Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder.
CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.