Volume status and arterial blood pressures are associated with arterial stiffness in hemodialysis patients.

BACKGROUND: Arterial stiffness is a strong predictor of mortality in hemodialysis patients. In this study, we aimed to investigate possible relations of arterial stiffness with volume status determined by bioimpedance analysis and aortic blood pressure parameters. Also, effects of a single hemodialysis session on these parameters were studied. METHODS: A total of 75 hemodialysis patients (M/F: 43/32; mean age: 53 ± 17) were enrolled. Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure were measured by applanation tonometry before and after hemodialysis. Extracellular fluid and total body fluid volumes were determined by bioimpedance analysis. RESULTS: Carotid-femoral pulse wave velocity (9.30 ± 3.30 vs 7.59 ± 2.66 m/s, p < 0.001), augmentation index (24.52 ± 9.42 vs 20.28 ± 10.19, p < 0.001), and aortic pulse pressure (38 ± 14 vs 29 ± 8 mmHg, p < 0.001) significantly decreased after hemodialysis. Pre-dialysis carotid-femoral pulse wave velocity was associated with age (r2 = 0.15, p = 0.01), total cholesterol (r2 = 0.06, p = 0.02), peripheral mean blood pressure (r2 = 0.10, p = 0.005), aortic-mean blood pressure (r2 = 0.06, p = 0.02), aortic pulse pressure (r2 = 0.14, p = 0.001), and extracellular fluid/total body fluid (r2 = 0.30, p < 0.0001). Pre-dialysis augmentation index was associated with total cholesterol (r2 = 0.06, p = 0,02), aortic-mean blood pressure (r2 = 0.16, p < 0.001), and aortic pulse pressure (r2 = 0.22, p < 0.001). Δcarotid-femoral pulse wave velocity was associated with Δaortic-mean blood pressure (r2 = 0.06, p = 0.02) and inversely correlated with baseline carotid-femoral pulse wave velocity (r2 = 0.29, p < 0.001). Pre-dialysis Δaugmentation index was significantly associated with Δaortic-mean blood pressure (r2 = 0.09, p = 0.009) and Δaortic pulse pressure (r2 = 0.06, p = 0.03) and inversely associated with baseline augmentation index (r2 = 0.14, p = 0.001). In multiple linear regression analysis (adjusted R2 = 0.46, p < 0.001) to determine the factors predicting Log carotid-femoral pulse wave velocity, extracellular fluid/total body fluid and peripheral mean blood pressure significantly predicted Log carotid-femoral pulse wave velocity (p = 0.001 and p = 0.006, respectively). CONCLUSION: Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure significantly decreased after hemodialysis. Arterial stiffness was associated with both peripheral and aortic blood pressure. Furthermore, reduction in arterial stiffness parameters was related to reduction in aortic blood pressure. Pre-dialysis carotid-femoral pulse wave velocity was associated with volume status determined by bioimpedance analysis. Volume control may improve not only the aortic blood pressure measurements but also arterial stiffness in hemodialysis patients.

Evaluation of malnutrition with blood ghrelin and fecal elastase levels in acute decompensated heart failure patients.

