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Cardiac rupture (CR) is a life-threatening mechanical complication of acute myocardial infarction (MI). CR subsumes 3 pathogenetic entities in descending order of frequency including (i) free wall rupture (FWR), (ii) ventricular septal rupture (VSR) and (iii) papillary muscle rupture (PMR). The incidence of CR decreased from 6.2% to 3.2% in parallel with a progressive use of revascularization procedures and implementation of potent medication [5,6]. In particular, the incidence of CR was highest in patients with a ST elevation myocardial infarction (STEMI, 0.9%) and lower in patients with non-ST elevation myocardial infarction (NSTEMI, 0.17%) or unstable angina (0.25%) [8]. Before use of reperfusion therapy, the incidence of VSR was 1–3% [1,6]. Obviously, the incidence of VSR is declining (0.2–0.3%) in parallel with the decreasing incidence of CR since the inception of thrombolytic therapy [7,8]. With the implementation of percutaneous coronary interventions (PCI), VSRhas becomean even rarermechanical complication. Although reperfusion therapy reduces the size of the infarctedmyocardium, it can also provoke hemorrhagic dissection or reperfusion injury, thus potentially accelerating the onset of VSR [3,4,9]. Consequently, time from MI to onset of VSR may have been reduced from 5 days to 1 day in patients receiving reperfusion therapy [1,3,6,9]. Notably, the intra-hospital mortality rate without surgical repair is about 74%–90%. Despite numerous improvements in surgical techniques, mortality rate remains high (20–45%) even in patients undergoing surgical repair, particularly when the RCA is the culprit lesion and cardiogenic shock is involved [3,6]. We present a challenging case of a complex cardiac rupture complicating a silent subacute myocardial infarction which still should be remembered as a potential differential diagnosis though it has decreasing frequency.

Postinfarction posterior ventricular septal rupture mimicking a biventricular free wall rupture with extracardiac left-to-right shunt