Determinants of mortality after myocardial infarction in patients with advanced renal dysfunction

Citation
Jn. Beattie et al., Determinants of mortality after myocardial infarction in patients with advanced renal dysfunction, AM J KIDNEY, 37(6), 2001, pp. 1191-1200
Citations number
41
Categorie Soggetti
Urology & Nephrology
Journal title
AMERICAN JOURNAL OF KIDNEY DISEASES
ISSN journal
02726386 → ACNP
Volume
37
Issue
6
Year of publication
2001
Pages
1191 - 1200
Database
ISI
SICI code
0272-6386(200106)37:6<1191:DOMAMI>2.0.ZU;2-U
Abstract
Previous studies using administrative data have shown high mortality in pat ients with renal failure requiring dialysis after acute myocardial infarcti on (AMI). There has been little investigation into the mortality after AMI in those with advanced renal disease who are not on dialysis therapy. We an alyzed a prospective coronary care unit registry of 1,724 patients with ST segment elevation myocardial infarction admitted over an 8-year period at a single tertiary-care center. Those not on chronic dialysis therapy were st ratified into groups based on corrected creatinine clearance, with cutoff v alues of 46.2, 63.1, and 81.5 mL/min/72 kg. Dialysis patients (n = 47) were considered as a fifth comparison group. Older age, black race, diabetes, h ypertension, previous coronary disease, and heart failure were incrementall y more common across increasing renal dysfunction strata. There were also g raded increases in the relative risk for atrial and ventricular arrhythmias , heart block, asystole, development of pulmonary congestion, acute mitral regurgitation, and cardiogenic shock. Primary angioplasty, thrombolysis, an d P-blockers were used less often across the risk strata (P < 0.0001 for al l trends). There was an early mortality hazard (age-adjusted relative risk, 8.76; P < 0.0001) for those with renal dysfunction but not on dialysis the rapy for the first 60 months, followed by graded decrements in survival acr oss increasing renal dysfunction strata. The excess mortality in this popul ation appears to be mediated through arrhythmias, adverse hemodynamic event s, and the lower use of mortality-reducing therapy. (C) 2001 by the Nationa l Kidney Foundation, Inc.