Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.

Fischell, Tim A.; Bausback, Kurt N.; McDonald, Thomas V.

doi:10.1172/jci114747

Cited by 61 publications

(17 citation statements)

References 36 publications

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“…Vasoconstrictive responses after balloon angioplasty have been reported [33] and attributed either to altered coronary artery autoregulation [34], or local effects of platelet-derived vasoactive substances such as serotonin [35]. However, these changes in vascular tone distal to the site of angioplasty disappear usually within the first days after intervention and are unlikely to persist up to 6 months after intervention.…”

Section: Vascular Dysfunction After Drug-eluting Stent Implantationmentioning

confidence: 99%

Local vascular dysfunction after coronary paclitaxel-eluting stent implantation

Togni¹,

Räber²,

Cocchia³

et al. 2007

International Journal of Cardiology

101

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Section: Vascular Dysfunction After Drug-eluting Stent Implantationmentioning

confidence: 99%

Local vascular dysfunction after coronary paclitaxel-eluting stent implantation

Togni¹,

Räber²,

Cocchia³

et al. 2007

International Journal of Cardiology

101

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“…A series of recent studies has related epicardial coronary vasoconstriction that has been reported early after PTCA 46,47 to ␣-adrenergic activation. 48 -52 Gregorini et al 48 observed a constrictor response not only of the culprit segment and a distal segment of the vessel that underwent PTCA but also of the nonmanipulated control vessel.…”

Section: ␣-Adrenergic Coronary Vasoconstriction During Interventionsmentioning

confidence: 99%

α-Adrenergic Coronary Vasoconstriction and Myocardial Ischemia in Humans

et al. 2000

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Abstract-The use of quantitative coronary angiography, combined with Doppler and PET, has recently been directed at the study of ␣-adrenergic coronary vasomotion in humans. Confirming prior animal experiments, there is no evidence of ␣-adrenergic coronary constrictor tone at rest. Again confirming prior experiments, responses to ␣-adrenoceptor activation are augmented in the presence of coronary endothelial dysfunction and atherosclerosis, involving both ␣ 1 -and ␣ 2 -adrenoceptors in epicardial conduit arteries and microvessels. Such augmented ␣-adrenergic coronary constriction is observed during exercise and coronary interventions, and it is powerful enough to induce myocardial ischemia and limit myocardial function. Recent studies indicate a genetic determination of ␣ 2 -adrenergic coronary constriction. (Circulation. 2000;101:689-694.)Key Words: coronary disease Ⅲ ischemia Ⅲ microcirculation Ⅲ nervous system Ⅲ receptors, adrenergic, alpha U nder normal circumstances, small coronary arteries and arterioles with a diameter of Ͻ300 m are the principal determinants of coronary vascular resistance. 1 These vessels receive autonomic innervation, and their diameter is altered by activation of these nerves. 2 In animal experiments, there is little ␣-adrenergic coronary vasomotor tone at rest, and the increase in coronary blood flow during sympathetic activation is only somewhat blunted. When the coronary circulation, however, is impaired by hypercholesterolemia, 3 endothelial dysfunction, 4 exhaustion of autoregulation, 5 or severe coronary stenosis, 6,7 ␣-adrenergic vasoconstriction becomes unrestrained and powerful enough to reduce coronary blood flow and initiate myocardial ischemia. 8 Both ␣ 1 -and ␣ 2 -adrenoceptors mediate coronary vasoconstriction, and there is a gradient with ␣ 1 -adrenoceptors more predominant in larger vessels and a reverse gradient with ␣ 2 -adrenoceptors more predominant in the microcirculation. 5,9 Surprisingly, isolated coronary arterioles of a size that constricts in vivo to ␣ 1 -adrenoceptor activation are unresponsive in vitro, 10 and cardiomyocytes on ␣ 1 -adrenergic activation release endothelin, which causes arteriolar constriction. 11 In the past, the study of ␣-adrenergic coronary vasoconstriction in humans has been limited by a lack of adequate techniques to quantify coronary blood flow and myocardial perfusion. In the last decade, quantitative coronary angiography has allowed quantification of the diameter of coronary arteries to Ϸ0.5 mm. Study of the human coronary microcirculation is indirect 12 and relies on parameters such as coronary flow velocity, measured invasively with Doppler flow probes, or myocardial blood flow, quantified noninvasively with PET. 13 Recently, these techniques have become widely available and directed toward the study of ␣-adrenergic coronary vasoconstriction in humans. Moreover, selective ␣ 1 -and ␣ 2 -agonists and -antagonists are now available for clinical use. The antagonist approach is used to study the endogenous ␣-adrenergic coronary vasocon...

