Unstable plaques hide in heavily calcified coronary arteries.

Background: The napkin-ring sign (NRS) was accepted as unstable plaques at coronary computed tomography angiography (CCTA). However, the incidence is relatively low. We sought to assess whether the newly defined diamond-attenuation-sign [DAS, defined as a qualitative plaque feature in a mixed plaque (MP) on CCTA cross-section images by the presence of two features: a visual calcification (in the shape of a diamond) accompanied by an annular-shape lower attenuation plaque tissue surrounding the lumen like a ring], could be accurately identified as unstable atherosclerotic plaques. Methods: Eight heart transplant recipients (8 male; mean age, 48.5±11.6 years; range, 37-65 years) underwent CCTA exams prior to heart transplant surgery. Segment-based CCTA sections were independently evaluated for various plaque patterns including non-calcified plaque (NCP) with NRS (NCP-NRS), NCP without NRS (NCP-non-NRS), MP with DAS (MP-DAS), MP without DAS sign (MP-non-DAS), and calcified plaque (CP). Results: NCP-NRS plaques in 6.4% (23/358), NCP-non-NRS plaques in 24.0% (86/358), MP-DAS plaques in 18.2% (65/358), MP-non-DAS plaques in 20.1% (72/358), and calcified-plaques in 7.0% (25/358) of all cases. The specificity and positive predictive values of the MP-DAS and NCP-NRS signs to identify unstable plaque features were excellent (97.1% vs. 98.6%, 90.8% vs. 87.0%, respectively). DAS plaques were more frequently seen on CCTA exams than that of NRS (39.3% vs. 13.3%, respectively, P=0.001). The diagnostic performance of MP-DAS to identify unstable coronary lesions was superior compared to NCP-NRS [area under the receiver operating characteristic curve (ROC), 0.756; 95% CI: 0.717-0.791 vs. 0.558; 95% CI: 0.514-0.600, respectively, P<0.001]. Conclusions: Both the DAS and NRS had a high specificity and positive predictive value for the presence of unstable lesions. DAS was a better identification of unstable atherosclerotic plaques in the assessment of plaque-calcification-pattern (PCP).

Subendocardial Involvement as an Underrecognized Cardiac MRI Phenotype in Myocarditis.

Background Subendocardial late gadolinium enhancement (LGE) detected with cardiac MRI in myocarditis represents a diagnostic dilemma, since it may resemble myocardial ischemia. Purpose To explore and compare the histopathologic characteristics and clinical features and outcomes in patients with myocarditis with and without subendocardial involvement at cardiac MRI. Materials and Methods This retrospective study evaluated 39 patients with myocarditis pathologically proven by means of either endomyocardial biopsy or explant pathologic findings between 2015 and 2020. Patients were divided into two groups according to cardiac MRI phenotype: 18 with subendocardial involvement (mean age ± standard deviation, 40 years ± 17; 10 women) and 21 with no subendocardial involvement (mean age, 35 years ± 11; six women). The median follow-up period was 784 days (interquartile range [IQR], 90-1123 days). The Student t test, Mann-Whitney U test, and univariable Cox regression were used for statistical analyses. Results In the 18 patients with subendocardial involvement, 12 (67%) had lymphocytic myocarditis and six (33%) had giant cell myocarditis. Patients with subendocardial involvement compared with those without subendocardial involvement had lower left ventricular ejection fraction (mean ± standard deviation, 27% ± 11 vs 41% ± 19; P = .004), larger LGE extent (median, 13% [IQR, 10%-22%] vs 5% [IQR, 2%-17%]; P < .001), higher rates of cardiac death or transplant (eight of 18 patients [44%] vs one of 21 patients [4.8%]; P = .006), higher probability of giant cell myocarditis (six of 18 [33%] vs one of 21 [4.8%]; P = .02), and more major adverse cardiovascular events (MACE) (15 of 18 [83%] vs seven of 21 [33%]; P = .002). In a subgroup of patients with comparable LGE extent (median, 15% vs 16%; P = .40) and left ventricular ejection fraction (median, 27% vs 31%; P = .26), the prognostic difference in terms of MACE remained (15 of 17 patients [88%] vs five of 10 [50%]; P = .02). Conclusion Subendocardial involvement detected with cardiac MRI in myocarditis indicated more severe clinical features, including a higher frequency of severe lymphocytic myocarditis or giant cell myocarditis and worse prognosis. © RSNA, 2021 See also the editorial by de Roos in this issue.

