Post-Myocardial Infarction Ventricular Septal Defect: No Reprieve From Doom?

Ventricular septal defect (VSD) complicating acute myocardial infarction (AMI) represents a rare but life-threatening condition with almost 100% of mortality if left untreated. Current standard treatment is based on surgical closure, although percutaneous closure devices may be valid alternatives in patients at high operative risk. Independently from the surgical or transcatheter approach, timing of intervention is crucial, as a linear correlation between acute-phase treatments (<14 days) and higher mortality has been described. Early surgery brings the risk of recurrent ventricular rupture, whereas delayed approach allows easier repair in scarring tissue but may be rendered impossible by irreversible hemodynamic deterioration and death while waiting for intervention. On these bases, current American guidelines recommend early surgery for all patients, whereas European guidelines consider delayed repair for those who respond well to aggressive therapy.,

The Current Case

In the case presented by Bachini et al, in this issue of JACC: Case Reports, the patient required an early treatment because of hemodynamic instability in spite of the intra-aortic balloon pump (IABP) placement. The patient was deemed not suitable for surgery owing to the high operative risk and, consequently, underwent percutaneous closure of VSD. Although the procedure was successful, the patients eventually died secondary to progressive VSD and refractory cardiogenic shock. This case confirms the frustrating persistently high mortality associated with VSD, independently of surgical or percutaneous therapeutic approaches. A probable explanation for such high mortality is the progression of VSD beyond the initial defect by fall of eschars from the surrounding weakened and necrotic myocardium.

New Considerations in Treating VSD

Given the high rates of therapeutic failure for VSD, it is essential to consider novel approaches to treatment. First, understanding that the VSD will progress in the days following the transcatheter septal closure, it is essential to plan the secondary intervention as soon as the initial hemodynamic improvement has been obtained. Second, stabilizing the patient is paramount to gaining time before the secondary intervention and left ventricle (LV) assist devices other than IABP might play an important role as a bridge to subsequent repair.

At present, the best management for the bridge therapy has not been established. Medical therapy has a limited role in the context of VSD, whereas IABP is widely used as a bridge therapy to VSD repair, as indicated also by guidelines., It lowers LV afterload, decreases myocardial oxygen demand (reducing systolic wall tension and increasing coronary perfusion pressure), thus improving myocardial supply-demand balance. Cardiac output increases with improved ventricular ejection and possibly contractility, secondary to increased coronary blood flow. Hemodynamic effects in the context of VSD are summarized in Figure 1. In addition to its hemodynamic effects, its advantages are the large availability in the catheterization laboratories and its ease of use.

Figure 1

Hemodynamic Parameters in the Context of Ventricular Septal Rupture at Baseline and After Placement of Left Ventricle Assist Devices

Parameters measured by Harvi Software (PVLoops). PA = pulmonary artery; PCWP = pulmonary capillary wedge pressure; Qp:Qs = pulmonary-to-systemic blood flow ratio; VSD = ventricular septal defect.

Alternatively, Impella pump placement has been suggested as a promising therapy. Although clinical data are few, the notable LV unloading might result in reduced filling pressures and afterload. Whether LV unloading and improved coronary blood flow will reduce the progression of VSD remains hypothetical. Theoretically, it may be considered the most “physiological” device, by significantly reducing the flow across the VSD, as demonstrated in computational models.

Conversely, extracorporeal-membrane-oxygenation (ECMO) increases LV pre- and afterload and myocardial oxygen consumption that may limit its cardioprotective effect. Although it is commonly used in cardiogenic shock, with VSD it may increase the shunt and, in turn, filling pressures. Thus, it is not surprising that in a recent cohort report, ECMO use was associated with independent excess mortality. Although combination of Impella and ECMO might represent an interesting solution from a hemodynamic standpoint, the large bore sheaths required may increase vascular and bleeding complications affecting, in turn, short-term survival.,

Conclusions

Post-infarction VSD remains a severe condition burdened by considerable mortality. Transcatheter approach is feasible, allowing earlier hemodynamic stabilization, but is frustrated by progression of VSD and plans for reintervention—transcatheter or surgical—have to be discussed early. As profoundly deteriorated clinical conditions at time of intervention (eg, cardiogenic shock, cardiac arrest) have poor prognoses, improved hemodynamic support is paramount. Further studies should focus on possible roles of improved LV support in both pre- and post-operative phases.

Funding Support and Author Disclosures

Dr Russo has received a fellowship training grant from EAPCI, sponsored by Edwards Lifesciences. Dr Enriquez-Sarano consults for Edwards, ChemImage, Cryolife, and HighLife. Dr Taramasso is a consultant for Abbott, Edwards Scientific, Boston Scientific, Shenqi Medical, 4tech, Simulands, MTeX, Occlufit, CoreMedic, and MEDIRA; and receives consultancy fees from Mitraltech.