Experimental & Clinical Cardiology最新文献

Objective: To investigate the relationship between serum uric acid levels and pulmonary hypertension in patients with idiopathic pulmonary artery hypertension (IPAH).

Methods: Serum uric acid levels were measured in 86 patients (mean [± SD] age 35.2±12.3 years; 36 men) with IPAH. Pulmonary arterial pressure and ventricular function were assessed using echocardiography. Serum uric acid levels were also measured in 40 healthy subjects (35.9±11.6 years of age; 15 men).

Results: Serum uric acid levels in IPAH patients were higher compared with control subjects (405±130 μmol/L versus 344±96 μmol/L; P<0.05). Fifty-two (60.4%) of the 86 patients with IPAH had elevated serum uric acid levels. The pulmonary systolic pressure and mean pulmonary pressure in the high uric acid group were higher than in the normal uric acid group (P<0.05). The left and right ventricular ejection fractions were lower in the high uric acid group compared with the normal uric acid group (P<0.05). Serum uric acid levels were correlated with the mean pulmonary arterial pressure (r=0.387; P<0.01) and New York Heart Association class (r=0.41; P<0.01). There was also an inverse correlation between uric acid levels and the left (r=-0.550; P<0.01) and right ventricular ejection fractions (r=-0.481; P<0.05).

Conclusion: Serum uric acid levels are associated with IPAH severity and the severity of ventricular dysfunction.

Background: The authors previously reported a murine model of left ventricular hypertrophy (LVH) and regression using a suture technique of transverse aortic arch constriction and subsequent removal. A number of issues have limited the widespread adoption of this method. The present study assessed a modification of this model using a titanium clip.

Methods: Male C57BL/6 mice (n=95) underwent minimally invasive aortic banding for three, four or six weeks with or without subsequent band removal for one week. Hearts were evaluated both structurally and functionally using heart weight/body weight ratios, transthoracic echocardiography and direct left ventricular pressure measured using catheterization.

Results: Clip banding resulted in a threefold gradient across the transverse aortic arch. Pressure overload induced concentric LVH by three weeks that progressively decompensated. By six weeks, hearts were significantly dilated, with poor left ventricular function. Clips were removed in a minimally invasive procedure after each time point. When overloaded for either three or four weeks, removal of the clip with subsequent pressure relief enabled regression of LVH and restoration of function. When removed after six weeks of banding, mouse hearts were unable to reverse remodel and maintained elevated left ventricular end-diastolic pressures and lung congestion.

Conclusions: The application and removal of a titanium clip successfully induced pressure overload and relief associated with the serial development and reversal of LVH. Compared with similar models using suture ligation and release, this method was found to be a simple, effective (no slipped bands) and reproducible method to study murine LVH, heart failure and its regression.

To the authors' knowledge, the present report represents the first case in the medical literature in which an ST-segment elevation during the recovery phase of an exercise stress test indicated significant left main coronary artery stenosis. Although the patient did not complain of chest pain during the test, the ST-segment elevation persisted 20 min into recovery.

Background: The chronic effects of ganglionic plexi (GP) ablation on atrial fibrillation (AF) inducibility have not been elucidated.

Objective: To investigate the effect of Wenxin Keli (WK) on the inducibility of AF and atrial substrate remodelling after epicardial GP ablation.

Methods: Twenty dogs were randomly divided into a sham-operated group, a GP ablation group and a WK-treated group. All animals underwent a left thoracotomy at the fourth intercostal space. AF inducibility was assessed by burst rapid pacing at the right atrium. Both the GP ablation group and the WK-treated group received four major GP ablations. In the WK-treated group, dogs were treated with oral WK once per day, and all animals were allowed to recover for eight weeks, after which AF inducibility and AF duration were measured again.

Results: After eight weeks of WK treatment, AF inducibility was lower than in the GP ablation group, and was similar to that of the sham-operated group. Compared with the sham-operated group, the levels of atrial natriuretic peptide (ANP), tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-6 in right atrial tissues were increased in GP ablation group (143.6±33.7 pg/mg versus 206.2±41.4 pg/mg, P=0.02; 75.3±12.1 pg/mg versus 141.3±64 pg/mg, P=0.03; and 175.1±42.5 pg/mg versus 351.7±101 pg/mg, P<0.01, respectively). There were no significant differences in levels of ANP, TNF-α and IL-6 in atrial tissues between the sham-operated group and WK treated group. Expression of connexin 43 in atrial tissues was increased after eight weeks of GP ablation, while WK administration inhibited connexin 43 remodelling.