Reversing pathology in a preclinical model of Alzheimer's disease by hacking cerebrovascular neoangiogenesis with advanced cancer therapeutics.

BACKGROUND: Cognitive decline leading to dementia, accompanied by the accumulation of amyloid-beta (Aß) in neuritic plaques together with the appearance of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein (tau), are previously noted hallmarks of Alzheimer's disease (AD). We previously discovered hypervascularity in brain specimens from AD patients and consistent with this observation, we demonstrated that overexpression of Aß drives cerebrovascular neoangiogenesis leading to hypervascularity and coincident tight-junction disruption and blood-brain barrier (BBB) leakiness in animal models of AD. We subsequently demonstrated that amyloid plaque burden and cerebrovascular pathogenesis subside when pro-angiogenic Aß levels are reduced. Based on these data, we propose a paradigm of AD etiology where, as a compensatory response to impaired cerebral blood flow (CBF), Aß triggers pathogenic cerebrovascular neoangiogenesis that underlies the conventional hallmarks of AD. Consequently, here we present evidence that repurposing anti-cancer drugs to modulate cerebrovascular neoangiogenesis, rather than directly targeting the amyloid cascade, may provide an effective treatment for AD and related vascular diseases of the brain. METHODS: We explored whether the anti-cancer drug, Axitinib, a small molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors (VEGFR) can inhibit aberrant cerebrovascular neoangiogenic changes, reduce Aß deposits and reverse cognitive decline in an animal model of AD. One month post-treatment with Axitinib, we employed a battery of tests to assess cognition and memory in aged Tg2576 AD mice and used molecular analysis to demonstrate reduction of amyloid plaques, BBB leakage, hypervascularity and associated disease pathology. FINDINGS: Targeting the pro-angiogenic pathway in AD using the cancer drug, Axitinib, dramatically reduced cerebrovascular neoangiogenesis, restored BBB integrity, resolved tight-junction pathogenesis, diminishes Aß depositions in plaques and effectively restores memory and cognitive performance in a preclinical mouse model of AD. INTERPRETATION: Modulation of neoangiogenesis, in an analogous approach to those used to treat aberrant vascularization in cancer and also in the wet form of age-related macular degeneration (AMD), provides an alternative therapeutic strategy for intervention in AD that warrants clinical investigation. FUNDING: None.

Resection of Cardiac Pheochromocytoma With Cardiopulmonary Bypass.

We report a case of a 21-year-old man with a cardiac pheochromocytoma involving the right atrium and extending to the right ventricular inflow tract, which was diagnosed by somatostatin receptor scintigraphy. For the preoperative evaluation, we chose multiple methods of imaging to accurately describe the anatomic extent and location of the tumor and its surrounding tissues, which showed that no major coronary artery ran through the tumor. The tumor was resected with disease-free margins effectively and safely with the use of cardiopulmonary bypass and with cardiac arrest. The patient remained asymptomatic at the 3-month follow-up.

Safety and efficacy of superior vena cava isolation using the second-generation cryoballoon ablation in a canine model.

