Administration of glycoprotein IIb-IIIa inhibitors in patients with ST-segment elevation myocardial infarction.

Patients with ST-segment elevation acute myocardial infarction require immediate reperfusion therapy. Reperfusion therapy can be provided by either pharmacologic or mechanical means. Pharmacologic reperfusion therapy consists of administering fibrinolytics, whereas mechanical reperfusion consists of performing percutaneous intervention, usually with stent placement. Each approach has been shown to decrease mortality, but each has disadvantages in establishing flow in the infarct-related artery. Regardless of the approach, during an acute myocardial infarction, activation and externalization of glycoprotein (GP) IIb-IIIa receptors occur on the surface of platelets. The GP IIb-IIIa inhibitors block the binding of fibrinogen to these platelet receptors. These inhibitors have been investigated in combination with both reperfusion strategies. The goal of adding GP IIb-IIIa inhibitor therapy to either reperfusion approach is to obtain better early, complete, and sustained reperfusion. Subsequently, this should lead to better clinical outcomes for patients with ST-segment elevation acute myocardial infarction. Although no mortality benefit has been seen with the addition of GP IIb-IIIa inhibitor therapy, ischemic complications have been reduced significantly.

Syndrome of inappropriate antidiuretic hormone-induced hyponatremia associated with amiodarone.

The syndrome of inappropriate antidiuretic hormone (SIADH), the most common cause of euvolemic hyponatremia, is due to nonphysiologic release of arginine vasopressin from the posterior pituitary. Hyponatremia induced by SIADH can be caused by several conditions, such as central nervous system disorders, malignancies, various nonmalignant lung diseases, hypoadrenalism, and hypothyroidism. A 67-year-old man developed hyponatremia consistent with SIADH. Although common comorbid conditions associated with SIADH were excluded as possible causes, his medical history and drug regimen were extensive. However, he had been taking spironolactone, amiodarone, and simvastatin for less than 3 months. Amiodarone was discontinued based on a case report suggesting that this drug can cause SIADH-induced hyponatremia. The patient's serum sodium level began to rise within 3 days of discontinuation and returned to normal within 1 month. Although SIADH-induced hyponatremia occurs only rarely, it should be recognized as a possible adverse effect of amiodarone.