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Cardiac Surgery Unit, Magna Graecia University, Viale Europa Localitá Germaneto, Catanzaro, 88100 Italy
(Email: frankono{at}libero.it).
We would like to thank Foroughi and colleagues [1] for their discussion and stimulating comments.
We agree that more focused evaluation between pedicled or skeletonized left internal mammary artery (LIMA) grafts should be related to endpoints that directly refer to the conduit itself or to the downstream myocardium. Anterolateral myocardial kinetics reflect LIMA to left anterior descending coronary artery (LAD) function. Perioperative troponins relate to both the effectiveness of myocardial revascularization and the quality of myocardial protection. However, when hospital outcomes are considered enzymatic leakage, myocardial functional recovery and the incidence of perioperative acute myocardial infarction (AMI) must be considered. Moreover, collateral circulation in patients undergoing three-vessel revascularization [2] may mask graft malfunction in the territory supplied by the graft. The potential for remote perioperative AMI exists in patients with LIMA to LAD graft failure and a well-developed collateral circulation [2]. However, when wall motion score indices (WMSI) were calculated for the nine segments nourished by the LAD, our postoperative echocardiographic results were comparable between the two groups:
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It is not possible to discriminate how much troponin is released from each ventricular segment. Malfunctioning or nonfunctioning grafts, however, correlate with an acute troponin rise [3]. Therefore, troponin values below the cut-off level for perioperative AMI exclude myocardial ischemia in the anterolateral segments.
The goal of our study was to evaluate intraoperative functional behavior of pedicled versus skeletonized LIMAs. We completely agree that endothelial damage during harvesting has a significant impact on short-term and long-term graft patency [4]. Neither intraoperative pulsation nor free-flow excludes the risk of postoperative graft malfunction [1, 5]. We think the most important advantage of transit-time flowmetry (TTF) analysis is the potential to objectively investigate graft function and detect early graft dysfunction, even if digital pulsation or preoperative free-flows are satisfactory. It is common knowledge that unsatisfactory TTF results occur with apparent "good pulsation" or good preoperative free-flow [5], or both. We assess TTF results about 30 minutes after protamine administration (in a "pro-thrombotic state") when endothelial damage or other types of lesions affecting graft function can be ruled out. This practice may be responsible for the predictive value of TTF on angiographic "mid-term" follow-up [6].
Endothelial damage is responsible for impaired nitric oxide induced vasodilation [4]; vessel caliber is a well-known determinant of flow [7]. Other factors, such as progression of atherosclerosis, risk-factors, comorbidities, and so forth determine long-term graft patency. Therefore to attribute graft patency to a single surgical variable, such as the harvesting technique may be a mistake. Moreover, when LIMA graft function is considered, previous reports are biased by intraluminal injection of papaverine; a limited number of enrolled patients; isolated free-flow evaluation; absence of evaluation of graft functional reserve; absence of stratification according to the type of conduit; and the quality of the coronary bed and the type of grafted vessel [8]. For example, the importance of the target vessel on TTF evaluation is clearly defined [7].
As already reported [8], surgeons are assured of satisfactory revascularization when the diastolic flow pattern, together with high maximum, mean, minimum flows, and low pulsatility index (PI) (< 4) are found [5, 6, 8]. Accordingly, low flows (especially in cases of chronic occluded coronaries or severely diseased coronary beds) with preserved diastolic pattern and PI, do not mandate graft revision. Intraoperative recruitment of graft flow reserve (GFR) by intra-aortic balloon pump similarly demonstrates the potential for coronary flow augmentation. Therefore, we consider safe a GFR to be greater than 1.5.
In conclusion, it is our institutional practice to revise any graft in which unexpected or unexplained TTF findings are encountered, or in which GFR was not recruited [5, 6, 8].
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