Endothelial constitutive nitric oxide synthase, angiotensin converting enzyme, angiotensin II type 1 receptor gene polymorphisms and endothelial functions in healthy individuals.

INTRODUCTION: Endothelial dysfunction is recognized as an early and initiating event in the pathogenesis of coronary artery disease. Gene polymorphisms of endothelial constitutive nitric oxide synthase (ecNOS), angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) have been found to be associated with atherosclerosis.  We aimed to investigate the possible effects of ecNOS, ACE and AT1R gene polymorphisms on endothelial functions in healthy population. MATERIALS AND METHODS: In 255 healthy subjects (male/female: 119/136 mean age 35.1±2.3 years)  ecNOS, ACE and AT1R gene polymorphisms were assessed by polymerase chain reaction (PCR). Endothelium dependent (EDD, flow-mediated) and endothelium independent vasodilation (EID) were measured by high resolution brachial artery ultrasound and 0.5 mg sublingual nitroglycerine respectively. RESULTS: ecNOS and ACE genes had no significant effect on EDD and EID. However, subjects with AT1RAC+CC genotypes had lower EDD compared to subjects with AT1RAA genotype in females (19.4 ± 6.6% vs 21.5 ± 7.8%, p = 0.041). EDD and EID were significantly negatively associated with  age, body mass index, serum creatinine, glucose, uric acid and hemoglobin levels. When the data on age, uric acid, BMI, glucose, creatinine, and hemoglobin were split into 3 as low-1/3, mid-1/3 and  high 1/3, there was significant graded decrease in EDD and EID with these parameters. In multiple regression analysis, age and presence of AT1RAC+CC genotype  retained as significant independent factors predicting endothelial functions. CONCLUSIONS: Gene polymorphisms of endothelial constitutive nitric oxide synthase and  angiotensin converting enzyme had no effect on endothelial functions. However, the presence of angiotensin II type 1 receptor polymorhism (AT1RAC+CC genotype) seemed to adversely affect the endothelial functions as reflected by impaired endothelium dependent and independent vasodilatation in healthy individuals.

Drugs with blocking effects on the renin-angiotensin-aldosterone system do not improve endothelial dysfunction long-term in hypertensive patients.

In essential hypertension, endothelial dysfunction has been documented many times and correlates with prognosis. The influence of the renin-angiotensin-aldosterone system (RAAS) on endothelial dysfunction has also been studied. The present study investigated the duration of the effects of RAAS-blocking drugs on endothelial function in 44 consecutive, never-treated, outpatients with mild to moderate hypertension. Patients (11 per group) received an angiotensin receptor blocker (ARB; irbesartan 300 mg/day or valsartan 160 mg/day) or an angiotensin-converting enzyme inhibitor (ACEi; fosinopril 10 mg/day or quinapril 20 mg/day). If target blood pressure (< 140/90 mmHg) was not achieved, 12.5 mg/day hydrochlorothiazide was added. Endothelial function, assessed by measuring brachial artery diameter, did not change significantly after 6 weeks, 1 year or 3 years of treatment in any group. Across all groups, endothelium-dependent and -independent vasodilation increased significantly after 6 weeks but, after 1 year, decreased below baseline and was at a similar level after 3 years; groups did not differ significantly. Both ACEi and ARB had similar effects on endothelial function; improvement occurred at the start of treatment but was not maintained. Endothelial dysfunction may be a resistant or irreversible feature of hypertension, requiring high doses of antihypertensive drugs and above-average patient compliance.

Is there any relationship between serum and urine neopterin and serum interferon-gamma levels in the activity of Behcet's disease?

