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Ann Thorac Surg 2000;70:341-342
© 2000 The Society of Thoracic Surgeons
a Departments of Cardiothoracic Surgery and Anaesthesia, Royal Melbourne Hospital, PO Box 2135, Parkville, Victoria, Australia 3050
e-mail: alistair.royse{at}nwhcn.org.au
To the Editor
We thank Dr Wendler and colleagues for their letter regarding our paper [1] and also their own recent publication [2].
Conduit flow is dependent on several factors including the resistance of the conduit and coronary vascular bed (including variable flow from the native coronary circulation), metabolic demand of the myocardium, the systemic blood pressure and size of the patient. Our patients varied considerably in size with body surface area (BSA) mean ± SE (range) of 1.85 ± 0.03 (1.67–2.17)m2. Flows indexed to BSA were also reported.
We do not hydrostatically vasodilate conduits as per Mills [3], where the conduit may be dilated more than is possible by pharmacological relaxation of the arterial smooth muscle. A hydrostatically dilated left internal mammary artery (LIMA) may return to normal size and flow within a short period of time. It is possible that our method of intraluminal vasodilation resulted in a lesser degree and perhaps more variable vasodilation than Wendler and colleagues [2]. Our concentration of papaverine (1 mg/mL) may have been less effective at vasodilating the conduits than that used by Dr Wendler (2.5 mg/mL). No macroscopic vasospasm was present in any of the conduits. All measurements against no resistance (free-flow) [1] were performed sequentially within a 2 minute period after construction of the Y graft [4]. The elevated flow of the composite conduit relates entirely to the reduced resistance of two conduits in parallel compared to one.
Transit-time Doppler was validated in our study by simultaneous collection of blood from the conduits and was accurate. Consequently, the flows reported were accurate [1]. Our study accurately measures conduit flow reserve (CFR) since the initial conduit flow was recorded when there was no resistance (bleeding freely from the conduit). All postoperative studies injecting adenosine or other agents lower resistance of the coronary vasculature (but not to zero). Therefore all postoperative studies will underestimate the true CFR. Consequently, we would argue that intraoperative assessment of CFR is possibly more valid.
The flow measurement after completion of grafting, was performed approximately 5 minutes after the release of the conduit clamp, but before removal of the aortic clamp (ie no native coronary flow). This period allowed myocardial reperfusion, tying of the final anastomosis and tacking of the conduit to the heart. During grafting we administer 500 ml of blood cardioplegia every 7–14 minutes. By the time of measurement we would expect most, if not all, of the oxygen debt to be repaid and so would not expect significant hyperemic coronary vasodilation during this recording. The metabolic demand of the reperfused quiescent heart may be less than the beating, ejecting heart, with reduced blood flow requirements. Native coronary flow is abolished in the presence of an applied aortic clamp and re–established upon its release.
Prior studies have documented LIMA to left anterior descending graft flows of 33–42 mL/min [1]. We argue that composite conduit flow to the whole heart after bypass of 82 ± 13 mL/min is consistent with these prior studies and slightly more than the baseline flow recorded by Wendler and colleagues [2] at 1 and 6 months postoperatively. Baseline and maximal conduit flows for both series were similar.
These two studies [1, 2] were conducted at different time frames using different methods and are therefore not directly comparable. Nevertheless, finding that CFR exceeded actual conduit flow to all three coronary territories by a factor of approximately 2 or more should satisfy most surgeons of the adequacy of composite arterial conduit based on the LIMA.
References
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