Endoplasmic Reticulum Is Involved in Myocardial Injury in a Miniature Swine Model of Coronary Artery Stenosis Exposed to Acceleration-Associated Stress.

This study aimed to investigate the effects of myocardial injury in a minimally-invasive miniature swine model with different levels of coronary artery stenosis (CAS) and exposed to maximal tolerated +Gz. Proximal left anterior descending branch was ligated in 20 swine. Five swine underwent a sham operation. A trapezoid acceleration curve was used for +Gz stress. Pathological changes of myocardial tissue were detected by H&E staining. Apoptotic cardiomyocytes were detected by TUNEL. GRP78 and CHOP were investigated by immunohistochemistry and western blot. CAS models were successful in 18 animals.Compared with the sham-operated group (+8.00±0.71 Gz), the maximal tolerated +Gz values of the moderate stenosis (+6.00±0.89 Gz, P<0.05) and severe stenosis groups (+5.20±0.84 Gz, P<0.05) were decreased.Compared with sham animals (12.16±1.25%), after exposure to maximum +Gz, apoptotic cells of the moderate (43.53±8.42%, P<0.05) and severe stenosis group (60.50±9.35%, P<0.05) were increased, MDA content was increased (1.89 and 4.91 folds, respectively, P<0.05), and SOD activity was reduced (-13.66% and -21.71%, respectively). After exposure to maximum +Gz, GRP78 protein expression was low in the sham-operated (0.29±0.05) and mild stenosis groups (0.35±0.04), while expression was high in the moderate (0.72±0.04, P<0.05) and severe stenosis groups (0.65±0.07, P<0.05). CHOP protein expression was not observed in the sham-operated group, while expression was high in the moderate and severe stenosis groups. These results indicated that Under maximum exposure to +Gz stress, different levels of CAS led to different levels of myocardial injury. Endoplasmic reticulum response is involved in the apoptosis of cardiomyocytes after +Gz stress.

PPARG, AGTR1, CXCL16 and LGALS2 polymorphisms are correlated with the risk for coronary heart disease.

PURPOSE: Our study was designed to explore the interaction between genes of PPARG, AGTR1, CXCL16 and LGALS2 and further investigate the association between genes polymorphisms and coronary heart disease (CHD). METHODS: 90 CHD patients and 80 healthy individuals were enrolled in our study. Gene chip technology was used for checking four single nucleotide polymorphisms (SNPs) (PPARG rs1152002, AGTR1 rs5186, CXCL16 rs3744700 and LGALS2 rs7291467). MDR software was used to analyze gene-gene interactions. Odds ratio (OR) with 95% confidence interval (CI) were employed to evaluate the association of genes and CHD risk. RESULTS: Genotypes and alleles distribution in case and control groups showed significant difference (P<0.05). And there exists interaction among genes. The model of PPARG×CXCL16 showed effects on the occurrence of CHD (OR=2.92, 95% CI=1.44-5.94). Meanwhile, the PPARG×AGTR1×CXCL16×LGALS2 model was associated with CHD susceptibility (OR=3.97, 95% CI=2.01-7.84). Moreover, we found that PPARG×LGALS2×CXCL16, was the best interaction model and it could significantly increase the risk for CHD (OR=3.37, 95% CI=1.71-6.63). CONCLUSION: PPARG rs1152002, AGTR1 rs5186, CXCL16 rs3744700 and LGALS2 rs7291467 polymorphisms may be closely related to the development of CHD. Moreover, there exist gene-gene interactions among these susceptibility genes.

Modification of atrioventricular node in a special condition treating paroxysmal supraventricular tachycardia.

Modification of atrioventricular node is a usual and necessary operation to cure atrioventricular nodal reentrant tachycardia (AVNRT). In this operation, atrioventricular block is the most severe complication and its prevention is of our great concern. This complication always occurs under some special circumstances with potential risk. So, it is very important to realize such conditions, as in this paper. A patient with paroxysmal palpitation for 10 years, aggravating to shortness of breath with chest distress for 1 year; cardiac electrophysiological examination found slow conduction in both antegrade and retrograde paths of reentrant loop, and typical AVNRT could be induced. During effective ablation there was no junctional rhythm. In some special cases, modification of atrioventricular node should not only rely on the junctional rhythm to determine the ablation effect, but also on the time of cardiac electrophysiological examination, as such to avoid the severe complication of atrioventricular block caused by excessive ablation.

