Plasma Endothelin-1 Levels in Stable and Unstable Angina

Qiu, Shiqiang; Théroux, Pierre; Marcil, Michel; Solymoss, B.

doi:10.1159/000175848

Cited by 56 publications

(21 citation statements)

References 21 publications

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“…Higher plasma levels of endothelin-1 were also seen in patients with unstable angina pectoris [17]. Though this elevation did not correlate with other clinical or laboratory characteristics, the increase was more pronounced in patients whose subsequent clinical course was complicated by acute coronary events [15].…”

Section: Discussionmentioning

confidence: 99%

“…Elevated plasma endothelin level or enhanced endothelin expression was reported in patients suffering from several cardiovascular diseases, such as congestive heart failure [4, 5, 6], pulmonary hypertension of different origins [7, 8, 9, 10, 11], atherosclerosis [12], vasospastic angina pectoris [13], myocardial infarction [14], unstable angina pectoris [15, 16, 17]and some other cardiovascular diseases. [18].…”

Section: Introductionmentioning

confidence: 99%

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Time Course of Endothelin-1 Plasma Level in Patients with Acute Coronary Syndromes

Vojáček¹,

Kolář²,

Lisý³

et al. 1999

Cardiology

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An elevated plasma level of endothelin-1 was reported in several cardiovascular conditions including unstable angina pectoris and myocardial infarction. The present study was designed to evaluate the time course of the endothelin-1 release in unstable angina pectoris and to assess its relationship to the development of myocardial infarction and coronary vessel occlusion. The cohort studied included 32 patients with the clinical diagnosis of unstable angina pectoris who had been admitted to the coronary care unit and subsequently underwent coronary angiography (group A). Fourteen patients with chronic stable angina pectoris referred to routine diagnostic coronary angiography served as the control group (group B). A significant difference in the endothelin-1 plasma level was found between both groups, the values being 10.2 ± 5.3 and 6.0 ± 3.1 pg/ml (p < 0.01), respectively. There were, however, no significant differences between the following subdivisions of group A: patients with and without subsequent myocardial infarction; those with angiographically documented occlusion of at least one major branch of the coronary artery and no occlusion; and finally, those with persisting symptoms of angina pectoris and with favorable response to treatment. Neither was there any difference found among the subgroups differing in the time interval between the onset of chest pain and blood sampling. The time course of endothelin plasma concentrations showed elevated values lasting for more than 96 h after the index episode of prolonged chest pain. No correlation with the subsequent clinical course could be inferred. Thus, plasma endothelin level was elevated in patients with unstable angina pectoris and myocardial infarction and the increase persisted for several days after the onset of symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Time Course of Endothelin-1 Plasma Level in Patients with Acute Coronary Syndromes

Vojáček¹,

Kolář²,

Lisý³

et al. 1999

Cardiology

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“…20 Increased ET levels can be detectable in these patients. 2,3 On the other hand, these patients often suffer from heart failure, and they may profit from the ability of molsidomine to unmask the positive inotropic effect of endogenous ET-1. BQ 610 can also reveal the positive inotropy of ET-1.…”

Section: Discussionmentioning

confidence: 99%

“…Increased ET plasma concentrations have been reported in patients with angina, 2,3 myocardial infarction, 4,5 or heart failure. 6 Drugs that antagonize or block the effects of ET-1 may consequently be of importance in the treatment of these diseases.…”

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confidence: 99%

Inotropic Effects of Endothelin-1

et al. 1999

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Abstract-In vivo studies could not detect a positive inotropy of endothelin (ET)-1 as described in in vitro experiments.ET-induced direct positive inotropy, which seems to be mediated by ET B receptors, may be antagonized in vivo by an indirect cardiodepressive effect owing to an ET-induced coronary vasoconstriction via ET A receptors. This study compares the effects of a dose of 1 nmol/kg ET-1 alone on myocardial contractility and myocardial energy metabolism with the effects of 1 nmol/kg ET-1 after pretreatment with 5 mg/kg molsidomine or with 100 g/kg of the ET A receptor antagonist BQ 610. We investigated the effects of ET-1 versus saline controls in open-chest rats. In addition to measurements in the intact circulation, myocardial function was examined by isovolumic registrations independent of peripheral vascular effects. We also studied the effect of ET-1 on myocardial high-energy phosphates. Pretreatment with molsidomine and BQ 610 attenuated the ET-induced reduction of cardiac output (ET-1: Ϫ62%; molsidomineϩET-1: Ϫ47%; BQ 610ϩET-1: Ϫ27% different from controls). After a transient initial vasodilation, ET-1 raised total peripheral resistance (ET-1: ϩ190%; molsidomineϩET-1: ϩ171%; BQ 610ϩET-1: ϩ89%). BQ 610 was more effective in preventing ET-induced vasoconstriction. The increase of isovolumic peak first derivative of left ventricular pressure (ET-1: Ϫ2%; molsidomineϩET-1: ϩ16%; BQ 610ϩET-1: ϩ19%) after pretreatment with molsidomine or BQ 610 indicates that these drugs unmask the positive inotropy of ET-1. ET-induced myocardial ischemia was abolished by molsidomine and BQ 610. Key Words: endothelin Ⅲ BQ 610 Ⅲ molsidomine Ⅲ contractility Ⅲ phosphates, high-energy Ⅲ rats T he peptide endothelin (ET)-1 is the most potent vasoconstrictor known to date, 1 and it is involved in the development of several diseases. Increased ET plasma concentrations have been reported in patients with angina, 2,3 myocardial infarction, 4,5 or heart failure. 6 Drugs that antagonize or block the effects of ET-1 may consequently be of importance in the treatment of these diseases. Two different ET receptors have been characterized (the ET A 7 and the ET B 8 receptors), and many selective and nonselective ET receptor antagonists have been synthesized. Nevertheless, until now it has been unclear whether selective or nonselective ET receptor antagonists should be used in therapy. In addition to its important vascular effects, several experiments with isolated cardiac tissues demonstrated a positive inotropic effect of ET-1. 9 -12 In isolated hearts 13,14 and in in vivo studies, 15,16 ET-1 showed a controversial effect on myocardial contractility. In a previous in vivo study with rats, we could not detect the described positive inotropy of ET-1. 17 We supposed that the potent vasoconstrictive effect of ET-1 might cause myocardial ischemia with consecutive cardiodepression, thereby masking the described direct positive inotropic effect of ET-1 in vivo. Our hypothesis was confirmed by the fact that the combination of ET-1 with high do...

