Does the Reduction in Systolic Blood Pressure Alone Explain the Regression of Left Ventricular Hypertrophy?

Verdecchia, P.; Ospedale, R.

doi:10.1097/00004872-200406002-01435

Cited by 6 publications

(7 citation statements)

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“…[2][3][4] Although the fall in BP is paralleled by a reduction in LVM, [27][28][29] a stronger correlation between changes in 24-hour BP and changes in LVM (as compared with casual BP) was reported. 30 In accordance with other studies, 27-29 our results clearly suggest that, after adjustment for pretreatment LVMI, the most powerful determinant of LVMI reduction is the change in systolic BP resulting from treatment. Of interest, it was suggested by Devereux et al 28 that the benefit of BP reduction on LV remodeling cannot be fully appreciated unless the duration of follow-up is Ն3 years (as in the present study).…”

Section: Du Cailar Et Al Left Ventricular Mass Sodium and Aldosteronesupporting

confidence: 92%

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

et al. 2010

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Abstract-In essential hypertension, the regression of left ventricular hypertrophy is an important goal of treatment. In addition to treatment-associated changes in blood pressure (BP), the roles of other determinants of left ventricular hypertrophy regression, including dietary sodium intake, deserve investigation. In the present study, the change in echographic left ventricular mass index (LVMI) was assessed in 182 patients with never-treated essential hypertension at baseline and after 3 years of treatment by angiotensin converting enzyme inhibitors or angiotensin II receptor antagonists given at recommended doses and associated with other antihypertensive agents. Treatment was associated with satisfactory control of BP (Ͻ140/90 mm Hg) in 64% of patients, and left ventricular hypertrophy prevalence decreased from 56% to 39%. Twenty-four-hour urinary sodium was positively related to LVMI at baseline and at the end of the study, independently of age, sex, and systolic BP. Supine plasma aldosterone concentration was correlated with LVMI only at baseline but not in multivariate analysis. In response to treatment, the percentage of change in LVMI was positively correlated with the absolute changes in systolic BP, urinary sodium, and plasma aldosterone concentration, independently of baseline LVMI. The population was divided into 3 tertiles according to final values of gender-specific urinary sodium. When, within each urinary sodium tertile, patients were divided into those with plasma aldosterone concentration below and above the median (11.6 ng/dL), LVMI progressively increased across sodium tertiles only in patients with high plasma aldosterone concentration. Systolic BP was similar across all of the groups. In conclusion, aldosterone requires the presence of high dietary salt for the expression of its unfavorable effect on the heart. (Hypertension. 2010;56:865-870.)Key Words: left ventricular hypertrophy Ⅲ sodium intake Ⅲ hypertension Ⅲ aldosterone Ⅲ renin-angiotensin blockade A lthough left ventricular hypertrophy (LVH) is considered as an adaptative mechanism that preserves cardiac pump function in the presence of pressure or volume overload, it also represents a preclinical disease strongly predictive of cardiovascular morbidity and mortality in hypertension. 1 Moreover, some evidence indicates that reduction or aggravation of LVH, respectively, improves or enhances the risk of subsequent complications. [2][3][4] In the Pressioni Arteriose Monitorate e Loro Associazioni cohort of 398 treated subjects with essential hypertension, a prevalence of LVH of 19% was found when adequate control (Ͻ140/90 mm Hg) of blood pressure (BP) was achieved, whereas the prevalence of LVH was 29% in the presence of uncontrolled BP. 5 Because a number of treated patients exhibit levels of left ventricular mass (LVM) that exceed the need to sustain cardiac workload, it was suggested that nonhemodynamic factors may modulate or consistently influence the regression of LVH. 6 During the last decade, dietary sodium and aldosterone wer...

