Regarding ACE inhibitors in heart failure management, all of the following statements are true EXCEPT:

Question

Accepted Answer

B. They reduce mortality in both systolic and diastolic heart failure. ## ACE Inhibitors in Heart Failure: Mechanism and Evidence

### Mortality Benefit Profile
**Key Point:** ACE inhibitors reduce mortality in systolic heart failure (reduced ejection fraction, HFrEF) but do NOT reduce mortality in isolated diastolic heart failure (HFpEF) — they improve symptoms only.

The landmark trials (CONSENSUS, SOLVD) demonstrated mortality reduction in HFrEF. However, trials in HFpEF (CHARM-Preserved, I-PRESERVE) showed symptomatic benefit without mortality reduction.

### Why the Other Statements Are Correct

| Feature | Mechanism | Clinical Relevance |
|---------|-----------|--------------------|
| **Dry cough** | Bradykinin accumulation in pulmonary epithelium (ACE also degrades bradykinin) | Occurs in 10–20% of patients; reversible on drug cessation |
| **Angioedema contraindication** | Risk of recurrent/severe angioedema if prior history exists | Absolute contraindication; risk ~30% if prior ACE-I angioedema |
| **Vasodilation mechanism** | Reduced angiotensin II → decreased SVR and preload | No direct inotropic effect; benefit is hemodynamic, not contractile |

### Clinical Pearl
**High-Yield:** ACE inhibitors are first-line in HFrEF (Class I recommendation) but are NOT recommended as monotherapy in HFpEF unless there is concurrent hypertension or post-MI state.

[cite:Harrison 21e Ch 281]

Answer

A. They improve symptoms and reduce hospitalisation primarily through vasodilation rather than inotropic effects

Answer

C. They cause a dry cough due to bradykinin accumulation in the lungs

Answer

D. They are contraindicated in patients with a history of angioedema from any cause

Regarding ACE inhibitors in heart failure management, all of the following statements are true EXCEPT:

Explanation

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