Heart Failure After Acute ST Segment Elevation Myocardial Infarction, The Need for Selective Aldosterone Blockade

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US Cardiology 2006;2005:2(1):191-195


There are several situations in which high-risk myocardial infarction (MI) patients can be identified. These include:

  • a large amount of necrosis, i.e. marked sinustachycardia (ST) segment elevation, marked troponin T elevation, multiple lead electrocardiogram (ECG) changes or extensive left ventricle (LV) dysfunction as measured by brain natriuretic peptide (BNP) or echocardiogram;
  • patients with diabetes and abnormal hemoglobin A1Cs;
  • renal disease manifested by elevated creatinine or microalbuminurea; and
  • on-going inflammation as manifested by C-reactive protein (CRP).

The national registry for MI (NRMI) consists of 190,518 patients.1 Following their acute MI, 36,303 patients had heart failure ((HF) 19%).These patients were classified in Killip class 2 or 3. In that registry, the hospital mortality was 21.4% in patients with HF compared with 7.2% in patients without HF. In the NRMI registry, none of the patients were treated with a potassium-sparing diuretic, such as aldactone or eplerenone.

Estimation of Risk

In a recent study in which ejection fraction was measured within 24 hours after the onset of the MI, ejection fractions 45% (120 patients) had a 2.5% 30-day mortality, whereas ejection fractions less than 45% (81 patients) had a 25.9% 30-day mortality.2 Early mortality was therefore captured in this study.

One of the conclusions that can be drawn is that these high-risk patients with poor ejection fraction may benefit from angiotensin-converting enzyme (ACE) inhibition, angiotensin receptor blockers (ARBs), anti-coagulation, aldosterone blockade, beta-blockers, aspirin, statins, glycoprotein 2B 3A receptor blockers, and angiography to assess coronary pathology.

The Renin Angiotensin Aldosterone System and the Aldosterone Hypothesis

The renin angiotensin (RAS) is more appropriately referred to as the renin angiotensin aldosterone system (RAAS). It is common knowledge that angiotensinogen in the presence of renin becomes angiotensin 1, which in the presence of an ACE becomes angiotensin 2. There are alternative pathways for the production of angiotensin 2, but when produced from angiotensin 1, angiotensin 2 can be blocked by an ACE inhibitor.Angiotensin 2 has several pathophysiologic effects on the cardiovascular (CV) system that can be blocked by ARBs.


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