Alteration in regulation of myocardial blood flow in one-vessel coronary artery disease determined by positron emission tomography

Sambuceti, Gianmario; Parodi, Oberdan; Marcassa, Claudio; Neglia, Danilo; Salvadori, Piero A.; Giorgetti, Alejandro; Bellina, Riccardo; Sacco, Sonia Di; Nista, N; Marzullo, Paolo; Testa, Roberto; LʼAbbate, Antonio

doi:10.1016/0002-9149(93)90348-g

Cited by 67 publications

(15 citation statements)

References 27 publications

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“…Nevertheless, CFR remained significantly lower in remote segments than in controls after L-NMMA. This is in line with previous observations in CAD patients reporting an impaired hyperemic response in remote territories supplied by an angiographically normal coronary artery (5,23).…”

Section: Discussionsupporting

confidence: 93%

Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses

Kaufmann

Rimoldi

Gnecchi‐Ruscone

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Kaufmann PA, Rimoldi OE, Gnecchi-Ruscone T, Luscher TF, Camici PG. Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses. Am J Physiol Heart Circ Physiol 293: H2178-H2182, 2007. First published July 27, 2007; doi:10.1152/ajpheart.01292.2006.-We studied the impact of systemic infusion of the nitric oxide synthase (NOS) inhibitor N G -monomethyl-L-arginine (L-NMMA) on coronary flow reserve (CFR) in patients with coronary artery disease (CAD). We have previously demonstrated that CFR to adenosine was significantly increased after systemic infusion of L-NMMA in normal volunteers but not in recently transplanted denervated hearts. At baseline, myocardial blood flow (MBF; ml ⅐ min Ϫ1 ⅐ g Ϫ1 ) was measured at rest and during intravenous administration of adenosine (140 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ) in 10 controls (47 Ϯ 5 yr) and 10 CAD patients (58 Ϯ 8 yr; P Ͻ 0.01 vs. controls) using positron emission tomography and 15 O-labeled water. Both MBF measurements were repeated during intravenous infusion of 10 mg/kg L-NMMA. CFR was calculated as the ratio of MBF during adenosine to MBF at rest. CFR was significantly higher in healthy volunteers than in CAD patients and increased significantly after L-NMMA in controls (4.00 Ϯ 1.10 to 6.15 Ϯ 1.35; P Ͻ 0.0001) and in patients, both in territories subtended by stenotic coronary arteries (Ͼ70% luminal diameter; 2.06 Ϯ 1.13 to 3.21 Ϯ 1.07; P Ͻ 0.01) and in remote segments (3.20 Ϯ 1.23 to 3.92 Ϯ 1.62; P Ͻ 0.05). In conclusion, CFR can be significantly increased in CAD by a systemic infusion of L-NMMA. Similarly to our previous findings in normal volunteers, this suggests that adenosine-induced hyperemia in CAD patients is constrained by a mechanism that can be relieved by systemic NOS inhibition with L-NMMA. coronary circulation; autonomic nervous system; ischemic heart disease; cardiac imaging; positron emission tomography IT IS WELL ESTABLISHED THAT myocardial ischemia is a powerful stimulus for vasodilatation of coronary resistive vessels. The vasodilator response is reported to be near maximal for ischemic times of up to 15-20 s, while no further changes are observed for longer ischemic times (16).Experimental studies in animals have proven that intracoronary or intravenous infusion of adenosine achieves a degree of coronary vasodilatation comparable to that obtained after a period of ischemia of 15-20 s. In normal humans, intravenous infusion of 140 g/kg adenosine produces an increase in myocardial blood flow (MBF) approximately fourfold above the resting value with no further increase at higher adenosine doses (12,29).In a recent study in normal volunteers (15), we demonstrated that hyperemic MBF measured during the combined intravenous infusion of adenosine (140 g/kg) and the nitric oxide synthase (NOS) inhibitor N G -monomethyl-L-arginine (L-NMMA; 10 mg/ kg) was 53% higher than that during infusion of adenosine alone. This effect seems to necessitate an intact cardiac innervation, since no increase in MBF during ...

