the use of calcium-channel blockers and beta blockers has been shown to exert some protective effects on AF recurrence, probably through prevention of ionic remodelling and paid off endogenous angiotensin II production, their use was 3 times higher in CTAF than in these previous trials. There are many potential explanations for this observed lack buy Cilengitide of effect: the overall characteristics of the patient populace enrolled in CTAF, the variations in clinical characteristics of patients treated with RAS inhibition, or the type of AF required to get an intrinsic antiarrhythmic result with RAS inhibitors. First, crucial differences in patient populations between the previously published information, and our study may, at least partially, explain the apparent difference. The protective effect of RAS inhibition has been demonstrated in patients with impaired LVEF, early post MI, symptomatic CHF regardless of LVEF or hypertension with LVH. In comparison, CTAF enrolled not many patients with one of these conditions and excluded significantly symptomatic CHF patients. In the high-risk conditions of CHF or LVH, the upsurge in angiotensin II levels and its tissue effects through the mitogen-activated physical form and external structure protein kinase system may trigger atrial structural remodelling, including loss of myocytes, disorganization of the sarcoplasmic reticulum and LVH, changes in electrical and structural remodelling induced by AF may be more moderate and, consequently, treatment with RAS inhibitor may be less effective. Our are concordant with a post hoc analysis of AFFIRM. But, our seem to be in contradiction with a little, open label study from Hong Kong evaluating amiodarone alone or in combination with losartan or perindopril for the prevention of AF recurrence in patients with lone paroxysmal AF. Both agents were powerful for symptomatic AF prevention, but not for documented asymptomatic AF. Even though interesting, this trial can’t give a definitive solution due to this indicator disparity and the lack of details about the specific Cabozantinib molecular weight percentage of patients in AF at random assignment. On another hand, people in CTAF who were receiving RAS inhibitors were older, more often hypertensive and had more prolonged AF than those who were not handled with RAS inhibitors. But, the occurrence of AF repeat between the two groups was the same, which may claim that RAS blockade had a beneficial effect in the high-risk group. In addition to various patient populations, the significance of electric re-modelling and drug therapy at baseline may possibly also have played a role. While rapid atrial pacing shortens the atrial effective refractory period, increases AF length and might cause atrial cardiomyopathy, these changes could be attenuated with using RAS antagonists experimentally and in patients with chronic AF starting electrical cardioversion. AF length can be a known key determinant of electrical remodelling and AF repeat, and only 350-watt of the CTAF people had AF longer than a week.