BACKGROUND: Behcet's disease (BD) is a chronic, inflammatory, multisystem vasculitic disorder. There is no reliable laboratory marker that indicates disease activity. Neopterin is an immunological marker of cellular immune activation, which is secreted by monocytes/macrophages as a result of interferon-gamma (IFN-gamma) secretion by activated T lymphocytes. OBJECTIVE: We aimed to investigate serum and urine neopterin levels in BD patients. METHODS: Forty-five patients who were diagnosed according to the criteria of the International Study Group for BD and 45 age- and sex-matched healthy controls were enrolled in the study. Disease activity was considered by clinical findings. Serum and urine neopterin levels and serum IFN-gamma levels were measured. RESULTS: The mean values of serum and urine neopterin levels were 12.68 +/- 4.87 nmol/L and 167.53 +/- 148.73 micromol/mol creatinine, respectively, in BD patients (P = 0.000 and P = 0.008, respectively), which were statistically significantly different from the control group. However, there was no significant statistical difference between serum and urine neopterin levels of the clinically active and inactive patients. It was also found that the mean value of serum IFN-gamma levels was higher in healthy controls than in BD patients (P = 0.000). CONCLUSIONS: We conclude that serum and urinary neopterin measurement can not be used as a reliable laboratory marker as the BD patients' serum and urinary neopterin levels do not increase in the active stage even though these levels increase when compared to healthy controls.

Traumatic lingual ulcer in a child: Riga-Fede disease.

Riga-Fede disease RFD is an extremely rare, benign inflammatory disorder characterized by reactive, traumatic ulceration of the oral mucosa especially located on the tongue. It is most commonly associated with natal or neonatal teeth in newborns. Mucosal lesions are often caused by repetitive traumatic damage due to backward and forward motions of the tongue over the lower incisors. Failure to diagnose and treat these lesions properly may result in inadequate food intake, growth retardation and permanent lingual deformity. We report a 15-month-old healthy infant with tongue ulcer diagnosed as RFD based on history and clinical features.

Evaluation of activatory and inhibitory natural killer cell receptors in non-segmental vitiligo: a flow cytometric study.

BACKGROUND: Recent observations established the role of altered cellular immunity and autoimmune hypothesis in the pathogenesis of vitiligo. There have been several reports discussing T-cell and natural killer (NK) cell populations, but NK cell receptors were not evaluated in vitiligo. OBJECTIVE: The purpose of this investigation was to assess the role of T and NK cells as well as activatory and inhibitory NK cell receptor alterations in the pathogenesis of vitiligo and whether any aberrations were correlated with clinical findings of the disease. PATIENTS/METHODS: Fifty-three patients with non-segmental vitiligo and 45 age- and sex-matched healthy controls were enrolled in the study. The percentages of lymphocytes, granulocytes, monocytes and CD3, CD4, CD8, CD14, CD16, CD56, CD45, CD45RA, CD54RO, CD28, CD80, CD94, CD158a, KIR3DL-1 receptors as well as CD94, CD158a, KIR3DL-1 receptors on CD16(+) cells were detected by using flow cytometry. The patient and control groups were compared in terms of the results of flow cytometric analysis, and the results were assessed regarding the type and activity of vitiligo. RESULTS: The percentages of CD16(+)CD56(+), CD3(+)CD16(+)CD56(+), CD8(+) and CD45RO(+) cells were significantly increased in vitiligo group compared with the controls. No difference was detected between the patients and control groups in percentages of CD3(+), CD4(+), CD3(-)CD16(+)CD56(+), CD28(+), CD45(+), CD45RA(+), CD94(+), CD158a(+) and KIR3DL-1(+) cells. The percentage of CD16(+)CD158a(+) cells was significantly decreased in a randomized selected group of vitiligo patients. There were no differences in percentage expression of studied cell surface antigens between patients in the active or stable period. CD3(+) cells were significantly increased in generalized form, and CD45RO(+) cells were significantly increased in acral/acrofacial form when compared with the other types of vitiligo. CONCLUSIONS: These results indicate further evidence for T and NK cell abnormalities in non-segmental vitiligo. The present data show that NK cell activation may be responsible in the pathogenesis of vitiligo in conformity with decreased inhibitory and increased activatory NK cell receptors.

Heart rate variability in diabetes patients.