OBJECTIVES: Exocrine pancreatic dysfunction may contribute to malnutrition and lack of appetite in the advanced stages of heart failure. Nutritional assessment was carried out on patients diagnosed with mild or moderate/severe heart failure. Fecal elastase levels are an indicator of pancreatic exocrine function and ghrelin is an appetite hormone which is also investigated for its contribution to malnutrition. STUDY DESIGN: This is an observational study. 52 patients (32 males, 20 females) aged over eighteen years and hospitalized for acute decompensated heart failure (ADHF) were included in the study. They were compared with 31 people (16 male, 15 female) of the same age as Control Group (C). Patients in New York Heart Association (NYHA) stages 1 and 2 were grouped as mild (miADHF), while those in NYHA stages 3 and 4 were grouped as moderate/severe ADHF (seADHF). Fecal and blood samples were taken at admission. In ADHF patients, exocrine pancreatic functions and their relationship with malnutrition were evaluated. Statistical analyses were performed using Tukey's test, the independent-sample t-test, the Kruskal-Wallis test, the Mann-Whitney U-test, the chi-square test and Pearson's bivariate correlation analysis. RESULTS: Significantly decreased fecal elastase levels were found when moderate/severe ADHF patients and the control group were compared. (C 278.9±144.8, miADHF 336.6±181.7, seADHF 168.7±153.6, p=0.002). 10 seADHF patients (50%) had severe, 4 (20%) moderate, and 6 (30%) mild pancreatic insufficiency. Ghrelin levels were higher in seADHF patients compared to C and miADHF patients (C 69.7±34.6, miCHF 82.5±48.2, SeADHF 105.0±78.1 p=0.361). CONCLUSION: Fecal elastase and ghrelin hormone levels can contribute to the determination of malnutrition in ADHF patients.

Diagnostic and prognostic significance of survivin levels in malignant pleural effusion.

UNLABELLED: We aimed to evaluate the diagnostic and prognostic value of measuring survivin levels, which is an inhibitor of apoptosis in pleural effusions. METHODS: Group I, malignant (MPE) (n = 51); Group II, tuberculosis (TPE) (n = 18); Group III transudative (TE) (n = 9) effusions were enrolled prospectively. We used ELISA to analyze 78 effusions. The value for the differential diagnosis and the correlation between survivin and survival in MPE were analyzed. RESULTS: Survivin level was 41.75 ± 76.20 in MPE, 15.83 ± 10.92 in TPE and 8.33 ± 8.67 in TE. When the patients divided two groups as malignant and non-malignant pleural effusion (non-MPE), survivin level was significantly higher in MPE (41.75 ± 76.20) than in non-MPE (13.33±2.05) (p = 0.012). The cutoff value for survivin levels detected by ROC curve analysis was 7.5 pg/ml, with sensitivity and specificity values of 72%, 44%, respectively. Survivin had no discriminative power in differentiating exudative effusions of MPE from TPE (p = 0.405). There was no correlation between survivin level and age, sex, location, fluid pH, glucose, protein, albumine and ADA level while there was significant moderate correlation with fluid LDH (r = 0.49; p < 0.001). Survivin levels can distinguish patients who had poor prognosis (median survival 75 days, n = 24) and those who had good prognosis (median survival 219 days, n = 27, p = 0.03) in MPE. In conclusion, survivin expression levels detected with ELISA had no discriminative power in differentiating exudative effusions included MPE and TPE. Elevated survivin levels are associated with poor survival in MPE. Our results suggest that survivin may be a potential prognostic marker in MPE.

Hypervolemia rather than arterial calcification and extracoronary atherosclerosis is the main determinant of pulse pressure in hemodialysis patients.

INTRODUCTION: Pulse pressure (PP) has been reported as an independent predictor of cardiovascular mortality in hemodialysis patients. In this study, we aimed to investigate association of PP with echocardiographic and vascular structural changes such as atherosclerosis and arterial calcifications in HD patients. PATIENTS AND METHODS: In this cross-sectional study, 108 chronic hemodialysis patients (49 male, 59 female, mean age: 46 ± 13 years) were included. Biochemical analyses, echocardiographic and high-resolution carotid Doppler examinations were done. Aortic wall and coronary artery calcifications were measured with electron beam computed tomography. The degree of carotid artery stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. RESULTS: PP was strongly correlated with systolic (r: 0.82) and diastolic (r: 0.33) blood pressure, left ventricular mass index (r: 0.58), left ventricle end diastolic diameter (r: 0.38) and weakly correlated with aortic wall calcification score (r: 0.26) and carotid plaque score (r: 0.27), but not with coronary artery calcification score. Patients with carotid plaque had higher PP than patients without plaque (50 ± 16 mmHg versus 44 ± 14 mmHg, P = 0.05). Patients were divided into three groups according to aortic wall calcification score. PP was significantly higher in patients with higher aortic wall calcification (54 ± 16 mmHg) than patients with lower aortic wall calcification (44 ± 15 mmHg, P = 0.04). However, on multivariate linear regression analysis for predicting PP, the only significant factor retained was left ventricle end diastolic diameter. CONCLUSION: PP was weakly associated with large vessel calcification and atherosclerosis in hemodialysis patients. The bulk of the effect on PP seems to be due to hypervolemia.

