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Ann Thorac Surg 1996;61:1816-1817
© 1996 The Society of Thoracic Surgeons


Case Report

Repair of Postinfarction Ventricular Septal Defect on a Beating Heart

Toshiki Takahashi, MD, Keishi Kadoba, MD, Kazuhiro Taniguchi, MD, Yoshiki Sawa, MD, Hiroshi Imagawa, MD, Takafumi Masai, MD, Hikaru Matsuda, MD

First Department of Surgery, Osaka University, Medical School, Osaka, Japan

Accepted for publication November 9, 1995.


    Abstract
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 Footnotes
 Abstract
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Two elderly patients with postinfarction ventricular septal defect underwent repair by endocardial patch with infarct exclusion on a beating heart under normothermic cardiopulmonary bypass with ultra–short-acting ß-blocker infusion. Their hemodynamic states soon recovered, and postoperative angiographic studies showed improvement of cardiac function and no residual shunt. Ultra–short-acting ß-blocker has the potential to facilitate safe repair of postinfarction ventricular septal defect on a beating heart, and this operative approach can be beneficial for myocardial protection.


    Introduction
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 Introduction
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Postinfarction ventricular septal defect (VSD) often induces cardiogenic shock and requires operative treatment early after myocardial infarction. Although the operative mortality of this disease has decreased during the past 3 decades, it is still relatively high [1, 2]. On the other hand, ß-blockers recently have been found to facilitate operative procedures on beating hearts [35]. Confronted with patients in whom postinfarction VSD developed with circulatory deterioration, we successfully operated on these patients with a beating heart using normothermic cardiopulmonary bypass (CPB) with ultra–short-acting ß-blocker infusion (esmolol), for avoidance of global myocardial ischemia and damage to the normal metabolic processes as well as peripheral perfusion.


    Case Reports
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Patient 1
A 63-year-old man with diabetes mellitus experienced an inferior myocardial infarction and began to have unremitting dyspnea 10 days later. He was referred to our hospital for treatment of refractory congestive heart failure. Echocardiography with color-flow Doppler echocardiography and cardiac catheterization showed a large VSD at the midportion of the septum, poor left ventricular (LV) function, and severe coronary three-vessel disease. He underwent urgent operation consisting of saphenous vein grafting to the left anterior descending coronary artery and first diagonal, and repair by endocardial equine pericardial patch (Edwards Laboratories AG, Switzerland) with infarct exclusion [1] on a beating heart under normothermic CPB with LV venting and esmolol infusion. Esmolol was administered through the central venous line after CPB was begun. Initial administration was a bolus of 30 mg/kg, followed by a continuous infusion of 3 mg•kg-1•min-1. Immediately after administration, LV contractions became weak and the heart rate decreased to about 40 beats/min, which recovered within about 40 minutes after cessation of esmolol administration. The performance of the distal anastomosis was aided by intraluminal vessel occluders and the Visuflow Surgical Site Visualization Wand (Research Medical, Inc, Midvale, UT). The LV venting and artificially flaccid contraction prevented LV distention and facilitated enough exposure of the posterior wall without aortic valve incompetence when the heart was lifted. The CPB time was 191 minutes. Extubation was done within 10 hours after the operation, and the postoperative course was uneventful. The maximum serum creatine kinase MB fraction was 14 IU/L. Cardiac catheterization 2 weeks after the operation showed improvement of LV wall motion in the anterior lesion, with an ejection fraction of 0.44, intact patent grafts, and no residual shunt.

Patient 2
A 79-year-old woman experienced an anterior myocardial infarction. After recovery from this, she suddenly had an episode of dyspnea 3 days later. Her dyspnea soon became severe and unremitting even at rest, and she was referred to our hospital. On her arrival, she began to have circulatory collapse and required institution of the percutaneous cardiopulmonary system. Echocardiography with color-flow Doppler echocardiography and cardiac catheterization showed a large VSD near the apex and 99% stenosis in the proximal portion of the left anterior descending coronary artery. She was also found to have renal and liver dysfunction (serum creatinine level, 3.3 mg/dL; total bilirubin level, 2.8 mg/dL; prothrombin time, 19%). She underwent emergent repair of postinfarction VSD [1] in a same fashion as in patient 1. Cardiac contractions became weak and the heart rate decreased to about 60 beats/min after the administration of esmolol. She was weaned off CPB, and use of the percutaneous cardiopulmonary system was begun about 40 minutes after discontinuation of esmolol. The CPB time was 138 minutes. Her hemodynamic state improved, and the percutaneous cardiopulmonary system was removed 2 days after the operation. The maximum serum creatine kinase MB fraction was 5 IU/L. Cardiac catheterization performed 23 days after the operation showed improvement of LV wall motion without the anterior lesion, with an ejection fraction of 0.63 and no residual shunt.


