Neurohormonal and clinical responses to high- vs. low-dose enalapril therapy in chronic heart failure

Tang, Wen; Vagelos, Randall H.; Yee, Yin‐Gail

doi:10.1016/s1062-1458(02)00654-2

Cited by 19 publications

(28 citation statements)

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“…18,19 Incomplete inhibition of the vascular converting enzyme was not related to the duration of ACE inhibitor therapy. This finding, albeit collected in a cross-sectional study, contrasts with results reported by other investigators who noted an increase in AI/AII conversion over time.…”

Section: Clinical Characteristics Of 34 Subjectsmentioning

confidence: 97%

Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure

et al. 2002

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Background-Plasma aldosterone levels are elevated in patients with chronic heart failure (CHF) taking angiotensinconverting enzyme (ACE) inhibitors. Elevated aldosterone levels may reflect incomplete inhibition of the vascular converting enzyme during long-term ACE inhibition. We simultaneously measured plasma aldosterone levels and the degree of inhibition of the vascular converting enzyme in patients with CHF. Methods and Results-Thirty-four subjects with CHF receiving the maximum recommended doses of ACE inhibitors for a duration of 3 to 105 months were studied. The pressor response to exogenous angiotensin I (AI) was measured and normalized for the pressor response to angiotensin II (AII) to assess inhibition of the vascular converting enzyme (AII/AI ratio). Aldosterone levels were determined by solid-phase radioimmunoassay. Eleven of the 34 subjects had plasma aldosterone levels above the upper limit of normal, ie, Ͼ15.0 ng/dL. Seven of these 11 subjects (64%) had an AII/AI ratio Յ0.05, indicating complete inhibition of the vascular converting enzyme. In the entire cohort, the AII/AI ratio did not correlate with the duration of ACE inhibitor therapy. Conclusions-Plasma aldosterone levels are elevated in patients with CHF during long-term ACE inhibitor therapy despite complete inhibition of the vascular converting enzyme. Complete inhibition of the vascular converting enzyme does not obviate the need for aldosterone receptor blockade in patients with CHF.

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Section: Clinical Characteristics Of 34 Subjectsmentioning

confidence: 97%

Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure

et al. 2002

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“…The benefits of mineralocorticoid receptor antagonists in ambulatory HF patients are now widely established, with such treatment reducing mortality and readmissions in patients with advanced as well as paucisymptomatic HF 19,20 . Importantly, aldosterone breakthrough occurs in many HF patients despite treatment with an angiotensin-converting enzyme inhibitor at an adequate dose 21 . Although decongestive treatment with loop diuretics further boosts systemic and intrarenal aldosterone production, there is a lack of data regarding the use of mineralocorticoid receptor antagonists in decompensated HF 3 .…”

Section: Conflict Of Interest: None Declaredmentioning

confidence: 99%

Determinants and impact of the natriuretic response to diuretic therapy in heart failure with reduced ejection fraction and volume overload

et al. 2015

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“…The study found that ANP, BNP, and norepinephrine levels were significantly lower in the 40-mg/d group compared with the 10-mg/d group. 26 In contrast, Tang et al 19 suggested that neurohormonal changes were not significantly affected by higher ACE inhibition. Seventy-five patients with EF <40% were randomized to enalapril 40 mg or 5 mg once daily and evaluated over a 30-week follow-up.…”

Section: Neurohormonal and Immunologic Activitymentioning

confidence: 94%

“…17,18 Reactivation of the converting enzyme can be suppressed by increasing the dose of the ACE inhibitor. 19 Nussberger et al 20 showed that angiotensin II levels decrease in a dose-dependent fashion with quinapril (2. 21 In severe HF, however, dose dependency of angiotensin II was not evident, as demonstrated in a study using enalapril.…”

Section: Neurohormonal and Immunologic Activitymentioning

confidence: 99%

What is the Optimal Angiotensin‐Converting Enzyme Inhibitor Dose in Heart Failure?

Thomas

Geltman

2006

Congestive Heart Failure

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Doses of angiotensin‐converting enzyme (ACE) inhibitors used in the landmark heart failure trials that demonstrated survival benefit are rarely reached in routine practice. The authors review the current literature regarding optimal dosing of ACE inhibitors in heart failure with specific focus on neurohormonal, functional capacity, and clinical outcomes. Neurohormonal studies have shown that lower ACE inhibitor dosing may provide inadequate suppression of the renin‐angiotensin‐aldosterone system. Higher doses of ACE inhibitors have resulted in greater increments in exercise and functional capacity. Clinically, patients on high‐dose ACE inhibitor therapy had significant reductions in all‐cause mortality or hospitalization, cardiovascular hospitalizations, and heart failure‐specific hospitalizations. There is, however, conflicting evidence, and so continued uncertainty exists regarding optimal dosing. Despite underutilization of ACE inhibitors, there is insufficient evidence to support lower doses. Likewise, limited data exist for doses higher than those used in the landmark trials. Clinicians should therefore attempt to reach target doses in heart failure whenever possible.

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Neurohormonal and clinical responses to high- vs. low-dose enalapril therapy in chronic heart failure

Cited by 19 publications

References 0 publications

Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure

Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure

Determinants and impact of the natriuretic response to diuretic therapy in heart failure with reduced ejection fraction and volume overload

What is the Optimal Angiotensin‐Converting Enzyme Inhibitor Dose in Heart Failure?

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