Remote postconditioning consisted of 1 min isc/1 min rep protects the ischemic rabbit heart in vivo, independently of the site of the remote artery. This intervention seems to confer a stronger protection than the classic postconditioning.
Despite current optimal treatment, the morbidity and mortality of coronary heart disease remain significant worldwide and open the way for the development of novel cardioprotective therapies. In the last two decades, a remarkable scientific effort has focused on the limitation of infarct size. Important input from experimental studies has led the way in this direction. However, clinical and preclinical results using various cardioprotective strategies to attenuate reperfusion injury have generally not been applicable for every day clinical practice. Protection of the ischemic myocardium is known to occur as a result of ischemic preconditioning (PC), in which repetitive brief periods of ischemia protect the heart from a subsequent prolong ischemic insult. Although PC is a powerful form of protection, it is of limited clinical application for obvious ethical and practical reasons. Another endogenous form of cardioprotection, similar to PC but applicable at the time of reperfusion, termed postconditioning (PostC), has been recently described. Short series of repetitive cycles of brief reperfusion and re-occlusion of the coronary artery applied at the onset of reperfusion, reduce the infarct size and coronary artery endothelial dysfunction. At present, pharmacological PC and PostC are possible alternative methods that may substitute pharmaceutical treatments the short ischemic insults. Adenosine, nicorandil and other agents have been already used as pharmacological mimetics of ischemic PC in multicenter trials. We summarize the recent research efforts on novel therapeutic strategies and on the design of new compounds, based on the accumulated knowledge of the ligands, receptors and intracellular signaling pathways of PC and PostC.
The aim of this study was to assess the effectiveness of chronic medical treatment with oral propranolol and its influence on heart rate variability in patients with vasovagal syndrome. A spectral frequency domain analysis was used for the estimation of heart rate variability characteristics. Thirty-six patients, mean age 49 +/- 17 years, with a history of recurrent syncope and positive tilt testing were involved in the study. All patients received oral propranolol (five patients also had a dual chamber inhibited DDI pacemaker implanted) for a mean time 12 +/- 6 months. One patient complained of syncope during this follow-up. The tilt test repeated in 29 patients during follow-up was negative in 28. In 20 patients treatment was discontinued for 4 days and a new tilt test was then performed. Eleven of these 20 patients (55%) had a positive test (P < 0.001 compared with the group in which treatment was continued). In the group of 11 patients in whom the tilt test became positive again after medical treatment had been withdrawn (mean age 43 +/- 20 years) and in 11 asymptomatic controls (mean age 52 +/- 19 years), with no history of syncope and negative tilt testing, the heart rate variability was assessed. The increase in the low frequency component from rest to the maximum value of heart rate variability during tilt testing was higher in the vasovagal group than in the controls (2.6 +/- 1.2 vs 1.5 +/- 0.7 P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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