Maximum loading of carpal bones during movements: a finite element study.

BACKGROUND: Maximum stresses show critical points on an object because failure may start from the area close to maximum stress points. However, there appears no study on maximum loading points of carpal bones. PURPOSE: To clarify the loading pattern of each carpal bone during wrist movements. METHODS: A finite element wrist model was designed using a three-dimensional reconstruction of computed tomographic images from the distal end of radius and ulna to the proximal third of metacarpals. Loading was performed in neutral, 45° of flexion and extension, 5° of radial and 25° of ulnar deviation, and maximum loading points were plotted. RESULTS: In each position except for extension, minimum loads were carried by triquetrum, while minimum loads were carried by capitatum in extension. Maximum loads were carried by trapezium in neutral and ulnar deviation and flexion but by scaphoideum in radial deviation and extension. CONCLUSION: Studies on maximum loading of each bone are a new approach and may help to improve the knowledge on wrist mechanics.

A novel parameter for the diagnosis of acute pulmonary embolism: the T-wave peak-to-end interval.

OBJECTIVE: Acute pulmonary embolism (APE) is a very common disease that must be diagnosed and treated quickly and accurately to reduce significant morbidity and mortality rates. Acute pulmonary embolism is associated with numerous electrocardiographic (ECG) changes including prolonged QT interval with global T-wave inversion. The aim of the study was to investigate the relationship between the T-wave peak-to-end interval and diagnosis of APE, which has never been investigated in the literature. PATIENTS AND METHODS: Seventy-three patients who were suspected of having APE took part in the present study. The Local Ethics Committee of Istanbul University, Turkey, approved the study protocol. Forty-one of the patients were diagnosed as having APE using computed tomography. Surface ECGs were taken in the initial assessment at admission. The Tp-Te interval was identified as the interval from the peak of the T-wave to the end of the T-wave. The measurements of the Tp-Te interval were taken using precordial leads. All measurements were compared using appropriate statistical tests. Statistical analysis was performed using SPSS version 22.0. RESULTS: We enrolled 73 patients to the study, 41 of which were diagnosed as having APE. Men comprised 54% of the APE group. The mean ages in the APE (+) and APE (-) groups were 59.5 ± 14.5 years and 61±9.2 years, respectively. There was a significant increase in Tp-Te results in V1 (p<0.01). The Tp-Te interval was 74.21 ± 20.81 in the APE (+) group, whereas it was 59.73 ± 12.82 in APE (-) group (p<0.01). CONCLUSIONS: Acute pulmonary embolism (APE) is a mortal condition and as such, rapid and accurate diagnosis is very important. Surface ECG can be used to measure Tp-Te in patients admitted to the emergency room with suspected APE in the differential diagnosis as a fast and easily accessible tool.

The relationship between T-wave peak-to end interval and ST segment recovery on intracoronary ECG during primary PCI.

OBJECTIVE: T-wave peak to end interval (TPE) is a measure of repolarization dispersion, which has been reported as a major arrhythmogenic factor post acute myocardial infarction. The aim of our study was to investigate the changes in TPE in this patient population with regard to peri-procedural intracoronary ECG findings. PATIENTS AND METHODS: Forty-four patients (34 male and mean age of 54.9 ± 10.9 years) with acute STEMI were included. Intracoronary ECG was performed during primary PCI. TPE indices were calculated before and after the procedure. Measurement of the intracoronary ST-segment was carried out before and just after coronary blood flow was established in the infarct related artery. Intracoronary ST-segment resolution (IC-STR) was defined as ≥ 1 mm compared to baseline. RESULTS: There was no difference with respect to baseline characteristics when patients with IC-STR were compared with patients without IC-STR. TPE values decreased significantly after primary PCI in patients with IC-STR (80.9 ± 22.8 ms vs. 65.8 ± 14.4 ms; p < 0.001) whereas they did not change significantly after PCI in patients without IC-STR (79.2 ± 20.9 ms vs. 68.5 ± 16.3 ms; p = 0.18). CONCLUSIONS: TPE measured from surface ECG recordings is significantly reduced in STEMI patients with successful reperfusion after primary PCI, as determined by IC-ECG recordings.

