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Journal of Cardiovascular Magnetic Resonance 05/2012; 12:1-2. · 3.72 Impact Factor
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ABSTRACT: Small studies suggest that postconditioning reperfusion interrupted by brief repetitive cycles of reocclusions, may protect the myocardium in the clinical setting.
To test the hypothesis that postconditioning limits infarct size in relation to the area at risk in patients with ST elevation myocardial infarction (STEMI).
76 patients (aged 37-87 years) eligible for primary percutaneous coronary intervention due to STEMI were randomised to standard percutaneous coronary intervention (n = 38) or postconditioning, consisting of four cycles of 60 s reperfusion and 60 s of reocclusion before permanent reperfusion (n = 38).
The area at risk was determined from angiographic abnormally contracting segments. Infarct size was quantified from delayed enhancement MRI on days 6-9. Infarct size, expressed in relation to the area at risk, did not differ between the control group (44%; 30, 56) (median and quartiles) and the post-conditioned group (47%; 23, 63). The slope of the regression lines relating infarct size to the area at risk differed between the two groups. Infarct size was significantly (p = 0.001) reduced by postconditioning in patients with large areas at risk. The area under the curve and peak troponin T release and CKMB during 48 h did not differ between patients in the control and postconditioning groups.
This prospective, randomised trial suggests that postconditioning does not reduce infarct size in patients with STEMI in the overall study group. The data indicate that postconditioning may be of value in patients with large areas at risk. Clinical trial registration information Karolinska Clinical Trial Registration (http://www.kctr.se). Unique identifier: CT20080014.
Heart (British Cardiac Society) 11/2010; 96(21):1710-5. · 4.22 Impact Factor
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ABSTRACT: In order to determine myocardial salvage, accurate quantification of myocardium at risk (MaR) is necessary. We present a validated novel automatic segmentation algorithm for quantification of MaR by myocardial perfusion SPECT (MPS) in patients with acute coronary occlusion.
Twenty-nine patients with coronary occlusion were injected with a perfusion tracer before reperfusion, and underwent rest MPS within 4 hours. The MaR was quantified using the proposed algorithm (Segment software), the software Quantitative Perfusion SPECT (QPS) and by manual segmentation. The Segment MaR algorithm used a threshold of 55% of maximal counts and an a priori model based on normal coronary artery perfusion territories. The MaR was 30 ± 10% left ventricular mass (%LVM) by manual segmentation, 31 ± 12%LVM by Segment, and 36 ± 14%LVM by QPS. There was a good agreement between automatic and manual segmentation for both of the algorithms with a lower bias for Segment (.8 ± 4.0%LVM) than for QPS (5.8 ± 5.8%LVM) when compared to manual segmentation.
The Segment MaR algorithm can be used to correctly assess MaR from MPS images in patients with acute coronary occlusion without access to tracer-specific normal database. The MaR in relation to final infarct size enables determination of myocardial salvage.
Journal of Nuclear Cardiology 05/2010; 17(5):831-40. · 2.67 Impact Factor
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ABSTRACT: Final infarct size following coronary occlusion is determined by the duration of ischemia, the size of myocardium at risk (MaR) and reperfusion injury. The reference method for determining MaR, single-photon emission computed tomography (SPECT) before reperfusion, is impractical in an acute setting. The aim of the present study was to evaluate whether MaR can be determined from the contrast enhanced myocardium using steady-state free precession (SSFP) cine cardiovascular magnetic resonance (CMR) performed one week after the acute event in ST-elevation myocardial infarction (STEMI) patients with total coronary occlusion.
Sixteen patients with STEMI (age 64 +/- 8 years) received intravenous 99 m-Tc immediately before primary percutaneous coronary intervention. SPECT was performed within four hours. MaR was defined as the non-perfused myocardial volume derived with SPECT. CMR was performed 7.8 +/- 1.2 days after the myocardial infarction using a protocol in which the contrast agent was administered before acquisition of short-axis SSFP cines. MaR was evaluated as the contrast enhanced myocardial volume in the cines by two blinded observers. MaR determined from the enhanced region on cine CMR correlated significantly with that derived with SPECT (r2 = 0.78, p < 0.001). The difference in MaR determined by CMR and SPECT was 0.5 +/- 5.1% (mean +/- SD). The interobserver variability of contrast enhanced cine SSFP measurements was 1.6 +/- 3.7% (mean +/- SD) of the left ventricle wall volume.
Contrast enhanced SSFP cine CMR performed one week after acute infarction accurately depicts MaR prior to reperfusion in STEMI patients with total occlusion undergoing primary PCI. This suggests that a single CMR examination might be performed for determination of MaR and infarct size.
Journal of Cardiovascular Magnetic Resonance 01/2010; 12(1):25. · 3.72 Impact Factor
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ABSTRACT: Concentrations of cardiac troponins (cTn) in serum or plasma may be elevated in several disease states other than acute coronary syndromes. In heart failure and end stage renal disease, cardiac troponin T (cTnT) correlates positively with left ventricular mass index (LVMI). Exercise-induced elevation of cardiac troponins in well-trained athletes has been confirmed by several reports but the aetiology and clinical significance is unclear. In the present study, we measured baseline concentrations of cardiac markers and investigated whether or not serum cTnT is associated with left ventricular hypertrophy (LVH) in professional football players.
Twenty-three male professional football players with a mean age of 23 years (range 18-32) were studied. Echocardiography and blood sampling were carried out approx 24h after a training session. Serum cTnT, other cardiac markers and plasma brain natriuretic peptide (BNP) were compared with LVMI.
cTnT was only detectable in one subject. The prevalence of elevated cardiac troponin I (cTnI), creatine kinase MB (CKMB) and creatine kinase was higher than for cTnT. cTnI concentrations were higher in football players than in controls. LVMI did not correlate with any of the cardiac markers. Plasma BNP concentrations were normal in all subjects.
Serum cTnT concentrations were not elevated in healthy professional football players with LVH. This argues against the hypothesis that LVH per se may cause increased cTnT. The finding of higher cTnI in football players than in non-athletic controls should be confirmed and the aetiology elucidated.
Journal of Science and Medicine in Sport 11/2007; 10(5):291-6. · 3.03 Impact Factor
