Neurocardiac Injury After Cerebral and Subarachnoid Hemorrhages.

Cerebrovascular events are associated with high mortality and morbidity rates. Neurocardiac injury after a subarachnoid hemorrhage and cerebral hemorrhage further worsen clinical outcomes. Excess catecholamine-induced cardiotoxicity is currently the most widely accepted pathophysiologic mechanism. Awareness of neurocardiac injury and the cardiac manifestations associated with it will allow for early diagnosis and appropriate management.

Prosthetic Valve Thrombosis: Diagnosis and Management.

St. Jude mechanical prosthesis is the most commonly used prosthetic device with least valvular complications with excellent hemodynamics. However, prosthetic valve thrombosis is one of the serious complications, with rates between 0.03% and 0.13% per patient-year depending on the type of anticoagulation used and compliance to the therapy. Transthoracic echocardiography (TTE) is the initial screening tool (class I) that would provide clues for the assessment of valvular hemodynamics. Fluoroscopy is an alternate imaging modality for the assessment of mechanical leaflet motion, especially in patients when prosthetic valves are difficult to image on TTE or transesophageal echocardiography. A complete fluoroscopic evaluation of a prosthetic valve includes assessment of valvular motion and structural integrity. Opening and closing angles can be measured fluoroscopically to determine whether a specific valve is functioning properly. We discuss a case of a 91-year-old man with thrombosis of bileaflet mechanical mitral prosthesis that was demonstrated on real-time fluoroscopy (not evident on TTE). An algorithmic approach to diagnosis and management of prosthetic heart valve thrombosis is outlined.

Neurogenic stress cardiomyopathy associated with subarachnoid hemorrhage.

Cardiac manifestations are recognized complications of subarachnoid hemorrhage. Neurogenic stress cardiomyopathy is one complication that is seen in acute subarachnoid hemorrhage. It can present as transient diffuse left ventricular dysfunction or as transient regional wall motion abnormalities. It occurs more frequently with neurologically severe-grade subarachnoid hemorrhage and is associated with increased morbidity and poor clinical outcomes. Managing this subset of patients is challenging. Early identification followed by a multidisciplinary team approach can potentially improve outcomes.

Existing drugs and agents under investigation for pulmonary arterial hypertension.

Pulmonary arterial hypertension is a progressive and debilitating disorder with an associated high morbidity and mortality rate. Significant advances in our understanding of the epidemiology, pathogenesis, and pathophysiology of pulmonary hypertension have occurred over the past several decades. This has allowed the development of new therapeutic options in this disease. Today, our selection of therapeutic modalities is broader, including calcium channel blockers, prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, and soluble guanylate cyclase stimulators, but the disease remains fatal. This underscores the need for a continued search for novel therapies. Several potential pharmacologic agents for the treatment of pulmonary arterial hypertension are under clinical development and some promising results with these treatments have been reported. These agents include rho-kinase inhibitors, long-acting nonprostanoid prostacyclin receptor agonists, tyrosine protein kinase inhibitors, endothelial nitric oxide synthase couplers, synthetically produced vasoactive intestinal peptide, antagonists of the 5-HT2 receptors, and others. This article will review several of these promising new therapies and will discuss the current evidence regarding their potential benefit in pulmonary arterial hypertension.

ST elevation myocardial infarction after tranexamic acid: first reported case in the United States.

Antifibrinolytic agents, such as tranexamic acid (TA), aprotinin, and E-aminocaproic acid, have been extensively used in the past 2 decades to prevent blood loss from traumatic or postoperative bleeding. For example, the Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 2 (CRASH-2) trial demonstrated that there was a significant reduction in all-cause mortality in trauma patients treated with TA (relative risk=0.91, P=0.003) and death due to bleeding (relative risk=0.85, P=0.007). This article reports the case of a 56-year-old woman without any previous cardiac history who was admitted to the hospital for an elective right hip arthroplasty and who received 1 dose of 10 mg/kg of TA. Her immediate postoperative course was complicated by hypotension and chest pain, and an electrocardiogram showed ST segment elevation in the inferior leads. Emergent coronary angiography showed complete occlusion of the distal right coronary artery that was successfully treated with thrombectomy and percutaneous coronary intervention. An extensive literature search showed only 4 cases of myocardial infarction in the setting of TA administration, all of which were outside the United States.

Severe amiodarone induced pulmonary toxicity.

A known complication of Amiodarone therapy is Amiodarone induced Pulmonary Toxicity (APT). Several features of this adverse effect make it difficult to diagnosis and treat. The case of a 63-year-old male with classic radiographic and histologic findings of APT is discussed. Clinical presentation, pathophysiology, diagnostic findings, and treatment strategies are reviewed. The patient was successfully managed with pulse high dose steroid therapy.