scholarly journals P962 The Remodeling Index risk stratifies patients with hypertensive left ventricular hypertrophy

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
T T Le ◽  
J Bryant ◽  
B Ang ◽  
B Su ◽  
S Cook ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Wall Thickness ◽  
Prognostic Value ◽  
Ventricular Hypertrophy ◽  
Fold Increase ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Single Measure ◽  
Hypertensive Patients ◽  
Remodeling Index

Abstract Funding Acknowledgements National Medical Research Council BACKGROUND Hypertensive left ventricular hypertrophy (LVH) is associated with increased cardiovascular events. The authors previously developed the Remodeling Index (RI) that incorporated LV volume and wall-thickness in a single measure of advanced hypertrophy in hypertensive patients. PURPOSE This study examined the mechanisms and prognostic potential of the RI in reference with current LVH classifications. METHODS Cardiovascular magnetic resonance (CMR) was performed in 400 asymptomatic hypertensive patients. The newly derived RI ([(EDV)^1/3]/t; where EDV is LV end-diastolic volume and t is the maximal wall thickness across 16 myocardial segments) stratified hypertensive patients into 3 groups: without LVH, LVH with normal RI (LVH_Normal-RI) and LVH with low RI (LVH_Low-RI). The primary outcome was a composite of all-cause mortality, acute coronary syndromes, strokes and decompensated heart failure. RESULTS LVH_Low-RI was associated with increased LV mass index, fibrosis burden, impaired myocardial function and elevated biochemical markers of myocardial injury and wall stress. Over 18.3 ± 7.0 months (601.3 patient-years), patients with LVH_Low-RI had more than a 5-fold increase in adverse events compared to those with LVH_Normal-RI (11.6 events/100patient-years versus 2.0 events/100 patient-years, respectively; log-rank P < 0.001; Figure A). The RI provided incremental prognostic value over and above a model consisting of clinical variables and LVH (P = 0.02). Conversely concentric and eccentric LVH were associated with adverse prognosis (4.5 events/100patient-years versus 6.0 events/100patient-years, respectively; log-rank P = 0.62) that was similar as the natural history of hypertensive LVH (5.1 events/100patient-years). CONCLUSIONS The RI provides mechanistic insights and prognostic value that improves risk-stratification of hypertensive LVH. Abstract P962 Figure.

scholarly journals The remodelling index risk stratifies patients with hypertensive left ventricular hypertrophy

2020 ◽  
Author(s):  
Thu-Thao Le ◽  
Vanessa Lim ◽  
Rositaa Ibrahim ◽  
Muh-Tyng Teo ◽  
Jennifer Bryant ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Adverse Events ◽  
Wall Thickness ◽  
Prognostic Value ◽  
Ventricular Hypertrophy ◽  
Troponin I ◽  
Left Ventricular ◽  
Single Measure ◽  
Hypertensive Patients ◽  
Clinical Variables

Abstract Aims  Hypertensive left ventricular hypertrophy (LVH) is associated with increased cardiovascular events. We previously developed the remodelling index (RI) that incorporated left ventricular (LV) volume and wall-thickness in a single measure of advanced hypertrophy in hypertensive patients. This study examined the prognostic potential of the RI in reference to contemporary LVH classifications. Methods and results  Cardiovascular magnetic resonance was performed in 400 asymptomatic hypertensive patients. The newly derived RI (EDV3t, where EDV is LV end-diastolic volume and t is the maximal wall thickness across 16 myocardial segments) stratified hypertensive patients: no LVH, LVH with normal RI (LVHNormal-RI), and LVH with low RI (LVHLow-RI). The primary outcome was a composite of all-cause mortality, acute coronary syndromes, strokes, and decompensated heart failure. LVHLow-RI was associated with increased LV mass index, fibrosis burden, impaired myocardial function and elevated biochemical markers of myocardial injury (high-sensitive cardiac troponin I), and wall stress. Over 18.3 ± 7.0 months (601.3 patient-years), 14 adverse events occurred (2.2 events/100 patient-years). Patients with LVHLow-RI had more than a five-fold increase in adverse events compared to those with LVHNormal-RI (11.6 events/100 patient-years vs. 2.0 events/100 patient-years, respectively; log-rank P < 0.001). The RI provided incremental prognostic value over and above a model consisting of clinical variables, LVH and concentricity; and predicted adverse events independent of clinical variables, LVH, and other prognostic markers. Concentric and eccentric LVH were associated with adverse prognosis (log-rank P = 0.62) that was similar to the natural history of hypertensive LVH (5.1 events/100 patient-years). Conclusion  The RI provides prognostic value that improves risk stratification of hypertensive LVH.

