A Web-Based Virtual Microscopy Platform for Improving Academic Performance in Histology and Pathology Laboratory Courses: A Pilot Study.

Virtual microscopy (VM) has been utilized to improve students' learning experience in microscope laboratory sessions, but minimal attention has been given to determining how to use VM more effectively. The study examined the influence of VM on academic performance and teacher and student perceptions and compared laboratory test scores before and after VM incorporation. A total of 662 third-year students studying histology and 651 fourth-year students studying pathology were divided into two groups. The light microscopy (LM) group used a light microscope in 2014 and 2015, while the LM + VM group used the VM platform and a light microscope in 2016 and 2017. Four factors positively predict laboratory scores (R square, 0.323; P < 0.001): (i) the pathology course and test-enhanced learning, (ii) the VM platform and experience, (iii) medical students and lecture scores, and (iv) female students. The LM + VM group exhibited less score variability on laboratory examinations relative to their mean than the LM group. The LM + VM group was also associated with fewer failing grades (F grade; odds ratio, 0.336; P < 0.001) and higher scores (A grade; odds ratio, 2.084; P < 0.001) after controlling for sex, school, course, and lecture grades. The positive effect of the VM platform on laboratory test grades was associated with prior experience using the VM platform and was synergistic with more interim tests. Both teachers and students agreed that the VM platform enhanced laboratory learning. The incorporation of the VM platform in the context of test-enhanced learning may help more students to master microscopic laboratory content.

Thromboelastography characterized CD36 null subjects as slow clot formation and indicative of hypocoagulability.

BACKGROUND: Platelet CD36 is the receptor for oxidized low-density lipoprotein and collagen. The conventional platelet test cannot distinguish CD36-null subjects from normal expression subjects. Thromboelastography (TEG) testing can analyze global hemostasis. TEG testing data on CD36-null subjects are not available. METHODS: Our subjects were 40 apheresis platelet donors, including 8 CD36-null individuals. We grouped the donors according to the platelet CD36 expression levels to assess the effects of platelet CD36 expression levels on TEG measurement variables. RESULTS: The whole blood TEG test revealed that CD36-null subjects had prolonged reaction time of fibrin formation (TEG R time) and a slower rate to build up cross-linked fibrin (TEG α angle). The final maximal amplitudes of clot formation showed little difference between CD36-null individuals and normal expression individuals. Correlation analysis showed that CD36 expression levels were negatively correlated with TEG R time (r = -0.342, p = 0.031) and positively correlated with the TEG α angle (0.379, p = 0.016). TEG testing on apheresis platelet samples with diminished heterocellular interaction did not reveal differences between CD36-null and normal expression individuals. A subanalysis of the data of a group of healthy subjects showed that platelet CD36 levels correlated positively with platelet-monocyte aggregates (PMAs). Low PMA can diminish heterocellular interaction and likely explain the abnormal TEG results observed in CD36-null individuals. CONCLUSION: TEG distinguishes CD36-null subjects from normal CD36 expression subjects as having a slower rate of fibrin formation and reassessment of TEG-based diagnostic monitoring is necessary for CD36 null subjects.

Intermediate CD14++CD16+ monocyte predicts severe coronary stenosis and extensive plaque involvement in asymptomatic individuals.

Circulating leukocyte subtypes and monocyte subsets are independent predictors of cardiovascular events. We hypothesized that an increased leukocyte subtype would predict severe coronary stenosis and extensive plaque involvement. We retrospectively analyzed clinical, laboratory, and coronary CT data in a total of 588 asymptomatic adults (69% men; mean age, 57 ± 9 years) undergoing a general health check-up. Intermediate CD14++CD16+ monocyte count had the strongest association with mixed and calcified plaque scores, whereas the numbers of neutrophils and classical CD14++CD16- monocytes were significantly associated with non-calcified plaque score. Only high CD14++CD16+ monocyte count (>12 cells/µL) significantly predicted extensive plaque involvement [odds ratio 3.16 (95% confidence interval 1.84-5.43), P < 0.001; quartile 4 vs. 1-3] and severe coronary stenosis [3.67 (1.84-7.33), P < 0.001; quartile 4 vs. 1-3] after adjustments for Framingham Risk Score (FRS), metabolic syndrome, and C-reactive protein. The CD14++CD16+ monocyte count, when added to FRS, significantly reclassified 30.4 and 26.7% of the overall and 50.2 and 36.2% of the intermediate-risk population (FRS 6-20%) for predicting extensive plaque involvement and severe coronary stenosis, respectively. Thus, in asymptomatic individuals, intermediate CD14++CD16+ monocyte could independently predict severe CAD and improve risk stratification.

