Introduction
Cardiogenic shock (CS) is a spectrum of phenotypes and multiorgan failure (MOF). Recent works [1] approach the typification, but no continuous hemodynamic patterns has been associated with these phenotypes nor MOF.
Methods
295 AMI-CS patients (SBP ≤90 mmHg, vasopressor use, cardiac index ≤2.2 L/min/m2, or lactate ≥2 mmol/L) and pulmonary artery (PA) catheter. Cut-off values were used to divide in 3 phenotypes cardiac [C0] (no organ involvement), cardiorenal [CR] (eGFR <45 ml/min/1.73 m2), and cardiometabolic [CM] (renal+hepatic [AST or ALT >3 ULN]) [2] SCAI definitions were used [3]. MODS score defines MOF as ≥2 organs [4]; AKI (rise Cr >0.3 mg/dL) and electric instability (VT/VF). Repeated measures ANOVA was used to compare 24 h hemodynamic data. 30-day mortality hazard ratios were obtained (Fig. 1E).
Results
C0 represent 64.41% (190), CR 14.91% (44) and CM 20.68% (61). SCAI C was more in C0 (24.74 vs 0, 0%), E in the CM (23.16, 38.64 vs 63.93%); SCAI D had differences in CR and CM (61.36 vs 36.07%). C0 were younger (59, vs CR 66, CM 62; p<0.001); diabetes was more common in CM (60.66) vs CR (56.82) or C0 (42.63%) (p=0.024). Hypertension predominates in CR (72.73 vs CM 57.38, C0 44.21%). GRACE score was lower in C0 (180.64, 157–206) against CR (211.07, 186.5–237), CM (218, 195–247) (p<0.001). AKI was higher in CR, CM (79.55, 86.89 vs 65.79%, p<0.001), as hemodialysis (18.18 and 34.43 vs 6.32, p<0.001) compared to C0. In CM: leukocytes, BUN, Cr, AST, ALT, and CRP were higher with lower levels of eGFR and platelets. C0 had fewer vasoactive requirements (p<0.001). IABP (p=0.741) and VT/FV (p=0.687) had no differences. MOF prevalence was C0 62.6% vs CR 86.4% and CM 96.7% (p<0.001). MODS ≥4 was C0 39.5, CR 65.9, CM 85.2% and SOFA ≥7 was C0 32.6, CR 63.6, CM 83.6%. Mortality was higher in CR (56.82%) and CM (54.1%) compared to C0 (39.47%, p=0.032) (p=0.001, Fig. 1A). RAP (p<0.001, Fig. 2A), PCWP (0.007, Fig. 2C), cardiac output (<0.001, Fig. 2B), index (0.001), power (0.001), perfusion pressure (PP = MAP-RAP, 0.028) and PAPi (0.043) discriminate the C0 phenotype.
AKI had lower survival (p<0.001, Fig. 1B) related to lower SBP (<0.001), DBP (0.003), MAP (<0.001, Fig. 2F) cardiac output (0.002), index (<0.001), power (<0.001, Fig. 2E), and PP (<0.001, Fig. 2D) and higher RAP (0.003), PADP (0.024), PAMP (0.011), PCWP (0.001). Electrical instability had lower survival (p<0.001, Fig. 1C), lower SBP (0.004), DBP (0.011), MAP (0.001, Fig. 2G), cardiac outpu t(0.036), index (0.019), power (0.003, Fig. 2I), PP (0.002, Fig. 2H) and higher PAMP (0.04). Finally, multiorgan failure had a decreased survival (p=0.016, Fig. 1D), higher heart rates (p=0.018), RAP (0.001, Fig. 2K), PCWP (<0.001), PADP (0.02) and lower SBP (0.017), DBP (0.002), MAP (<0.001) cardiac output (<0.001), index (0.004), power (<0.001), PP (<0.001, Fig. 2J), PAPi (<0.001, Fig. 2L).
Conclusions
We demonstrated associations with hemodynamic trajectories across time, which has not been reported before, could reveal AMI-CS phenotypes and related organ dysfunction patterns.
Funding Acknowledgement
Type of funding sources: None.
