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521.

Background

Patients with atrial myocardial infarction (ATMI) have frequent cardiac and noncardiac complications. However, ATMI is uncommonly diagnosed because of its nonspecific ECG changes. Our objective was to analyze the ECG characteristics of ATMI in patients with inferior STEMI.

Hypothesis

Electrocardiographic P wave parameters can help in diagnosis of ATMI.

Methods

We evaluated 932 patients who underwent coronary angiography and recruited 39 patients with ATMI and 33 patients without ATMI with inferior STEMI for a retrospective study. Twelve‐lead ECGs were obtained to measure P‐wave parameters in diagnosis of ATMI. P‐wave parameters and PR‐segment displacement were compared in patients with and without ATMI.

Results

In inferior leads, PWD and PWDisp were significantly longer in the ATMI group than in the non‐ATMI group (limb lead II, 109.79 ±15.51 ms and 86.65 ±5.02 ms, respectively; P < 0.001; limb lead III, 108.31 ±12.51 ms and 85.27 ±7.47 ms, P < 0.001; aVF, 106.49 ±13.68 ms and 83.01 ±7.89 ms, P < 0.001; PWDisp, 41.67 ±10.72 ms and 25.18 ±5.17 ms, P < 0.001). By contrast, PWA was significantly lower in the ATMI group than in the non‐ATMI group (limb lead II, 0.96 ±0.18 mV and 1.39 ±0.22 mV, respectively; P < 0.001; limb lead III, 0.90 ±0.11 and 1.21 ±0.23, P < 0.001; aVF, 0.88 ±0.17 and 1.26 ±0.28, P < 0.001). PR‐segment displacement was found in 8 (20.5%) patients with ATMI. A PWD ≥95.5 ms in lead DII diagnosed ATMI with a higher sensitivity and specificity (90%, 94%) than did PWA or PWDisp.

