Divergent hemometabolic dynamics: understanding the differences between acute myocardial infarction and heart failure related cardiogenic shock

Abstract Background Understanding the hemodynamic trajectories between acute myocardial infarction(AMI) & non-AMI cardiogenic shock(CS) is crucial for tailored management. Purpose Describe different hemometabolic patterns in AMI vs AMI-CS, AMI vs AMI-CS survivors & AMI vs AMI-CS non-survivors. Methods 354 AMI & 81 Non-AMI CS patients with PAC-hemodynamics were included. ANOVA of repeated measures was used to compare trajectories. Cox regression analysis for hazard ratios of conventional cut-off values hemometabolic goals & ideal with Youden index for LVSWi at baseline & 24h(Fig2B/C). Results AMI-CS were older(62 vs 52,P<0.001), exhibit a higher prevalence of smoking, dyslipidemia, HTN, & DM2(P<0.05). HF history & AF were more prevalent in Non-AMI-CS(P<0.001). AMI-CS had lower heart rate, respiratory rate, BUN, pH; higher LVEF, hemoglobin, leucocytes, platelets, glucose, Cl-, Na+, AST, ALT, LDH(P<0.05). Treatment modalities, AMI-CS had higher mechanical circulatory support (P<0.001). AKI was more common in non-AMI(P=0.004). There were no differences in number of vasoactives(P=0.46), but non-AMI had more dobutamine use(P<0.001). MODS score, organ failures, VT/VF, Phenotype, SCAI, and mortality(46.9 vs 47.7% Non-AMI vs AMI-CS) had no differences(P>0.05). Dynamics congestion associated with phenotypes & SCAI are shown in Fig 2A. SBP(F=12.39,P<0.001), DBP(4.72,0.03) & MAP(9.98,0.002) (Fig1A) had differences in AMI vs non-AMI-CS, but none were seen in survivors(P>0.05), only in non-survivors (SBP 17.52, <0.001; DBP 6.59, 0.011 & MAP 13.98, <0.001). RAP(7.4,0.007) & PCWP(53.51,<0.001) (Fig1B/C) also differ among AMI vs non-AMI & non-survivors(5.69,0.018 & 28.77,<0.001); but only PCWP differs across survivors(27.49,<0.001). Cardiac output & index(Fig1D)(13.65,<0.001 & 18.88,<0.001) had both differences among survivors(4.17,0.042 & 6.67,0.01) & non-survivors(10.98,<0.001 & 13.57,<0.001). Cardiac power, index, & CPIRAP(Fig1E) also had this behavior being higher in AMI. Coronary perfusion pressure (Fig1F) differs among all 3 classes (P<0.001), AMI vs non-AMI(F=31.17), survivors(11.63) & non-survivors(25.81). Perfusion pressure only had in AMI vs non-AMI(15.91,<0.001) & non-survivors(20.39,<0.001). PAPI(Fig1G) had differences in AMI vs non-AMI(F=9.3,P=0.002) & non-survivors(8.69,<0.001). API(Fig1H) differs across all spectrums(14.87 groups, 5.89 survivors & 11.61 non-survivors). Finally, LVSWi & RVSWi(Fig1I/J) had differences among AMI vs non-AMI in all categories: groups(22.5 & 14.27 both <0.001), survivors(7.88,0.005 & 9.29,0.003) & non-survivors(21.27,<0.001 & 5.17, 0.024). In the metabolic, only lactate(Fig1K) shows differences in AMI vs non-AMI(5.46,0.02) & non-survivors(8.02,0.005); no differences were noted in survivors. Hazard ratios were assessed with the whole cohort, AMI, & non-AMI; full data is shown in Fig 2B/C. Conclusion Our investigation elucidates nuanced hemodynamic disparities between AMI vs non AMI-CS, even in survivors and non-survivors of CS.Figure 1.Hemodynamic trajectoriesFigure 2.Alluvial. B/C Baseline & 24h goals