ABSTRACT
Background: Cardiogenic shock is a leading cause of mortality in patients with acute myocardial infarction. Objectives: The authors sought to compare clinical characteristics, hospital trajectory, and drug and device use between patients with ST-segment elevation myocardial infarction-related cardiogenic shock (STEMI-CS) and those without (non-ST-segment elevation myocardial infarction complicated by cardiogenic shock [NSTEMI-CS]). Methods: We analyzed data from 1,110 adult admissions with cardiogenic shock complicating acute myocardial infarction (AMI-CS) across 17 centers within Cardiogenic Shock Working Group. The primary end point was in-hospital mortality. Results: Our study included 1,110 patients with AMI-CS, of which 731 (65.8%) had STEMI-CS and 379 (34.2%) had NSTEMI-CS. Most patients were male (STEMI-CS: 71.6%, NSTEMI-CS: 66.5%) and White (STEMI-CS: 53.8%, NSTEMI-CS: 64.1%). In-hospital mortality was 41% and was similar among patients with STEMI-CS and NSTEMI-CS (43% vs 39%, P = 0.23). Patients with out-of-hospital cardiac arrest had higher in-hospital mortality in patients with NSTEMI-CS (63% vs 36%, P = 0.006) as compared to patients with STEMI-CS (52% vs 41%, P = 0.16). Similar results were observed for in-hospital cardiac arrest in patients with STEMI-CS (63% vs 33%, P < 0.001) and NSTEMI-CS (60% vs 32%, P < 0.001). Only 27% of patients with STEMI-CS and 12% of NSTEMI-CS received both a drug and temporary mechanical circulatory support device during the first 24 hours, which increased to 78% and 61%, respectively, throughout the course of the hospitalization (P < 0.001 for both). Conclusions: Despite increasing use of inotropic and vasoactive support and mechanical circulatory support throughout the hospitalization, both patients with STEMI-CS and NSTEMI-CS remain at increased risk for in-hospital mortality. Randomized controls trials are needed to elucidate whether timing and sequence of escalation of support improves outcomes in patients with AMI-CS.
ABSTRACT
Background Recent prospective multicenter data from patients with advanced heart failure demonstrated that left ventricular assist device (LVAD) support combined with standard heart failure medications, induced significant cardiac structural and functional improvement, leading to high rates of LVAD weaning in selected patients. We investigated whether preintervention myocardial and systemic inflammatory burden could help identify the subset of patients with advanced heart failure prone to LVAD-mediated cardiac improvement to guide patient selection, treatment, and monitoring. Methods and Results Ninety-three patients requiring durable LVAD were prospectively enrolled. Myocardial tissue and blood were acquired during LVAD implantation, for measurement of inflammatory markers. Cardiac structural and functional improvement was prospectively assessed via serial echocardiography. Eleven percent of the patients showed significant reverse remodeling following LVAD support (ie, responders). Circulating tumor necrosis factor alpha, interleukin (IL)-4, IL-5, IL-6, IL-7, IL-13, and interferon gamma were lower in responders, compared with nonresponders (P<0.05, all comparisons). The myocardial tissue signal transducer and activator of transcription-3, an inflammatory response regulator, was less activated in responders (P=0.037). Guided by our tissue studies and a multivariable dichotomous regression analysis, we identified that low levels of circulating interferon gamma (odds ratio [OR], 0.06; 95% CI, 0.01-0.35) and tumor necrosis factor alpha (OR, 0.05; 95% CI, 0.00-0.43), independently predict cardiac improvement, creating a 2-cytokine model effectively predicting responders (area under the curve, 0.903; P<0.0001). Conclusions Baseline myocardial and systemic inflammatory burden inversely correlates with cardiac improvement following LVAD support. A circulating 2-cytokine model predicting significant reverse remodeling was identified, warranting further investigation as a practical preintervention tool in identifying patients prone to LVAD-mediated cardiac improvement and device weaning.
