Histological and ultrastructural features of giant cell myocarditis: report of 3 cases / 中华病理学杂志

<p><b>OBJECTIVE</b>To identify clinical and pathological features of giant cell myocarditis.</p><p><b>METHODS</b>Clinical presentation and follow-up data of three patients with giant cell myocarditis were collected.Gross, histopathological, immunohistological and ultrastructural findings of extransplantated hearts of the patients were documented.</p><p><b>RESULTS</b>Grossly, multifocal involvement of the myocardium with variably dilated cardiac chambers were observed in all 3 cases.Histological examination revealed pronounced focal inflammatory infiltrates with multinucleated giant cells. Multinucleated giant cells were positive for CD68 and CD11b immunostains but were negative for CD163 in all cases. Transmission electron microscopy showed that the multinucleated giant cells derived from fusion of several macrophages with adherent lymphocytes and secretary cells. Clinically, the overall patient condition improved in all three cases after heart transplantation.One patient experienced acute cellular rejection (2R level) 4 months after transplantation, but recovered after treatment. One patient developed multinucleated giant cells observed in heart biopsy two weeks after transplantation.</p><p><b>CONCLUSIONS</b>Giant-cell myocarditis is a rare disease of adult, and cardiac transplantation could improve the clinical outcome. Multinucleated giant cell in the myocarditis lesions were derived from macrophages, likely participating in the immune response. Endomyocardial biopsy is important for the diagnosis of giant cell myocarditis.</p>

Association between clinical features and histopathological findings in patients with left ventricular non-compaction cardiomyopathy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the association between clinical and histopathological features in patients with left ventricular non-compaction cardiomyopathy (LVNC).</p><p><b>METHODS</b>Histopathological examinations were made on 11 LVNC recipient hearts from June 2004 to June 2014 in Fuwai Hospital, myocardial ultrastructure changes were detected using transmission electron microscopy. Association between clinical and pathological features were analyzed.</p><p><b>RESULTS</b>Patients were (24 ± 11) years old. There were 6 patients with mucus matrix LVNC, 3 patients with fibrous fatty infiltration, and 2 patients with cardiomyocytes proliferation. The gross morphological changes of LVNC hearts were characterized by numerous and prominent trabeculations with deep intratrabecular recesses in left ventricular myocardium. Ratios of the thicker noncompacted endocardial layer (N) and thin epicardial compacted layer (C) (N/C ratio) were ≥ 2.0, and the most serious lesions were located in the left ventricular apex, and followed by the left ventricular free wall. Histological microscopic examinations evidenced numerous matrix-like material and immature cardiomyocytes on endocardial tissue. Transmission electron microscopy revealed mitochondrial abnormalities on morphology, number, and distribution, underdeveloped cardiomyocytes and anomalies of intercalated disc structure, increased deposition of extracellular matrix-like substance and perinuclear glycogen. Pathological changes on cytoplasmic matrix and intercalated disc were present in all three tissue types of LVNC in this cohort and mitochondria hyperplasia was detected in patients with fibrous fatty infiltration. Heart weight ≥ 350 g is often associated with increased number of mitochondria. Increased cytoplasmic matrix was often detected in patients with LVEF ≥ 30% while intercalated disc anomalies were often detected in patients with LVEF < 30%.</p><p><b>CONCLUSION</b>Histological changes were closely related clinical features in patients with LVNC.</p>

Myocardial changes in heart transplantation recipients with primary restrictive cardiomyopathy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the histopathological features of primary restrictive cardiomyopathy (PRCM).</p><p><b>METHODS</b>Nine extransplanted hearts from heart transplantation recipients were examined. Gross and histopathological findings were observed, photographed and final pathological diagnosis was compared to clinical diagnosis. The myocardial ultrastructure changes were determined using transmission electron microscopy.</p><p><b>RESULTS</b>The hallmark pathologic feature of PRCM was distinguished by myocardial cell degeneration and hyperplastic collagen fibrils around the myocardial cells.Fibrosis was severer in left ventricle free wall than in ventricular septum and right ventricle. The degree of myocardial cell degeneration and poloidal disorder were severer in patients with reduced ejection fraction (EF) than in patients with preserved EF. Transmission electron microscope evidenced severe interstitial fibrosis, myofibrillar changes of sarcomere structure, abnormalities both on intercalated disc number and distribution.</p><p><b>CONCLUSIONS</b>PRCM is characterized by hyperplastic collagen fibrils around the cardiomyocytes. Fibrosis is severer in left ventricle than in right ventricle. Sarcomere dysplasia is the main cause of PRCM, and ultrastructural examination is helpful for PRCM diagnosis.</p>

