Heart Failure Prevention Post–Myocardial Infarction: 5 Things to Know

Musa A. Sharkawi, MBBCh; Ajar Kochar, MD, MHS

Disclosures

May 28, 2020

Editorial Collaboration

Medscape &

4. Early initiation of an aldosterone antagonist for patients with EF ≤ 40% and HF or diabetes reduces the risk for mortality and sudden cardiac death.

The EPHESUS trial showed that there was a 15% relative risk reduction of all-cause mortality in patients who were treated with eplerenone compared with patients who received placebo. This effect, however, was time-dependent and attenuated if the drug was added 7 days after index MI. Therefore, the ACCF/AHA STEMI guidelines recommend that "an aldosterone antagonist should be given to patients with STEMI and no contraindications who are already receiving an ACE inhibitor and beta-blocker and who have an EF ≤0.40 and either symptomatic HF or diabetes mellitus."

It is important for clinicians to keep in mind that aldosterone antagonists should not be given to men with a serum creatinine level ≥ 2.5 mg/dL or to women with a creatinine level ≥ 2.0 mg/dL, or to male and female patients with a serum potassium level ≥ 5.0 mEq/L.

In all of the drug classes noted thus far—ACE inhibitors, beta-blockers, and aldosterone antagonists—it is crucial to uptitrate the dosages to the optimal levels studied in trial during and after the hospitalization period.

5. New pharmacologic and nonpharmacologic therapies to prevent HF in patients post-MI are on the horizon, pending additional trial data.

The PARADIGM-HF trial showed that combination therapy with the angiotensin inhibitor sacubitril and the ARB valsartan was superior to enalapril in reducing the risk of HF-associated death and of hospitalization in patients with symptomatic HF and reduced EF.

As a neprilysin inhibitor, sacubitril not only prevents the degradation of natriuretic peptides (the group of hormones that have potent effects on sodium and fluid balance), but also inhibits the renin-angiotensin-aldosterone system, reducing sympathetic drive and exerting antihypertensive and antiproliferative effects. On the basis of results from the PARADIGM-HF trial, the ongoing PARADISE-MI trial is evaluating whether sacubitril/valsartan might also reduce the incidence and severity of HF among post-MI patients with LVEF ≤ 40%.

Another class of medications developed for the treatment of type 2 diabetes, the sodium-glucose cotransporter-2 (SGLT2) inhibitors have shown promise in improving cardiovascular outcomes. The DAPA-HF trial showed that patients with symptomatic HF and an EF ≤ 40% who received dapagliflozin had a lower risk for worsening HF or death from cardiovascular causes compared with patients who received placebo, regardless of the presence or absence of diabetes. Building on previously published data, the ongoing EMMY trial aims to evaluate the effects of empagliflozin on biomarkers of HF in post-MI patients with and without type 2 diabetes.

Preclinical studies suggested that mechanical unloading of the myocardium reduces myocardial oxygen demand when it is performed prior to revascularization, and that this may in turn attenuate reperfusion injury and reduce infarct size. A small feasibility pilot trial, DTU-STEMI, demonstrated that this strategy of LV unloading followed by immediate reperfusion is as safe as LV unloading followed by a 30-minute delay to reperfusion. A larger upcoming trial, STEMI-DTU, will study patients with anterior STEMI to assess the effects of LV unloading on infarct size using a mechanical circulatory support device (Impella CP). It is important to note that there have been no trial data to date suggesting improvement in clinical outcomes with the use of any form of mechanical circulatory support in the setting of MI.

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