BACKGROUND: The safety and efficacy of superior vena cava (SVC) isolation (SVCI) using second-generation cryoballoon (CB) ablation remains unknown. METHODS: Electrical isolation of SVC was attempted using the second-generation CB ablation catheter in 14 canines. Ablation duration was randomized to either 90 s (7 canines) or 120 s (7 canines). SVC venography was performed to identify the SVC-right atrium (RA) junction. The 28-mm CB was positioned above SVC-RA junction. Repeat electrophysiological assessment in the live animals was conducted 40-60 days post-ablation, after which animals were euthanized for histological examination. RESULTS: Acute SVCI was successfully performed in all canines. No significant differences in numbers of freezes (1.7 ±â€¯0.8 vs. 1.5 ±â€¯0.5, p = 0.658), time to isolation (TTI) (24.3 ±â€¯8.1s vs. 22.7 ±â€¯9.0s, p = 0.297), temperature at isolation (-23.4 ±â€¯12.5 °C vs. -21.5 ±â€¯11.1 °C, p = 0.370), and nadir temperature (-51.2 ±â€¯6.2 °C vs. -53.3 ±â€¯7.0 °C, p = 0.195) were observed between the 90-s and 120-s groups. There were no procedural complications except one transient sinus bradycardia in the 120-s group. After ablation, animals survived for 51 ±â€¯5 days. Chronic SVCI was achieved in 6 of 7 (85.7%) SVCs in the 90-s group and 7 of 7 SVCs (100%) in the 120-s group (p = 0.299). Histological analysis revealed that a circumferential transmural lesion was achieved in all isolated SVCs. No sinus node (SN) and phrenic nerve injuries were observed. The minimum distance between ablation lesion and SN was 5.1 ±â€¯3.0 mm. CONCLUSIONS: The second-generation CB ablation catheter is both safe and effective in achieving SVC isolation in a canine model. Effective SVCI was found in the 90-s dosing strategy.

Met-Hemoglobin Is a Biomarker for Poor Oxygen Delivery in Infants Following Surgical Palliation.

BACKGROUND: Infants with cyanotic congenital heart disease demonstrate wide fluctuations in hemoglobin (Hb), oxygen saturation, and cardiac output following palliation. Methemoglobin (Met-Hb), the product of Hb oxidation, may represent a compensatory mechanism during hypoxia and may be utilized as a biomarker. METHODS: Arterial and venous Met-Hb levels were obtained from infants requiring palliation. The primary outcome was to describe the relationship between Met-Hb and other indices of tissue oxygenation (venous saturation, estimated arteriovenous oxygen difference [Est AV-Diff], and lactate). Secondary outcomes were to determine the impact of elevated Met-Hb levels ≥1.0% and the effect of red blood cell (RBC) transfusion on Met-Hb levels. RESULTS: Fifty infants and 465 Met-Hb values were studied. Venous Met-Hb levels were significantly higher than arterial levels (venous: 0.84% ± 0.36% vs arterial: 0.45% ± 0.18%; P < .001). Venous Met-Hb demonstrated a significant inverse relationship with venous oxygen saturation (R = -0.6; P < .001) and Hb (R = -0.3, P < .001) and a direct relationship with the Est AV-Diff (R = 0.3, P < .001). A total of 129 (29.6%) venous Met-Hb values were elevated (≥1.0%) and were associated with significantly lower Hb and venous saturation levels and higher Est AV-Diff and lactate levels. Methemoglobin levels decreased significantly following 65 RBC transfusions (0.94 ± 0.40 vs 0.77 ± 0.34; P < .001). Linear mixed models demonstrated that higher venous Met-Hb levels were associated with lower measures of tissue oxygenation and not related to any preoperative clinical differences. CONCLUSION: Methemoglobin may be a clinically useful marker of tissue oxygenation in infants following surgical palliation.

Hepatocyte growth factor inhibits tubular epithelial­myofibroblast transdifferentiation by suppression of angiotensin II via the JAK2/STAT3 signaling pathway.

