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Published in Thomas F. Lüscher, Paul M. Vanhoutte, The Endothelium: Modulator of Cardiovascular Function, 2020
Thomas F. Lüscher, Paul M. Vanhoutte
The levels of thromboxane B2 in the coronary sinus are elevated during attacks of coronary vasospasm, an observation which is consistent with an augmented activation of the platelets.926,1030,1220,1434 However, the levels of the prostanoid are normal early on during the ischemia. Inhibitors of cyclooxygenase or selective inhibitors of thromboxane synthetase do not reduce the frequency or duration of the ischemic attacks, i.v. prostacyclin usually does not influence the number, severity, or duration of the spontaneous or provoked ischemic episodes.175 Thus, in coronary vasospasm platelet activation is likely to be a consequence rather than a cause of variant angina.
Neural Regulation of Coronary Blood Flow*
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
David D. Gutterman, Michael J. Brody, Melvin L. Marcus
More recently, Gutstein et al. (1984) provided evidence that electrical stimulation in lateral hypothalamus produces coronary vasoconstriction. Rat coronary arteries were perfusion-fixed during central electrical stimulation (hypothalamus) and compared to similarly prepared animals not stimulated. Morphometric analysis showed reduced mean luminal diameter and cross-sectional areas in coronary vessels from experimental animals. The authors interpreted these data as evidence of centrally mediated coronary vasospasm of large coronary arteries. Such responses may correspond to α-adrenergic mediated large coronary vasospasm observed in humans (Yasue et al., 1974; Ricci et al., 1979; Chierchia, 1983).
High PAI Activity as an Indicator of Disease Activity in Rest Angina
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
By emergency coronary angiography cardiologists often find thrombosis superimposed on the severe atherosclerotic lesions occurring in patients with acute ischemic syndromes. On the other hand, some patients with angina pectoris and/or acute myocardial infarction have no significant atherosclerotic lesions. In the latter case, it is most likely that coronary vasospasm contributes to the pathogenesis. However, few reports exist on the role of the fibrinolytic system in this type of angina patient In mis chapter, the significance of the fibrinolytic components in patients with rest angina resulting from coronary vasospasm will be discussed.
Advances in the available pharmacotherapy for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
Published in Expert Opinion on Pharmacotherapy, 2023
Antonio Greco, Simone Finocchiaro, Dominick J. Angiolillo, Davide Capodanno
Approximately two thirds of ACS are caused by the rupture of a lipid-laden coronary plaque, resulting into occlusive (STEMI) or non-occlusive (NSTEMI) thrombosis [7]. Plaque erosion is the second most common mechanism of ACS (~25%), with a platelet-rich thrombus developing on a denuded endothelial surface [8]. Calcific nodules represent another cause of ACS (~5%): consisting of nodular calcification protruding into the lumen with superimposed thrombus, they are associated with a high incidence of major adverse cardiovascular events (MACE) [9]. Coronary vasospasm (~1-5%), spontaneous coronary artery dissection (~1-4%) and coronary embolism (~1-3%) are additional causes of ACS [10–12]. In addition, ~6% of MI consists of MI with nonobstructive coronary arteries (MINOCA), which is more common in women and non-Caucasians [13–16]. Finally, also the unbalance between oxygen demand and supply to the heart (e.g. sustained tachyarrhythmia, severe bradyarrhythmia, severe hypertension, respiratory failure, shock, severe anemia or hypotension) can cause a MI [17].
Coronary vasospasm as an etiology of recurrent ventricular fibrillation in the absence of coronary artery disease: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Binita Bhandari, Tejaswi Kanderi, Keerthi Yarlagadda, Mehreen Qureshi, Saketram Komanduri
Management of VF is time-sensitive as it can cause sudden cardiac death if not immediately reverted and also involves diagnostic testing to delineate the cause of VF if possible. Defibrillation remains the mainstay of treatment to prevent significant mortality during acute episodes as well as to prevent further VF episodes. The literature on VF caused by coronary vasospasm is evolving, and a range of presentations from mild chest discomfort to myocardial infarction and life-threatening arrhythmias and sudden cardiac death have been reported [13]. Our patient had recurrent hospital admissions (Figure 5) with chest pain and ST elevations noted on ECG leading to a coronary catheterization. Once ACS was ruled out, VFib was attributed to coronary vasospasm, which was further supported by recurrent episodes with potential anginal attacks but a decrease in the frequency of ICD shocks with the management of coronary vasospasm by calcium channel blockers and nitrates.
Feasibility of right coronary artery first ergonovine provocation test
Published in Acta Cardiologica, 2021
Hyun Seok Ham, Ki-Hun Kim, Jino Park, Yeo-Jeong Song, Seunghwan Kim, Dong-Kie Kim, Sang-Hoon Seol, Doo-Il Kim
The diagnosis of coronary spasm has an important clinical significance because such condition can cause acute coronary syndrome, fatal arrhythmias, transient heart failure, and sudden cardiac death [1–3]. However, several coronary spasms develop unpredictably, are spontaneously resolved in a few minutes, and can be misdiagnosed as other organ symptoms, which are related to the underestimated burden of coronary vasospasm [1,4]. Therefore, the provocation test for vasospasm has been performed, and coronary angiography using pharmacological intracoronary (IC) provocation is recommended for the verification of unexplained chest pain among patients with normal or unobstructed coronary arteries based on the international guidelines [5–7]. Although the safety of the pharmacological provocation test is well-known, the specific procedure-related factors such as standardised provocation protocol or methods remain uncertain. The Japanese Circulation Society (JCS) guidelines suggested the use of the LCA first then RCA sequence as the method of IC ergonovine provocation test; however, no concrete reasons for such sequence were given [6,8]. For provocation test on both coronary arteries, the diagnostic catheter should be changed to the other type inevitably in most cases. This may provoke catheter-induced arterial spasm and lead to a false-positive response.