Contribution of endothelium-derived nitric oxide to coronary arterial distensibility: An in vivo two-dimensional intravascular ultrasound study

Sudhir, Krishnankutty; Mullen, William L.; Hausmann, Dirk; Fitzgerald, Peter J.; Chou, Tony M.; Yock, Paul G.; Chatterjee, Kanu

doi:10.1016/0002-8703(95)90322-4

Cited by 25 publications

(12 citation statements)

References 36 publications

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“…Using such techniques, endothelium-derived NO has been shown to regulate large arterial stiffness in the ovine iliac artery. 40 Similar observations have been made in the human coronary circulation using ultrasound-derived measurement of distensibility, 41 and in the human brachial artery for elasticity, compliance, and PWV. 42 Conversely, drugs that lead to an increase in local NO levels such as glyceryl trinitrate 42 and acetylcholine, 43 reduce arterial stiffness in human muscular arteries.…”

Section: Local Studiessupporting

confidence: 59%

Nitric Oxide and the Regulation of Large Artery Stiffness

2004

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Section: Local Studiessupporting

confidence: 59%

Nitric Oxide and the Regulation of Large Artery Stiffness

2004

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“…We have also shown that in healthy young men, acute administration of E increases the response to ACh in a rapid time frame that suggests a nongenomic mechanism of action (7), an effect also observed in many other settings (4 -6, 8, 9). The mechanisms underlying these nongenomic effects of E on the vasculature are presently uncertain, although there is evidence that receptors located in the endothelial cell plasma membrane, which may be related to the classical estrogen receptors, are involved (19,20), or that E acts either on the vascular endothelium (4,5,9) or directly on vascular smooth muscle cells (10,11,21,22).…”

Section: Discussionmentioning

confidence: 99%

Rapid Potentiation of Endothelium-Dependent Vasodilation by Estradiol in Postmenopausal Women Is Mediated via Cyclooxygenase 2

Calkin

Sudhir

Honisett

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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Estrogens influence cardiovascular function through direct and indirect effects and via genomic and nongenomic mechanisms. The pathways underlying the nongenomic mechanisms are not completely understood. Estrogen-induced responses in vascular cells have been shown to influence prostaglandins and cyclooxygenase (COX), a key enzyme in the production of prostaglandins, with two isoforms, COX-1 and COX-2. We investigated the effects of prostaglandins on the acute potentiation by 17beta-estradiol (E) of acetylcholine (ACh)-mediated vasodilation in the cutaneous vasculature. Using a double-blind placebo-controlled design, we assessed skin blood flow in 32 healthy, postmenopausal women by laser Doppler velocimetry with direct current iontophoresis of ACh and sodium nitroprusside before and after 6-wk treatment periods with aspirin (a nonspecific COX-1 and COX-2 inhibitor), diclofenac (predominantly a COX-2 inhibitor, which also inhibits COX-1), celecoxib (a specific COX-2 inhibitor), given at anti-inflammatory doses, or placebo. Blood flux values before iontophoresis of ACh did not differ between the treatment groups or after E administration, excluding a direct cutaneous vasodilator effect of the treatments or of E. Acute E administration enhanced the response to ACh after aspirin, diclofenac, and placebo; however, this effect was completely abolished with celecoxib treatment (P < 0.05). E had no effect on sodium nitroprusside-mediated vasodilation after any of the treatments. We conclude that the COX-2 pathway plays a specific role in the rapid E-induced potentiation of cholinergic vasodilation in postmenopausal women.

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“…Thus it would be of interest to investigate the extent to which vascular distensibility, as measured by IVUS, is related to vulnerable plaque markers at necropsy examination. Finally, as vascular compliance has been shown to depend on nitric oxide mediated smooth muscle cell relaxation,9 differences in endothelial function between stable and unstable plaques may be reflected in differences in both remodelling and compliance.…”

Section: Discussionmentioning

confidence: 99%

“…Although the trigger mechanisms for these different forms of remodelling in response to plaque accumulation are incompletely understood, alterations in flow dynamics—and in particular shear stress—at the surface of the endothelial cell are thought to play a critical role in plaque formation and vessel response 78 As the ability of the vessel to distend is dependent on intact endothelial function,9 vessel compliance may influence the remodelling pattern. Preliminary data show that eccentric plaques have better remodelling capability,10 which may result from better distensibility and preserved endothelial function 11…”

mentioning

confidence: 99%

Coronary artery compliance and adaptive vessel remodelling in patients with stable and unstable coronary artery disease

Jeremias

2000

Heart

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Objective-To test the hypothesis that patients with unstable coronary syndromes show accentuated compensatory vessel enlargement compared with patients with stable angina, and that this may in part be related to increased coronary artery distensibility. Design and patients-In 23 patients with unstable coronary syndromes (10 with non-Q wave myocardial infarction and 13 with unstable angina), the culprit lesion was investigated by intravascular ultrasound before intervention. The vessel cross sectional area (VA), lumen area (LA), and plaque area (VA minus LA) were measured at end diastole and end systole at the lesion site and at the proximal and distal reference segments. Similar measurements were made in 23 patients with stable angina admitted during the same period and matched for age, sex, and target vessel. Calculations were made of remodelling index (VA at lesion site ÷ VA at reference site), distensibility index ([( A/A)/ P] × 10 3 , where A is the luminal area change in systole and diastole and P the diVerence in systolic and diastolic blood pressure measured at the tip of the guiding catheter during a cardiac cycle), and stiVness index ([ln(P sys /P dias )]/( D/D), where P sys is systolic pressure, P dias is diastolic pressure, and D is the diVerence between systolic and diastolic lumen diameters). Positive remodelling was defined as when the VA at the lesion was > 1.05 times larger than at the proximal reference site, and negative remodelling when the VA at the lesion was < 0.95 of the reference site. Results-Mean (SD) LA at the lesion site was similar in both groups (4.03 (1.8) v 4.01 (1.93) mm 2 ), while plaque area was larger in the unstable group (13.29 (4.04) v 8.34 (3.6) mm 2 , p < 0.001). Remodelling index was greater in the unstable group (1.14 (0.18) v 0.83 (0.15), p < 0.001). Positive remodelling was observed in 15 patients in the unstable group (65%) but in only two (9%) in the stable group (p < 0.001). Negative remodelling occurred only in two patients with unstable symptoms (9%) but in 17 (74%) with stable symptoms. At the proximal reference segment, the diVerence in LA between systole and diastole was 0.99 (0.66) mm 2 in the unstable group and 0.39 (0.3) mm 2 in the stable group (p < 0.001), and the calculated coronary artery distensibility was 3.09 (2.69) and 0.94 (0.83) per mm Hg in unstable and stable patients, respectively (p < 0.001). The stiVness index was lower in patients with unstable angina (1.95 (0.94) v 3.1 (0.96), p < 0.001). Conclusions-Compensatory vessel enlargement occurs to a greater degree in patients with unstable than with stable coronary syndromes, and is associated with increased coronary artery distensibility. (Heart 2000;84:314-319)

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Contribution of endothelium-derived nitric oxide to coronary arterial distensibility: An in vivo two-dimensional intravascular ultrasound study

Cited by 25 publications

References 36 publications

Nitric Oxide and the Regulation of Large Artery Stiffness

Nitric Oxide and the Regulation of Large Artery Stiffness

Rapid Potentiation of Endothelium-Dependent Vasodilation by Estradiol in Postmenopausal Women Is Mediated via Cyclooxygenase 2

Coronary artery compliance and adaptive vessel remodelling in patients with stable and unstable coronary artery disease

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