Escalating Temporary Mechanical Circulatory Support In Worsening Cardiogenic Shock: Feasibility In Advanced Heart Failure Therapy Candidates
Isseh IN, Gorgis S, Dagher C, Sharma S, Basir MB, and Parikh S. Escalating Temporary Mechanical Circulatory Support In Worsening Cardiogenic Shock: Feasibility In Advanced Heart Failure Therapy Candidates. Journal of Cardiac Failure 2020; 26(10):S55.
Journal of Cardiac Failure
Background: Temporary mechanical circulatory support (tMCS) can be used in cardiogenic shock (CS) as a bridge to advanced heart failure therapies (AHFT) (durable LVAD, cardiac transplantation). tMCS escalation in worsening CS has never been studied and prognostication in this cohort is needed, particularly in candidates for AHFT. We evaluated potential predictors of survival and outcomes of those that received AHFT.
Methods: From 07/2016-07/2018 we identified patients with worsening CS shock requiring tMCS escalation. Worsening CS was defined as persistent hypotension; increasing doses of vasopressors/inotropes; worsening end-organ perfusion parameters; and/or worsening invasive hemodynamics. tMCS escalation was defined as adding/exchanging tMCS device to existing tMCS. Potential prognostic variables were evaluated in ROC curves. All statistical tests were performed with a two-sided p value=05.
Results: 81 consecutive patients (61±14y, 73%m) had worsening CS shock requiring tMCS escalation. Devices used were IABP, Impella (2 5, CP, 5 0), ECMO and Tandem (TandemHeart, TandemLife, ProtekDuo). Survival to discharge was 32%. Etiology of shock was heterogeneous (33% AMI; 62% decompensated heart failure). 62% were transfers from outside hospitals. Utilization of a PA catheter pre-escalation was associated with improved survival compared to absence of a PA catheter (40% vs 18%, p=0.05). ROC curves demonstrated prognostic thresholds associated with survival: age <53y (80% specificity) and pre-escalation cardiac power output (CPO) >0.92 Watts (87% specificity). While prognostic thresholds associated with mortality were: age >69 y (81% specificity), BMI >35 kg/m2 (81% specificity), pre-escalation cardiac power output (CPO) <0.53 Watts (82% specificity), pre-escalation lactate >3 mmol/L (81% specificity). AUC was greatest in post-escalation blood pressure indicating persistence of hypotension post-escalation (SBP <85 mmHg; MAP <67 mmHg) was associated with a dismal prognosis (specificity 92% for both for predicting mortality). 7 patients went on to receive AHFT (49±13.4y, 57%m) with a mean BMI 32±11.4 kg/m2. 6 received durable LVAD during index hospitalization, 4 of which survived. 4 underwent transplant in subsequent hospitalizations, all of which survived. Majority had decompensated heart failure as etiology of shock (NICM=5, ICM=1, AMI=1) and received tMCS escalation within 1 day (n=6). All patients were classified as Stage D SCAI CS at the time of escalation and 5 received vasopressors/inotropes. Majority of patients had a PA catheter at time of escalation (n=6). Overall survival was higher in the AHFT compared to those that did not receive AHFT (n=5, 71% vs n=21, 28.4%, p=0.03).
Conclusions: tMCS escalation in worsening CS incurs poor survival overall (32%). tMCS escalation is feasible in stabilizing patients with worsening CS that are candidates for AHFT.