Does coronary flow reserve assessed by blood flow velocity analysis reflect absolute coronary flow reserve?

Takeuchi, Masaaki; Nohtomi, Yuichi; Kuroiwa, Akio

doi:10.1002/(sici)1097-0304(199607)38:3<251::aid-ccd6>3.0.co;2-7

Cited by 11 publications

(10 citation statements)

References 16 publications

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“…Coronary blood flow was calculated from the coronary blood flow velocity and the coronary artery diameter,22 using the formula: coronary blood flow (CBF, ml/min) = (πD 2 )/4 × PVi × HR…”

Section: Methodsmentioning

confidence: 99%

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Endogenous endothelin maintains coronary artery tone by endothelin type A receptor stimulation in patients undergoing coronary arteriography

Kyriakides

Kremastinos

Bofilis

et al. 2000

Heart

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Objective-To examine the contribution of endothelin type A (ET A ) receptor stimulation by endogenously generated endothelin-1 (ET-1) to the maintenance of coronary vascular tone in humans. Design-Controlled clinical study. Setting-Tertiary cardiovascular referral centre. Patients-14 subjects were studied, seven with normal coronary arteries and seven with coronary artery disease, mean (SEM) age, 53 (2) years. Interventions-After diagnostic coronary arteriography, BQ-123 (a selective ET A receptor antagonist; 100 nmol/min) in 0.9% saline, was infused into the left coronary artery at a rate of 1 ml/min for 60 minutes. Eight control subjects received saline alone. Main outcome measures-Blood flow velocity in the left anterior descending coronary artery, measured using a Doppler flow guidewire; coronary arteriography performed at baseline and immediately at the end of the BQ-123 or saline infusion to measure the diameter of proximal and distal left anterior descending coronary artery segments. Results-The diameter of the proximal segment increased by 6 (2)%, while that of the distal segment increased by 12 (3)% after BQ-123 (both p < 0.05 v baseline). Coronary blood flow increased from 75 (10) to 92 (10) ml/min and coronary vascular resistance decreased from 1.99 (0.36) to 1.44 (0.22) mm Hg/ml/min after BQ-123 (both p < 0.05 v baseline). The response to BQ-123 of patients with and without coronary artery disease was similar. There was no eVect of saline in the controls. Conclusions-Endogenously produced ET-1 contributes to the maintenance of basal coronary artery tone in humans by ET A receptor stimulation. The role of ET B receptors remains to be defined. (Heart 2000;84:176-182) Keywords: endothelins; arteries; blood flow; coronary circulation; angiographyThe endothelins are a family of 21 amino acid peptides with potent and characteristically sustained vasoconstrictor and vasopressor actions.1 Endothelin-1 (ET-1) is the predominant isopeptide generated by the vascular endothelium.2 ET-1 binds to at least two receptors. The ET A receptor appears to be the major one, causing vasoconstriction in arteries, while the ET B receptor mediates the release of endothelium dependent vasodilator substances and is also present in some resistance and capacitance arteries, where it can contribute to vasoconstriction.3 ET-1 may play a role in the pathophysiology of several conditions associated with vasoconstriction, including chronic heart failure, hypertension, Raynaud's disease, and renal failure.3 4 Recently described inhibitors of endothelin converting enzyme and endothelin receptor antagonists may therefore have therapeutic potential as vasodilator drugs in these conditions. Endogenous production of ET-1 contributes importantly to the maintenance of basal peripheral vascular tone 5 and blood pressure 6 in healthy volunteers, mainly through an eVect on ET A receptors. In contrast, the main eVect of endogenous ET-1 on ET B receptors in resistance arteries appears to be vasodilatation. ET-1 constricts human epicardi...

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“…Coronary blood flow was calculated from the coronary blood flow velocity and the coronary artery diameter,22 using the formula: coronary blood flow (CBF, ml/min) = (πD 2 )/4 × PVi × HR…”

Section: Methodsmentioning

confidence: 99%

“…Coronary vascular resistance was calculated from the mean arterial pressure (MAP, mm Hg), and coronary blood flow using the formula22: coronary vascular resistance (CVR, mm Hg/ml/min) = MAP/CBF…”

Section: Methodsmentioning

confidence: 99%

Endogenous endothelin maintains coronary artery tone by endothelin type A receptor stimulation in patients undergoing coronary arteriography

Kyriakides

Kremastinos

Bofilis

et al. 2000

Heart

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“…To obtain the maximal LAD flow velocity for the evaluation of coronary flow reserve (17)(18)(19), 8 mg of papaverine (Papaverine HCl; Dainippon Pharmaceutical. Co., Ltd., Osaka, Japan) was injected into the left coronary artery as a bolus of 10 ml saline solution for 1 min, and the maximal LAD flow velocity was measured (20)(21)(22).…”

Section: Study Protocolmentioning

confidence: 99%

Effects of Nicardipine on Coronary, Vertebral and Renal Arterial Flows in Patients with Essential Hypertension.

et al. 2003

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used rather than diuretics or β blockers. The acute effects of blood pressure reduction by DPCs on the blood flows in target organs, i.e., the coronary, vertebral and renal artery blood flows in hypertensive patients, have not been well studied.In the present study we measured hemodynamic variables and coronary, vertebral and renal blood flow velocity using a Doppler guidewire and evaluated the acute effect of nicardipine infusion on hemodynamics and on coronary, vertebral and renal artery flows in patients with essential hypertension.

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“…Based on the assumption of a good correlation between coronary reserve derived from absolute flow and that derived from flow velocity, 35 coronary flow velocity was used instead of indirectly calculated coronary blood flow. The underestimation of coronary reserve that might have resulted seems of little magnitude, since major coronary arteries make only a minor contribution to coronary resistance.…”

Section: Study Limitationsmentioning

confidence: 99%

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

Frimm¹,

Pereira²,

Rodrigues

et al. 2005

Clinical Cardiology

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SummaryBackground: The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively.Hypothesis: Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).Methods: Fractional shortening (%) and end-systolic stress (10 3 ·dyn·cm Ϫ2 ) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/ stress (cm 2 ·dyn Ϫ1 ) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening ≥ 30), HTN2 (19 patients, 20 ≤ fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted.Results: Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 ± 16, HTN1 = 72 ± 23, HTN2 = 143 ± 32, HTN3 = 186 ± 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 ± 0.6, HTN1 = 3.4 ± 1.0, HTN2 = 3.1 ± 1.0, HTN3 = 2.6 ± 1.1), but coronary reserve/stress was reduced in both

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Does coronary flow reserve assessed by blood flow velocity analysis reflect absolute coronary flow reserve?

Cited by 11 publications

References 16 publications

Endogenous endothelin maintains coronary artery tone by endothelin type A receptor stimulation in patients undergoing coronary arteriography

Endogenous endothelin maintains coronary artery tone by endothelin type A receptor stimulation in patients undergoing coronary arteriography

Effects of Nicardipine on Coronary, Vertebral and Renal Arterial Flows in Patients with Essential Hypertension.

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

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