Pretreatment with cyclosporine (CsA) decreases infarct size 24h after myocardial ischemia/reperfusion (I/R). The goal of this study was to determine effects of CsA pretreatment on long-term cardiac function after I/R-injury. Rats were randomly assigned to group1: vehicle-only, group2: CsA-5mg/kg/day, and group3: CsA-12.5mg/kg/day given orally for three days prior to I/R-injury (30 min of left anterior descending coronary artery occlusion). Post-I/R survival and cardiac function were evaluated 14 days after I/R-injury by echocardiography and invasive hemodynamic measurements. Rats with I/R-injury showed increased left ventricular pressure (LVEDP) compared to rats without I/R-injury (p<0.005). Although CsA initially decreased infarct size, no differences of LVEDP were seen 14 days after I/R-injury (vehicle: 21.2±8.9 mmHg, CsA-5mg/kg/day: 21.5±0.7 mmHg, CsA-12.5mg/kg/day: 20.5±9.4 mmHg). Ejection fraction and fractional shortening were decreased compared to baseline, but showed no differences between groups. On day 14, a dose-dependent increase in left ventricular end diastolic diameter was seen (p<0.001). CsA pretreatment was associated with a dose-dependent decrease in post-I/R-survival (vehicle: 56%, CsA-5mg/kg/day: 32%, CsA-12.5mg/kg/day: 16%; p=0.017). CsA pretreatment did not improve long-term cardiac function despite decreased infarct size 24h after I/R-injury, but increased post-I/R mortality significantly. Poor cardiac function after CsA pretreatment might be caused by left ventricular dilation.
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Heart rate variability (HRV) reflects periodic changes taking place in heart rhythm, which are controlled by the autonomic nervous system (ANS) and external factors. The aim of the present study was to assess the relationship between HRV and the level of intelligence using the Raven Advanced Matrices Test in 95 men (mean age 41.6 ±3.7SD yr) who experienced myocardial infarction during two years preceding the psychophysiological examination. HRV was analyzed from the EEG signal recordings in the time and spectral domains. It was found that post-myocardial infarct men of the higher than average intelligence had significantly increased HRV; the finding was reflected in the analysis of both time and frequency domains. Although both sympathetic and parasympathetic components showed an increase in the frequency domain, the former did disproportionately more, achieving substantial predominance. The results indicate that active mental processes and attitude, linked to a higher intelligence level, might be a beneficial prognostic marker, as is higher HRV, for the overall post-infarction cardiac mortality and for return of such subjects back to normal life. The corollary is that the assessment of IQ in post-infarction patients seems a simple screening method that may help presage the health and social course the patient takes.
This paper constitutes a report of our experience in the assessment of left ventricle contraction using MRI (Philips 0,5T Gyroscan T5/II) and includes a suggestion of the study method directed towards establishing the role of different patterns of ventricle contraction in general ventricle function. In 29 patients, 22 men and 7 women, (average age 55.3) with history of myocardial infarction, electrocardiographically gated MR images encompassing the entire heart in the anatomic long and short axis planes were acquired. Significant positive correlations between long axis shortening and area length ejection fraction were found on four chamber view images: r = 0.605 at p<0.05 and on two chamber view images: r = 0.554 at p<0.05.
It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC4 concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.
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In recent decades a significant raise in the incidence of myocardial infarction among young women has been recorded. It is presumed that, apart from the classical risk factors, other reasons exist for premature atherosclerosis in young women, related to the homeostasis of gonadal hormones. The aim of the study was to analyze the levels of gonadal hormones (estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone) measured in the luteal phase, in 65 normally menstruating women post myocardial infarction (MI) and to investigate a possible relationship between the hormone profile and selected coronary artery disease (CAD) risk factors. The levels of gonadal hormones: estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone were measured in the luteal phase. All examined women had normal mean levels of gonadal hormones. In the post MI patients leading a sedentary life style, a significantly lower mean progesterone concentration was observed (16.29 ± 9.11 versus 29.43 ± 21.14 nmol/l, p = 0.05) and significantly higher mean testosterone concentration (2.34 ± 0.98 versus 1.76 ± 1.09 nmol/l, p = 0.05) when compared to patients from the same group, but leading a more active life. In obese post MI women (BMI ≥ 30 kg/m2) a lower mean concentration of progesterone was detected (18.02 ± 8.12 versus 26.16 ± 14.72 nmol/l, p = 0.05), than in slimmer patients from the same group. In post MI women with a positive family history for CAD, a significantly higher mean concentration of testosterone was detected (2.31 ± 1.22 versus 1.67 ± 0.74 nmol/l, p = 0.05) than in patients with no family history. The results suggest a correlation between levels of gonadal hormones and classical CAD risk factors.
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