Open AccessThe Effects of Glibenclamide, a K ATP Channel Blocker, on the Warm‐Up Phenomenon
Author(s) -
Ferreira Beatriz M. A.,
Moffa Paulo J.,
Falcão Andrea,
Uchida Augusto,
Camargo Paulo,
Pereyra Pascual,
Soares Paulo R.,
Hueb Whady,
Ramires Jose A. F.
Publication year - 2005
Publication title -
annals of noninvasive electrocardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.494
H-Index - 48
eISSN - 1542-474X
pISSN - 1082-720X
DOI - 10.1111/j.1542-474x.2005.00650.x
Subject(s) - glibenclamide , medicine , angina , heart rate , cardiology , diabetes mellitus , blood pressure , rate pressure product , ischemia , st depression , myocardial ischemia , ischemic preconditioning , anesthesia , myocardial infarction , endocrinology
Background: The warm‐up phenomenon observed after the second of two sequential exercise tests is characterized by an increased time to ischemia and ischemic threshold, and the latter is related to ischemic preconditioning. Previous studies have demonstrated that a single dose of glibenclamide, a cardiac ATP‐sensitive K (K ATP ) channel blocker, prevents ischemic preconditioning. This study aimed to investigate the effects of chronic treatment with glibenclamide during two sequential exercise tests. Methods: Forty patients with angina pectoris were divided into three groups: 20 nondiabetics (NDM), 10 patients with diabetes in treatment with glibenclamide (DMG) and 10 diabetic patients with other treatments (DMO). All patients underwent two consecutive exercise tests. Results: Heart rate and rate‐pressure product at 1.0 mm ST‐segment depression significantly increased during the second exercise test in NDM group (121.3 ± 16.5 vs 127.3 ± 15.3 beats/min, P < 0.001, and 216.7 + 43.1 vs 232.1 ± 43.0 beats·min −1 ·mmHg·10 2 , P < 0.001), and in DMO group (114.1 ± 19.6 vs 119.6 ± 18.1 beats/min, P = 0.001, and 199.8 ± 36.6 vs 222.2 ± 29.2 beats·min −1 ·mmHg·10 2 , P = 0.019), but it did not change in patients in DMG group (130.7 ± 14.5 vs 132.1 ±14.7 beats/min, P = ns, and 251.7 ± 47.2 vs 250.3 ± 42.8 beats·min −1 ·mmHg·10 2 , P = ns). In the three groups, NDM, DMO, and DMG, the time to 1.0 mm ST‐segment depression during the second exercise test was greater than during the first (225.0 ± 112.5 vs 267.0 ± 122.3 seconds, P = 0.006; 187.5 ± 54.0 vs 226.5 ± 74.6 seconds, P = 0.029 and 150.0 ± 78.7 vs 186.0 ± 81.9 seconds, P < 0.001). Conclusion: The chronic use of glibenclamide may have mediated the loss of preconditioning benefits in the warm‐up phenomenon, probably through its KATP channel‐blocker activity, but without acting upon the tolerance to exercise.