“Diseases desperate grown by desperate appliances will be relieved or not at all” (Shakespeare, Hamlet IV 8–10)

The mortality of patients who develop cardiogenic shock following myocardial infarction remains high, despite modern management with medical and interventional treatment.1 Although an invasive approach to revascularisation may have a favourable impact upon mortality in comparison to medical treatment alone, the 30 day mortality of the aggressively treated patients in the SHOCK (should we emergently revascularize occluded coronaries for cardiogenic shock) trial was a discouraging 47%.2 The majority of patients who develop cardiogenic shock have severe left ventricular systolic dysfunction as a consequence of large regions of infarcted or ischaemic myocardium, which underlies a clinical course characterised by progressive haemodynamic deterioration. In contrast, acute haemodynamic deterioration may also result from rupture of the left ventricular free wall, ventricular septum, and papillary muscles. Free wall rupture is by far the most common of all ruptures and usually results in sudden death. Ventricular septal defect and papillary muscle rupture are less frequent but more amenable to intervention; in the SHOCK registry, these two mechanical complications were present in only 8% of all patients presenting with shock.3 Nonetheless, the relative infrequency of these mechanical complications should not belie their importance as a potentially reversible cause of cardiogenic shock.4-8

Often, myocardial rupture occurs in patients with small areas of infarction and well preserved systolic function of the left ventricle.4 ,5 ,7 ,8 The latter results in an increased shear stress in the area of necrosis or at its boundaries leading to the mechanical disruption. The therapeutic implications are obvious and elegantly simple—the correction of the mechanical complication may leave the patient with relatively intact ventricular function, which in turn may be a powerful predictor of a favourable long term …