Intra-coronary administration of soluble receptor for advanced glycation end-products attenuates cardiac remodeling with decreased myocardial transforming growth factor-β1 expression and fibrosis in minipigs with ischemia-reperfusion injury

Background  The cardioprotective effects of soluble receptor for advanced glycation end-products (sRAGE) have not been evaluated in large animals and the underlying mechanisms are not fully understood. This study aimed to evaluate the effects of intra-coronary administration of sRAGE on left ventricular function and myocardial remodeling in a porcine model of ischemia-reperfusion (I/R) injury.
Methods  Ten male minipigs with I/R injury were randomly allocated to receive intra-coronary administration of sRAGE (sRAGE group, n=5) or saline (control group, n=5). Echocardiography was performed before and 2 months after infarction. Myocardial expression of transforming growth factor (TGF)-β1 was determined by immunohistochemistry and fibrosis was evaluated by Sirius red staining.
Results  As compared with the baseline values in the control animals, left ventricular end-diastolic volume (from (19.5±5.1) to (32.3±5.6) ml, P <0.05) and end-systolic volume (from (8.3±3.2) to (15.2±4.1) ml, P <0.05) were significantly increased, whereas ejection fraction was decreased (from (61.6±13.3)% to (50.2±11.9)%, P <0.05). No obvious change in these parameters was observed in the sRAGE group. Myocardial expression of TGF-β1 was significantly elevated in the infarct and non-infarct regions in the control group, as compared with sRAGE group (both P <0.01). Fibrotic lesions were consistently more prominent in the infarct region of the myocardium in the control animals (P <0.05). 
Conclusion  Intra-coronary sRAGE administration attenuates RAGE-mediated myocardial fibrosis and I/R injury through a TGF-β1-dependent mechanism, suggesting a clinical potential in treating RAGE/ligand-associated cardiovascular diseases.

     

Effects of shenmai injection on pulmonary aquaporin 1 in rats following traumatic brain injury

Background  Aquaporin-1 (AQP1) has involved in fluid transport in diverse pulmonary edema diseases. Our study aimed to explore the dynamic changes of AQP1 in pulmonary water metabolism in rats following traumatic brain injury (TBI) and the protective effect provided by shenmai injection.

Methods  Sixty male Sprague Dawley rats weighting 280–300 g were randomly divided into three groups: the normal control group, the model group and the shenmai injection (SMI) group. One piece skull was taken away without injuring cerebral tissue in normal control group, while rats in model group and SMI group were subject to free fall injury in the cerebral hemisphere. Rats in model group received intraperitoneal normal sodium (15 ml/kg) at one hour post-injury and the same dose of shenmai injection instead in SMI group, respectively. The expression of AQP1 was detected by immunohistochemical analysis and semi-quantitative RT-PCR at 0 hour, 10 hours, 72 hours and 120 hours after TBI. Arterial blood gas analysis and lung wet to dry were also measured.

Results  AQP1 was mainly presented in the capillary endothelium and slightly alveolar epithelial cells in three groups, but the expression of AQP1 in the normal control group was positive and tenuous, weakly positive in the model and SMI groups, respectively. Compared with normal control group, AQP1 mRNA levels were down regulated in the model and SMI groups at 10 hours, 72 hours and 120 hours (P <0.05). While AQP1 mRNA levels in the SMI group was up-regulated than that in the model group (P <0.05). Lung wet to dry weight ratio (W/D) in the model and SMI groups at 10 hours were higher than that in normal control group (P <0.05). Compared with normal control group, PaO₂ was markedly lower in the model and SMI groups (P <0.05), but there were no statistically significant differences between model and SMI groups (P >0.05).

Conclusions  The decreased AQP1 expression may be involved in the increased lung water content and dysfunction of pulmonary water metabolism following TBI. The treatment with SMI could improve water metabolism by promoting AQP1 expression.

     

Effect of repaglinide and gliclazide on glycaemic control, early-phase insulin secretion and lipid profiles in

Background  Both repaglinide and gliclazide are insulin secretagogues widely used in the treatment of type 2 diabetes. They stimulate insulin secretion through distinct mechanisms and may benefit patients from different aspects. The present study was to evaluate the effects of repaglinide or gliclazide on glycaemic control, insulin secretion, and lipid profiles in type 2 diabetes patients.