The ratio of epicardial to body fat improves the prediction of coronary artery disease beyond calcium and Framingham risk scores.

The association between epicardial fat and coronary artery disease (CAD) might be affected by general adiposity. We aimed to determine whether the percentage of epicardial adipose tissue (%EAT), defined as the mass ratio of epicardial fat to body fat, could improve prediction of asymptomatic CAD. We consecutively enrolled 846 adults who underwent coronary computed tomography angiography as part of a health check-up and assessed their coronary stenosis severity and epicardial fat mass. Body fat mass was measured by bioelectrical impedance analysis. Subjects with CAD history, hyperthyroidism, pitting edema, or subjects taking diuretics or thiazolidinedione were excluded. Obstructive CAD was defined as at least one coronary artery with 50 % or greater obstruction, and severe CAD was defined as 70 % or greater obstruction. The %EAT had the maximum area under the curve for predicting the presence of CAD and superior discriminative performance to EAT and other EAT-indexed parameters. Multivariable logistic regression analysis revealed that %EAT >0.41 % was a predictor of obstructive CAD [odds ratio 3.59 (95 % confidence interval 2.28-5.64)], and %EAT >0.47 % was a predictor of severe CAD [4.01 (2.01-7.99)] after adjustment for calcium score and Framingham risk score. This prediction was more pronounced in subjects with higher body fat percentage (≥25 % for men and ≥35 % for women), Framingham risk score (≥10 %), or calcium score (≥100). A spillover of body fat at epicardium over a critical threshold is associated with significant coronary stenosis. This association was independent of obesity, coronary calcium burden, and Framingham risk factors.

The Emerging Roles of Coronary Computed Tomographic Angiography: Acute Chest Pain Evaluation and Screening for Asymptomatic Individuals.

UNLABELLED: Coronary computed tomographic angiography (CCTA) has been widely available since 2004. After that, the diagnostic accuracy of CCTA has been extensively validated with invasive coronary angiography for detection of coronary arterial stenosis. In this paper, we reviewed the updated evidence of the role of CCTA in both scenarios including acute chest pain and screening in asymptomatic adults. Several large-scale studies have been conducted to evaluate the diagnostic value of CCTA in the context of acute chest pain patients. CCTA could play a role in delivering more efficient care. For risk stratification of asymptomatic patients using CCTA, latest studies have revealed incremental benefits. Future studies evaluating the totality of plaque characteristics may be useful for determining the role of noncalcified plaque for risk stratification in asymptomatic individuals. KEY WORDS: Acute chest pain • Computed tomography • Coronary artery disease • Health screening • Stable angina.

High-fat diet induces cardiomyocyte apoptosis via the inhibition of autophagy.

PURPOSE: Excessive fat intake induces obesity and causes cardiac injury. Intracellular degradation process involving destruction of long-lived proteins and organelles maintains homeostasis for cells under stress. The purpose of this study was to explore the relation of high-fat diet (HFD)-induced cardiac injury and intracellular degradation process with regard to autophagy and ER stress. METHODS AND RESULTS: HFD feeding for 24 weeks induced hyperglycemia, hyperlipidemia, and cardiac hypertrophy in adult male C57BL/6 mice. In the heart, PARP cleavage, an indicator of apoptosis, levels of LC3-II and p62, indicators of autophagy, and CHOP, indicator of ER stress, were increased. A palmitate-treated cardiomyoblast (H9C2) cell culture was examined to explore how HFD induced myocardial injury. Excessive palmitate (400 µM) treatment induced apoptosis and increased the number of autophagosomes and acid vacuoles of H9C2 cells. Besides, it elevated the expression of LC3-II, p62, and PARP cleavage. Induction of autophagy by rapamycin ameliorated palmitate-induced apoptosis, while inhibition of autophagy by 3-methyladenine or LC3 siRNA exacerbated palmitate-induced apoptosis. Palmitate treatment also induced CHOP expression which is associated with ER stress. CONCLUSION: HFD can cause cardiac injury by induction of apoptosis which is associated with autophagy dysregulation and ER stress. In addition, autophagy deficiency augments cardiac apoptosis, suggesting that autophagy serves as a pro-survival role in lipotoxic condition.

