Several fluid retentive states such as heart failure, cirrhosis of the liver, and syndrome of inappropriate antidiuretic hormone secretion are associated with inappropriate elevation in plasma levels of arginine vasopressin (AVP), a neuropeptide that is secreted by the hypothalamus and plays a critical role in the regulation of serum osmolality and in circulatory homeostasis. The actions of AVP are mediated by three receptor subtypes V 1a , V 2 , and V 1b . The V 1a receptor regulates vasodilation and cellular hypertrophy while the V 2 receptor regulates free water excretion. The V 1b receptor regulates adrenocorticotropin hormone release. Conivaptan is a nonpeptide dual V 1a /V 2 AVP receptor antagonist. It binds with high affinity, competitively, and reversibly to the V 1a /V 2 receptor subtypes; its antagonistic effect is concentration dependent. It inhibits CYP3A4 liver enzyme and elevates plasma levels of other drugs metabolized by this enzyme. It is approved only for short-term intravenous use. Infusion site reaction is the most common reason for discontinuation of the drug. In animals conivaptan increased urine volume and free water clearance. In heart failure models it improved hemodynamic parameters and free water excretion. Conivaptan has been shown to correct hyponatremia in euvolemic or hypervolemic patients. Its efficacy

Introduction: Cardiac abnormalities can be seen with subarachnoid hemorrhage. To date, there have been isolated case reports of transient left ventricular apical ballooning cardiomyopathy, also known as Takotsubo cardiomyopathy in patients suffering from subarachnoid hemorrhage.

GP (glycoprotein) IIb/IIIa inhibitors are routinely used in patients with acute coronary syndromes. There have been reported platelet counts of below 20 × 10^9/L within hours of administering the drug. We present a case of a 44 years old man with inferior wall myocardial infarction and third-degree heart block who was admitted for cardiac catheterization. The patient successfully underwent percutaneous intervention to right coronary artery and eptifibatide was given per protocol. 6 h post-eptifibatide initiation, platelets dropped from 288 × 10^9/L to 24 × 10^9/L. Eptifibatide was stopped and a CBC (complete blood count) was repeated after 2 hours. The platelets had further dropped to undetectable levels showing 0 × 10^9/L. The patient remained completely asymptomatic.Pseudo-thrombocytopenia was ruled out on peripheral smear. Platelet transfusion was considered, however, platelets started to rise few hours after stopping of Eptifibatide. Twelve hours later, platelet count reached 4 × 10^9/L. It continued to show a positive trend and reached up to a level of 293 × 10^9/L after 5 days. Patient was discharged in a stable condition. Due to this rare but significant phenomenon, patients on these drugs should have their platelet count closely monitored. It is also very rare not to have any symptoms after such critically low platelet levels.

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