Results 241 to 250 of about 63,499 (283)
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Current Opinion in Cardiology, 1999
Severe atherosclerotic narrowing of one or more coronary arteries is responsible for myocardial ischemia and angina pectoris in most patients with stable angina pectoris. The coronary arteries of patients with stable angina also contain many nonobstructive plaques, which are prone to fissures or rupture resulting in presentation of acute coronary ...
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Severe atherosclerotic narrowing of one or more coronary arteries is responsible for myocardial ischemia and angina pectoris in most patients with stable angina pectoris. The coronary arteries of patients with stable angina also contain many nonobstructive plaques, which are prone to fissures or rupture resulting in presentation of acute coronary ...
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2023
Abstract This chapter outlines the guidance on Stable angina. It provides a clear overview for the junior doctor in a clinical setting.
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Abstract This chapter outlines the guidance on Stable angina. It provides a clear overview for the junior doctor in a clinical setting.
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▼Ivabradine for stable angina?
Drug and Therapeutics Bulletin, 2008Up to 1 in 25 people in Europe and the USA have stable angina, with symptoms that may limit function and quality of life.1,2 Beta-blockers are usually used in initial symptomatic treatment, but may cause unwanted effects.3–6 They are also contraindicated in some patients (e.g.
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Treatment of Stable Angina Pectoris
American Journal of Therapeutics, 2011Management of stable angina pectoris includes antianginal medications, medications to prevent progression of atherosclerosis, and aggressive treatment of causative risk factors. Antianginal medications commonly used include nitrates, beta-blockers, calcium channel blockers, and ranolazine. Antiplatelet agents, statins, and angiotensin-converting enzyme
Chandrasekar, Palaniswamy +1 more
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The Prognosis in Stable and Unstable Angina
Cardiology Clinics, 1991The average annual mortality in unselected patients with chronic stable angina is 4%. Mortality is increased in male patients and in patients who have risk factors such as hypertension, previous MI, or abnormal ECGs. We do not routinely recommend cardiac catheterization in the initial management of patients with stable angina unless the patient ...
T C, Hilton, B R, Chaitman
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Ranolazine for chronic stable angina
The Lancet, 2008Ranolazine is a new and unique antianginal drug that has been approved for the treatment of chronic stable angina pectoris. The drug is administered as a sustained-release formulation. Although the drug's mechanism of action has not been fully elucidated, current thinking is that ranolazine, a selective inhibitor of late sodium influx, attenuates the ...
David T, Nash, Stephen D, Nash
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Optimal Treatment of Stable Angina
Cardiology, 2008Angina pectoris due to coronary artery disease is a common manifestation of myocardial ischemia. Reduction of oxygen demand (β-blockers) and relief of coronary vasoconstriction (calcium blocker or nitrate) are additive approaches to controlling ischemia.
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Management of Chronic Stable Angina
Critical Care Nursing Clinics of North America, 2017Chronic stable angina (CSA) is a symptomatic problem that is precipitated by ischemic heart disease. CSA is diagnosed when symptoms are present for at least 2 months without changes in severity, character, or triggering circumstances. This article is a summary of current treatment strategies aimed to prevent progression of atherosclerosis, and ...
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Advances in the Management of Stable Angina
Journal of Managed Care Pharmacy, 2006To describe the approved uses, pharmacology, pharmacodynamics, pharmacokinetics, efficacy, safety, and place in therapy of ranolazine, the first new antianginal drug therapy introduced in more than 20 years for the treatment of chronic angina.The mechanism of action of ranolazine is unknown, but it may involve inhibition of the late sodium current in ...
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Pathophysiology of Stable Angina Pectoris
Cardiology Clinics, 1991The pathophysiology of stable angina is discussed with respect to anatomic substrate, coronary and systemic hemodynamic mechanisms, the dynamic nature of coronary artery stenoses, and determinants of myocardial oxygen consumption. Cellular mechanisms involved in ischemia and the transduction of these changes into angina are also reviewed.
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