A 62-year-old man was admitted for spontaneous constrictive, intense chest pain. He was not overweight (weight, 65 kg; height, 168 cm), but he had a 10-year history of hypertension, which was treated with diuretics and a beta blocker. He also had a history of renal dysfunction.

On admission, the patient no longer complained of chest pain, which stopped spontaneously after 20 minutes. His heart rate was 74 beats/ minute, and his blood pressure was 145/75 mm Hg on both arms. Results of the physical examination were normal. An electrocardiogram showed a sinus rhythm and signs of left ventricular hypertrophy with flattened T waves. The patient’s biological markers showed no troponin release, a moderately increased brain natriuretic peptide level (300 pg/mL), a normal D-dimers concentration, and a high creatinine level (200 µmol/L).

The suspected diagnosis was acute aortic syndrome, but echocardiography showed only left ventricular hypertrophy with normal systolic left ventricular function, and there was no valve disease or aortic abnormality. Results of a second biological troponin assessment performed 4 hours later were positive, allowing the physician to diagnose acute coronary syndrome, without troponin release, namely non–ST-segment elevation acute myocardial infarction (MI), according to the “new” definition of MI.¹

The patient was treated with combination oral antiplatelet therapy (aspirin and clopidogrel [Plavix]), unfractionated heparin, and statins. Some guidelines-recommended treatments could not be given, such as beta-blockers (because of the left ventricular dysfunction), and angiotensin-converting enzyme (ACE) inhibitors, low-molecular-weight heparin, and statins (because of the renal dysfunction). An invasive strategy (ie, coronary angioplasty) was not recommended, also because of the renal dysfunction, and therefore no glycoprotein (GP) IIb/IIIa inhibitors were given.

In this case, the degree of renal dysfunction was overestimated. The creatinine clearance was > 30 mL/min/m², despite the high creatinine value. Thus, it would be important to recognize this patient as a high-risk patient, not only because of his age and troponin release, but also because of the renal dysfunction. According to the Global Registry of Acute Coronary Events (GRACE) score,² the probability of death was 4% in the hospital and 10% at 6 months, and the probability of death or MI was 19% in the hospital and 35% at 6 months!

Despite the patient’s renal dysfunction and his high-risk level, it would be important to use all effective and guidelines-recommended treatments, including low-molecular-weight heparin instead of unfractionated heparin (or even 2.5 mg fondaparinux [Arixtra],³ according to the results of the Organization to Assess Strategies in Acute Ischemic Syndromes (OASIS)-6 study³; an ACE inhibitor⁴; an early invasive procedure (coronary angioplasty) after specific preparation and evaluation of the risk of contrast-induced nephropathy⁵; and a IIb/IIIa inhibitor in view of the possible invasive procedure.⁶

This case report illustrates the importance of accurate assessment of renal function in acute coronary syndrome patients. Sometimes, renal dysfunction is overestimated and leads to underutilization of recommended treatments.

References
1. Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000; 36(3): 959-969.

2. Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital mortality in the global registry of acute coronary events. Arch Intern Med. 2003; 163(19):2345-2353.

3. Yusuf S, Mehta SR, Chrolavicius S, et al. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA. 2006; 295(13):1519-1530.

4. Mann JF, Gerstein HC, Pogue J, et al. Renal insufficiency as a predictor of cardiovascular outcomes and the impact of ramipril: the HOPE randomized trial. Ann Intern Med. 2001; 134(8):629-636.

5. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004; 44(7): 1393-1399.

6. Januzzi JL, Cannon CP, DiBattiste PM, et al. Effects of renal insufficiency on early invasive management in patients with acute coronary syndromes (the TACTICS-TIMI 18 trial). Am J Cardiol. 2002; 90(11): 1246-1249.