Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease

Pacold, Ivan; Hwang, Ming H.; Lawless, Christine E.; Diamond, Peter; Scanlon, Patrick J.; Loeb, Henry S.

doi:10.1016/0002-9149(86)90729-0

Cited by 32 publications

(21 citation statements)

References 7 publications

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“…Pacold et al 19 found a moderate reduction in maximum hyperemia with indomethacin, but several other investigations using indomethacin, 18 ASA, 21 and ibuprofen 22 have not shown any effect. Our results, however, indicate that PGs are important regulators of metabolic vasodilation in patients with atherosclerosis.…”

Section: Vasodilator Pgsmentioning

confidence: 92%

“…26,27 In humans with atherosclerosis, indomethacin has been shown to reduce resting CBF and increase CVR [17][18][19] ; these effects are associated with increased MABP, estimated myocardial oxygen demand, and arteriovenous oxygen extraction. 17,19 Although estimated myocardial workload did not increase in the present study, our findings are otherwise consistent with these previous investigations.…”

Section: Vasodilator Pgsmentioning

confidence: 99%

“…12,16 Previous studies have shown that cyclooxygenase inhibition with indomethacin reduces resting CBF in patients with coronary artery disease. 17 Although it has been confirmed by others, 18,19 some have speculated that the effects of indomethacin are not due to PG inhibition. 18 However, experimental studies have suggested that PGs are not essential for coronary metabolic vasodilation.…”

mentioning

confidence: 92%

“…18 However, experimental studies have suggested that PGs are not essential for coronary metabolic vasodilation. 20 In humans, there has been conflicting evidence regarding the effect of cyclooxygenase inhibition on metabolic vasodilation, 18,19,21,22 and its effect on conduit vessel flow-mediated coronary artery dilation is unknown. Therefore, we aimed to determine the contribution of endothelium-derived NO and PG to resting CBF and to pacing-induced metabolic vasodilation and flow-mediated dilation.…”

mentioning

confidence: 99%

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Contribution of Vasodilator Prostanoids and Nitric Oxide to Resting Flow, Metabolic Vasodilation, and Flow-Mediated Dilation in Human Coronary Circulation

et al. 1999

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Background-Endothelial dysfunction is associated with atherosclerosis and may contribute to ischemic syndromes. We assessed the contribution of endothelium-derived nitric oxide (NO) and vasodilator prostanoids to resting blood flow, metabolic vasodilation, and flow reserve in the human coronary circulation. Methods and Results-Coronary hemodynamics were assessed before and after inhibition of vasodilator prostanoids and NO with intracoronary aspirin (acetylsalicylic acid [ASA]) and N

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Section: Vasodilator Pgsmentioning

confidence: 92%

Section: Vasodilator Pgsmentioning

confidence: 99%

mentioning

confidence: 92%

mentioning

confidence: 99%

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Contribution of Vasodilator Prostanoids and Nitric Oxide to Resting Flow, Metabolic Vasodilation, and Flow-Mediated Dilation in Human Coronary Circulation

et al. 1999

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“…Some investigators also found indications that i.v. and oral treatment with indomethacin has negative effects on coronary flow and ventricular performance in humans: using the thermodilution technique, coronary vasoconstriction was found despite an increase in myocardial oxygen demand in adult patients with coronary artery disease (4)(5)(6). Moreover, Appleton et al (6), who analyzed LV function after indomethacin administration in the newborn baby using M-mode echocardiography, reported that myocardial function during the diastolic phase was affected, whereas systolic function was not changed.…”

mentioning

confidence: 99%

Myocardial Perfusion and Performance after Indomethacin Administration in Newborn Lambs

et al. 1993

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ABSTRACT. Indomethacin is a drug widely used to achieve pharmacologic closure of a patent ductus arteriosus in the premature infant. In several vascular beds (brain, kidney, intestine), indomethacin has been shown to cause vasoconstriction. Possible negative effects on myocardial blood flow and performance could be deleterious in premature infants with limited cardiac reserve. Before, during, and 30 and 60 min after administration of 1 mg.kg-' of indomethacin in nine newborn lambs, we measured coronary blood flow velocity (Doppler flow probe around the left circumflex coronary artery), left ventricular (LV) pressure (by tip manometer) and volume (by conductance catheter technique), cardiac output, arterial pressure, arterial and venous saturations and calculated systemic and coronary vascular resistance, LV systolic function by the endsystolic pressure-volume relationship, and myocardial oxygen extraction. To investigate the effect of indomethacin on the flow regulation of the coronary vascular bed, we measured coronary flow and LV function under different levels of myocardial demand, achieved by stepwise occluding of the descending aorta. During indomethacin infusion, coronary and systemic vascular resistance increased significantly (by 43 and 76%, respectively), resulting in an increase in arterial pressure from 10.2 to 16.9 kPa, whereas neither coronary flow nor LV systolic function changed despite the increase in afterload. Thirty and 60 min after indomethacin, coronary and systemic vascular resistance had returned to baseline levels and LV systolic function remained unchanged. The relationship between coronary flow and cardiac demand was not different before or after indomethacin. These results suggest that indomethacin may transiently impair the ability of the newborn heart to respond to increased myocardial demand by causing coronary vasoconstriction but does not impair myocardial performance, either at baseline or in response to increasing demand. (Pediatr Res 33: 295-301,1993) Abbreviations CO, cardiac output E,,, end systolic elastance ESPVR, end-systolic pressure-volume relationship HR, heart rate IVC, inferior vena cava LV, left ventricle MFVcor, mean coronary flow velocity Pao, aortic pressure

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Cyclooxygenase 2 inhibition and thrombosis: Comment on the article by Crofford et al

McMurray¹

2001

Arthritis & Rheumatism

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Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease

Cited by 32 publications

References 7 publications

Contribution of Vasodilator Prostanoids and Nitric Oxide to Resting Flow, Metabolic Vasodilation, and Flow-Mediated Dilation in Human Coronary Circulation

Contribution of Vasodilator Prostanoids and Nitric Oxide to Resting Flow, Metabolic Vasodilation, and Flow-Mediated Dilation in Human Coronary Circulation

Myocardial Perfusion and Performance after Indomethacin Administration in Newborn Lambs

Cyclooxygenase 2 inhibition and thrombosis: Comment on the article by Crofford et al

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