Acute stent thrombosis in the setting of cocaine abuse following percutaneous coronary intervention.

The treatment of acute coronary syndrome (ACS) in patients with documented cocaine abuse has always presented significant challenges. Issues related to medication compliance, the potential risks of beta adrenergic blockade, and possible continued cocaine abuse postmyocardial infarction necessitate a unique, individualized approach to these patients. Recent data in the era of extensive percutaneous coronary interventions (PCI) and intracoronary stent (ICS) implantation have raised questions regarding the safety of ICS in patients who may revert to cocaine abuse postacute coronary syndrome as a result of the potentially higher risk of stent thrombosis in these patients. While the precise reason as to why cocaine use may increase the risk of stent thrombosis is not fully understood, it is likely the result of a confluence of factors, including coronary vessel vasoconstriction, impaired vascular compliance, as well as the platelet-activating effect of cocaine. We present the case a 46-year-old male with a history of cocaine abuse who presented with an acute stent thrombosis 2 days post-PCI likely as a result of cocaine abuse on the day of discharge following initial stent implantation for a non-ST-elevation myocardial infarction (NSTEMI). We also review the literature regarding the safety of PCI in cocaine abusers.

Drug treatment of orthostatic hypotension and vasovagal syncope.

Orthostatic hypotension is a common problem, estimated to occur in 5 out of every 1000 individuals and in as many as 7% to 17% of patients in an acute care setting. Moreover, orthostatic hypotension may be more prominent in elderly patients due to the increased intake of vasoactive medications and concomitant decrease in physiologic function, such as baroreceptor sensitivity, often seen with aging. Orthostatic hypotension is a fall in blood pressure on assuming an upright position. Absolute cutoffs for the drop in blood pressure are often difficult to determine because different patients exhibit varying degrees of tolerance to falls in blood pressure. Therefore, strict numerical criteria may lead to underdiagnosis and improper intervention. A thorough review of patient symptomatology combined with appropriate clinical tests should be employed to narrow the vast differential diagnosis and pinpoint the etiology. The fall in blood pressure seen in orthostatic hypotension results from the inability of the autonomic nervous system to adequately compensate for the 500 mL blood that is estimated to pool in the lower extremities on assuming an upright posture. The decrease in venous return results in a concomitant decrease in cardiac output and thus hypoperfusion of the cerebral circulation, possibly resulting in syncope or various other symptoms. A complete investigation should consider hypovolemia, removal of offending medications, primary autonomic disorders, secondary autonomic disorders and, of course, vasovagal syncope, the most common cause of syncope. Although further research is still necessary to rectify the disease process responsible for orthostatic hypotension, patients suffering from this disorder can effectively be treated through a combination of nonpharmacologic treatment, pharmacologic treatment and patient education. Agents such as fludrocortisone, midodrine and erythropoietin show promising results as therapeutic adjuncts. Treatment for recurrent vasovagal syncope includes increased salt intake, and various drug treatments, most of which are still under investigation.