Acute Exacerbation Impairs Right Ventricular Function in COPD Patients.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) may impair right ventricular (RV) function. Tissue Doppler imaging (TDI) is helpful in the noninvasive evaluation of RV longitudinal function. The aim of this study was to assess the impact of acute COPD exacerbation on RV function assessed by TDI. METHODS: The study included 30 COPD patients who had acute exacerbation and 30 controls. RV function was assessed echocardiographically during acute exacerbation and after recovery. In addition to conventional echocardiographic parameters, tricuspid annular plane systolic excursion, tricuspid annulus peak systolic velocity (Sa), and TDI-derived isovolumic myocardial acceleration (IVA) were determined. RESULTS: During exacerbation, COPD patients had a significantly larger RV and higher pulmonary artery systolic pressure, with significantly lower IVA, Sa and tricuspid annular plane systolic excursion compared to controls. After recovery, IVA and Sa significantly increased, while RV diameter and pulmonary artery systolic pressure significantly decreased to levels similar to controls. There were statistically significant, but modest correlations between IVA and Sa (r=0.441, p=0.003), tricuspid annular plane systolic excursion (r=0.628, p<0.001), pulmonary artery systolic pressure (r=-0.391, p=0.002) and RV diameter (r=-0.309, p=0.018). Sa correlated with pulmonary artery systolic pressure (r=-0.350, p=0.007) and RV diameter (r=-0.344, p=0.008). CONCLUSIONS: COPD exacerbations have a negative impact on RV function. TDI-derived IVA and Sa may be used in the assessment of subclinical RV dysfunction in COPD patients with exacerbation.

Aspirin resistance in patients with acute ischemic stroke.

Aspirin is used in ischemic stroke therapy. However, some patients are not responsive to the antithrombotic action of aspirin. The aim of this study was to assess the prevalence of aspirin resistance in stroke patients and its association with mortality. One-hundred and six patients (mean age 64.9 ± 14.6 years, 53 male) with acute ischemic stroke were consecutively recruited. All subjects were taking aspirin regularly. Aspirin responsiveness was determined by Ultegra Rapid Platelet Function Assay-ASA (VerifyNow Aspirin). Aspirin resistance was defined as aspirin reaction unit (ARU) ≥ 550. Aspirin resistance was detected in 35 patients. There were not any significant differences in age, gender and comorbidities between aspirin-resistant and aspirin-sensitive patients. The mean National Institute of Health Stroke Scale (NIHSS) scores of the aspirin-resistant and aspirin-sensitive patients were 15 ± 3 and 12 ± 5, respectively (p = 0.006). Twenty-seven patients had a history of prior ischemic stroke and eight of them had aspirin resistance. Eleven patients died in-hospital and a total of 43 patients died during 2 years. Both the in-hospital and 2-year mortality rates were significantly higher in patients with aspirin resistance (20 vs. 5.6%, p = 0.038 and 60.0 vs. 31.0%, p = 0.004, respectively). Regression analysis revealed aspirin resistance [odds ratio (OR) 3.097, 95% confidence interval (CI) 1.070-8.959, p = 0.037] as an independent predictor of 2-year mortality, as well as age (OR 1.051, 95% CI 1.003-1.102, p = 0.038) and NIHSS scores (OR 1.208, 95% CI 1.016-1.437, p = 0.033). Aspirin resistance is not uncommon in patients with acute ischemic stroke and is associated with short and long term mortality in these patients.

Polymorphisms of the angiotensin-converting enzyme and angiotensinogen gene in patients with atrial fibrillation.

Activation of the renin-angiotensin system (RAS) is associated with atrial fibrillation (AF). The aim of this study was to investigate the relation between AF and polymorphisms in RAS. One hundred and fifty patients with AF, 100 patients with no documented episode of AF and 100 healthy subjects were consecutively recruited into the study. The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and the M235T, A-20C, and G-6A polymorphisms of the angiotensinogen gene were genotyped. Patients with AF had significantly lower frequency of II genotype of ACE I/D and higher frequency of angiotensinogen M235T polymorphism T allele and TT genotype and G-6A polymorphism G allele and GG genotype compared with the controls. AF patients had significantly larger left atrium, higher left ventricular mass index (LVMI) and higher frequency of significant valvular pathology. ACE I/D polymorphism II genotype, angiotensinogen M235T polymorphism TT genotype and G allele and GG genotype of angiotensinogen G-6A polymorphism were still independently associated with AF when adjusted for left atrium, LVMI and presence of significant valvular pathology. Genetic predisposition might be underlying the prevalence of acquired AF. Patients with a specific genetic variation in the RAS genes may be more liable to develop AF.

Aspirin resistance in patients with chronic renal failure.

