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Transient left ventricular apical ballooning syndrome is characterized by reversible left ventricular wall motion abnormalities, chest pain or dyspnea, ST-segment elevation, and mild elevation of cardiac enzyme levels in the absence of obstructive coronary artery disease. The pathophysiology of the syndrome is still unknown. The probable mechanism is supposed to be a catecholamine discharge. We report the case of a 66-year-old woman with recently diagnosed pheochromocytoma who presented with chest pain and ST-segment elevation. Coronary angiography revealed normal coronaries and apical dyskinesia at ventriculography. A similar episode of chest pain occurred 4 years ago with same angiographic findings and reversible inferobasal akinesia. In-hospital course was uneventful and the patient was discharged from the hospital 4 days later with treatment of aspirin 1 × 100 mg, metoprolol 1 × 50 mg, lisinopril 1 × 10 mg, and atorvastatin 1 × 20 mg. At 2 years follow-up after the event, the patient remained asymptomatic.  相似文献   
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Congenital absence of uterus and vagina, the Mayer-Rokitansky-Küster-Hauser Syndrome (MRKHS), results from defective müllerian duct development during female embryogenesis; it is the second most common cause of primary amenorrhea. Atypical forms of MRKHS (type B) represent a heterogeneous group of disorders with associated anomalies of other organ systems which frequently includes the renal and skeletal systems and several individually occurring malformations.We report two cases with MRKHS in which we diagnosed situs inversus totalis incidentally during radiologic examinations. Abdominal situs inversus describes the mirror-image arrangement of the intra-abdominal organs in the abdominal cavity and it is characterized by the presence of multiple congenital anomalies.In this report we attempt to question whether the association between MRKHS and situs inversus is a rare feature of the müllerian dysgenetic spectrum or whether it is the result of random association.  相似文献   
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The aim of this study was to determine left ventricular (LV) morphology and aortic function in power athletes and to compare them with normal subjects. Thirty-two elite male wrestlers and 15 age-matched healthy male controls were included. All subjects underwent echocardiographic examination. Measurements included LV cavity dimension at systole and diastole, wall thickness, diastolic parameters, and aortic diameter, 3cm above aortic valve, at systole and diastole. Left ventricular mass and mass index were found to be higher in the athletes than in control subjects. The aortic distensibility index was found to be reduced in the athletes compared with controls (2.53 ± 0.91 vs 3.94 ± 1.77cm2dyne–1 10–6, P = 0.003), while the aortic stiffness index was significantly higher in the athletes than in controls (9.12 ± 3.23 vs 6.65 ± 2.35, P = 0.02). However, LV end-systolic wall stress was lower in the athletes than in controls. Furthermore, transmitral early (E) and late (A) peak velocity, peak velocity of the myocardial systolic wave (S m), and early (E m) and atrial (A m) diastolic waves at the inferior wall were higher in the athletes than in controls. Reduced aortic distensibility in elite power athletes may be one of the cardiovascular adaptation factors which affect LV hypertrophy.  相似文献   
25.
The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 ± 12.8 and 149.2 ± 17.3mmHg, respectively. Mean DBP decreased from 93.7 ± 8.2 to 87.7 ± 10.3mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% ± 24.3% before and 58.3% ± 18.1% after the treatment. The same variables with ristocetin were 66.8% ± 21.6% and 60.8% ± 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.  相似文献   
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Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.  相似文献   
28.
BackgroundThe information on electrocardiographic features of patients with coronavirus disease 2019 (COVID-19) is limited. Our aim was to determine if baseline electrocardiographic features of hospitalized COVID-19 patients are associated with markers of myocardial injury and clinical outcomes.MethodsIn this retrospective, single center cohort study, we included 223 hospitalized patients with laboratory-confirmed COVID-19. Clinical, electrocardiographic and laboratory data were collected and analyzed. Primary composite endpoint of mortality, need for invasive mechanical ventilation, or admission to the intensive care unit was assessed.ResultsForty patients (17.9%) reached the primary composite endpoint. Patients with the primary composite endpoint were more likely to have wide QRS complex (>120 ms) and lateral ST-T segment abnormality. The multivariable Cox regression showed increasing odds of the primary composite endpoint associated with acute respiratory distress syndrome (odds ratio 7.76, 95% CI 2.67–22.59; p < 0.001), acute cardiac injury (odds ratio 3.14, 95% CI 1.26–7.99; p = 0.016), high flow oxygen therapy (odds ratio 2.43, 95% CI 1.05–5.62; p = 0.037) and QRS duration longer than >120 ms (odds ratio 3.62, 95% CI 1.39–9.380; p = 0.008) Patients with a wide QRS complex (>120 ms) had significantly higher median level of troponin T and pro-BNP than those without it. Patients with abnormality of lateral ST-T segment had significantly higher median level of troponin T and pro-BNP than patients without.ConclusionsThe presence of QRS duration longer than 120 ms and lateral ST-T segment abnormality were associated with worse clinical outcomes and higher levels of myocardial injury biomarkers.  相似文献   
29.

Background

Polycystic ovary syndrome (PCOS) is related to metabolic syndrome, insulin resistance, and cardiovascular metabolic syndromes. This is particularly true for individuals with central and abdominal obesity because visceral abdominal adipose tissue (VAAT) and epicardial adipose tissue (EAT) produce a large number of proinflammatory and proatherogenic cytokines. The present study aimed to determine whether there are changes in VAAT and EAT levels which were considered as indirect predictors for subclinical atherosclerosis in lean patients with PCOS.

Methods

The clinical and demographic characteristics of 35 patients with PCOS and 38 healthy control subjects were recorded for the present study. Additionally, the serum levels of various biochemical parameters were measured and EAT levels were assessed using 2D-transthoracic echocardiography.

Results

There were no significant differences in mean age (p?=?0.056) or mean body mass index (BMI) (p?=?0.446) between the patient and control groups. However, the body fat percentage, waist-to-hip ratio, amount of abdominal subcutaneous adipose tissue, and VAAT thickness were higher in the PCOS patient group than in the control group. The amounts of EAT in the patient and control groups were similar (p?=?0.384). EAT was correlated with BMI, fat mass, waist circumference, and hip circumference but not with any biochemical metabolic parameters including the homeostasis model assessment of insulin resistance index or the levels of triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein (HDL) cholesterol. However, there was a small positive correlation between the amounts of VAAT and EAT. VAAT was directly correlated with body fat parameters such as BMI, fat mass, and abdominal subcutaneous adipose thickness and inversely correlated with the HDL cholesterol level.

Conclusions

The present study found that increased abdominal adipose tissue in patients with PCOS was associated with atherosclerosis. Additionally, EAT may aid in the determination of the risk of atherosclerosis in patients with PCOS because it is easily measured.
  相似文献   
30.
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