Study quantifies dangers of renal disease after heart attackBMJ 2004; 329 doi: http://dx.doi.org/10.1136/bmj.329.7468.702-a (Published 23 September 2004) Cite this as: BMJ 2004;329:702
Even mild renal disease, as measured by the glomerular filtration rate (GFR), is a major risk factor for cardiovascular complications after myocardial infarction.
Although renal failure has been associated with one of the highest risks in determining outcome after a heart attack, until now the influence of milder degrees of renal impairment was less well defined (New England Journal of Medicine 2004;351:1285-91).
In the current study, researchers from the valsartan in acute myocardial infarction trial (VALIANT) led by Dr Nagesh Anavekar of the cardiovascular division at Brigham and Women's Hospital, Boston, Massachusetts, identified 14 527 patients who had had acute myocardial infarction complicated by clinical or radiological signs of heart failure or left ventricular dysfunction, or both. Patients in the study had been randomly assigned to receive captopril or valsartan, or both.
Although the rate of renal events increased with declining estimated GFRs, the adverse outcomes were predominantly cardiovascular, with a progressive increase in the risk of death from cardiovascular causes, reinfarction, congestive heart failure, stroke, or resuscitation after cardiac arrest.
Each reduction of 10 units in the estimated GFR was associated with a hazard ratio for death and non-fatal cardiovascular outcomes of 1.10 (95% confidence interval 1.08 to 1.12), which was independent of the treatment assignment. Unadjusted Kaplan-Meier estimates of three year mortality were 14.1% (13.0% to 15.2%) in the group with an estimated GFR of at least 75.0 ml/min per 1.73 m2 of body surface area, 20.5% (18.8% to 22.2%) in the group with an estimated GFR of 60.0-74.9 ml/min per 1.73 m2, and 28.9% (27.0% to 30.8%) in the group with an estimated GFR of 45.0-59.9 ml/min per 1.73 m2. Thee year mortality reached 45.5% (42.1% to 48.9%) in the group with an estimated GFR of <45.0 ml/min per 1.73 m2.
“Among patients who have had a myocardial infarction, any degree of preexisting renal impairment should be considered a potent, independent, and easily identifiable risk factor for cardiovascular complications,” the authors wrote.
The risk of cardiovascular disease began to rise once the GFR dropped below 60 ml/min per 1.73 m2. This value corresponds to a serum creatinine level of 1.0-1.7 mg/dl (88.4-150.3 micromol per litre) for people over 40 years old, depending on exact age, sex, and race.
Blockade of the renin-angiotensin system with either angiotensin converting enzyme inhibitors or angiotensin-receptor blockers is known to reduce the progression of renal disease. In VALIANT, all patients received effective inhibitors of the renin-angiotensin system, yet a lower GFR estimated at baseline was also still associated with adverse cardiovascular outcomes.
The analysis had several limitations. The authors could not comment on the effect of the duration of renal dysfunction on the risk of adverse cardiovascular outcomes, and they did not examine the influence of changes in renal function on risk, possibly related to therapy.