Reproducibility of chronic and acute infarct size measurement by delayed enhancement-magnetic resonance imaging.

OBJECTIVES: The aim of this study was to evaluate the reproducibility of acute and chronic infarct size (IS) by delayed enhancement (DE) magnetic resonance imaging (MRI). BACKGROUND: Infarct size measurements can be used as surrogate end point to reduce the sample size in studies comparing different reperfusion strategies in myocardial infarction (MI). Delayed enhancement MRI is a rather new technique, and so far infarct IS reproducibility has not been established appropriately. METHODS: In 21 patients (10 acute MI and 11 chronic MI), IS was assessed repeatedly on consecutive days by DE-MRI. Reproducibility, interobserver, and intraobserver variabilities were assessed and compared by the Bland-Altman method. RESULTS: Acute and chronic IS were 17.1 +/- 19.6% (range 5.1% to 69.8%) of LV mass (%LV) and 16.9 +/- 9.9 %LV (range 2.0% to 36.0%), respectively. Infarct size difference (bias) between scan I and scan II was -0.5 %LV, and limits of agreement were +/-2.4 %LV. Mean bias (-0.7 %LV) and limits of agreement (+/-3.2%) were slightly higher for acute in comparison with chronic MI with -0.4 +/- 1.3 %LV. Intraobserver and interobserver variability was low with a mean bias of 0.3 %LV (limits of agreement +/- 1.7 %LV) and -0.7 %LV (limits of agreement +/- 2.2 %LV), respectively. CONCLUSIONS: Infarct size measurement by DE-MRI is an excellent tool for IS assessment, owing to its excellent repeatability in chronic and acute MI. It has therefore the potential to serve as a surrogate end point to uncover advantages of new reperfusion strategies.

Functional and morphological skeletal muscle abnormalities correlate with reduced electromyographic activity in chronic heart failure.

BACKGROUND: Exercise intolerance and early muscle fatigue are key symptoms in patients with chronic heart failure (CHF). In advanced stages of the disease, profound metabolic abnormalities have been described finally leading to a catabolic state with progressive loss of muscle bulk. The aim of this study was to investigate morphological, functional and electromyographical parameters of the skeletal muscle in CHF. METHODS: We included 17 patients with CHF and 12 age-matched healthy controls (left ventricular ejection fraction 25+/-2 versus 68+/-1%, body mass index 26.6+/-0.8 versus 28.0+/-1.0 kg/m2; P=NS) in this study. Cross-sectional area (CSA) of the thigh was assessed by computed tomography. Under electromyographical control, maximal and submaximal (30%) isometric strength as well as the relative decrease of muscle strength of the quadriceps muscle over a period of 20 s were determined. RESULTS: Patients with CHF showed a significant reduction of muscle CSA (134.8+/-5.3 versus 165.2+/-7.4 cm2, P=0.002) as compared with healthy controls. The maximal quadriceps muscle strength was found to be significantly reduced in patients with CHF (226.7+/-22.3 versus 286.9+/-17.1 N, P<0.05) who also exhibited a higher extent of muscular fatigability (-2.18+/-0.33 versus -0.54+/-0.20 N/s, P<0.01). Electromyographic activity at 30% submaximal contraction showed a lower increase in patients with CHF (66+/-22 versus 114+/-36%; P<0.05) indicating impaired muscle fibre recruitment. Furthermore, a significant correlation between muscular fatigability and reduced electromyographic activity was found in CHF (r=0.84; P<0.001). CONCLUSIONS: Our findings demonstrate an impaired electromyographic activity and muscular function in patients with CHF suggesting a new pathomechanism contributing to functional abnormalities of the skeletal muscle in advanced stages of this disease.