Methods  A total of 47 newly diagnosed type 2 diabetes patients were randomized 1:1 to receive a 4-week treatment with repaglinide or gliclazide. The standard mixed meal tolerance test was performed before and after the treatment. Plasma glucose (PG), insulin concentration, and lipid profiles were measured. The area under insulin concentration curve (AUC_ins) and the early-phase insulin secretion index (ΔI₃₀/ΔG₃₀) were calculated.

Results  After the trial, fasting and postprandial PG and postprandial insulin improved significantly in both groups (P <0.05). The maximum insulin concentration occurred earlier in the repaglinide group than that in the gliclazide group. AUC_ins increased in both groups (P <0.05), but no significant difference was found between groups. ΔI₃₀/ΔG₃₀ increased in both groups (P <0.05), especially in the repaglinide group (P <0.05). Triglyceride and total cholesterol decreased significantly in the repaglinide group in some time points, while no significant change was observed in the gliclazide group.

Conclusions  Repaglinide and gliclazide had similar effects on glycaemic control and total insulin secretion,while repaglinide had more effects on improvements in β-cell function and lipid metabolism.

     

Depression, anxiety and influencing factors in patients with acute pulmonary embolism

Background  Psychological distress has been widely studied in many cardiovascular and pulmonary diseases, but the condition in acute pulmonary embolism (APE) is unknown. The purpose of this study was to investigate levels of depression and anxiety and their influencing factors in APE patients. 

Methods  Sixty consecutive patients with APE were subjected to investigation of depression and anxiety by the Beck Depression Inventory and State-Trait Anxiety Inventory, and 60 community-based subjects were enrolled as controls. APE patients were stratified as high-risk, intermediate-risk and low-risk according to the disease severity. Scores of depression and anxiety were compared by statistical analysis using paired t tests between APE patients and controls, and by analysis of variance within the APE patients with the three risk stratification. Factors influencing depression and anxiety were evaluated. 

Results  The mean age of the patients (38 males and 22 females) was (52±12) years. APE patients displayed higher scores of depression (P=0.04) and anxiety (P=0.001) compared with controls. Patients in the high-risk group displayed higher scores of depression (P=0.004) and anxiety (P=0.001) compared with those in the intermediate- and low-risk groups. Depression scores were highly correlated with anxiety scores (r=0.60, P <0.001). Both depression and anxiety inversely related to risk stratification (P <0.01), age (P <0.05), and arterial blood oxygen pressure (PaO₂) (P <0.05). Linear regression analysis showed that PaO₂ was independently inversely related to both depression (P <0.01) and anxiety (P <0.05); risk stratification and age were independently inversely related to anxiety (P <0.05).  

Conclusions  Patients of APE suffered high levels of depression and anxiety, which were negatively influenced by PaO₂, risk stratification and age.  

     

Effect and cost of perioperative use of antibiotics in coronary artery bypass grafting: a randomized controlled study

Background  Bacterial infections remain a serious complication following coronary artery bypass grafting (CABG). The objective of the study was to determine the effectiveness of a guideline for the appropriate use of antibiotics in CABG during the perioperative period.

Methods  Six hundred and fourteen hospitalized patients who had undergone CABG from January to June 2006 were randomly allocated to an intervention group and a control group. The data on the hospital stay, days of antibiotic used, types of prophylactic antibiotics used, surgical wound infection and pulmonary infection and antibiotic costs for the patients were compared.

Results  The postoperative hospitalization days of the intervention group were significantly fewer than that for the control group (P <0.05). The time of antibiotic use and post-infection treatment time were also significantly less in the intervention group than in the control group (P <0.05). The average hospital daily cost and total cost of antibiotics were less in the intervention group than in the control group (P <0.05). Compared with the control group, prophylactic antibiotic use in the intervention group was more reasonable.

Conclusions  The guideline for the appropriate use of antibiotics in CABG during the perioperative period is effective strategies for reducing antibiotic costs, the time of antibiotic use and post-infection treatment time without compromising the patients’ clinical outcome.

     

Repairing cartilage defects using chondrocyte and osteoblast composites developed using a bioreactor

Background  Articular cartilage injury is a common disease, and the incidence of articular wear, degeneration, trauma and sports injury is increasing, which often lead to disability and reduced quality of life. Unfortunately repair of articular cartilage defects do not always provide satisfactory outcomes.

Methods  Chondrocyte and osteoblast composites were co-cultured using a bioreactor. The cartilage defects were treated with cell-β-tricalcium phosphate (β-TCP) composites implanted into osteochondral defects in dogs, in vivo, using mosaicplasty, by placing chondrocyte-β-TCP scaffold composites on top of the defect and osteoblast-β-TCP scaffold composites below the defect.