Tubular epithelial­myofibroblast transdifferentiation (TEMT) is important in the development of chronic renal failure. The present study investigated whether hepatocyte growth factor (HGF) inhibits TEMT, and whether this function may be associated with the inhibition of angiotensin II (AngII) and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Human HK­2 kidney proximal tubular cells were divided into 4 groups and treated with AngII (1x10­6 M), HGF (8x10­3 M), AngII plus HGF or control conditions, followed by an assessment of apoptosis induction and the expression levels of α­smooth muscle actin (α­SMA), which is a marker of TEMT. as well as the activation level of JAK2, phosphorylated (p)­JAK2, STAT3 and p­STAT3 signaling pathways. In HK­2 cells, α­SMA mRNA and protein expression levels increased following treatment with AngII, however, decreased expression was observed following exposure to HGF. HGF counteracted the AngII­induced increase in the expression of α­SMA in HK­2 cells. Similar expression profiles were observed for the phosphorylated forms of JAK2 and STAT3, indicating the possible involvement of this signaling pathway. The results demonstrated that treatment of cells with AngII was associated with the induction of apoptosis when compared with the control. By contrast, treatment with HGF attenuated AngII­induced apoptosis. The results suggested that HGF may inhibit TEMT by inhibiting AngII through the JAK2/STAT3 signaling pathway in HK­2 cells and HGF may prevent apoptosis induced by AngII. The present study provides a basis for understanding the mechanisms involved in the inhibition of TEMT by HGF, which requires further investigation.

Protective effect of olmesartan against cardiac ischemia/reperfusion injury in spontaneously hypertensive rats.

Olmesartan, as a new angiotensin II receptor blocker, has shown beneficial effects on cardiovascular diseases. Nevertheless, the effect of olmesartan on ischemia/reperfusion (I/R) injury in the hypertensive heart has not been investigated. Therefore, the present study aimed to investigate the effect of olmesartan on I/R injury in spontaneously hypertensive rats (SHRs). Experimental groups were designed with a 2×2 factorial design for olmesartan and I/R effects. In the I/R group, the left anterior descending coronary artery (LAD) was ligated for 40 min followed by a 180-min reperfusion. In the sham group, SHRs underwent the same surgical procedure as the I/R group, with the exception that the suture passed under the LAD without being tightened. In the Olm-I/R group, the SHRs received olmesartan (5 mg/kg) for 4 weeks prior to surgery and other procedures were the same as for the I/R group. In the Olm-sham group, the SHRs received olmesartan (5 mg/kg) for 4 weeks prior to surgery and other procedures were the same as for the sham group. Infarct size was measured for the I/R and Olm-I/R groups. Blood pressure (BP), serum creatine kinase (CK), left ventricular mass index (LVMI), high mobility group box 1 (HMGB1) protein expression levels and hypoxia-inducible factor-1α (HIF-1α) mRNA expression levels were measured for all four groups. Olmesartan significantly reduced BP and LVMI in the olmesartan-treated SHRs compared with those in the SHRs that were not treated with olmesartan. HMGB1 and HIF-1α expression levels were significantly decreased in the Olm-sham and Olm-I/R groups compared with those in the sham and I/R groups, respectively. The proportional increase in HIF-1α expression due to I/R was greater in the olmesartan-treated rats than in the untreated rats. Serum CK levels were significantly reduced in the Olm-I/R group compared with those in the I/R group. In conclusion, olmesartan ameliorates left ventricular hypotrophy and protects the heart against I/R injury in addition to lowing BP in SHRs. The protective effect of olmesartan may be partly due to its antioxidative and anti-inflammatory properties.

Management of focal atrial tachycardias originating from the atrial appendage with the combination of radiofrequency catheter ablation and minimally invasive atrial appendectomy.

BACKGROUND: Focal atrial tachycardias (ATs) originating from the left and the right atrial appendage (AA) were the most difficult to eliminate. OBJECTIVE: To evaluate the safety and long-term efficacy of minimally invasive surgical atrial appendectomy in combination with radiofrequency catheter ablation (RFCA) in the management of focal atrial appendage tachycardias (AATs). METHODS: We included 42 consecutive patients with 42 AATs confirmed by activation mapping and contrast venography. Thirty of them were successfully managed with RFCA (RFCA-successful group), while the remaining 12 (28.6%) finally resorted to video-assisted thoracoscopic atrial appendectomy owing to RFCA failure (resort-to-surgery group). We searched for predictors of RFCA failure, and the need for surgery by using a binomial logistic regression model. RESULTS: In the RFCA-successful group, 6 (20.0%) patients experienced recurrence and re-do ablation and 11 (36.7%) AATs originated from distal AAs. In the resort-to-surgery group, the tachycardias involved exclusively distal AAs and required more RFCA attempts compared with those of the RFCA-successful group (1.58 ± 0.51 vs 1.20 ± 0.41; P = .0165). During atrial appendectomy, incessant ATs were terminated immediately after resection of the AA at the base. Long-term success was achieved in all 42 patients with a follow-up of 29.1 ± 17.5 months. No complications occurred. Fourteen patients with tachycardia-induced cardiomyopathy recovered fully. We identified origin at distal AATs and longer time to tachycardia termination by ablation as predictors of RFCA failure and the need for surgical intervention. CONCLUSION: ATs originating from the distal portion of AA were more refractory to RFCA. The combination of catheter ablation and video-assisted thoracoscopic atrial appendectomy was an effective strategy to manage AATs.