Relationship between HLA molecules and late restenosis after coronary stent placement.

OBJECTIVE: The objective of this study is to confirm whether there is relation between the human leucocyte antigen (HLA) locus and restenosis after percutaneous coronary intervention (PCI) holds in our patient population and whether it can be useful as a prognostic factor. METHODS: We examined the HLA phenotypes in 46 consecutive patients (39 men, 7 women, mean age of 57 ± 9 years) who had successful stent implantation in the coronary artery. Selective coronary arteriography was performed 6 months after coronary stenting to assess the presence of restenosis. The HLA phenotyping was performed for HLA-A,-B,-C antigens by Terasaki microlymphocytotoxicity technique and for HLA-DR alleles with PCR-SSP technique. RESULTS: Restenosis(R+) was present in 12 (26.1%) patients (11 men, 1 woman, mean age of 57 ± 10 years). For HLA Class I antigens frequency of HLA-B62 and HLA-CW2 antigen was slightly higher in restenotic patients but did not reach statistical significance. For HLA-DR alleles restenotic patients had higher frequencies for HLA-DRB1(∗)01(R+ %25, R- %14.7), and HLA-DR11(R+ %41.7, R- %20.6), without reaching statistical significance and lower frequencies for DR7(R+ %0, R- %17.6) and D13(R+%8.3, R- %32.4) and HLA-DR53 (R+ %25, R- %35.3) without reaching statistical significance. CONCLUSION: In conclusion, results show that there was no relationship between the development of restenosis and HLA-subtypes.

High sensitivity C-reactive protein in spontaneous bacterial peritonitis with nonneutrocytic ascites.

BACKGROUND/AIMS: Diagnosis of spontaneous bacterial peritonitis in cirrhotic ascites is based on a polymorphonuclear leukocyte count of ascitic fluid equal or greater than 250/mm3 in the presence of clinical signs. There is a small number of patients with positive ascitic fluid culture whose polymorphonuclear leukocyte count is less than 250/mm3. In this study, we assessed the diagnostic value of serum high sensitivity C-reactive protein in spontaneous bacterial peritonitis with nonneutrocytic ascites. METHODOLOGY: Patients with decompensated cirrhosis were enrolled in three groups. Group 1: Signs and symptoms of peritonitis plus a polymorphonuclear leukocyte count of ascitic fluid equal or greater than 250/mm3. Group 2: Signs and symptoms of peritonitis, but polymorphonuclear leukocyte count of ascitic fluid less than 250/mm3. Group 3: No signs and symptoms of peritonitis and polymorphonuclear leukocyte count of ascitic fluid less than 250/mm3. Ceftriaxone was started in Groups 1 and 2. Serum level of hsCRP was repeated after the 2nd day of the antibacterial treatment. RESULTS: Mean levels of serum hsCRP were 68.4 mg/dl, 68.3 mg/dl and 6.5 mg/dl in Groups 1, 2 and 3 respectively. Those levels were significantly higher in Groups 1 and 2 compared to Group 3 (p < 0.0001). After the 2nd day of ceftriaxone, serum hsCRP decreased to a mean level of 9.0 mg/dl in Group 1 and to 9.1 mg/dl in Group 2. CONCLUSION: These findings indicate that elevated hsCRP levels may discriminate patients with and without spontaneous bacterial peritonitis even in the presence of nonneutrocytic ascites, and may have utility in the assessment of treatment response.

Left ventricular thickness is increased in nonhypertensive Turner's syndrome.