Results  Electron microscopy revealed that the induced chondrocytes and osteoblast showed fine adhesive progression and proliferation in the β-TCP scaffold. The repaired tissues in the experimental group maintained their thickness to the full depth of the original defects, as compared with the negative control group (q=12.3370, P <0.01; q=31.5393, P <0.01).

Conclusions  Perfusion culture provided sustained nutrient supply and gas exchange into the center of the large scaffold. This perfusion bioreactor enables the chondrocytes and osteoblasts to survive and proliferate in a three-dimensional scaffold.

     

Preconditioning of intravenous parecoxib attenuates focal cerebral ischemia/reperfusion injury in rats

Background  Several studies suggest that cyclooxygenase-2 (COX-2) contributes to the delayed progression of ischemic brain damage. This study was designed to investigate whether COX-2 inhibition with parecoxib reduces focal cerebral ischemia/reperfusion injury in rats.

Methods  Ninety male Sprague-Dawley rats were randomly assigned to three groups: the sham group, ischemia/reperfusion (I/R) group and parecoxib group. The parecoxib group received 4 mg/kg of parecoxib intravenously via the vena dorsalis penis 15 minutes before ischemia and again at 12 hours after ischemia. The neurological deficit scores (NDSs) were evaluated at 24 and 72 hours after reperfusion. The rats then were euthanized. Brains were removed and processed for hematoxylin and eosin staining, Nissl staining, and measurements of high mobility group Box 1 protein (HMGB1) and tumor necrosis factor-α (TNF-α) levels. Infarct volume was assessed with 2,3,5-triphenyltetrazolium chloride (TTC) staining.

Results  The rats in the I/R group had lower NDSs (P <0.05), larger infarct volume (P <0.05), lower HMGB1 levels (P <0.05), and higher TNF-α levels (P <0.05) compared with those in the sham group. Parecoxib administration significantly improved NDSs, reduced infarct volume, and decreased HMGB1 and TNF-α levels (P <0.05).

Conclusions  Pretreatment with intravenous parecoxib was neuroprotective. Its effects may be associated with the attenuation of inflammatory reaction and the inhibition of inflammatory mediators.

     

Erythropoietin decreases carbon tetrachloride-induced hepatic fibrosis by inhibiting transforming growth factor-beta

Background  In addition to hematopoietic effect, the erythropoietin is known as a multifunctional cytokine with anti-fibrosis and organ-protective activities. The purpose of this study was to evaluate the effect of recombinant human erythropoietin (rhEPO) on hepatic fibrosis and hepatic stellate cells (HSCs).

Methods  Carbon tetrachloride (CCl₄) induced hepatic fibrosis mice models were used for in vivo study and HSCs line for in vitro study. CCl₄ and rhEPO (0, 200 or 1000 U/kg) was injected intraperitoneally in BALB/c mice three times a week for 4 weeks. Immunohistochemistry and immunoblotting were performed to evaluate expressions of transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), and fibronectin in explanted liver. Immunoblotting of α-SMA, phophorylated Smad-2 and Smad-2/3 was performed in HSCs treated with TGF-β1 and/or rhEPO.

Results  Expressions of TGF-β1, α-SMA, and fibronectin were increased in CCl₄ injected mice livers, but significantly attenuated by co-treatment with CCl₄ and rhEPO. Co-treatment of rhEPO markedly suppressed fibrosis in Masson’s trichrome compared with treatment of only CCl₄. TGF-β1 increased phosphorylated α-SMA, Smad-2 expressions in HSCs, which were decreased by rhEPO co-treatment.

Conclusions  Treatment of rhEPO effectively suppressed fibrosis in CCl₄-induced liver fibrosis mice models. Anti-fibrosis effect of rhEPO could be related to inhibition of TGF-β1 induced activation of HSCs.

     

Pioglitazone ameliorates nonalcoholic steatohepatitis by down-regulating hepatic nuclear factor-kappa B and cyclooxygenases-2 expression in rats

Background  Pioglitazone is effective in nonalcoholic steatohepatitis (NASH), but the mechanisms of action are not completely understood. This study was designed to investigate the effects of pioglitazone on hepatic nuclear factor-kappa B (NF-κB) and cyclooxygenases-2 (COX-2) expression in NASH rats.

