Prostaglandin E1 (PGE1) has been shown to limit infarct size, improve coronary blood flow, inhibit platelet aggregation, and reduce both left ventricular (LV) preload and afterload in experimental animals. Its use in the therapy of patients with acute myocardial infarction (AMI) and congestive heart failure (CHF) has not, however, been reported. Five patients with AMI of less than 12 hours' duration and LV dysfunction were studied to assess the hemodynamic effects of IV infusion of PGE1. PGE1 in the concentration of 0.4 microgram/ml was infused at a rate of 0.003 microgram2kg/min (3 ng . kg-1 . min-1) to a maximum rate of 0.021 microgram/kg/min (21 ng . kg-1 . min-1) for a total time of up to 90 minutes. There was an insignificant increase in heart rate, with significant decreases in mean arterial blood pressure and systemic vascular resistance. Pulmonary capillary wedge pressure declined from 21 +/- 3 to 15 +/ 1 mm Hg (p less than 0.05), mean pulmonary artery pressure and pulmonary vascular resistance decreased (p less than 0.05), mean pulmonary artery pressure and pulmonary vascular resistance decreased (p less than 0.05), with increases in cardiac index from 2.38 +/- 0.08 to 2.89 +/- 0.58 L/min/m2 (p less than 0.01) and stroke volume from 51 +/- 17 to 59 +/- 20 ml/beat (p less than 0.05). No major cardiac or extracardiac side effects were encountered during PGE1 infusion. One patient had transient nausea which did not require discontinuation of the drug. PGE1 is an effective vasodilator and deserves further application in therapy for AMI patients with CHF.
Blunt and penetrating chest trauma as a cause of hemopericardium with subsequent cardiac tamponade and/or constrictive pericarditis due either to the presence of intrapericardial clotted blood or chronic inflammation has been well described.1-3 We describe here an unusual patient who presented with massive organized intrapericardial hematoma with the hemodynamic characteristics of chronic constrictive pericarditis 4 years after suffering blunt chest trauma. The diagnostic studies, including two-dimensional echocardography and cardiac CT scan which aided in establishing the preoperative diagnosis of the etiology of the constriction, are demonstrated. A 25-year-old man with a ?-month history of ankle swelling and a 2-month history of abdominal swelling was admitted for evaluation. Four years prior to admission, the patient was involved in a motor vehicle accident in which he suffered chest trauma from the steering wheel. No chest x-ray examination was obtained at that time. He described hemoptysis associated with that incident. During the 3-Y2 year interim he denied any subsequent chest trauma. His major symptom at the time of admission was dyspnea on exertion. On physical examination he appeared chronically ill. There was marked jugular venous distention with prominent x and y descent. An early diastolic sound was present on cardiac examination, and the point of maximal intensity was only faintly palpable in the sixth intercostal space at the anterior axillary line. There was marked tense ascites, the liver was palpable 13 cm below the right costal margin and was not pulsatile, and trace pretibial edema was present. An ECG demonstrated sinus tachycardia and low voltage. Chest x-ray examination revealed bilateral costophrenic angle blunting and cardiomegaly. The left heart border was markedly irregular and "tented" (Fig. 1). Cardiac catheterization revealed elevated end-diastolic pressures with equalization of diastolic pressures between the right atrium, right ventricle, and left ventricle. The intracardiac pressures were (mm Hg): right atrium (mean 15), right ventricle (30/15) with characteristic diastolic dip and plateau, pulmonary artery (30/19), and pulmonary artery wedge (mean 19). No significant (greater than 10 mm Hg) respiratory variation in pressures was noted. Cineangiography by contrast injection into the low right
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