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Ann Thorac Surg 1999;68:1118-1120
© 1999 The Society of Thoracic Surgeons
a Research Center and Department of Surgery, Montreal Heart Institute, Montreal, Canada
b Hôpital Lariboisiére, Paris, France
c Institut de Recherches Internationales Servier, Paris, France
Address reprint requests to Dr Perrault, Montreal Heart Institute, 5000 Belanger St. E, Montreal, PQ, Canada H1T 1C8;
e-mail: lpperrau{at}icm.umontreal.ca
as originally published in 1996:
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We have previously reported the effects of hemostatic devices on the endothelial function of coronary arteries in a porcine model reproducing the conditions of beating heart coronary artery bypass surgery. These methods included clamping of the coronary artery with bulldog clamps, gas jet insufflation, extravascular balloon occlusion [1], and snaring of the vessel on silicone tubings [2]. These experiments have shown that clamping produces a significant coronary endothelial dysfunction and gas jet insufflation but to a lesser degree, as demonstrated by the impaired endothelium-dependent relaxations to the receptor-operated agonist serotonin while endothelium-independent relaxations were maintained. Extravascular balloon occlusion and snaring caused no significant endothelial dysfunction assessed in organ chamber experiments. Because of the recent development of shunt catheters for perfusion during the construction of the anastomosis on the beating heart, experiments were conducted to determine the effects of these devices on coronary endothelial function in the same model. In brief, under general anesthesia and after median sternotomy, 2-mm experimental silicone perfusion catheters (not available commercially) (n = 6) and a 2.5-mm Anastaflo device (Research Medical Inc, Midvale, UT) (n = 6) matched to the size of the target artery were inserted in vivo through a 3-mm arteriotomy in the left anterior descending artery (Fig 1). The devices were applied for 15 minutes after which they were removed and the hearts were explanted and the coronary arteries dissected out in the standard fashion [1, 2]. Rings in contact with the catheters proximal and distal to the arteriotomy were harvested for the experiments (Fig 2). Coronary rings remote from the arteriotomy sites served as controls.
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(Table 1). There was a significant decrease in endothelium-dependent relaxations to serotonin (10-10 to 10-5 M) in both the perfusion catheter and Anastaflo groups compared with control coronary arteries (Fig 3). There were no significant differences in endothelium-independent relaxations to the exogenous NO donor, Sin-1 (10-5 M, data not shown). These results show that intravascular catheters cause a significant endothelial dysfunction in normal porcine coronary arteries of the same magnitude as the intentional removal of the endothelium by endoluminal rubbing of the intimal surface often used in physiological studies [3]. The fact that contractile function and endothelium-independent relaxations were unaffected by the use of intravascular devices demonstrates the integrity of the underlying smooth muscle cells. Compared with intravascular devices, extravascular techniques create a lesser degree of endothelial functional damage. The effect of intravascular devices on the endothelium may not cause severe untoward consequences in severely atherosclerotic arteries, which are often dysfunctional. However, the unfavorable profile observed should raise caution in surgeons, because intravascular devices and insufflation of gas within the lumen of the coronary artery may favor coronary vasospasm in the acute period after surgery at the site of insertion because of the loss of endothelial coverage. Moreover, the endothelial denudation associated with insertion and removal of the catheters is followed by the regeneration of endothelial cells, which present a selective dysfunction of Gi-protein-mediated relaxations that can lead to a reduced bioavailibility of endothelial nitric oxide and loss of the protective effects of nitric oxide on smooth muscle proliferation and platelet aggregation. With exposure of the basement membrane and collagen fibers, the injured surface becomes a preferential site for platelet aggregation and activation of the coagulation pathway, possibly favoring the development of intimal hyperplasia at the site of endothelial injury, which can lead to premature graft failure [4]. Finally, because most patients who undergo coronary artery bypass surgery probably have a significant endothelial dysfunction of their coronary arteries associated with advanced atherosclerosis [5], additional injury to the endothelium from devices may not contribute to the progression of disease within the vessel wall unless the smooth muscle cell layer is injured. This would explain the satisfactory clinical results in most patients whose coronary arteries are probed during surgery, a procedure we do not recommend using routinely because intimal injury may have severe consequences. Indeed, iatrogenic left main stenosis has been reported after angioplasty or the use of rigid catheters inserted in the coronary ostia during aortic valve replacement secondary to intimal trauma [6]. Nevertheless, further studies are needed to assess the effect of hemostatic devices used in minimally invasive coronary artery bypass surgery or continuous cardioplegia on atherosclerotic arteries with endothelial dysfunction to render this type of physiological evaluation more relevant to the current practice of cardiac surgery.
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), Anastaflo catheter (
), and controls (
). Statistically significant differences between the two preparations from the indicated concentration: **p < 0.001.