Partial ventricular septal defect (Pacman® Heart)
1 Servei de Cardiologia, Hospital Universitari Dr Josep Trueta, Avda. De França, s/n, 17001 Girona, Spain
2 Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands
Received 29 September 2006; accepted after revision 9 September 2007.
* Corresponding author. Tel: +34 627296108; fax: +34 972226050. E-mail address: bet.pujol{at}gmail.com
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Abstract |
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Complete ventricular septal defects (VSD) can be congenital (estimated prevalence 0.5% in live births) (Roguin N, et al. High prevalence of muscular ventricular septal defect in neonates. J Am Coll Cardiol 1995;26:1545–1548) or may be a complication of acute myocardial infarction (estimated incidence in the era of thrombolysis 0.2%) [Crenshaw BS, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27–32]. In this paper, we report two unique cases of partial VSD.
Keywords: Ventricular septal defect
Complete ventricular septal defects (VSD) can be congenital (estimated prevalence 0.5% in live births)1 or may be a complication of acute myocardial infarction (estimated incidence in the era of thrombolysis 0.2%).2 In this paper, we report two unique cases of partial VSDs.
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Case 1 |
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A 76-year-old male was treated with Streptokinase because of a 2-h-old acute inferior myocardial infarction. A routinely made transthoracic two-dimensional echocardiography revealed akinesia of the infero-posterior walls, mild aortic valve disease, and non-transmural loss of myocardial tissue in the inferoseptum without interventricular communication or evidence for a left-to-right shunt (Figure 1). Surgical repair was not done because of absent left-to-right shunting. An echocardiogram obtained 3 weeks later showed some extension of the septal defect that remained stable from that moment at repeat echocardiograms.
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Case 2 |
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A 70-year-old asymptomatic male was referred because of a cardiac murmur. Transthoracic two-dimensional echocardiography revealed severe aortic stenosis (peak pressure gradient 93 mmHg, aortic valve area 0.8 cm2), mild left ventricular (LV) hypertrophy, and preserved LV function. A non-transmural loss of myocardial tissue was observed in the inferoseptum (Figure 2) without interventricular communication or evidence for a left-to-right shunt. Follow-up echocardiograms at 6 and 12 months showed no changes in aortic stenosis severity, LV function or septal defect size.
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In patients undergoing thrombolysis for acute myocardial infarction, the extent of necrosis, advanced age, hypertension, female sex, and the absence of smoking are associated with an increased risk for ventricular septal rupture.2 It generally occurs within the first week after infarction, with the highest incidence on the first day and on days 3 through 5.3 Our acute myocardial infarction patient had only a partial VSD. Surprisingly, the other patient without a history of myocardial infarction and preserved LV function showed also a partial VSD, most likely of congenital origin. To the best of our knowledge partial VSDs were not described before in the literature. They can be easily recognized by the appearance of a ‘Pacman’ (a mouth opening in diastole and closing in systole, see Figure 2) in the muscular wall.
Conflict of interest: none declared.
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References |
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TopAbstractCase 1Case 2References |
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- Roguin N, Du ZD, Barak M, Nasser N, Hershkowitz S, Milgram E. High prevalence of muscular ventricular septal defect in neonates. J Am Coll Cardiol (1995) 26:1545–1548.[Abstract]
- Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation (2000) 101:27–32.
[Abstract/Free Full Text] - Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med (2002) 347:1426–1432.
[Free Full Text]
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