Background: Cardiogenic shock (CS) continues to have hospital mortality rates of 30-50% despite medical advances. Approximately 40-50% of these patients present a history of Diabetes or Insulin resistance (IR). This article aims to analyze the evidence published on the influence of IR on myocardial metabolism and its possible impact in CS.
Methods: A narrative review of the literature was conducted using Scoupus, PubMed and Google Scholar searches, focusing on studies published between 2012 and 2025. Using the following combination of MeSH terms and Boolean operators: “Cardiogenic Shock AND Insulin Resistance”; “Cardiogenic Shock AND Myocardial Metabolism”; “Insulin Resistance AND Myocardial Energy Metabolism”; “Cardiogenic Shock AND Hyperglycemia”; and “Cardiogenic Shock AND Lactate.” Original articles, systematic reviews, and experimental studies evaluating insulin resistance, myocardial metabolism, energy substrate utilization, and cardiogenic shock or related critical conditions in English or Spanish were included.
Outcome: Metabolic research indicates that under conditions of critical stress IR shifts myocardial substrate utilization toward fatty acids, decreasing glucose uptake due to alteration of the IRS-1/PI3K/Akt pathway. Fatty acid oxidation is 10-12% less oxygen efficient and exacerbates energy imbalance in conditions of hypoperfusion and hypoxia. Observational cohorts demonstrate that markers of IR, including HOMA-IR and the triglyceride-to-glucose ratio (TyG), are associated with a significant increased risk of CS and in-hospital mortality. With odds ratios ranging 1.3 to 1.4 compared to healthy patients. This suggests IR reflects the severity of the condition and may act as an active mediator of myocardial dysfunction. Experimental models of CS have shown early mitochondrial dysfunction, reduced oxidative phosphorylation and accumulation of lipotoxic intermediates. On a clinical scale, observational studies have reported that patients with serum lactate levels exceeding 4 mmol/L are associated with increased in-hospital mortality and poorer functional recovery. In addition, neurohormonal activation accompanied by inflammatory cytokines like IL-6 and TNF-a contributes to multiorgan dysfunction in up to 40-60% of patients with cardiogenic shock. Catecholamines and cortisol release exacerbates IR and perpetuates the metabolic response cycle. Despite this evidence, metabolic assessment is rarely systematically integrated into the management of CS.
Conclusion: Insulin resistance represents a central, though often underestimated, component in the pathophysiology of cardiogenic shock. Its impact on myocardial metabolism contributes to energy inefficiency and progressive cardiac dysfunction. Recognizing and understanding these metabolic alterations could open up new therapeutic opportunities aimed at improving the prognosis for these patients.
