Evaluation of thromboxane production and complement activation during myocardial ischemia in patients with angina pectoris.

Montalescot, Gilles; Drobinski, G; Maclouf, Jacques; Maillet, F; Salloum, J.; Ankri, Annick; Kazatchkine, Michel D.; Eugene, L.; Thomas, Daniel; Grosgogeat, Y

doi:10.1161/01.cir.84.5.2054

Cited by 35 publications

(16 citation statements)

References 48 publications

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“…In this study, patients with relatively higher ischaemic thresholds who developed ischaemia only after 2 min of peak-rate pacing were selected for final analysis; the results obviously demonstrated comparable evidence of electrocardiographic and biochemical parameters. The present study appeared to contradict other results [9,25,30, 311 since we obtained decreased plasma thromboxane levels from the CS blood at 2 min of peak-pacing in patients with pacing-induced ischaemia. This presentation was comparable with a decreased (but not negative) myocardial lactate extraction.…”

Section: Transmyocardial Plasma Thromboxane Az Level and Lactate Extrcontrasting

confidence: 99%

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

et al. 1998

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1. Myocardial thromboxane A2 production increases in patients with pacing-induced ischaemia and correlates with a decrease in myocardial lactate extraction. The release of myocardial thromboxane A2 before any lactate production was observed in patients with unstable angina. This study was proposed to clarify whether the early thromboxane A2 release contributed to the ongoing myocardial ischaemia and to determine which metabolites can be attributed to the thromboxane A2 release. Thirty-five patients with chest pain and positive treadmill exercise test underwent atrial pacing to the predicted maximal heart rate. The pacing was maintained at this peak rate for 10 min, then ceased. Blood samples of the ascending aorta and coronary sinus were drawn simultaneously at rest, at 2 and 10 min of peak-pacing, and 5 and 10 min after termination of the pacing; samples were used for analyses of lipid profiles, prostacyclin, thromboxane A2, lactate and lipid peroxides on plasma and low-density lipoprotein particles. 2. Twenty out of 35 patients who displayed pacing-induced ischaemia were documented by electrocardiographic evidence of ST depression > 2 mm developing after 2 min of peak-pacing [ischaemic group, ST delta(+)]. They had (i) negative fractional lactate extraction; (ii) pacing-induced decreases of plasma thromboxane A2 levels in the coronary sinus blood (564 +/- 57 versus 479 +/- 47 ng/l, P < 0.05) at 2 min of peak-pacing; the data increased at 10 min of peak-pacing (564 +/- 57 versus 620 +/- 60 ng/l, P < 0.05), then returned to baseline levels at 5 and 10 min post-pacing; (iii) significantly increased lipid peroxides on low-density lipoprotein of the coronary sinus blood at 2 and 10 min of peak-pacing (each P < 0.001), as well as at 5 min post-pacing (P < 0.05); (iv) significant correlation between thromboxane A2 levels and lipid peroxides on low-density lipoprotein of the coronary sinus blood samples. 3. In ST delta(+) patients, myocardial thromboxane synthesis changed before lactate production and correlated with the increase of lipid peroxides on low-density lipoprotein of the coronary venous blood. This implies that lipid peroxides on low-density lipoprotein participate in thromboxane production and play a determinative role in pacing-induced ischaemia.

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Section: Transmyocardial Plasma Thromboxane Az Level and Lactate Extrcontrasting

confidence: 99%

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

et al. 1998

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“…56,58,75,76,78 Daily aspirin doses as low as 30 mg to 50 mg inactivate the platelet cyclo-oxygenase-1 enzyme and inhibit thromboxane production . [79][80][81] Studies comparing lower (75 mg to 150 mg) with higher aspirin doses have consistently found comparable ischemic event rates with either dose when used as monotherapy or when combined with the P2Y 12 inhibitor clopidogrel . [56][57][58][59][60]78 The efficacy of ticagrelor seems to be decreased in patients treated with higher aspirin doses (≥300 mg daily) versus lower aspirin doses (≤100 mg daily) .…”

Section: Aspirin Dosing In Patients Treated With Dapt: Recommendationmentioning

confidence: 99%

2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention, 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Di

et al. 2016

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“…In summary, these results provide further support for the importance of TxA 2 in eliciting arrhythmias and may have special significance in cases where the level of TxA 2 is elevated above normal. One obvious example is the increase in TxA 2 during myocardial ischemia (18,29). However, another example involves the recent reports that Vioxx, an inhibitor of the inducible form of COX-2, may increase the risk of cardiovascular problems.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane A₂-induced arrhythmias in the anesthetized rabbit

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Kosloski

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Experiments were conducted in the anesthetized rabbit to investigate mechanisms for arrhythmias that occur after left atrial injection of the thromboxane A(2) (TxA(2)) mimetic U-46619. Arrhythmias were primarily of ventricular origin, dose dependent in frequency, and TxA(2) receptor mediated. The response was receptor specific since arrhythmias were absent after pretreatment with a specific TxA(2) receptor antagonist (SQ-29548) and did not occur in response to another prostaglandin, PGF(2alpha). Alterations in coronary blood flow were unlikely the cause of these arrhythmias because coronary blood flow (as measured with fluorescent microspheres) was unchanged after U-46619, and there were no observable changes in the ECG-ST segment. In addition, arrhythmias did not occur after administration of another vasoconstrictor (phenylephrine). The potential involvement of autonomic cardiac efferent nerves in these arrhythmias was also investigated because TxA(2) has been shown to stimulate peripheral nerves. Pretreatment of animals with the beta-adrenergic receptor antagonist propranolol did not reduce the frequency of these arrhythmias. Pretreatment with atropine or bilateral vagotomy resulted in an increased frequency of arrhythmias, suggesting that parasympathetic nerves may actually inhibit the arrhythmogenic activity of TxA(2). These experiments demonstrate that left atrial injection of U-46619 elicits arrhythmias via a mechanism independent of a significant reduction in coronary blood flow or activation of the autonomic nervous system. It is possible that TxA(2) may have a direct effect on the electrical activity of the heart in vivo, which provides significant implications for cardiac events where TxA(2) is increased, e.g., after myocardial ischemia or administration of cyclooxygenase-2 inhibitors.

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Evaluation of thromboxane production and complement activation during myocardial ischemia in patients with angina pectoris.

Cited by 35 publications

References 48 publications

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

Thromboxane A₂-induced arrhythmias in the anesthetized rabbit

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Evaluation of thromboxane production and complement activation during myocardial ischemia in patients with angina pectoris.

Cited by 35 publications

References 48 publications

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

Thromboxane A2-induced arrhythmias in the anesthetized rabbit

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Thromboxane A₂-induced arrhythmias in the anesthetized rabbit