ACE inhibitors captopril and enalapril induce regression of left ventricular hypertrophy in hypertensive patients with chronic renal failure

Dyadyk, A. I.; Bagriy, A. E.; Lebed, I A; Yarovaya, N.F.; Schukina, Elena V.; Тарадин, Г. Г.

doi:10.1093/ndt/12.5.945

Cited by 58 publications

(28 citation statements)

References 9 publications

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“…12 Dyadyk and co-workers demonstrated a 20% reduction in LV mass index over 12 months in ESRD patients treated with either captopril or enalapril. 13 There have been no clinical trials of treatment for ACS or CHF in patients with ESRD. We have recently shown that CKD patients, including ESRD, in the setting of ST-segment elevation MI (STEMI), significantly benefit from the use of aspirin and β-blockers.…”

Section: Discussionmentioning

confidence: 99%

Mortality benefit of angiotensin-converting enzyme inhibitors after cardiac events in patients with end-stage renal disease

McCullough

Sandberg

Yee

et al. 2002

J Renin Angiotensin Aldosterone Syst

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Hypothesis/introductionThe risks and benefits of angiotensin-converting enzyme (ACE) inhibitors in patients with end-stage renal disease (ESRD) after cardiac events are unknown. We sought to determine the independent effect of ACE inhibitors (ACE-I) on long-term mortality in ESRD patients after cardiac events. Materials and methodsWe analysed a prospective coronary care unit registry and identified 527 ESRD patients, 368 with complete data on medications prescribed, over eight years at a single, tertiary centre. ResultsThe overall mean age was 64.4+13.8 years with 54.9% men, and 59.2% African-American. A total of 143/386 (37.0%) were prescribed ACE-I during the hospital stay for cardiac reasons, including congestive heart failure (CHF) 52.8% and acute coronary syndromes (ACS) 47.2%. There were no significant differences in the rates of hypotension or arrhythmias in those who were treated with ACE-I versus those who were not. Survival analysis over three years, adjusted for known confounders, demonstrated a 37% reduction in all-cause mortality in those who received ACE-I, (p=0.0145). ConclusionsIn the setting of coronary care unit admission for CHF and ACS, ESRD patients selected for ACE-I, did not have increased rates of adverse haemodynamic or arrhythmic complications. The use of ACE-I conferred an independent mortality reduction over long-term follow-up. IntroductionWe and others have demonstrated that chronic kidney disease (CKD) including end-stage renal disease (ESRD) requiring renal-replacement therapy are independent risk factors for morbidity and mortality after a variety of cardiac events.

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Section: Discussionmentioning

confidence: 99%

Mortality benefit of angiotensin-converting enzyme inhibitors after cardiac events in patients with end-stage renal disease

McCullough

Sandberg

Yee

et al. 2002

J Renin Angiotensin Aldosterone Syst

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“…Clinical studies on LVH regression after ACE inhibition in essential hypertension [22, 23]and in patients with chronic renal failure [24, 25]indicate that the renin-angiotensin-aldosterone system might play a role in the development of LVH [26]. Moreover, it was proposed that the regression caused by ACE inhibition in chronic renal failure was independent of its antihypertensive effects [27].…”

Section: Discussionmentioning

confidence: 99%

No Association between Deletion-Type Angiotensin-Converting Enzyme Gene Polymorphism and Left-Ventricular Hypertrophy in Hemodialysis Patients

Yildiz¹,

Akkaya

Hatemi

et al. 2000

Nephron

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Left-ventricular hypertrophy (LVH), a bad prognostic sign, is a common finding in hemodialysis patients. The aim of the study was to analyze factors, including angiotensin-converting enzyme (ACE) genotype that may have an effect on the development of LVH in hemodialysis patients. Seventy-nine hemodialysis patients (42 males, 37 females, mean age 37.7 ± 13.1 years) and 82 age- and sex-matched normotensive healthy controls (40 males, 42 females, mean age 35.6 ± 5.7 years) were included. Left-ventricular mass index (LVMI) was higher in the hemodialysis group compared to controls (170.1 ± 69.3 versus 84.9 ± 15.7 g/m², p < 0.001). Fourty-three hypertensive patients in the hemodialysis group had an increased LVMI compared to 36 normotensive hemodialysis patients (194.2 ± 75.5 versus 141.2 ± 48.0 g/m², p < 0.001). On univariate analysis, LVMI was found to be correlated with blood pressure (r = 0.38, p < 0.001), time spent on dialysis (r = 0.22, p = 0.02) and hemoglobin levels (r = –0.21, p = 0.03). No correlation was found between LVMI and age (r = 0.09, p = 0.22), predialytic creatinine (r = 0.09, p = 0.21) and albumin (r = –0.10, p = 0.18). On multivariate analysis for the predictors of LVMI, blood pressure, time spent on dialysis and hemoglobin levels were also found to be significant. LVMI in DD, ID and II genotypes were 155.0 ± 71.2, 181.6 ± 60.6, and 163.6 ± 83.4 g/m², respectively (p > 0.05). No association between LVMI and DD genotype was found. ACE genotype distribution was similar in hemodialysis patients and healthy controls. It was concluded that LVH in hemodialysis patients was mainly related to hypertension, anemia and time spent on dialysis and the DD genotype had no effect on LVMI in hemodialysis patients.

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“…Hence this points to the presence of other factors in the pathogenesis. However hypertension must be aggressively pursued in patients with renal failure as treatment has resulted in a modest amelioration of LVH (Dyadyk, Bagriy et al 1997). It also seems that the activation of the renin angiotensin aldosterone axis seems to be a factor independent of hypertension.…”

Section: Uremic Cardiomyopathymentioning

confidence: 99%

“…In conjunction with this Pirola et al have also shown that angiotensin II also stimulated the release of PTH (Pirola, Wang et al 1993;Okano, Wu et al 1994) and in the next section we will discuss how PTH seems to be an important factor in causing fibrosis and LVH. It has been shown that treatment with ACE inhibitors causes regression of LVH independent of hypotensive effects (Cannella, Paoletti et al 1997;Dyadyk, Bagriy et al 1997;Vlahakos, Hahalis et al 1997). This lends more credibility to the idea that cardiac fibrosis may be an important factor in the pathogenesis of uremic cardiomyopathy.…”

Section: Uremic Cardiomyopathymentioning

confidence: 99%

Cardiotonic Steroids and Cardiac Fibrosis

Vetteth¹,

Malhotra²,

Shapiro³

2012

Cardiomyopathies - From Basic Research to Clinical Management

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ACE inhibitors captopril and enalapril induce regression of left ventricular hypertrophy in hypertensive patients with chronic renal failure

Cited by 58 publications

References 9 publications

Mortality benefit of angiotensin-converting enzyme inhibitors after cardiac events in patients with end-stage renal disease

Mortality benefit of angiotensin-converting enzyme inhibitors after cardiac events in patients with end-stage renal disease

No Association between Deletion-Type Angiotensin-Converting Enzyme Gene Polymorphism and Left-Ventricular Hypertrophy in Hemodialysis Patients

Cardiotonic Steroids and Cardiac Fibrosis

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