    Comment
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The operative mortality of repair of postinfarction VSD is worst in patients treated early after infarction, those with cardiogenic shock, and those whose VSD is located inferiorly [1, 2]. Komeda and associates [1] reported repair by endocardial pericardial patch with infarct exclusion, which avoided further damage to the right ventricle. This operative technique is relatively simple and is expected to improve the outcome of patients with postinfarction VSD.

Myocardial protection and preservation of normal metabolic processes in major organs are also important factors to improve the operative outcome in such deteriorated patients. Terminal warm blood cardioplegia [6] and continuous warm blood cardioplegia [7] were reported to be beneficial for myocardial protection in patients with poor ventricular function. Recently, Sweeney and Frazier [3] advocated coronary bypass operations on heart beating using a ventricular assist device with ß-blocker infusion for severely ill and high-risk patients. This approach does not require aortic cross-clamping and provides superior myocardial protection, perhaps achieved by coupling mechanical ventricular decompression with the patient's own normal or augmented coronary flow. We applied esmolol in the repair of postinfarction VSD on the beating heart under normothermic CPB. In addition, a ß-blocker may be beneficial for protecting against extension of myocardial necrosis after acute myocardial infarction [8]. Although the heart continued to beat, it was flaccid because of the esmolol infusion, and repair of the postinfarction VSD was technically easy in both patients. Esmolol was cleared rapidly without any serious side effects, and both patients were weaned easily from the circulatory assist system. However, they required about 40 minutes for LV contractions and heart rate to recover. The CPB time was therefore a little longer than normal in both patients.

In conclusion, ultra–short-acting ß-blocker has the potential to facilitate safe operative procedures for postinfarction VSD on the beating heart under normothermic CPB, and this approach can be beneficial for myocardial protection, especially in patients with high operative risk.


    Footnotes
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 
Address reprint requests to Dr Matsuda, First Department of Surgery, Osaka University Medical School 2-2, Yamadaoka, Suita, Osaka 565, Japan.


    References
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 Footnotes
 Abstract
 Introduction
 Case Reports
 Comment
 References
 

  1. Komeda M, Fremes SE, David TE. Surgical repair of postinfarction ventricular septal defect. Circulation 1990;82(Suppl 4):243–7.
  2. Skillington PD, Davies RH, Luff AJ, et al. Surgical treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990;99:798–808.[Abstract]
  3. Sweeney MS, Frazier OH. Device-supported myocardial revascularization: safe help for sick hearts. Ann Thorac Surg 1992;54:1065–70.[Abstract/Free Full Text]
  4. Lonn U, Peterzen B, Granfeldt H, Casimir-Ahn H. Coronary artery operation with support of the Hemopump cardiac assist system. Ann Thorac Surg 1994;58:519–23.[Abstract/Free Full Text]
  5. Olearchyk AS. Calcified ascending aorta and coronary artery disease. Ann Thorac Surg 1994;59:1013–5.
  6. Teoh KH, Christakis GT, Weisel RD, et al. Accelerated myocardial metabolic recovery with terminal warm blood cardioplegia. J Thorac Cardiovasc Surg 1986;91:888–95.[Abstract]
  7. Lichtenstein SV, Ashe KA, Dalati HE, Cusimano RJ, Panos A, Slutsky AS. Warm heart surgery. J Thorac Cardiovasc Surg 1991;101:269–74.[Abstract]
  8. Reimer KA, Rasmussen MM, Jennings RB. Reduction by propranolol of myocardial necrosis following temporary coronary occlusion in dogs. Circ Res 1973;33:353–60.[Abstract/Free Full Text]



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This Article
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Hiroshi Imagawa
Hikaru Matsuda
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Right arrow Articles by Takahashi, T.
Right arrow Articles by Matsuda, H.
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Right arrow Articles by Takahashi, T.
Right arrow Articles by Matsuda, H.


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