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Ann Thorac Surg 1999;67:893
© 1999 The Society of Thoracic Surgeons
a Montreal Heart Institute, Research Center, 5000 Bélanger St E, Montréal, PQ H1T 1C8, Canada
b Hôpital Lariboisière, 2, rue Ambroise Pare, 150 France, 75475 Paris Cedex 10, France
c Institut de Recherches Internationales Servier, Courbevoie, France
To the Editor
We would like to commend the authors [1] of this paper for their elegant study demonstrating the injurious effects of gas insufflation on the coronary endothelium used for minimally invasive coronary artery bypass graft (MIDCAB) procedures or for continuous blood cardioplegia. We support their conclusions in exerting caution with the use of this method for keeping the surgical field dry, as the consequences of the injury may be underestimated or may nor appear until late in the postoperative evolution. We have published in the Annals of Thoracic Surgery papers demonstrating the functional consequences of gas jet insufflation and other devices on a similar model of porcine coronary arteries, which caused a significant decrease in endothelium-dependent relaxations to 5-hydroxytryptamine in coronary arterial segments adjacent to the arteriotomy [2, 3]. This finding was initially surprising to us because the gas jet was directed tangentially at the arteriotomy at a standard flow and distance. A large number of experiments were performed to ensure that the findings were not artifactual. The absence of impairment of endothelium-independent relaxations found in those experiments is in concordance with the findings of Burfeind’s group of a type II injury according to the Ip classification [4], which suggests the absence of injury to the smooth muscle cells. Moreover, the morphologic studies done with silver nitrate staining comparing the effects of bulldog clamps, gas jet insufflation, and an extravascular balloon occluding device on the endothelial coverage showed that only the latter device caused minimal denudation of endothelial cells. Burfeind and colleagues also reported an unpublished observation of endothelial damage by intraluminal shunts and occluders. We have tested the effects of those types of devices on the endothelial reactivity and found profound impairment of endothelium-dependent relaxations with both [5].
The final point concerns the obvious limitation of both their study and ours in which experiments were performed in normal porcine coronary arteries. Although we agree that the normal endothelium probably has a greater protective and recuperative capacity than a dysfunctional one, two issues should be kept in mind. The first is that regenerated endothelium after denudation is dysfunctional as shown by endothelial function studies and affects preferentially the Gi protein-mediated relaxations in the early stages [6]. Second, it is probable that the majority of patients who eventually need coronary artery bypass graft procedures have a significant endothelial dysfunction of their coronary arteries, as do most patients with advanced arteriosclerosis [7]. Thus, it is possible that additional injury to the endothelium from devices may not further adversely affect the progression of disease in the blood vessel wall unless the layer of smooth muscle cells is injured. This would explain the lack of detrimental effects or adverse results in patients in whom coronary arteries are routinely probed for the sake of measurement and evaluation of the outflow during coronary artery bypass graft operations, which we do not recommend. Notwithstanding, the need for studies evaluating the consequences of the various devices and techniques used for control of the target coronary arteries during MIDCAB or continuous cardioplegia on arteriosclerotic arteries with endothelial dysfunction remains.
References
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