Conclusions: Epicardial GP ablation can induce atrial substrate remodelling, including Cx43 upregulation and increased levels of ANP, TNF-α and IL-6. These changes may be suppressed by long-term oral WK administration.

Background: Despite the widespread clinical use of cyclooxygenase (COX) inhibitors, dilemmas regarding the potential impact of these drugs on the cardiovascular system persist.

Objective: To estimate the effects of different COX inhibitors (meloxicam, acetylsalicylic acid [ASA] and SC-560) on cardiac function and coronary flow in isolated rat hearts, with special focus on the L-arginine/nitric oxide system.

Methods: The hearts of eight-week-old male Wistar albino rats (n=72; 12 rats per group; body mass 180 g to 200 g) were retrogradely perfused according to the Langendorff technique at gradually increased perfusion pressure (40 cmH2O to 120 cmH2O). After control experiments, the hearts were perfused with the following drugs: 100 μM ASA, alone or in combination with 30 μM N(ω)-nitro-L-arginine monomethyl ester (L-NAME), 0.3 μM meloxicam with or without 30 μM L-NAME, 3 μM meloxicam with or without 30 μM L-NAME, 30 μM L-NAME and 0.25 μM SC-560. In the control and experimental groups, the following parameters of heart function were continuously recorded: maximum rate of left ventricular pressure development, minimum rate of left ventricular pressure development, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate and mean blood pressure. Coronary flow was measured flowmetrically. The amount of released NO2 (-) was determined spectrophotometrically in coronary venous effluent.

Results: While meloxicam and SC-560 were found to have an adverse influence on cardiac function and coronary perfusion, ASA did not negatively affect the intact model of the heart.

Conclusion: It appeared that interaction between COX and the L-arginine/nitric oxide system truly exists in coronary circulation and may explain the causes of the observed effects.

Hypertrophic cardiomyopathy (HCM) is a disease with an autosomal-dominant pattern of inheritance associated with a variety of disease courses, age of onset, symptom severity, left ventricular outflow obstruction and risk for sudden cardiac death. Left ventricular systolic function is typically normal in most HCM patients using conventional echocardiographic indexes; however, myocardial systolic and diastolic function are reduced, and the mechanism of myocardial dysfunction remains unclear. Echocardiography is an invaluable tool for the diagnosis and assessment of hemodynamic condition, evaluation of therapy and outcome, and follow-up of patients with HCM. The recent advent of speckle tracking imaging provides a novel index for the noninvasive assessment of left ventricular myocardial dysfunction, and has been confirmed by many studies. A search for original articles focusing on HCM and its associated twist and untwist mechanisms was performed in the MEDLINE and PubMed databases with no date restrictions. All articles identified were English-language, full-text publications. The reference lists of identified articles were also searched for additional articles and reviews.

Cardiovascular diseases are threatening human health with rising morbidity and mortality rates. Gamma-glutamyltransferase (GGT) has been found to be involved in the pathogenesis of cardiovascular diseases, especially coronary artery disease, and the prognosis of cardiovascular disease may be predicted by increasing GGT levels. GGT levels are related to cardiovascular emergencies of chronic heart failure, and an elevated GGT level has been shown to be an independent predictive maker for cardiac death and cardiac transplantation. Investigation of the role of GGT in the mechanism of cardiac diseases will be helpful in developing preventive strategies and treatment methods.

Background: Although hematological parameters have been associated with prognosis in patients with various cardiovascular diseases, their relationship with coronary collateral (CC) circulation in patients with stable coronary artery disease (CAD) is unknown.

Objective: To investigate the relationship between hematological parameters and CC vessel development in patients with stable CAD.

Methods: A total of 96 patients who underwent coronary angiography were retrospectively enrolled. All study participants had at least one occluded major coronary artery. Development of CCs was classified using the method of Rentrop. Rentrop grades of 0 and 1 indicate poor CCs, whereas grades 2 and 3 indicate good CCs. Hematological parameters, including mean platelet volume (MPV) and neutrophil/lymphocyte (N/L) ratio, were measured. Multivariate logistic regression analysis was performed to identify independent variables.

