left ventricular mass index (LVMI) decreased significantly. The decrease of LVMI is significant only in patients who had LVH before operation. In analysis of factors associated with net LVMI decrease (ΔLVMI; post-operative LVMI - pre-operative LVMI), only pre-operative LVMI (r = -.783, p < .001), and ΔSBP (r = .472, p = .036) significantly correlated with ΔLVMI. In conclusion, LVH in PA could be significantly reversed by adrenalectomy. Pre-operative LVMI and ΔSBP were associated with the degree of LVMI decrease. LVH in PA could be significantly reversed by adrenalectomy. Pre-operative LVMI and ΔSBP were associated with the degree of LVMI decrease.

Angiotensin II Receptor Blocker, Valsartan, Increases Myocardial Blood Volume and Regresses Hypertrophy in Hypertensive Patients

Although a reduction in myocardial blood volume (MBV), an in vivo index of the myocardial microvasculature, measured by myocardial contrast echocardiography in patients with hypertension (HT), can be demonstrated, it is still unknown whether a decreased MBV can be improved by antihypertensive treatment. Eleven HT patients (mean age 58 years, 7 men) with left ventricular hypertrophy (LVH) and 10 age- and sex-matched normal controls were studied. Harmonic power Doppler images were acquired at end-diastole of every 6(th) beat and MBV was calculated as 10(X/10)x100%, where X (dB) is myocardial contrast intensity minus the contrast intensity of the adjacent intracavity blood pool. Baseline blood pressure (BP) and left ventricular mass index (LVMI) in the HT patients were higher and MBV was lower than in the controls (2.52 +/-0.37% vs 3.31 +/-0.61%, P<0.01). MBV did not correlate with mean BP, but was inversely correlated with LVMI (r=0.61, P<0.01). After treatment with valsartan for 6 months, LVMI significantly decreased and MBV increased (2.72 +/-0.26%, P<0.05 vs baseline) in the patients with HT. There was a significant inverse correlation between the changes in MBV and those of LVMI (r=0.62, P<0.05), but not between MBV and mean BP. Valsartan, an angiotensin II receptor blocker, corrected the decreased MBV in association with regression of LVH in patients with HT.

L-Carnitine Supplementation Decreases the Left Ventricular Mass in Patients Undergoing Hemodialysis

Patients on long-term hemodialysis become deficient in carnitine and are frequently treated with carnitine supplementation to offset their renal anemia, lipid abnormality and cardiac dysfunction. The therapeutic value of carnitine supplementation on left ventricular hypertrophy (LVH) in patients with normal cardiac systolic function remains uncertain. The cardiac morphology and function of 10 patients given 10 mg/kg of L-carnitine orally, immediately after hemodialysis sessions 3 times per week for a 12-month period were compared with 10 untreated control patients. Using echocardiography, left ventricular fractional shortening (LVFS) and left ventricular mass index (LVMI) were measured before and after the study period. As a result, amounts of serum-free carnitine increased from 28.4+/-4.7 to 58.5+/-12.1 micromol/L. The LVMI decreased significantly from 151.8+/-21.2 to 134.0+/-16.0 g/m(2) in treated patients (p<0.01), yet the LVMI in untreated control patients did not change significantly (ie, from 153.3+/-28.2 to 167.1+/-43.1 g/m(2)). However, LVFS values remained unchanged in both groups. Although L-carnitine promoted a 31% reduction in erythropoietin requirements, hematocrit and blood pressure did not change during the study period. Supplementation with L-carnitine induced regression of LVH in patients on hemodialysis, even for those with normal systolic function.

