title: Ischemic changes on rubidium-82 positron emission tomography imaging are associated with left ventricular functional and volumetric change independent of metabolic properties and echocardiographic functional variables in ischemic cardiomyopathy.
abstract: Positron emission tomography (PET) imaging allows identification of stress-induced ischemia and myocardial viability in patients with ischemic cardiomyopathy. We assessed the left ventricular (LV) functional response to vasodilator stress in patients with advanced ischemic cardiomyopathy undergoing pharmacologic stress (PET) perfusion and metabolic imaging. Additionally, we aimed to determine if mitral regurgitation (MR), right ventricular (RV) dysfunction and diastolic function influenced the observed LV responses to pharmacologic stress. In 161 patients (81% men; 65 ± 13 years), PET and echocardiography were performed within a week for noninvasive evaluation of myocardial ischemia and viability (scored using 17-segment model), as well as ventricular and valvular function. Patients were stratified based on ischemic defects in any segments versus hibernation/scar defects only. The LV volumes, EF by gating and transient ischemic dilatation (TID) index were generated automatically. Wall thickening (WT) scores were determined visually. The subgroup with reversible/ischemic segments on PET imaging (N = 55) exhibited greater end-systolic (ESV) and end-diastolic volume (EDV) enlargement during stress (13 ± 22 and 16 ± 43 ml increase respectively, vs. 0 ± 18 ml [P < 0.0001] and 2 ± 24 ml [P = 0.01]), a decrease in LVEF during stress (mean -3% vs. +2%), and greater TID indices (mean 1.13 ± 0.18 vs. 1.02 ± 0.12) compared to hibernation/scar only (N = 92). In addition, mean WT scores during stress declined significantly only in the ischemic subgroup (P < 0.0001 for regional LAD, non-LAD and global wall thickening scores). The prevalence and the severity of MR and RV dysfunction did not differ between groups. By univariate analysis, global and LAD territory segmental ischemia, global sum stress score (SSS), TID index, resting EF, ESV enlargement during stress, as well as global WT changes correlated with post-stress LVEF decline. Multivariate predictors included SSS, resting LVEF, and ESV change. Ischemic changes on vasodilator PET imaging are associated with global LV functional decline and volumetric dilatation, presumably due to stunning effect. Severity of RV dysfunction and MR had limited impact on the above changes.
authors.affiliation: Department of Nuclear Medicine, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
authors.forename: Raymond C
authors.initials: RC
authors.lastname: Wong
authors.forename: Manuel D
authors.initials: MD
authors.lastname: Cerqueira
authors.forename: Richard C
authors.initials: RC
authors.lastname: Brunken
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D009202:Cardiomyopathies / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D016009:Chi-Square Distribution; D015150:Echocardiography, Doppler; D018619:Echocardiography, Doppler, Pulsed; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000503:physiopathology; D015999:Multivariate Analysis; D017202:Myocardial Ischemia / Q000150:complications*; D055414:Myocardial Perfusion Imaging / Q000379:methods*; D049268:Positron-Emission Tomography; D011237:Predictive Value of Tests; D012042:Registries; D012189:Retrospective Studies; D012414:Rubidium Radioisotopes; D012720:Severity of Illness Index; D013318:Stroke Volume; D014665:Vasodilator Agents; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
chemical_list: D012414:Rubidium Radioisotopes; D014665:Vasodilator Agents
references.citation: J Nucl Cardiol. 2006 Nov;13(6):e121-51
references.pmid: 17174789
references.citation: Circulation. 1999 Sep 7;100(10):1035-42
references.pmid: 10477527
references.citation: J Am Coll Cardiol. 1996 Jun;27(7):1612-20
references.pmid: 8636545
references.citation: Eur J Nucl Med Mol Imaging. 2008 Feb;35(2):336-42
references.pmid: 17912523
references.citation: J Nucl Cardiol. 2007 Jul;14(4):529-36
references.pmid: 17679061
references.citation: J Nucl Med. 2007 Mar;48(3):349-58
references.pmid: 17332611
references.citation: J Am Soc Echocardiogr. 2005 Dec;18(12):1440-63
references.pmid: 16376782
references.citation: Circulation. 2006 Aug 1;114(5):e84-231
references.pmid: 16880336
references.citation: J Nucl Cardiol. 2004 Jul-Aug;11(4):440-9
references.pmid: 15295413
references.citation: J Nucl Cardiol. 2004 May-Jun;11(3):253-62
references.pmid: 15173772
references.citation: J Nucl Cardiol. 1996 Mar-Apr;3(2):96-104
references.pmid: 8799234
references.citation: J Nucl Med. 2007 May;48(5):783-93
references.pmid: 17475968
references.citation: J Am Coll Cardiol. 2003 Dec 3;42(11):1921-8
references.pmid: 14662253
references.citation: J Nucl Cardiol. 2008 Nov-Dec;15(6):745-53
references.pmid: 18984449
references.citation: J Nucl Cardiol. 2004 Sep-Oct;11(5):542-50
references.pmid: 15472639
references.citation: J Nucl Cardiol. 2005 May-Jun;12(3):268-75
references.pmid: 15944531
references.citation: J Am Coll Cardiol. 2003 Oct 1;42(7):1206-7
references.pmid: 14522481