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“…2 Elevated plasma concentrations of ET have been observed in patients suffering from diverse cardiovascular diseases, such as congestive heart failure, [3][4][5] pulmonary hypertension 6 and angina pectoris. [7][8][9] In patients with acute myocardial infarction (AMI) particularly, the cardiac ET system is markedly activated 10,11 and plasma concentrations of ET-1 are elevated. 12 Little is known, however, about the relationship between plasma ET-1 concentrations, mortality and left ventricular (LV) systolic function in human AMI subjects.…”

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confidence: 99%

Clinical Significance of Acute-Phase Endothelin-1 in Acute Myocardial Infarction Patients Treated With Direct Coronary Angioplasty

Katayama

Yano

Nakashima

et al. 2005

Circ J

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ndothelins (ET) are 21-amino-acid peptides produced by the endothelium and which play important roles in cardiovascular physiology and pathophysiology. 1 The most important ET produced by the endothelium is ET-1, which has an important role in the vasoconstriction of the peripheral arterial system and also of the coronary vascular bed. 2 Elevated plasma concentrations of ET have been observed in patients suffering from diverse cardiovascular diseases, such as congestive heart failure, 3-5 pulmonary hypertension 6 and angina pectoris. [7][8][9] In patients with acute myocardial infarction (AMI) particularly, the cardiac ET system is markedly activated 10,11 and plasma concentrations of ET-1 are elevated. 12 Little is known, however, about the relationship between plasma ET-1 concentrations, mortality and left ventricular (LV) systolic function in human AMI subjects.The object of the present study was to determine whether clinical prognosis after AMI may be predicted from acutephase plasma ET-1 concentrations, and to assess whether there might be any relationship between plasma ET-1 concentrations and LV systolic function. Methods Patient PopulationThe study population comprised 110 consecutive patients (79 males, 31 females; 68±11 years, range 40-93) presenting with a first AMI, admitted and enrolled between March 2003 and June 2004. Diagnosis of AMI was done according to the following criteria: (1) complaint of chest pain and/or discomfort; (2) electrocardiographic ST segment elevation of ≥0.1 mV in 2 or more limb leads, or ≥0.2 mV in 2 or more precordial leads, or new left bundlebranch block; and (3) elevation of total serum creatine kinase (CK) more than twice the upper limit of the normal range. We excluded patients with renal failure on admission (serum creatinine >2.5 mg/dl), patients with old myocardial infarction (MI), patients who reached the institution >6 h after onset, and patients who died <24 h after onset (ie, at the time of blood sampling). We diagnosed anterior MI in 54 patients. Subjects were divided into 2 groups according to the median plasma ET-1 concentration: <2.9 pg/ml (L group, n=55) and ≥2.9 pg/ml (H group, n=55). We distinguished between angina pectoris episodes <24 h before the onset of AMI from general angina pectoris, to take into account ischemic pre-conditioning. Treatment StrategyFollowing oral administration of 200 mg of aspirin and 200 mg of ticlopidine, all patients successfully underwent direct percutaneous coronary intervention (PCI) within 8 h of the onset of symptoms. In 18 patients, conventional plain

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Plasma Endothelin-1 Levels in Stable and Unstable Angina

Cited by 56 publications

References 21 publications

Time Course of Endothelin-1 Plasma Level in Patients with Acute Coronary Syndromes

Time Course of Endothelin-1 Plasma Level in Patients with Acute Coronary Syndromes

Inotropic Effects of Endothelin-1

Clinical Significance of Acute-Phase Endothelin-1 in Acute Myocardial Infarction Patients Treated With Direct Coronary Angioplasty

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