Pathological changes, TGF-ß1 expression, and the effects of hepatocyte growth factor in 5/6 nephrectomized rats.

Several studies have shown that hepatocyte growth factor (HGF) ameliorates chronic renal failure, but its mechanism of action is unclear. This study was designed to test the delivery of HGF in the PCI-neo vector, using the 5/6 nephrectomized rat as a model for chronic renal failure, and to confirm that this protective function is associated with decreased protein expression of transforming growth factor-beta1 (TGF-ß1). Rats were randomly divided into the following groups: Control (untreated), PCI-neo (vector control), 5/6 nephrectomy, and PCI-neo-HGF. Rats were sacrificed at both the fifth and ninth week after 5/6 nephrectomy. Kidney specimens were used for pathological examination (hematoxylin-eosin staining), and detection of TGF-ß1 protein (Western blot and immunohistochemistry) expression. Blood urea nitrogen, serum creatinine, and 24-h urinary protein excretion (UPE) were increased, renal interstitium was seriously injured, and TGF-ß1 protein expression was elevated in 5/6 nephrectomized rats compared to control rats at either time point. Red blood cell and hemoglobin levels decreased in the ninth week after 5/6 nephrectomy. PCI-neo-HGF expression ameliorated the aforementioned changes and decreased TGF-ß1 expression, not only in the fifth week, but also in the ninth week after surgery. The process of renal injury in the 5/6 nephrectomized rat was consistent with that of chronic renal failure. The increase in TGF-ß1 expression was maintained after 5/6 nephrectomy. HGF relieved chronic renal failure, this protection was associated with down-regulation of TGF-ß1 protein expression, and the protective effects were long-term and stable after 5/6 nephrectomy.

[Clinico-pathological characteristics of infective endocarditis associated with congenital heart disease: an analysis of 74 cases in single center].

OBJECTIVE: To assess the changing profile of infective endocarditis (IE) in patients with congenital heart disease (CHD) from 1998 to 2009 in our hospital. METHODS: Clinical characteristics of IE patients with CHD underwent surgical treatment during 1998 - 2009 in our hospital were evaluated. The coincidence rate between clinical and pathological diagnosis were analyzed. RESULTS: There were 74 IE cases associated with CHD during the 12 years, accounting for 33.6% of all patients with IE receiving surgery during this time period. Mean age was higher for patients treated in 2006 - 2009 than patients treated in 2002 - 2005 [(38.7 ± 14.6) years vs. (28.4 ± 12.8) years, P = 0.003].Bicuspid aortic valve (accounting for 52.2%) was the most frequent congenital heart disease and the age of these patients was younger than patients with other congenital heart diseases. IE in CHD affected the left heart structures in 83.8% (62/74) of all cases, 47 in aortic valve (75.8%). Blood cultures were performed in 29.7% of the patients (22/74) and the positive rate was 59.1% (13/22). Streptococci viridans were the most common causative organisms. Echocardiography was performed in all patients and 66.3% echocardiographic records were positive, IE was diagnosed in 53 patients (71.7%) before operation. The operative mortality was 2.7%. CONCLUSION: Congenital heart disease, especially bicuspid aortic valve, is the most common underlying disease for IE. Combined analysis of clinical, echocardiographic and blood culture results are essential for increasing the diagnosis rate of IE.

