Key result
Intravenous insulin (2 U) similarly decreased arterial glucose by 30% (P<0.001) and increased myocardial glucose uptake 3-fold (P<0.001) in both CAD and control patients.
Why the study?
Does intravenous insulin alter cardiac metabolic and hemodynamic parameters differently in patients with stable coronary artery disease compared to controls?
Does intravenous insulin alter cardiac metabolic and hemodynamic parameters differently in patients with stable coronary artery disease compared to controls?
Intravenous insulin shifts myocardial metabolism from free fatty acids to carbohydrates without altering hemodynamics, which may be beneficial during ischemia in patients with stable CAD.
Answers are grounded in this paper and cite their sources.
May support metabolic shift toward glucose in stable CAD; leaves open ischemic outcome benefit, needing prospective trials.
To assess the effects of insulin in stable coronary artery disease (CAD), 2 U i.v. insulin was given to 9 control and 10 CAD patients during coronary sinus catheterization. Hemodynamic and metabolic data were obtained before and for 90 min after insulin injection. Insulin induced no changes in heart rate, mean aortic pressure, rate-pressure product, coronary sinus flow, or coronary resistance. Metabolic changes were similar in both groups and included 1) 30% decrease of arterial glucose (P less than .001) and 3-fold increase of myocardial glucose uptake (P less than .001), 2) 1.5- to 2.5-fold elevation of arterial lactate (P less than .001) and myocardial lactate usage (P less than .001), respectively, 3) 50-70% suppression of arterial levels (P less than .001) and myocardial uptake of free fatty acids (P less than .01), and 4) 10% reduction of myocardial net oxygen consumption (P less than .05). Myocardial citrate efflux increased in the CAD patients (P less than .05), whereas alanine release rose only in control patients (P less than .01), suggesting that glucose enters glycogen production in the CAD patients and pyruvate production in the control patients to a high degree. Myocardial glutamate uptake remained unchanged. In conclusion, insulin sensitivity was not altered in CAD. The insulin-induced shift from myocardial free fatty acid to carbohydrate usage may be beneficial to the ischemic heart by increasing glycogen stores, saving oxygen, and inhibiting an excess free-fatty acid concentration, which may be toxic during ischemia.
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Thomassen et al. (1989) studied Stable coronary artery disease (CAD) (n=19). Insulin vs. Control patients was evaluated on Hemodynamic and metabolic changes (including arterial glucose and myocardial glucose uptake) (p=<0.001). Intravenous insulin (2 U) similarly decreased arterial glucose by 30% (P<0.001) and increased myocardial glucose uptake 3-fold (P<0.001) in both CAD and control patients.
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