Diabetes mellitus can cause cardiovascular autonomic neuropathy and is associated with increased cardiovascular deaths. We investigated cardiovascular autonomic neuropathy in diabetics and healthy controls by analysis of heart rate variability. Thirty-one diabetics and 30 age- and sex-matched controls were included. In the time domain we measured the mean R - R interval (NN), the standard deviation of the R - R interval index (SDNN), the standard deviation of the 5-min R - R interval mean (SDANN), the root mean square of successive R - R interval differences (RMSSD) and the percentage of beats with a consecutive R - R interval difference > 50 ms (pNN50). In the frequency domain we measured high-frequency power (HF), low-frequency power (LF) and the LF/HF ratio. Diabetes patients had lower values for time-domain and frequency-domain parameters than controls. Most heart rate variability parameters were lower in diabetes patients with chronic complications than in those without chronic complications.

The role of HLA molecules in susceptibility to chronic rheumatic heart disease.

Only a small fraction of the streptococcal pharyngitis progress to rheumatic carditis, which implies that environmental, host and microbial factors interact to cause an aberrant immune response against the antigens of the microorganism that cross-react with cardiac tissues. Although there are numerous studies and a general consensus on the relation between human leucocyte antigen (HLA) class II antigens and rheumatic heart disease (RHD), the details and the culprit antigens are still controversial. The study was undertaken to examine 100 patients with chronic RHD and 100 controls for HLA class I and class II antigens for differences in prevalence. All samples were typed at the HLA-DRB1/3/4/5 and DQB1 loci by the sequence-specific primer (PCR-SSP) method at low resolution. For HLA class I antigens, HLA-B13 frequency was marginally increased in patients with RHD compared to controls without reaching statistical significance. For class II antigens, RHD patients had higher frequencies for HLA-DRB1*01 (RHD 24%, controls 10%), DRB1*04 (RHD 35%, controls 26%), DRB1*07 (RHD 18%, controls 11%) and HLA-DQB1*02 (RHD 32%, controls 17%) without reaching statistical significance, and significantly lower frequencies for DRB1*13 (Pc < 0.003, OR: 5.69), DRB5* (Pc < 0.003, OR: 33) and DRB3* (Pc = 0.03, OR: 2.66) compared to controls. It was concluded that host, microbial and environmental factors collude to create acute rheumatic fever (RF) and chronic rheumatic valve disease. The HLA-DRB1*13, DRB5* and DRB3* were protective against the development of rheumatic valve damage.

Suicide attempt with clopidogrel.

We report the case of a 49-year-old male who took an overdose of 1650 mg of clopidogrel with suicidal intent. The patient developed abnormalities of platelet aggregation, but never developed symptoms. Clopidogrel is a commonly prescribed drug. Reports of overdose of clopidogrel were very rarely reported in the literature.

Genetic polymorphisms and endothelial dysfunction in patients with essential hypertension: a cross-sectional case-control study.

BACKGROUND: Both in animal models and humans an association between endothelial constitutive nitric oxide synthase (ecNOS) gene polymorphism and the development of hypertension has been found. However, the relation between ecNOS polymorphism and endothelial function in patients with hypertension has not been systematically studied. Genes of the renin-angiotensin system include the angiotensin-converting enzyme (ACE) gene, and the angiotensin II type 1 receptor (ATIR) gene, and have been associated with essential hypertension. However, no consistent data are available about the relation between polymorphisms of these genes and the presence of endothelial dysfunction in such patients. OBJECTIVES: To assess the presence of genetic polymorphisms and of endothelial dysfunction in patients with essential hypertension. To determine the effects of gene polymorphisms on endothelial dysfunction in these subjects. METHODS: In 129 patients with essential hypertension and the same number of age-matched controls polymorphisms of the ecNOS gene, ACE gene, and AT1R gene were analysed by polymerase chain reactions. Endothelial function was assessed by maximal endothelial dependent vasodilation in response to reactive hyperaemia using high resolution ultrasound examinations of the brachial arteries. To assess correlation between genetic markers, endothelial function, and the presence of hypertension both univariate and multivariate analyses were used including Pearson's and Spearman's correlation coefficients, and multiple logistic regressions. RESULTS: The size of endothelium-dependent vasodilation between patients and controls differed by 16% (p<0.02). However, the presence of genetic polymorphisms of the ecNOS, ACE, and AT1R genes did not significantly differ between patients and controls. Neither were there any statistically significant differences in endothelial function between various genotypes of the three genes. This was so for both the patients and the controls, although in all of these comparisons the controls overall displayed a slightly better endothelial function than the patients did. Multiple regression analysis with endothelial dysfunction as dependent and the presence of gene polymorphisms as independent variables did not reveal any significant correlation either. CONCLUSION: A significant relation between endothelial dysfunction and essential hypertension was demonstrated. However, no relations between genetic markers and the presence of essential hypertension or between endothelial dysfunction and genetic markers were established. The failure of our study to demonstrate the latter may be due to confounders. Also, other genes may be more important in the pathogenesis of endothelial dysfunction and essential hypertension. The current study underscores that endothelial dysfunction and hypertension are not simple genetic disorders, and that they are, essentially, multicausal.