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“…These findings are in accordance with other studies that demonstrated an impaired coronary flow reserve immediately after balloon angioplasty, compared with normal values of the control group, due to an increased baseline coronary blood flow. 10,16 Several mechanisms have been postulated for the observed increase in baseline flow velocity after PTCA, such as (1) failure of the peripheral arterial vascular bed to vasoconstrict appropriately on the sudden increase in distal coronary pressure produced by coronary angioplasty, (2) epicardial vasoconstriction at the site of the Doppler guidewire tip mediated by a myogenic response and/or neural mechanisms, 17,18 or (3) the influence of drug therapy. 19,20 However, all patients were treated with nitroglycerin during the procedure, and there was no difference in drug therapy (nitrates, calcium antagonists, ␤-blockers, or ACE inhibitors) between patients with and without impaired CFR after PTCA.…”

Section: 6mentioning

confidence: 99%

Immediate and Long-Term Effect of Balloon Angioplasty or Stent Implantation on the Absolute and Relative Coronary Blood Flow Velocity Reserve

et al. 1998

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Background-There is controversy regarding the immediate and long-term effects of PTCA on the coronary flow reserve. Methods and Results-A total of 54 patients with 1-vessel disease and normal left ventricular function were studied after balloon angioplasty (nϭ34) or stent implantation (nϭ20). Distal coronary blood flow velocity reserve (CFR) was defined as the ratio of adenosine-induced hyperemic versus baseline blood flow velocity with a 0.014-in Doppler guidewire. The relative CFR was defined as the ratio of the distal CFR and the reference CFR measured in the normal adjacent coronary artery. Hemodynamic and angiographic measurements were performed before and directly after balloon angioplasty or stent implantation and at 6-month follow-up. CFR after PTCA Յ2.5 was defined as an impaired CFR. Immediately after PTCA, CFR improved toward the range of the reference artery CFR. In both the balloon-treated and the stent-treated groups, initial high CFR values decreased and impaired CFR values increased at follow-up toward the values of the reference CFR in patients without restenosis. Impaired CFR after balloon angioplasty (33%) or stent implantation (58%) in patients without restenosis was related to an increased baseline flow velocity that normalized at follow-up. Patients with an increase of CFR after stenting were characterized by an unaltered baseline flow velocity and an increased adenosine-induced hyperemic flow velocity. Conclusions-An impaired CFR (Յ2.5) is a frequent finding after balloon angioplasty or stent implantation as a result of a high baseline flow velocity. Normalization of impaired CFR at follow-up in patients without restenosis was associated with a decline of the baseline flow velocity after both balloon angioplasty and stent implantation, supporting the contention that this phenomenon relates to a slow recovery of autoregulation of the microvascular bed. (Circulation. 1998;98:2133-2140.)Key Words: angioplasty Ⅲ stents Ⅲ blood flow I n a classic study, Gould et al 1 introduced the curvilinear relationship between coronary lesion severity and flow reserve distal to the narrowing. Subsequently, several clinical studies evaluated this relationship in the setting of coronary angioplasty using digital subtraction techniques, 2 intracoronary blood flow velocity and pressure measurements, 3,4 or PET.5 A recently published large, multicenter trial (DEBATE study) demonstrated that impaired coronary flow reserve (Յ2.5) immediately after balloon angioplasty was associated with a high incidence of recurrent angina, need for revascularization procedures, and a high restenosis rate. 6 The hypothesis that impaired coronary flow reserve after balloon angioplasty is due to residual lumen obstruction was supported by studies showing a normalization of impaired coronary flow reserve after optimal vascular lumen enlargement by stent implantation. 7,8 However, other studies demonstrated a spontaneous improvement of impaired coronary flow reserve after balloon angioplasty without adjunctive coronary intervention du...

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Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.

Cited by 61 publications

References 36 publications

Local vascular dysfunction after coronary paclitaxel-eluting stent implantation

Local vascular dysfunction after coronary paclitaxel-eluting stent implantation

α-Adrenergic Coronary Vasoconstriction and Myocardial Ischemia in Humans

Immediate and Long-Term Effect of Balloon Angioplasty or Stent Implantation on the Absolute and Relative Coronary Blood Flow Velocity Reserve

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