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.

Impaired coronary flow reserve in metastatic cancer patients treated with sunitinib.

PURPOSE: Hypertension is one of the major side effects of sunitinib, an angiogenesis inhibitor used in the treatment of metastatic renal cell carcinomas (mRCC) and gastrointestinal stromal tumors (GIST). Endothelial dysfunction, an early and reversible event in the pathogenesis of atherosclerosis, is suggested to be one of the possible underlying mechanisms of hypertension caused by angiogenesis inhibitors. Coronary flow reserve (CFR) measurement by trans-thoracic Doppler echocardiography (TTDE) reflects coronary microvascular and endothelial functions, as a cheaper and an easy screening test. We have used TTDE to evaluate endothelial function and coronary microvascular function in mRCC and GIST patients under sunitinib treatment. METHODS: Eighteen metastatic cancer patients (16 mRCC and 2 GIST) on sunitinib treatment and 27 healthy subjects were enrolled in this cross-sectional study. Thyroid stimulating hormone (TSH), lipid profile, creatinine, hemoglobin, glucose, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), anthropometric and physical parameters of patients were recorded. CFR recordings were performed by the Vivid 7 echocardiography device. RESULTS: CFR was significantly lower in patients when compared with controls (1.82±0.4 vs 2.71±0.8, respectively; p < 0.001). Impaired CFR was found in 13 (72%) patients whereas all controls had normal CFR values. CFR was inversely correlated with the duration of sunitinib treatment (r=-0.36, p =0.01), high sensitivite (hs) CRP (r = -0.574, p =0.01) and ESR (r = - 0.5, p = 0.02). CONCLUSION: Our findings indicate that CFR is significantly impaired in cancer patients on sunitinib treatment. There is an inverse correlation between CFR and duration of sunitinib treatment and inflammation markers.

Neutrophil-to-lymphocyte ratio, insulin resistance, and endothelial dysfunction in patients with autosomal dominant polycystic kidney disease.

Endothelial dysfunction (ED), insulin resistance (IR), and inflammation are risk factors for increased cardiovascular morbidity and mortality in autosomal dominant polycystic kidney disease (ADPKD). ADPKD patients may have increased carotid intima-media thickness (CIMT) and decreased coronary flow velocity reserve (CFVR). The neutrophil-to-lymphocyte ratio (NLR) was introduced as a marker to determine inflammation in various disorders. We aimed to investigate the relationship between NLR and IR, CFVR, CIMT, and the left ventricular mass index (LVMI) in normotensive ADPKD patients. Twentynine ADPKD patients (age 38.8 ± 10.2 years; 8 men and 21 women) and 19 healthy controls (age 33.8 ± 7.4 years; 8 men and 11 women) were included in this cross-sectional study. CFVR was calculated with echocardiography as the ratio of hyperemic to baseline diastolic peak coronary flow velocities. CIMT was measured in the distal common carotid artery by using a 10-MHz linear echocardiography probe. HOMA-IR was calculated NLR was calculated as the ratio of the neutrophil and lymphocyte counts. Age, sex, body mass index, and levels of glucose, creatinine, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, C-reactive protein (CRP), microalbuminuria, and creatinine clearance were similar between ADPKD patients and healthy subjects. NLR, CIMT, LVMI, and HOMA-IR were significantly higher and CFVR values were significantly lower in patients with ADPKD compared to that in healthy subjects. NLR showed positive correlation with CIMT, HOMA, insulin, glucose, and HDL cholesterol levels, while it was inversely correlated with CFVR and albumin level in all subjects. In patients with ADPKD, NLR showed positive correlation with HDL cholesterol level and inverse correlation with LVMI and albumin level. NLR that was found to be increased in patients with ADPKD may be a readily available marker of inflammation and ED.

Insulin resistance and coronary flow velocity reserve in patients with autosomal dominant polycystic kidney disease.