Results: The MPV and N/L ratio were significantly higher in the poor CC group compared with the good CC group. Negative correlations were found in the analyses comparing Rentrop score with MPV and N/L ratio (r=-0.274; P=0.012 and r=-0.339; P=0.001, respectively). In multivariate analysis, the N/L ratio was independently related to CC circulation (OR 0.762 [95% CI 0.587 to 0.988]; P=0.04).

Conclusion: The results suggest that N/L ratio and MPV are associated with poor CCs, and a high N/L ratio is a significant predictor of poor CC development in patients with stable CAD.

Background/objective: Left ventricular (LV) circumferential or longitudinal shortening may be impaired in patients with type 2 diabetes mellitus (DM). In the present study, patients with type 2 DM without myocardial ischemia and combined impairment of circumferential and longitudinal (C+L) shortening were studied to assess the prevalence and factors associated with this condition.

Methods: Data from 386 patients with type 2 DM enrolled in the SHORTening of midWall and longitudinAl left Ventricular fibers in diabEtes study were analyzed. One hundred twenty healthy subjects were used to define C+L dysfunction. Stress-corrected midwall shortening and mitral annular peak systolic velocity were considered as indexes of C+L shortening and classified as low if <89% and <8.5 cm/s, respectively (10th percentiles of controls).

Results: Combined C+L dysfunction was detected in 66 patients (17%). The variables associated with this condition were lower glomerular filtration rate (OR 0.98 [95% CI 0.96 to 0.99], greater LV mass (OR 1.05 [95% CI 1.02 to 1.08]), high pulmonary artery wedge pressure (OR 1.23 [95% CI 1.04 to 1.44]) and mitral annular calcifications (OR 3.35 [95% CI 1.71 to 6.55]). Considering the entire population, the relationship between stress-corrected midwall shortening and peak systolic velocity was poor (r=0.20), and the model was linear. The relationship was considerably closer and nonlinear in patients with combined C+L dysfunction (r=0.61; P<0.001), having the best fit by cubic function.

Conclusions: Combined C+L dysfunction was present in one-sixth of patients with type 2 DM without myocardial ischemia. This condition was associated with reduced renal function, worse hemodynamic status and structural LV abnormalities, and may be considered a preclinical risk factor for heart failure.

Transresveratrol (t-resveratrol; 3,5,4'-trihydroxy-trans-stilbene) is a polyphenolic compound found in fresh grapes, grape juice and wine, and has been found to reduce the total cholesterol level in hypercholesterolemic rats. The objective of the present study was to assess the effects of t-resveratrol on platelet-neutrophil complex formation and neutrophil reactive oxygen species (ROS) status in control and hypercholesterolemic rats using a modified flow cytometric method. Rats (n=80) were divided into five groups (control, ethanol, resveratrol, hypercholesterolemic and resveratrol-administered hypercholesterolemic groups), comprising 16 animals per group. Serum levels of lipids and H2O2 were determined using commercially available kits, while platelet-neutrophil complex formation and neutrophil ROS status were determined using a modified flow cytometric method. Serum total cholesterol and low-density lipoprotein cholesterol levels were found to be increased and the high-density lipoprotein cholesterol level was found to be decreased in the HC group compared with the control group (P<0.001). Treatment of HC rats with t-resveratrol significantly lowered total cholesterol and low-density lipoprotein cholesterol levels (P<0.001). In the hypercholesterolemic group, levels of serum H2O2 platelet-neutrophil complex formation and neutrophil ROS status were significantly increased (P<0.001). On the other hand, in the resveratrol-administered hypercholesterolemic group, serum H2O2 levels, platelet-neutrophil complex formation and neutrophil ROS status were decreased compared with the hypercholesterolemic group (P<0.001). Serum H2O2 levels, platelet-neutrophil complex and neutrophil ROS status were positively correlated with one another. The present study is the first to demonstrate the protective effect of t-resveratrol against hypercholesterolemia-induced platelet-neutrophil complex formation and neutrophil ROS burst. Further investigations on its plausible role in antihypercholesterolemic treatment are warranted.