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Title of Journal: J Nucl Cardiol

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Abbravation: Journal of Nuclear Cardiology

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Springer US

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DOI

10.1016/0165-7992(90)90136-8

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ISSN

1532-6551

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Warranty period of normal stress myocardial perfus

Authors: Wanda Acampa Mario Petretta Renato Cuocolo Stefania Daniele Valeria Cantoni Alberto Cuocolo
Publish Date: 2013/10/04
Volume: 21, Issue: 1, Pages: 50-56
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Abstract

We evaluated the relationship between diabetes and temporal characteristics of cardiac risk at longterm followup in a propensity scorematched cohort of diabetic and nondiabetic patients with normal stress myocardial perfusion singlephoton emission computed tomography MPSWe studied 828 consecutive patients with suspected or known coronary artery disease and normal perfusion at stress MPS To account for differences in baseline characteristics between diabetics and nondiabetics we created a propensity scorematched cohort considering clinical variables and stress type After matching clinical characteristics were comparable in 260 diabetic and 260 nondiabetic patients All patients were followed for at least 1 year median 53 months Endpoint events were cardiac death or nonfatal myocardial infarction At Cox analysis diabetes hazard ratio 39 P  01 and poststress left ventricular ejection fraction LVEF ≤45 hazard ratio 41 P  01 were independent predictors of events At parametric analysis nondiabetic patients with poststress LVEF 45 remained at low risk for the entire length of followup while the highest probability of events and the major risk acceleration was observed in patients with diabetes and poststress LVEF ≤45After a normal stress MPS diabetic patients are at higher risk for cardiac events than nondiabetic subjects also after balancing clinical characteristics and stress type by propensity score analysis The warranty period of a normal stress MPS varies according to diabetic status and poststress LVEFStress myocardial perfusion singlephoton emission computed tomography MPS has taken a central role in risk stratify patients with suspected or known coronary artery disease CAD It has been shown that risk stratification incorporated in a testing strategy reduces the overall cost and enhances the effectiveness of testing12 Risk stratification by normal stress MPS may identify patients with and without CAD who do not require further intervention Although the presence of a normal scan should reassure that patients prognosis is excellent in diabetic patients a normal MPS seems to be less encouraging than in nondiabetic subjects34 In particular Giri et al3 demonstrated that despite the survival during the first 2 years of followup was identical in patients with symptoms suggestive of CAD and normal MPS irrespective to diabetic status the event rates increased after 2 years in diabetics but not in nondiabetics The duration of the lowrisk status after a normal stress MPS depends on several factors such as clinical characteristics that may influence the natural progression of CAD5 Outcomebased multivariable risk adjustment models can to some extent account for confounding covariates However concerns for residual bias may limit interpretation of results6 Thus we sought to evaluate the relationship between diabetes and the temporal characteristics of cardiac risk at longterm followup in a propensity scorematched cohort of diabetic and nondiabetic patients with normal stress MPSAll patients underwent stress technetium99m sestamibi gated MPS by physical exercise or dipyridamole stress test according to the recommendations of the European Association of Nuclear Medicine and European Society of Cardiology7 In all patients betablocking medications and calcium antagonists were withheld for 48 hours and longacting nitrates for 12 hours before testing For patient undergoing exercise test symptomlimited treadmill standardized protocols were performed with monitoring of heart rate and rhythm blood pressure and electrocardiography ECG Test endpoints were achievement of 85 maximal predicted heart rate horizontal or downsloping STsegment depression 2 mm STsegment elevation 1 mm moderate to severe angina systolic blood pressure decrease 20 mm Hg blood pressure 230/120 mm Hg dizziness or clinically important cardiac arrhythmia For dipyridamole stress test patients were instructed not to consume products containing caffeine for 24 hours before the test Dipyridamole was infused at dose of 0142 mg·kg−1·minute−1 intravenous over 4 minutes A dose of 100 mg of aminophylline was administered intravenously in the event of chest pain or other symptoms or after significant ST depressionAt peak exercise or 4 minutes after completion of dipyridamole infusion a bolus of 370 MBq of Tc99m sestamibi was intravenously injected Patients continued the exercise for additional 60 seconds after tracer injection For both types of stress heart rate blood pressure and 12lead ECG data were recorded at rest at the end of each stress stage at peak stress and in the delay phases at rest Maximal degree of STsegment change at 80 ms after the Jpoint of the ECG was measured and assessed as horizontal downsloping or upsloping For both types of stress imaging was started 30 minutes after tracer injection using a dualhead rotating gamma camera ECAM Siemens Medical Systems Hoffman Estates IL USA equipped with a lowenergy highresolution collimator and connected with a dedicated computer system8 No attenuation or scatter correction was used For gating a cardiac cycle was divided into eight frames The RR interval and heart rate histogram were recorded to monitor arrhythmia An average RR interval of ±15 was accepted for gating Perfusion imaging was reconstructed by summing the gated data at each projection into an “ungated” raw data file before low phase prefiltering and ramp filtered back projection An automated software program esoft 25 QGS/QPS CedarsSinai Medical Center Los Angeles CA was used to calculate left ventricular LV volumes and ejection fraction EF and the scores incorporating both the extent and severity of perfusion defects using standardized segmentation of 17 myocardial regions9 Briefly this commercial package determines reconstruction limits for the projection dataset reconstruct the projection images into transaxial images using standard filtered backprojection and then reorient the transaxial images into shortaxis images LV contours were checked visually and manually adjusted if the computergenerated automatic contours were found to be incorrect Quantitative defect extent and severity were defined from sexspecific normal limits and summed stress score was obtained by adding the scores of the 17 segments 0 = normal to 4 = absent perfusion of the stress images A poststress LVEF 45 and a summed stress score 3 were considered normal10 The cutoff of 45 was chosen for reduced poststress LVEF according to previous data demonstrating that it was the optimal threshold for the prediction of hard cardiac events11Patient followup was obtained by use of a questionnaire that was assessed by a phone call to all patients and/or general practitioners or cardiologists and by review of hospital or physicians’ records by individuals blinded to the patient’s test results The primary endpoint was the occurrence of cardiac death or nonfatal myocardial infarction whichever occurred first Cardiac death defined as due to acute myocardial infarction ventricular arrhythmias refractory heart failure or cardiogenic shock was confirmed by review of death certificate hospital chart or physician’s records Nonfatal myocardial infarction was defined based on the criteria of typical chest pain elevated cardiac enzyme levels and typical ECG alterations The date of the last examination or consultation was used to determine the length of followup