[The relationship between hyperuricaemia and clinic pathology of IgA nephropathy].

OBJECTIVE: To analyze the correlation between the level of serum uric acid and the clinical and pathological features of IgA nephropathy. METHODS: Totally 148 patients diagnosed as IgA nephropathy by renal biopsy in our hospital from January 2007 to December 2010 were divided into hyperuricaemic group (41 cases) and non-hyperuricaemic group (107 cases) according to the level of serum uric acid. The clinical parameters and renal pathology grade were compared. RESULTS: There were significant differences between hyperuricaemic group and non-hyperuricaemic group in the incidences of hypertension (63.4% vs 38.3%), disease duration [(18.90 ± 10.12) months vs (9.46 ± 3.91) months] and body mass index [(22.81 ± 3.60) kg/m(2) vs (15.32 ± 2.54) kg/m(2)] (all P < 0.05), while no differences in age and sex (both P > 0.05). The blood urea nitrogen (BUN) [(8.93 ± 4.28) mmol/L vs (5.21 ± 2.18) mmol/L], creatinine (Cr) [(155.96 ± 107.72) µmol/L vs (79.52 ± 40.01) µmol/L], serum triglycerides [(2.11 ± 1.06) mmol/L vs (1.86 ± 1.20) mmol/L] and 24-hour urine protein amount [(4328.16 ± 1434.25) mg/24 h vs (2885.10 ± 1388.15) mg/24 h] were significantly different between the two groups (all P < 0.05). The percentage of Lee's grade I + II in hyperuricaemic group was 12.2%, and IV + V grade was 39.0%, while percentage of Lee's grade I + II in non-hyperuricaemic group was 25.2%, and IV + V grade was 16.9% (P < 0.05). Tubulointerstitial lesions (TIL) grade III + IV was more in hyperuricaemic group, which was 68.3%, while TIL grade II was more in non-hyperuricaemic group, which was 76.6%. Renal artery damage grade II + III was more in hyperuricaemic group, which was 73.2%, while renal artery damage grade 0 + I was more in non-hyperuricaemic group, which was 69.2%. CONCLUSIONS: The level of serum uric acid was related with 24-hour urine protein amount, blood pressure and kidney function in IgA nephropathy, and Lee's grade, TIL grade and renal artery damage grade were severe in hyperuricaemic group.

Surgical treatment for primary mitral valve tumor: a 25-year single-center experience.

OBJECTIVE: Primary mitral valve (MV) tumor is a rare lesion, and to date, there have been few larger surgical series of MV tumors. We retrospectively analyzed 11 cases of primary MV tumors regarding clinical and pathological features, surgical procedure and long-term outcomes. METHODS: From November 1983 to December 2008, we operated on 11 patients (age 36.3 ± 17.7 years, weight 55.4 ± 11.2 kg) with primary MV tumors. Symptoms were cardiac in 8 cases (72.7%) and neurologic in 3 (26.3%). Surgical procedures included en bloc excision and MV repair in 8 cases and tumor resection and MV replacement in 3. No radiotherapy or chemotherapy was given to patients with malignant tumors. RESULTS: Pathological diagnosis was papillary fibroelastoma in 3 cases, myxoma in 3, lymphangioma in 1, lipoma in 1, hemangioma in 1 and sarcoma in 2. No early deaths or complications occurred. Late death occurred in 2 patients with sarcoma 1 year postoperatively. At the latest follow-up, with a maximum of 25 years (mean 10.6 ± 8.8), the 9 survivors were in New York Heart Association functional class I with normal MV function and no echocardiographic evidence of local recurrence. CONCLUSIONS: The majority of primary MV tumors are benign. They can cause cardiac or neurologic symptoms and should be excised as soon as a diagnosis is made. For benign tumors, valve-sparing resection and valve repair are often possible with excellent long-term outcomes. The prognosis of malignant MV tumors is poor.

[Clinical implication of microvasculopathy in patients post heart transplantation].

