Explore chapters and articles related to this topic
Pathophysiology of Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Jacob Cao, John O'Sullivan, Sean Lal
Ranolazine is a novel anti-anginal drug. Its main effect is mediated through inhibition of the late sodium channel current but it may also have effects on glucose and fatty acid metabolism. Experimental models of cardiac ischemia-reperfusion injury have shown that ranolazine treatment reduced fatty acid and enhanced glucose metabolism with associated increase in ATP generation. However, human trials of ranolazine in heart failure are lacking.
Coronary Artery Disease
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Sodium channel blockers and sinus node inhibitors can also be used for stable angina. Ranolazine is a sodium channel blocker that treats chronic angina. Common adverse effects include constipation, dizziness, headache, and nausea. Ivabradine, a sinus node inhibitor, inhibits the inward sodium/potassium current in the gated channel in sinus node cells. It slows down the heart rate without causing decreased contractility. Ivabradine is used for chronic stable angina pectoris when there is a normal sinus rhythm, and the patient cannot tolerate beta-blockers. It is also used in combination with beta-blockers when the patient’s symptoms are not adequately controlled only by a beta-blocker, and the heart rate is more than 60 beats per minute.
Angina pectoris in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Wilbert S. Aronow, William H. Frishman
Ranolazine was approved by the FDA for treatment of patients with chronic stable angina pectoris in January 2006. Ranolazine was approved for use as combination therapy when angina is not adequately controlled with other antianginal drugs. The recommended dose of sustained release ranolazine is 750 or 1000 mg twice daily. Ranolazine may be effective in patients with microvascular angina and endothelial dysfunction (116).
What is the current value of beta-adrenoreceptor antagonists for angina?
Published in Expert Opinion on Pharmacotherapy, 2022
Jayakumar Sreenivasan, Urvashi Hooda, Wilbert S. Aronow
Ischemic heart disease is one of the leading causes of mortality worldwide [1]. Management of patients with stable ischemic heart disease involves risk modification, anti-platelet therapy, anti-anginal pharmacotherapy, and selective coronary revascularization for refractory angina despite maximal medical therapy. Clinical trials comparing revascularization and medical therapy showed that revascularization does not provide a survival benefit or improve exercise tolerance in patients with stable angina. Guidelines recommend beta-blockers, calcium channel blockers, and nitrates as the first-line anti-anginal agents. Ranolazine is used as a second-line agent in patients unable to tolerate first-line anti-anginal agents due to side effects or as a combination therapy with first-line agents in patients with residual angina. Ivabradine, nicorandil, and trimetazidine are other newer drugs that are being studied for angina. Although current guidelines recommend a hierarchical approach to the treatment of angina, there is no evidence for the superiority of one anti-anginal agent over the others. Beta-adrenoreceptor blockers have been used for chronic coronary artery disease since the 1960s. Beta-blockers significantly reduce mortality in patients with recent myocardial infarction and left ventricular dysfunction, while there is limited evidence to support such a mortality benefit in stable ischemic heart disease with normal ejection fraction. This editorial inspects the evidence behind the current use and future of beta-blockers for the treatment of angina.
Cardiac arrhythmias in pregnant women: need for mother and offspring protection
Published in Current Medical Research and Opinion, 2020
Theodora A. Manolis, Antonis A. Manolis, Evdoxia J. Apostolopoulos, Despoina Papatheou, Helen Melita, Antonis S. Manolis
Importantly, it has been reported that the 9-month postpartum period is associated with a significantly increased risk of cardiac events in patients with LQTS, particularly in women with the LQT2 genotype77. Thus, close follow-up is recommended in such patients during the postpartum period. Ranolazine78 and mexiletine79 (former FDA category C agent) have been suggested as an add-on therapy to prevent cardiac events in select LQT3 patients80; however, there are limited data for using these drugs during pregnancy. Finally, pregnant patients previously fitted with an implantable cardioverter defibrillator (ICD), including LQTS patients, do not appear to have an increased risk for adverse complications during pregnancy77,81.
Pharmacological management of atrial fibrillation in patients with heart failure with reduced ejection fraction: review of current knowledge and future directions
Published in Expert Review of Cardiovascular Therapy, 2020
Ranolazine is an anti-anginal medication which inhibits the late sodium current, potassium and calcium channels, decreases early and delayed afterdepolarizations, and increases the atrial effective refractory period [130]. The anti-AF effects arise from atrial-selective inhibition of peak Ina [131]. In canine models, ranolazine suppressed AF in the setting of HF [132]. In humans, it has shown efficacy in decreasing AF burden and has an additive effect with amiodarone to convert to SR [133–136]. It patients with HFrEF the combination of ranolazine and amiodarone converts post-operative AF more rapidly than amiodarone alone [137]. Early data also suggest ranolazine is safe in structural heart disease [135,136]. Given its anti-anginal properties, it may be particularly useful in ICM patients with HFrEF and AF. Further work is needed to better understand how this multifaceted medication can be incorporated into clinical practice and if it can meaningfully impact clinical outcomes in HFrEF and AF.