The diagnostic value of troponin T and myoglobin levels in acute myocardial infarction: a study in Turkish patients.

This study compares the diagnostic value of troponin T (TnT) and myoglobin with creatinine kinase (CK) for myocardial infarction (MI) in a tertiary care centre in a developing nation. The study group comprised 33 acute myocardial infarction patients and 27 healthy controls. Receiver operating characteristic curves for TnT, myoglobin and CK were drawn and areas under the curve calculated. At admission, myoglobin levels had greater diagnostic sensitivity than TnT or CK levels. After 2 h, myoglobin and TnT had equal sensitivity and specificity, whereas CK still had lower sensitivity than myoglobin and TnT. After 4 h there was no difference between the tests. It was concluded that myoglobin levels on admission and TnT at 2 h had the greatest diagnostic rate, whereas all the tests were similar after 4 h for MI.

Doxazosin, but not amlodipine decreases insulin resistance in patients with chronic renal failure: a prospective, randomized-controlled study.

Insulin resistance (IR) in chronic renal failure (CRF) is well-known. In this randomized-controlled study, we aimed to compare the effect of doxazosin and amlodipine on IR in patients with CRF. Fifteen patients with CRF (male/female: 5/10, mean age: 46 +/- 13 years) and 9 controls (male/female: 3/6, mean age: 35 +/- 8 years) were included. Patients and controls had no family history of diabetes mellitus. Homeostasis model assessment (HOMA) was calculated as a marker of IR. Patients were grouped randomly to doxazosin (n = 8; 2-4 mg/day) and amlodipine (n = 7; 5-10 mg/day) arms. Baseline biochemical analysis (fasting serum glucose, BUN, creatinine, uric acid, cholesterol and cholesterol subgroups) and parameters related with insulin metabolism (insulin, C peptide, HOMA) were similar between amlodipine and doxazosin groups. There was no difference in age, gender and body mass index among study groups. The follow-up time was 12 weeks. Patients with CRF had higher HOMA (1.83 +/- 0.55 vs 1.00 +/- 0.36, p = 0.001), fasting insulin (8.06 +/- 1.98 vs 4.46 +/- 1.31 IU/l, p < 0.001) and serum triglyceride levels (197 +/- 136 vs 112 +/- 67 mg/dl, p = 0.04) as compared to controls. Serum HDL cholesterol levels were significantly lower in patients with CRF than controls (40 +/- 10 vs 57 +/- 14 mg/dl, p = 0.02). HOMA significantly decreased after doxazosin (1.91 +/- 0.45 vs 1.41 +/- 0.21, p = 0.02), however, no difference was found after amlodipine. Also, fasting insulin levels were decreased after a 12-week doxazosin therapy from 8.17 +/- 1.22 vs 6.58 +/- 0.84 IU/l, p = 0.02), but no change was seen after amlodipine. Lipid parameters did not significantly change during the study period in 2 groups. No adverse effect requiring drug discontinuation was observed during the 12-week period in the study groups. In conclusion, doxazosin decreases IR in patients with CRF, whereas amlodipine has no effect. This may be of advantage in the treatment of hypertension in this group of patients for preventing some long-term complication of IR.