Endothelial progenitor cells in primary aldosteronism: a biomarker of severity for aldosterone vasculopathy and prognosis.

CONTEXT: Primary aldosteronism (PA) is associated with a higher incidence of cardiovascular events, probably through mineralocorticoid receptor (MR)-dependent endothelial cell dysfunction, in comparison with essential hypertension (EH). OBJECTIVE: Our objective was to investigate the number and function of endothelial progenitor cells (EPC) in PA and the relationship with arterial stiffness and disease progression. DESIGN AND SETTING: We conducted a prospective study of the change of EPC number and outcome of PA patients after treatment at a tertiary medical center. PRIMARY OUTCOMES: Changes in arterial stiffness and EPC number after treatment and the curability of hypertension were assessed. PATIENTS: A total of 113 PA patients (87 patients diagnosed with aldosterone-producing adenoma, 26 with idiopathic hyperaldosteronism) and 55 patients with EH participated. RESULTS: PA patients had higher arterial stiffness than EH patients (P = 0.006), with a lower numbers of circulating EPC and endothelial colony-forming units (P < 0.05). The differences were ameliorated at 6 months after unilateral adrenalectomy or treatment with spironolactone. Expression of MR was identified in the EPC. The number of circulating EPC was inversely correlated with the plasma aldosterone concentration (P = 0.021), arterial stiffness (P = 0.029) and serum high-sensitivity C-reactive protein (P = 0.03). High-dose aldosterone (10(-5) and 10(-6) m) attenuated EPC proliferation and angiogenesis in vitro. Among the 45 patients who underwent unilateral adrenalectomy, 32 (71%) were cured of hypertension. The preoperative number of EPC [log(EPC number percent) >-3.6] predicted the curability of hypertension after adrenalectomy (P = 0.003). CONCLUSIONS: The relative deficiency of EPC in PA patients may contribute to aldosterone vasculopathy, which can be reversed by adrenalectomy and spironolactone. High aldosterone levels attenuated EPC proliferation and angiogenesis. Circulating EPC number may be a valuable biomarker to identify PA patients with a high incidence of arterial stiffness and to predict postoperative residual hypertension of aldosterone-producing adenoma.

Using clinical cardiovascular risk scores to predict coronary artery plaque severity and stenosis detected by CT coronary angiography in asymptomatic Chinese subjects.

We aimed to determine whether the Framingham risk score (FRS), systematic coronary risk evaluation (SCORE), and Chinese multi-provincial cohort study (CMCS) could predict anatomic severity of coronary plaques. From January 2007 to October 2010, we performed a contrast-enhanced 64-slice or 256-slice multidetector computed tomography coronary angiography as part of a health check-up protocol in 806 asymptomatic subjects (70.5% male, 56 ± 9 year-old). Risk scores significantly correlated with calcium volume score, plaque stenosis score and plaque distribution score (P < 0.001). Of the 3 risk scores, the SCORE system showed the best correlation. Overall, 180 (22%) and 37 (5%) subjects were found to have stenosis of 50-69% and more than 70% in at-least one coronary artery segment, respectively. In the prediction of the presence of obstructive CAD (≥ 50% diameter stenosis), all risk scores had similar discrimination. In the prediction of severe CAD (≥ 70% diameter stenosis), FRS and CMCS had similar area under curves but SCORE discriminated better than FRS (P < 0.05). The optimal cutoff point to predict obstructive CAD was 9.54% for FRS, 1.05% for CMCS, and 0.95% for SCORE, whereas to predict severe CAD was 9.63, 1.05, 1.15% for FRS, CMCS, SCORE, respectively, with a sensitivity of 0.61-0.70 and a specificity of 0.55-0.66. Cardiovascular risk scores are associated with the severity and extent of coronary artery plaque. The stronger association might translate into a better discrimination using SCORE. These findings will aid in the appropriate selection or recalibration of the risk assessment system for cardiovascular disease screening.

