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Nonobstructive Coronary Heart Disease and Coronary Artery Vasospasm
Published in Mark C Houston, The Truth About Heart Disease, 2023
To diagnose CA-VS, you may need to wear an ambulatory monitor for up to 48 hours. The monitor records your heart's electrical impulses, even during sleep. If you have chest pain, this usually will show up on the electrocardiogram (EKG) that indicates coronary spasm. However, not all patients show EKG changes during every episode.
Cardiac Emergencies in Obstetrics
Published in Sanjeewa Padumadasa, Malik Goonewardene, Obstetric Emergencies, 2021
Sanjeewa Padumadasa, Sanjeewa Rajapakse
Low-dose aspirin is safe during pregnancy, but there is limited evidence available regarding the safety of clopidogrel. Beta-blockers can be used, and nifedipine is the drug of choice when coronary spasm is suspected. Newer antiplatelets and statins are contraindicated in pregnancy.
Rational Medical Therapy of Functional GI Disorders
Published in Kevin W. Olden, Handbook of Functional Gastrointestinal Disorders, 2020
Richard M. Sperling, Kenneth R. McQuaid
Cardiac Causes Atypical chest pain occurs in up to 50% of patients with mitral valve prolapse, although this may be partially attributable to ascertainment bias (30). Coronary spasm can take place in patients with normal coronary arteries; this is characterized on EKG by ST-segment elevation during pain and may be provoked by an ergonovine challenge during coronary arteriography.
Complete invasive diagnosis of patients with ischemia with nonobstructive coronary arteries: why it matters
Published in Expert Review of Molecular Diagnostics, 2022
Jasmine Melissa Madsen, Jacob Thomsen Lønborg, Thomas Engstrøm
Endothelial-dependent dysfunctions of both the microcirculation and epicardial arteries may be assessed with provocative testing including vasoactive drugs such as acetylcholine, acting on the endothelial cells and the vascular smooth muscle cells, triggering epicardial or arteriolar vasoconstriction in dysfunctional endothelium [3]. Following infusion with acetylcholine, patients with INOCA due to an endothelial-dependent dysfunction will develop electrocardiogram changes and angina. However, if the dysfunction is due to microvascular spasm, no changes in the diameter of the epicardial coronary arteries will arise, whereas the epicardial vessels will change diameter if the dysfunction is caused by epicardial spasm [13]. Thus, coronary spasm mainly relies on an enhanced vasoreactivity of the vascular smooth muscle cells often with a coexisting endothelial dysfunction [6]. Up to two-thirds of patients with INCOA is caused by endothelial dysfunction and up to 20% of these patients have mixed microvascular and epicardial spasm [13].
Angina due to coronary artery spasm (variant angina): diagnosis and intervention strategies
Published in Expert Review of Cardiovascular Therapy, 2021
Thanh Ha Nguyen, Gao-Jing Ong, Olivia C Girolamo, Viviane De Menezes Caceres’, Armin Muminovic, Yuliy Y Chirkov, John D Horowitz
It has become apparent over the past 20 years that CAS may involve predominant constriction of either large or small coronary vasculature. Whereas the form of ‘variant angina’ described by Prinzmetal et al. [1] probably relates to either focal or diffuse spasm of large coronary arteries, as illustrated in Figure 1, microvascular coronary spasm is manifest by the presence of the coronary slow flow phenomenon (CSFP), defined as TIMI-2 flow in at least one major coronary artery, in the absence of recent myocardial infarction [31]. CSFP is generally present chronically (thus requiring no provocative testing: if indeed provocative testing is performed, many patients develop diffuse spasm) (Figure 2), but worsens in severity during symptomatic crises [32] and can be ameliorated both by the (currently unavailable) T-channel-selective calcium antagonist mibefradil [33] and by intracoronary injection of the dihydropyridine L-channel calcium antagonist nicardipine [34]. Both forms of CAS are identically characterized clinically, including the occurrence of angina predominantly at rest, with severe symptomatic crises, and poor symptomatic responses to organic nitrates [35].
Pathobiology and evolving therapies of coronary artery vasospasm
Published in Baylor University Medical Center Proceedings, 2021
Monish A. Sheth, Robert J. Widmer, Hari K. Dandapantula
Coronary artery vasospasm (CAV) is defined as an “exacerbated, nonspecific contractile response of epicardial coronary artery smooth muscle to various stimuli” or a “reversible, focal and intense coronary vasoconstriction that typically occurs in an epicardial conduit artery segment.”1 Prinzmetal2 is credited with the first description of chest pain secondary to coronary spasm in 1959. CAV has been shown to manifest in both normal coronary arteries and in coronary arteries with underlying atherosclerotic lesions. In a classic study by Bertrand et al,3 focal spasms were noted more in patients who complained of angina at rest than in patients with exertional angina, atypical chest pain, valvular heart disease, and cardiomyopathy. CAV was noted in 20% of patients with recent myocardial infarction (MI) compared with 6.2% of patients with a history of MI. Coronary spasm was superimposed on fixed atherosclerotic lesions in 60% of the patients with observed spasm. There are significant ethnic differences in CAV. The incidence of CAV is higher in Korean and Japanese individuals than in Western cohorts.4 The overall prognosis of CAV was found to be better in a Japanese population with survival as the main endpoint.5