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PubMed · 185472

Myocardial ischemia.

R Gorlin
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Abstract

Myocardial ischemia results from an imbalance of energy supply and demand. Because of the essentially aerobic nature of myocardial metabolism and the high oxygen extraction from the blood, ischemia is usually equatable with limitation of blood supply. Coronary atherosclerosis is a patchy disorder, and therefore, ischemia usually occurs in segmental fashion throughout the topography of the heart. Ischemia is invariably seen earliest and most intensely in the deep or subendocardial layers of myocardium. Ischemia leads to biochemical disruption, including initiation of glycolysis, which in turn causes electrophysiological and mechanical disturbances. Myocardial ischemia can be induced naturally or experimentally in the human subject in a variety of ways, some of which have been studied in the laboratory.

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Angina PectorisCold TemperatureCoronary CirculationCoronary DiseaseEatingElectric StimulationElectrophysiologyEnergy MetabolismGlycolysisHeartHumansLactatesMyocardial ContractionMyocardiumPhysical ExertionSleepSmokingStress, PsychologicalSynaptic TransmissionJournal Article

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R Gorlin. 1976. Myocardial ischemia.. https://pubmed.ncbi.nlm.nih.gov/185472/

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PubMed2007

Effect of a hypoglycemic agent on ischemic preconditioning in patients with type 2 diabetes and stable angina pectoris.

OBJECTIVE: Ischemic preconditioning is an increased tolerance to myocardial ischemia during the second of two consecutive exercise tests. ATP-sensitive K(+) channel blockers, such as glinides and sulfonylurea drugs, can induce loss of ischemic preconditioning. This study aimed to investigate the effects of repaglinide, a hypoglycemic agent with an affinity for myocardial ATP-sensitive K (+)channels, on the results of consecutive exercise tests in patients with diabetes and multivessel coronary artery disease. METHODS: Forty-two patients with type 2 diabetes and chronic stable angina pectoris, and two-vessel or three-vessel disease participated in this study. The patients underwent two consecutive treadmill exercise tests (phase 1). On the day after these exercise tests, 2 mg of oral repaglinide was given to the patients. One week later, two exercise tests were repeated consecutively (phase 2). RESULTS: All patients achieved 1.0-mm ST-segment depression during the four exercise tests (T1, T2, T3, and T4). In phase 2, seven patients improved in time to onset of 1.0-mm ST-segment depression. The worsening of the time to onset of 1.0-mm ST-segment depression in phase 2 demonstrated ischemic preconditioning block in 83.3% of patients (P=0.0001). Even the postexercise electrocardiographic parameters (ST-segment depression morphology and magnitude and arrhythmias) were significantly different between the groups with and without pharmacologic ischemic preconditioning block (P=0.031). CONCLUSIONS: Repaglinide, an oral hypoglycemic agent with ATP-sensitive K(+) channel-blocker activity, eliminated the myocardial ischemic preconditioning in patients with coronary disease and diabetes.

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