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A favorable outcome of a post-myocardial infarction ventricular septal rupture/Miyokart enfarktusu sonrasi ventrikuler septal rupturun olumlu sonucu.


Usually, the ventricular septal rupture is a devastating complication of the myocardial infarction (1), leading to death, in case of the unoperated patient. Additional investigations are essential in the correct hemodynamic assessment, especially the first introduced in clinical practice for this disease, the echocardiography (2). Long-term mortality is reduced if the patient with acquired ventricular septal defect is emergently operated, if there is significant hemodynamic alteration (3).

The aim of our study is to reveal the spontaneous, rare evolution toward healing of a ventricular septal rupture, acquired after a myocardial infarction.

Case Report

A-45-year- old patient, previously diagnosed with Wolf-Parkinson-White syndrome (5 years ago), was hospitalized with subacute anteroseptal myocardial infarction (September 2011). One week ago, after excessive alcohol consumption, he had chest pain for 6 hours, exacerbated by physical effort. At the moment of admission, the serum biomarkers for myocardial infarction were normal, as well as other laboratory data, with the exception of the gamma-glutamil-transpeptidase 150 IU/l (normal values: <40 IU/l). He also had echocardiographic kinetic changes-dyskinesia of the anteroseptal wall, hypokinesia of all the other left ventricular walls, ejection fraction--30%. The electrocardiogram revealed only the Wolf-Parkinson-White syndrome: the delta wave was hiding the Q-waves because the conduction was via the accessory pathway, as Brackbill et al. (4) also remarked. He was conservatory treated (delayed admission--after one week). The epicardial coronary arteries were normal at angiography (the vasospasm was the incriminated mechanism for myocardial infarction). After discharge, he interrupted the medication and he performed inadequate physical efforts. He underwent a cardiological examination in October 2011 (4 weeks after the first admission), for small efforts dyspnea and palpitations. He had a left parasternal systolic murmur, produced by a ventricular septal defect, revealed by Doppler echocardiography (Fig. 1). Left ventricle was dilated with an altered ejection fraction (30%); this diminished myocardial contractility was explained by chronic alcohol consumption (50g per day; elevated gamma-glutamil-transpeptidase: 125 IU/l, normal values < 40 IU/l) and by the associated hypothyroidism (thyroid stimulating hormone: 7 IU/l, normal values: 0.5-4.5 IU/l). His electrocardiography presented the same aspect as 5 years ago: WolfParkinson-White syndrome (Fig. 2). The patient refused the electrophysiological studies for ablative therapy. Repeated episodes of paroxysmal supraventricular tachycardia were detected on 24 hours electrocardiographic Holter recording. The medical recommended treatment consisted of: acetylsalicylic acid 100 mg/day, ramipril 5 mg/day, atorvastatin 80 mg / day, levothyroxine 100 [micro]g/day. He did not come to reevaluation for one year, even if he was invited to an examination every month. In October 2012, it was an unexpected surprise to find that he had no systolic murmur at physical examination. Doppler echocardiography revealed that there was no ventricular septal defect anymore (Fig. 3). The same aspect of fibrotic scar with no interventricular communication was documented through 3D echocardiography and transesophageal echocardiography (Video 1. See corresponding video/movie images at Our team also performed a thoracic computed tomography angiography, which revealed the same fibrotic scar of the subaortic ventricular septum (Fig. 4). He still had arrhythmias and the echocardiographic aspect of dilated cardiomyopathy, but his effort tolerance was better. The patient respected the recommended cardiological treatment, but he continued to consume alcohol on a daily basis and refused to follow the endocrinological treatment for hypothyroidism.


The spontaneous closure of post-infarction ventricular septal rupture is very rare. Only 5 patients were reported (5-7) until the presented case. The mechanism of the closure in these 5 cases was the formation of a clot. At the presented patient, the mechanism was probably the proliferation of the fibrous tissue, proven by the echocardiographic aspect of the damaged ventricular septum, after one year of evolution. This mechanism was mentioned as leading to a spontaneous closure of the congenital ventricular septal defects in young and middle-aged adults (8); therefore, it can be similar for the acquired post-infarction ventricular septal defect, where the clot was not involved in this closure.


The case presented rare physiopathological mechanisms for the associated pathologies and their evolution: a myocardial infarction with normal coronary angiography, a mechanical complication of the myocardial infarction (ventricular septal rupture, spontaneously closed), recurrent arrhythmias, chronic alcohol consumption and hypothyroidism.


The authors declare that they have no potential conflicts of interest to disclose.


We would like to give our thanks to doctors Liliana Gheorghe, Marius Savin and Drago? Negru (University of Medicine and Pharmacy "Gr.T. Popa", lasi, Radiology Department), who provided the thoracic computer tomography angiography -of the patient.

Video 1. 3D echocardiography and transesophageal echocardiography: fibrotic scar, without interventricular communication


(1.) Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med 2002; 347: 1426-32. [CrossRef]

(2.) Panidis IP Mintz GS, Goel I, McAllister M, Ross J. Acquired ventricular septal defect after myocardial infarction: detection by combined two-dimensional and Doppler echocardiography. Am Heart J 1986; 111: 427-9. [CrossRef]

(3.) Alter P Maisch B, Moosdorf R. Long-term survival with acquired ventricular septal defect after myocardial infarction. Ann Thorac Surg 2004; 78: 2178-80. [CrossRef]

(4.) Brackbill TA, Done JT, Murphy GW, Barold SS. The diagnosis of myocardial infarction in the WPW Syndrome. Chest 1974; 65: 493-9. [CrossRef]

(5.) Williams RI, Ramsey MW. Spontaneous closure of an acquired ventricular septal defect. Postgard Med J 2002; 78: 425-6. [CrossRef]

(6.) Huang G, Antonini-Canterin F Pavan D, Piazza R, Cassin M, Burelli C, et al. Spontaneous closure of postinfarction ventricular septal rupture. A case report. Ital Heart J 2003; 4: 484-7.

(7.) Mittal CM, Aslam N, Mohan B, Tandon R, Sood N, Wander GS. Spontaneous closure of post-myocardial infarction ventricular septal rupture. Tex Heart Inst J 2011; 38: 596-7.

(8.) Amash NM, Warnes CA. Ventricular septal defects in adults. Annals of Internal Medicine 2001; 135: 812-24. [CrossRef]

Paloma Manea, Rodica Ghiuru, Flavia Cociorva *, Mircea Balasanian *, Grigore Tinica *

1st Medical Department and *Department of Cardiovascular Surgery, "Gr. T. Popa", lasi University of Medicine and Pharmacy, lasi-Romania

Address for Correspondence/Yaz??ma Adresi: Dr. Paloma Manea, 1st Medical Department, University of Medicine and Pharmacy "Gr. T. Popa" Iasi, Romania, Str. Universitatii nr. 16, 700115

Phone: +4072 256 97 70


Available Online Date/Cevrimici Yayin Tarihi: 22.04.2013

doi: 10.5152/akd.2013.117
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Article Details
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Title Annotation:Case Reports/Olgu Sunumlari
Author:Manea, Paloma; Ghiuru, Rodica; Cociorva, Flavia; Balasanian, Mircea; Tinica, Grigore
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Date:Jun 1, 2013
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