The authors report the first emergent angiographic assessment of the coronaries with accompanying echocardiography in a 64-year-old man with dermatomyositis, who presented with ST segment elevation and cardiac specific enzyme derangements highly suggestive of myocardial infarction in the presence of acute pancreatitis. Both studies revealed no anatomical or functional evidence of obstructive coronary disease. Although the mechanism of electrocardiogram abnormalities found in acute pancreatitis remains to be elucidated fully, the authors propose a direct cardiac toxic effect by the pancreatic proteolytic enzymes to account for these changes and we recommend an angiographic approach as the first step to avoid the potentially lethal administration of thrombolytic therapy or potent anticoagulation.

The inhibitory actions of Ang II on K(ATP) appear to be mediated by an increase in the subsarcolemmal ATP concentration that results from the inhibition of adenylate cyclase activities via AT1 receptors/PTX-sensitive G proteins.

No abstract

We present a 64-year-old woman who was brought to the emergency department after suffering a motor vehicle accident, involving multiple soft tissue and bone trauma. Even though she was free from cardiovascular symptoms for the last three years, her past medical history of aorto-coronary bypass surgery prompted preoperative consultation. The diagnostic images showed a unique visualization of an ascending aortic traumatic pseudoaneurysm by transthoracic and transoesophageal echocardiogram as well as with cardiac catheterization.

A 20-year-old man without past medical history was admitted for diffuse left-sided and retrosternal chest pain after he was "told and forced to swallow crystal rocks." He denied any prior symptomatology and denied cough. In the emergency department, he had a normal physical examination and laboratory studies. The ECG, however, showed diffuse ST-segment elevations ( Figure 1). He was admitted to the Coronary Care Unit. Within 6 hours of admission, he developed a pericardial friction rub. His urine toxicology screening was positive for cocaine. The chest x-ray was consistent with the diagnosis of pneumopericardium (Figure 2).On the second hospital day, the patient underwent both an esophageal contrast study with gastrografin and a cardiac echocardiogram. Both were normal. Subsequent chest x-rays showed a slow resolution of his pneumopericardium (Figures 3 and 4).Cocaine-induced pneumopericardium has seldom been reported, and its mechanism remains elusive. In the present case, we postulate that the likely use of "crack" cocaine with solid contaminants in the crystalline mass could have caused a microscopic esophageal tear and eventually produced a leak of air into the pericardial sac that was self-contained. The patient was discharged in stable condition on the fourth hospital day.