Search

Reconstruction of the anatomy of the proximal humerus is a prerequisite to achieving good long-term clinical results after shoulder arthroplasty. Modern, adjustable prostheses have greater flexibility of inclination, retroversion, and medial and dorsal offset in comparison with older prostheses. Such improvements should allow for better reconstruction of the centre of rotation compared to older prostheses. Reconstruction of the humeral head centre was assessed in 106 modern adjustable (Affinis) and 47 second-generation prostheses. All reconstructions were compared both to the preoperative state and the unoperated shoulder. To describe the pre- and postoperative states, the geometry and position of the humeral head in relation to the glenoid were analysed on patient radiographs. Applying the defined parameters, modern adjustable prostheses showed better reconstruction than second generation prostheses. Parameter values measured in reconstructions using fourth generation prostheses were comparable to those of the unoperated shoulder, but differed significantly from the preoperative state. Second generation prostheses, in contrast, only show non-specific differences in parameter values. This suggests that an approximate reconstruction of normal anatomy can be achieved using a modern fourth generation prosthesis. Reconstruction of the complex anatomy of the proximal humerus is significantly better with modern adjustable prostheses compared to second generation prostheses. Improved clinical outcome can therefore be predicted in a functional and intact rotator cuff. The advantage of using modern prostheses systems over older models is clearly demonstrated in this study.

Objective: We aimed to share the features of 45 patients with firearm injuries related head traumas and our experiences in their treatments. Methods: Our cases consisted of 36 males 45 patients in total between the ages of 18-65, who were brought to the emergency service of our hospital due to firearm injuries. For this retrospective study, it was accessed to the patient data from the archival records of our hospital. The demographical data of the patients like age and gender, and the records such as type of injury, injured area in head, diagnosis, treatment and follow ups were reviewed. Results: There were sinus injury related epidural haemorrhages in 8 of patients who underwent urgent surgical intervention (17.8%). In 18 of the patients (39.95%) who underwent surgery had supratentorial injuries and 7 (15.55%) had infratentorial injuries. All these 25 patients (55.50%) who underwent surgery had multiple intracranial injuries (compression fracture + subdural haemorrhage + contusion + pneumocephalus + SAH + brain edema). Four of these 6 patients with multiple injuries had abdominal injuries. Two patients had haemopneumothorax. There were vertebra and extremity injuries in 2 patients with abdominal injuries. Conclusions: Brain injuries occurring with the firearm head injuries are seen as multiple injuries and their rate of mortality is quite higher.

The correct approach to the lumbar disc hernia is subject to debate. Although a rare case of lumbar disc herniation with spontaneous regression, to be seen and is a well-known phenomenon commonly reported. But the underlying mechanism has not been fully clarified. Proposed mechanisms are enzymatic degradation and phagocytosis, dehydration and the retraction of a herniated disc in the annulus fibrosus. Cauda equina syndrome, despite the progressive narcotic pain goes outside and progressive neurological deficits, conservative treatment should be given priority to patients. Think about the possibility that spontaneously regressed with medical treatment and follow-up of disc herniation, should not rush to surgery. In our case, the level of lumbar disc herniation was presented on spontaneously regressed patients. The patient's clinical condition is improved in accordance with the resolution of the disc herniation and this is confirmed by magnetic resonance imaging.