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Section: Du Cailar Et Al Left Ventricular Mass Sodium and Aldosteronesupporting

confidence: 92%

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

et al. 2010

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“…It is generally believed that SBP has greater association with LVH compared with DBP. 6,7 However, the change in emphasis towards SBP has assumed importance only recently. Moreover, lowering SBP is not always beneficial for lowering cardiovascular risk.…”

Section: Introductionmentioning

confidence: 99%

Diastolic blood pressure reduction contributes more to the regression of left ventricular hypertrophy: a meta-analysis of randomized controlled trials

et al. 2013

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Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor; however, the key strategy necessary for LVH regression in hypertensive patients is not clear. A meta-analysis was conducted to study the effect of blood pressure reduction on LVH regression. We explored the relationship between different degrees of systolic blood pressure (SBP)/diastolic blood pressure (DBP) reduction and LVH regression. A total of 17 randomized controlled trials comprising 2196 hypertensive patients (mean age, 56.3 years; 64.1% were men) were identified. Different degrees of SBP and DBP reductions were significantly associated with LVH regression: SBP reduction ≥20 mm Hg (SBPM20) (weighted mean difference (WMD): 14.35 g m(-2); 95% confidence interval (CI): 10.44, 18.26; P<0.0001); SBP reduction <20 mm Hg (SBPL20 group) (WMD: 14.82 g m(-2); 95% CI: 9.83, 19.8(2); P<0.0001); DBP reduction ≥10 mm Hg (DBPM10 group) (WMD: 15.17 g m(-2); 95% CI: 11.86, 18.48; P<0.0001); and DBP reduction <10 mm Hg (DBPL10 group) (WMD: 11.76 g m(-2); 95% CI: 3.75, 19.76; P=0.004). Significant regression of LVH was found in the DBPM10 group compared with the SBPM20, SBPL20 and DBPL10 groups (P<0.0001). The most significant decrease in LVH was seen in patients with a mean age over 60 years in the DBPM10 group. Moreover, the renin-angiotensin system inhibitor was found to be the most effective antihypertensive drug for LVH regression. This meta-analysis result indicates that proper DBP reduction plays an important role in the regression of echocardiographic LVH in hypertensive patients.

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“…In fact LVH is a potent marker and predictor of subsequent mortality and morbidity, including the risk of sudden death [7,8]. Associated hypertension, in particular severe or moderate hypertension, compounds the risk and it has been shown that systolic blood pressure is the principal determinant of LVH regression in hypertensive humans [34]. Evidence in the literature supports the theory that reversal of LVH is possible and this holds potential for the reduction of CV events with timely treatment.…”

Section: Resultsmentioning

confidence: 99%

Echocardiographic Left Ventricular Hypertrophy (LVH) and Prognosis – A Meta-Analysis

Hilton¹

2018

J Med - Clin Res & Rev

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Background: Different formulae and partition values define left ventricular hypertrophy (LVH) using echocardiography. This diagnostic systematic review investigates further various formulae and cut-points and their predictive potential. Methods: Searches of Medline, EMbase, the Cochrane Library, reference lists and conference proceedings were conducted. Statistical analysis was performed using Meta-test version 0.6 and Epi-info statistical programs. Studies included cohort studies or randomised controlled trials (RCTs) of hypertensive persons where baseline LVH was measured and clinical outcome ascertained. Results: 24 studies were identified that included subjects with outcomes such as all-cause mortality, cardiac death, non-fatal cardiovascular (CV) events and/or stroke. Of 10 studies assessing all-cause mortality, 6 were analyzed with the combined relative risk (RR), sensitivity and specificity values being 2.10 (95% CI 1.79-3.24), 57% and 68% respectively. Conclusion: LVH is associated with an approximate two fold increased risk for all-cause mortality.

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Does the Reduction in Systolic Blood Pressure Alone Explain the Regression of Left Ventricular Hypertrophy?

Cited by 6 publications

References 0 publications

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

Diastolic blood pressure reduction contributes more to the regression of left ventricular hypertrophy: a meta-analysis of randomized controlled trials

Echocardiographic Left Ventricular Hypertrophy (LVH) and Prognosis – A Meta-Analysis

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