Comparison of three doses of enalapril in preventing left ventricular remodeling after acute myocardial infarction in the rat / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats, especially evaluating the efficacy of low dose enalapril.</p><p><b>METHODS</b>AMI was induced by ligating the left coronary artery in 149 female SD rats. 48 hours after the procedure, the 97 surviving rats were randomized to one of the following four groups: (1) AMI controls (n = 24), (2) high-dose (10 mg x kg(-1) x d(-1), n = 25), (3) middle-dose (1 mg x kg(-1) x d(-1), n = 23), and (4) low-dose (0.1 mg x kg(-1) x d(-1), n = 25) enalapril groups. In addition, sham-operated (n = 13) and normal rats (n = 10) were randomly selected to serve as non-infarction controls. Enalapril was delivered by direct gastric gavage. After 4 weeks of therapy, hemodynamic studies were performed, then the rat hearts were fixed with 10% formalin and pathology analysis was performed. Exclusive of the dead rats and those with MI size < 35% or > 55%, complete experimental data were obtained from 67 rats, which were comprised of (1) AMI controls (n = 13), (2) high-dose enalapril (n = 13), (3) middle-dose enalapril (n = 12), (4) low-dose enalapril (n = 12), (5) sham-operated (n = 8) and (6) normal (n = 9) groups.</p><p><b>RESULTS</b>There were no significant differences among the four AMI groups in infarction size (all P > 0.05). Compared with the sham-operated group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), absolute and relative weight (LVAW, LVRW) in AMI group were all significantly increased (all P < 0.001), while maximum LV pressure rising and dropping rates (+/- dp/dt) and their corrected values by LV systolic pressure (+/- dp/dt/LVSP) were all significantly reduced in the AMI control group (P < 0.01 - 0.001), indicating LVRM occurred and LV systolic and diastolic functions were impaired. Compared with the AMI group, LVEDP, LVV, LVAW and LVRW were all significantly decreased in the three enalapril groups (control P < 0.001), with the reduction of LVEDP, LVV and LVAW being more significant in high-dose than in low-dose enalapril groups (all P < 0.05), and the +/- dp/dt/LVSP were significantly increased only in the high and middle-dose enalapril groups (P < 0.01).</p><p><b>CONCLUSIONS</b>High, middle and low doses of enalapril were all effective in preventing LVRM after AMI in the rat, with low dose enalapril being effective and high dose superior. As for LV functional improvement, only high and middle-dose enalapril were effective.</p>

Autopsy Study on the Causes of Coma in Cases with Congenital Heart Disease Following Cardiac Surgery after Extracorporeal Circulation / 中国胸心血管外科临床杂志

Objective　To observe the morphological changes of brain and to analyze the cause of coma after open-heart surgery in cases suffered from congenital heart disease.　Methods　Twenty six autopsy cases were collected from Jan. 1973 to Sep. 1999 in Fuwai Hospital. Their duration of coma was 1 day to 40 days and all of them died earlier later following cardiac surgery. Their surgical procedure, extracorporeal circulation time, and other clinical records and autopsy findings were reviewed. 　Results　The brain lesions included intracranial hemorrhages (n＝11), cerebral edema (n＝11), encephalitis and encephalomingitis (n＝3), and cerebromalacia (n＝1). Intracranial hemorrhages occurred in epidural (n＝3), subdural (n＝3), subarachoid spaces (n＝4), and intracerebral parenchyma (n＝1). The causes of coma were deduced as follows: lower cardiac output (n＝7), air embolism (n＝3), pneumonia (n＝3) and other infections (n＝2), pulmonary hypertension (n＝2), and the unknown causes of coma (n＝9). But the 6 out of the last 9 cases showed longer duration (more than 100 min) of extracorporeal circulation. Intracranial hemorrhages occurred more frequently in cases with waking period than those without after cardiac operation, and vice versa the cerebral edema. 　Conclusion　Intracranial hemorrhage and cerebral edema were the main changes of brain in the patients suffered from coma, but its causes were complex and difficult to analyze. These results suggest that further improved heart preservation, shorter time of extracorporeal circulation and effective treatment of infection would be benefit to the prevention of coma.