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I have been suffering from chronic angina for about seven years. At the beginning everything was not horrible at all. I just had minor discomfort in my chest after eating and sometimes also used to wake up in the night from pain in my chest. But with the time the symptoms increased in number and their severity. I have been diagnosed with chronic angina in 2007 and since that time I am constantly trying to find a medication that will help me cope with the symptoms and live my life as a normal human being. The problem was not only in the unpleasant sensation that I used to experience but also in the risk of developing a more serious form of the disease that could even require a surgery. Since the time I was put on Ranolazine things has got much easier as the drug is very effective. It helps me control my angina and I no longer feel the pain. According to my doctor, currently there is no risk of serious complications. And all this is due to Ranolazine which turned out to be a real salvation for me. Now I can sleep normally, and all the symptoms I had are easily eliminated with one pill of Ranolazine. Try out the drug if your problem is chronic angina and you haven't found your best medication yet.

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None of the study participants had epicardial coronary artery disease (as required by the enrollment criteria); 7 of 11 patients underwent coronary angiography, which showed no significant coronary stenosis, and 4 of 11 patients underwent noninvasive stress testing, which showed no evidence of myocardial ischemia.

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Due to the difficulties in obtaining myocardial tissue samples and assessing substrate flux in humans, little is known about myocardial substrate metabolism in HF patients.

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Together with our findings using the isolated distal saphenous artery, ranolazine probably exerts its vasodilatatory effect on the pre-capillary arterioles via a direct action on both the endothelium and the smooth muscle cells.

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Stable angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arms, typically elicited by exertion or emotional stress and relieved by rest or nitroglycerin, and it is caused by an imbalance between myocardial oxygen supply and myocardial oxygen consumption.

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On the other hand, its effect on the INaL is quite promising for the electrophysiology community, as some evidence exists that ranolazine can decrease the incidence of atrial fibrillation and ventricular tachyarrhythmias.

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The subject, who was in the ranolazine group, had been inappropriately enrolled into the study with advanced chronic kidney disease.

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As such, in one embodiment, the invention is directed to a method for reducing the undesirable side effects of dronedarone or pharmaceutically acceptable salt or salts thereof comprising coadministering a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof.

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In vivo studies on the effects of heart failure should take into consideration the impact these differences in circulating FFA and ketone bodies have on myocardial substrate metabolism (e.

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In another embodiment, the intravenous delivery of ranolazine may be temporarily discontinued for 1-3 hrs and then restarted at the same or lower dose for patients experiencing adverse events deemed to be treatment related.

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To our knowledge, this is the only study to investigate the effects of HF on select populations of cardiac mitochondria ().

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Progressive loss of myocardial ATP due to a loss of total purines during the development of heart failure in dogs: a compensatory role for the parallel loss of creatine.

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The formulation of claim 4, wherein the tablet comprises a first layer comprising dronedarone or a pharmaceutically acceptable salt thereof and a second layer comprising ranolazine formulated for sustained release.

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When added to a regimen of maximal dose amlodipine, ranolazine significantly reduced the frequency of angina episodes per week compared with placebo (2.

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Examples of structural alerts include alkylating electrophilic centers, unstable epoxides, aromatic amines, azo-structures, N-nitroso groups, and aromatic nitro-groups (Ashby and Paton 1994).

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During the treatment period, subjects returned to the clinic for efficacy and safety assessments at weeks 6, 12, 18, and 24 and ET visits for subjects who prematurely discontinued the study.

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