Standardizing the definition of hyperenhancement in the quantitative assessment of infarct size and myocardial viability using delayed contrast-enhanced CMR.

PURPOSE: To evaluate a standardized definition of delayed hyperenhancement in the analysis of contrast-enhanced cardiac magnetic resonance (ceCMR) imaging. PATIENTS AND METHODS: CeCMR was performed in 15 patients with chronic ischemic heart disease. Delayed hyperenhancement was analyzed both by visual analysis by an experienced team of observers, and after thresholding the window setting of the images at 2, 3, 4, 5, and 6 SD above the mean signal intensity of remote, normal myocardium in the same slice. In each patient, total infarct size (TIS) and segmental infarct extent (SIE) were calculated. RESULTS: TIS and SIE were 22.9 +/- 12.2 mL and 32 +/- 28% after visual analysis. Thresholding the window setting at 2, 3, 4, and 6 SD above signal intensity of remote caused a 40%, 31%, and 17% increase (p < 0.007) and a 7% decrease (p = NS) in TIS, and a 75%, 41%, and 16% increase and 22% decrease in SIE (p < 0.001), respectively. There was no difference between visual analysis and analysis after thresholding at 5 SD. CONCLUSION: Analyzing ceCMR with a standardized definition of hyperenhancement related to the signal of remote, nonenhanced myocardium may result in considerable overestimation of infarct size at the usual cut-off of 2 SD.     

Use of lornoxicam for analgesia in the early postoperative period

Lornoxicam was used for analgesia in 64 patients on days 1-2 after extensive interventions. The drug efficiency and safety were evaluated depending on the dose and route of administration. Intravenous infusion of lornoxicam in a daily dose of 24 mg (basic therapy) did not involve the use of opioids in 35% patients and its analgesic effect was higher than that of promedol monotherapy. Combined therapy with lornoxicam and promedol allows reduction of promedol dose by 25-50% and the incidence of untoward effects by 27-44%.     

Accuracy of one- and two-dimensional algorithms with optimal image plane position for the estimation of left ventricular mass: a comparative study using magnetic resonance imaging.

The commonly recommended one-dimensional (ID) and two-dimensional (2D) algorithms for left ventricular (LV) mass calculation are limited by assumptions about ventricular geometry and image plane position. To assess the accuracy of these algorithms after eliminating errors associated with image plane position, LV mass was calculated from high quality cardiovascular magnetic resonance imaging (CMR) data sets using ID (modified cube formula; MCF) and 2D algorithms [area-length (AL) and truncated ellipsoid (TE) methods], and the summation of slices (SS) method as reference technique in 25 patients with LV aneurysms, 15 patients with hypertrophic cardiomyopathy, and 10 healthy subjects. Each algorithm in each group overestimated LV mass compared to SS (p <0.05 and p<0.001). In each patient group, the smallest bias to the reference method was observed for the TE algorithm (p<0.001 vs. MCF and p < 0.05 vs. AL). The LV mass interval encompassing the limits of agreement was 120-220 g for MCF, 100-148 g for AL, and 80-136 g for TE. The interstudy reproducibility of the SS technique for the assessment of LV mass was superior compared to the ID and 2D algorithms. We conclude that despite the use of optimized image plane position ID and 2D algorithms are inaccurate for calculation of LV mass in ventricles with normal and distorted LV geometry. Thus, 3D imaging techniques, such as CMR, should be preferred when assessing LV mass.     

Physical exercise and atherosclerosis: proatherogenic effects of high and moderate intensity static exercise on blood lipid transport system

Effects of high (100 and 80 kg) and moderate (60 kg) intensity static leg exercise on blood serum lipoproteins and apolipoproteins (apo) A1 and B were studied in healthy subjects (n=11) and patients with coronary heart disease and class I angina (n=11). Static leg exercise with loads exceeding 60 kg were associated with atherogenic changes of blood lipid transport system: elevation of levels of triglycerides, apoprotein B and apo B/A ratio both in healthy subjects and patients, and of total and low density lipoprotein cholesterol in patients. These post exercise changes were more pronounced in the presence of fasting hyperlipidemia and their severity increased with increase in duration of exercise. Static leg exercise did not increase concentration of high density lipoprotein cholesterol. For prevention of post exercise atherogenic dyslipidemia it is expedient to supplement strength training programs with dynamic exercise of moderate intensity.     

Voluntary exercise does not affect stress-induced tachycardia, but improves resistance to cardiac arrhythmias in rats

1. It is currently unknown whether long-term voluntary exercise has enduring cardioprotective effects in animal models. 2. The present study was conducted in three groups of rats: (i) sedentary controls (n = 6); (ii) 24 h runners (n = 8; unlimited access to running wheels); and (iii) 2 h runners (n = 8; access to running wheels limited to 2 h daily). After termination of the 6 week exercise protocol, all rats were implanted with the telemetric electrocardiogram transmitters and were studied 1 week later. 3. Resting heart rate (HR) values in the control rats, 24 h runners and 2 h runners were 372 ± 7, 361 ± 9 and 298 ± 5 b.p.m., respectively (P < 0.05 for 2 h runners vs controls). The high-frequency spectral power in the control rats, 24 h runners and 2 h runners was 3.9 ± 0.2, 4.3 ± 0.3 and 5.3 ± 0.3 s2, respectively (P < 0.05 for 2 h runners vs controls), whereas intrinsic HR was 383 ± 3, 377 ± 2 and 346 ± 3 b.p.m., respectively (P < 0.001 for 2 h runners vs controls). Restraint stress provoked tachycardia of similar magnitude in all groups. 4. After completion of telemetric studies, haemodynamic indices and susceptibility to cardiac arrhythmias were assessed in anaesthetized animals, there were no major between-group differences in HR, arterial pressure, contractility indices or sensitivity to β-adrenoceptor stimulation (dobutamine) or blockade (atenolol). The effective refractory period in the control rats, 24 h runners and 2 h runners was 49 ± 2, 55 ± 2 and 60 ± 4 ms, respectively (P = 0.054 for 2 h runners vs controls). A significantly higher dose of aconitine was required to provoke ventricular arrhythmias in the 24 h and 2 h running groups compared with controls (489 ± 76, 505 ± 88 and 173 ± 33 μg, respectively; P < 0.05). 5. We conclude that, in rats, long-term voluntary exercise has enduring cardioprotective effects mediated at the level of both the central nervous system and the heart.     

Epigenetic changes in the rat livers induced by pyrazinamide treatment

Drug-induced liver injury, including drug-induced hepatotoxicity during the treatment of tuberculosis infection, is a major health problem with increasingly significant challenges to modern hepatology. Therefore, the assessment and monitoring of the hepatotoxicity of antituberculosis drugs for prevention of liver injury are great concerns during disease treatment. The recently emerged data showing the ability of toxicants, including pharmaceutical agents, to alter cellular epigenetic status, open a unique opportunity for early detection of drug hepatotoxicity. Here we report that treatment of male Wistar rats with antituberculosis drug pyrazinamide at doses of 250, 500 or 1000 mg/kg/day body weight for 45 days leads to an early and sustained decrease in cytosine DNA methylation, progressive hypomethylation of long interspersed nucleotide elements (LINE-1), and aberrant promoter hypermethylation of placental form glutathione-S-transferase (GSTP) and p16(INK4A) genes in livers of pyrazinamide-treated rats, while serum levels of bilirubin and activity of aminotransferases changed modestly. The early occurrence of these epigenetic alterations and their association with progression of liver injury specific pathological changes indicate that alterations in DNA methylation may be useful predictive markers for the assessment of drug hepatotoxicity.