Background and Objective: The slow coronary flow (SCF) phenomenon is an angiographic observation and a well-recognized clinical entity characterized by delayed opacification of vessels in a normal coronary angiogram due to reasons yet unclear. Thyroid hormones exert significant effects on plasma homocysteine (Hcy) levels and microvascular resistance. Recently, several investigators have consistently reported that elevation of the plasma Hcy level can severely disturb vascular endothelial function and play a role in the pathogenesis of SCF. Accordingly, we investigated the levels of plasma Hcy and thyroid hormones and their relationship in patients with SCF. Method: Forty-four patients with angiographically proven SCF (Group I) (mean age 55.5 ± 10.4 years, 26 males) and 44 cases with normal coronary flow (NCF) pattern (Group II) (mean age 53.9 ± 11 years, 22 males) with similar risk profiles were enrolled in the study. Coronary flow patterns of the cases were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. The coronary TIMI frame counts were calculated separately for each coronary artery and their average was determined as the mean TIMI frame count for each subject. Serum levels of free tri-iodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH) and Hcy were measured. Patients with thyroid disease or on medications with a potential to affect thyroid functions were excluded. Results: There were no statistically significant differences between the groups concerning the demographic characteristics and major cardiovascular risk factors. Mean TIMI frame counts of SCF and NCF groups were 45.9 ± 12 and 23.3 ± 3.7, respectively. fT4 (ng/dl) and TSH (µIU/ml) levels of the two groups were similar (p > 0.05). The level of fT3, the active metabolite of the thyroid hormone family, was dramatically reduced in the SCF group when compared to the NCF group (2.3 ± 0.2 vs. 3.0 ± 0.3, p = 0.0001, respectively). Plasma Hcy levels of patients with SCF were found to be significantly higher than controls (12.2 ± 4.9 vs. 8.5 ± 2.9, p = 0.0001, respectively). Correlation analysis showed a significant negative correlation between the plasma fT3 and Hcy levels and the mean TIMI frame counts (r = –0.31, p = 0.003 vs. r = –0.66, p = 0.0001). Moreover, there was a significant positive correlation between the plasma Hcy levels and the mean TIMI frame counts (r = 0.58, p = 0.0001). Also, fT3 was the only significant determinant of the variance of Hcy in multiple regression analysis (r = –0.30, p = 0.005). Conclusion: fT3 levels were decreased and plasma Hcy levels were increased significantly in patients with SCF as compared to controls. This finding suggests that thyroid hormones and/or (?) a possible disturbance in their metabolism may be responsible for the elevated levels of plasma Hcy in patients with SCF and may play a role in the pathogenesis of the SCF phenomenon.

Background and objective Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B(12) and folate in food, leading ultimately to an increase in circulating Hcy levels. Methods Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B(12), and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. Results Mean TIMI frame count was 46.3 +/- 8.7 in group I and 24.3 +/- 2.9 in Group II (p = .0001). Vitamin B(12) levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 +/- 4.3 vs. 17.1 +/- 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 +/- 5.6 vs. 7.9 +/- 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 +/- 5.3 vs. 7.5 +/- 2.7, p = .0001) and folate levels were reduced (13.9 +/- 4.7 vs. 18.6 +/- 4.9, p = .0001) in patients with H. pylori infection, while vitamin B(12) levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = -.33, p = .002 vs. r = -.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -.21, p = .03). Conclusion Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.

Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry. We enrolled 105 patients (71 females, mean age, 49.2 +/- 13.6 years) with recently diagnosed and untreated hypertension (blood pressure140 and/or 90 mmHg, fasting glucose110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 +/- 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 +/- 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 +/- 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 +/- 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) x Immunoreactive Insulin (microU/mL)/405, for the assessment of IR. There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003). Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index.

BACKGROUND AND OBJECTIVE: Coronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima-media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. METHOD: The study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. RESULTS: Plasma homocysteine levels (μmol/l) and carotid intima-media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4±4.9 vs. 8.5±2.8, P=0.0001; 0.75±0.08 vs. 0.69±0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8±4.4 vs. 16.5±5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima-media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). CONCLUSION: Homocysteine levels and carotid intima-media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis. © 2006 Lippincott Williams & Wilkins.

