Ann Thorac Surg 2003;75:1315-1317
© 2003 The Society of Thoracic Surgeons
Case report
Postinfarction ventricular septal defect in a patient without coronary lesions
Gianantonio Nappi, MDa*,
Luca Salvatore De Santo, MDa,
Michele Torella, MDa,
Maurizio Cotrufo, MD, FECTSa
a Department of Cardio-Thoracic and Respiratory Sciences, Second University of Naples, V. Monaldi Hospital, Naples, Italy
Accepted for publication September 27, 2002.
* Address reprint requests to Prof Nappi, Department of Cardio-Thoracic and Respiratory Sciences, Second University of Naples, V. Monaldi Hospital, Via L. Bianchi 5, 80131 Naples, Italy
e-mail: gianantonio.nappi{at}unina2.it
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Abstract
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A 46-year-old man with polycystic kidney disease was referred to our institution for ventricular septal defect complicating myocardial infarction. Cardiac catheterization disclosed normal coronary arteries and absence of myocardial bridging. None of the more frequent causes of thrombosis were present, and histopathology proved negative for acute myocarditis. The surgical procedure was successful and the 11-month follow-up uneventful.
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Introduction
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In the thrombolytic era, postinfarction ventricular septal defect (VSD) is becoming uncommon. Nevertheless, 30-day mortality for surgically treated patients still reaches 47%, and those undergoing medical treatment experience even worse outcomes. Total occlusion of the infarct-related artery with minimal collaterals is the common underlying angiographic pattern [1, 2]. The pathophysiology of acute coronary events in patients with angiographically normal coronary arteries is still unclear [3, 4].
This case report describes the successful surgical treatment of a VSD in a patient with intact epicardial coronary arteries and polycystic kidney disease (PKD). This disease is frequently associated with cardiovascular abnormalities, namely, aneurysms of the coronary arteries leading to ischemic myocardial injury [5].
A 46-year-old man was admitted to a peripheral hospital for typical chest pain that had begun 2 hours before. The patient had a history of PKD and medically treated hypertension but did not report tobacco smoking or use of cocaine. Blood pressure was normal, and physical examination revealed neither S3 nor rales. Electrocardiography showed sinus rhythm (86 beats/min) and ST elevation in the right precordial leads, as well as in leads II, III, and aVf, with reciprocal change in I and aV1. Cardiac troponin I and T were 55 and 34 ng/mL, respectively, and creatine kinase–MB reached 455 U/L. Blood chemistry was normal except for mild kidney failure (creatinine 1.7 mg/dL, blood urea nitrogen 74 mg/dL), in accordance with previous chemistry screenings. Serum lipid profile, erythrocyte sedimentation, along with coagulation factors (prothrombin activity, activated thromboplastin time, and antithrombin III) proved normal. Thrombolysis was contraindicated both by active peptic ulcer and by risk for intracerebral bleeding. The patient was treated with analgesic medications and was sent for primary percutaneous coronary intervention to our department 3 hours later. In the course of transportation, the patient became severely dyspneic as well as oliguric, and systolic arterial pressure fell to less than 85 mm Hg. At admission into the intensive care unit, cardiac troponin I and T were 83 and 64 ng/mL (normal values <0.08 ng/mL). Echocardiographic evaluation showed marked akinesis of the inferior wall and of the basal segment of the posterior interventricular septum, along with a dilated right ventricle that was globally hypokinetic. Left ventricular ejection fraction was 40%. Doppler evaluation disclosed the presence of a VSD approximately 20 mm wide, with left to right shunt. No intracardiac or vascular embolic source was detected. Relief of dyspnea (rales were present over >50% of lung fields) and partial hemodynamic compensation was achieved through insertion of an intraaortic balloon pump (IABP) with percutaneous femoral artery puncture, intravenous infusion of enoximone (5 µg-1 · kg-1 · min-1) and loop diuretics. The patient was then sent for cardiac catheterization, which disclosed intact nonaneurysmatic coronary arteries and absence of myocardial bridging. By placement of a Swan-Ganz catheter, a central venous pressure of 20 mm Hg was measured, pulmonary pressure of 55 mm Hg, and wedge pressure of 21 mm Hg. Qs/Qp was 2.8:1. Surgical procedure was performed 2 hours after hospital admission. After a median sternotomy, arterial perfusion was obtained through the ascending aorta, which was free of macroscopic atherosclerotic changes and venous drainage with bicaval cannulation. A sump was introduced in the left ventricle through the right superior pulmonary vein, and hypothermic (30°C nasopharyngeal temperature) cardiopulmonary bypass was instituted. Cardioplegic arrest was obtained with infusion in the aortic root of hypothermic crystalloid solution. Surgical exploration disclosed an infarcted area extending from the mid right posterior descending to the apex. The septum was approached through the infarcted left ventricular wall with a longitudinal incision parallel to the posterior descending coronary artery, extending from the base of the heart to the apex. Detachment of the midportion of the interventricular septum from the inferior wall was observed creating a VSD of 3 x 2 cm. This was excluded using a 3 x 2, triangular patch of bovine pericardium following the technique of David and colleagues [6]. Specimens for histopathologic studies were collected during the procedure. The patient was extubated on postoperative day 2. The IABP and inotropic support weaning were completed within 72 hours. Qs/Qp approached normal values, and echocardiographic evaluation demonstrated absence of left to right shunt. Blood test for anticardiolipin antibodies and lupus anticoagulant proved negative. Levels of C protein, S protein, and homocysteine, which were determined during the hospitalization, fell in the normal range. Pathologic examination showed typical contraction band necrosis: stretched myofibrils, nuclear pyknosis, mitochondrial damage, vascular congestion, and neutrophilic infiltration. Such a pattern was compatible with an infarct duration of less than 24 hours. Postoperative course was uneventful, and patient was discharged days after the operation. Echocardiographic follow-up at 5 and 11 months disclosed left ventricular ejection fraction of 58% and moderate impairment of the inferior wall.
