BACKGROUND: Ischemic preconditioning (IP) is a cardioprotective phenomenon, induced by brief episodes of myocardial ischemia, which is supposed to affect not only the myocardium, but also the entire cardiovascular system. Considering that patients with coronary artery disease (CAD) have also been described to present impaired aortic mechanical properties, we tried to investigate the possible influence of the late phase of IP on aortic distensibility in patients with CAD. METHODS: Fifty patients, aged 48 to 72 (mean, 57+/-6 years), with angiographically confirmed CAD and exercise-induced myocardial ischemia, underwent two treadmill exercise testings (ETs). The second ETs was performed the next day. Thallium-201 scintigraphy was performed during the first and the second ET. Aortic distensibility was evaluated before each exercise testing by a non-invasive technique, using two-dimensional guided M-mode transthoracic echocardiography and arterial pressure was measured simultaneously at the brachial artery by sphygmomanometry. RESULTS: The patients were divided in 2 groups according to the extent of myocardial ischemia at peak exercise of the second test, compared to the first test. In 35 (70%) of the studied patients ischemia signs were reduced during the second ET (Group A), while in the rest 15 (30%) of the patients (Group B) no improvement or even worsening of the observed ischemia signs was demonstrated by the studied exercise parameters and the extent of myocardial ischemia in thallium-scintigraphy. Increased aortic distensibility during the second measurement was found in 33 (94%) of the 35 patients of Group A but only in 1 (7%) of the 15 patients of Group B. Aortic distensibility was found to be significantly improved in patients of Group A, while it was found to be worsened in Group B patients. CONCLUSIONS: The aortic distensibility alteration could be used as an index of influence of ischemic preconditioning to exercise-induced myocardial ischemia, which could be considered indicative of the systemic effects of IP in humans.
BACKGROUND:Ischemic preconditioning (IP) is a cardioprotective phenomenon, induced by brief episodes of myocardial ischemia, which is supposed to affect not only the myocardium, but also the entire cardiovascular system. Considering that patients with coronary artery disease (CAD) have also been described to present impaired aortic mechanical properties, we tried to investigate the possible influence of the late phase of IP on aortic distensibility in patients with CAD. METHODS: Fifty patients, aged 48 to 72 (mean, 57+/-6 years), with angiographically confirmed CAD and exercise-induced myocardial ischemia, underwent two treadmill exercise testings (ETs). The second ETs was performed the next day. Thallium-201 scintigraphy was performed during the first and the second ET. Aortic distensibility was evaluated before each exercise testing by a non-invasive technique, using two-dimensional guided M-mode transthoracic echocardiography and arterial pressure was measured simultaneously at the brachial artery by sphygmomanometry. RESULTS: The patients were divided in 2 groups according to the extent of myocardial ischemia at peak exercise of the second test, compared to the first test. In 35 (70%) of the studied patientsischemia signs were reduced during the second ET (Group A), while in the rest 15 (30%) of the patients (Group B) no improvement or even worsening of the observed ischemia signs was demonstrated by the studied exercise parameters and the extent of myocardial ischemia in thallium-scintigraphy. Increased aortic distensibility during the second measurement was found in 33 (94%) of the 35 patients of Group A but only in 1 (7%) of the 15 patients of Group B. Aortic distensibility was found to be significantly improved in patients of Group A, while it was found to be worsened in Group B patients. CONCLUSIONS: The aortic distensibility alteration could be used as an index of influence of ischemic preconditioning to exercise-induced myocardial ischemia, which could be considered indicative of the systemic effects of IP in humans.