Circadian fluctuations of tissue plasminogen activator antigen and plasminogen activator inhibitor-1 antigens in vasospastic angina

Sakata, Kazuki; Hoshino, Tsuneo; Yoshida, Hiroshi; Ono, Norihisa; Ohtani, Seiji; Yokoyama, Shinya; Mori, Noriko; Kaburagi, Tsuneo; Kurata, Chinori; Urano, Tetsumei; Takada, Yumiko; Takada, Akikazu

doi:10.1016/0002-8703(92)90964-w

Cited by 35 publications

(10 citation statements)

References 28 publications

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“…A peak in the morning and in the afternoon of ischemia-related conditions, such as the myocardial infraction [22,34,35], anginal crisis [36][37][38], and strokes, [39,40] has been reported. These episodes have been related to morning variations of the endothelial function [41] and of thrombogenesis biochemical markers [42][43][44][45][46]. Durgan et al [47] demonstrated that there is a relation between the date time and the tolerance to reperfusion-ischemia in cardiomyocytes of isolated mice, being the lowest tolerance during the morning time.…”

Section: Discussionmentioning

confidence: 99%

Sudden death circadian rhythm in Chagasic patients compared to non-Chagasic patients

Márques

Mendoza

Suárez

et al. 2017

Chronobiology International

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Section: Discussionmentioning

confidence: 99%

Sudden death circadian rhythm in Chagasic patients compared to non-Chagasic patients

Márques

Mendoza

Suárez

et al. 2017

Chronobiology International

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“…3 As with acute myocardial infarction, a circadian periodicity is present with attacks recurring at approximately the same time in the 24-hour period. [4][5][6] The attacks are severe and are accompanied by syncope, inferior ST-segment elevation and transient AV block, suggestive of acute transient occlusion of the RCA, a frequent site in Prinzmetal angina. 7 Coronary angiography showed a single non-critical obstruction in the distal part of the RCA.…”

Section: Discussionmentioning

confidence: 99%

Multifocal spasm with acetylcholine in Prinzmetal angina

Michels¹,

Baars²

2008

NHJL

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A 60-year-old female patient with Prinzmetal angina and a single non-critical (<50%) focal obstruction in the right coronary artery was referred for percutaneous coronary intervention. Coronary angiography with provocative testing using incremental doses of acetylcholine demonstrated diffuse mild vasoconstriction and multifocal hyperreactive vasoconstriction in apparently normal coronary segments but not at the site of the nonsignificant obstruction. We refrained from intervention and advised avoidance of β-blockade, and continuation of medical therapy with nitrates and calcium antagonists. (Neth Heart J 2008;16: 134-6.)Keywords: Prinzmetal angina, acteylcholine, multifocal spasm A 60-year-old female was awakened early one morning with extreme chest discomfort radiating to both her arms. She felt weak and light-headed and she fainted when she tried to get up. She regained consciousness quickly without sequelae. Upon arrival at the hospital she was without symptoms. The ECG was normal. Physical examination revealed no abnormalities. During her hospital stay she had two more early morning episodes of chest discomfort with inferior ST-segment elevation and second degree as well as complete AV block (figure 1). She is a cigarette smoker with no other classical risk factors. Coronary angiography in the absence of ischaemia revealed a normal left coronary artery and a mild fixed coronary obstruction in the distal segment of the right coronary artery (RCA). The diagnosis of Prinzmetal angina was made. 1 She was treated with calcium antagonists and nitrates. She was referred for percutaneous coronary intervention (PCI) of the non-critical obstruction ( figure 2A), but we decided to perform a provocative test with selective intracoronary infusions of acetylcholine in incremental doses. 2 Infusion of acetylcholine at the third dose level (50 µg) induced diffuse mild vasoconstriction and multifocal hyperreactive vasoconstriction (spasm) in apparently normal coronary segments but not at the site of the alleged culprit lesion (figure 2B). The mild constriction and spasms were promptly resolved by intracoronary nitroglycerin ( figure 2C). We refrained from PCI and advised an intensification of the therapy with calcium antagonists, nitrates, aspirin and statins, and avoidance of β-blockade and smoking. DiscussionThis patient presented with classical Prinzmetal (variant) angina. She is a cigarette smoker with no other classical risk factors. 3 As with acute myocardial infarction, a circadian periodicity is present with attacks recurring at approximately the same time in the 24-hour period. [4][5][6] The attacks are severe and are accompanied by syncope, inferior ST-segment elevation and transient AV block, suggestive of acute transient occlusion of the RCA, a frequent site in Prinzmetal angina. 7 Coronary angiography showed a single non-critical obstruction in the distal part of the RCA. Intuitively we held spasm at this site responsible for the attacks, but later we realised that spasm may develop at sites other than the fixed...

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“…[6][7][8][9]15 Aspirin and heparin should be administered in the acute setting on the basis of the association of vasospasm with increased thrombus formation. 15,17 Initially, patients with vasospasm may receive b-blockers as standard therapy for acute coronary syndrome. 18 However, if there is a known stimulant exposure (eg, cocaine or amphetamines), b-blockers should be avoided because of paradoxically increased coronary arterial tone and increased incidence of arrhythmias.…”

Section: Discussionmentioning

confidence: 99%