[Hibernating myocardium and the 'no reflow' phenomenon: a study of absolute regional myocardial perfusion and glucose metabolism using positron emission tomography in chronic and acute heart disorders].

Positron emission tomography (PET) is a powerful tool for in vivo measurements of physiologic processes such as regional myocardial blood flow and metabolism. Myocardial blood flow is often studied using radioactive labeled ammonia (13NH3) while myocardial metabolism can be investigated using 18F-fluorodeoxyglucose (FDG). Moreover, the use of appropriate kinetic models allows quantification of these processes. In this study, myocardial viability in both chronic and acute heart disease was investigated by the use of positron emission tomography. In this context, viable refers to dysfunctioning areas of the myocardium in which functional recovery is observed after revascularization. In patients suffering chronic coronary artery disease, PET findings of flow and metabolism were correlated with myocardial ultrastructure. In dysfunctional myocardial segments, normal 13NH3 uptake or decreased 13NH3 uptake with relatively increased FDG uptake (PET mismatch) indicates the possibility for functional recovery after bypass surgery. Since absence of scar tissue in these segments is likely to be required for functional recovery, it was not surprising that little fibrosis was found in myocardial biopsies taken in PET mismatch areas. The biopsies also revealed the presence of viable myocardial cells showing a variable loss of contractile material. The contractile material was replaced by glycogen. One could wonder about the time course needed for functional recovery after restoration of blood flow in the presence of a considerable amount of cells lacking a normal contractile apparatus. It would therefore be interesting to study functional recovery at different time points in patients with variable amounts of these myolytic cells. Probably, recovery of contractility would be slower in myocardial areas with a larger amount of abnormal cells. Another question that arises is the meaning of the increased FDG signal in dysfunctional, though viable myocardium. At first sight, glycogen storage in myolytic cells seems an excellent candidate to explain the increased intake of FDG in PET mismatch areas. However, in this study, in areas considered nonviable by PET, similar amounts of myolytic cells were found. Histologically altered cells might represent a structural and protective adaptation to long term hypoperfusion or to repetitive episodes of ischemia. Another possibility for the increased FDG uptake is an enhancement of glucose utilization in the mismatch areas not only in the myolytic cells, but also in the morphologically normal cell fractions. In patients with a PET mismatch pattern, significant recovery of flow and function was observed after surgery with a significant decrease in glucose utilization. Although it would have been interesting to histologically study the fate of myolytic cells in these recovered areas, this was not possible for obvious ethical reasons. In areas considered non viable by PET expressing a concordant decrease of 13NH3 and FDG uptake (PET match), no recovery of function, flow or metabolism was noted at follow-up. Another study was conducted in our department in infarct patients in which regional myocardial blood was measured within 24 hours after successful thrombolysis. The aim was to investigate the presence of impaired tissue perfusion in the acute stage and to evaluate its effect on recovery of flow, metabolism and function. In about 30% of patients with a TIMI 3 patent vessel, seriously impaired tissue flow was observed in the acute stage. Whether this impairment was due to irreversible damage to capillaries or myocytes, to reperfusion injury or to the presence of multiple distal thrombi remains unknown. Most patients showing severely impaired regional myocardial blood flow in the acute stage revealed absence of viable myocardium on follow-up PET NH3/FDG scans.