Increased QT dispersion in hemodialysis patients improve after renal transplantation: a prospective-controlled study.

Increased QT dispersion (QTd), predicting patients with risk of malignant arrhythmia, have recently been reported in hemodialysis patients (HDp). In this prospective study, we aimed to investigate changes in QTd and signal averaged-ECG (SAECG) in HDp after transplantation. Twenty-seven HDp (M/F:18/9, mean age 30+/-8 years) and 24 controls (M/F:14/10, mean age 33+/-6 years) were included. All QT parameters (QTmax, Qtmin, and QTd) were increased in HDp. QTmax and QTd started to decrease at the first month after transplantation. Percentage change in QTd at the third month was significantly correlated with percentage change in LV mass index (r=0.45, P=0.04), serum calcium (r=-0.47, P=0.02) and intact parathyroid hormone (r=0.68, P=0.01). In multivariate regression analysis, only percent chance in LV mass index was retained as significant. As for analysis of SAECG, 4 of the 23 (17%) HDp has abnormal late potentials which disappeared after transplantation. HDp with LV hypertrophy had higher filtered-QRS duration compared to patients without hypertrophy (110+/-12 vs. 97+/-11 msec, P=0.01). It was concluded that increased QTd and presence of late potentials improved early after renal transplantation. These changes were mainly associated with the regression of the LV mass.

Effect of left atrial size and function on P-wave dispersion: a study in patients with paroxysmal atrial fibrillation.

BACKGROUND: Paroxysmal atrial fibrillation (PAF), a common arrhythmia, is caused by the fractionated and nonhomogeneous propagation of sinus impulse. HYPOTHESIS: This study was undertaken to examine the effect of left atrial (LA) dimension and function on P-wave dispersion (deltaP) in unselected patients with PAF and health controls. METHOD: In this study, 62 consecutive patients with PAF (32 men, 30 women, mean age 55+/-11 years) and 62 age- and gender-matched healthy controls (33 men, 29 women, mean age 52+/-13 years) were studied to compare the effect of LA size, volume, and function on deltaP (difference between maximum and minimum P-wave duration on 12-lead electrocardiogram). RESULTS: P-wave dispersion in patients with PAF and normal LA diastolic diameter (LAD) was longer than that in controls with normal LA size (53+/-8 vs. 34+/-8 ms, p < 0.001). P-wave dispersion increased in patients with PAF (62+/-12 vs. 53+/-8 ms, p = 0.003) and controls (40+/-7 vs. 34+/-8 ms, p = 0.005) with increased LAD. Presence or absence of PAF did not interact with LAD for their effect on deltaP (2 x 2 analysis of variance test p = 0.20). In the PAF group, deltaP correlated with LAD (r = 0.43, p = 0.002), LA diastolic volume (r = 0.6, p < 0.001), and LA ejection fraction (AEF) (r = - 0.33, p = 0.05). The AEF was preserved when LAD increased in the patients without PAF (0.52+/-0.07 vs. 0.57+/-0.10, p = NS), however was significantly decreased in the PAF group (0.37+/-0.12 vs. 0.49+/-0.10, p = 0.01). On multivariate logistic regression analysis, only deltaP retained significance on development of PAF. CONCLUSION: It was concluded that deltaP increased in patients with PAF and normal LA size. In controls with increased LA size, deltaP increased but did not reach the levels attained in patients with PAF. The AEF was decreased in patients with PAF but was preserved in those without PAF. These findings can be explained by the changes in LA microarchitecture which concurrently decreased atrial myocardial contraction, increased deltaP, and predisposed to PAF.

Comparison of the effects of enalapril and losartan on posttransplantation erythrocytosis in renal transplant recipients: prospective randomized study.