Issue Highlights

HomeCirculationVol. 113, No. 12Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published28 Mar 2006https://doi.org/10.1161/circ.113.12.1549Circulation. 2006;113:1549RELATIONSHIP BETWEEN HOMOCYSTEINE AND MORTALITY IN CHRONIC KIDNEY DISEASE, by Menon et al.Prior studies relating plasma homocysteine to the risk of cardiovascular disease in the general population have yielded inconsistent results. Reduced glomerular filtration rate (GFR) is a risk factor for cardiovascular disease, and plasma homocysteine is related inversely to GFR. Therefore, the association of plasma homocysteine with cardiovascular disease in some earlier reports may have been confounded by inadequate adjustment for GFR. In this issue of Circulation, Menon and colleagues relate homocysteine levels to all-cause and cardiovascular mortality in patients with stages 3 to 4 chronic kidney disease enrolled in the Modification of Diet in Renal Disease Study who were followed up for a median duration of 10 years. The authors observed that plasma homocysteine levels increased with worsening GFR. In analyses adjusting for GFR (measured by the renal clearance of 125I-iothalamate), plasma homocysteine was not associated with all-cause or cardiovascular mortality. These observations suggest that plasma homocysteine may be a marker of severity of kidney disease rather than an independent risk factor in patients with stages 3 to 4 chronic kidney disease. See p 1572.IMPACT OF DIABETES MELLITUS ON REGRESSION OF ELECTROCARDIOGRAPHIC LEFT VENTRICULAR HYPERTROPHY AND THE PREDICTION OF OUTCOME DURING ANTIHYPERTENSIVE THERAPY: THE LOSARTAN INTERVENTION FOR ENDPOINT (LIFE) REDUCTION IN HYPERTENSION STUDY, by Okin et al.Research has established that left ventricular hypertrophy (LVH) is associated with excess morbidity and mortality. Moreover, recent observational and randomized data support the concept that LVH regression improves prognosis. Whether the benefits of LVH regression are equivalent across various patient subgroups is, however, uncertain. Dr Okin and colleagues examined over 9000 patients with hypertension in the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study, 1195 of whom had diabetes, to understand the benefits of LVH regression in patients with diabetes. Consistent with prior studies, the investigators observed that the prevalence of LVH was greater among patients with diabetes. However, with a mean follow-up of about 5 years, patients with diabetes had less electrocardiographic LVH regression. Surprisingly, though the mortality benefit of hypertension treatment in diabetes is established, LVH regression per se was not predictive of improved prognosis in those with diabetes. The data of Okin et al suggest that the pathogenesis of the poor prognosis associated with LVH in diabetes is multifactorial and merits further investigation. See p 1588.WOMEN HAVE HIGHER LEFT VENTRICULAR EJECTION FRACTIONS THAN MEN INDEPENDENT OF DIFFERENCES IN LEFT VENTRICULAR VOLUME: THE DALLAS HEART STUDY, by Chung et al.The clinical utility of ejection fraction is widely accepted, and despite the well-recognized pitfalls, it remains an important predictor of outcome in multiple different cardiac diseases. In general, common cutpoints have been applied to men and women. In this week’s journal, Chung et al acquired cardiac magnetic resonance imaging in 1435 women and 1183 men from the Dallas Heart Study. This carefully performed study in a probability-based sample of Dallas residents aged 30 to 65 demonstrated that the median left ventricular ejection fraction in women (75%) is higher than in men (70%); this is secondary to a higher stroke volume. This gender-associated difference in stroke volume is independent of end-diastolic volume and other evaluated confounders. Future work will be needed to assess the importance of this finding in the study of cardiovascular diseases. See p 1597.Visit http://circ.ahajournals.org:Clinician UpdateGastrointestinal Complications of Dual Antiplatelet Therapy. See p e655.Images in Cardiovascular MedicineSevere Left Atrial Edema and Heart Failure After Atrial Fibrillation Ablation. See p e659.Serial High-Spatial-Resolution, Multisequence Magnetic Resonance Imaging Studies Identify Fibrous Cap Rupture and Penetrating Ulcer Into Carotid Atherosclerotic Plaque. See p e660.Diffuse Infiltration of Lymphoma of the Myocardium Mimicking Clinical Hypertrophic Cardiomyopathy. See p e662. Download figureDownload PowerPointCorrespondenceSee p e665. Previous Back to top Next FiguresReferencesRelatedDetails March 28, 2006Vol 113, Issue 12 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.113.12.1549 Originally publishedMarch 28, 2006 PDF download Advertisement