Preinfarction angina (PA) and early reperfusion of infarct-related arteries have been shown to reduce infarct size in patients with acute myocardial infarction (AMI). The beneficial effects of PA on infarct size have been attributed to the development of ischemic preconditioning and faster coronary recanalization in patients treated with thrombolytic therapy (TT).To evaluate the effect of PA on clinical coronary reperfusion time in patients with AMI receiving successful TT.Seventy-five patients presenting with AMI (within 6 h after the initial onset of symptoms) were studied. All patients received TT and were evaluated with coronary angiography (CA) at predischarge. The patients were divided into two groups: group 1 (PA-positive) comprised those who experienced a new onset of prodromal angina within 72 h before the onset of AMI. Group 2 (PA-negative) comprised those who had a sudden onset of AMI without the preceding angina. The successful myocardial reperfusion criteria after TT were ST segment resolution of 50% or greater, the appearance of reperfusion arrhythmias and the resolution of chest pain. The time of reperfusion criteria was recorded after TT. CA was performed in all patients at predischarge. Patients with no patent infarct-related arteries on CA and clinical failure of reperfusion were excluded from the study.Clinical characteristics, risk factors and angiographic findings did not differ significantly between the groups. The time interval from the start of continuous chest pain to TT was also similar between the groups. The left ventricular ejection fraction was higher and there were less frequent ventricular arrhythmias in patients with PA than in those without PA (47.9+/-7.4 versus 44.4+/-8.1, P=0.041, and 17.1% versus 37.5%, P=0.043, respectively). The clinical reperfusion time was significantly shorter in the patients with PA than in those without PA (68.2+/-24.5 min versus 81.4+/-19.3, P=0.012). The clinical reperfusion time was positively correlated with age and the time interval from the start of continuous chest pain to TT but inversely related to the presence of PA.In patients with AMI preceded by PA, TT resulted in more rapid clinical reperfusion than in patients without PA. Thus, earlier myocardial reperfusion may account for smaller infarct size and better prognosis in patients with PA.

Obstructive sleep apnea (OSA) has a critical association with cardiovascular mortality and morbidity. Carotid intima-media thickness (IMT), flow-mediated dilatation (FMD) and aortic stiffness are early signs of atherosclerosis. The presence of subclinical atherosclerosis was assessed in OSA patients using these parameters.40 patients with OSA showing an apnea-hypopnea index (AHI)or =5 (mean age 51.3 +/- 9 years, 32 males) and 24 controls (AHI5, mean age 51.9 +/- 5.2 years, 19 males) were enrolled in the study. In all subjects, polysomnographic examination and recordings were performed during sleep. IMT of the carotid artery, endothelium-dependent/-independent vasodilation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography.The demographic data of the patients with OSA and controls were not significantly different. Subjects with OSA demonstrated higher values of aortic stiffness (7.1 +/- 1.88 vs. 6.42 +/- 1.56, respectively) and IMT (0.85 +/- 0.13 vs. 0.63 +/- 0.11 mm, p = 0.0001, respectively) but lower distensibility (9.47 +/- 1.33 vs. 11.8 +/- 3.36 cm(2)/dyn/10(6)) and FMD (4.57 +/- 1.3 vs. 6.34 +/- 0.83%, p = 0.0001, respectively) than the controls. The respiratory disturbance index correlated positively with aortic stiffness and IMT and negatively with distensibility and FMD.We observed blunted endothelium-dependent dilatation, increased carotid IMT and aortic stiffness in patients with OSA compared with matched control subjects. This is evident in the absence of other diseases, suggesting that OSA is an independent cause of atherosclerosis. These simple and non-invasive methods help to detect subclinical atherosclerosis in OSA.

Angiotensin-converting enzyme (ACE) is a key enzyme in the production of angiotensin II and thus may participate in the modulation of cardiac growth. The cloning of the ACE gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of the study is to analyse the ACE gene I/D polymorphisms in healthy young subjects and to evaluate its relationship to left ventricular mass and functions.38 women and 40 men (mean age 21.1 +/- 1.7 and 21.4 +/- 1.7 years) were studied. They underwent complete echocardiographic assessment and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood by polymerase chain reaction. Thickness of interventricular septum (IVS) and posterior wall (LVPW) and left ventricular mass (LVM) and LVM index (LVMI) were measured by M-mode. Left ventricular ejection fraction (LVEF) was calculated by Simpson's method.There was no statistically significant difference among the DD, DI and II genotypes, concerning age, body mass index, heart rate, systolic and diastolic blood pressures.The thickness of IVS (9.5 mm), LVPW (9.0 mm), LVM (204.5 g) and LVMI (105.5 g/m2) in DD genotypes were higher than both DI (8.3 mm; 8.1 mm; 168.1 g; 90.9 g/m2) and II genotypes (8.2 mm; 7.0 mm; 141.7 g; 77.8 g/m2) in men, but not in women. LVEF among the 3 genotypes were not statistically different.Our findings suggest that left ventricular hypertrophy is partially determined by genetic disposition especially in men but not in women.

