Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome

INTRODUCTION: It is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event. METHOD: Fifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5–10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T(3)), free T(3), thyroxine (T(4)), free T(4), troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group. RESULTS: The T(3 )and free T(3 )levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T(4), free T(4 )and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T(3 )and free T(3 )levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T(3), free T(3), T(4 )and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively). CONCLUSION: TFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state

Comparison of right ventricular functions according to infarct localization using advanced echocardiographic methods in myocardial infarction with ST elevation

Objectives: In this study, we aimed to compare the effectsof infarct localization in patients with ST ElevatedMyocardial Infarction (STEMI) on the right ventricular(RV) functions by using advanced echocardiographicmethods.Materials and methods: A total of 89 patients withSTEMI were included into the study and patients weredivided to three groups as anterior, isolated-inferior andinferior+RV MI groups. In addition to standard echocardiographicmesurements, RV tissue doppler, RV EjectionFraction (RVEF), Myocardial performance index (MPI)and TAPSE measurements of all patients were performedbetween 24-72 hours after the event.Results: Compared to groups, RV functions in inferior MIwith RV involvement group were deteriorated. Tricuspidannular plane systolic excursion (TAPSE) value for theinferior MI with RV involvement (19±1mm) group werelower than those for Inferior MI group without RV involvement(23±1mm) and anterior MI (23±1mm) (p<0.05). TheRV MPI value for inferior MI group with RV involvement(0.76±0.14) were found to be higher than those for anterior(0.64±0.1) and inferior MI (0.56±0.1) group withoutRV involvement (p<0.05). Peak Sm (r = -0.35, p =0.01), TAPSE (r = -0.47, p<0.001) and RV EF (r = -0.46,p<0.001) showed a negative correlation with RV MPI value.Furthermore, RV tricuspid E/A rate (r = -0.19, p = 0.7)and RV free wall tissue doppler Em/Am rate (r = -0.26, p =0.01) displayed a negative correlation with RV MPI value.Conclusions: Use of advanced methods addition to theconventional echocardiographic methods in STEMI patients,could produce more valuable information to evaluateRV functions and provide a positive impact on treatmentstrategies.Key words: Acute myocardial infarction, right ventricle,echocardiography, TAPSE, MP

Physico-chemical foundations underpinning microarray and next-generation sequencing experiments

Hybridization of nucleic acids on solid surfaces is a key process involved in high-throughput technologies such as microarrays and, in some cases, next-generation sequencing (NGS). A physical understanding of the hybridization process helps to determine the accuracy of these technologies. The goal of a widespread research program is to develop reliable transformations between the raw signals reported by the technologies and individual molecular concentrations from an ensemble of nucleic acids. This research has inputs from many areas, from bioinformatics and biostatistics, to theoretical and experimental biochemistry and biophysics, to computer simulations. A group of leading researchers met in Ploen Germany in 2011 to discuss present knowledge and limitations of our physico-chemical understanding of high-throughput nucleic acid technologies. This meeting inspired us to write this summary, which provides an overview of the state-of-the-art approaches based on physico-chemical foundation to modeling of the nucleic acids hybridization process on solid surfaces. In addition, practical application of current knowledge is emphasized

Plasma brain natriuretic peptide as a surrogate marker for cardioembolic stroke

<p>Abstract</p> <p>Background</p> <p>Cardioembolic stroke generally results in more severe disability, since it typically has a larger ischemic area than the other types of ischemic stroke. However, it is difficult to differentiate cardioembolic stroke from non-cardioembolic stroke (atherothrombotic stroke and lacunar stroke). In this study, we evaluated the levels of plasma brain natriuretic peptide in acute ischemic stroke patients with cardioembolic stroke or non-cardioembolic stroke, and assessed the prediction factors of plasma brain natriuretic peptide and whether we could differentiate between stroke subtypes on the basis of plasma brain natriuretic peptide concentrations in addition to patient's clinical variables.</p> <p>Methods</p> <p>Our patient cohort consisted of 131 consecutive patients with acute cerebral infarction who were admitted to Kagawa University School of Medicine Hospital from January 1, 2005 to December 31, 2007. The mean age of patients (43 females, 88 males) was 69.6 ± 10.1 years. Sixty-two patients had cardioembolic stroke; the remaining 69 patients had non-cardioembolic stroke (including atherothrombotic stroke, lacunar stroke, or the other). Clinical variables and the plasma brain natriuretic peptide were evaluated in all patients.</p> <p>Results</p> <p>Plasma brain natriuretic peptide was linearly associated with atrial fibrillation, heart failure, chronic renal failure, and left atrial diameter, independently (F_4,126= 27.6, p < 0.0001; adjusted R²= 0.45). Furthermore, atrial fibrillation, mitral regurgitation, plasma brain natriuretic peptide (> 77 pg/ml), and left atrial diameter (> 36 mm) were statistically significant independent predictors of cardioembolic stroke in the multivariable setting (Χ²= 127.5, p < 0.001).</p> <p>Conclusion</p> <p>It was suggested that cardioembolic stroke was strongly predicted with atrial fibrillation and plasma brain natriuretic peptide. Plasma brain natriuretic peptide can be a surrogate marker for cardioembolic stroke.</p