Methods  Thirty Sprague-Dawley male rats were randomly assigned to a control group (n=10), NASH group (n=10), and pioglitazone treatment group (n=10). Liver tissues were processed for histology by hematoxylin & eosin and Masson stained. Serum alanine aminotransferase (ALT), cholesterol, triglyceride, fasting blood glucose (FBG), fasting insulin (FINS) levels and biochemical parameters of antioxidant enzyme activities, tumor necrosis factor alpha (TNF-α), prostaglandin E₂ (PGE₂) levels in serum and liver were measured. The mRNA and protein expression of peroxisome proliferator-activated receptor gamma (PPARγ), NF-κB and COX-2 were determined by real-time polymerase chain reaction, Western blotting and immunohistochemistry. One-way analysis of variance (ANOVA) and Wilcoxon’s signed-rank test was used for the statistical analysis.

Results  There were severe steatosis, moderate inflammatory cellular infiltration and fibrosis in NASH rats. After pioglitazone treatment, steatosis, inflammation and fibrosis were significantly improved compared with the NASH group (χ²=20.40, P <0.001; χ²=20.17, P <0.001; χ²=13.98, P=0.002). Serum ALT, cholesterol, triglyceride, FBG, FINS levels were significantly elevated in the NASH group (P <0.05). In the NASH group, total anti-oxidation competence (T-AOC), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and malondialdehyde (MDA) levels in serum and liver were conspicuous disordered than those parameters in the control group. Meanwhile, TNF-α and PGE₂ levels in serum and liver were significantly increased compared with the control group. Immunohistochemistry showed NF-κB and COX-2 expression in liver was significantly elevated. However, PPARγ level was decreased in the NASH group. Real-time PCR and Western blotting revealed mRNA and protein expression of COX-2 were increased in the NASH group compared with the control group (0.57±0.08 vs. 2.83±0.24; 0.38±0.03 vs. 1.00±0.03, P <0.001 and P=0.004, respectively). After pioglitazone intervention, all of those parameters markedly improved (P <0.05 or P <0.01).

Conclusion  Down-regulating hepatic NF-κB and COX-2 expression, at least in part, is one of the possible therapeutic mechanisms of pioglitazone in NASH rats.

     

Effects of bone marrow-derived endothelial progenitor cell transplantation on vein microenvironment in a rat model of chronic thrombosis

Background  Endothelial progenitor cells (EPCs) have been used in both experimental studies and clinical treatments of limb ischemia, as well as in the construction of engineered vascular tissue. The objective of this study was to investigate the effects of transplanted bone marrow-derived EPCs on the vein microenvironment in a rat model of chronic vein thrombosis.
Methods  Mononuclear cells were isolated from the bone marrow of immature rats by density gradient centrifugation, cultured, and then transplanted into experimentally induced thrombi into inferior vena cava through the femoral vein. Vascular endothelial growth factor (VEGF), angiopoietin-1 (ANG-1)  and monocyte chemotactic protein-1 (MCP-1) mRNA and protein expression levels were measured by real-time quantitative polymerase chain reaction and Western blotting of thrombi and adjacent caval walls 28 days post-transplantation.
Results  Levels of VEGF, ANG-1, and MCP-1 mRNA in EPC-transplanted thrombi were 100%, 230.7%, and 212.5% of levels detected in the sham-operated group (P<0.01), and 99.9%, 215.4%, and 177.8% of levels detected in the experimental control group (P< 0.01). VEGF, ANG-1 and MCP-1 protein levels exhibited a similar trend.
Conclusions  Transplanted bone marrow-derived EPCs appear to alter the vein microenvironment in experimentally induced chronic vein thrombosis by upregulating cytokines associated with thrombic organization and recanalization.

     

Partial liquid ventilation decreases tissue and serum tumor necrosis factor-α concentrations in acute lung injury model of immature piglet induced by oleic acid

Background  Pediatric patients are susceptible to lung injury. Acute lung injury in children often results in high mortality. Partial liquid ventilation (PLV) has been shown to markedly improve oxygenation and reduce histologic evidence of injury in a number of lung injury models. This study was designed to examine the hypothesis that PLV would attenuate the production of local and systemic tumor necrosis factor (TNF)-α in an immature piglet model of acute lung injury induced by oleic acid (OA).

Methods  Twelve Chinese immature piglets were induced acute lung injury by OA. The animals were randomly assigned to two groups of six animals, (1) conventional mechanical ventilation (MV) group and (2) PLV with 10 ml/kg FC-77 group.