BACKGROUND: Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). AIM: The aim of this study was to investigate coronary flow velocity reserve (CFVR) as a marker of endothelial dysfunction, carotid intima media thickness (CIMT) as a marker of subclinical organ damage and insulin resistance (IR) as a cardiovascular risk factor in patients with ADPKD. METHODS: Twenty-two normotensive ADPKD patients with well-preserved renal function and 19 healthy subjects were included in the study. Creatinine clearances were calculated by the Cockcroft-Gault formula. The homeostasis model of IR (HOMA-IR) was used to measure IR. CIMT was measured by high-resolution vascular ultrasound. CFVR was calculated as the ratio of hyperaemic to baseline diastolic peak velocities by echocardiography. RESULTS: There was no significant difference between the two groups regarding age, gender, body mass index, systolic and diastolic blood pressures, cholesterol and triglyceride levels. However, CIMT and HOMA-IR were significantly increased and CFVR was significantly decreased in patients with ADPKD compared with healthy subjects. CONCLUSIONS: The findings of decreased CFVR, increased CIMT and increased IR suggest that cardiovascular risk is elevated even in the early stages of ADPKD.

Long-term prognostic value of coronary flow velocity reserve in renal transplant recipients.

BACKGROUND: In this prospective study, we sought to investigate the long-term prognostic value of coronary flow reserve (CFR) and carotid intima media thickness (IMT) estimates in renal transplant recipients without known coronary artery disease. METHODS: The 20 renal transplant recipients included in this study underwent CFR recordings performed by trans-thoracic Doppler echocardiography (TTDE) and carotid IMT measured by carotid Doppler ultrasonography. RESULTS: During a 3-year follow-up only one patient experienced a cardiac event. The baseline CFR and carotid IMT values of the patients were 1.77 ± 0.47 and 0.67 ± 0.15 mm, respectively. After 3 years of follow-up, there were no significant differences compared with baseline measurements with regard to CFR and IMT values. CFR values at the third year of follow-up showed significant correlation with age as well as IMT at baseline and at the third year. Upon multivariate analysis, baseline carotid IMT (ß = -0.562; P = .05) was a significant independent predictor of CFR at the third year. CONCLUSION: Carotid IMT showed a greater predictive value for impaired CFR in renal transplant recipients. CFR was not an independent predictor for cardiovascular events among renal transplant recipients within the first 3 years of follow-up measurements.

Kirschner wire fixation for scaphoid fractures: an experimental study in synthetic bones.

We have studied the biomechanical stability in vitro of three different Kirschner (K) wire configurations in three types of simulated scaphoid waist fractures. The fractures were created with a saw in Sawbones models. There were three fracture patterns: perpendicular to the long axis of the scaphoid model; and 30° and 20° oblique to that. Two 1.2 mm. K-wires were used in each scaphoid. The three configurations were: parallel; 20° oblique; and crossing. The oblique or crossing configurations of K-wires were the most stable depending on the fracture pattern.

Investigation of early atherosclerotic changes in acromegalic patients.

BACKGROUND: Functional and morphological changes of endothelium were risk factors for mortality attributed to atherosclerosis. Studies investigating early atherosclerotic alterations and the effect of the treatment of acromegaly on these alterations gave conflicting results. OBJECTIVE: Surrogate markers of early atherosclerotic changes, i.e. brachial artery flow-mediated dilation (FMD) and carotid artery intima-media-thickness (IMT) in active and inactive acromegalic patients were compared with control subjects matched to patients for age, sex and cardiovascular risk factors to find out the direct effects of growth hormone (GH)/insulin-like growth factor-1 excess. METHODS: In 14 active acromegalics and their 14 matched controls, 14 inactive acromegalics and their 14 matched controls, carotid artery IMT and FMD of brachial artery were measured. Inactive acromegalics were in remission for at least 1 year. RESULTS: Active acromegalics had higher IMT than matched controls and inactive acromegalics (0.85 +/- 0.20 mm, 0.64 +/- 1.77 mm, 0.66 +/- 0.20 mm respectively; p < 0.005, p < 0.05) and IMT of inactive acromegalics was not different from their matched controls (0.61 +/- 0.12 mm). FMD was significantly lower in active acromegalics than in matched controls and inactive acromegalics (2.910 +/- 2.00 mm, 6.5 +/- 2.81 mm, 5.68 +/- 2.9 mm respectively; p < 0.005, p < 0.05). FMD of inactive acromegalics was not significantly different from their matched controls (7.96 +/- 3.12 mm). A significant inverse relationship was found between GH and FMD in active acromegalics (r = -0.659, p = 0.010). CONCLUSION: In active acromegalics, early atherosclerotic changes are not only attributed to the high prevalence of risk factors, but also to the abnormal GH secretion itself.