BACKGROUND: Turner's syndrome (TS), the most frequent congenital anomaly in newborn girls, is associated with various cardiovascular abnormalities, predominantly bicuspid aortic valves and aortic coarctation. The causes of the left ventricular hypertrophy (LVH) and ECG findings associated with TS are unknown. We used echocardiography to assess cardiac structure and function in normotensive patients with TS. METHOD: Thirty-one patients with TS and 30 healthy women were enrolled in this comparative study. Twelve-lead ECG, 24-hour-ambulatory ECG recording, and echocardiography were performed. RESULTS: With 24-hour-ambulatory ECG recording, the mean heart rate (HR) of TS women was higher than non-TS women. With echocardiographic examination, the interventricular septum diastolic thickness, left ventricle posterior wall diastolic thickness (LVPW), the LV mass index (LVMI), and left atrial diameter index (LADi) were significantly higher in TS women compared with controls. Mitral flow A velocity was significantly higher and the ratio of early to late diastolic filling was significantly lower in TS patients. CONCLUSION: HR, LV wall thicknesses, LVMI and the LADi are significantly increased in normohypertensive TS women. There is also subclinical diastolic dysfunction in these patients.

Atrial and ventricular arryhthmogenic potential in Turner Syndrome.

BACKGROUND: P-wave dispersion (Pd), corrected P-wave dispersion (Pdc), QT-wave dispersion (QTd), and corrected QT-wave dispersion (QTdc) parameters were not assessed in Turner Syndrome (TS) before. The aim of this study is to investigate the cardiac arrhythmogenic potential in patients with TS. METHODS: Thirty-one patients with TS and 30 healthy women were enrolled in the study. For this purpose 12-lead electrocardiogram (ECG) and 24-hour ambulatory ECG recordings were performed. RESULTS: Pd, Pdc, QTd, and QTdc were significantly higher in patients with TS. On 24-hour ambulatory ECG recording, the mean heart rate (HR) was higher, while the mean of all RR intervals between normal beats (MeanNN), the standard deviation of all the RR intervals (SDNN), the square root of the mean of the squared differences of two consecutive RR intervals (rMSSD), and the percentage of the beats with consecutive RR interval difference more than 50 milliseconds (pNN50) were lower in TS. CONCLUSION: There were significant increases in Pd, Pdc, QTd, and QTdc in patients with TS and they may be features of the disease. The frequency of supraventricular arrhythmias was increased. There also was a significant deterioration of sympathetic and parasympathetic components of autonomic function as assessed by heart rate variability (HRV) in Turner patients.

Changes in left ventricular outflow and intraventricular flow patterns in hypertension and controls: a Doppler echocardiographic study.

OBJECTIVE: It has been previously reported that intraventricular flow patterns in some hypertensive patients with left ventricular hypertrophy, change to patterns similar to flow profiles of hypertrophic cardiomyopathy. The purpose of the study was to assess left ventricular outflow and mid-septal intraventricular flow patterns in hypertensive and normotensive patients. METHODS: Left ventricular outflow and mid-septal flows of 68 patients (41 men, mean age 53 +/- 14 years) and 45 non-hypertensive healthy controls (26 men, mean age 43 +/- 16 years) were assessed with Doppler echocardiography. Acceleration slope, pre-ejection period (PEP), and velocity-time integrals of the flows were recorded at the level and 1, 2 and 4 cm below the aortic valve. M-mode parameters of left ventricular wall thicknesses, dimensions and ejection fractions were also recorded. The data was analysed with the paired Student's t test with pre-hoc Bonferoni correction of the level of significance (0.05/4 = 0.0125) for multiple comparisons. RESULTS: In normotensive patients the acceleration slope uniformly and statistically significantly decreased beneath the aortic annulus and PEP was unchanged. In hypertensive patients the acceleration slope steepened (1596 +/- 531 vs. 1948 +/- 700 cm/sec, p < 0.05) and PEP decreased (108 +/- 23 vs. 98 +/- 20 msec, p < 0.05) 1 cm below the aortic valve and later reverted to the normal pattern of decrease seen in normotensive patients. CONCLUSION: The increase in acceleration slope and decrease in PEP in the subvalvular region may represent the changing contraction pattern in the hypertensive patients, causing protrusion of the upper septum into left ventricular outflow track and may have a role in the genesis of systolic murmurs.

Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.

BACKGROUND: Accelerated atherosclerosis and vascular calcification are common in chronic haemodialysis (HD) patients. In this study, we aimed to investigate the relationship between left ventricular hypertrophy (LVH) in HD patients and atherosclerosis and vascular calcification measured by electron beam computed tomography (EBCT). METHODS: In a cohort of 118 HD patients (52 male, 66 female, mean age: 46+/-13 years), we measured biochemical parameters, including BUN, creatinine, albumin, haemoglobin, C-reactive protein and fibrinogen levels, and performed echocardiography, high-resolution B-mode carotid ultrasonography and EBCT in 85 of them. The degree of stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. Carotid plaque scores were calculated by summing the degrees of stenosis measured at all locations. RESULTS: LVH was detected in 89 of the patients (75%). Plaque-positive patients had higher left ventricular mass index (LVMI) than plaque-negative patients (175+/-59 vs 143+/-46 g/m2, P = 0.003). LVMI was correlated with systolic blood pressure (r = 0.62, P<0.001), pulse pressure (r = 0.58, P<0.001), haemoglobin levels (r = - 0.25, P = 0.008), carotid plaque score (r = 0.32, P = 0.001) and coronary (CACS) and aortic wall calcification score (AWCS) (r = 0.34, P = 0.002 and r = 0.43, P<0.001, respectively). Multiple linear regression analysis (model r = 0.76) showed the independent factors related to LVMI to be systolic blood pressure, pulse pressure, CACS and presence of carotid plaques. CONCLUSION: Extra-coronary atherosclerosis and vascular calcification are associated with LVH in HD patients. Whether the treatment of atherosclerosis or vascular calcification may cause regression of or even prevent LVH in HD patients remains to be seen.

Structural, functional and autonomic changes in the cardiovascular system in growth hormone deficient patients.

BACKGROUND: Growth hormone deficiency (GHD) is known to cause higher rates of cardiovascular mortality. The purpose of the study was to analyze the structural and functional changes in the heart and investigate their relation to autonomic function as assessed with heart rate variability (HRV). METHODS: Eleven untreated GHD patients (mean age 50.4 +/- 10.7 years, M/F: 3/8) and 15 age- and sex-matched healthy persons (mean age 45.3 +/- 10.4 years, M/F: 5/10) were compared. Both groups were examined with echocardiography, HRV, and exercise testing and findings were analyzed. RESULTS: The groups were similar in height, weight, body mass index, body surface area, systolic and diastolic blood pressure, heart rate. The GHD patients had lower exercise duration and metabolic equivalent (MET) compared to controls (7.94 +/- 1.26 vs. 9.8 +/- 1.9 min, P < 0.001, for MET 8.85 +/- 0.86 vs. 10.7 +/- 2.23, P = 0.03). On echocardiography, GHD patients had lower interventricular septum diastolic diameter (9 +/- 0.89 vs. 10.7 +/- 0.88 mm, P < 0.001) and posterior wall thickness (8.4 +/- 0.93 vs. 9.8 +/- 0.91 mm, P = 0.002), and lower left ventricle mass index (90.9 +/- 20 vs. 112 +/- 8 g/m2, P = 0.01). Left ventricular ejection fraction was lower in the GHD patients (57.4 +/- 5.12% vs. 65.5 +/- 4.1%, P < 0.001). Time and frequency domain heart rate variability parameters, SDNN, SDANN, VLF, LF ve LF/HF were lower in GHD patients compared to controls. There was a significant correlation between left ventricle diastolic diameter and LF (r = 0.62, P = 0.02). CONCLUSION: GHD seemed to cause decreased left ventricle mass and decreases in the sympathetic components of HRV that may have a bearing on the increased cardiovascular risk seen in these patients.