Results  Compared with MV group, the PLV group had better cardiopulmonary variables (P <0.05). These variables included heart rate, mean blood pressure, blood pH, partial pressure of arterial oxygen (PaO₂), PaO₂/inspired O₂ fraction (FiO₂) and partial pressure of arterial carbon dioxide (PaCO₂). PLV reduced TNF-α levels both in plasma and tissue compared with MV group (P <0.05).

Conclusion  PLV provides protective effects against TNF-α response in OA-induced acute lung injury in immature piglets.

     

Effect of Ulinastatin donor-pretreatment on liver graft during cold preservation in rats

Background  Donor-pretreatment with ulinastatin may influence the liver graft during cold preservation. The aim of this research was to determine whether pretreatment of donor liver with Ulinastatin can attenuate cold preservation injury, and to explore the mechanism by which Ulinastatin affects the donor liver graft. 

Methods  One hundred and forty-four Wistar rats were divided into the Ulinastatin treatment group (T group) pretreated with Ulinastatin 50 000 U/kg and control group (C group) treated with 0.9% normal saline via peritoneal injection prior to the anesthetization. After the abdominal cavity was opened and perfused with cold Ringer’s lactate solution, the liver was harvested. The harvested liver was preserved in cold Ringer’s lactate solution for 0, 2, 6, 24 hours, at which time the liver tissue was sampled for determination of dry weight and wet weight, Na⁺-K⁺-ATPase and Ca²⁺-ATPase activity, lactic acid dehydrogenase (LDH) activity, lactic acid and malondialdehyde levels. Light microscopy and electron microscopy were used to observe liver morphology. The liver cold-preservation solution was taken for measurement of aspartate aminotransferase (AST) and alanine transaminase (ALT) levels. Correlation between ATPase activity and lactic acid level was analyzed by SPSS 13.0 for Windows.

Results  The morphology in the T group had improved cell boundaries vs. the C group at each time point. Dry weight to wet weight in the T group was lower than in the C group at 6 hours (P <0.05), but the difference was not significant at 24 hours. ALT levels in the T group were lower than that in the C group at 6 hours (P <0.05) and 24 hours (P <0.01). AST levels in the T group were lower than those in the C group at 2 hours (P <0.05), 6 hours (P <0.01) and 24 hours (P <0.01). Na⁺-K⁺-ATPase activity in the T group was higher than in the C group and the mean difference between two groups was significant at 0 hour (P <0.05) and 2 hours (P <0.05). Ca²⁺-ATPase activity in the T group was higher than in the C group with the mean difference between two groups significant at 2 hours (P <0.05). The T group had increased lactic acid levels at 0 hour (P <0.01) and 2 hours (P <0.05) compared with the C group, but there was no influence on the LDH activity at the same time. There were no obvious differences in the levels of malondialdehyde between the two groups at any time point. A linear correlation between Na⁺-K⁺-ATPase activity and lactic acid levels (r=0.295, P <0.05) was found.

Conclusions  Donor-pretreatment with ulinastatin may protect the cells in a liver graft from ischemia injury during cold preservation; the mechanism may be due to its promotion for cell glycolysis and its preservation of ATPase activity.

     

Detection of carboxyhemoglobin in patients with hepatic encephalopathy due to hepatitis B virus-related cirrhosis

Background  The heme oxygenase/carbon monoxide (HO/CO) system plays an important role in the development of hepatic fibrosis. The level of the HO/CO can be directly obtained by determining the carboxyhemoglobin (COHb) level. The aims of this study were to reveal the significance of COHb in patients with hepatitis B virus-related cirrhosis (HBC) complicated by hepatic encephalopathy (HE), and to further investigate the influence of the HO/CO pathway on the end-stage cirrhosis, hoping to find a reliable indicator to evaluate the course of HBC.

Methods  According to the diagnostic criteria, 63 HBC inpatients with HE were enrolled in group H. Patients regaining awareness with current therapies were categorized into group P-H. Comparisons were made with a control group (group N) consisting of 20 health volunteers. The levels of COHb, partial pressure of oxygen (PaO₂) and oxygen saturation (SaO₂) were determined by arterial blood gas analysis method. The incidences of hepatorenal syndrome (HRS), upper gastrointestinal bleeding, esophagogastric varices and spontaneous bacterial peritonitis (SBP) in group H were recorded. COHb levels in different groups were compared, and the correlations of COHb levels with HE grades (I, II, III, and IV), PaO₂, SaO₂ and hypoxemia were analyzed.

