Objective:To observe influence of cardiac resynchronization therapy (CRT ) on ventricular remodeling and inflammation in patients with chronic heart failure (CHF) .Methods :A total of 84 CHF patients treated in our hospital from Jun 2012 to Feb 2015 were selected , according to randam number table , they were randomly and e‐qually divided into routine treatment group (received routine medication ) and combined treatment group (received CRT based on routine treatment group) .Left ventricular ejection fraction (LVEF) ,left ventricular end -diastolic dimension (LVEDd) ,6min walking distance (6MWD) ,levels of high sensitive C reactive protein (hsCRP) ,inter‐leukin (IL)‐6 and tumor necrosis factor (TNF)–αwere compared between two groups before and three months after treatment .Results:Compared with before treatment ,three months after treatment ,there were significant rise in LVEF and 6MWD ,and significant reductions in LVEDd ,levels of hsCRP ,IL‐6 and TNF‐α in combined treatment group ( P<0.05 or < 0.01 ) ,while there were no significant improvements in above indexes in routine treatment group .Compared with routine treatment group ,there were significant rise in LVEF ± [(29.42 ± 4.32)%vs .(37.16 ± 4.72)% ] and 6MWD [ (232.66 ± 40.54) m vs .(304.12 ± 51.65) m] ,and significant reductions in LVEDd [ (64.35 ± 7.81) mm vs .(57.64 ± 6.12) mm] ,levels of hsCRP [ (23.21 ± 3.45)μg/ml vs .(16.31 ± 2.02)μg/ml] ,IL‐6 [ (22.08 ± 3.82)μg/ml vs .(15.79 ± 2.09)μg/ml] and TNF‐α[ (32.66 ± 5.66)μg/ml vs .(23.23 ± 3.12)μg/ml] in combined treatment group , P<0.05 or <0.01. Conclusion:CRT can significantly reduce levels of hsCRP ,IL‐6 and TNF‐αin CHF patients ,which may be the main mechanism delaying ventricular remodeling and improving cardiac function .

This study examined the protective effect of ischemic postconditioning (IPoC) and minocycline postconditioning (MT) on myocardial ischemia-reperfusion (I/R) injury in atherosclerosis (AS) animals and the possible mechanism. Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model. AS rabbits were randomly divided into 3 groups: (1) I/R group, the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h; (2) IPoC group, the myocardial ischemia lasted for 35 min, and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles (R20s/I20s×3)], and then reperfusion was sustained for 12 h; (3) MT group, minocycline was intravenously injected 10 min before reperfusion. The blood lipids, malondialdehyde (MDA), superoxide dismutase (SOD), soluble cell adhesion molecule (sICAM), myeloperoxidase (MPO), and cardiac troponin T (cTnT) were biochemically determined. The myocardial infarction size (IS) and apoptosis index (AI) were measured by pathological examination. The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the AS models were successfully established. The myocardial IS, the plasma levels of MDA, sICAM, MPO and cTnT, and the enzymatic activity of MPO were significantly decreased, and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group (P<0.05 for all). The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group (all P<0.05). It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits, and the mechanisms involved anti-oxidation, anti-inflammation, up-regulation of bcl-2 expression and down-regulation of caspase-3 expression. Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.

This study examined the protective effect of ischemic postconditioning (IPoC) and minocycline postconditioning (MT) on myocardial ischemia-reperfusion (I/R) injury in atherosclerosis (AS) animals and the possible mechanism. Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model. AS rabbits were randomly divided into 3 groups: (1) I/R group, the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h; (2) IPoC group, the myocardial ischemia lasted for 35 min, and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles (R20s/I20s×3)], and then reperfusion was sustained for 12 h; (3) MT group, minocycline was intravenously injected 10 min before reperfusion. The blood lipids, malondialdehyde (MDA), superoxide dismutase (SOD), soluble cell adhesion molecule (sICAM), myeloperoxidase (MPO), and cardiac troponin T (cTnT) were biochemically determined. The myocardial infarction size (IS) and apoptosis index (AI) were measured by pathological examination. The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the AS models were successfully established. The myocardial IS, the plasma levels of MDA, sICAM, MPO and cTnT, and the enzymatic activity of MPO were significantly decreased, and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group (P<0.05 for all). The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group (all P<0.05). It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits, and the mechanisms involved anti-oxidation, anti-inflammation, up-regulation of bcl-2 expression and down-regulation of caspase-3 expression. Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.
Animals ; Atherosclerosis ; physiopathology ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Minocycline ; pharmacology ; Myocardial Reperfusion Injury ; physiopathology ; Rabbits ; Reperfusion Injury ; physiopathology