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Section: Discussionsupporting

confidence: 93%

Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses

Kaufmann

Rimoldi

Gnecchi‐Ruscone

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…40,41 A similar finding in transplant patients is not unexpected. A functional abnormality in the resistance bed and an absolute decline in microvascular cross-sectional area are 2 possible explanations.…”

Section: Sources Of Variability Of Cfrsupporting

confidence: 70%

Heterogeneity of Coronary Flow Reserve in the Examination of Multiple Individual Allograft Coronary Arteries

et al. 1999

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Background-Epicardial and resistance vessel function in the transplanted heart has been evaluated primarily in regions supplied by a single vessel. Heterogeneity of flow among multiple perfusion fields as a marker of early endothelial dysfunction in the microcirculation has not been evaluated previously. This study tested the hypothesis that increased variability of coronary flow reserve (CFR) among multiple vascular regions would be associated with allograft coronary vasculopathy. Methods and Results-One hundred six posttransplant patients undergoing cardiac catheterization had measurement of CFR in at least 3 major epicardial vessels. Patients were divided into those with minimal angiographic abnormalities (nϭ37) and those with no angiographic abnormalities (nϭ69). The ranges, coefficients of variation, and univariate and multivariate regression analyses of CFR were computed to determine the major clinical factors influencing the degree of variability.

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“…[2][3][4][5][6][7][8][9] We used a canine model of LAD stenosis that slightly reduced resting epicardial LAD flow but did not affect LAD bed microsphere flow so that ischemia was not present. We evaluated LCx coronary flow reserve with and without concurrent LAD stenosis using an adenosine A 2A receptorspecific agonist 23 ; thus, hypotension, which might confound the measurement of flow reserve, was avoided.…”

Section: Discussionmentioning

confidence: 99%

“…1 In addition to the effects of a stenosis on flow reserve within its own bed, coronary stenosis and occlusion also decrease flow reserve in adjacent nonstenotic beds in both experimental animal models and clinical populations. [2][3][4][5][6][7][8][9] …”

mentioning

confidence: 99%

Effect of Coronary Stenosis on Adjacent Bed Flow Reserve

Pacella

Villanueva

2006

Circulation

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Background-During coronary stenosis, flow reserve in the adjacent nonstenotic bed decreases, but the microvascular mechanisms are unknown. Because myocardial contrast echocardiography (MCE) assesses microvascular physiology, we used it to relate flow reserve to intramyocardial blood volume in the adjacent bed. Methods and Results-A noncritical left anterior descending (LAD) stenosis was created in 10 dogs. MCE was performed and myocardial blood flow was measured with neutron-activated microspheres and flow probes. Data were collected at baseline, hyperemia, and hyperemia and stenosis. Hyperemia was induced with an A 2A receptor agonist. MCE acoustic intensity in the LAD and left circumflex (LCx) regions were fit to the following: yϭA(1-e Ϫ␤t ), where A, ␤, and Aϫ␤ reflect intramyocardial blood volume, red cell velocity, and flow, respectively. During hyperemia alone, LCx probe and microsphere flows and MCE-derived red cell velocity increased from baseline (30Ϯ14 versus 125Ϯ62 mL/min, PϽ0.0005; 1.5Ϯ0.5 versus 6.6Ϯ2.0 mL · min Ϫ1 · g Ϫ1 , PϽ0.0005; and 0.53Ϯ0.14 versus 0.96Ϯ0.45 second

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Alteration in regulation of myocardial blood flow in one-vessel coronary artery disease determined by positron emission tomography

Cited by 67 publications

References 27 publications

Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses

Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses

Heterogeneity of Coronary Flow Reserve in the Examination of Multiple Individual Allograft Coronary Arteries

Effect of Coronary Stenosis on Adjacent Bed Flow Reserve

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