One of the consequences associated with acute myocardial infarction is the development of ventriculoseptal rupture.1 Once present, there is rapid progression to cardiogenic shock; however, the options available for successful management of this condition are limited. While early operative management is important for closure of this defect, the mortality associated with early operative intervention is high.2,3
Surgical delay, however, can lead to worsening of cardiogenic shock, with a high mortality as well. An alternative in some patients is to carry out percutaneous closure of such defects, though this has been performed with limited success. In light of the profound cardiogenic shock and the inability to perform effective early surgical intervention, the use of percutaneous assist devices can play an important role as a temporizing measure till further destination therapy.4
We describe here a case of a man who developed ventriculoseptal rupture with cardiogenic shock after a large myocardial infarction and later received hemodynamic support with a TandemHeart assist device, allowing myocardial recovery and eventual definitive therapy with surgical closure of the defect.
A 73-year-old male with a history of hypertension and hyperlipidemia presented to an outside institution with a complaint of sudden onset chest pain. A diagnosis of acute inferior wall myocardial infarction was made and the patient was taken to the catheterization lab for emergent coronary intervention. A single drug-eluting stent was placed in the right coronary artery; however, the patient’s post-percutaneous coronary intervention (PCI) course was marred by the development of cardiogenic shock within 24 hours. An intra-aortic balloon pump (IABP) was eventually placed and vasopressors administered for hemodynamic support. Attempts to withdraw IABP support were unsuccessful due to persistent shock. An echocardiogram showed worsening cardiac function with severe, right-sided hypokinesis and a new 1.8 cm ventriculoseptal defect, with a prominent left to right shunt. The patient’s resting left ventricular ejection fraction remained at 65%. After ten days at the outside hospital, the patient was transferred to our center for further management while on dobutamine, dopamine, and an IABP.
Upon arrival at our center, the patient was normotensive at 122/79 mmHg, with a heart rate of 90 bpm on 3 mcg of dopamine and dobutamine while on 1:1 IABP support, with oxygen saturations of 99% while on 3 liters of oxygen. He was alert and oriented. Cardiac exam showed jugular venous distention with clear lungs on auscultation and a harsh 3/6 holosystolic murmur, heard best at the 5th intercostal space.
Repeat echocardiographic examination showed a stable 1.8 cm ventricular septal rupture (VSR). Interventional cardiology was initially consulted to assist with percutaneous closure of the defect; however, the defect was deemed too large for closure with an occluder. Surgery was therefore asked to evaluate the patient. Due to the friable nature of the tissue, surgery felt that waiting would be the best option to repair the ruptured septum successfully.
The next day, the patient decompensated further while on 1:1 IABP and inotropic and vasopressor support, and developed pulmonary edema. His renal function also deteriorated significantly, with a creatinine of 4.0, up from his baseline of 0.7, necessitating continuous veno-venous hemofiltration. Since the patient was considered too high risk for surgery, it was decided to place a left ventricular assist device. Unfortunately, in light of the large septal defect, the Impella 5.0 (Abiomed), which was initially considered, was not a good option, because its cannula requires LV placement. Therefore, the TandemHeart device (CardiacAssist) was considered as a temporizing measure, with eventual plans for surgical repair. The goal was to reverse the patient’s cardiogenic shock and stabilize him so that he could undergo surgical repair in a few days.
Therefore, under intracardiac echocardiographic guidance, a transseptal puncture was performed, and a 21 French (Fr) cannula, which had been advanced through the femoral vein, was placed into the left atrium. A second cannula was placed in the left common iliac artery via left common femoral access. A 15 Fr cannula was chosen over a 17 Fr due to mild to moderate iliac stenosis. Left ventricular support was then successfully initiated with 3L support at 6000 RPM.
While on the TandemHeart, the patient’s hemodynamic profile improved remarkably, and he was taken off the balloon pump and weaned down to minimal pressor support. Seven days later, the patient was taken to the operating room for surgical correction of the VSR. The VSR was repaired with a Hemashield graft (Atrium Medical/Maquet), and infarctectomy of the right ventricle was performed. A bypass graft was also placed using the saphenous vein on the left anterior descending artery. At the end of the procedure, the TandemHeart was explanted and the patient was then transferred to the coronary care unit in a stable condition.
The patient fared well after the procedure, and was weaned off all pressors with a stable hemodynamic profile. Unfortunately, three weeks later, the patient developed severe gram-negative sepsis with positive cultures from his urine and the site of harvestation of the saphenous vein. As his condition worsened, his family decided to withdraw all care, and the patient expired soon after.
Myocardial infarctions can result in mechanical, arrhythmic and inflammatory complications. Those associated with mechanical dysfunction include papillary muscle rupture, ventricular free wall rupture, development of ventricular aneurysms and ventriculoseptal ruptures as well. VSRs complicate approximately 0.5-2% of all myocardial infarctions.1,5,6 However, mortality with this complication is 85-92.5% if left untreated, due to the unusually high hemodynamic loads that are placed on an already compromised heart, with the development of resultant cardiogenic shock.6 While the mainstay of treatment has historically been surgical repair, the mortality with immediate surgical repair stands at 20-55%, and 95% in those who have undergone medical treatment only, at 30 days.6,7 Also of note is the fact that operative mortality is 54.1% if repair of this defect is carried out within 7 days of an MI, and it reduces to 18.4% if performed 7 days after an MI.2 Unfortunately, these patients have a poor cardiac profile with a very tenuous hemodynamic status, which necessitates some form of early intervention to lower mortality.