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone.

PURPOSE: To study the effect of exercise training on the myocardial perfusion in the postinfarct myocardium. MATERIALS AND METHODS: Twenty-nine patients with stable chronic myocardial infarction were randomly assigned to either a training group (N = 17) or a control group (N = 12). The training group received a 3-month exercise program. Cardiovascular MR was first performed before the training to establish a baseline, and subsequently performed once again upon conclusion of the program. Late gadolinium enhancement was used both to define the infarct and remote zones and to quantify the ratio of the residual viable myocardium (VMR) within the infarct zone. The myocardium was divided into subendocardial and subepicardial layers with equal thickness. The interval change of myocardial perfusion reserve (MPR) was computed for each zone and layer. The association between the exercise-induced perfusion change and VMR was analyzed for layers of the infarct zone. RESULTS: In the training group, the remote zone showed significantly increased MPR. The infarct zone showed no perfusion change in the subendocardial layer, but it demonstrated significantly increased MPR in the subepicardial layer. In the infarct zone, the change in MPR was associated with VMR. CONCLUSION: In chronic myocardial infarction, the exercise-induced perfusion change in the infarct zone is proportional to the amount of residual viable myocardium.

Plasma fatty acids and the risk of metabolic syndrome in ethnic Chinese adults in Taiwan.

BACKGROUND: Evidence of predictive power of various fatty acids on the risk of metabolic syndrome was scanty. We evaluated the role of various fatty acids, including saturated fat, monounsaturated fat, transfat, n-6 fatty acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), for the risk of the metabolic syndrome in Taiwan. RESULTS: A nested case-control study based on 1000 cases of metabolic syndrome and 1:1 matched control subjects. For saturated fat, monounsaturated fat and transfat, the higher the concentration the higher the risk for metabolic syndrome: participants in the highest quintile had a 2.22-fold (95% confidence interval [CI], 1.66 to 2.97) higher risk of metabolic syndrome. In addition, the participants in higher EPA quintiles were less likely to have the risk of metabolic syndrome (adjusted risk, 0.46 [0.34 to 0.61] for the fifth quintile). Participants in the highest risk group (low EPA and high transfat) had a 2.36-fold higher risk of metabolic syndrome (95% CI, 1.38 to 4.03), compared with those in the lowest risk group (high EPA and low transfat). For prediction power, the area under ROC curves increased from 0.926 in the baseline model to 0.928 after adding fatty acids. The net reclassification improvement for metabolic syndrome risk was substantial for saturated fat (2.1%, P = 0.05). CONCLUSIONS: Plasma fatty acid components improved the prediction of the metabolic syndrome risk in Taiwan.

Prediction model for high glycated hemoglobin concentration among ethnic Chinese in Taiwan.

BACKGROUND: This study aimed to construct a prediction model to identify subjects with high glycated hemoglobin (HbA1c) levels by incorporating anthropometric, lifestyle, clinical, and biochemical information in a large cross-sectional ethnic Chinese population in Taiwan from a health checkup center. METHODS: The prediction model was derived from multivariate logistic regression, and we evaluated the performance of the model in identifying the cases with high HbA1c levels (> = 7.0%). In total 17,773 participants (age > = 30 years) were recruited and 323 participants (1.8%) had high HbA1c levels. The study population was divided randomly into two parts, with 80% as the derivation data and 20% as the validation data. RESULTS: The point-based clinical model, including age (maximal 8 points), sex (1 point), family history (3 points), body mass index (2 points), waist circumference (4 points), and systolic blood pressure (3 points) reached an area under the receiver operating characteristic curve (AUC) of 0.723 (95% confidence interval, 0.677- 0.769) in the validation data. Adding biochemical measures such as triglycerides and HDL cholesterol improved the prediction power (AUC, 0.770 [0.723 - 0.817], P = < 0.001 compared with the clinical model). A cutoff point of 7 had a sensitivity of 0.76 to 0.96 and a specificity of 0.39 to 0.63 for the prediction model. CONCLUSIONS: A prediction model was constructed for the prevalent risk of high HbA1c, which could be useful in identifying high risk subjects for diabetes among ethnic Chinese in Taiwan.

