Abstract
Infarct associated ventricular septal defects (VSDs) are associated with considerable morbidity and mortality and are typically treated via an open surgical approach with the assistance of full mechanical bypass support in the setting of cardiogenic shock. We present two patients with infarct related VSDs and cardiogenic shock (CS) following acute ST segment elevation myocardial infarction (STEMI) and a review of the literature. Each patient successfully underwent percutaneous transcatheter closure of infarct related VSDs and initiation of extracorporeal membrane oxygenation (ECMO) via a portable miniaturized system that resulted in improvement in the patients’ hemodynamics.
1
Introduction
Ventricular septal rupture (VSR) is a rare but well described mechanical complication resulting from acute myocardial infarction (MI) and subsequent myocardial necrosis . In the pre-thrombolytic era, VSR and subsequent ventricular septal defects (VSDs) developed within the first week and presented in 1% to 2% of all post infarct patients. In-hospital mortality occurred in approximately 50% of post surgical and in nearly 100% of medically managed patients .
Those who developed VSR associated CS have an even higher reported mortality of 87%–100% . Treatment with emergency surgery was associated with an operative mortality of 60% compared to 54.1% if surgery was performed within 7 days and 18.4% if surgery occurred after seven days . Surgical repair of VSD is associated with patch dehiscence, potential enlargement of the necrotic area, and possible development of a new VSD and is associated with a 13%–31% mortality rate .
Percutaneous catheter-based therapy potentially offers a treatment strategy associated with a reduction in morbidity and possibly mortality. First described by Lock et al., many ventricular septal occlusion devices have been used for this purpose . The Amplatzer® Multi-Fenestrated “Cribriform” Septal Occluder, developed for multi-fenestrated atrial septal defects, has recently been successfully used to treat post-infarct related VSD with minimal residual shunting or device dislocation .
VSD associated CS results in a compromised left ventricular ejection fraction as the stroke volume is partially ejected into the right ventricle. This results in poor tissue perfusion and increased right ventricular pressures. ECMO has been recognized as a viable therapy in CS patients by decompressing the left ventricle (LV) and improving LV geometry . Successful surgical repair of the VSD is predicated on patients being placed on cardiopulmonary bypass and then on full hemodynamic support to allow the repair of the LV to mature. In recent years, miniaturized portable ECMO (mECMO) has been implemented in the cardiac catheterization laboratory for the treatment of patients with cardiac arrest, cardiogenic shock, or complications from acute myocardial infarction.
In this paper, we will review the literature supporting transcatheter repair of an infarct related VSD and hemodynamic support with mECMO in the context of the clinical care of two patients.
2
Case 1
A 75-year-old female presented with an acute anterior ST segment elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI) of her left anterior descending artery (LAD) with three bare metal stents. Post PCI, she developed CS requiring inotropes and placement of an intra-aortic balloon pump (IABP). Transthoracic echocardiography (TTE) revealed a large VSD with left to right shunting on color flow Doppler ( Fig. 1 ). She was transferred to our tertiary center for advanced treatment options. Given her critically ill condition, she was deemed to be inoperable. The decision was made to pursue transcatheter closure of the VSD and initiation of mECMO.
Angiography and transesophageal echocardiogram (TEE) demonstrated an irregular, apical VSD with left to right shunting ( Figs. 2, 3 ). Using a 6 Fr MP1 catheter, a 0.035″ × 260 cm wire was advanced through the VSD into the left pulmonary artery where it was snared by an 18 mm–30 mm EN Snare (Merit Medical, South Jordan UT) and externalized via the right common femoral vein ( Fig. 4 ). This wire was exchanged for a 0.035” × 300 cm Amplatzer 6 mm “J” tip wire (St. Jude Medical, Minneapolis MN) with a 6 Fr MP1. Two dimensional TEE suggested a very large defect without sufficient apical tissue for repair. Three dimensional TEE revealed a large defect, but one with circumferential tissue onto which a device could adhere. Given the large defect and potentially significant area of necrotic tissue, a 35 mm Amplatzer® Multi-Fenestrated “Cribriform” Septal Occluder was delivered and deployed across the defect via a 9 Fr TorqVue catheter (St. Jude Medical, Minneapolis MN) ( Figs. 4, 5 ). The Qp/Qs improved from 1.93 to 1.03 and the blood pressure rose from 85/54 to 120/80.
In order to achieve hemodynamic support and to decompress the LV to facilitate healing, percutaneous placement of the portable mECMO cannulas was achieved with a 21 Fr Bio-Medicus Multi-Stage Femoral venous cannula and a 15 Fr Bio-Medicus Femoral arterial cannula (Medtronic, Minneapolis MN). The side port of the arterial cannula was connected to a 5 Fr sheath placed via an antegrade fashion for distal limb perfusion. The mECMO circuit (Maquet Cardiohelp, Rastaat Germany) was initiated at 3 L/min. The patient underwent decanalization on post procedure day 2 without complications, had all pressors stopped on post-op day 3, and was transferred to a rehabilitation facility 2 weeks later. Repeat TTE revealed no further shunt ( Fig. 6 ).
2
Case 1
A 75-year-old female presented with an acute anterior ST segment elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI) of her left anterior descending artery (LAD) with three bare metal stents. Post PCI, she developed CS requiring inotropes and placement of an intra-aortic balloon pump (IABP). Transthoracic echocardiography (TTE) revealed a large VSD with left to right shunting on color flow Doppler ( Fig. 1 ). She was transferred to our tertiary center for advanced treatment options. Given her critically ill condition, she was deemed to be inoperable. The decision was made to pursue transcatheter closure of the VSD and initiation of mECMO.
Angiography and transesophageal echocardiogram (TEE) demonstrated an irregular, apical VSD with left to right shunting ( Figs. 2, 3 ). Using a 6 Fr MP1 catheter, a 0.035″ × 260 cm wire was advanced through the VSD into the left pulmonary artery where it was snared by an 18 mm–30 mm EN Snare (Merit Medical, South Jordan UT) and externalized via the right common femoral vein ( Fig. 4 ). This wire was exchanged for a 0.035” × 300 cm Amplatzer 6 mm “J” tip wire (St. Jude Medical, Minneapolis MN) with a 6 Fr MP1. Two dimensional TEE suggested a very large defect without sufficient apical tissue for repair. Three dimensional TEE revealed a large defect, but one with circumferential tissue onto which a device could adhere. Given the large defect and potentially significant area of necrotic tissue, a 35 mm Amplatzer® Multi-Fenestrated “Cribriform” Septal Occluder was delivered and deployed across the defect via a 9 Fr TorqVue catheter (St. Jude Medical, Minneapolis MN) ( Figs. 4, 5 ). The Qp/Qs improved from 1.93 to 1.03 and the blood pressure rose from 85/54 to 120/80.