Septal ruptures frequently occur in areas where the myocardial tissue has undergone necrosis after an episode of ischemia. The average time from infarction to rupture due to underlying necrosis is estimated at 3-5 days.8
Knowing the evolution of the infarct and the time it takes for the tissue to undergo necrosis is important, since early mechanical intervention can fail due to the friability of the underlying tissue. Other factors that need to be taken into account, besides the timing of the intervention and knowing the progression of disease, are the size and location of the defect. It is the size that predicts the degree of shunting, the extent of hemodynamic compromise, and in some cases, the likelihood of survival as well. The worst prognosis is also typically seen with posterior VSRs.9 This is due to the involvement of a large portion of the right ventricular wall along with basal segments of the heart.10
In this situation, physicians are usually presented with two options. The first is to pursue immediate surgical closure, while the second is to delay surgery, stabilize the patient, and wait for the necrotic borders to heal, in order to allow for better technical success at repair. Unfortunately, as mentioned earlier, immediate surgery is associated with a high mortality as well. Two of the major reasons why early surgical intervention has poor outcomes are the necrotic borders of the VSR, usually poor for suturing, and most of important of all, the underlying cardiogenic shock. If, however, surgery can be delayed for a certain amount of time, to allow for recovery of ventricular function and resolution of shock, outcomes can indeed be improved. This can be achieved with the use of percutaneously placed left ventricular assist devices, which allow for stabilization of the hemodynamic status of the patient and encourage better overall outcomes.
We suggest using the TandemHeart in such a situation, as a bridge to further therapy. The TandemHeart works by unloading the left ventricle, removing blood via a cannula placed in the left atrium by way of a transseptal puncture. The blood is directed to an axial pump that redirects this oxygenated blood back into the circulation through the femoral artery. The reduction in preload helps reduce the workload of the ventricle, improves mean arterial pressure along with microvascular perfusion and systemic perfusion, and reduces myocardial oxygen demand, allowing the ventricle to recover.11
Such an approach can reverse cardiogenic shock and help reduce mortality in those who are very sick. This also creates a delay for surgery, which allows the necrotic tissue to undergo fibrosis, thus permitting the sutures to hold after surgery. This strategy for medical stabilization and reversal of cardiogenic shock secondary to mechanical complications of acute myocardial infarction using the TandemHeart device, followed by surgical repair of the VSR, has the potential to become a new paradigm in the treatment of this complication.
There is limited evidence in literature of this approach of using percutaneous ventricular assist devices (pVADs) for ventricular support. La Torre et al have reported the use of the Impella 5.0 LVAD in patients with post-MI VSRs, and report mortality rates of 40% after approximately 8-23 days of left ventricular assist.12 Gregoric et al have also reported the successful use of a TandemHeart device as a bridge to surgical repair.13
In conclusion, we can state that the mortality with VSR post MI is indeed high. The reason for mortality is the cardiogenic shock that develops with the VSR. Surgical repair is deemed high risk due to the underlying hemodynamic instability and also due to the inability to carry out effective surgical repair. The use of pVADs such as the TandemHeart allows for reversal of the cardiogenic shock and permits stabilization of the patient, which can give physicians enough time to carry out effective surgical repair when feasible. Such a strategy can indeed potentially improve outcomes, but further studies are required to validate this pathway.
This case received a double-blind peer review from members of the Cath Lab Digest editorial board.
Dr. Ansari and Dr. Sadanandan report no actual or potential financial disclosures or conflicts of interest regarding the content herein.
The authors can be contacted via Dr. Saihari Sadanandan at email@example.com.
- Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med. 2002 Oct 31; 347(18): 1426-1432.
- Arnaoutakis GJ, Zhao Y, George TJ, Sciortino CM, McCarthy PM, Conte JV. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg. 2012 Aug; 94(2): 436-443; discussion 443-444. doi: 10.1016/j.athoracsur.2012.04.020.
- Radford MJ, Johnson RA, Daggett WM, Jr., Fallon JT, Buckley MJ, Gold HK, et al. Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival. Circulation. 1981 Sep; 64(3): 545-553.
- Halpern DG, Perk G, Ruiz C, Marino N, Kronzon I. Percutaneous closure of a post-myocardial infarction ventricular septal defect guided by real-time three-dimensional echocardiography. Eur J Echocardiogr. 2009 Jun; 10(4): 569-571. doi: 10.1093/ejechocard/jep021.
- Di Summa M, Actis Dato GM, Centofanti P, Fortunato G, Patane F, Di Rosa E, et al. Ventricular septal rupture after a myocardial infarction: clinical features and long term survival. J Cardiovasc Surg (Torino). 1997 Dec; 38(6): 589-593.
- Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1110-6.
- Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000 Jan 4-11; 101(1): 27-32.
- Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture. Ann Thorac Surg. 1986 Jun; 41(6): 683-691.
- Moore CA, Nygaard TW, Kaiser DL, Cooper AA, Gibson RS. Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival. Circulation. 1986 Jul; 74(1): 45-55.
- Bolooki H. Emergency cardiac procedures in patients in cardiogenic shock due to complications of coronary artery disease. Circulation. 1989 Jun; 79(6 Pt 2): I137-I148.
- Basra SS, Loyalka P, Kar B. Current status of percutaneous ventricular assist devices for cardiogenic shock. Curr Opin Cardiol. 2011 Nov; 26(6): 548-554. doi: 10.1097/HCO.0b013e32834b803c.
- La Torre MW, Centofanti P, Attisani M, Patane F, Rinaldi M. Posterior ventricular septal defect in presence of cardiogenic shock: early implantation of the impella recover LP 5.0 as a bridge to surgery. Tex Heart Inst J. 2011; 38(1): 42-44.
- Gregoric ID, Bieniarz MC, Arora H, Frazier OH, Kar B, Loyalka P. Percutaneous ventricular assist device support in a patient with a postinfarction ventricular septal defect. Tex Heart Inst J. 2008; 35(1): 46-49.