Verapamil and vasospastic angina: underuse in the elderly population

The first case of Prinzmetal angina was described in 1959 by Prinzmetal, et al. Since this description, several triggering factors have been associated with vasospastic angina (VA) and included: illicit drugs such as cocaine, amphetamine or marijuana, but also bitter-orange, alcohol, butane, chemotherapy drugs, over-the-counter medication and different antibiotics. Smoking is also a major risk factor for developing VA. Thus, except for smoking, many of conventional atherosclerosis risk factors do not appear to be applicable to VA. However, vasospastic angina can also occur without any triggering factor. It is established that coronary spasm plays an important role not only in the pathogenesis of variant angina but also in ischemic disease in general, including resting and effort angina, acute myocardial infarction (AMI) and sudden death. In approximately one in ten patients with AMI, angiography does not reveal any obstructive coronary artery disease. The classical symptoms are represented by recurrent resting angina with spontaneous remission. A circadian pattern has been noted and VA preferentially occurs in the morning hours. Complications of VA included AMI, malignant ventricular arrhythmia and even sudden cardiac arrest or death. Conflicting results exist on the VA pathophysiology. In fact, proposed mechanisms responsible for this disease entity are the hyperactivity of sympathetic nervous system associated with a vagal withdrawal or a reduced nitric oxide synthase and endothelial dysfunction. A genetic predisposition has also been evoked. Calcium channel blockers (CCBs) are the first-line therapy for VA. These agents have been shown to reduce symp-