scholarly journals Suppression of aldosterone mediates regression of left ventricular hypertrophy in patients with hypertension

2011 ◽  
Vol 12 (4) ◽  
pp. 483-490 ◽  
Author(s):  
Anne-Catherine Pouleur ◽  
Hajime Uno ◽  
Margaret F Prescott ◽  
Akshay Desai ◽  
Evan Appelbaum ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Wall Thickness ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Plasma Aldosterone ◽  
Plasma Aldosterone Concentration ◽  
Hypertensive Patients ◽  
Blood Pressure Targets ◽  
Direct Renin Inhibitor

Background: High circulating aldosterone levels stimulate myocardial fibrosis and left ventricular hypertrophy (LVH). However, it is not clear whether suppression of aldosterone directly contributes to LVH regression in hypertensive patients. Methods: The Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial randomised 465 hypertensive overweight subjects with LVH to the direct renin inhibitor aliskiren 300 mg, losartan 100 mg or the combination and followed patients for 9 months. All patients were treated to standard blood pressure targets. Left ventricular (LV) mass index (LVMI) and LV wall thickness (LVWT) were assessed by cardiac magnetic resonance. A subset of 136 patients who had plasma aldosterone concentration (ALDO) measured at baseline and study end was analysed. Results: At baseline, plasma ALDO was modestly related to systolic blood pressure, LVMI, and wall thickness (all, p < 0.05). Aliskiren, either alone or in combination, was associated with a significantly greater reduction from baseline to 9 months in plasma aldosterone than losartan alone ( p < 0.02). Reduction in ALDO was related to reduction in LVMI even after adjustment for baseline ALDO, BP reduction and treatment group ( p for trend = 0.042). Conclusion: In hypertensive patients with increased LVWT, aliskiren alone or in combination with the angiotensin receptor blocker losartan provides greater reduction in aldosterone compared to losartan alone. Moreover, suppression of aldosterone was associated with reduction of LVH, independently of the change in SBP, suggesting that suppression of aldosterone, a known mediator of LVH, may be particularly important for LVH regression and as a target for therapy.

A common variant of the eNOS gene (E298D) is an independent risk factor for left ventricular hypertrophy in human essential hypertension

2009 ◽  
Vol 117 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Ying Xin ◽  
Xiaodong Song ◽  
Hao Xue ◽  
Zhe Liu ◽  
Xiaojian Wang ◽  
...  
Keyword(s):  
Risk Factor ◽  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Wall Thickness ◽  
Ventricular Hypertrophy ◽  
Critical Role ◽  
Left Ventricular ◽  
Enos Gene ◽  
Case Control Studies ◽  
Hypertensive Patients