Endothelial dysfunction in peritoneal dialysis patients with and without failed renal transplants.

BACKGROUND: Endothelial dysfunction (ED) is a common, early abnormality that predisposes patients to develop atherosclerosis and cardiovascular events; inflammation is associated with atherosclerosis and malnutrition. Patients with failed transplants are usually complicated by inflammation; however, ED in this group of patients has not been well defined. In this cross-sectional study, we sought to investigate ED among naïve peritoneal dialysis (nPD) patients who were never transplanted as well as patients with failed renal transplants who were re-starting peritoneal dialysis (fTxPD). METHODS: Twenty-five nPD patients (15 female/10 males; mean age, 44 +/- 11 years), and 12 fTxPD patients (4 males; mean age, 37 +/- 10 years) were included in the study. Coronary flow reserve (CFR) measurements were used to evaluate ED. Serum creatinine, calcium, phosphorus, total cholesterol, albumin, hemoglobin, and intact parathyroid hormone (iPTH) were measured. Also, highly sensitive C-reactive protein (hs-CRP) levels and weekly Kt/V were determined as possible confounding factors. Results were compared between the 2 groups. RESULTS: There were no significant differences regarding age, gender, mean systolic and diastolic blood pressures, or smoking status. Mean duration on PD, peritoneal transport characteristics, PD modality and doses, frequency of peritonitis episodes, as well as serum creatinine, calcium, phosphorus, total cholesterol, albumin, hemoglobin and iPTH levels were similar between the 2 groups. Weekly Kt/V of both groups were similar as well. However, hs-CRP levels were significantly higher (34 +/- 52 vs 6.7 +/- 7.5 mg/L; P = .017) and CFR significantly lower among patients with fTxPD compared with nPD patients (1.52 +/- 0.20 vs 1.91 +/- 0.53; P = .022). CONCLUSION: ED was more prominent among patients with failed transplants than nPD cases, suggesting that the failed allograft may be responsible for this abnormality.

Endothelial function and endothelial nitric oxide synthase intron 4a/b polymorphism in primary hyperparathyroidism.

BACKGROUND AND AIM: Patients with symptomatic primary hyperparathyroidism (pHT) have increased cardiovascular morbidity and mortality. Endothelial nitric oxide synthase (eNOS) intron 4a/b polymorphism is associated with coronary artery disease and hypertension in various populations. Our aim is to evaluate endothelial function in patients with pHT during pre-operative hypercalcemic and post-operative normocalcemic periods and to determine whether intron 4a/b polymorphism of eNOS gene influences endothelial function. SUBJECTS AND METHODS: Forty patients with pHT (age 48.48+/-11.64 yr) were examined pre-operatively and reexamined 5.8+/-1.9 months after parathyroidectomy. Forty-three healthy subjects (age 47.13+/-8.14 yr) were served as control group. Endothelial function was determined by flow-mediated dilation of brachial artery (FMD). eNOS4a/b polymorphism was detected by polymerase chain reaction. RESULTS: FMD was significantly lower in patients pre-operatively compared with controls (8.48+/-1.78% vs 19.49+/-2.34%, p<0.001). FMD improved significantly after parathyroidectomy (16.19+/-2.16%, p<0.001 compared with pre-operative measurements), but was still significantly lower than controls (p<0.001). The distribution of eNOS4a/b genotype frequencies was not significantly different between patients and controls. Logistic regression analysis showed that increased serum calcium (>2.47 mmol/l) and PTH concentrations (>7.75 pmol/l) were significant independent predictors of lower FMD (<16.7%). ENOS4a/b polymorphism did not enter in this model. CONCLUSION: Impaired endothelial function in patients with pHT improves after successful parathyroid surgery. No compelling data are evident to suggest that eNOS4a/b polymorphism modifies the endothelial function in patients with pHT.