[Brain natriuretic peptide and left ventricular remodeling after emergency percutaneous coronary intervention in acute myocardial infarction patients].

OBJECTIVE: To investigate the effect of emergency percutaneous coronary interventional (PCI) treatment on plasma brain natriuretic peptide (BNP) levels and left ventricular remodeling in patients with acute myocardial infarction (AMI). METHODS: This study included 118 patients with AMI and 20 healthy volunteers (their results were regarded as normal reference). Fifty-two patients who underwent successful emergency PCI 6-12 hours after onset were named as PCI group, and 66 patients rejected or in whom emergency PCI failed served as the control group. Plasma BNP levels were determined with Triage rapid assay at admission,at 12, 24, 48, 72 hours and 7, 14, 28 days after admission for both groups. Left ventricular ejection function (LVEF) was assessed by echocardiography with the modified Simpson's equation on 3-5 days and 28 days. Same assay was performed for 20 healthy volunteers. RESULTS: Plasma BNP levels of both groups were significantly higher at admission than those of volunteers. There was significant difference in BNP levels between two groups at corresponding time points (all P<0.01). In PCI group, BNP level peaked during 12-24 hours after admission, whereas two peaks of elevation of BNP levels were detected in control group, the first peak appeared during 12-24 hours and the second peak on 7 days after admission. Plasma BNP levels in PCI group were significantly lower than those of control group at corresponding time points (all P<0.01). There was no difference in LVEF level between two groups on 3-5 days after admission. LVEF level after emergency PCI was significantly higher than that of control group on 28 days after admission (P<0.01). CONCLUSION: Emergency PCI lowers plasma BNP level and improve LVEF level in patients with AMI, and it may reverse ventricular remodeling.

[Mechanism of percutaneous myocardial laser revascularization in the treatment of experimental cardiac ischemia].

OBJECTIVE: To evaluate the cardiac angiogenesis after percutaneous myocardial laser revascularization (PMR). METHODS: The left anterior descending coronary arteries of 10 healthy mongrel dogs weighing 14 - 18 kg were ligated partially so as to construct a model of chronic cardiac ischemia. Then the dogs were randomly divided into 2 groups of 5 dogs: PMR and control groups. Cardiogenesis Holmium: YAG laser system was used to make endomyocardial channels (15 +/- 3 channels/dog) in the ischemic ventricular walls in PMR group 2 weeks after the ligation. Sham procedure was conducted on the control group. Myocardial perfusion was examined by single photon emission computed tomography (SPECT) and left ventricle ejection fraction (LVEF) was examined by cardiac ultrasound before the ligation and 1, 4, and 12 weeks after PRM in the PMR group and before and 3, 6, and 14 weeks after the ligation in the control group. In the PRM group one dog was killed after the SPECT and LVEF examination 1 and 4 weeks after the PRM respectively and the remaining 3 dogs were killed after the SPECT and LVEF examination 12 weeks after the PRM. The dogs in the control group were killed after the SPECT and LVEF examination 14 weeks after the ligation. Myocardial pathology and cardiac angiogenesis analysis were conducted in both groups. RESULTS: Three months after PMR or coronary artery ligation, the SPECT scores of the PMR and control groups decreased from 3.2 +/- 0.6 and 3.1 +/- 0.5 to 0.3 +/- 0.2 and 1.2 +/- 0.3 respectively (both P < 0.05), the LVEF of the 2 groups increased from 42.6 +/- 6.5 and 43.2 +/- 8.7 to 55.8 +/- 7.6 and 42.6 +/- 6.5 respectively (both P < 0.05). Microscopy showed that the amount of micrangii was 45.6 +/- 7.4 vessel/field in the PMR region of the PRM group, significantly much more than that in the non-ischemic region of the PRM group (18.2 +/- 4.7), the ischemic region of the control group (21.4 +/- 5.6), and the non-ischemic region of the control group (17.3 +/- 6.9, all P < 0.05). CONCLUSION: PMR promotes angiogenesis in the ischemic myocardial wall, thus improving the blood perfusion of ischemic myocardium and global cardiac systolic function.