Biomedical subjects

Peng-Sheng Chen

Publications and source records attributed to Peng-Sheng Chen.

93 records · Page 6Linked to original sources

PubMedDate not supplied

Scar formation after ischemic myocardial injury in MRL mice.

INTRODUCTION: MRL is a strain of mice with the unusual ability to recover from injuries without forming scar tissue. It was recently reported that the MRL mice can recover with little or no scar formation following a cryogenically induced myocardial infarction of the right ventricle. These findings suggest that scarless recovery from myocardial injury is possible in mammalian ventricles. If applicable to humans, these results could have significant clinical implications in the management of patients with myocardial infarction. However, myocardial infarction in human patients usually results from ischemic injury instead of cryoinjury. Myocardial infarction usually occurs in the left ventricle. METHODS: We performed a prospective study creating left ventricular myocardial infarction in 32 MRL mice using coronary ligation. RESULTS: Among them, 21 mice survived surgery and had myocardial infarction documented by delayed contrast-enhanced magnetic resonance imaging (MRI) 35+/-10 days after surgery. All 21 mice had evidence of myocardial infarction in follow-up MRI performed 116+/-21 days after surgery. The infarct size was 27+/-12% of the area of visualized myocardium during the first MRI study and was 29+/-11% during the second MRI study (P=NS). Large myocardial infarction with aneurysm formation was documented by histological examinations in all 21 mice. The ventricular aneurysm showed transmural infarction with replacement fibrosis and mummified necrotic myocardium surrounded by collagenous scar tissue. Occasional surviving myocytes are present within the aneurysm. CONCLUSION: Ischemic myocardial injury in MRL mice is not followed by scarless recovery.

Animals↗

PubMedDate not supplied

Irreversible intrapulmonary vascular changes after pulmonary vein stenosis complicating catheter ablation for atrial fibrillation.

BACKGROUND: Pulmonary vein stenosis is a recognized complication of catheter ablation of arrhythmias emanating from the pulmonary vein; however, there is little information on secondary effects of pulmonary vein stenosis on lung tissue. METHODS AND RESULTS: A 55-year-old man with a history of paroxysmal atrial fibrillation refractory to antiarrhythmic medication had radiofrequency ablation in April 2003 and July 2003. Although these procedures were successful in resolving the patient's arrhythmia, they were complicated by the development of pulmonary vein stenosis of all four veins and pulmonary hypertension requiring patch annuloplasty of the pulmonary veins in October 2003. The patient was referred to our center for pulmonary vein stent placement in December 2003, June 2004, and August 2004, each time for recurrent hemoptysis. Due to persistent hemoptysis over the next several months, the patient underwent left lower lung lobectomy in September 2005. Microscopic examination of the lung showed marked medial thickening and intimal hyperplasia of large and small pulmonary veins and arteries, as well as focal organizing thrombi in the small arteries. The lung tissue showed extensive hemosiderin deposition indicative of prior hemorrhage. CONCLUSION: Chronic pulmonary vein stenosis after radiofrequency ablation of atrial fibrillation results in irreversible venous and arterial morphologic changes throughout the lung, including areas both close to, and remote from, the site of catheter ablation. Because there are persistent pathological changes remote from the ablation site causing the pulmonary hypertension, stenting the site of ablation to reopen large pulmonary veins may not be effective in treating the pulmonary hypertension.

Atrial Fibrillation↗

PubMedDate not supplied

Distribution of cardiac nerves in patients with diabetes mellitus: an immunohistochemical postmortem study of human hearts.

BACKGROUND: Autonomic neuropathy and functional cardiac denervation are complications of diabetes mellitus (DM). It is unknown if DM patients show histopathologic evidence of cardiac denervation. METHODS AND RESULTS: Nine sites were sampled at fixed distances from the atrioventricular valves from 27 postmortem hearts. Sections were stained with antibodies to S100 protein and to neurofilament (NF). Samples were visualized by light microscopy using the avidin-biotin peroxidase technique. The amount of cardiac nerves was graded blindly using semiquantitative methods according to the following criteria: Grade 0=presence of nerves in the epicardium only; Grade 1=strictly perivascular nerves; Grade 2=Grade 1 and nerve sprouts between myocardial cells sporadically; Grade 3=Grade 2 and nerve sprouts throughout the myocardium and endocardium. Specimens were divided into four groups. Control group consisted of patients with neither myocardial infarction (MI) nor DM. Experimental groups consisted of MI (n=7), MI with DM (n=6), and DM without MI (n=8). Average age of all patients was 57.3+/-15.7 years. No age differences existed among groups. Heterogeneous nerve distribution existed in all groups. S100-positive nerve density for control, MI, DM and MI, and DM without MI are 1.95+/-0.40, 1.66+/-0.54, 1.54+/-0.37, and 1.81+/-0.14, respectively (P=ns). NF-positive nerve density in the same groups were 1.10+/-0.18, 1.31+/-0.24, 1.13+/-0.12, and 1.19+/-0.42, respectively (P=ns). No differences in nerve densities between anterior and inferoposterior sections of the left ventricle existed. CONCLUSION: In postmortem human hearts, cardiac nerve distribution was heterogeneous among normal, MI, and DM patients. No evidence of cardiac denervation in patients with DM was demonstrated.

Autonomic Nervous System↗