Myocardial Glucose Metabolism Assessed by Positron Emission Tomography and the Histopathologic Findings of Microvessels in Syndrome X

Abstract

Background Syndrome X has been recognized as a disease that is primarily reflected in the cardiac microvasculature. Myocardial metabolism in this condition has been studied, but not in relation to small vessel pathology. Methods and ResultsIn order to examine the relationship between myocardial metabolism and small vessel pathology, 24 consecutive patients with syndrome X (7 men, 17 women; mean age 58 years) were evaluated by the thallium exercise stress test, positron emission tomography using F-18 fluoro-deoxyglucose (FDG), and an endomyocardial biopsy. All patients showed either diffuse or focal increase in the myocardial uptake of FDG, but only 17 patients (71%) showed hypoperfused areas with partial or complete redistribution in the thallium study. Quantification of myocardial FDG uptake revealed that the value in syndrome X patients was 10-fold higher than in controls (p<0.0001). Histopathological examination revealed that in syndrome X there is an extensive increase in smooth muscle cells and thickening of the vascular wall, even in capillary vessels, and the small vessel lumen was markedly narrowed. There was a significant inverse correlation between FDG myocardial uptake and the microvessel luminal area. Conclusions In syndrome X patients, myocardial FDG uptake is increased extensively, which is strongly associated with narrowed myocardial microvasculature. (Circ J 2004; 68: 220 -226)

Coronary microvascular dysfunction in women: an overview of diagnostic strategies

“…Further insight into the pathophysiology of CMD was provided by Satake et al ., who noted increased myocardial 18 F fluoro-deoxyglucose (FDG) uptake in 24 subjects (17 women) with CMD undergoing FDG PET as compared to 11 controls [56]. Endomyocardial biopsy in these subjects revealed significant increase in smooth muscle cells and thickening of the vascular wall, even in capillary vessels and the small vessel lumen was markedly narrowed.…”

Are Low Total Serum Antioxidant Status and Elevated Levels of C-Reactive Protein and Monocyte Chemotactic Protein-1 Associated With Cardiac Syndrome X?

“…Increases in the generation of proinflammatory cytokines, cell adhesion molecules, and growth factors can elicit inflammatory and proliferative changes in the vessel walls, resulting in microvascular dysfunction. 6,7 In this study, we attempted to determine whether total serum antioxidant status, as well as the levels of C-reactive protein (CRP) and monocyte chemotactic protein-1 (MCP-1), might be associated with cardiac syndrome X.…”

Phenotypic differences between microvascular and macrovascular smooth muscle cells and their contribution to coronary microvascular dysfunction

“…Recently, Zhao et al [33] have demonstrated that cardiomyocyte ATP depletion directly leads to hyperpolarization of neighbouring microvascular SMC via gap junctions, reducing intracellular Ca 2+ levels and causing vasorelaxation to increase myocardial blood flow. Whether gap junctions are inhibited in CMD in microvascular SMC has yet to be determined; however, gap junctions between cardiomyocytes and endothelial cells are depleted in CMD in a diabetes setting [34] . It is possible that a similar depletion occurs with SMC in CMD, leading to defects in vasorelaxation.…”