Case Report: Post-Infarct Ventricular Septal Defect Closure
Poster #: 045
Session/Time: B
Author:
Thomas Anthony Cook, BS
Mentor:
Matthew Summers, MD
Research Type: Case Report
Abstract
INTRODUCTION:
Ventricular septal defect (VSD) following acute myocardial infarction is a rare but deadly complication that carries mortality rates exceeding 90% when left untreated. Interventricular septum rupture typically arises 3-5 days post-infarction when myocardial tissue is most friable. The sudden development of a left-to-right shunt leads to volume overload of the right ventricle, pulmonary vasculature, and left atrium, precipitating severe biventricular failure and cardiogenic shock.
CASE INFORMATION:
A 65-year-old female with hypertension, uncontrolled type 2 diabetes, and obesity presented to a local emergency department with acute onset of shortness of breath and chest discomfort. An electrocardiogram showed anterolateral ST-segment elevations and a portable chest x-ray displayed an enlarged cardiac silhouette and increased pulmonary vascular markings concerning for cardiogenic shock. She was intubated and transferred to a tertiary care center where coronary angiography demonstrated total thrombotic occlusion of the left anterior descending artery. Emergent PCI was performed, but despite successful intervention, the patient developed worsening cardiogenic shock. Transesophageal echocardiography revealed a post-infarct VSD, prompting intra-aortic balloon pump (IABP) placement. During hospitalization, the patient developed ventricular tachycardia arrest (hospital day 8), acute kidney injury requiring continuous renal replacement therapy (CRRT), and ventilator-associated pneumonia, and she remained in refractory shock despite vasoactive inotropic support. On hospital day 12, percutaneous VSD closure was undertaken with fluoroscopic and echocardiographic guidance. Hemodynamics improved as Qp:Qs fell from 2.5 to 1.6 after placement of a 24-mm Amplatzer occluder device. Echocardiography confirmed stable device position with minimal residual shunt. The IABP was replaced during the procedure and removed successfully on hospital day 14. Postoperatively, the patient developed worsening sepsis and lactic acidosis despite broad-spectrum antibiotics and CRRT. On day 16, her condition deteriorated further, and comfort measures were initiated before she expired on hospital day 17.
DISCUSSION:
This case highlights the challenges of managing a post-infarct VSD, one of the most feared mechanical complications of acute coronary artery occlusion. Historically, untreated post-infarct VSD carries a mortality rate exceeding 90% within two weeks, reinforcing the need for urgent intervention. Closure can be achieved surgically via a patch repair with infarct exclusion or percutaneously using a transcatheter occluder device. Optimal timing of post-infarct VSD repair remains controversial. Immediate repair within 7 days of infarction, usually within 24-72 hours of VSD diagnosis, is required in patients with refractory cardiogenic shock. Delaying intervention to ≥ 7 days after infarction, however, allows infarcted myocardium to fibrose, strengthening tissue for suturing or device anchoring and has been associated with improved procedural success and reduced mortality rates. In this patient, delayed percutaneous closure successfully reduced shunting and enabled IABP removal, but systemic complications ultimately dictated prognosis.
CONCLUSION:
This case demonstrates both the potential and limitations of delayed percutaneous closure of post-infarct VSD. Although the intervention successfully reduced left-to-right shunting and allowed for weaning of IABP support, progressive sepsis and cardiogenic shock resulted in mortality. Early recognition, prompt initiation of mechanical circulatory support, and nuanced decisions regarding timing and modality of repair remain essential in managing this fatal complication of acute myocardial infarction.
Ventricular septal defect (VSD) following acute myocardial infarction is a rare but deadly complication that carries mortality rates exceeding 90% when left untreated. Interventricular septum rupture typically arises 3-5 days post-infarction when myocardial tissue is most friable. The sudden development of a left-to-right shunt leads to volume overload of the right ventricle, pulmonary vasculature, and left atrium, precipitating severe biventricular failure and cardiogenic shock.
CASE INFORMATION:
A 65-year-old female with hypertension, uncontrolled type 2 diabetes, and obesity presented to a local emergency department with acute onset of shortness of breath and chest discomfort. An electrocardiogram showed anterolateral ST-segment elevations and a portable chest x-ray displayed an enlarged cardiac silhouette and increased pulmonary vascular markings concerning for cardiogenic shock. She was intubated and transferred to a tertiary care center where coronary angiography demonstrated total thrombotic occlusion of the left anterior descending artery. Emergent PCI was performed, but despite successful intervention, the patient developed worsening cardiogenic shock. Transesophageal echocardiography revealed a post-infarct VSD, prompting intra-aortic balloon pump (IABP) placement. During hospitalization, the patient developed ventricular tachycardia arrest (hospital day 8), acute kidney injury requiring continuous renal replacement therapy (CRRT), and ventilator-associated pneumonia, and she remained in refractory shock despite vasoactive inotropic support. On hospital day 12, percutaneous VSD closure was undertaken with fluoroscopic and echocardiographic guidance. Hemodynamics improved as Qp:Qs fell from 2.5 to 1.6 after placement of a 24-mm Amplatzer occluder device. Echocardiography confirmed stable device position with minimal residual shunt. The IABP was replaced during the procedure and removed successfully on hospital day 14. Postoperatively, the patient developed worsening sepsis and lactic acidosis despite broad-spectrum antibiotics and CRRT. On day 16, her condition deteriorated further, and comfort measures were initiated before she expired on hospital day 17.
DISCUSSION:
This case highlights the challenges of managing a post-infarct VSD, one of the most feared mechanical complications of acute coronary artery occlusion. Historically, untreated post-infarct VSD carries a mortality rate exceeding 90% within two weeks, reinforcing the need for urgent intervention. Closure can be achieved surgically via a patch repair with infarct exclusion or percutaneously using a transcatheter occluder device. Optimal timing of post-infarct VSD repair remains controversial. Immediate repair within 7 days of infarction, usually within 24-72 hours of VSD diagnosis, is required in patients with refractory cardiogenic shock. Delaying intervention to ≥ 7 days after infarction, however, allows infarcted myocardium to fibrose, strengthening tissue for suturing or device anchoring and has been associated with improved procedural success and reduced mortality rates. In this patient, delayed percutaneous closure successfully reduced shunting and enabled IABP removal, but systemic complications ultimately dictated prognosis.
CONCLUSION:
This case demonstrates both the potential and limitations of delayed percutaneous closure of post-infarct VSD. Although the intervention successfully reduced left-to-right shunting and allowed for weaning of IABP support, progressive sepsis and cardiogenic shock resulted in mortality. Early recognition, prompt initiation of mechanical circulatory support, and nuanced decisions regarding timing and modality of repair remain essential in managing this fatal complication of acute myocardial infarction.