Percutaneous mitral balloon valvuloplasty in rheumatic mitral stenosis without heparin.

BACKGROUND AND AIM OF THE STUDY: Customarily, heparin is used to prevent embolic complications arising during percutaneous mitral balloon valvuloplasty (PMBV), but this may prolong hospital stay and increases the risk of bleeding, hemopericardium and cardiac tamponade. The study aim was to assess in-hospital complications of PMBV performed without heparin. METHODS: Rheumatic mitral stenosis patients undergoing PMBV between February 1997 and March 2000, either with (18 males, 91 females; mean age 37.5 +/- 8.8 years) or without (15 males, 119 females; mean age 37.5 +/- 15.1 years) heparin at conventional doses, were included in the study. Neurologic and cardiac examinations were conducted after PMBV and repeated before discharge from hospital. RESULTS: There was no statistically significant difference between groups in terms of age, gender, NYHA class, presence of atrial fibrillation, spontaneous echo contrast, left atrial appendix thrombus, left atrial diameter and mitral valve echo score. There was no difference between groups with regard to procedural success, mitral valve area and gradient attained, or rates of mitral insufficiency. Ten patients in the heparin group required transesophageal echocardiography (TEE) guidance during PMBV (p <0.001). The mean duration of PMBV was greater in the heparin group due to increased use of TEE guidance during septal puncture. During follow up, no patients in the non-heparin group had hemopericardium, cardiac tamponade, embolic event or death; by comparison, in the heparin group one patient had hemopericardium and one had a cardiac tamponade. No major bleeding episode requiring transfusion occurred in either group, but six and 10 cases of minor bleeding at access sites occurred in the non-heparin and heparin groups, respectively (p = NS). Duration of hospitalization was statistically longer in the heparin group than in the non-heparin group. CONCLUSION: Avoidance of heparin did not lead to an increase in embolic complications. The vascular access sites were withdrawn early, thereby reducing the duration of hospital stay and time to ambulation. This method did not cause any increase in numbers of vascular complications and blood transfusions.

Angiotensin converting enzyme gene polymorphism and development of post-transplant erythrocytosis.

BACKGROUND: An increased activation of the renin-angiotensin system probably plays a major role in the development of post-transplant erythrocytosis (PTE). It is known that deletion type polymorphism (DD) in the angiotensin converting enzyme (ACE) gene is associated with higher circulating angiotensin II (AII) levels. The aim of this study was to investigate the effect of ACE gene polymorphism on development of PTE. METHODS: 86 PTE patients (male/female: 68/18, mean age: 32 +/- 10 years) and 68 consecutively transplanted non- PTE patients (male/female: 38/30, mean age: 31 +/- 10 years) were included; 140 patients (91%) had been transplanted from living donors; 92 patients (60%) had hypertension. ACE gene polymorphism was determined by polymerase chain reaction (PCR). RESULTS: The mean time to appearance of PTE was 8.8 +/- 7.9 (range of 1-53) months. DD genotype was detected in 65 patients. PTE patients had a higher prevalence of hypertension (70% vs. 46%, p=0.003) and a lower frequency of DD genotype (34% vs. 54%, p=0.014) as compared to non-PTE patients [OR: 2.2 (1.14-4.25, 95% CI)]. PTE developed more frequently in male patients (68/106: 64%) than females (18/48: 38%) (p=0.002). Patients with DD genotype had a significantly longer leading time to PTE in Kaplan-Meier survival analysis with log-rank (136 +/- 15 vs. 92 +/- 13 months, p=0.015). In Cox regression analysis, hypertension (p=0.002) and recipient ACE genotype (p=0.013) were retained as independent variables for predicting PTE development. CONCLUSIONS: PTE develops more frequently in male, hypertensive renal transplant recipients with good allograft function. DD-type ACE gene polymorphism seems to protect against PTE development.

