BACKGROUND:
Patients presenting with cardiogenic shock (CS) are at risk of developing mixed shock (MS), characterized by distributive-inflammatory phenotype. However, no objective definition exists for this clinical entity.
METHODS:
We assessed the frequency, predictors, and prognostic relevance of MS complicating CS, based on a newly proposed objective definition. MS complicating CS was defined as an objective shock state secondary to both an ongoing cardiogenic cause and a distributive-inflammatory phenotype arising at least 12 hours after the initial CS diagnosis, as substantiated by predefined longitudinal changes in hemodynamics, clinical, and laboratory parameters.
RESULTS:
Among 213 consecutive patients admitted at 2 cardiac intensive care units with CS, 13 with inflammatory-distributive features at initial presentation were excluded, leading to a cohort of 200 patients hospitalized with pure CS (67±13 years, 96% Society of Cardiovascular Angiography and Interventions CS stage class C or higher). MS complicating CS occurred in 24.5% after 120 (29–216) hours from CS diagnosis. Lower systolic arterial pressure (
P
=0.043), hepatic injury (
P
=0.049), and suspected/definite infection (
P
=0.013) at CS diagnosis were independent predictors of MS development. In-hospital mortality (53.1% versus 27.8%;
P
=0.002) and hospital stay (21 [13–48] versus 17 [9–27] days;
P
=0.018) were higher in the MS cohort. At logistic multivariable analysis, MS diagnosis (odds ratio [OR], 3.00 [95% CI, 1.39–6.63];
P
adj
=0.006), age (OR, 1.06 [95% CI, 1.03–1.10] years;
P
adj
<0.001), admission systolic arterial pressure <100 mm Hg (OR, 2.41 [95% CI, 1.19–4.98];
P
adj
=0.016), and admission serum creatinine (OR, 1.61 [95% CI, 1.19–2.26];
P
adj
=0.003) conferred higher odds of in-hospital death, while early temporary mechanical circulatory support was associated with lower in-hospital death (OR, 0.36 [95% CI, 0.17–0.75];
P
adj
=0.008).
CONCLUSIONS:
MS complicating CS, objectively defined leveraging on longitudinal changes in distributive and inflammatory features, occurs in one-fourth of patients with CS, is predicted by markers of CS severity and inflammation at CS diagnosis, and portends higher hospital mortality.