Troponin elevation in acute ischemic stroke (TRELAS) - protocol of a prospective observational trial

<p>Abstract</p> <p>Background</p> <p>Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.</p> <p>Methods/Design</p> <p>The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. >= 0.05 μg/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.</p> <p>Discussion</p> <p>TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.</p> <p>Trial registration</p> <p>clinicaltrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01263964">NCT01263964</a></p

Simultaneous Occurrence of a Large Asymptomatic Prolapsing Left Atrial Myxoma with a Cutaneous Squamous Cell Carcinoma

Synchronous myxoma of the heart and other malignancies are extremely rare. We report a case of a 64-year-old man who had a large left atrial myxoma that obstructed the mitral valve, as well as an unrelated, coexistent cutaneous squamous cell carcinoma in the sacral area. During the preoperative evaluation for non-cardiac surgery, the tumor was diagnosed coincidentally by echocardiographic examination. Echocardiography findings were consistent with a large left atrial myxoma originating from the posterior wall and prolapsing into the left ventricular cavity through the mitral valve, causing mitral stenosis. The mass was successfully completely excised. Histologic examination of the mass confirmed the diagnosis of cardiac myxoma. We report a casual echocardiographic finding of a left atrial myxoma that obstructed the mitral valve outflow tract, and an unrelated, synchronous cutaneous squamous cell carcinoma in the sacral area

Discovery of autophagy as a universal mechanism for sex steroid synthesis in human ovary and testis

We recently discovered that lipophagy is a key mechanism to provide free cholesterol required for steroid biosynthesis in human ovary and testis. Pharmacological or genetic inhibition of autophagy by silencing of the autophagy-related (ATG) genes BECN1 (BECLIN1) and ATG5 resulted in a significant reduction in basal and gonadotropin-stimulated estradiol, progesterone (P4) and testosterone production in the ex-vivo explant tissue and cell culture models for ovary and testis. We also described a new mechanism of action for gonadotropin hormones, i.e., follicle stimulating hormone (FSH) and human chorionic gonadotropin (hCG)/luteinizing hormone (LH), in this process. They augment the production of sex steroid hormones by upregulating the expression of ATG genes, the accelerating autophagic flux and promoting LDs sequestration into autophagosomes and degradation in lysosomes. Furthermore, we detected several molecular aberrations at different steps of lipophagy-dependent P4 production in the ovary of women with defective luteal function. Our findings might have important clinical implications by opening a new avenue for the understanding and treatment of a wide range of diseases varying from reproductive disorders to sex hormone-producing neoplasms and hormone dependent malignancies, such as carcinomas of breast, endometrium, and prostate. Abbreviations: ACAT, Acyl-coenzyme A-cholesterol-acyl-transferase; AMBRA1, autophagy and beclin 1 regulator 1; ATG, autophagy-related; BECN1, BECLIN1; hCG, human chorionic gonadotropin; E2, estradiol; FSH, follicle stimulating hormone; GABARAP, GABA type A receptor-associated protein; GCs, luteinized granulosa cells; IVF, in vitro fertilization; LAMP2A, lysosomal associated membrane protein 2A; LDs, lipid droplets; LDLs, low-density lipoproteins; P4: progesterone; PCOS, polycystic ovary syndrome; SOAT1: Sterol-O-acetyltransferase; MAP1LC3B, microtubule associated protein 1 light chain 3 beta; PLIN3, perilipin 3; STAR, steroidogenic acute regulatory protein; SQSTM1, sequestosome-1