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Comment
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Adult PKD is frequently associated with cardiovascular abnormalities. These include hypertension, mitral valve prolapse, mild dilation of the aortic root, abdominal aneurysms, and predisposition to aortic, mitral, and tricuspidal valve regurgitation reminiscent of Marfan’s syndrome. Although the exact molecular mechanisms of adult PKD are not well established, a generalized defect of collagen structure is hypothesized. The most severe vascular problems are typical intracranial aneurysms with a high incidence of subarachnoid hemorrhage and a high mortality rate [5]. Reports of aneurysmal dilation of the coronary arteries in patients with adult PKD and stress-induced angina pectoris or myocardial infarction have also been published. In the present case, none of the characteristic features of this disease were found.
Pathophysiology, characteristics, and prognosis of myocardial infarction with angiographically normal coronary arteries are still under investigation. Cocaine abuse, hypercoagulable states, myocardial bridges, coronary embolism, trauma, and vasospasm together with acute myocarditis are among the most frequently reported causes. Age less than 50 years, current cigarette smoking, and a positive family history of premature coronary disease is the usual risk profile of such patient subset [3, 4].
Myocardial bridges determining angiographic systolic narrowing are disclosed in up to 4.5% of the patients, and usually affect the middle segment of the left anterior descending. Continuous mechanical endothelial damage leading to premature arteriosclerosis at the site of myocardial bridge, appear to be the main determinants of ischemia. These events lead to angina pectoris, myocardial infarction, life-threatening ventricular arrhythmias, and even ventricular septal defect [2].
Primary antiphospholipid syndrome, hyperhomocysteinemia, and dysfunction of proteins S or C systems have also been addressed as causes of cardiac microvascular disease and myocardial infarction [4].
Myocardial infarction with normal coronary arteries appears to be less severe, with fewer complications during the acute phase and superior freedom from recurrence, cardiac failure, and death when compared with myocardial infarction due to severe atherosclerotic disease [3].
In the reported case, only the patient’s age fitted the usual risk factor profile. His angiographic pattern was completely normal, and screening for known etiologic causes proved negative. Interestingly, myocardial infarction was rapidly complicated by ventricular septal rupture (less than 5 hours from symptom onset). Despite the fact that inferior infarcts tends to have worse outcomes, and that VSDs located in the inferobasal portion of the septum are more difficult to approach during surgery, the procedure was successful and the postoperative course uneventful. Preoperative IABP insertion, early left and right cardiac catheterization, and VSD patch exclusion surgical technique proved a valuable management strategy. The diagnostic process, although accurate and extensive, was unable to disclose the exact pathophysiology.
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References
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- Crenshaw B.S., Granger C.B., Birnbaum Y., et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. Circulation 2000;101:27-32.[Abstract/Free Full Text]
- Tio R.A., Ebels T. Ventricular septal rupture caused by myocardial bridging. Ann Thorac Surg 2001;72:1369-1370.[Abstract/Free Full Text]
- Ammann P., Marschall S., Kraus M., et al. Characteristics and prognosis of myocardial infarction in patients with normal coronary arteries. Chest 2000;17:333-338.
- Lagana B., Baratta L., Tubani L., Golluscio V., Delfino M., Fanelli F.R. Myocardial infarction with normal coronary arteries in a patient with primary antiphospholipid sindrome: case report and literature review. Angiology 2001;52:785-788.
- Torres V.E. Cystic disease of the kidney. In: Massry S.G., Glassock R.J., eds. Textbook of nephrology. Philadelphia: Lippincott Williams & Wilkins, 2001:896-911.
- David T.E., Dale L., Sun Z. Postinfarction ventricular septal rupture: repair by endocardial patch with infarct exclusion. J Thorac Cardiovasc Surg 1995;110:1315-1322.[Abstract/Free Full Text]
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Abstract
Introduction
