**Post Myocardial Infarction Ventricular Septal Defect**

Michael S. Firstenberg and Jason Rousseau

*Division of Cardiac Surgery, The Ohio State University Medical Center, Columbus, USA* 

#### **1. Introduction**

28 Front Lines of Thoracic Surgery

Carpentier A.; Adams D; Filsoufi F. (2010). Carpentier's Reconstructive Valve Surgery,

Savage E; Bolling S, (2006). Atlas of Mitral Valve Repair, Lippincott Williams & Wilkins,

Society of Thoracic Surgeons. J AmColl Cardiol 2008;52:e1–e142.

Elsevier, ISBN: 978-0-7216-9168-8 USA

ISBN – 13:978-0-7817-4692-2 USA

JS. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and

> With advances in the management of acute myocardial infarction (AMI) the incidence of mechanical complications continues to decline. Nevertheless, when they occur, unfortunately, despite similar advances and growing experiences in the surgical management of these problems, morbidity and mortality remain high. Post-myocardial infarction ventricular septal defects (PI-VSD) have fascinated and challenged clinicians for years. The timing of presentation can be quite variable, as they tend to occur in patients several days after their initial cardiovascular insult (acute PI-VSD) – and unfortunately, they can occur in patients who appear to have been making significance progress on the road to recovery. In addition, although more rare, some patients might not present until weeks, if not longer, after their infarction with symptoms that prompt the discovery of a chronic PI-VSD. Early PI-VSDs tend to be catastrophic and typically result in early death. The pathophysiology is also variable and complex, but common themes include: 1) worsening cardiac output, often with manifestations of shock and end-organ damage, from acute left ventricular (LV) dysfunction and from increased left-right shunting, 2) acute right ventricular (RV) dysfunction from a sudden increase in pressure, volume, and flow from left to right shunts, and 3) pulmonary hypertension also from the increase in RV flow. Definitive management remains surgical, however controversies continue to exist regarding the timing of surgery and the role of concomitant coronary revascularization. Unfortunately, despite early repair and standardization of techniques, both short and long-term outcomes remain less than ideal.

### **2. History**

As with many cardiovascular conditions, post-myocardial infarction ventricular septal defects (PI-VSD) were described first at autopsy (Latham, 1845) and then pre-mortum in 1923, many years before the pathophysiology was understood (Brunn, 1923). It was not until 1934 that the association with coronary artery disease was described (Sager, 1934). The first report of a surgical repair came in 1956 when Denton Cooley described the surgical management in a patient 9 weeks after the initial diagnosis (Cooley, 1956). With advances in cardiovascular surgery and peri-operative management of the cardiac surgery patient there were increasing reports of survival in what was previously felt to be a lethal problem. Most of the successful cases occurred in patients who presented in congestive heart failure many

Post Myocardial Infarction Ventricular Septal Defect 31

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

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

Transthoracic echocardiography (TTE) remains the cornerstone of the non-invasive assessment of PI-VSD (Kishon, 1993). TTE is indicated in any patient who presents with evidence of acutely impaired ventricular function or in unexplained hemodynamic deterioration suggests a mechanical complication following an acute myocardial infarction (Buda, 1991). Echocardiography has the benefit of being able to assess both left and right ventricular function, the presence of potentially co-existing and confounding valvular diseases – typically mitral regurgitation, and with color flow imaging it can be 100% specific and sensitive in diagnosing a PI-VSD. Despite the utility of TEE in the acute assessment of a deterioritating patient, a high index of suspicion is needed when looking for a PI-VSD as traditional echo windows might miss a small or apical defect. Large pericardial effusions

the pulmonary artery is then diagnostic for a ventricular septal defect.

defect.

**4.1 Echocardiography** 

might suggest an associated free wall rupture.

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 end-organ failure.
