Myocardial fibrosis in patients with symptomatic obstructive hypertrophic cardiomyopathy: correlation with echocardiographic measurements, sarcomeric genotypes, and pro-left ventricular hypertrophy polymorphisms involving the renin-angiotensin-aldosterone system

IntroductionHypertrophic cardiomyopathy (HCM) is a heterogeneous disorder of the cardiac sarcomere, resulting in myocyte hypertrophy and disarray, interstitial fibrosis, and cardiac dysfunction. Our aim was to determine whether the amount of fibrosis in HCM correlates with echocardiographic measures of diastolic dysfunction, presence of HCM-susceptibility mutations, or polymorphisms in the renin-angiotensin-aldosterone system (RAAS).MethodsSurgical specimens from patients with obstructive HCM undergoing septal myectomy at the Mayo Clinic (2001–2004) were examined and compared with autopsy-derived tissues from age- and sex-matched normal controls. Digital image analysis was used to quantitate the fibrosis in representative microscopic sections. Genotyping was performed for myofilament-HCM using polymerase chain reaction, high-performance liquid chromatography, and direct DNA sequencing. RAAS polymorphism status was similarly established.ResultsThe study included 59 HCM cases and 44 controls. Patients with HCM exhibited more fibrosis (mean 17%, range 3–45%) than controls (mean 8%, range 3–17%) (P<.0001). A significant relationship existed between amount of fibrosis and maximum wall thickness (P=.02), left ventricular ejection fraction (P=.02), and peak early/late diastolic mitral annulus velocity (E/A ratio) (P=.002). Although there was no association between amount of fibrosis and myofilament-HCM genotype status or polymorphisms in the RAAS cascade, there was a trend toward more fibrosis in patients with ≥1 C-encoding allele in CYP11B2-encoded aldosterone synthase.ConclusionsPatients with HCM undergoing septal myectomy had significantly more myocardial interstitial fibrosis than controls. The amount of fibrosis in HCM patients correlated with degree of septal hypertrophy and left ventricular systolic and diastolic function. Notably, neither mutations in cardiac myofilament proteins or polymorphisms in RAAS exhibited strong associations with severity of myocardial fibrosis.     

Histopathological characteristics and oxidative injury secondary to atrial fibrillation in the left atrial appendages of patients with different forms of mitral valve disease

BackgroundThe prevalence of atrial fibrillation (AF) and the frequency cardioversion of AF postoperatively are different in different forms of mitral valve disease. We hypothesized that these differences would relate to different extent of histopathological characteristics and oxidative injury in different forms of mitral valve diseases.MethodsLeft atrial appendages were obtained from 24 patients of mitral valve disease with or without AF undergoing mitral valve surgery. Control data were obtained from left appendages of 4 persons in normal sinus rhythm (SR) died of traffic accident. Histopathology, immunohistochemistry, Western blotting and enzyme kinetics examination were performed to assess the extent of histopathological characteristics and oxidative injury.ResultsThe average cross-sectional diameter of atrial myocyte of mitral stenosis (MS)+AF, MS+SR, mitral regurgitation (MR)+AF, MR+SR and control was 25.62±7.56 μm, 20.20±9.34 μm, 21.69±7.00 μm, 13.93±4.32 μm and 9.81±2.34 μm, respectively. Significantly statistical difference was found between each group (P<.05).Increased degree of atrial interstitial fibrosis was seen both in MS and MR with AF patients compared to other groups (P<.05), and the extent of fibrosis was more remarkable in MR patients compared to MS patients (P<.05).The extent of 3-nitrotyrosine (3-NT) immunoreactivity significantly increased in the patients with MS and AF compared to those of MR and AF (P<.05), and the immunoprevalence of 3-NT was significantly increased in patients of MS and SR compared to those of MR and SR (P<.05). Correlation analysis demonstrated a negative correlation between creatine kinase (CK) activity and extent of 3-NT immunoreactivity in atrial tissues (r=?0.382, P<.05).Significant decreases in CK activity were observed in myocardium from all patients of mitral valve disease with or without AF compared to controls (P<.05).Western blotting demonstrating an increased prevalence of 3-NT formation in CK-MM was detected compared to control group (P<.05). Correlation analysis demonstrated a negative correlation between CK-MM activity and extent of CK-MM tyrosine nitration (r=?0.446, P<.05).ConclusionsIn different forms of mitral valve disease with different cardiac rhythm, the extent of histopathological characteristics and oxidative injury are different. Histopathological characteristics and oxidative injury not only relate to mitral valve disease but also relate to the development and sustain of AF.     