A prediction model for the risk of incident chronic kidney disease.

BACKGROUND: Chronic kidney disease is a health burden for the general population. We designed a cohort study to construct prediction models for chronic kidney disease in the Chinese population. METHODS: A total of 5168 participants were followed up during a median of 2.2 (interquartile range, 1.5-2.9) years, and 190 individuals (3.7%) developed chronic kidney disease, defined by a glomerular filtration rate of less than 60 mL/min/1.73 m(2). RESULTS: We developed a point system to estimate chronic kidney disease risk at 4 years using the following variables: age (8 points), body mass index (2 points), diastolic blood pressure (2 points), and history of type 2 diabetes (1 point) and stroke (4 points) for the clinical model, with the addition of uric acid (2 points), postprandial glucose (1 point), hemoglobin A1c (1 point), and proteinuria 100 mg/dL or greater (6 points) for the biochemical model. Similar discrimination measures were found between the clinical model (area under the receiver operating characteristic curve, 0.768; 95% confidence interval (CI), 0.738-0.798) and the biochemical model (area under the receiver operating characteristic curve, 0.765; 95% CI, 0.734-0.796). The area under the receiver operating characteristic curve of the clinical model was 0.667 (95% CI, 0.631-0.703) for the external validation data from community-based cohort participants. The optimal cutoff value for the clinical model was set as 7, with a sensitivity of 0.76 and a specificity of 0.66. CONCLUSION: We constructed a clinical point-based model to predict the 4-year incidence of chronic kidney disease. This prediction tool may help to target Chinese subjects at risk of developing chronic kidney disease.

Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization.

AIMS: To explore whether exercise can improve cardiac function in a post-myocardial infarction (MI) rabbit model and to determine contributing factors in the left ventricle (LV). METHODS AND RESULTS: Adult male New Zealand White rabbits (2.5-3 kg) underwent MI by ligation of the left anterior descending coronary artery. For 8 weeks after surgery, sham-operated, and post-MI rabbits were housed under sedentary conditions or assigned to a 4-week treadmill exercise protocol at a speed of 1.0 km/h for 30 min 5 days per week, then sacrificed. The non-infarcted region of the LV was harvested for further analysis. MI decreased left ventricular ejection fraction (LVEF) and increased thiobarbituric acid reactive substances (TBARS) generation in the LV. Exercise improved the cardiac function of MI rabbits. Left ventricular LC3II/LC3I (microtubule-associated protein light chain 3) in the MI group was 2.1-fold higher than that of the sham group, exercise significantly decreased LC3II/LC3I in the MI group. MI down-regulated the expression of heart-type fatty acid binding protein (h-FABP), and exercise up-regulated h-FABP. In addition, LVEF had a significantly positive correlation with h-FABP and a negative correlation with LC3II/LC3I. CONCLUSION: Exercise induced change in autophagic function and fatty acid utilization may contribute to the improvement in ventricular function in the infarcted heart.

High-density lipoprotein-cholesterol trajectory pattern, associated lifestyle and biochemical factors among Taiwanese.

