Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting.

To investigate whether systemic endothelial function on forearm resistance vessels is related to angiographic restenosis after coronary stenting, 47 men who underwent elective coronary stenting were divided into 2 groups according to the presence (n = 20) or absence (n = 27) of in-stent restenosis 6 months after the procedure. Another 19 risk factor-matched men with normal coronary angiograms served as the control group. Forearm blood flow was assessed by venous occlusive plethysmography. Basal forearm blood flow was similar between restenosis, nonrestenosis, and control groups (2.63 +/- 0.19, 2.58 +/- 0.14, and 3.23 +/- 0.13 ml/100 ml forearm tissue per minute, respectively). In all 3 groups, forearm blood flow increased significantly during reactive hyperemia (5.75 +/- 0.7, 11. 32 +/- 1.23, and 14.52 +/- 1.36 ml/100 ml forearm tissue per minute, p <0.05, respectively) and remained unchanged after sublingual administration of nitroglycerin. The percentage change of forearm blood flow during reactive hyperemia was significantly lower in the restenosis group (117.3 +/- 18.3%) than in the nonrestenosis group (354.2 +/- 46.5%, p <0.01). This difference was still present after sublingual nitroglycerin (37.6 +/- 21.2% vs 226.4 +/- 40.5%, p <0. 01). In contrast, percentage change of hyperemic forearm blood flow was significantly lower in patients with angina (117.5 +/- 49.5%) than in those without angina (290.1 +/- 37.4%, p <0.05) at follow-up. In all patients, the angiographic loss index was correlated negatively to the percentage change of hyperemic forearm blood flow (r = -0.33, p <0.01) and positively to the percentage change of forearm vascular resistance during reactive hyperemia (r = 0.33, p <0.01). In patients with angiographic restenosis after coronary stenting, forearm reactive hyperemia was more impaired compared with those without angiographic restenosis. Systemic endothelial dysfunction might be either a marker or one of the confounding factors in the development of late restenosis after coronary stenting.

[1]  M. Chang,et al.  Early alteration of coronary hemodynamics in late restenosis after coronary angioplasty. , 1999, Japanese heart journal.

[2]  M. Creager,et al.  Hyperhomocyst(e)inemia is associated with impaired endothelium-dependent vasodilation in humans. , 1997, Circulation.

[3]  R Busse,et al.  Nitric oxide attenuates the release of endothelium-derived hyperpolarizing factor. , 1996, Circulation.

[4]  M. Yacoub,et al.  Endothelin-1 stimulates proliferation of human coronary smooth muscle cells via the ET(A) receptor and is co-mitogenic with growth factors. , 1999, Atherosclerosis.

[5]  B Dupuis,et al.  Role of endothelial cells in restenosis after coronary angioplasty , 1996, Fundamental & clinical pharmacology.

[6]  M. Creager,et al.  Endothelial release of nitric oxide contributes to the vasodilator effect of adenosine in humans. , 1995, Circulation.

[7]  A. Sheikhzadeh,et al.  Cardiac release and kinetics of endothelin after uncomplicated percutaneous transluminal coronary angioplasty. , 1998, The American journal of cardiology.

[8]  T. Ogihara,et al.  Converting enzyme inhibitor improves forearm reactive hyperemia in essential hypertension. , 1997, Hypertension.

[9]  T Endo,et al.  Role of nitric oxide in reactive hyperemia in human forearm vessels. , 1994, Circulation.

[10]  M. Kunitomo,et al.  Excessive salt or cholesterol intake alters the balance among endothelium-derived factors released from renal arteries in spontaneously hypertensive rats. , 1999, Journal of cardiovascular pharmacology.

[11]  R. Kernoff,et al.  Local intramural delivery of L-arginine enhances nitric oxide generation and inhibits lesion formation after balloon angioplasty. , 1997, Circulation.

[12]  D. Baim,et al.  Mechanisms of restenosis and redilation within coronary stents--quantitative angiographic assessment. , 1993, Journal of the American College of Cardiology.

[13]  D. Harrison,et al.  Endothelium-dependent vascular relaxation is abnormal in the coronary microcirculation of atherosclerotic primates. , 1990, Circulation.

[14]  A. Sollevi,et al.  The role of myogenic relaxation, adenosine and prostaglandins in human forearm reactive hyperaemia. , 1987, The Journal of physiology.

[15]  C. Pepine,et al.  Circadian variation in coronary tone in patients with stable angina. Protective role of the endothelium. , 1995, Circulation.

[16]  Å. Kilbom,et al.  Endogenous prostaglandins as local regulators of blood flow in man: effect of indomethacin on reactive and functional hyperaemia. , 1976, The Journal of physiology.

[17]  A. Yeung,et al.  Close relation of endothelial function in the human coronary and peripheral circulations. , 1995, Journal of the American College of Cardiology.

[18]  A. Takeshita,et al.  Characteristics of Responses to Salt Loading and Deprivation in Hypertensive Subjects , 1982, Circulation research.

[19]  M. Joyner,et al.  Contribution of nitric oxide and prostaglandins to reactive hyperemia in human forearm. , 1996, Journal of applied physiology.

[20]  A. Yeung,et al.  Flow-induced vasodilation of the human brachial artery is impaired in patients <40 years of age with coronary artery disease. , 1996, The American journal of cardiology.

[21]  M. Muggeo,et al.  Non-invasive detection of early endothelial dysfunction in hypercholesterolaemic subjects. , 1995, Atherosclerosis.

[22]  A. Takeshita,et al.  Limited Maximal Vasodilator Capacity of Forearm Resistance Vessels in Normotensive Young Men with a Familial Predisposition to Hypertension , 1982, Circulation research.

[23]  T. Hedner,et al.  Enhanced acetylcholine and P2Y-receptor stimulated vascular EDHF-dilatation in congestive heart failure. , 1999, Cardiovascular research.

[24]  A. Buda,et al.  Intimal hyperplasia after balloon injury is attenuated by blocking selectins. , 1997, Circulation.

[25]  P. Ganz,et al.  Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans. , 1996, The American journal of physiology.

[26]  K. Kugiyama,et al.  Flow-mediated, endothelium-dependent dilatation of the brachial arteries is impaired in patients with coronary spastic angina. , 1997, American heart journal.

[27]  R. Cohen,et al.  Endothelium-dependent hyperpolarization. Beyond nitric oxide and cyclic GMP. , 1995, Circulation.

[28]  R. Cannon,et al.  Impaired forearm vasodilator reserve in patients with microvascular angina. Evidence of a generalized disorder of vascular function? , 1987, The New England journal of medicine.

[29]  Y. L. Chen,et al.  Electron microscopic studies of phenotypic modulation of smooth muscle cells in coronary arteries of patients with unstable angina pectoris and postangioplasty restenosis. , 1997, Circulation.