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Updated: Jul 19, 2026

Surgical Swine Model of Chronic Cardiac Ischemia Treated by Off-Pump Coronary Artery Bypass Graft Surgery
Published on: March 27, 2018
Coronary vasodilatory capacity and flow reserve in normal myocardium supplied by bypass grafts late after surgery
R Campisi1, J Czernin, H L Karpman
1Department of Molecular and Medical Pharmacology, UCLA School of Medicine, University of California, Los Angeles 90095-6948, USA.
Insights
Coronary artery bypass surgery patients show reduced myocardial flow reserve years later, regardless of graft type. This suggests non-obstructive changes, not graft blockages, impact blood flow in bypass patients.
Area of Science:
- Cardiovascular Surgery
- Nuclear Cardiology
- Myocardial Perfusion Imaging
Background:
- Coronary artery bypass surgery (CABS) is a primary treatment for myocardial ischemia.
- Long-term evaluation of myocardial blood flow and flow reserve in normally perfused areas after CABS is limited.
- Comparative analysis of vasodilation responses in arterial versus venous bypass conduits is not well-established.
Purpose of the Study:
- To assess myocardial blood flow and flow reserve in normally perfused myocardium late after CABS.
- To compare pharmacologic vasodilation responses between arterial and venous bypass grafts.
Main Methods:
- Positron emission tomography (PET) with N-13 ammonia was used to quantify myocardial blood flow.
- Measurements were taken at rest and during dipyridamole-induced hyperemia.
- 15 patients 9 years post-CABS and 10 healthy volunteers were studied.
Main Results:
- Resting myocardial blood flow was similar between CABS patients and controls, and across saphenous vein and internal mammary artery grafts.
- Hyperemic myocardial blood flow and flow reserve were significantly lower in CABS patients compared to controls (p <0.005 and p <0.02, respectively).
- No significant difference in hyperemic response or flow reserve was observed between arterial and venous grafts.
Conclusions:
- Myocardium supplied by bypass grafts exhibits reduced vasodilatory capacity years after surgery, irrespective of conduit type.
- Findings suggest non-obstructive intimal changes in grafts or native vessel disease, rather than flow-limiting stenoses, are responsible.
- PET imaging demonstrates impaired myocardial flow reserve in bypass patients, highlighting potential long-term functional changes.
Abstract:
Coronary artery bypass surgery is used widely for treating myocardial ischemia. However, blood flow and flow reserve of normally perfused myocardium subtended by bypass grafts have not been evaluated late after surgery. Also, it is unknown whether pharmacologic vasodilation evokes comparable myocardial flow responses in arterial and venous conduits. Myocardial blood flow was quantified at rest and during dipyridamole hyperemia using N-13 ammonia and positron emission tomography (PET) in 15 patients 9 +/- 3 years after bypass surgery and in 10 healthy volunteers. Blood flow was analyzed in 26 territories subtended by bypass grafts with normal wall motion and normal perfusion. Myocardial blood flow at rest did not differ between patients and controls (0.65 +/- 0.14 vs 0.68 +/- 0.16 ml/ g/min) and was similar in normal myocardium subtended by saphenous vein (n = 16) and internal mammary artery grafts (n = 10; 0.64 +/- 0.13 vs 0.66 +/- 0.15 ml/g/min). However, the hyperemic response in normal myocardium supplied by bypass grafts was less than that in controls (1.61 +/- 0.33 vs 2.04 +/- 0.30 ml/g/min, p <0.005). No differences between territories supplied by venous and arterial conduits were observed (1.61 +/- 0.35 vs 1.63 +/- 0.32 ml/g/min). Normal myocardium subtended by bypass grafts exhibited a lower flow reserve than that in controls (2.54 +/- 0.51 vs 3.16 +/- 0.85, p <0.02). Myocardial flow reserve was almost identical in regions supplied by venous and arterial grafts (2.55 +/- 0.48 vs 2.52 +/- 0.58). The similar reduction in vasodilatory capacity together with the normal PET polar map findings during dipyridamole argue against flow limiting stenoses in both venous and arterial bypass conduits late after revascularization. Rather, nonobstructive proliferative fibrointimal changes of the bypass conduits or atherosclerosis of the native resistance vessels might account for this finding.
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