Conclusions

This study suggests P‐wave parameters might be considered ECG findings in diagnosis of ATMI in patients with inferior STEMI.  相似文献   
522.
Background It has been shown that interleukin-35 (IL-35) subunits are strongly expressed in atherosclerotic plaques in humans. Therefore, it is considered to play a role in atherosclerosis.Objectives In this study, IL-35 levels were compared with the control group in patients with stable coronary artery disease (CAD), and the association between IL-35 levels and the lesion type, lesion severity and extension was investigated with the Gensini score (GS) and the Syntax score (SS) in the patient group.Methods Sixty patients (18 female and 42 male) with CAD diagnosed by coronary angiography, who presented with typical chest pain and positive noninvasive cardiac stress test, and 46 patients (18 female and 28 male) with normal coronary lumenogram, were included in this study. Gensini and Syntax scores were calculated in the patient group, and these values were compared with IL-35 levels. Non-normally distributed variables were analyzed by the Mann-Whitney U test, whereas normally distributed parameters were assessed by Student’s t-test. The difference between categorical variables were evaluated by the Chi-square or Fisher test. P-values<0.05 were considered as statistically significant.Results No significant differences were observed between patients and the control group in terms of demographic characteristics and laboratory findings. Compared to the control group, IL-35 levels of the CAD group were considerably lower (36.9±63.9 ng/ml vs. 33.2±13.2 ng/ml, p<0.008). Although not statistically significant, IL-35 levels were higher in patients with low SS than among those with high SS (33.2±13.7 vs. 31.8±8.9, p=0.51). The IL-35 values of the patients with high GS were significantly lower than in patients with low GS (35±17.4 vs. 30.7±8.6, p=0.043).Conclusion It has been shown that IL-35 levels can be a new biomarker for stable CAD, and IL-35 is associated with the extension of CAD.  相似文献   
523.
Gamma-aminobutyric acid (GABA) dysfunction is a known feature of alcoholism. We investigated GABA-B receptor activity in 3-week abstinent alcoholics using the growth hormone (GH) response to baclofen, a GABA-B receptor agonist. The study aimed to investigate the relationship between GABA-B receptor activity and alcohol withdrawal. GH response to baclofen was measured in alcohol-dependent males without depression (n = 22) who were on day 21 of alcohol abstinence and in healthy control male subjects (n = 23). After 20mg baclofen was given orally to the subjects, blood samples for GH assay were obtained every 30 min for the subsequent 150 min. The patients were divided into two subgroups (continuing withdrawal and recovered withdrawal subgroups) according to their withdrawal symptom severity scores on day 21 of alcohol cessation. Baclofen administration significantly altered GH secretion in the controls, but not in the patients. When GH response to baclofen was assessed as DeltaGH, it was lower in the patients with continuing withdrawal symptoms than in the controls and in the recovered withdrawal group. Impaired GH response to baclofen in all patients mainly pertained to the patients whose withdrawal symptoms partly continued. Our results suggest that reduced GABA-B receptor activity might be associated with longer-term alcohol withdrawal symptoms in alcoholic patients.  相似文献   
524.
INTRODUCTION: Experimental and clinical studies demonstrated that the renin-angiotensin system (RAS) affects the pathogenesis of atherosclerosis and prognosis of coronary heart disease (CHD). The aim of this study was to investigate the genotype distribution and the allele frequencies of three RAS genes polymorphisms and their effects on premature CHD in a Turkish population. MATERIALS AND METHODS: One-hundred and fifteen Turkish patients with premature CHD and 128 controls were included into the study. Angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT1) receptor and angiotensinogen (AGT) gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The patients group showed an increased frequency of the ACE D allele compared with controls (65% vs. 35%, p = 0.0001). There was a significant association between the DD genotype and premature CHD (ACE DD vs. ID and II; odds ratio [OR] = 2.82 [CI 95% 1.33 2.91, p = 0.002]). Also, we observed increased premature CHD risk associated with higher frequencies of the AGT MM genotype in patients when compared with controls (AGT MM vs. TT and MT, OR = 1.92 [CI 95% 1.11-3.33, p = 0.018]). We found a significant association between AT1-receptor AA genotype and decreased risk of premature CHD (AT1R AA vs. AC and CC, OR = 0.57[CI 95% 0.34-0.95, p = 0.03]). CONCLUSIONS: We demonstrated that increased premature CHD risk is associated with higher frequencies of the ACE DD and AGT MM genotypes. These findings indicate a synergistic contribution of ACE DD and AGT MM polymorphisms to the development of premature CHD. Also, our results suggest that family history, smoking, diabetes, hypertension, obesity and ACE DD genotype were independent risk factors for premature CHD.  相似文献   
525.
526.
To investigate plasma tumor necrosis factor-alpha (TNF-α) levels as an indicator to reflect the magnitude of the destructive inflammatory phase and articular cartilage damage after a knee trauma. Eighteen mature Wistar Albino male rats were divided into two groups equal in number. Nine animals underwent anterior cruciate ligament transection (ACLT) of the right knees, while nine animals had a sham procedure. All animals were killed at the end of 8 weeks; serum TNF-α levels were analyzed with enzyme linked-immunosorbent assay, and the osteoarthritic changes of articular cartilage were evaluated by a histopathological method using OARSI (Osteoarthritis Research Society International) osteoarthritis cartilage histopathology assessment system score. Serum TNF-α levels and OARSI scores showed significant difference between two groups. Despite 8 weeks after the initial trauma, ACLT group still demonstrated elevated levels of plasma TNF-α indicating the ongoing inflammatory phase. Serum TNF-α levels were also found to be correlated with the OARSI osteoarthritis cartilage histopathology assessment system scores. Post-traumatic local TNF-α overproduction as a proinflammatory cytokine is known to have a major role in cartilage matrix degradation. In this study, elevated plasma TNF-α levels were considered as the consequence of the early local inflammatory response to altered knee biomechanics. Degree of articular cartilage damage found to be consistent with plasma TNF-α levels suggest that monitoring plasma TNF-α levels may be a simple and reliable method to reflect the magnitude of destruction during the ongoing inflammatory phase of OA.  相似文献   