OBJECTIVE: Assess the clinical implication of microvasculopathy detected by endomyocardial biopsy samples in patients post heart transplantation. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

[Association between dysplastic development of ventricular wall and primary cardiomyopathy: pathomorphological observations on 92 hearts from transplant recipients.].

OBJECTIVE: To investigate the morphological characteristics and types of ventricular wall with dysplastic development and their associations to primary cardiomyopathy. METHODS: Ninety-two hearts from heart transplant patients were studied soon after explanation from 2004 to 2007. Gross examination/measurement, histopathology and photography were performed. RESULTS: Dysplastic development of ventricular wall could be evidenced in patients with various heart diseases but more often in patients with primary cardiomyopathy, though the extension and distribution of dysplastic development of ventricular wall varied between patients with or without primary cardiomyopathy. Severe dysplastic development of ventricular wall is associated with clinical dysplastic cardiomyopathy. The range of extension and degree of dysplasia in the ventricular wall correlated positively to heart dilation/failure and time point of heart failure development. The incidence of severe ventricular wall dysplasia was 27.17% in all transplanted hearts and was 43.1% (25/58) in hearts diagnosed as primary cardiomyopathy (P < 0.05). The main pathological changes of dysplastic hearts were: (1) extensive proliferative hypertrophy of the heart wall, (2) fibrous/fat or fat/fibrous tissue replacement of normal myocardium, (3) disarrangement of myocardial fibers, (4) dysplastic change in the medium-sized intramural arteries. Dysplastic cardiomyopathy was presented mainly as a combination of several forms of dysplasia. The same clinical manifestations of dysplastic cardiomyopathy patients did not always show the same pathologic changes. Fibrous-fat tissue replacement was commonly found in dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Disarrangement of myocardium was often accompanied by hypertrophic cardiomyopathy. Dysplasia of intramural arteries could result in heart dilatation due to myocardial ischemia. CONCLUSION: Dysplasia of ventricular wall is a common variation of heart structure. Only severe or diffuse types of dysplasia is associated with cardiomyopathy, especially primary cardiomyopathy.

[Pathologic features of arrhythmogenic right ventricular cardiomyopathy with severe heart failure].

OBJECTIVES: To study the pathologic features of arrhythmogenic right ventricular cardiomyopathy (ARVC) in the phase of heart failure. METHODS: Eight cases underwent heart transplantation in Fuwai Hospital during the period from May, 2004 to July, 2007 with pathologic diagnosis of ARVC were studied. The age of patients ranged from 15 to 54 years. They had history of palpitation and syncope for 1 to 22 years. Severe heart failure was diagnosed according to the New York Heart Association Classification System. The recipient hearts were examined and the following parameters were evaluated: weight of heart, presence of cardiac dilatation, myocardial hypertrophy, fatty infiltration, fibrosis, parietal thrombosis and myocarditis. The degree of left ventricular involvement was also analyzed. RESULTS: Of the 8 cases studied, 7 cases with prominent right ventricular lesion (fibrofatty replacement) were classified as classic type. One case with prominent left ventricle lesion and mild right ventricle involvement was classified as left predominant type. No biventricular type and no pure fatty infiltration were found. The cases of classic type showed moderate to severe dilatation of right ventricle, sometimes with aneurysm formation. Left ventricle was involved in 6 cases, which showed diffuse interstitial fibrosis, patchy fibrous replacement and subepicardial fatty infiltration. Mild to moderate dilatation of left ventricle, myocardial hypertrophy and vacuolation were also observed in these cases. The case of left predominant type had severe hypertrophy and dilatation of left ventricle, with prominent diffuse interstitial fibrosis and transmural fatty infiltration. Besides, 3 cases showed left ventricular hypertrophy and parietal thrombosis in both ventricles. Focal lymphocytic myocarditis was noted in 1 case. CONCLUSIONS: Left ventricular involvement is common in the heart failure phase of ARVC. Extensive interstitial fibrosis, marked hypertrophy and degeneration of myocardial fibers, as well as severe cardiac dilatation with organized thrombi, represent the major pathologic changes which resembles dilated cardiomyopathy.