CARDIOGENIC SHOCK COMPLICATING ST ELEVATION MYOCARDIAL INFARCTION: CONFLICTING DEFINITIONS AND THE IMPACT OF PRIMARY PERCUTANEOUS CORONARY INTERVENTION
2021
BACKGROUND In a stark contrast to ∼5% in-hospital mortality in all comer ST Elevation Myocardial Infarction (STEMI) patients, nearly 50% of STEMI patients complicated by cardiogenic shock (STEMI-CS) die during their hospital admission. Despite advancements in pharmaco-mechanical therapies treating STEMI-CS, mortality has remained unchanged. Failure to improve mortality-rate is partly due to our inability to objectively define and identify CS in a "pre-shock state". As per the current guidelines/major studies, CS is defined as either (1) systolic blood pressure (SBP) ≤ 90mmHg, (2) cardiac-index (CI) 2 mmol/L; these parameters are used interchangeably. Here, we wish to address this problem by (1) evaluating consecutive STEMI patients to identify the incidence of CS based on the above 3 parameters, (2) evaluating the concordance between the above 3 parameters in CS patients, and (3) determining the impact of primary percutaneous coronary intervention (PPCI) on these 3 parameters. METHODS AND RESULTS Consecutive patients with STEMI confirmed with electrocardiography were prospectively recruited upon presentation to the cardiac catheterization lab. Hemodynamic parameters were evaluated continuously pre- and post-PPCI using a whole-body impedance based non-invasive technology. Systolic blood pressure (SBP) and lactate were measured before and after PPCI. Sixty-eight STEMI patients were recruited; 22/68 (32%) were female and the mean age was 65.8±1.5 years (34 – 90 years). At presentation pre-PPCI, mean SBP was 126±4 mmHg; mean CI was 2.8±0.1 L/min/m2 and mean lactate was 3.0±0.5 mmol/L. Based upon SBP, CI and lactate, 12.7%, 23.5% and 37.3% patients were in CS. Poor correlation was observed between these parameters. Post-PPCI, CI (pre-PCI: 2.5±0.1 vs. post-PCI: 2.8±0.1 L/min/m2; p=0.00001) increased, whereas SBP (Pre-PCI: 125±4 vs. post-PCI: 112±3 mmHg; p=0.00006), and lactate (Pre-PCI: 3.2±0.53 vs. post-PCI: 2.4±0.5 mmol/L; p=0.004) decreased. CONCLUSION Our study is the first to describe, (1) poor congruity between the current parameters defining CS, (2) PPCI improves CI and reduces lactate, likely aborting impending CS and associated mortality, and (3) that SBP is a suboptimal tool for assessing CI in the setting of STEMI. With ongoing recruitment and 1-month follow-up, we wish to identify outcome [death at 30-days, prolonged (>96 hours) in-hospital stay due to heart failure, refractory arrhythmias, need for inotropic support and/or mechanical circulatory support, including intra-aortic balloon pump insertion during the index hospital admission] associated hemodynamic marker(s) that may help us identify high-risk STEMI patients in a timely fashion.
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