527.
In recent years, in addition to neurological examination and neuroradiologic examinations, attempts have been made to assess the severity of post-traumatic brain injury and to obtain an early idea of patient prognosis using biochemical markers with a high degree of brain tissue specificity. One such enzyme is neuron-specific enolase (NSE). This study investigates the correlation between serum NSE levels, Glasgow Coma Score, and prognosis measured by Glasgow Outcome Scores in head trauma patients. This was a prospective study conducted with 80 trauma patients presenting to the Emergency Department. Patients were divided into four groups. The first group consisted of patients with general body trauma, but no head trauma. The second group had minor head trauma. The third group had moderate head trauma, and the fourth group had severe head trauma. The relationship between subjects' admission NSE levels and admission and discharge Glasgow Coma Scores (GCS) and Glasgow Outcome Scores (GOS) 1 month later was examined. A receiver operating characteristic (ROC) analysis was performed using a serum NSE cutoff level of 20.52 ng/mL and a GOS of 3 or less as the definition of poor neurologic outcome. There was a significant difference in the NSE levels between group 1 (general trauma) and group 3 (moderate head trauma). There was also a statistically significant difference in NSE levels between group 1 (general trauma) and group 4 (severe head trauma) (p < 0.05). There was a statistically significant inverse relationship between NSE levels and GOS as determined within groups 3 (moderate) and 4 (severe head trauma) (p < 0.05). When NSE levels were compared with admission GCS, it was found that GCS fell as NSE levels rose. There was no significant correlation between NSE and GCS within groups 3 (moderate) or 4 (severe). There was a statistically significant correlation within group 2 (mild) (p < 0.05). By ROC analysis, serum NSE was 87% sensitive and 82.1% specific in predicting poor neurologic outcome in the study patients. The area under the curve was 0.931. This study shows that initial serum NSE levels in moderate and severe head trauma patients correlate inversely with GOS 1 month later, but only within the moderate and severe head trauma groups. However, serum NSE was 87% sensitive and 82.1% specific in predicting poor neurologic outcome in all of the study patients. This derived cutoff value now needs to be prospectively validated.  相似文献   
528.
Clinical Rheumatology - The aim of this study was to compare the carotid-femoral pulse wave velocity (CFPWV), aortic stiffness index (ASI), and aortic distensibility values of fibromyalgia patients...  相似文献   
529.
BACKGROUND: The renin-angiotensin system (RAS) and endothelial nitric oxide (NO) affect the pathogenesis of atherosclerosis and prognosis of coronary artery disease (CAD). Previous epidemiologic data suggested that genetic factors are more likely to affect young rather than old people. Our objective was to investigate the association between the polymorphisms of eNOS (Glu298Asp) and the RAS genes and premature CAD in a Turkish population. METHODS: A total of 115 Turkish patients with premature CAD and 83 controls were included in the study. ACE I/D, AT1R A/C, AGT T/M and eNOS Glu298Asp gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: It was found that increased premature CAD risk is associated with higher frequencies of the ACE DD [OR: 2.600 (CI 95% 1.395-4.847, p=0.002)], AGT MM [OR=2.407 (CI 95% 1.267-4.573, p=0.007)] and eNOS 894TT [OR=17.000 (CI 95% 3.952-73.125, p<0.001)] genotypes. Carriers of ACE DD+eNOS 894TT (p=0.002), AGT MM+eNOS 894TT (p=0.001), AT1R AA+eNOS 894TT and AT1R non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD. CONCLUSIONS: This study indicates a synergistic contribution of RAS genes (ACE I/D, AGT T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature CAD.  相似文献   
530.
Postprandial lipoprotein metabolism is suggested to play a role in the pathogenesis of atherosclerosis. In this study, we investigated postprandial lipemia and its relationship to cardiovascular risk factors in patients with overt and subclinical hypothyroidism. Twentynine female patients with TSH levels greater than 5 μIU/mL and 12 euthyroid control female subjects were included in the study. Fifteen patients had subclinical hypothyroidism and 14 had overt hypothyroidism. All subjects underwent an oral lipid tolerance test. If triglyceride levels increased by 80% or more, subjects were considered postprandial lipemia positive. Control, overt hypothyroid, and subclinical hypothyroid groups were not statistically different with respect to anthropometric measurements, fasting blood C-reactive protein, uric acid, homocysteine, glucose, insulin, lipoprotein (a), apolipoprotein B levels, and homeostasis model assessment index. Fasting triglyceride levels correlated positively with TSH levels. Postprandial lipemia frequency was higher in overt hypothyroid subjects than in the control group. The subclinical hypothyroid group did not differ from the hypothyroid group with respect to postprandial lipemia frequency. In subjects with TSH levels higher than 5 μIU/mL, PPL risk was increased sevenfold. The results of this study show that postprandial triglyceride metabolism is affected in hypothyroidism.  相似文献   
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