Objective - Both left ventricular hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth-promoting effect on cardiomyocytes. The purpose of this study was to examine the relationship between left ventricular structure, function and IR in patients with EH. Methods - We enrolled 73 patients (21 men, mean age 51.7 ± 9.2 years) with untreated hypertension (BP > 140 and/or 90 mm Hg, fasting glycaemia < 110 mg/dl) and 64 healthy subjects without diabetes mellitus and hypertension (21 men, mean age 48.9 ± 10.6 years) constituted the control group. In all subjects, transthoracic echocardiography was performed and blood samples were taken. Homeostasis model assessment (HOMA) was calculated by the formula: HOMA-index = fasting blood glucose (mg/dl) * immunoreactive insulin (μU/ml)/405 for the assessment of IR. Hypertensive patients were divided in two groups by mean HOMA index values. Each subject was examined for LV end-diastolic diameter, septal and posterior wall thickness, LV mass index (LVMI), fractional shortening (FS), mitral inflow velocity pattern, atrial filling fraction (AFF), left ventricular outflow velocity pattern and the total ejection isovolume index (TEI index). Results - The HOMA index (p < 0.001), LVMI (p < 0.001), AFF (p < 0.0001), peak A velocity (p < 0.028), septal (p < 0.0001) and posterior (p < 0.0001) wall thickness were significantly higher and FS (p < 0.001), E/A ratio (p < 0.0001) were significantly lower in hypertensive patients than healthy controls. LVMI (p < 0.01) and septal wall thickness (p < 0.001) were significantly higher in those hypertensive patients with a higher HOMA index. The HOMA-index was univariately related to the TEI index (r = 0.27, p = 0.01) and septal wall thickness (IVS) (r = 0.29, p = 0.01) by Pearson correlation analysis in hypertensive patients. LVMI, FS and mitral inflow velocity pattern were not related to the HOMA index. The TEI index (R 2 = 0.20, p = 0.0001) and IVS (R2 = 0.12, p = 0.002) were significantly related to the HOMA-index as an independent variable by stepwise regression analysis. Conclusions - These results demonstrated that hypertensive patients had both abnormal cardiac structure and function and higher IR index. In our study group, the effect of hypertension on cardiac structure and function was correlated with IR. Our results suggested that IR might be an important factor causing left ventricular dysfunction and wall thickness in non-diabetic patients with EH.

Background: Physiologic adaptations in an athlete’s heart include increased left and right ventricular chamber size, left ventricular wall thickness and mass. Angiotensin-converting enzyme (ACE) is a key enzyme in angiotensin II production causing cardiac hypertrophy. The cloning of the ACE gene has made it possible to identifya deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. Therefore, the ACE genes, which have been shown to be polymorphic, could be candidate genes for large-artery stiffness. Methods: 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic examination, and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood. The aortic diameter was recorded by M-mode echocardiography at a level 3 cm above the aortic valve. Aortic systolic diameter was measured at the time of full opening of the aortic valve, and diastolic diameter was measured at the peak of QRS. Aortic strain, stiffness index and distensibility were calculated. Results: Left ventricular mass index and left ventricular ejection fraction were significantly higher in athletes than controls (p < 0.001). The aortic distensibility index and strain were significantly greater in athletes compared with controls (respectively: 5.8 ± 2.7 vs. 4.7 ± 1.8 cm–2 dyn–1 10–6, p = 0.017; 12.3 ± 2.4 vs. 9.3 ± 3.1, p < 0.001). The aortic stiffness index was significantly lower in athletes than in controls (4.8 ± 1.9 vs. 6.1 ± 2.1, p < 0.001). The aortic distensibility index and strain were statistically different in ACE DD vs. DI groups and DD vs. II groups of athletes. The aortic stiffness index was statistically different in ACE DD vs. II groups of athletes. Aortic parameters were similar according to ACE genotypes in controls. Conclusion: The results of this study indicate that aortic distensibility was increased by prolonged training in endurance athletes, particularly in those with the ACE II genotype. This effect represents an extracardiac adaptation to chronic prolonged training in athletes.

