Abstract
We report the case of a 38-year-old man with a long-standing history of a small ventricular septal defect presented with chest pain. Electrocardiography revealed sinus rhythm, ST-segment elevation in leads V1–6. The chest X-ray showed mild cardiomegaly. He underwent cardiac catheterisation laboratory to primary coronary angioplasty. Coronary angiography showed normal coronary arteries. Aortic root angiography revealed type A aortic dissection. Transthoracic and transesophageal echocardiography showed aortic dissection in ascending aorta and a perimembranous ventricular septal defect. Thoracoabdominal CT angiography confirmed the aortic dissection before the surgery.
The patient underwent cardiac surgery immediately. The ventricular septal defect and aortic dissection were repaired successfully. The postoperative recovery was uneventful and he has thus far remained asymptomatic at 6 months’ follow-up.
1
Introduction
Acute aortic dissection (AAD) is an extremely fatal disorder, with a mortality rate of 1% per hour during the first 24 h after the onset of chest pain . The extension of aortic dissection into the coronary arteries may cause acute myocardial infarction. Ventricular septal defects (VSDs) are common congenital heart defects , but there have been no reports of these defects in association with acute myocardial infarction and an acute aortic dissection in the literature.
We herein present a first case report of acute myocardial infarction due to aortic dissection in a patient with ventricular septal defect.
2
Case
A 38-year-old man with a long-standing history of a small ventricular septal defect was admitted to our clinic with complaint of chest pain. He had never been advanced for operative repair and had no other coronary risk factor without smoking. On physical examination, arterial blood pressure was 120/60 mmHg, heart rate was 98 bpm, and a Grade 5/6 pansystolic murmur was noticed at the left sternal border. The presenting electrocardiography revealed sinus rhythm, ST-segment elevation in leads V1–6 and reciprocal ST-segment depression in leads DII, DIII, and aVF, suggesting an anterior wall acute myocardial infarction (AMI). Chest X-ray showed mild cardiomegaly. Troponin T, CK, and CK-MB values were elevated. Medical therapy consisting of clopidogrel, aspirin, intravenous nitroglycerine, and intravenous heparin was given. He underwent cardiac catheterisation laboratory instantly to primary coronary angioplasty. Coronary angiography showed normal right coronary artery. But the left coronary artery could not be catheterized initially. Aortic root angiography, which was performed to investigate the left coronary artery, revealed Stanford type A aortic dissection, mild aortic regurgitation, and normal right coronary artery ( Fig. 1 ). Transthoracic and transesophageal echocardiography confirmed aortic dissection in ascending aorta and concomitant perimembranous VSD, with left to right shunting, and a systolic gradient of 65 mmHg was measured between the two ventricles ( Fig. 2 ). Thoracoabdominal CT angiography (CTA) was performed to corroborate the aortic dissection before the surgery. A Stanford type A aortic dissection extending from the ascending aorta to the iliac arteries was recognized by thoracoabdominal CTA ( Fig. 3 ). The patient underwent cardiac surgery immediately. A graft replacement from the ascending aorta to the hemi aortic arch was carried out successfully and the small ventricular septal defect was closed with several interrupted sutures. The postoperative recovery was uneventful. At follow-up (1 year), he continued to enjoy an excellent result.
2
Case
A 38-year-old man with a long-standing history of a small ventricular septal defect was admitted to our clinic with complaint of chest pain. He had never been advanced for operative repair and had no other coronary risk factor without smoking. On physical examination, arterial blood pressure was 120/60 mmHg, heart rate was 98 bpm, and a Grade 5/6 pansystolic murmur was noticed at the left sternal border. The presenting electrocardiography revealed sinus rhythm, ST-segment elevation in leads V1–6 and reciprocal ST-segment depression in leads DII, DIII, and aVF, suggesting an anterior wall acute myocardial infarction (AMI). Chest X-ray showed mild cardiomegaly. Troponin T, CK, and CK-MB values were elevated. Medical therapy consisting of clopidogrel, aspirin, intravenous nitroglycerine, and intravenous heparin was given. He underwent cardiac catheterisation laboratory instantly to primary coronary angioplasty. Coronary angiography showed normal right coronary artery. But the left coronary artery could not be catheterized initially. Aortic root angiography, which was performed to investigate the left coronary artery, revealed Stanford type A aortic dissection, mild aortic regurgitation, and normal right coronary artery ( Fig. 1 ). Transthoracic and transesophageal echocardiography confirmed aortic dissection in ascending aorta and concomitant perimembranous VSD, with left to right shunting, and a systolic gradient of 65 mmHg was measured between the two ventricles ( Fig. 2 ). Thoracoabdominal CT angiography (CTA) was performed to corroborate the aortic dissection before the surgery. A Stanford type A aortic dissection extending from the ascending aorta to the iliac arteries was recognized by thoracoabdominal CTA ( Fig. 3 ). The patient underwent cardiac surgery immediately. A graft replacement from the ascending aorta to the hemi aortic arch was carried out successfully and the small ventricular septal defect was closed with several interrupted sutures. The postoperative recovery was uneventful. At follow-up (1 year), he continued to enjoy an excellent result.