BACKGROUND: The aim of this prospective randomized study was to compare the safety and efficacy of enalapril (E) and losartan (L) in the treatment of posttransplantation erythrocytosis and the effect of the ACE genotype on response to therapy. METHODS: Twenty-seven (24 male and 3 female, mean age 34+/-8 years) renal transplant recipients with erythrocytosis were treated either with E (15 patients) (10 mg/day) or L (12 patients) (50 mg/day) for 8 weeks. RESULTS: The hemoglobin levels were significantly decreased in the L (17.1+/-0.7 to 15.9+/-1.3 g/dl, P=0.01) and E groups (17.4+/-1.1 to 14.9+/-2.2 g/dl, P=0.001). Among the responders who discontinued treatment, there was a trend for longer time to relapse in the L group (7.38+/-3.75 months; 95% confidence interval: 0.03-14.7) compared with the E group (2.75+/-0.70 (95% confidence interval: 1.37-4.13) (P=0.11). Decrease in hemoglobin was more prominent with E compared with L (-3.26+/-0.65 vs. -1.70+/-0.39 g/dl, P=0.05). Decrease in hemoglobin levels between DD and non-DD genotype groups was similar (-2.0+/-1.5 vs. -1.7+/-2.3 g/dl, P=0.69). CONCLUSIONS: Enalapril caused a greater decrease but faster relapse in hemoglobin levels compared with losartan in patients with posttransplantation erythrocytosis. The DD type polymorphism had no effect on response.

Cardiac and intestinal amyloidosis in a renal transplant recipient with familial Mediterranean fever.

In Turkey, familial Mediterranean fever (FMF) is an important cause of nephrotic syndrome and endstage renal disease due to renal deposition of AA type amyloid. We report a case of living-related donor renal transplant recipient with FMF and renal AA type amyloidosis, who died of progressive heart failure due to cardiac involvement. The patient also had intractable diarrhea caused by biopsy-proven intestinal amyloidosis. The patient was on 1 mg/day colchicine. Although he was attack-free throughout the post-transplant period, intestinal and clinically significant cardiac amyloidosis, which implied the presence of sustained inflammation and continuing amyloid deposition, appeared three years after renal transplantation. Cardiac deposition of AA amyloid may cause clinically significant heart disease, leading to cardiovascular mortality after renal transplantation for end-stage renal disease in FMF patients.

QT dispersion and signal-averaged electrocardiogram in hemodialysis and CAPD patients.

OBJECTIVE: The aim of this study was to compare QT dispersion (QTd) and signal-averaged electrocardiogram (SA-ECG) parameters that may predict risk of malignant arrhythmias in patients on hemodialysis (HD), on continuous ambulatory peritoneal dialysis (CAPD), and in controls. SETTING: Controlled cross-sectional study in a tertiary-care setting. PATIENTS: 28 HD (M/F 18/10; mean age 32 +/- 9 years), 29 CAPD (M/F 17/12; mean age 34 +/- 10 years), and 29 healthy controls (M/F 17/12; mean age 32 +/- 8 years) were included. INTERVENTIONS: On ECG, minimum (QTmin) and maximum (QTmax) QT duration and their difference (QTd) were measured. In SA-ECG, duration of filtered QRS, HFLA signals less than 40 microV, and RMS voltage (40 ms) were also measured. RESULTS: Higher serum Ca2+ and lower K+ levels were found in CAPD compared to HD. All QT parameters were increased in HD and CAPD compared to controls. QT dispersion was significantly prolonged in HD compared to CAPD. In HD, QTd was correlated with left ventricular (LV) mass index (r = 0.53, p = 0.004), but not in CAPD (r = -0.09, p = 0.63). QT dispersion was significantly prolonged in patients with LV hypertrophy compared to patients without hypertrophy on HD (68 +/- 18 ms vs 49 +/- 18 ms, p = 0.008). In the analysis of SA-ECG, 3 of the 28 (11%) HD and 2 of the 29 (7%) CAPD patients had abnormal late potentials. Patients on HD and CAPD had significantly higher filtered-QRS duration compared to controls (105 +/- 15 ms and 104 +/- 12 ms vs 95 +/- 5 ms, respectively, p = 0.04). Patients with LV hypertrophy had higher filtered-QRS duration compared to patients without hypertrophy (109 +/- 12 ms vs 95 +/- 8 ms, p < 0.001). CONCLUSION: Dialysis patients had prolonged QTd and increased filtered-QRS duration in SA-ECG compared to controls. Patients on HD had longer QTd than patients on CAPD. QTd has been correlated to LV mass index in HD, but not in CAPD. This difference might be due to the effect of different dialysis modalities on electrolytes, especially the higher serum Ca2+ levels.

