Chest pain associated with moderator band pacing.

A 65-year-old man was evaluated for chronic chest pain that had been present for 8 years after placement of a dual-chamber implantable cardioverter-defibrillator to treat inducible ventricular tachycardia. Previous coronary angiography had revealed nonobstructive coronary artery disease and a left ventricular ejection fraction of 0.45 to 0.50, consistent with mild idiopathic nonischemic cardiomyopathy. Evaluation with chest radiography and transthoracic echocardiography showed the implantable cardioverter-defibrillator lead to be embedded within the right ventricle at the moderator band, which had mild calcification. Treatment included extraction of the dual-coil lead and placement of a new single-coil right ventricular lead at the mid septum. The patient had complete relief of symptoms after the procedure. This case shows that chest pain can be associated with the placement of a right ventricular implantable cardioverter-defibrillator lead in the moderator band and that symptomatic relief can occur after percutaneous lead extraction and the implantation of a new right ventricular lead to the mid septal region.

A case report of vinorelbine monotherapy-related acute bronchospasm and non-ST elevation acute coronary syndrome.

Vinorelbine is a semi-synthetic vinca-alkaloid with a broad spectrum anti-tumor activity. The dose-limiting toxicity of vinorelbine is neutropenia and leucopenia which is seen in majority of the patients. The previous case reports on the cardiac toxicity occurred mainly in combination therapy of vinorelbine with cisplatin or carboplatin. We offer evidence that acute coronary syndrome and resultant diastolic heart failure developed as a result of acute bronchospasm due to intravenous vinorelbine monotherapy.

Symptomatic repetitive right ventricular outflow tract ventricular tachycardia in pregnancy and postpartum.

Idiopathic ventricular tachycardias, which occur in patients without structural heart disease, are a common entity, representing up to 10% of all ventricular tachycardias evaluated by cardiac electrophysiology services. Pregnancy can increase the incidence of various cardiac arrhythmias. Factors that can potentially promote arrhythmias in pregnancy include the effects of hormones, changes in autonomic tone, hemodynamic perturbations, hypokalemia, and underlying heart disease. Ventricular arrhythmias in pregnancy are repetitive monomorphic ventricular premature complexes and couplets that frequently originate at the right ventricular outflow tract. New onset symptomatic repetitive right ventricular outflow tract ventricular tachycardia during pregnancy has been inadequately reported in the literature. We present a case of symptomatic repetitive right ventricular outflow tract tachycardia that started during pregnancy and continued in the postpartum period, requiring curative treatment with electrophysiology study and radiofrequency ablation.

Acute pulmonary edema associated with direct current cardioversion in a structurally normal heart.

The transthoracic application of synchronized direct current cardioversion (DCC) is widely used to terminate atrial fibrillation, atrial flutter, and other supraventricular tachyarrhythmia. DCC is a highly effective method for acute restoration of sinus rhythm. Although DCC is a relatively safe and frequently performed procedure, data on potential side effects are very rarely reported in the literature. The most serious complications associated with DCC are thromboembolism and intracranial hemorrhage. The true incidence of postcardioversion pulmonary edema is not known, but it is estimated to occur in 1% to 3% of patients, particularly those with coexistent heart disease. We report on a patient with a structurally normal heart who developed acute pulmonary edema after undergoing DCC. The patient had no evidence of myocardial injury according to an electrocardiogram and cardiac biomarkers. The patient was treated with intravenous diuretics. After 4 days, the pulmonary edema resolved.

Spontaneous coronary artery dissection in a woman on fenfluramine.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome, cardiogenic shock, and sudden cardiac death in women of reproductive age who have no traditional risk factors for coronary artery disease. The etiology, prognosis, and treatment of SCAD remain poorly defined. Coronary angiography is the gold standard for diagnosis. Management includes medical therapy and revascularization procedures using percutaneous intervention and coronary artery bypass grafting. Possible mechanisms of SCAD include rupture of atherosclerotic plaque or vasa vasorum, hemorrhage between the outer media and external lamina with intramedial hematoma expansion, and compression of the vessel lumen. We report a case of SCAD in a 39-year-old woman presenting with ST-elevation myocardial infarction midway through her menstrual cycle. Her medications included fenfluramine for obesity and hydrochlorothiazide, amlodipine, and atenolol for hypertension.

Calciphylaxis: a rare association with alcoholic cirrhosis. Are deficiencies in protein C and S the cause?

Calciphylaxis is a rare condition of induced systemic hypersensitivity in which tissues respond to appropriate challenging agents with a sudden local calcification. It is characterized by acute calcium deposition in the medial layer of small and intermediate dermal vasculature that can lead to epidermal ischemia, ulceration, and necrosis. Calciphylaxis typically occurs in patients with end-stage renal disease who are undergoing dialysis and who have secondary hyperparathyroidism. Even in this population the incidence is less than 1%. The cause of calciphylaxis is unknown. However, it has been suggested that deficiencies of protein C and protein S may play a role in the pathophysiology of this disorder. Our patient is the fourth with cirrhosis to be reported to have developed calciphylaxis and adds further evidence that low levels of these anticoagulant factors may be an important etiologic factor for development of calciphylaxis. This report should alert the clinician that calciphylaxis occurs in patients with cirrhosis and should stimulate further research concerning the possible role of protein C and protein S deficiency in calciphylaxis.

Spontaneous negative pressure changes: an unusual cause of noncardiogenic pulmonary edema.

The principal physiologic mechanism underlying the formation of negative pressure pulmonary edema (NPPE) is thought to be the creation of excessive negative intrathoracic force from inspiration against a critical obstruction of the upper airway. The increased subatmospheric transpulmonary pressures result in transudation of fluid from the pulmonary capillaries to the interstitium and alveoli. The clinical picture is that of pulmonary edema. Aggressive diagnostic and therapeutic intervention can be avoided if the syndrome is recognized early. This report highlights the clinical features of NPPE and serves as a reminder to the clinician that although NPPE can cause significant morbidity, conservative supportive therapy typically results in a good outcome.

Simvastatin-induced lactic acidosis: a rare adverse reaction?

Simvastatin, a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, is a commonly used cholesterol-lowering agent. The long-term safety profile of simvastatin, established over 10 years of clinical use, is excellent. HMG-CoA reductase inhibitors block 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis. However, other important nonsterol compounds, such as coenzyme Q10 (CoQ10), are also derived from the same synthetic pathway. CoQ10 is an essential carrier in the mitochondrial respiratory chain that participates in oxidative phosphorylation. Simvastatin and other HMG-CoA reductase inhibitors have been documented to lower serum concentrations of CoQ10. It has been suggested that the adverse effect of myopathy caused by HMG-CoA reductase inhibitors is due to CoQ10 deficiency in the tissue mitochondria. Documentation of this cause-and-effect phenomenon, however, has been lacking. We offer evidence that lactic acidosis may develop as a complication of simvastatin therapy. Our patient also manifested the well-known HMG-CoA reductase inhibitor drug toxicities of rhabdomyolysis and hepatitis. The occurrence of these known adverse events with lactic acidosis in our patient suggests that interference of the mitochondrial respiratory chain may play a role in the toxicity of this class of drugs.