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Insulin prolongs the QTc interval in humans
A Gastaldelli1, M Emdin, F Conforti
1Metabolism Unit and Coronary Division, Consiglio Nazionale delle Ricerche Institute of Clinical Physiology, Department of Internal Medicine, University of Pisa School of Medicine, 56126 Pisa, Italy.
Summary
Physiological hyperinsulinemia prolongs ventricular repolarization, affecting the Q-T interval. This effect is linked to insulin-induced hypokalemia and increased adrenergic activation, not insulin sensitivity.
Area of Science:
- Cardiology
- Endocrinology
- Physiology
Background:
- Insulin is known to hyperpolarize plasma membranes.
- The effect of insulin on ventricular repolarization, specifically the Q-T interval, has not been extensively studied.
Purpose of the Study:
- To investigate whether physiological hyperinsulinemia affects ventricular repolarization in healthy individuals.
- To explore the relationship between insulin levels, Q-T interval, and factors like heart rate, norepinephrine, and serum potassium.
Main Methods:
- Electrocardiographic monitoring was performed on 35 healthy volunteers.
- Hyperinsulinemia was induced using a euglycemic insulin clamp (1 mU/min/kg).
- Q-T interval was measured and corrected for heart rate (QTc) using Bazett's formula.
Main Results:
- Hyperinsulinemia led to a prompt and consistent increase in QTc (from 420 ms to 428 ms).
- Heart rate and plasma norepinephrine levels increased during the insulin clamp.
- Fasting serum potassium decreased during insulin infusion, and QTc was inversely related to serum potassium levels.
Conclusions:
- Physiological hyperinsulinemia acutely prolongs ventricular repolarization (QTc) independently of insulin sensitivity.
- Insulin-induced hypokalemia and adrenergic activation contribute to the prolongation of the Q-T interval.
- These findings highlight a direct electrophysiological effect of insulin on the heart.