Comorbidity burden in patients with cardiogenic shock: a cardiogenic shock working group analysis

Background Comorbidity burden is a major determinant of prognosis in patients with cardiovascular diseases and represents a growing global challenge. However, the prognostic impact of comorbidity burden on outcomes in cardiogenic shock (CS) remains insufficiently characterized, particularly regarding its variation across CS subtypes. Purpose To characterize the prevalence and distribution of comorbidities in CS, assess its impact on outcome, and identify high-risk comorbidity patterns in acute myocardial infarction-related (AMI) and heart failure-related (HF) CS. Methods CS patients from the multicenter Cardiogenic Shock Working Group (CSWG) registry (2020–2024) were analyzed. The impact of distinct chronic conditions (hypertension, diabetes, atrial fibrillation, chronic kidney disease, peripheral vascular disease, chronic obstructive pulmonary disease (COPD), asthma, liver disease, anemia, history of stroke, severe valve disease, coronary artery disease, history of HF and MI), their combinations, and cumulative burden on clinical outcome (primary endpoint: in-hospital mortality) were assessed. Univariable and multivariable logistic regression models were performed, adjusted for age, sex, lactate, creatinine, out-of-hospital cardiac arrest and CS etiology (for all-cause CS analyses). Results Among 6,815 CS patients (53.6% HF-CS, 26.5% AMI-CS), 6087 (89.3%) presented with at least one comorbidity, and 4390 (64.4%) with three or more, with higher comorbidity burden in HF-CS compared to AMI-CS. Across distinct comorbidities, COPD was the strongest predictor of in-hospital mortality in HF-CS (aOR 1.36, 95% CI 1.08–1.71, p<0.01), while a history of MI conferred the highest mortality risk in AMI-CS (aOR 1.50, 95% CI 1.09–2.06, p=0.01). Distinct high-risk comorbidity combinations associated with in-hospital mortality varying across CS subtypes, including COPD plus anemia (aOR 1.54, 95% CI 1.08-2.16, p=0.01) or COPD plus severe valve disease (aOR 1.57, 95% CI 1.10-2.24, p=0.01) in HF-CS, and COPD plus stroke (aOR 3.40, 95% CI 1.59-7.62, p<0.01) or COPD plus history of MI (aOR 2.34, 95% CI 1.36-4.07, p<0.01) in AMI-CS. In-hospital mortality increased with rising comorbidity burden, escalating from 32.9% to 36.5% to 44.5% in AMI-CS (1–3, 4–6, ≥7 comorbidities) and from 18.5% to 24.5% to 27.5% in HF-CS, and remained independently associated with higher mortality after adjustment across both subtypes (Figure 1A/B). A critical threshold at 5–7 comorbidities marked a disproportionate rise in mortality (Figure 1C). Conclusions In this real-world CS cohort, comorbidity burden was highly prevalent, varied across subtypes, and was independently associated with mortality. Integrating subtype-specific characteristics of chronic conditions into early CS risk stratification is essential to identify high-risk subgroups and optimize clinical decision-making in CS management.