Effect of diurnal variability of heart rate on development of arrhythmia in patients with chronic obstructive pulmonary disease.

We examined the possible effect of diurnal variability of heart rate on the development of arrhythmias in patients with chronic obstructive pulmonary disease (COPD). Forty-one COPD patients (M/F: 39/2, mean age: 59+/-8.5 years) and 32 (M/F: 27/5, mean age: 57+/-11 years) healthy controls were included. Twenty-four hour ECG recordings were analyzed for atrial fibrillation (AF) or ventricular premature beats (VPB), and circadian changes in heart rate variability (HRV) were assessed by dividing the 24-h period into day-time (08:00-24:00 h) and night-time (24:00-08:00 h) periods. Night-time total (TP), low frequency (LF) and high frequency (HF) powers were similarly lower from day-time parameters in AF(-) COPD patients (HF 3.91+/-1 vs. 4.43+/-1.04 ms(2), P=0.001) and controls (HF 3.95+/-0.72 vs. 4.82+/-0.66 ms(2), P<0.001). The LF/HF ratios were also significantly reduced in the same patient groups (AF(-) COPD 1.35+/-0.21 vs. 1.27+/-0.19, P=0.04, controls 1.43+/-0.14 vs. 1.24+/-0.09, P<0.001). Night-time TP and LF were increased, HF unchanged and LF/HF significantly increased (1.11+/-0.25 vs. 1.19+/-0.27, P<0.05) in AF(+) COPD patients. Frequency of VPB was correlated with corrected QT dispersion (QTc(d)) (r=0.52, P=0.001) and the day-time/night-time HF ratio (r=0.43, P=0.02). Patients with QTc(d)>or=60 ms did not have the expected increase in night-time HF and had a statistically insignificant increase in LF/HF ratio. In COPD patients with QTc(d)<60 ms, circadian changes in HRV parameters were parallel with the controls. We concluded that COPD patients with arrhythmia had circadian HRV disturbances such as unchanged night-time parasympathetic tone and disturbed sympatho-vagal balance in favor of the sympathetic system all day long, which may explain the increased frequency of arrhythmia.

Left ventricular hypertrophy and endothelial dysfunction in chronic hemodialysis patients.

BACKGROUND: Endothelial dysfunction (ED), which is a risk factor for atherosclerosis, has been reported recently in chronic hemodialysis (CHD) patients. In this study, we aim to investigate the association of ED and presence of left ventricular hypertrophy (LVH) in CHD patients. METHODS: One hundred four CHD patients (47 men, 57 women; mean age, 45 +/- 12 years) and 49 age- and sex-matched controls were included. Mean time on dialysis therapy was 62 months. Echocardiographic examination and flow-mediated endothelium-dependent (EDD) and endothelium-independent dilatation (EID) of the brachial artery, measured by high-resolution ultrasonography, a noninvasive method for assessing endothelial function, were performed on a nondialysis day. RESULTS: LVH was detected in 72 CHD patients (69%). Patients with LVH had a lower EDD (9.3% +/- 6.1% versus 12.1% +/- 8.3%; P = 0.06), but the difference was not significant. Mean EID was significantly lower in CHD patients with LVH (13.6% +/- 7.6% versus 18.6% +/- 9.8%; P = 0.008). Left ventricular mass index (LVMI) correlated with both EDD (r = -0.22; P = 0.03) and EID (r = -0.32; P = 0.002). Patients with LVH had a greater rate of hypertension (35 of 72 versus 7 of 32 patients; P = 0.02) and lower hemoglobin levels (11.0 +/- 1.8 versus 11.8 +/- 1.6 g/dL [110 +/- 18 versus 118 +/- 16 g/L]; P = 0.05). CHD patients had a lower EDD (10.2% +/- 6.9% versus 20.9% +/- 7.6%; P < 0.001) and EID (15.0% +/- 8.5% versus 27.8% +/- 8.5%; P < 0.001) compared with controls. In linear regression analysis for predicting LVMI, presence of hypertension, hemoglobin level, and EID, but not EDD, were found to be independent variables. CONCLUSION: EID, which may reflect decreased elasticity of arteries, contributes to the development of LVH in CHD patients, in addition to hypertension and anemia.

