Late presenting acute myocardial infarction with evolving cardiogenic shock
Presenter
James Xu, MBBS, FRACP, Northwell Health North Shore University Hospital, Manhasset, NY
James Xu, MBBS, FRACP1, Gaurav Rao, M.D.2 and Perwaiz M. Meraj, M.D., FSCAI1, (1)Northwell Health North Shore University Hospital, Manhasset, NY, (2)Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Westbury, NY
Title
Late presenting acute myocardial infarction with evolving cardiogenic shock
Introduction
Global registries suggest an increase in percutaneous revascularization and early use of left-ventricular assist devices in patients presenting with acute myocardial infarction and cardiogenic shock (CS), with improvement in patient survival. However, mortality remains high in this high-risk population. We present a case of late-presenting acute myocardial infarction complicated by CS and subsequent non-cardiac clinical deterioration despite successful hemodynamic support and wean to explant.
Clinical Case
A 77 year old non-smoking male was admitted to hospital with late presentation ST-elevation myocardial infarction and Killip class III heart failure. He had been experiencing severe chest pain over the preceding 24 hours. Past history includes hypertension treated with losartan 50mg daily. On arrival, blood pressure was 98/56 mmHg and heart rate 56 bpm. Electrocardiogram (EKG) showed sinus rhythm with broad right bundle branch block pattern and residual anterior and inferior ST-segment elevation. Chest X-ray confirmed pulmonary edema. Laboratory results showed creatinine 2.63 mg/dL, lactate 3.4 mmol/L and hemoglobin 16.1 g/dL. He initially received diuretic treatment for heart failure, however with worsening hypotension requiring inotropic and vasopressor support. Bedside transthoracic echocardiogram confirmed severe left ventricular dysfunction. EKG evolved into a left bundle branch block pattern and he was bradycardic at 44 bpm in secondary degree AV block. Urgent cardiac catheterization was performed via right femoral venous and arterial access. Temporary transvenous right ventricular pacing was initiated at 60 bpm, and a 40cc Sensation Plus intra-aortic balloon pump was placed. Hemodynamic assessment showed pulmonary artery saturation 51%, Fick cardiac index 1.67, cardiac power output 0.56 Watts, pulmonary artery pulsatility index 1.1. Selective coronary angiography revealed left dominant coronary circulation with complete occlusion of the left anterior descending artery (LAD) at the proximal segment and mild disease in the other arteries. Hemodynamic parameters continued to worsen, and hemodynamic support was rapidly escalated to an Impella CP device (Abiomed, MA). Following this, percutaneous coronary intervention (PCI) was performed with successful placement of 2 drug eluting stents from proximal to ostial LAD (Synergy 2.75x24mm + 3.5x8mm) and establishment of TIMI 3 flow in all branches. The Impella device was kept in situ post procedurally. With improving hemodynamics this was explanted without complications after 72 hours. Unfortunately, the patient developed pneumonia with distributive shock during his subsequent in-hospital convalescence and passed away.
Discussion
Left ventricular devices such as the Impella reduce cardiac work-load and improve coronary and end-organ perfusion in patients with CS. Analysis of data from the cVAD Registry suggested that earlier initiation of Impella hemodynamic support prior to PCI may significantly improve outcomes. In the current case, the patient initially presented with SCAI Stage B (beginning) CS, which soon evolved into SCAI Stage C (classic) CS, with appropriate escalation and initiation of hemodynamic support prior to revascularization. Our case highlights that CS patients can be treated with successful wean to explant of the hemodynamic support device when a systemic shock team approach is utilized, however many times patient demise is due to non-cardiac causes.