Results  The COHb level in group P-H ((1.672±0.761)%) was significantly higher than that in group N ((0.983±0.231)%) (P <0.01), and the level in group H ((2.102±1.021)%) was significantly higher than groups P-H and N (P <0.01). A positive correlation was observed between the COHb concentration and the grade of HE (r_s=0.357, P=0.004). There were no significant differences of COHb levels between HE patients with and without complications such as esophagogastric varices ((2.302±1.072)% vs. (1.802±1.041)%, P >0.05) or the occurrence of SBP ((2.960±0.561)% vs. (2.030±1.021)%, P >0.05). Compared with HE patients with HRS, the level of COHb was significantly higher in HE patients without HRS ((2.502±1.073)% vs. (1.981±1.020)%, P=0.029). The COHb level had a negative correlation with PaO₂ (r=−0.335, P=0.007) while no statistically significant relationship was found with SaO₂ (r=−0.071, P >0.05). However, when the above two parameters met the diagnostic criteria of hypoxemia, the COHb concentration increased ((2.621±0.880)% vs. (1.910±0.931)%, P=0.011).

Conclusions  COHb is a potential candidate to estimate the severity and therapeutic effect of HE. The levels of COHb may be tissue-specific in cirrhotic patients with different complications.

     

Changes in plasma hydrogen sulfide and nitric oxide levels and their clinical significance in children with Kawasaki disease

Background  Cardiac involvement is the most common complication of Kawasaki disease (KD); however, the underlying mechanisms are not understood. The present study was designed to investigate changes in plasma hydrogen sulfide (H₂S) and nitric oxide (NO) levels in the acute and recovery stages of KD children and to examine their clinical significance.

Methods  Thirty-five KD patients and 32 healthy children were enrolled in the study. KD patients were divided into two subgroups: a non-cardiac involvement group and a cardiac involvement group. Plasma H₂S levels were measured using the sulfur-sensitive electrode method and plasma NO levels and NO synthase activity were determined using the nitrate reductase method both before and after intravenous immune globulin (IVIG) therapy.

Results  Plasma H₂S levels significantly decreased in KD patients during the acute phase of the disease and NO levels were significantly increased, compared with the control group (P <0.01). After treatment with IVIG, both plasma H₂S and NO levels significantly increased (P <0.01). The plasma levels of H₂S were significantly lower in the cardiac involvement group compared with the non-cardiac involvement group (P <0.05).

Conclusion  H₂S and NO may play a role in the pathophysiological process of inflammation during the acute phase of KD. Endogenous H₂S may exert protective effects with respect to cardiac complications in KD.

     

Relationship of left heart size and left ventricular mass with exercise capacity in chronic heart failure

Background  Impaired exercise capacity is one of the most common clinical manifestations in patients with chronic heart failure (CHF). The severity of reduced exercise capacity is an indicator of disease prognosis. The aim of the current study was to investigate the association between left heart size and mass with exercise capacity.

Methods  A total of 74 patients were enrolled in the study, with 37 having congestive heart failure (left ventricular ejection fraction (LVEF) <0.45) and the other 37 with coronary heart disease (by coronary angiography) serving as the control group (LVEF >0.55). Echocardiography and cardiopulmonary exercise test were performed. The multiply linear regression model was used to evaluate the association between echocardiogrphic indices and exercise capacities.

Results  The study showed that left ventricular end diastolic / systolic diameter (LVEDD/LVESD), left atrial diameter (LAD) and left ventricular mass index (LVMI) were significantly enlarged in patients with chronic heart failure compared with controls (P <0.01). The VO₂AT, Peak VO₂, Load AT, and Load Peak in chronic heart failure patients were also significantly reduced compared with controls (P <0.05), VE/VCO₂ slope was increased in patients with chronic heart failure (P <0.01). Multivariate linear regression analysis indicated that the patients’ exercise capacity was significantly associated with the left heart size and mass, however, the direction and/or strength of the associations sometimes varied in chronic heart failure patients and controls. Load AT correlated negatively with LVEDD in chronic heart failure patients (P=0.012), while Load AT correlated positively with LVEDD in control patients (P=0.006). VE/VCO₂ slope correlated positively with LAD (B=0.477, P <0.0001) in chronic heart failure patients, while the VE/VCO₂ slope correlated negatively with LAD in control patients (P=0.009).

Conclusion  The study indicates that the size of LVEDD and LAD are important determinants of exercise capacity in patients with CHF, which may be helpful to identify exercise tolerance for routine monitoring of systolic heart failure.