Association of monocyte chemoattractant protein 1 (MCP-1) gene polymorphism with lupus nephritis in Egyptian patients

Background and study aimMonocyte chemoattractant protein-1 (MCP-1) is a member of CC chemokine that plays an important role in the recruitment of monocytes/macrophages into renal tubulointerstitium. A biallelic A/G polymorphism at position ∼2518 in the MCP-1 gene was found to regulate MCP-1 expression. MCP-1 and its A/G gene polymorphism have been implicated in the pathogenesis of some renal diseases. The aim of the study was to investigate the role of the MCP-1 gene polymorphism as early predictors of the development of glomerulonephropathy in SLE patients. We also aimed to measure the serum and urinary levels of MCP-1 in patients with SLE, to find out its relation to clinical disease activity.Methods140 SLE patients (100 with nephritis and 40 without nephritis) and 80 controls were included in this study. MCP-1 gene polymorphism was analyzed by polymerase chain reaction. Serum and urine MCP-1 level were measured using high-sensitivity enzyme-linked immunosorbent assay.ResultsThe A/A genotype was more common in controls than in SLE patients, whereas both the A/G (P < 0.000) and G/G (P < 0.000) genotypes were more frequent in SLE patients. Carriers of G allele of the MCP-1 ∼2518 polymorphism had more than 7 fold increased risk to develop glomerulo-nephropathy in patients with SLE. High MCP-1 circulating levels production from patients with A/G and G/G genotypes was significantly higher than in A/A genotype. In addition there were significant differences in the mean levels of serum MCP-1 (P < 0.001) and urinary MCP-1 (P < 0.001) between patients and controls.ConclusionThe present study provides a new evidence that the presence of MCP-1 A (-2518) G gene polymorphism and high circulating MCP-1 levels can play an important role in the development of SLE and nephropathy in Egyptians.     

Genotype-phenotype associations between chymase and angiotensin—converting enzyme gene polymorphisms in chronic systolic heart failure patients

PurposeAngiotensin II, which plays a crucial role in the myocardial remodeling process of heart failure, is generated via the angiotensin-converting enzyme and chymase pathways. We studied angiotensin-converting enzyme and chymase-1 polymorphisms in patients with systolic heart failure and the correlation with clinical status and left ventricular function.MethodsWe genotyped 195 patients with heart failure and systolic left ventricular dysfunction (ejection fraction <40%) for angiotensin-converting enzyme insertion (I)/deletion (D) and chymase-1 (−1903G/A) polymorphisms. Heart failure etiology and patients' clinical manifestations were analyzed in relation to genotype subtypes.ResultsThe chymase-1 −1903 GG genotype was associated with a nonischemic heart failure etiology (χ² = 6.67, P = 0.009). In the group of heart failure patients, the odds ratio of chymase-1 GG genotype having a nonischemic etiology was 2.48 (95% CI 1.23–5.00). The chymase-1 GG genotype was associated with lower ejection fraction (P = 0.005). Conversely, the angiotensin-converting enzyme D allele had no detectable impact on systolic heart failure phenotype.ConclusionsIn patients with chronic systolic heart failure, the chymase-1 polymorphism was related to nonischemic etiology of heart failure. Patients homozygous for the G allele had a significantly greater reduction in systolic left ventricular function.     

Obese and diabetic KKAy mice show increased mortality but improved cardiac function following myocardial infarction

