A 52-year-old man was admitted to the emergency department with a 2-hour history of typical ischemic chest pain. He had type 2 diabetes mellitus, hypertension, dyslipidemia, and peripheral vascular disease. He did not smoke and was not overweight, although there was a strong family history of premature coronary disease. Results of the physical examination showed that the patient had hypotension, sinus tachycardia, and diaphoresis; no clinical evidence of left ventricular failure was present. Electrocardiography results showed anteroseptal ST-segment depression. The patient was given prescriptions for oxygen, nitrates, and opiates. Loading doses of aspirin and clopidogrel (Plavix) were administered, along with lowmolecular-weight heparin and a glycoprotein IIb/IIIa antagonist. Urgent coronary angiography showed a thrombus within the left anterior descending artery, and a drug-eluting stent was inserted; no other flow-limiting atherosclerotic coronary disease was noted.

The patient returned to the coronary care unit and remained pain free. He received intravenous insulin for 24 hours and then was given his usual oral hypoglycemic agents, including metformin (Fortamet, Glucophage, Riomet) and glyburide (Diabeta, Micronase). His cardiologist ensured that evidence-based secondary preventative therapies were provided, including aspirin, clopidogrel, a statin, a ß-adrenoreceptor antagonist, and an angiotensin-converting enzyme inhibitor. His blood pressure and lipid levels met current targets suggested by the American Heart Association. Attendance at cardiac rehabilitation classes was arranged, and the patient was discharged free of symptoms 4 days after the index event. His left ventricular function appeared well preserved on routine follow-up echocardiography 1 month later.

Was this man's long-term prognosis improved by the regimen of evidence-based treatment he received? Could more be done to improve his outcome?