dc.creator | Farmakis D., Xanthopoulos A., Triposkiadis F. | en |
dc.date.accessioned | 2023-01-31T07:37:39Z | |
dc.date.available | 2023-01-31T07:37:39Z | |
dc.date.issued | 2021 | |
dc.identifier | 10.1016/j.hjc.2021.01.012 | |
dc.identifier.issn | 11099666 | |
dc.identifier.uri | http://hdl.handle.net/11615/71469 | |
dc.description.abstract | The once dominant plaque-centric model of the pathophysiology and management of coronary artery disease (CAD) has long been questioned by a bulk of experimental and clinical evidence suggesting, among others, that coronary artery obstruction is not synonymous with myocardial ischaemia, ischaemia may occur in the absence of obstructive lesions and may persist after successful coronary revascularization, while elective revascularization provides little or no prognostic benefit. As a result, a paradigm shift has been suggested taking into consideration the multifactorial aspect of CAD such as microvascular disease and the consequences of ischemia at the level of cardiomyocyte. In this paper, we propose an alternative approach to the medical management of patients with chronic CAD and stable angina, based on the properties of the drugs currently available in the anti-ischemic armamentarium in relation to the pathophysiology of myocardial ischemia. In this approach, pharmacological therapy is organized into three steps, including disease-modifying therapy for all patients with chronic CAD, pathophysiology-based anti-ischaemic therapy for patients with stable angina and symptomatic therapy in patients with persistent anginal symptoms. © 2021 Hellenic Society of Cardiology | en |
dc.language.iso | en | en |
dc.source | Hellenic Journal of Cardiology | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85101009404&doi=10.1016%2fj.hjc.2021.01.012&partnerID=40&md5=ede26c4091820ecc9ec78f63162065c1 | |
dc.subject | acetylsalicylic acid | en |
dc.subject | beta adrenergic receptor blocking agent | en |
dc.subject | calcium channel | en |
dc.subject | canakinumab | en |
dc.subject | colchicine | en |
dc.subject | diltiazem | en |
dc.subject | hydroxymethylglutaryl coenzyme A reductase inhibitor | en |
dc.subject | ivabradine | en |
dc.subject | metoprolol | en |
dc.subject | nicorandil | en |
dc.subject | ranolazine | en |
dc.subject | sodium glucose cotransporter 2 | en |
dc.subject | ticagrelor | en |
dc.subject | verapamil | en |
dc.subject | anemia | en |
dc.subject | angiography | en |
dc.subject | cardiovascular risk | en |
dc.subject | coronary artery disease | en |
dc.subject | dyspnea | en |
dc.subject | Editorial | en |
dc.subject | heart failure | en |
dc.subject | heart left ventricle ejection fraction | en |
dc.subject | heart left ventricle function | en |
dc.subject | heart muscle ischemia | en |
dc.subject | heart rate | en |
dc.subject | hemodynamics | en |
dc.subject | human | en |
dc.subject | ischemic heart disease | en |
dc.subject | microangiopathy | en |
dc.subject | non ST segment elevation myocardial infarction | en |
dc.subject | oxygen consumption | en |
dc.subject | sinus rhythm | en |
dc.subject | stable angina pectoris | en |
dc.subject | tachycardia | en |
dc.subject | vasoconstriction | en |
dc.subject | coronary artery disease | en |
dc.subject | heart muscle ischemia | en |
dc.subject | stable angina pectoris | en |
dc.subject | Angina, Stable | en |
dc.subject | Coronary Artery Disease | en |
dc.subject | Humans | en |
dc.subject | Myocardial Ischemia | en |
dc.subject | Hellenic Cardiological Society | en |
dc.title | A critical appraisal of the pharmacological management of stable angina | en |
dc.type | other | en |