Azra Meryem Tanrikulu

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.

P Wave Dispersion Increases during Hemodialysis Sessions

Background/Aims: Atrial fibrillation (AF) is common among hemodialysis (HD) patients and is associated with high mortality. P wave dispersion (PWD) is a noninvasive electrocardiographic marker of paroxysmal AF. Our aim was to evaluate the effect of HD session on PWD. Methods: Twenty-five patients (mean age 63 years, 10 males) with sinus rhythm and undergoing chronic HD treatment were included. Blood samples were drawn and 12-lead electrocardiograms were recorded immediately before HD session, at the 2nd hour during HD and at the end of the HD session. The difference between maximum and minimum P wave durations was calculated as PWD. Results: PWD significantly increased during HD sessions compared with predialysis values (41 ± 12 vs. 21 ± 10 ms, respectively, p < 0.001), then decreased to a value of 24 ± 7 ms at the completion of HD, which was not significantly different from the predialysis values. PWD during HD was significantly correlated with predialysis systolic and diastolic blood pressure (r = 0.42, p = 0.037, and r = 0.59, p = 0.002, respectively) and predialysis serum potassium level (r = 0.44, p = 0.031). Linear regression model revealed that predialysis diastolic blood pressure (p = 0.002), predialysis serum potassium level (p = 0.037) and the amount of ultrafiltration (p = 0.048) were the significant predictors of prolonged PWD during HD. Conclusion: PWD increases significantly during HD sessions. This may increase the risk of AF episodes during HD. High diastolic blood pressure and serum potassium level before HD and ultrafiltration amount may predict prolonged PWD during HD.

Aspirin Resistance in Hypertensive Patients

J Clin Hypertens (Greenwich). 2010;12:714–720. ©2010 Wiley Periodicals, Inc.

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.

Pleural Fluid Amino-Terminal Brain Natriuretic Peptide in Patients With Pleural Effusions

BACKGROUND: Definite diagnosis of transudative or exudative pleural fluids often presents a diagnostic dilemma. The aim of this study was to evaluate whether amino-terminal brain natriuretic peptide (NT-proBNP) levels in pleural fluid has a diagnostic value for discriminating heart-failure-related pleural effusions from non-heart-failure effusions. METHODS: Sixty-six subjects (40 male, mean age 61 ± 18 y) with pleural effusions were included. Samples of pleural fluid and serum were obtained simultaneously from each subject. Biochemical analysis, bacterial and fungal culture, acid-fast bacilli smear and culture, and cytology were performed on the pleural fluid. RESULTS: Subjects with heart-failure-related pleural effusion had significantly higher pleural NT-proBNP levels than other subjects (P < .001). Pleural and serum NT-proBNP measures were closely correlated (r = 0.90, P < .001). An NT-proBNP cutoff value of ≥ 2,300 pg/mL in pleural fluid had a sensitivity of 70.8%, a specificity of 97.6%, and positive and negative predictive values of 94.4% and 85.4%, respectively, for discriminating transudates caused by heart failure from exudates. Eight heart-failure subjects were misclassified as exudates by Lights criteria, 5 of whom received diuretics before thoracentesis. All misclassified subjects had pleural NT-proBNP levels higher than 1,165 pg/mL, which predicted heart-failure-associated transudates with 95.8% sensitivity and 85.7% specificity. CONCLUSIONS: Pleural fluid NT-proBNP measurement in the routine diagnostic panel may be useful in differentiation of heart-failure-related pleural effusions and exudative pleural fluids with reasonable accuracy, especially in heart-failure patients treated with diuretics.

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 myocardialACE levels. DD genotype favours myocardial fibrosis and is associated with malignant ventricular tachycardia.The aim of this study was to explore ACE gene polymorphism inARVD patients. Methods. Twenty-nine patients with ARVD and 24 controls were included.AllARVD 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.

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.