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  3. Fifty years of progress in radionuclide assessment of myocardial perfusion
  4. Buccal caffeine for the routine reversal of Persantine
  5. Multimodality molecular imaging in predicting ventricular arrhythmias and sudden cardiac death
  6. Mentorship at Distance: A new initiative of the Journal of Nuclear Cardiology
  7. Safety of vasodilator stress myocardial perfusion imaging in patients with elevated cardiac biomarkers
  8. ASNC Model Coverage Policy: Single photon myocardial perfusion imaging
  9. A selection of recent, original research papers
  10. Effect of Bayesian-penalized likelihood reconstruction on [13N]-NH3 rest perfusion quantification
  11. Impaired cardiac PET image quality due to delayed 82 Rubidium dose delivery to the heart
  12. Complete somatostatin-induced insulin suppression combined with heparin loading does not significantly suppress myocardial 18F-FDG uptake in patients with suspected cardiac sarcoidosis
  13. Left ventricular mechanical dyssynchrony by phase analysis as a prognostic indicator in heart failure
  14. “Same-Patient Processing” for multiple cardiac SPECT studies. 1. Improving LV segmentation accuracy
  15. Optimizing quantitative myocardial perfusion by positron emission tomography for guiding CAD management
  16. Lessons learned from MPI and physiologic testing in randomized trials of stable ischemic heart disease: COURAGE, BARI 2D, FAME, and ISCHEMIA
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  18. Quantitative I-123 mIBG SPECT in differentiating abnormal and normal mIBG myocardial uptake
  19. Coronary steal: Revealing the diagnosis with quantitative cardiac PET/CT
  20. Life-Threatening Ventricular Arrhythmias: Current Role of Imaging in Diagnosis and Risk Assessment
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  22. Regadenoson pharmacologic rubidium-82 PET: A comparison of quantitative perfusion and function to dipyridamole
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  26. What have we learned from CONFIRM? Prognostic implications from a prospective multicenter international observational cohort study of consecutive patients undergoing coronary computed tomographic angiography
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  29. ASNC Announcement
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  31. New software methods to cope with reduced counting statistics: shorter SPECT acquisitions and many more possibilities
  32. Impact of time-of-flight on qualitative and quantitative analyses of myocardial perfusion PET studies using 13 N-ammonia
  33. Impact of time-of-flight on qualitative and quantitative analyses of myocardial perfusion PET studies using 13 N-ammonia
  34. Dual molecular imaging for targeting metalloproteinase activity and apoptosis in atherosclerosis: molecular imaging facilitates understanding of pathogenesis
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  36. Acute hyperglycemia causes microvascular damage, leading to poor functional recovery and remodeling in patients with reperfused ST-segment elevation myocardial infarction

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