Association between chronic hepatitis C infection and coronary flow reserve in dialysis patients with failed renal allografts.

BACKGROUND: Hepatitis C infection occurs frequently among patients with end-stage renal disease and increases the risk of atherosclerotic cardiovascular diseases. Endothelial dysfunction (ED) is an early event in the pathogenesis of atherosclerosis. It has been reported among patients treated with hemodialysis (HD), peritoneal dialysis (PD), or renal transplantation. The aim of the present study was to evaluate effects of chronic hepatitis C infection on ED in patients with failed renal transplants. METHODS: Twenty-six nondiabetic, anti-hepatitis C virus (HCV)-positive (15 females, mean age: 38 +/- 8 years) and 26 anti-HCV-negative patients (15 females, mean age: 36 +/- 5 years), all of whom had returned to PD or HD after renal transplant failure were studied to assess coronary flow reserve (CFR) by transthoracic Doppler echocardiography. Serum high-sensitivity C-reactive protein (hs-CRP) levels were measured as markers of chronic inflammation. CFR recordings and intima-media thickness measurements were performed using the Vivid 7 echocardiography device. RESULTS: Demographic and clinical characteristics of patients were similar between the two groups. Serum hs-CRP levels were significantly higher among HCV-positive patients versus HCV-negative counterparts. HCV-positive patients showed lower CFR measurement than HCV-negative ones. Also, a negative correlation was observed between serum hs-CRP levels and CFR values. CONCLUSION: CFR values are worse among anti-HCV-positive patients with failed renal transplants compared with anti-HCV-negative subjects. Graft dysfunction per se may aggravate a proinflammatory states thereby inducing ED. Furthermore, the presence of HCV is a greater trigger of ED among patients with renal failed grafts.

Coronary artery bypass grafting in a 12-year-old girl with familial hypercholesterolemia.

We present the case of a 12-year-old girl with familial hypercholesterolemia and coronary artery disease. She underwent triple-vessel coronary artery bypass grafting with bilateral pedicled internal mammary artery grafting without adverse events. Pediatric patients with familial hypercholesterolemia may present with premature coronary atherosclerosis requiring coronary artery bypass grafting. In situ internal mammary artery grafts should be the graft of choice.

Hepatitis C virus infection in hemodialysis patients is not associated with insulin resistance, inflammation and atherosclerosis.

BACKGROUND: Hepatitis C virus (HCV) infection is associated with increased levels of inflammatory markers and is also a significant risk factor for the development of Type 2 diabetes mellitus (DM) in the general population. In attempt to address this issue in chronic hemodialysis (HD) patients, we evaluated the relation of HCV infection with inflammatory markers, endothelial dysfunction, insulin resistance and atherosclerosis. METHODS: In a cohort of 72 HD patients (36 (50%) had a positive HCV EIA test and 36 (50%) had a negative anti-HCV test), we examined HCV antibody status, insulin resistance (HOMA-IR) and beta-cell function (HOMA-beta), serum inflammatory parameters (high sensitive C-reactive protein (CRP), fibrinogen and procalcitonin), and performed echocardiography, high-resolution brachial artery ultrasound and B-mode carotid Doppler examination to assess the vascular functions and atherosclerosis. RESULTS: There were no differences in age, gender, body mass index (BMI), primary disease, duration of dialysis, smoking status, laboratory parameters except glucose, total cholesterol and LDL cholesterol between anti-HCV-positive and anti-HCV-negative groups. The serum concentrations of glucose, total cholesterol and LDL cholesterol were significantly lower in the anti-HCV-positive patients than anti-HCV-negative patients (p = 0.04, p = 0.02, p = 0.01, respectively). There were no significant differences in inflammatory parameters, total insulin secretion (HOMA-beta, p = 0.76) and insulin resistance (HOMA-R, p = 0.91) between anti-HCV-positive and negative patients. The intima media thickness, carotid plaque score and brachial artery endothelium-dependent dilatation did not differ significantly between the two groups (p = 0.44, 0.45, and 0.17, respectively). CONCLUSION: HCV infection was not related to atherosclerosis and insulin resistance in hemodialysis patients. Since hemodialysis patients had a large number of uremia-related cardiovascular risk factors, the effect of HCV infection could disappear in this group of patients.

