title: Myocardial perfusion/metabolism mismatch and ventricular arrhythmias in the chronic post infarction state.
abstract: OBJECTIVE
  Ventricular arrhythmias have been shown to originate in the myocardial peri-infarct region due to irregular heterotopic conduction. Hypoperfused but viable myocardium is often localised in those areas and may be involved in the pathogenesis of arrhythmias. We tested the hypothesis that these myocardial perfusion/metabolism mismatches (MM) are significantly associated with ventricular arrhythmias in the chronic post infarction state.
  
  
  METHODS
  47 post infarction patients were included in the study. 33 suffered from ventricular arrhythmia whereas 14 did not. All patients underwent (99m)Tc tetrofosmin SPECT and (18)F-FDG PET. A region-of-interest(ROI)-analysis was used to assess viable myocardium based on predefined MM-criteria. Univariate analyses as well as a logistic regression model for the multivariate analysis were carried out.
  
  
  RESULTS
  94% of the arrhythmic patients displayed at least one MM-segment as compared to 64% of the non-arrhythmic patients. MM-segments and arrhythmia showed a statistically significant relation (p = 0.018). The logistic regression model predicted the occurrence or absence of arrhythmia in 85% of all cases. Multivariate analysis gave consistent results, after adjusting for symptomatic chronic heart failure (CHF), aneurysms and age.
  
  
  CONCLUSIONS
  Our results support the hypothesis that hypoperfused but viable myocardium represents an arrhythmogenic substrate and is a relevant risk factor for developing ventricular arrhythmias following myocardial infarction. Therefore, the detection of MM-segments allows the identification of patients with a higher risk for future cardiac events.
authors.affiliation: Abteilung Nuklearmedizin, Radiologie III, Universitätsklinikum Ulm, Robert-Koch-Strasse 8, 89081 Ulm, Germany. bernd-joachim.krause@medizin.uni-ulm.de
authors.forename: B J
authors.initials: BJ
authors.lastname: Krause
authors.forename: T D
authors.initials: TD
authors.lastname: Poeppel
authors.forename: M
authors.initials: M
authors.lastname: Reinhardt
authors.forename: E-G
authors.initials: EG
authors.lastname: Vester
authors.forename: M
authors.initials: M
authors.lastname: Yong
authors.forename: J
authors.initials: J
authors.lastname: Mau
authors.forename: B-E
authors.initials: BE
authors.lastname: Strauer
authors.forename: H
authors.initials: H
authors.lastname: Vosberg
authors.forename: H-W
authors.initials: HW
authors.lastname: Müller
mesh_terms: D003327:Coronary Disease / Q000000981:diagnostic imaging; D005260:Female; D019788:Fluorodeoxyglucose F18; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000000981:diagnostic imaging*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D015899:Tomography, Emission-Computed, Single-Photon; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging; D014693:Ventricular Fibrillation / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*
chemical_list: D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; C078700:technetium tc-99m tetrofosmin