QT interval dispersion (QTd) reflects inhomogeneity of repolarisation. Delayed cardiac repollarisation leading to the prolongation of the OT interval is a well-characterised precursor of arrhythmias. Obstructive sleep apnoea syndrome (OSAS) can cause cardiovascular complications, such as arrhythmias, myocardial infarction, and systemic and pulmonary hypertension. The aim of this study was to assess QTd in OSAS patients without hypertension. A total of 49 subjects without hypertension, diabetes mellitus, any cardiac or pulmonary diseases, or any hormonal, hepatic, renal or electrolyte disorders were referred for evaluation of OSAS. An overnight polysomnography and a standard 12-lead ECG were performed in each subject. According to the apnoea-hypopnoea index (AHI), subjects were divided into control subjects (AHI

Obstructive sleep apnoea syndrome (OSAS) might be a cause of heart failure. The present study aimed to assess left ventricular mass and myocardial performance index (MPI) in OSAS patients. A total of 67 subjects without any cardiac or pulmonary disease, referred for evaluation of OSAS, had overnight polysomnography and echocardiography. According to apnoea-hypopnoea index (AHI), subjects were classified into three groups: mild OSAS (AHI: 5-14; n=16), moderate OSAS (AHI: 15-29; n=18), and severe OSAS (AHI: ?30; n=33). Thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode, along with left ventricular mass (LVM) and LVM index (LVMI). Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Döppler echocardiography. There were no differences in age or body mass index among the groups, but blood pressures were higher in severe OSAS compared with moderate and mild OSAS. In severe OSAS, thickness of IVS (11.2 ± 1.1 mm), LVPW (11.4 ± 0.9 mm), LVM (298.8 ± 83.1 g) and LVMI (144.7 ± 39.8 g·m-2) were higher than in moderate OSAS (10.9 ± 1.3 mm; 10.8 ± 0.9 mm; 287.3 ± 74.6 g; 126.5 ± 41.2 g·m-2, respectively) and mild OSAS (9.9 ± 0.9 mm; 9.8 ± 0.8 mm; 225.6 ± 84.3 g; 100.5 ± 42.3 g·m-2, respectively). In severe OSAS, MPI (0.64 ± 0.14) was significantly higher than in mild OSAS (0.50 ± 0.09), but not significantly higher than moderate OSAS (0.60 ± 0.10). In conclusion, severe and moderate obstructive sleep apnoea syndrome patients had higher left ventricular mass and left ventricular mass index, and also left ventricular global dysfunction. Copyright©ERS Journals Ltd 2005.

PP-077 Vitamin D and PTH (Parathyroid hormone) are considered important primarily for calcium and phosporus homeostasis. However, in the recent years, vitamin D and PTH levels have been linked to cardiovascular disease and mortality. One hundred patients were included in the study. Patient group