A study of the relationships between angiotensin- converting enzyme gene, chymase gene polymorphisms, pharmacological treatment with ACE inhibitor and regression of left ventricular hypertrophy in essential hypertension patients treated with benazepril

Background: About 15–37% of the adult population worldwide suffers from hypertension. Hypertension is responsible for one-third of all global deaths. Left ventricular hypertrophy (LVH) is one of the most important characteristics of hypertension target organ damage and is also an independent risk factor for cardiovascular events. Therefore, effective regression of LVH is a main aim of hypertension treatment and also an important public health concern. However, few studies of the regression of LVH have been reported. In particular, little is known about the relationship between the genotypes of angiotensin-converting enzyme (ACE) and chymase (CMA) genes, and the effectiveness of antihypertensive drugs in regression of LVH.Aim: The study investigated whether the insertion/deletion (I/D) polymorphism of ACE gene and the A/B polymorphism of the CMA gene are related to the regression of LVH in essential hypertension patients who were participants in a long-term trial of therapy with benazepril.Subjects and methods: Data from 157 patients was collected and used in the analysis. The genotypes of ACE and CMA genes were identified by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Left ventricular mass (LVM) was measured by echocardiography, and left ventricular mass index (LVMI) was calculated.Results: Blood pressure was markedly reduced and heart rate was unchanged by long-term treatment with benazepril. Regression of LVH was observed. The mean reduction in LVMI was 41.50 ± 28.48 g m−2. Reduction of LVM, LVMI and percentage reduction of LVMI were more in the DD group than in the II and ID groups (P < 0.05). No significant difference in other indices was found in the different genotype groups of ACE (P > 0.05). No significant difference in all indices was found among the different genotype groups of CMA (P > 0.05). No interaction was found between the genotypes of ACE and CMA.Conclusion: Hypertension patients with the DD genotype are more likely to have regression of LVH when treated with benazepril than patients with other genotypes of ACE. No evidence was found to support an association between CMA genotype and regression of LVH in patients or to support the interaction between the two genes in regression of LVH.

Regression of Hypertensive Left Ventricular Hypertrophy by Losartan Compared With Atenolol

An echocardiographic substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was designed to test the ability of losartan to reduce left ventricular (LV) mass more than atenolol. A total of 960 patients with essential hypertension and LV hypertrophy (LVH) on screening ECG were enrolled at centers in 7 countries and studied by echocardiography at baseline and after 1, 2, 3, 4, and 5 years' randomized therapy. Clinical examination and blinded readings of echocardiograms in 457 losartan-treated and 459 atenolol-treated participants with > or =1 follow-up measurement of LV mass index (LVMI) were used in an intention-to-treat analysis. Losartan-based therapy induced greater reduction in LVMI from baseline to the last available study than atenolol with adjustment for baseline LVMI and blood pressure and in-treatment pressure (-21.7+/-21.8 versus -17.7+/-19.6 g/m2; P=0.021). Greater LVMI reduction with losartan was observed in women and men, participants >65 or <65 years of age, and with mild or more severe baseline hypertrophy. The difference between treatment arms in LVH regression was due mainly to reduced concentricity of LV geometry in both groups and lesser increase in LV internal diameter in losartan-treated patients. Antihypertensive treatment with losartan, plus hydrochlorothiazide and other medications when needed for pressure control, resulted in greater LVH regression in patients with ECG LVH than conventional atenolol-based treatment. Thus, angiotensin receptor antagonism by losartan has superior efficacy for reversing LVH, a cardinal manifestation of hypertensive target organ damage.