BackgroundIntroduction of the yellow obese gene (A^y) into mice (KKAy) results in obesity and diabetes by 5 weeks of age.MethodsUsing this model of type 2 diabetes, we evaluated male and female 6- to 8-month-old wild-type (WT, n=10) and KKAy (n=22) mice subjected to myocardial infarction (MI) and sacrificed at day (d) 7.ResultsDespite similar infarct sizes (50%±4% for WT and 49%±2% for KKAy, P=not significant), the 7d post-MI survival was 70% (n=7/10) in WT mice and 45% (n=10/22) in KKAy mice (P<.05). Plasma glucose levels were 1.4-fold increased in KKAy mice at baseline compared to WT (P<.05). Glucose levels did not change in WT mice but decreased 38% in KKAy post-MI (P<.05). End-diastolic and end-systolic dimensions post-MI were smaller and fractional shortening improved in the KKAy (5%±1% in WT and 10%±2% in KKAy, P<.05 for all). The improved cardiac function in KKAy was accompanied by reduced macrophage numbers and collagen I and III levels (both P<.05). Griffonia (Bandeiraea) simplicifolia lectin-I staining for vessel density demonstrated fewer vessels in KKAy infarcts (5.9%±0.5%) compared to WT infarcts (7.3%±0.1%, P<.05).ConclusionIn conclusion, our study in KKAy mice revealed a paradoxical reduced post-MI survival but improved cardiac function through reduced inflammation, extracellular matrix accumulation, and neovascularization in the infarct region. These results indicate a dual-role effect of obesity in the post-MI response.     

The effects of asymmetric ventricular filling on left–right ventricular interaction in the normal rat heart

Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P?<?0.001) and developed pressure (P?<?0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV?+?50?%, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV?+?50?% when RV volume was increased incrementally between 50 and 300?μl (P?<?0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P?<?0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV?+?50?% (P?<?0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P?<?0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation–perfusion characteristics within the lung.     

The role of human urotensin-II in patients with hypertrophic cardiomyopathy

Objective: Hypertrophic cardiomyopathy (HCM) is a genetic condition with the hallmark feature of left ventricular hypertrophy. Human Urotensin-II (hUT-II) is regarded as a cardiovascular autacoid/hormone, and it has cardiac inotropic and hypertrophic properties. Aims of this study were to elucidate the clinical significance of serum hUT-II levels as a potential new biomarker in patients with HCM.

Methods: This study included 40 HCM patients (60% males and 40% females) and were compared to 30 healthy control subjects (47% males and 53% females. All patients underwent extensive clinical, laboratory, and echocardiographic. Blood samples were taken to test for serum hUT-II levels by commercial ELISA Kit.

Results: Serum hUT-II was significantly higher (p < 0.01) in patients with HCM (15.8 ± 2.1 pmol/L) compared with healthy controls (3.3 ± 1.7 pmol/L). With regard to HCM patient, Serum hUT-II levels were significantly higher in the female with 16.3 ± 1.9 pmol/L than the male with 15.4 ± 2.2 pmol/L (p < 0.05). Among echocardiographic parameters, hUT-II was negatively associated with ejection fraction (r = -0.160, p = 0.324).

Conclusion: Results of the first study indicated that serum hUT-II levels were markedly elevated in patients with HCM. Serum hUT-II is a novel biomarker parameter that has clinical use in patients with the severity of LVH.     

Blended learning y predisposición al aprendizaje autodirigido en un programa de especialización dental

IntroductionOne of the challenges in higher education is to train professionals capable of maintaining lifelong learning. Because of it, the incorporation of ICT through strategies that involve online learning is essential. However, the success of its implementation depends on the ability of the student to self-manage their learning process. Therefore, the aim of this study was to relate levels of self-directed learning readiness of a specialization program students at the beginning of a scientific communication course with their satisfaction with the methodology implemented and it effectiveness on developing scientific communication competencies.Materials and methodsThree instruments were applied: Fisher, King & Tague's self-directed learning readiness scale B-learning strategy satisfaction questionnaire and Self-perceived scientific communication skills questionnaire. The relation between self-directed learning readiness and the results of the other questionnaires was evaluated.ResultsPositive correlations were observed between levels of willingness to learn and the dimensions of classroom activities (P<.01), interaction in face-to-face activities (P<.05) and teaching-learning activities (P<.05); between the levels of willingness to learn and the reading dimension of scientific articles (P<.01) and between the levels of self-confidence and the reading dimension of the scientific article (P<.05).ConclusionsSelf-direction in learning played an important role in the implementation of the educational strategy for these particular students.     

