Clinical implication of microvasculopathy in patients post heart transplantation / 中华心血管病杂志

<p><b>OBJECTIVE</b>Assess the clinical implication of microvasculopathy detected by endomyocardial biopsy samples in patients post heart transplantation.</p><p><b>METHODS</b>Light microscopic evaluations were performed in 278 endomyocardial biopsies harvested from 64 patients post heart transplantation for more than one year, microvasculopathy was defined as stenotic endothelial and/or medial disease.</p><p><b>RESULTS</b>The patients with stenotic microvasculopathy were younger than those without microvasculopathy (40.7 ± 15.9 vs. 49.4 ± 8.7, P < 0.05). The mean score of acute cellular rejection (0.83 ± 0.39 vs. 0.37 ± 0.32, P < 0.01) and the numbers of ≥ grade II acute rejection (0.84 ± 0.16 vs. 0.23 ± 0.10, P < 0.01) were significantly greater in stenotic microvasculopathy group compared to those of non-stenotic group. Multivariate regression analysis confirmed that stenotic microvasculopathy is the independent risk factor for the mean acute rejection score (OR = 3.40, 95%CI, 4.62 - 193.07, P < 0.01), but not for the Quilty lesion, coronary heart disease of donor, diabetes mellitus. Angiographically confirmed coronary vasculopathy and cardiac dysfunction (χ(2) = 0.94, P > 0.05 and χ(2) = 2.90, P > 0.05) were similar between microvasculopathy group and non-microvasculopathy group.</p><p><b>CONCLUSION</b>Post heart transplantation microvasculopathy is an immune-mediated phenomenon and associated with higher mean score of acute cellular rejection and higher numbers of ≥ grade II acute rejection but was not the prognostic risk factor for coronary vasculopathy and function reduction after heart transplantation.</p>

Clinicopathologic analysis of dilated heart in cardiac transplant recipients / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the pathologic features of dilated heart in cardiac transplant recipients, with clinicoradiologic correlation.</p><p><b>METHODS</b>Sixty recipient hearts from cardiac transplantation performed in Fuwai Hospital were analyzed by gross examination, histologic observation and electron microscopy. Clinicoradiologic correlation was available in 40 cases.</p><p><b>RESULTS</b>Amongst the 40 cases of dilated heart, 52.5% (21/40) were due to dilated cardiomyopathy, 22.5% (9/40) due to arrhythmogenic right ventricular cardiomyopathy, 15.0% (6/40) due to ischemic cardiomyopathy, and the remaining 10.0% (4/40) due to miscellaneous causes, including local noncompaction of ventricular myocardium, giant cell myocarditis, alcoholic cardiomyopathy and hypertensive cardiomyopathy. The discrepancy rate between clinical and pathologic diagnosis was 37.5% (15/40). The erroneous categories included arrhythmogenic right ventricular cardiomyopathy (7 cases), ischemic cardiomyopathy (5 cases), and giant cell myocarditis (1 case), which were all mistaken clinically as dilated cardiomyopathy. While ischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, noncompaction of ventricular myocardium and giant cell myocarditis have distinctive pathologic features, the diagnosis of alcoholic and hypertensive cardiomyopathies required clinicopathologic correlation. Dilated cardiomyopathy due to viral myocarditis was not identified in the cases studied.</p><p><b>CONCLUSION</b>Pathologic examination is essential in analysis of transplant recipient heart and helps to rectify clinical diagnostic discrepancy.</p>

Effects of atenolol and metoprolol on cardiomyocyte apoptosis and related gene expression after acute myocardial infarction in rats / 中国医学科学院学报

<p><b>OBJECTIVE</b>To compare the beneficial effects of Atenolol and Metoprolol on cardiomyocyte apoptosis and related gene expressions after acute myocardial infarction (AMI) in rats.</p><p><b>METHODS</b>AMI model was established with the ligation of anterior descending coronary artery in 251 randomly selected female SD rats. Twenty-four hours after operation, the 124 survivors were randomly assigned to AMI control group (MI group, n = 43), Atenolol group (group A, 10 mg x kg(-1) d(-1), n = 39), and Metoprolol group (group B, 20 mg x kg(-1) x d(-1), n = 42). Sham operation group (group S, n = 27) was also established. Two subgroup (48 h subgroup and 4 weeks subgroup) was randomly divided in each group according to the time points. Drugs were given to each treatment group by gastric gavage 24 h after ligation. Cardiomyocyte apoptosis was detected with terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) and DNA ladder. Bcl-2, bax and caspase-3 genes were detected with immunohistochemistry and Western blot analysis.</p><p><b>RESULTS</b>Compared with AMI control group, myocyte apoptosis rate (MAR) significantly decreased only in infarction area (P < 0.01) in group B. Bcl-2 expression was found to increase in myocytes of infarction, border and non-infarcted areas except for non-infarcted area of group A. Changes of the expressions of bax and caspase-3 was not significant. Four weeks after AMI, MAR was found to decrease significantly in scar, border and non-infarcted areas (P < 0.05, P < 0.01) in both group A and group B. No significant changes of bcl-2, bax and caspase-3 expressions was found except for a significant decrease of bax expression in non-infarcted area of group A. As indicated by Western blot, no significant change of the expressions of caspase-3, bcl-2 and bax were found in myocytes of group A and group B compared with AMI control group; however, bcl-2/bax ratio significantly increased to the same level of sham-operated group (P < 0.05).</p><p><b>CONCLUSION</b>Both Atenolol and Metoprolol treatment can reduce cardiomyocyte apoptosis in infarction/scar, border and non-infarcted areas after AMI, mainly through the increase of bcl-2 expression and bcl-2/bax ratio.</p>

