Adaptation of nonrevascularized human hibernating and chronically stunned myocardium to long-term chronic myocardial ischemia.
It is unknown whether human chronically ischemic dysfunctional myocardium degenerates over time or adapts to chronic ischemia. We studied whether perfusion, metabolism, and contractile function and reserve can be preserved in nonrevascularized human chronically stunned and hibernating myocardium. We studied 16 event-free, medically treated patients with ejection fractions of 31 +/- 2% and chronically stunned or hibernating myocardium in 56 +/- 5% of the left ventricle on technetium-99m sestamibi single-photon emission computed tomography/fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography. Patients underwent repeat single-photon emission computed tomography, positron emission tomography, and tissue Doppler echocardiography at rest and during stress at follow-up after 25 +/- 4 months, and we investigated whether measurements of myocardial viability remained stable over time. Patients were stable with respect to New York Heart Association class and global left ventricular function (30 +/- 2%, p = 0.81). Wall motion score was unaltered in hibernating myocardium and chronically stunned regions, and a contractile reserve by tissue Doppler stress echocardiography was preserved. Overall, 74% of hibernating myocardium and chronically stunned regions retained their initial perfusion/metabolism pattern at follow-up. In hibernating myocardium, initial and follow-up sestamibi uptakes (53 +/- 1% and 53 +/- 2%, p = 0.85) and FDG uptakes (76 +/- 1% and 74 +/- 1%, p = 0.21) did not differ. In chronically stunned regions, sestamibi uptake displayed a minor decrease at follow-up (70 +/- 1% vs 67 +/- 1%, p <0.01) and FDG uptake remained constant (68 +/- 2% and 67 +/- 1%, p = 0.21). In conclusion, myocardial perfusion, FDG uptake, and contractile function in nonrevascularized chronically stunned and hibernating myocardium adapt to chronic ischemia in patients who are free of events. In chronically stunned regions, adaptation may be less complete than in hibernating myocardium.
Wiggers
Henrik
H
Department of Cardiology, Skejby Hospital, Aarhus University Hospital, Aarhus, Denmark. henrikwiggers@dadlnet.dk
Nielsen
Søren Steen
SS
Holdgaard
Paw
P
Flø
Christian
C
Nørrelund
Helene
H
Halbirk
Mads
M
Nielsen
Torsten Toftegaard
TT
Egeblad
Henrik
H
Rehling
Michael
M
Bøtker
Hans Erik
HE
D000222:Adaptation, Physiological; D000368:Aged; D002908:Chronic Disease; D004452:Echocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D017682:Myocardial Stunning / Q000209:etiology / Q000503:physiopathology*; D049268:Positron-Emission Tomography; D013318:Stroke Volume; D015899:Tomography, Emission-Computed, Single-Photon