Assessment of left atrial appendage function and its relationship to pulmonary venous flow pattern by transesophageal echocardiography.

We evaluated left atrial appendage function and its relationship to pulmonary venous flow in 53 patients divided into four groups. Group 1 consisted of 10 normal subjects. Group 2 included 15 patients with significant pure mitral stenosis in sinus rhythm. In group 3, there were 13 patients with pure significant mitral stenosis and atrial fibrillation. Group 4 consisted of 15 patients with normal mitral valve and atrial fibrilltion. We found significant decrease in left atrial appendage ejection fraction and maximum emptying flow velocity, velocity time integral of systolic pulmonary venous flow in Groups 2, 3 and 4 in comparison with normal subjects. Systolic pulmonary venous flow velocity was significantly decreased in Groups 3 and 4. There was significant correlation between left atrial appendage ejection fraction and peak emptying flow velocity (r = 0.62, P < 0,001). Systolic peak pulmonary venous flow velocity was significantly correlated with left atrial appendage ejection fraction and maximum emptying flow velocity (r = 0.67, P = 0,01; r = 0.58, P < 0,001, respectively). There was also significant correlation between systolic pulmonary venous flow velocity time integral and left atrial appendage ejection fraction (r = 0.66, P = 0.001). When normals were excluded from analysis, all the correlations were still significant. We concluded that left atrial appendage is a contractile structure, and that systolic pulmonary venous flow velocity is influenced by left atrial appendage dysfunction. Therefore left atrial appendage function needs to be considered when interpreting Doppler transmitral and systolic pulmonary venous flow patterns.

The effect of fluvastatin of hyperlipidemia in renal transplant recipients: a prospective, placebo-controlled study.

Posttransplant hyperlipidemia is a common complication which may affect long term cardiovascular mortality. In this prospective, placebo-controlled study, 19 renal transplant recipients (11 male 8 female, mean age 31.2 +/- 8.4 years) with good allograft function (serum creatinine <2 mg/dl) more than 6 months after transplantation were included. All the patients had hyperlipidemia (serum cholesterol >230 mg/dl and/or LDL-cholesterol >130 mg/dl) despite dietary interventions. The patients were treated with a triple immunosuppressive regimen. After a 8-week period of placebo plus diet regimen, the patients were put on fluvastatin plus diet for another 8 weeks. The patients were followed for its effect on lipid parameters and side effects. After convertion to fluvastatin, serum cholesterol (263.0 +/- 31.6 vs 223.2 +/- 31.6 mg/dl, p = 0.001), LDL-cholesterol (174.4 +/- 28.3 vs 136.4 +/- 28.5 mg/dl, p = 0.002), Apolipoprotein (Apo) A1 (131.1 +/- 16.9 vs 114.7 +/- 18.4 mg/dl, p = 0.001) and Apo B (109.0 +/- 29.8 vs 97.3 +/- 31.5 mg/dl, p = 0.02) levels decreased significantly. Serum levels of triglycerides, VLDL-cholesterol and HDL-cholesterol levels did not vary under fluvastatin. Serum lipoprotein (a) levels were also unchanged during the whole study period (24.9 +/- 19.4 vs 23.1 +/- 19.8 mg/dl, p > 0.05). We concluded that fluvastatin effectively decreased atherogenic lipoproteins such as serum cholesterol, LDL-cholesterol, Apo B in posttransplant hyperlipidemia, however fluvastatin had no effect on another independent risk factor of atherogenesis, serum lipoprotein (a) levels.