BACKGROUND: Little is known about high-density lipoprotein-cholesterol (HDL-C) trajectory patterns among ethnic Chinese in Taiwan, or the effects of lifestyle and biochemical measurements on these trajectory patterns. METHODS AND RESULTS: This longitudinal study was based on 330 adult participants who underwent biochemical measurements annually from 2003 to 2006. As time progressed, HDL-C increased significantly; women had a consistently higher value (10 mg/dl) than men. An increase of 1 kg/m(2) in body mass index was associated with -1.00 +/-0.25 mg/dl HDL-C for women (P=0.0001) and -0.78 +/-0.11 mg/dl for men (P<0.0001). Current smoking was inversely associated with HDL-C in men only. Systolic blood pressure and exercise frequency were positively associated with HDL-C in men only. Compared with non-smokers, participants who smoked had a lower HDL-C level of -8.42 +/-4.90 mg/dl in women (P=0.09) and -3.60 +/-0.94 mg/dl in men (P=0.0001). In contrast, a 1-h increase in exercise frequency every week was related to an increased HDL-C level of 0.38 +/-0.28 mg/dl for women (P=0.18) and 0.53 +/-0.14 mg/dl for men (P=0.0001). CONCLUSIONS: An increase in HDL-C was shown over a 4-year period and gender-specific lifestyle factors were associated with HDL-C concentration among ethnic Chinese in Taiwan.

Postprandial glucose improves the risk prediction of cardiovascular death beyond the metabolic syndrome in the nondiabetic population.

OBJECTIVE: With increasing evidence about the cardiovascular risk associated with postprandial nonfasting glucose and lipid dysmetabolism, it remains uncertain whether the postprandial glucose concentration increases the ability of metabolic syndrome to predict cardiovascular events. RESEARCH DESIGN AND METHODS: This was an observational study of 15,145 individuals aged 35-75 years without diabetes or cardiovascular diseases. Postprandial glucose was obtained 2 h after a lunch meal. Metabolic syndrome was diagnosed using the criteria of the U.S. National Cholesterol Education Program Adult Treatment Panel III. Cardiovascular and all-cause deaths were primary outcomes. RESULTS: During a median follow-up of 6.7 years, 410 individuals died, including 82 deaths from cardiovascular causes. In a Cox model adjusting for metabolic syndrome status as well as age, sex, smoking, systolic blood pressure, LDL, and HDL cholesterol levels, elevated 2-h postprandial glucose increased the risk of cardiovascular and all-cause death (per millimole per liter increase, hazard ratio 1.26 [95% CI 1.11-1.42] and 1.10 [1.04-1.16], respectively), with significant trends across the postprandial glucose quintiles. Including 2-h postprandial glucose into a metabolic syndrome-included multivariate risk prediction model conferred a discernible improvement of the model in discriminating between those who died of cardiovascular causes and who did not (integrated discrimination improvement 0.4, P = 0.005; net reclassification improvement 13.4%, P = 0.03); however, the improvement was only marginal for all-cause death. CONCLUSIONS: Given the risk prediction based on metabolic syndrome and established cardiovascular risk factors, 2-h postprandial glucose improves the predictive ability to identity nondiabetic individuals at increased risk of cardiovascular death.

Cell therapy generates a favourable chemokine gradient for stem cell recruitment into the infarcted heart in rabbits.

AIMS: Stem cell recruitment into the heart is determined by a concentration gradient of stromal-derived factor 1 (SDF-1) from bone marrow to peripheral blood and from blood to injured myocardium. However, this gradient is decreased in chronic myocardial infarction (MI). This study evaluated the effect of cell therapy using bone marrow stromal cells (BMSCs) on an SDF-1 gradient in post-infarction rabbits. METHODS AND RESULTS: Myocardial infarction was induced in male New Zealand white rabbits (2.5-3 kg) by ligation of the left anterior descending coronary artery. Two months later, the rabbits were randomized to either saline or BMSC (2 x 10(6) autologous BMSCs injected into the left ventricular cavity) treatment. Four weeks after therapy, the SDF-1 gradients from bone marrow to blood and from blood to myocardium increased in the BMSC group compared with the saline group. This was accompanied by an increase in cells positive for CD34, CD117, and STRO-1 in the myocardium, resulting in more capillary density, better cardiac function, and a decrease in infarct size. CONCLUSION: Generation of an SDF-1 gradient towards the heart is a novel effect of BMSC-based cell therapy. This effect facilitates stem cell recruitment into remodelled myocardium and supports improvement in cardiac function.

Association of fasting and post-prandial hyperglycemia on the risk of cardiovascular and all-cause death among non-diabetic Chinese.

