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- W185533880 abstract "A 55-year-old man with known hypertension presented emergently with severe, acute-onset chest pain of 3 to 4 hours' duration, associated with vomiting and diaphoresis. The diagnosis was acute anterolateral-wall MI, and streptokinase was given as thrombolysis. On the 3rd day of hospitalization, the patient developed orthopnea and acute pulmonary edema. Examination revealed an apical pansystolic murmur. Transthoracic echocardiography (TTE) showed an apical ventricular septal defect (VSD) (size, 5–6 mm) with a peak gradient of 70 mmHg (Figs. 1 and and2).2). The patient refused surgery in favor of medical management. His condition improved with decongestive measures, and he was hemodynamically stable with intra-aortic balloon pump support. He was discharged from the hospital after 2 weeks in stable condition with strict instructions regarding follow-up after 1 week and monthly thereafter. He was placed on regular therapy with low-dose angiotensin-converting enzyme inhibitors, and he remained in stable condition in New York Heart Association (NYHA) functional class II. At the 6-year follow-up visit, the murmur had disappeared, and TTE revealed that a left ventricular clot had closed the VSD. The patient was monitored for another year. He remained in NYHA class II. Three-dimensional transesophageal echocardiography confirmed that the VSD was covered from the left ventricular side by the clot (Fig. 3).Fig. 1 Transthoracic echocardiogram (apical 4-chamber view) shows a ventricular septal defect (VSD) (arrow).Fig. 2 Two-dimensional transthoracic color-flow Doppler echocardiogram shows left-to-right flow through the ventricular septal defect.Fig. 3 Three-dimensional transesophageal echocardiogram (4-chamber view) shows the closure of the ventricular septal defect by a clot (asterisk)." @default.
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- W185533880 date "2011-01-01" @default.
- W185533880 modified "2023-09-23" @default.
- W185533880 title "Spontaneous closure of post-myocardial infarction ventricular septal rupture." @default.
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