Quadriceps muscle compensatory activations are delayed following anterior cruciate ligament reconstruction using hamstring tendon graft

BackgroundCompensatory and anticipatory quadriceps activation (CQA and AQA) in response to postural perturbations are essential for functional stability of the knee. This study aimed at investigating CQA and AQA before and after anterior cruciate ligament reconstruction (ACLR) using hamstrings graft.MethodsTwelve participants with ACLR and 12 healthy controls were exposed to 10 either unpredictable or predictable perturbations of the knee before ACLR (T1), two months (T2) and six months (T3) after surgery. Latencies of CQA and AQA in vastus lateralis (VL), rectus femoris (RF) and vastus medialis (VM) were measured.ResultsLatency of CQA was delayed in ACLR compared to controls at T1 for VL (105 ± 25 vs. 57 ± 9 ms; P < .001), RF (102 ± 23 vs. 56 ± 9 ms; P < .001) and VM (107 ± 24 vs. 66 ± 16 ms; P < .001), at T2 for VL (68 ± 14 vs. 55 ± 10 ms; P < .01) and at T3 for VL (105 ± 22 vs. 58 ± 7 ms; P < .001), RF (102 ± 22 vs. 58 ± 12 ms; P < .001) and VM (106 ± 20 vs. 63 ± 8 ms; P < .001). AQA occurred earlier in ACLR than in controls at T1 for VL (− 82 ± 64 vs. − 14 ± 11 ms; P < .05) and VM (− 105 ± 68 vs. -9 ± 12 ms; P < .05).ConclusionCQA are delayed following ACLR with hamstring graft and should be addressd by post-surgical rehabilitation.     

Mediastinal adipose tissue expresses a pathogenic profile of 11 β-hydroxysteroid dehydrogenase Type 1, glucocorticoid receptor,and CD68 in patients with coronary artery disease

ObjectiveCardiac visceral fat is accepted to be a new marker for cardiometabolic risk due to its association with increased cardiovascular risk factors. This study aimed to compare the expression of 11 beta hydroxysteroid dehydrogenases (11β-HSD)-1, glucocorticoid receptor (GCR), and CD68 in mediastinal and subcutaneous adipose tissues (MAT, and SAT, respectively) and to assess their possible relationships with the development of coronary artery disease (CAD).Methods and resultsExpression of 11β-HSD-1, GCR, and CD68 mRNA levels were measured by quantitative real-time polymerase chain reaction in MAT and SAT tissues of 37 patients undergoing coronary artery bypass grafting due to CAD (CAD group) and 19 non-CAD patients (controls) undergoing heart valve surgery. 11β-HSD-1 in MAT and SAT and GCR expression in MAT and SAT were found to be significantly increased in CAD group when compared with controls (P<.05, respectively). In CAD group, 11β-HSD-1 mRNA levels were found to be significantly higher in MAT compared to SAT (P<.05). CD68 mRNA levels were significantly higher in MAT of CAD group compared to controls (P<.05). Immunohistochemical analyses demonstrated the presence of CD68+ cells and increased 11β-HSD-1 expression in MAT of CAD group compared to SAT.ConclusionThe present study demonstrate that the mediastinal fat exhibits a pathogenic mRNA profile of 11β-HSD-1, GCR, and CD68. The identification of 11β-HSD-1 expression within the mediastinal fat, along with increased GCR expressions and the presence of CD68+ cells highlight that MAT potentially contributes to the pathogenesis of CAD.     

Suture configuration techniques have no effect on mid-term clinical outcomes of arthroscopic meniscus root repairs

BackgroundThe aim of this study was to evaluate the clinical and radiological outcomes of arthroscopic transtibial pullout repair (ATPR) for the medial meniscus with both two modified loop stitches (TLS) and two simple stitches (TSS) techniques.MethodsBetween January 2013 and January 2016, 41 patients who had undergone ATPR for medial root tears with TLS and TSS techniques were retrospectively evaluated. The mean age at operation was 53 years (range 45–58). The mean follow-up period was 44.6 months (range 26–64). Lysholm knee score was used for clinical evaluation before and after surgery. For all patients, meniscal extrusion distances in the coronal plane were measured using magnetic resonance imaging and were recorded both preoperatively and at final follow-up.ResultsThere was no difference in terms of meniscus extrusion measurements between groups preoperatively (P > .05). Postoperative meniscus extrusion measurements were 2.1 ± 0.3 and 2.9 ± 0.6 in TLS and TSS groups, respectively. The difference between groups was statistically significant (P < .01). The increase in postoperative Lysholm score was found to be statistically significant in both groups (P < .01). Postoperative Lysholm scores were 88.8 ± 3.7 and 87.6 ± 4.8 in TLS and TSS groups, respectively. The difference between groups was statistically insignificant (P > .05).ConclusionsThere was a significant improvement in Lysholm knee scores postoperatively in patients that underwent transtibial pullout medial meniscus posterior root repair regardless of meniscus reduction level and suture configuration types. Although TLS technique was superior to TSS technique in terms of meniscus reduction, this meniscus reduction did not create any clinical difference at clinical outcome.     