The role of post-prandial glucose on cardiovascular risk among Chinese adults without diabetes was investigated. In a median follow-up of 3.5 years on 16,590 participants, 95 cardiovascular deaths were found. The relative risk in the highest quintile post-prandial glucose was 1.61 (P for trend, 0.05) for cardiovascular death.

A proteomic study of the effects of ramipril on post-infarction left ventricular remodelling in the rabbit.

OBJECTIVES: In this study, we used a proteomic approach to investigate the potential proteins regulated by ramipril in post-infarction left ventricular remodelling in the rabbit. METHODS AND RESULTS: Myocardial infarction (MI) was induced in male New Zealand White rabbits (2.5-3 kg) by ligation of the left anterior descending coronary artery. Two months later, the rabbits were either left untreated (MI group) or were treated daily for one month with 0.1 mg/kg wt of ramipril (ramipril group), then sacrificed. One month of ramipril treatment resulted in a significant improvement in the LV ejection fraction (LVEF) and a decrease in hydroxyproline content. The protein profiles of LV tissue showed that ramipril caused upregulation of glutathione peroxidase, superoxide dismutase (SOD), and heart-type fatty acid binding-protein (h-FABP) and downregulation of HSP27 and cyclophilin A. Ramipril treatment caused an increase in catalase, glutathione peroxidase, and SOD activity in the LV tissue. Oxidized glutathione levels and the GSSG/GSH ratio in the heart tissue were lower in the ramipril group than in the MI group. CONCLUSIONS: Ramipril increased antioxidative protein expression and enzyme activity, which could partly explain the role of ramipril in attenuating LV remodelling. In addition, the present study identifies several potential protein targets which may help to explain the mechanism by which ramipril exerts its effect in post-infarction LV remodelling in the rabbit.

Effect of cardiac rehabilitation on myocardial perfusion reserve in postinfarction patients.

Cardiac rehabilitation is believed to increase myocardial perfusion reserve (MPR), but this has not been adequately studied because of poor delineation of infarcted myocardium in previous studies. The purpose of this study was to determine the effect of cardiac rehabilitation on MPR in the remote and infarcted myocardium with contrast-enhanced magnetic resonance imaging; 39 postinfarction patients were recruited for this study and randomly assigned to a training group (n = 20) or a nontraining group (n = 19). Those in the training group participated in a 3-month rehabilitation training program at an exercise intensity of 55% to 70% of peak oxygen uptake (VO2); those in the nontraining group continued their usual lifestyle. Nineteen age-, weight-, and height-matched subjects without cardiovascular risk factors were selected as healthy controls. After myocardial infarction, a reduction in perfusion reserve was seen not only in the infarcted myocardium, but also in the remote myocardium. In the training group, exercise capacity increased by 15% (p <0.01), to the same level as in healthy controls. The post-training MPR increased in both remote (30%, p <0.01) and infarcted myocardium (25%, p <0.05) and reached the same level as in healthy controls. The change in exercise capacity correlated with the change in MPR in the remote myocardium (r = 0.55, p <0.001 for peak VO2). In the nontraining group, exercise capacity and MPR were unchanged. In conclusion, cardiac rehabilitation improves perfusion reserve in both infarcted and remote myocardium, with a parallel increase in exercise capacity.

Brachial artery flow-mediated vasodilation in patients with cardiac syndrome X.

Cardiac syndrome X (CSX) differs from coronary artery disease (CAD) and is characterized by angina, positive stress test, and patent coronary arteries. The probable mechanism is a microvascular disorder associated with endothelial dysfunction. In this study, brachial artery flow-mediated vasodilation was used as well as the endothelin-1 assay to assess endothelial function in patients with cardiac syndrome X (CSX), coronary artery disease (CAD), and healthy controls. All subjects underwent a 2-step brachial artery flow-related vasodilatation test. Serum endothelin-1, one of the most potent constricting factors, was measured for all participants. Patients with CSX had a lower brachial artery dilation ratio than controls but higher than that of CAD patients. Control subjects and CSX patients had higher endothelin-1 levels than CAD patients. CSX patients were found to have worse endothelial function than healthy volunteers, but patients with CAD had even worse endothelium function than CSX patients.