Ventricular arrhythmias in patients with COPD are associated with QT dispersion.

STUDY OBJECTIVE: QT dispersion (QTd) and late potentials derived from signal-averaged ECG (SAECG) have been proposed as noninvasive predictors of cardiac arrhythmias that occur in patients with COPD. In this study, we aimed to investigate QTd and SAECG in patients with COPD. DESIGN: Cross-sectional study. SETTING: Teaching chest disease hospital and cardiology center in a university hospital. PATIENTS: Thirty patients with COPD (28 men and 2 women; mean +/- SD age, 60 +/- 9 years) and 31 age- and sex-matched control subjects (28 men and 3 women; mean age, 57 +/- 7 years) were included. MEASUREMENTS AND RESULTS: Respiratory function tests, arterial blood gas analyses, echocardiographic examinations, rhythm Holter recordings, and heart rate variability (HRV) analyses were performed in addition to the measurements of QT intervals and SAECG. Patients with COPD had higher rate of ventricular premature beats (VPBs) as compared to control subjects (924 +/- 493 beats vs 35 +/- 23 beats, p = 0.009). Eight patients with COPD (27%) had nonsustained runs of ventricular tachycardia (VT). QTd rates were significantly increased in patients with COPD as compared to control subjects (57.7 +/- 9.9 ms vs 37.5 +/- 8.2 ms, p < 0.001). On comparing patients with COPD with and without runs of VT, patients with VT had longer QTd (67 +/- 10 ms vs 55 +/- 8 ms, p = 0.001). However no difference in any HRV and late potential parameters were found between patients with COPD with and without runs of VT. VPB rates were strongly correlated with QTd in patients with COPD (r = 0.61, p < 0.001). On SAECG analysis, patients with COPD had significantly increased total QRS duration as compared to control subjects. Nine of the 30 patients with COPD (30%) had positive late potentials. However, QTd and VPB rates were also similar between patients with COPD with and without late potentials. CONCLUSIONS: The development of ventricular arrhythmia in patients with COPD was associated with increased QTd. Increased QTd may be associated with autonomic changes seen in patients with COPD.

Association between hepatitis C virus infection and development of posttransplantation diabetes mellitus in renal transplant recipients.

BACKGROUND: Posttransplantation diabetes mellitus (PTDM) is a metabolic complication of renal transplantation. A high prevalence of DM has been recently reported in patients with chronic hepatitis C virus (HCV) infection in the nontransplant population. The aim of this study was to investigate possible factors that may have a role in the development of DM, including HCV infection in renal transplant recipients. PATIENTS AND METHODS: This case-control study included 43 patients with PTDM (36 men, 7 women; mean age, 44+/-10 years) and 43 consecutive transplant patients who did not develop PTDM (30 men, 13 women; mean age, 37+/-11 years). Age, body mass index, high-dose steroid use, family history for DM and HCV, and presence of HLA-DR2, -DR3, and -DR4 were considered as possible factors for predicting PTDM. RESULTS: Patients with PTDM were older (P=0.002) and had a higher prevalence of family history of DM (61% vs. 9%, P<0.001) and a higher rate of HCV seropositivity (72% vs. 37%, P=0.002; odds ratio = 1.94; 95% confidence interval = 1.26-2.98). The prevalence of pancreatic autoantibodies (anti-glutamic acid decarboxylase, islet cell antibody) was similar between patients with and without PTDM. In logistic regression analysis (r = 0.61, P<0.001), age, family history, and HCV infection were independent variables for predicting development of PTDM. CONCLUSION: HCV infection was associated with the development of PTDM, in addition to family history and increased age. The rate of autoantibodies against pancreatic cells was not increased in patients with HCV, which suggested that nonimmunologic mechanisms were likely to have a role in the pathogenesis of PTDM.