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Nonobstructive Coronary Heart Disease and Coronary Artery Vasospasm
Published in Mark C Houston, The Truth About Heart Disease, 2023
In patients with CA-VS, the lumen of the coronary artery has no visible or documented plaque by coronary angiography, but the artery may have intense constriction or vasospasm that obstructs blood flow and causes anginal chest pain, tightness, pressure, shortness of breath, and, sometimes, an MI. A coronary artery spasm is a temporary tightening (constriction) of the muscles in the wall of one of the coronary arteries which can decrease or completely block blood flow to sections of the heart (Figure 16.1).
The Coronary Arteries: Atherosclerosis and Ischaemic Heart Disease
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Coronary artery spasm is a controversial topic for pathologists as it is impossible to detect on histological analysis and it is diagnosed by exclusion of other causes for myocardial infarction. During life, it is known as vasospasmic angina, is more common in females and can lead to ACS, MI and cardiac arrhythmias. It is presumed to be the cause of SCD when there is transmural myocardial ischaemic damage (acute and/or chronic) in the wall of the ventricle (in the absence of any coronary artery pathology [see Table 2.3]). The ischaemic damage is regional pointing to a regional arterial transient blockage/spasm. Thrombotic/embolic disease with lysis is a possibility in these cases, but there is no source for thrombosis or emboli found at autopsy. Hypercoagulable syndromes may be an explanation. It is also linked to drug use, particularly cocaine.26
Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
The skin may be pale due to peripheral vasoconstriction. Dilated pupils and hyperpyrexia may be present. Cocaine may lead to arrhythmias (Cregler and Mark, 1986; Benchimol et al., 1978), and thus to life-threatening cardiovascular events. Cardiac arrhythmias including ventricular premature beats, ventricular tachycardia and fibrillation, myocarditis, acute myocardial infarction, and sudden death have been observed, and there may not be underlying heart disease in precipitating the cardiac events (Isner et al., 1986). The subject may complain of chest pain and dyspnea, and coronary artery spasm with acute myocardial infarction have been documented in multiple case reports and studies (Coleman et al., 1982; Kossowsky and Lyon, 1984; Howard et al., 1985; Simpson and Edwards, 1986). Cocaine may induce coronary vasoconstriction (Schachne et al., 1984). Although there is the potential onset of cardiac dysfunction related to cocaine abuse, in a controlled medical environment the sympathomimetic effects of topical cocaine on cardiovascular function were not evident when patients with coronary artery disease were anesthetized (Barash et al., 1980).
Chest pain with ST-elevation in leads AVR, III, AVF, V1, V3R, V4R and V5R
Published in Clinical and Experimental Hypertension, 2023
Yuehai Wang, Yuqiang Zhang, Yan Wang, Changpeng Zhai, Jie Gao, Guangyong Huang, Shengjun Ma
It is not difficult to understand that the patient’s continuous multi lead ST-elevation and increased titer of serum troponin I suggest severe myocardial injury like STEMI. The reasons may come from the following three factors: firstly, the decrease of forward blood flow of pulmonary circulation and the increase of right ventricular pressure caused by bilateral multiple PE lead to the decrease of effective perfusion pressure of right coronary artery, which reduces the blood supply to right myocardium; Secondly, hypoxemia caused by bilateral multiple PE leads to the reduction of blood oxygen supply to the right cardiac muscle; Finally, the bilateral multiple PE increases the anterior and posterior load of the right heart, resulting in a serious contradiction between the supply and demand of oxygen in the blood of the myocardium. In addition, the titers of vasoconstrictors such as thromboxane A2, endothelin-1, and serotonin in the blood of patients with PE increased (1). Whether these substances can cause coronary artery spasm and reduce coronary blood flow remains to be determined. Therefore, the pathological mechanism of myocardial injury in this patient with PE is multifactorial (Figure 2).
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
Vasospastic angina can occur in patients with or without atherosclerotic vasculature. It can have focal or diffuse involvement of coronary arteries or epicardial microvasculature [3]. Multiple mechanisms have been proposed for the pathogenesis of coronary artery spasm including vascular smooth muscle hyperactivity, altered autonomic system, endothelial dysfunction, low–grade inflammation, electrolyte abnormalities, and oxidative stress. Vascular smooth muscle hyperactivity is considered a key factor [3]. The symptoms show diurnal variation, occurring more often at night. Increased fibrin formation and decreased fibrinolytic activity at night are considered to be the underlying mechanism [4]. Hyperinsulinemia, some genetic factors, and systemic vasomotor disorders like migraine or Raynaud’s phenomenon have also been associated with increased risk for this condition [5–7].
Coronary vasospasm complicating atrial fibrillation ablation: a case report and review of the literature
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Nirmal Guragai, Upamanyu Rampal, Rahul Vasudev, Pragya Bhandari, Atul Prakash, Hartaj Virk, Mahesh Bikkina, Shamoon Fayez
Coronary artery spasm post ablation is usually present with angina like symptoms. Calcium channel blockers and nitrates are the most appropriate therapy in these patients [12]. The prognosis of vasospastic angina is relatively good in general; however, it is known to be a cause of serious life-threatening ventricular-arrhythmias and resultant sudden cardiac death in some cases [13]. Coronary artery spasm is usually limited to a single coronary artery and can rarely cause ventricular arrhythmias. It is exceedingly rare to see spasm of multiple vessels leading to myocardial stunning causing ventricular fibrillation and cardiac arrest. The LVEF was acutely reduced to 20% in our patient which was attributed to myocardial stunning secondary to severe triple vessel spasm. In our case there was complete recovery of EF in a few days highlighting that favorable outcomes can be achieved with early identification of this rare complication and treatment using IC/IV nitrates with adequate hemodynamic support (percutaneous assist devices) in cases complicated by cardiogenic shock.