Effects of enalapril in heart failure: a double blind study of effects on exercise performance, renal function, hormones, and metabolic state.

Cleland, John G.F.; Dargie, Henry J.; Ball, Stephen G.; Gillen, G.; Hodsman, G P; Morton, John J.; East, B.W.; Robertson, Ian; Ford, Ian; Robertson, James I.

doi:10.1136/hrt.54.3.305

Cited by 266 publications

(55 citation statements)

References 49 publications

(6 reference statements)

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“…Angiotensin‐converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) have been shown in multiple large clinical trials to improve symptoms, reduce hospitalizations, and improve survival in patients with HF with reduced ejection fraction (HFrEF) 3, 4, 5, 6, 7. The American College of Cardiology (ACC)/American Heart Association (AHA) clinical guidelines make it a Class I, Level A recommendation to use ACEi/ARB therapy in patients with HFrEF both to “prevent symptomatic heart failure” and to “reduce morbidity and mortality.”8 In addition, the ACC/AHA HF Performance Measures recommend ACEi/ARB for outpatients with HFrEF and ACEi/ARB therapy at the time of hospital discharge for inpatients with HFrEF 9.…”

Section: Introductionmentioning

confidence: 99%

Initiation, Continuation, or Withdrawal of Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers and Outcomes in Patients Hospitalized With Heart Failure With Reduced Ejection Fraction

Gilstrap

Fonarow

Desai

et al. 2017

JAHA

118

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BackgroundGuidelines recommend continuation or initiation of guideline‐directed medical therapy, including angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers (ACEi/ARB), in hospitalized patients with heart failure with reduced ejection fraction.Methods and ResultsUsing the Get With The Guidelines‐Heart Failure Registry, we linked clinical data from 16 052 heart failure with reduced ejection fraction (ejection fraction ≤40%) patients with Medicare claims data. We divided ACEi/ARB‐eligible patients into 4 categories based on admission and discharge ACEi/ARB use: continued (reference group), started, discontinued, or not started on therapy. A multivariable Cox proportional hazard model was used to determine the association between ACEi/ARB category and outcomes. Most, 90.5%, were discharged on ACEi/ARB (59.6% continued and 30.9% newly started). Of those discharged without ACEi/ARB, 1.9% were discontinued, and 7.5% were eligible but not started. Thirty‐day mortality was 3.5% for patients continued and 4.1% for patients started on ACEi/ARB. In contrast, 30‐day mortality was 8.8% for patients discontinued (adjusted hazard ratio [HR adj] 1.92; 95% CI 1.32‐2.81; P<0.001) and 7.5% for patients not started (HR adj 1.50; 95% CI 1.12‐2.00; P=0.006). The 30‐day readmission rate was lowest among patients continued or started on therapy. One‐year mortality was 28.2% for patients continued and 29.7% for patients started on ACEi/ARB compared to 41.6% for patients discontinued (HR adj 1.35; 95% CI 1.13‐1.61; P<0.001) and 41.7% (HR adj 1.28; 95% CI 1.14‐1.43; P<0.001) for patients not started on therapy.ConclusionsCompared with continuation, withdrawal of ACEi/ARB during heart failure hospitalization is associated with higher rates of postdischarge mortality and readmission, even after adjustment for severity of illness.

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Section: Introductionmentioning

confidence: 99%

Initiation, Continuation, or Withdrawal of Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers and Outcomes in Patients Hospitalized With Heart Failure With Reduced Ejection Fraction

Gilstrap

Fonarow

Desai

et al. 2017

JAHA

118

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“…This effect may explain in part the reduction in plasma catecholamines in patients with congestive heart failure treated with ACE inhibitors 47 and the reduction in cardiac arrhythmias in such patients. 48 In the adrenal gland, concentrations of ACE are high in both the adrenal cortex and adrenal medulla. 20 Ang II receptors have a similar distribution.…”

Section: Role Of Tissue Angiotensin Converting Enzyme In Cardiovasculmentioning

confidence: 99%

Tissue angiotensin converting enzyme in cardiac and vascular hypertrophy, repair, and remodeling.

Johnston

1994

Hypertension

160

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A 52-year-old white man presented with a small full wall thickness anterior myocardial infarct. He L was given intravenous streptokinase, aspirin, and nitrates, and his course was uncomplicated.He had suffered mild essential hypertension for 10 years and had been treated over this period with moduretic (one tablet per day). His primary physician had excluded causes of secondary hypertension, and he had been told that his blood pressure control on the diuretic was satisfactory (documented at levels between 146 and 138 mm Hg systolic and 90 and 96 mm Hg diastolic). His serum cholesterol levels had been measured on several occasions, and the last reading was 6.8 mmol/dL (205 mg%).A chest radiograph performed in the hospital showed cardiomegaly, and his electrocardiogram showed high voltage over his anterior chest leads. An echocardiogram confirmed increased posterior and septal thicknesses, with normal fractional shortening. A radionuclide ventriculogram showed a left ventricular ejection fraction of 40%. Serum creatinine concentration was within normal limits, as were serum potassium and blood glucose levels.His blood pressure on presentation to the hospital with the myocardial infarction was 160/100 mm Hg and remained at this level for the first 24 hours. On the second day, 6.25 mg captopril was given and then 12.5 mg twice daily. His blood pressure fell to 150/95 mm Hg, and his captopril dose was increased to 25 mg twice daily.On discharge from the hospital, his blood pressure was 140/82 mm Hg. Six months later, on medical review, his blood pressure was 142/84 mm Hg, his cholesterol was 5.5 mg/dL, and his left ventricular hypertrophy had regressed.This man presents with a very common clinical and management problem: a middle-aged man with longstanding treated hypertension and left ventricular hypertrophy complicated by an acute myocardial infarct.Dr Johnston was an invited speaker at

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“…Other vasodilators enhancing angiotensin I1 levels will result in facilitation of noradrenaline synthesis and increasedg-receptor stimulation. Angiotensin converting enzyme inhibitors, on the other hand, have been shown to reduce circulating catecholamine levels (89,93,(95)(96)(97)(98). T h e combination of vasodilatation associated with a fall in angiotensin I1 and sympathetic nervous system activity may be the important feature that results in improved mortality in patients treated with these agents.…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

“…These agents produce vasodilatation in patients with heart failure where a major part of the increased peripheral vascular resistance is secondary to activation of this system. T h e two most commonly used agents are captopril and enalapril and a number of studies have shown that both agents are effective in producing short-and long-term haemodynamic and clinical improvement (87)(88)(89)(90)(91)(92)(93)(94). In addition to improving symptomatology and functional class, it has recently been shown that therapy with enalapril results in an improvement in prognosis in patients with severe congestive cardiac failure.…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

Therapeutic Progress—review Xxxiv: Congestive Cardiac Failure

Davies

1989

J Clin Pharm Ther

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Effects of enalapril in heart failure: a double blind study of effects on exercise performance, renal function, hormones, and metabolic state.

Cited by 266 publications

References 49 publications

Initiation, Continuation, or Withdrawal of Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers and Outcomes in Patients Hospitalized With Heart Failure With Reduced Ejection Fraction

Initiation, Continuation, or Withdrawal of Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers and Outcomes in Patients Hospitalized With Heart Failure With Reduced Ejection Fraction

Tissue angiotensin converting enzyme in cardiac and vascular hypertrophy, repair, and remodeling.

Therapeutic Progress—review Xxxiv: Congestive Cardiac Failure

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