The clinicopathological endomyocardial biopsy analysis in cardiac transplant recipients due to end-stage heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>Endomyocardial biopsies from 42 (35 males and 7 females, aged 43.3 years) heart transplant recipients due to end-stage heart failure between June 2004 and January 2006 in our institute were obtained for pathological studies.</p><p><b>METHODS</b>Sixteen patients underwent 1 endomyocardial biopsy (right ventricular septum) between 13 days to 5 months, 13 patients underwent second biopsy between 1.5 to 8 months and 10 patients underwent third biopsy between 3 to 8.5 months post transplantation. Specimen were stained by hematoxylin-eosin (HE) and Phosphotungstic Acid Hematoxylin (PTAH) and observed under light microscope and cardiac allograft rejection were evaluated according to the Revision of the 1990 working formulation for the standardization of nomenclature in the diagnosis of heart rejection in 2004.</p><p><b>RESULTS</b>The rejection grades were as follows: Grade 0 R in 31 biopsies; Grade 1 R (mild rejection 1990 grade 1A, 1B and 2.) in 30 biopsies; Grade 2 R (moderate rejection, 1990 grade 3A) in 3 biopsies; Grade 1 R cellular rejection companies with humoral rejection in 1 biopsy. Cellular rejection with Quilty effect was found in 2 biopsies. Ischemic myocardial injury presented in 4 biopsies. Quilty effect was observed in 1 biopsy. Cytomegalovirus or toxoplasmic myocarditis was not observed.</p><p><b>CONCLUSIONS</b>Endomyocardial biopsy (EMB) is a valuable diagnostic procedure for rejection surveillance in heart allograft recipients. The observed low rejection incidence and mild rejection from specimens of our heart recipients were comparable to the results of developed countries.</p>

Lung pathology of severe acute respiratory syndrome / 中国医学科学院学报

<p><b>OBJECTIVE</b>To study the morphological features of the lungs obtained from autopsies of severe acute respiratory syndrome (SARS) patients.</p><p><b>METHODS</b>Bilateral lungs from 7 patients died from SARS were carefully studied grossly and microscopically. All tissues from these cases were routinely processed and carefully studied.</p><p><b>RESULTS</b>All lungs from these cases were extremely expanded and became solid. Microscopically, the edema and fibrin exudates in the alveoli was the most common findings, especially in the early phase of the disease. The hyaline membrane was almost always present in the lungs of these cases. The organization of intra-alveolar fibrin exudates along with the interstitial fibrosis led to obliteration of alveoli and consolidation of lungs. The desquamation and hyperplasia of alveolar lining cells was also apparent. Foci of haemorrhage and lobular pneumonia, even diffuse fungal infection were frequently seen in these specimens. Micro-thrombus were easily found in these lungs.</p><p><b>CONCLUSIONS</b>The lung of SARS from autopsy is characterized by edema, intra-alveolar fibrin exudates, hyaline membrane formation, organization of intra-alveolar exudates and fibrosis, which lead to the obliteration of alveoli and consolidation of lungs.</p>

Morphological study of severe acute respiratory syndrome (SARS) / 中华病理学杂志

<p><b>OBJECTIVE</b>Seven cases of autopsy from SARS patients are studied to investigate the pathogenesis and the pathologic changes of the major organs.</p><p><b>METHODS</b>Detailed gross and microscopic examination of the autopsy specimen is performed, including lung, heart, liver, kidney, spleen and lymph nodes.</p><p><b>RESULTS</b>All of the lungs are markedly enlarged and consolidated. Microscopically, pulmonary edema is a prominent finding, especially at the early stage of the disease (5 days after the onset). The alveolar spaces are filled with fibrinous exudates and lined with hyaline membrane. In 5 cases that undergo over 3 weeks of the course, the main pattern is organization of intra-alveolar deposit, along with fibroblastic proliferation in the alveolar septa, which leads to obliteration of alveolar space and pulmonary fibrosis. All of the lungs show bronchopneumonia, scattered hemorrhage, and proliferation of alveolar epithelial cells with desquamation. Microthrombi are seen in 6 cases. Fungal infection is noted in 2 cases. One of them is disseminative, involving bilateral lungs, heart, and kidney; the other one is diagnosed in hilar lymph nodes. In immune system, hilar and abdominal lymph nodes are usually congested and hemorrhagic, with depletion of lymphocytes, and accompanied with subcapsular sinus histiocytosis. One of the cases shows enlargement of abdominal lymph nodes, which have reduced number of germinal centers. Spleen exhibits atrophy of white pulps, and even lost of white pulps in some areas. The red pulp is markedly congested and hemorrhagic. In 5 cases, cardiomegale is prominent. Thrombosis (2 cases), focal myocarditis (1 case), and fungal myocarditis (1 case) are observed. In addition, liver shows massive necrosis (1 case) and nodular cirrhosis (1 case).</p><p><b>CONCLUSIONS</b>Lung is the major organ affected by SARS, demonstrated as diffuse alveolar damage. It is postulated that viral infection induces severe damage of alveolar epithelial and capillary endothelial cells, leads to pulmonary edema, intra-alveolar fibrin deposit, and hyaline membrane formation. Consequently, intra-alveolar organization and alveolar septal fibrosis causes loss of alveolar spaces, eventually, pulmonary fibrosis and atelectasis. The immune system is often affected, and presented as depletion of lymphoid tissue in lymph nodes and spleen. Secondary infection is a common complication, which should be paid close attention in the management of SARS patients.</p>