Hypercholesterolemia attenuates the anti-ischemic effect of preconditioning during coronary angioplasty

• Published in: Chest Vol. 128; no. 3; p. 1623
• Main Authors: Ungi, Imre, Ungi, Tamás, Ruzsa, Zoltán, Nagy, Edit, Zimmermann, Zsolt, Csont, Tamás, Ferdinandy, Péter
• Format: Journal Article
• Language: English
• Published: United States 01-09-2005
• Subjects: Angioplasty, Balloon, Coronary - methods; Coronary Disease - complications; Coronary Disease - therapy; Electrocardiography; Female; Humans; Hypercholesterolemia - complications; Ischemic Preconditioning, Myocardial - methods; Male; Middle Aged; Myocardial Ischemia - diagnosis; Myocardial Ischemia - therapy
• ISSN: 0012-3692
• DOI: 10.1378/chest.128.3.1623

Cardioprotection by preconditioning is limited in some animal models of hypercholesterolemia. We studied ischemic preconditioning induced by coronary angioplasty in hypercholesterolemic and normocholesterolemic patients by means of a beat-to-beat analysis of ST segments.
Thirty coronary disease patients were classified into normocholesterolemic and hypercholesterolemic groups. Intracoronary ECG was recorded during three consecutive balloon inflations of 2-min duration with 5-min intervals.
In normocholesterolemic patients, the ST segment was continuously elevated during the occlusions and rapidly normalized after balloon deflations. Repeated occlusions significantly attenuated ST-segment elevation from 1.28 +/- 0.67 to 0.88 +/- 0.51 mV (p < 0.001) and decreased the time to normalization of ST segment. In hypercholesterolemic patients, the ST segment was rapidly elevated in the first 30 s of the first occlusion, and normalization of the ST segment was longer on the first reperfusion. However, in these patients, repeated occlusions abolished the initial elevation of the ST segment but did not attenuate maximal ST-segment elevation (1.24 +/- 1.11 mV vs 1.21 +/- 1.09 mV) and failed to decrease the time to normalization of the ST segment.
Hypercholesterolemia accelerates the evolution of myocardial ischemia, delays recovery on reperfusion, and deteriorates the anti-ischemic effect of preconditioning in humans.