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10.1097/FJC.0b013e3181a1b9e7 http://scihub22266oqcxt.onion/10.1097/FJC.0b013e3181a1b9e7 C4454281!4454281 !19333133     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19333133 &cmd=llinks): Failed to open stream: HTTP request failed! 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A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine |pdf=|usr=}}{{19333133 }} gab.com Text A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine JO: J Cardiovasc Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=19333133 #FOAvip Inhibition of the persistent or late Na current (INa) using ranolazine (Ranexa) represents a novel mechanism of action that was approved in the United States in 2006 and only recently in the European Union for use in patients with stable angina pectoris. In general, myocardial ischemia is associated with reduced adenosine triphosphate fluxes and decreased energy supply, resulting in severe disturbances of intracellular ion homeostasis in cardiac myocytes. In the recent years, increased late INa was suggested to contribute to this phenomenon by elevating intracellular Na concentration with subsequent rise in diastolic Ca levels by means of the sarcolemmal Na-Ca exchange system. Ranolazine, a specific inhibitor of late INa, reduces Na influx and hence ameliorates disturbed Na and Ca homeostasis. This is associated with a symptomatic improvement of angina in patients unlike other antianginal drugs without affecting heart rate or systemic blood pressure as shown in placebo-controlled studies. Therefore, ranolazine is a useful new option for patients with chronic stable angina not only as an add-on therapy. New clinical and experimental studies even point to potential antiarrhythmic effects, beneficial effects in diastolic heart failure, and under hyperglycemic conditions. In the present article, the relevant pathophysiological concepts for the role of late INa inhibition are reviewed and the most recent data from basic studies and clinical trials are summarized. Twit Text FOAVip A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine ????J Cardiovasc Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=19333133 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19333133 #FOAvip English Wikipedia <ref>{{Cite pmid|19333133 }}</ref> A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine #MMPMID19333133 Maier LS J Cardiovasc Pharmacol 2009[Oct]; 54 (4 ): 279-86 PMID19333133 show ga Inhibition of the persistent or late Na current (INa) using ranolazine (Ranexa) represents a novel mechanism of action that was approved in the United States in 2006 and only recently in the European Union for use in patients with stable angina pectoris. In general, myocardial ischemia is associated with reduced adenosine triphosphate fluxes and decreased energy supply, resulting in severe disturbances of intracellular ion homeostasis in cardiac myocytes. In the recent years, increased late INa was suggested to contribute to this phenomenon by elevating intracellular Na concentration with subsequent rise in diastolic Ca levels by means of the sarcolemmal Na-Ca exchange system. Ranolazine, a specific inhibitor of late INa, reduces Na influx and hence ameliorates disturbed Na and Ca homeostasis. This is associated with a symptomatic improvement of angina in patients unlike other antianginal drugs without affecting heart rate or systemic blood pressure as shown in placebo-controlled studies. Therefore, ranolazine is a useful new option for patients with chronic stable angina not only as an add-on therapy. New clinical and experimental studies even point to potential antiarrhythmic effects, beneficial effects in diastolic heart failure, and under hyperglycemic conditions. In the present article, the relevant pathophysiological concepts for the role of late INa inhibition are reviewed and the most recent data from basic studies and clinical trials are summarized. |Acetanilides/administration & dosage/pharmacology/*therapeutic use [MESH] |Angina Pectoris/*drug therapy/metabolism [MESH] |Animals [MESH] |Arrhythmias, Cardiac/*drug therapy/metabolism [MESH] |Clinical Trials as Topic [MESH] |Heart Failure, Diastolic/*drug therapy/metabolism [MESH] |Humans [MESH] |Piperazines/administration & dosage/pharmacology/*therapeutic use [MESH] |Ranolazine [MESH] |Sodium Channel Blockers/administration & dosage/pharmacology/*therapeutic use [MESH] |Sodium Channels/metabolism [MESH] |Sodium-Calcium Exchanger/metabolism [MESH]A novel mechanism for the treatment of angina, arrhythmias, and diasto(epmc).pdf DeepDyve Pubget Overpricing