eNOS (endothelial NO synthase) plays a critical role in the development of ventricular remodelling and cardiac hypertrophy. The purpose of the present study was to determine whether three common variants in NOS3 (the eNOS gene) are associated with the risk of LVH [LV (left ventricular) hypertrophy] in patients with essential hypertension. Three NOS3 genetic variants, −T786C (rs2070744), eNOS4a/b and +G894T (rs1799983), were genotyped in two independent case-control studies: the first study consisted of 1061 hypertensive patients with LVH and 1118 hypertensive patients without LVH, and the second sample consisted of 120 patients with LVH and 223 patients without LVH. Echocardiographic measurements were obtained in all of the hypertensive patients. Only the +G894T (E298D) variant of NOS3 was associated with a higher risk of LVH {OR (odds ratio), 1.67 [95% CI (confidence interval), 1.19–2.36]; P<0.01} in the first population, and replicated in the second population [OR, 1.41 (95% CI, 1.01–2.28); P<0.05] in a recessive model. Compared with carriers of the G allele (GT+GG), patients carrying the TT genotype had increased septal wall thickness (16.2%, P<0.01 and 11.7%, P<0.01 respectively), LV posterior wall thickness (8.3%, P<0.01 and 7.1%, P<0.01 respectively), LV mass index (14.0%, P<0.01 and 25.1%, P<0.01 respectively) and relative wall thickness (13.1%, P<0.01 and 16.2%, P<0.01 respectively) in the first and second populations. The results of the present study support that homozygosity for +G894T (E298D) in NOS3 is a genetic risk factor for the development of LVH in patients with hypertension.

Atrial natriuretic peptide gene promoter polymorphism is associated with left ventricular hypertrophy in hypertension

2007 ◽  
Vol 114 (2) ◽  
pp. 131-137 ◽  
Author(s):  
Hao Xue ◽  
Shuxia Wang ◽  
Hu Wang ◽  
Kai Sun ◽  
Xiaodong Song ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Wall Thickness ◽  
Ventricular Hypertrophy ◽  
Gene Promoter ◽  
Left Ventricular ◽  
Hypertensive Patients ◽  
Control Subjects

Recent studies suggest that the ANP (atrial natriuretic peptide)/NPRA (type A natriuretic peptide receptor) system modulates ventricular remodelling and cardiac hypertrophy in hypertension in Western populations. In the present study, we tested for any association between two SNPs (single nucleotide polymorphisms) in the ANP gene (one in the promoter and one exonic) with cardiac hypertrophy. We tested the hypothesis in 2118 hypertensive patients, including 945 with LVH [LV (left ventricular) hypertrophy] and 1173 without LVH, as well as 816 healthy control subjects. All subjects were genotyped for the −A2843G and A188G polymorphisms. We found that the GG genotype at position −2843 conferred a 2.2-fold risk for LVH compared with the AA or AG genotypes, including septal wall thickness (11.8±1.4 mm for GG compared with 10.9±1.4 and 10.7±1.3 mm for AA and AG respectively; P<0.01), posterior wall thickness (11.8±2.8 mm for GG compared with 10.6±1.2 and 10.6±1.4 mm for AA and AG respectively; P<0.01), LV mass index (62.7±13.6 g/m2.7 for GG compared with 57.9±8.6 and 57.8±8.4 g/m2.7 for AA and AG respectively; P<0.05) and relative wall thickness (50.7±10.8% for GG compared with 44.3±7.3 and 43.5±6.8% for AA and AG respectively; P<0.05). Plasma levels of ANP were significantly lower in the hypertensive patients with LVH carrying the GG genotypes compared with those carrying the AA or AG genotypes (P<0.01). No association of GG genotype with echocardiographic variables and plasma ANP levels was identified in hypertensive patients without LVH and in control subjects (P>0.05). No significant association between the A188G genotype and echocardiographic variables was found in either hypertensive patients or controls (P>0.05). In conclusion, our findings indicate that the −A2843G polymorphism in the ANP gene promoter might be a genetic risk factor for the development of LVH in patients with hypertension.

Common Carotid Artery Stiffness and Patterns of Left Ventricular Hypertrophy in Hypertensive Patients

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 651-659 ◽  
Author(s):  
Pierre Boutouyrie ◽  
Stéphane Laurent ◽  
Xavier Girerd ◽  
Athanase Benetos ◽  
Patrick Lacolley ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Left Ventricular Hypertrophy ◽  
Common Carotid Artery ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Hypertensive Patients ◽  
Artery Stiffness
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