Effects of nicotinic acid on endothelial cells and platelets

BackgroundInteractions between platelets and endothelial cells under inflammatory conditions lead to an increased expression of various activity markers of atherosclerosis in the vessel wall. The purpose of this study was to investigate possible protective effects of nicotinic acid in an in vitro endothelial cell model.MethodsAfter a 24-hour incubation period with nicotinic acid (1 mmol/l), human umbilical vein endothelial cells were stimulated for 1 h with lipopolysaccharide and were then incubated in direct contact with activated platelets. Following this incubation, the expression of CD40L and CD62P on platelets and the expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, uPAR, and MT1-MMP on endothelial cells were measured by flow cytometry. Supernatants were analyzed by ELISA for soluble MCP-1 and MMP-1.ResultsThe increased expression of VCAM-1 on endothelial cells by proinflammatory stimulation with activated platelets was significantly reduced through preincubation with nicotinic acid (P<.05). Furthermore, platelets in direct contact with preincubated endothelial cells showed a significant reduction in their CD62P and CD40L expression when compared to platelets incubated with untreated endothelial cells (P<.05). Treatment with nicotinic acid did not have a significant effect on ICAM-1, uPAR, and MT1-MMP expression on endothelial cells. Levels of soluble MCP-1 and MMP-1 in supernatants were lower after preincubation with nicotinic acid.ConclusionNicotinic acid inhibits platelet activation after platelets contacted nicotinic acid treated endothelial cells and inhibits VCAM-1 expression on human endothelial cells under inflammatory conditions. These findings suggest a possible pleiotropic therapeutic relevance of nicotinic acid in atherosclerosis.     

Clinical efficacy of Qili Qiangxin Capsule combined with exercise rehabilitation in the treatment of chronic heart failure

ObjectiveTo investigate the effect of Qili Qiangxin Capsule combined with cardiac exercise rehabilitation on patients with chronic heart failure (CHF).MethodsA total of 93 CHF patients admitted to Shanghai's Putuo District Central Hospital from March 2021 to December 2021 were included in the study and were randomly divided into the control group (46 cases) and the intervention group (47 cases). The control group received routine treatment, and the intervention group was treated with Qili Qiangxin Capsule as well as cardiac exercise rehabilitation that was routine for patients with CHF. The total effective rate, 6-min walking distance, left ventricular ejection fraction, B-type natriuretic peptide (BNP) level, left ventricular end-systolic diameter, and left ventricular end-diastolic diameter were compared in terms of the two groups.ResultsAfter three months of treatment, when compared with the control group, the total effective rate of the treatment on the patients in the intervention group increased significantly (87.23% vs 63.04%; P < 0.05). The 6-minute walking distance, BNP level, and the left ventricular end-diastolic diameter improved more drastically in the intervention group than in the control group, and the differences were statistically significant (P < 0.05). There was no significant difference in the other indicators before and after treatment (P > 0.05).ConclusionQili Qiangxin Capsule combined with cardiac exercise rehabilitation can significantly improve cardiac and motor function in patients with CHF.     

Association between cognitive function and asthma in adults

BackgroundCognitive deficits are associated with asthma globally; however, the association between cognitive function and asthma has not been fully elucidated.ObjectiveTo assess the relationship between asthma and cognitive function.MethodsA total of 202 patients with asthma aged older than 18 years were analyzed retrospectively from August 2019 to February 2020. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) test. We compared the associations of clinical parameters with cognitive function (MoCA, ≥23 vs <23) and lung function (forced expiratory volume in 1 second [FEV1], ≥70% vs <70%).ResultsOf the total participants, 89 (44.1%) indicated cognitive impairment, of whom23.1% were aged less than 65 years and 72.9% were aged 65 years or older. MoCA scores were significantly different according to age (24.91 ± 3.89 for ages <65 years vs 19.11 ± 5.11 for ages ≥65 years, P < .001) and lung function (23.29 ± 5.17 for FEV1 ≥70% vs 21.23 ± 5.21 for FEV1 <70%, P = .006), but not according to asthma control (22.35 ± 5.38 for nonsevere asthma vs 22.88 ± 4.91 for severe asthma, P = .55). Age (odds ratio [OR], 1.07; 95% confidence interval [CI], 1.014-1.13; P = .01), educational status (OR, 6.068; CI, 2.175-16.927; P = .001), and asthma duration (OR, 1.007; CI, 1.001-1.013; P = .02) were significantly associated with cognitive impairment.ConclusionCognitive impairment was largely observed in adults (44.1%) with asthma and was more prevalent in older adults than in younger adults. Longer asthma duration and lower lung function were more associated with cognitive dysfunction.     

Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function

Abstract. We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a moremarked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.     

Application of assisted portal under anterior horn of lateral meniscus for the treatment of discoid meniscus injury

PurposeThe assisted inferior anterolateral portal under anterior horn of the lateral meniscus (UAHLM portal) was applied to treat the lateral discoid meniscus injury conveniently and the clinical outcomes were evaluated.MethodsA retrospective review was conducted on 60 patients who underwent arthroscopic surgery with a symptomatic discoid lateral meniscus. Normal anterolateral/anteromedial portals assisted with UAHLM portal (1-2 cm inferior to the anterolateral portal) were used. All patients were followed up for 24–48 months (median, 33 months) and evaluated by MRI images and clinical outcomes including clinical findings, Lysholm scores and IKDC scores.ResultsAfter meniscus plasty with or without repair, most of the upper layer of lateral meniscuses was retained. A total of 54 patients (16 males and 38 females, 42 ± 17.8 years old) showed satisfactory clinical results without requiring reoperation after a median follow-up time of 33 months. At final follow-up, a full range of motion was achieved in all patients. MRI indicated the thickness of anterior horn of lateral meniscus was (5.38 ± 1.09 mm) before the operation and (4.04 ± 0.71 mm) after the operation at the 2-year follow-up; clinical outcomes were improved significantly than the baseline: positive McMurray test (50 vs. 2, P < 0.001), Lysholm score (64.9 ± 9.0 vs. 94.7 ± 4.9, P < 0.001), and IKDC score (54.4 ± 7.7 vs. 92.6 ± 4.3, P < 0.001). No significant complication was observed during the follow-up.ConclusionThus, this technique with assisted UAHLM portal was convenient for arthroscopic discoid meniscus plasty and meniscus repair and served as an effective method in patients with a symptomatic discoid lateral.     

Spontaneously occurring restrictive nonhypertrophied cardiomyopathy in domestic cats: a new animal model of human disease

BackgroundSpontaneously occurring small animal models of myocardial disease, closely resembling the human condition, have been reported for hypertrophic cardiomyopathy (in cats) and arrhythmogenic right ventricular cardiomyopathy (in cats and boxer dogs). Nonhypertrophied restrictive cardiomyopathy (RCM) is a well-recognized but relatively uncommon primary heart muscle disease causing substantial morbidity in humans. We describe RCM occurring in felines here as a potential model of human disease.MethodsWe used two-dimensional and Doppler echocardiography to define morphologic and functional features of RCM in 35 domestic cats (25 male; 10±4 years old) presenting to a subspecialty veterinary clinic. Ten underwent complete necropsy examination. Echocardiographic parameters of diastolic filling were compared to those in 41 normal controls.ResultsThe 35 cats presented with congestive heart failure (n=32), lethargy (n=2), or syncope (n=1), associated with thromboembolism in 5 and supraventricular tachyarrhythmias in 8. During an average 4.4-year follow-up period, 18 died or were euthanized due to profound heart failure, and 3 died suddenly; survival from clinical presentation to death was 0.1 to 52 months. Echocardiographic and necropsy examination showed biatrial enlargement, nondilated ventricular chambers, and normal wall thicknesses and atrioventricular valves. Histopathology demonstrated disorganized myocyte architecture and patchy replacement myocardial fibrosis. Pulsed Doppler demonstrated restrictive physiology with increased early (E) mitral filling velocity (1.1±0.3 m/s) and peak E to peak late (A) flow ratios (4.3±1.2), reduced A filling velocity (0.3±0.1 m/s), and shortened mitral deceleration time (40.7±9.3 ms; all P<.001 vs. controls), with preserved left ventricular systolic function.ConclusionsA primary myocardial disease occurring spontaneously in domestic cats is remarkably similar to restrictive nondilated and nonhypertrophied cardiomyopathy in man and represents another potential animal model for human disease.