BACKGROUND: Chronic renal failure (CRF) is associated with increased risk of cardiovascular morbidity and mortality. Aspirin resistance worsens clinical prognosis. The aim of this study was to explore the prevalence of aspirin resistance in CRF. METHODS: Two hundred and forty-five CRF patients (115 patients undergoing chronic hemodialysis and 130 patients with stage 3-4 chronic kidney disease [CKD]) and 130 patients with normal renal functions (control group) were consecutively recruited. All subjects were taking aspirin regularly. Aspirin responsiveness was determined by Ultegra Rapid Platelet Function Assay-ASA (VerifyNow Aspirin). Aspirin resistance was defined as aspirin reaction unit (ARU) =550. RESULTS: Aspirin resistance was detected in 53 patients undergoing hemodialysis, 32 patients with stage 3-4 CKD and 22 controls. The frequency of aspirin resistance was significantly higher in the CRF group compared with controls (34.7% vs. 16.9%, p<0.001) and in hemodialysis patients (46.1%) compared with stage 3-4 CKD patients (24.6%, p<0.001) and controls (16.9%, p<0.001). Multivariate analysis revealed female sex (odds ratio [OR] = 2.201; 95% confidence interval [95% CI], 1.173-4.129; p=0.014), hemodialysis (OR=3.636; 95%CI, 1.313-10.066; p=0.013) and HDL cholesterol (OR=0.974; 95% CI, 0.950-0.999; p=0.043) as independent predictors of aspirin resistance in this cohort of patients. CONCLUSION: Patients with CRF have higher frequency of aspirin resistance. This might further increase the risk of cardiovascular morbidity and mortality in these patients.

Acute exacerbation impairs endothelial function in patients with chronic obstructive pulmonary disease.

OBJECTIVES: The effect of acute exacerbation of chronic obstructive pulmonary disease (COPD) on brachial artery flow-mediated dilation (FMD) has not been examined. The aim of this study was to assess the endothelial function of COPD patients during acute exacerbations. STUDY DESIGN: The study included 30 consecutive patients (8 women, 22 men; mean age 64.2+/-10.9 years) who experienced acute exacerbation of COPD, defined according to the Anthonisen criteria (increased dyspnea, sputum, and sputum purulence). All patients received the same antibiotic and bronchodilator treatment. Endothelial function was assessed by brachial artery ultrasonography within the first 48 hours and after complete resolution of exacerbation symptoms. Flow-mediated dilation was defined as both the maximum absolute and maximum percentage changes in the vessel diameter during reactive hyperemia. The results were compared with those of 20 age-and sex-matched controls without COPD. RESULTS: The patient and control groups were similar in terms of age, gender, hypertension, diabetes, hyperlipidemia, coronary artery disease, heart rate, and blood pressure. Parameters of FMD during acute exacerbation were significantly lower than those obtained after recovery (absolute change: 0.23+/-0.12 mm vs. 0.38+/-0.17 mm, p<0.001; percentage change: 6.44+/-3.99% vs. 10.42+/-4.86%, p<0.001) and than those of the control group (absolute change: 0.36+/-0.13 mm, p=0.001; percentage change: 9.77+/-3.83%, p=0.003). Flow-mediated dilation increased significantly after recovery, yielding similar values to those of the controls. Improvements in FMD were significant in both sexes. CONCLUSION: Acute COPD exacerbation is associated with worsening endothelial function, increasing the risk for cardiovascular morbidity.

Perindopril decreases P wave dispersion in patients with stage 1 hypertension.

INTRODUCTION: Angiotensin-converting enzyme inhibitors prevent atrial fibrillation episodes by effective control of blood pressure and improving electrical and structural remodelling in the atria. Increased P wave dispersion (PWD) is a non-invasive electrocardiographic marker for paroxysmal atrial fibrillation. The aim of the study was to evaluate the effect of perindopril treatment on PWD in hypertensive patients. METHODS: Forty-eight hypertensive patients (mean age 57.4+/-11.8 years, 18 men) were included. Blood pressure values were determined and 12-lead electrocardiograms were recorded at the beginning and at the first week, first month, third month and sixth month of the perindopril treatment.The difference between maximum and minimum P wave durations was calculated as PWD. RESULTS: PWDs were significantly shortened at the first, third and sixth months (41.7+/-8.8 ms, 39.1+/-6.9 ms and 38.3+/-7.1 ms, respectively) compared with baseline and first-week measurements (54.3+/-9.2 ms and 49.0+/-9.1 ms, respectively, p<0.001). Baseline PWD was correlated with body mass index (r=0.32, p=0.026), while PWD at the sixth month of treatment was significantly correlated with left atrial volume index (r=0.30, p=0.042). Multiple linear regression analysis revealed that PWD at the sixth month was related to baseline PWD (p=0.001). CONCLUSION: Perindopril treatment significantly reduced PWD in hypertensive patients.

Angiotensin-converting enzyme gene polymorphism in arrhythmogenic right ventricular dysplasia: is DD genotype helpful in predicting syncope risk?

INTRODUCTION: Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterised by fibrofatty replacement of right ventricular myocytes and increased risk of ventricular arrhythmias and sudden cardiac death. Angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism affects myocardial ACE levels. DD genotype favours myocardial fibrosis and is associated with malignant ventricular tachycardia. The aim of this study was to explore ACE gene polymorphism in ARVD patients. METHODS: Twenty-nine patients with ARVD and 24 controls were included. All ARVD patients had documented sustained ventricular tachycardia. Thirteen patients had syncopal episodes. Six patients were resuscitated from sudden cardiac death. ACE gene polymorphism was identified by polymerase chain reaction technique. RESULTS: There was no significant difference in DD genotype frequency between ARVD patients and controls (44.8% vs. 45.8%, p=0.94). However, DD genotype frequency was significantly higher in ARVD patients with syncopal episodes compared to those without syncope (69.2% vs. 25.0%, p=0.017, odds ratio:6.750, 95% confidence interval: 1.318-34.565). DD genotype was detected in higher frequency also in patients with a family history of sudden cardiac death (66.7% vs. 39.1%,p=0.36). CONCLUSION: High prevalence of DD genotype in ARVD patients with syncope suggests that ACE I/D polymorphism might be useful in identifying high-risk patients for syncope.