Objectives - Early recognition and appropriate therapy of diastolic dysfunction (DD) is advisable to prevent further progression to diastolic or systolic heart failure and death. The mitral atrioventricular plane displacement (AVPD) method has been shown to be a reliable and simple technique to study left ventricular systolic function in patients, because the mitral annulus can be visualized in almost all patients even if the endocardial borders are difficult to trace. The aim of our study is to estimate the left ventricular ejection fraction by AVPD method (EF A V P D ), in addition to Teicholz's short axis method (EF-T) and Simpson's biplane method (EF-2D) in patients with DD. Material and methods - One hundred and two subjects were submitted to complete echocardiographic assessment, and DD was shown in 62 patients. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) using M-mode and left ventricular ejection fraction was calculated from the AVPD-mean in 62 patients with DD (mean age 55.67 ′ 5.65, 24 men and 38 women) and in 40 age-matched control subjects (mean age 54.07 ′ 6.96, 15 men and 25 women). There were no statistically significant group differences related to age, gender, heart rate or body mass index. However, in the patients with DD, presence of hypertension and/or diabetes mellitus was significantly higher than control subjects. Results - The systolic functions, as assessed by conventional measures in patients with DD and healthy subjects were not stastically different, and were within normal limits. The septal, anterior, lateral and posterior part of the atrioventricular plane values and AVPD-mean during systole were statistically lower in the DD group (12.35 ′ 1.42mm) compared with controls (15.32 ′ 1.38 mm) (p < 0.001). EF A V P D in patients with DD was statistically lower (62.97 ′ 7.85%) than healthy subjects (79.30 ′ 7.60%) (p < 0.001). Significant positive correlations between EF A V P D and EF-2D (r = 0.325, p < 0.01) and EF-T (r = 0.355, p < 0.01) and FS (r = 0.314, p < 0.01) were found. EF A V P D correlated only with velocity of mitral flow propagation (VPR) in diastolic function parameters (r = 0.374, p < 0.01). Conclusions - The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF A V P D in the DD group compared with controls.This indicated the presence of a statistically significant and mildly reduced left ventricular systolic function by the AVPD method in patients with DD. It might be suggested that DD might be combined with systolic dysfunction. However, isolated diastolic dysfunction is uncommon.The mitral AVPD is reproducible, widely applicable and a simple non-invasive method for the estimation of left ventricular systolic function in patients with DD.

Background: The association between the presence of diagonal earlobe crease (ELC) and coronary artery disease (CAD) still remains controversial. Objective: The aim of this study was to evaluate the association between bilateral ELC and CAD. Methods: 415 patients were examined for the presence or absence of bilateral ELC, angiographic evidence of CAD and coronary risk factors. The patients were divided into 2 groups according to angiographic evidence of CAD. Results: Bilateral ELC was significantly and positively correlated with CAD, hypertension, age, male gender, cigarette smoking and family history of CAD. The ELC was an independent variable for CAD. The observed sensitivity, specificity, positive predictive value and negative predictive value of the bilateral ELC for the diagnosis of CAD were in the following order: 51.3, 84.8, 89.4 and 41.2%. Conclusion: The presence of bilateral ELC was significantly associated with CAD and coronary risk factors. The bilateral ELC was an important dermatological indicator of CAD, and it might be a useful diagnostic tool in the clinical examination of patients.

Heart rate variability (HRV) is a useful tool for the detection of sympathetic-parasympathetic balance in the autonomic nervous system. Autonomic nervous system involvement in patients with rheumatoid arthritis (RA) has rarely been studied and has shown conflicting results. Our purpose was to determine if HRV showed changes in patients with RA in comparison with the normal population. Short-term analysis of HRV was performed for time-domain frequency in 42 patients with RA and 44 matched controls. In this analysis, patients displayed lower standard deviation of the mean than healthy subjects ( P0.0001). Patients tended to display higher pNN50 and root-mean-square of successive difference values than did healthy subjects, but these differences were not statistically significant (P0.05). In frequency domain analysis, the spectral measures of HRV showed reduced high-frequency (HF) values and an higher low-frequency (LF) values; as a result, the ratio between low and high frequencies (LF/HF), representative of sympathovagal modulation, was significantly increased (P=0.001, P=0.012, and P=0.003, respectively). Our data suggest an increase in sympathetic control of the heart rate in patients with RA. This increased sympathetic activity could play a key role in the development of ventricular tachyarrhythmias in RA and may be related to the higher incidence of sudden death in this disorder.