Left atrial geometric and functional remodeling in athletes.

The aim of this study was to evaluate left atrial (LA) volume and its changes with the phases of atrial filling, and to examine the effect of exercise capacity on these parameters. Using two-dimensional echocardiography, LA volumes were measured in 30 male endurance runners and 30 age-matched sedentary men (controls). Maximal oxygen consumption (VO2max) was measured using a metabolic chart during exercise. LA reservoir, pump, and conduit functions, kinetic energy and force were calculated. We found that athletes had higher LA volume and volume index (except the conduit volume), LA passive emptying fraction, and LA total emptying fraction compared to control subjects. We observed positive correlations between: VO2max and LA passive emptying fraction (r=0.49, p<0.05); VO2max and LA active emptying fraction (r=0.54, p<0.05); VO2max and LA kinetic energy (r=0.61, p<0.05); and VO2max and LA force (r=0.57, p<0.05). These findings suggest that atrial function reflects exercise capacity in athletes.

Impaired endothelium-dependent flow-mediated dilation in Behçet's disease: more prominent endothelial dysfunction in patients with vascular involvement.

Brachial artery endothelial dysfunction was shown previously in a small group of Behçet's disease (BD) patients. This study aimed to compare the endothelial function in BD patients with and without vascular involvement. The study group consisted of 25 BD patients with vascular involvement, 25 BD patients without any vascular disease and 46 healthy controls. Brachial artery flow-mediated (endothelium-dependent) dilation (FMD), nitroglycerine-induced dilation and carotid artery intima-media thickness were measured. FMD was impaired in patients with BD (10.41 +/- 3.85%) compared to healthy controls (14.41 +/- 3.39%, p < 0.001). FMD was significantly lower in BD patients with vascular involvement (8.80 +/- 3.63%) than those without any vascular disease (12.02 +/- 3.43%, p = 0.003). This study reveals that endothelial dysfunction documented by brachial artery FMD is a feature of BD, and it is more prominent in patients with vascular involvement.

Aortic distensibility and left ventricular diastolic functions in endurance athletes.

Aortic elastic properties are important determinants of left ventricular function. The aim of this study was to determine left ventricular diastolic function and aortic distensibility in endurance athletes. Thirty male runners and thirty age-matched healthy male controls took part in the study. All subjects underwent echocardiographic examination and cardiopulmonary exercise testing. Measurements included LV cavity dimension, standard and tissue Doppler parameters, and aortic diameter, 3 cm above aortic valve, at systole and diastole. Maximal oxygen uptake in athletes was higher than in controls. The aortic distensibility index was found to be higher in athletes compared with controls (5.37 +/- 1.50 vs. 3.37 +/- 1.48 cm (2) . dynes (-1) . 10 (-6), p < 0.001). While the aortic stiffness index in athletes was significantly lower than in controls (2.77 +/- 0.28 vs. 3.43 +/- 0.41, p < 0.001). Furthermore, transmitral early peak velocity (E) and late peak velocity (A), peak velocity of myocardial systolic wave (S (m)), early (E (m)) and atrial (A (m)) diastolic waves in athletes were higher than in controls. It seemed that the association of E (m) velocity with aortic distensibility was stronger than that of other LV parameters (coefficient = 0.74, p < 0.001) by using multiple linear regression. Increased aortic distensibility in endurance-trained athletes may cause better diastolic function as a physiological cardiovascular adaptation factor.

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.