**4. Diagnosis**

The diagnosis of a PI-VSD must be considered in the differential in any patient presenting with hemodynamic impairment, particularly in the context of a sudden deterioration in a patient who otherwise had been doing well, either during or after an AMI. As a PI-VSD presents in a similar manner as other mechanical complications of AMI, such a papillary muscle rupture (with acute mitral regurgitation), free wall rupture (with contained tamponade), or severe LV failure and pulmonary edema the initial diagnosis is often suspected during initial investigations and confirmed with additional imaging.

The typical presentation occurs in a patient who is otherwise recovering after initial management of an uncomplicated AMI. Patients often complain of recurrent chest pain from what is most likely new onset or recurrence of myocardial necrosis and will develop a new systolic murmur that can be harsh, pansystolic, and often-best ascultated at the left lower sternal border. Patients can often have a bundle branch block from disruption of the septal conduction system and will quickly deteriorate hemodynamically with findings suggestive of acute cardiogenic shock.

weeks after their initial acute event. It was these experiences that set the foundation for the belief that operative management should be delayed as long as possible to allow for scarring of the necrotic myocardium to provide for a more stable repair. As experiences grew – in terms of the initial diagnosis and surgical management – early repair was advocated, particularly in patients who were stable before hemodynamic deterioration and subsequent

The incidence of PI-VSD has decreased considerably over the years with advances in myocardial reperfusion strategies. Historically, up to 5% of all myocardial infractions were associated with mechanical complications such free-wall rupture, papillary muscle rupture, and PI-VSD (Agnihotri, 2008). With current treatment algorithms that advocate early and aggressive attempts at revascularization of the acute ischemic myocardial – such as thrombolytic therapy, early percutanous interventions with coronary stenting (PCI), and, less frequently, emergent coronary artery bypass surgery (CABG) – the overall incidence has dropped significantly. Large multi-centers studies evaluating the pathophysiologies of acute myocardial infarctions have shown a current incidence of approximately 0.2% of all AMI. With delays in therapies, or late clinical presentation, and the resulting increase in myocardial damage, this incidence increases up to 2%. Despite the relatively low risk of developing a PI-VSD, it account for a disproportionally high risk of mortality. Over 5% of all early deaths after AMI are attributed directly to the pathophysiologic complications of PI-

The timing of the development of a PI-VSD can be quite variable with the average time to clinical presentation is between 2 and 4 days, however presentation can be as few as a few

Patient risk factors include gender, with men at a greater risk than women (3:2 ratio), increasing age, and current smoking history. The mean age of presentation in GUSTO was

The diagnosis of a PI-VSD must be considered in the differential in any patient presenting with hemodynamic impairment, particularly in the context of a sudden deterioration in a patient who otherwise had been doing well, either during or after an AMI. As a PI-VSD presents in a similar manner as other mechanical complications of AMI, such a papillary muscle rupture (with acute mitral regurgitation), free wall rupture (with contained tamponade), or severe LV failure and pulmonary edema the initial diagnosis is often

The typical presentation occurs in a patient who is otherwise recovering after initial management of an uncomplicated AMI. Patients often complain of recurrent chest pain from what is most likely new onset or recurrence of myocardial necrosis and will develop a new systolic murmur that can be harsh, pansystolic, and often-best ascultated at the left lower sternal border. Patients can often have a bundle branch block from disruption of the septal conduction system and will quickly deteriorate hemodynamically with findings suggestive

suspected during initial investigations and confirmed with additional imaging.

end-organ failure.

VSD (Poulsen, 2008).

**4. Diagnosis** 

of acute cardiogenic shock.

hours after AMI or as long as several weeks.

62.5 years and ranged from 44 to 81 years (Crenshaw, 2000).

**3. Clinical presentation** 

With the acute clinical deterioration, a rapid assessment of the etiology is critical. Unlike other mechanical complications, such as papillary muscle rupture, PI-VSDs will have imagining confirming a left to right shunt – such as contrast injected into the left ventricle during catheterization crossing the defect into the RV and entering into the pulmonary arteries (Figure 1). Likewise, oxymetric assessment with right heart catheterization will demonstrate a "step-off" from the mixing of de-oxygenated RV blood with the oxygenation LV blood. Quantitative assessment of Qp:Qs will correlate with the size of defect.

Fig. 1. Representative cardiac catheterization in which contrast is injected into the left ventricular cavity and then crosses the defect into the right ventricle. Contrast flowing into the pulmonary artery is then diagnostic for a ventricular septal defect.
