Future Perspectives to Improve CHA2DS2VASc Score: The Role of Left Atrium Remodelling, Inflammation and Genetics in Anticoagulation of Atrial Fibrillation.

In 10% of ischemic strokes, non-valvular atrial fibrillation (NVAF) is detected retroactively. Milder, or even asymptomatic forms of NVAF have shown high mortality, thrombotic risk, and deterioration of cognitive function. The current guidelines for the diagnosis and treatment of AF contain "grey areas", such as the one related to anticoagulant treatment in men with CHA2DS2-VASc score 1 and women with score 2. Moreover, parameters such as renal function, patient weight or left atrium remodelling are missing from the recommended guidelines scores. Vulnerable categories of patients including the elderly population, high hemorrhagic risk patients or patients with newly diagnosed paroxysmal episodes of atrial high rate at device interrogation are at risk of underestimation of the thrombotic risk. This review presents a systematic exposure of the most important gaps in evaluation of thrombotic and hemorrhagic risk in patients with NVAF. The authors propose new algorithms and risk factors that should be taken into consideration for an accurate thrombotic and hemorrhagic risk estimation, especially in vulnerable categories of patients.

Remote Monitoring in Cardiac Resynchronization Therapy-First Experience in Romania with a CRT Virtual Ward.

BACKGROUND: Remote monitoring (RM) is becoming a standard of care for patients with cardiac resynchronization therapy (CRT). This technology combines the use of pacemakers or implantable cardioverter-defibrillators (ICD) and wireless communication to provide physicians with continuous, real-time information on the patient's cardiac activity. The purpose of the study was to evaluate if the remote monitoring technology in the follow-up CRT patients is feasible and safe. METHODS: A total of nine patients were enrolled in the study, implanted with a CRT system with wireless transmission capabilities. Immediately after the procedure received the RM, were enrolled in the virtual clinic and instructed by the doctor how to use the device at home. Regular virtual transmissions were made automatically every 3 weeks, respecting optimal transmission conditions. The accumulation of fluid in the lungs, atrial or ventricular tachyarrhythmia together with system integrity automatically activate alerts. RESULTS: One hundred and one transmissions were collected and analyzed from the virtual ward. Average follow-up was 7.7±4.8 months, longest follow-up was 18 months. None of the patients experienced complications during the study period, with three of them being follow-up solely through telemetric means by implanting physician. Treatment optimization was successfully conducted via phone consultations, when necessary, without any adverse events. CONCLUSIONS: The results of our study suggest that RM could be integrated into routine CRT management protocols, enhancing patients care and resource utilization.

Reduced Left Ventricular Twist Early after Acute ST-Segment Elevation Myocardial Infarction as a Predictor of Left Ventricular Adverse Remodelling.

BACKGROUND: The left ventricular (LV) remodelling process represents the main cause of heart failure after a ST-segment elevation myocardial infarction (STEMI). Speckle-tracking echocardiography (STE) can detect early deformation impairment, while also predicting LV remodelling during follow-up. The aim of this study was to investigate the STE parameters in predicting cardiac remodelling following a percutaneous coronary intervention (PCI) in STEMI patients. METHODS: The study population consisted of 60 patients with acute STEMI and no history of prior myocardial infarction treated with PCI. The patients were assessed both by conventional transthoracic and ST echocardiography in the first 12 h after admission and 6 months after the acute phase. Adverse remodelling was defined as an increase in LVEDV and/or LVESV by 15%. RESULTS: Adverse remodelling occurred in 26 patients (43.33%). By multivariate regression equation, the risk of adverse remodelling increases with age (by 1.1-fold), triglyceride level (by 1.009-fold), and midmyocardial radial strain (mid-RS) (1.06-fold). Increased initial twist decreases the chances of adverse remodelling (0.847-fold). The LV twist presented the largest area under the receiver operating characteristic (ROC) curve to predict adverse remodelling (AUROC = 0.648; 95% CI [0.506;0.789], p = 0.04). A twist value higher than 11° has a 76.9% specificity and a 72.7% positive predictive value for reverse remodelling at 6 months.

Dose-dependent effects of acetaminophen and ibuprofen on mitochondrial respiration of human platelets.

Acetaminophen and ibuprofen are widely used over-the-counter medications to reduce fever, pain, and inflammation. Although both drugs are safe in therapeutic concentrations, self-medication is practiced by millions of aged patients with comorbidities that decrease drug metabolism and/or excretion, thus raising the risk of overdosage. Mitochondrial dysfunction has emerged as an important pathomechanism underlying the organ toxicity of both drugs. Assessment of mitochondrial oxygen consumption in peripheral blood cells is a novel research field Cu several applications, including characterization of drug toxicity. The present study, conducted in human platelets isolated from blood donor-derived buffy coat, was aimed at assessing the acute, concentration-dependent effects of each drug on mitochondrial respiration. Using the high-resolution respirometry technique, a concentration-dependent decrease of oxygen consumption in both intact and permeabilized platelets was found for either drug, mainly by inhibiting complex I-supported active respiration. Moreover, ibuprofen significantly decreased the maximal capacity of the electron transport system already from the lowest concentration. In conclusion, platelets from healthy donors represents a population of cells easily available, which can be routinely used in studies assessing mitochondrial drug toxicity. Whether these results can be recapitulated in patients treated with these medications is worth further investigation as potential peripheral biomarker of drug overdose.

Considering Diastolic Dyssynchrony as a Predictor of Favorable Response in LV-Only Fusion Pacing Cardiac Resynchronization Therapy.

Background: CRT improves systolic and diastolic function, increasing cardiac output. Aim of the study: to assess the outcome of LV diastolic dyssynchrony in a population of fusion pacing CRT. Methods: Diastolic dyssynchrony was measured by offline speckle-tracking-derived TDI timing assessment of the simultaneity of E″ and A″ basal septal and lateral walls. New parameters introduced: E″ and, respectively, A″ time (E″T/A″T) as the time difference between E″ (respectively, A″) peak septal and lateral wall. Patients were divided into super-responders (SR), responders (R), and non-responders (NR). Results: Baseline characteristics: 62 pts (62 ± 11 y.o.) with idiopathic DCM, EF 27 ± 5.2%; 29% type III diastolic dysfunction (DD), 63% type II, 8% type I. Average follow-up 45 ± 19 months: LVEF 37 ± 7.9%, 34%SR, 61%R, 5%NR. The E″T decreased from 90 ± 20 ms to 25 ± 10 ms in SR with significant LV reverse remodeling (LV end-diastolic volume 193.7 ± 81 vs. 243.2 ± 82 mL at baseline, p < 0.0028) and lower LV filling pressures (E/E' 13.2 ± 4.6 vs. 11.4 ± 4.5, p = 0.0295). DD profile improved in 65% of R with a reduction in E/E' ratio (21 ± 9 vs. 14 ± 4 ms, p < 0.0001). Significant cut-off value calculated by ROC curve for LV diastolic dyssynchrony is E″T > 80 ms and A″T > 30 msec. Conclusions: The study identifies the cut-off values of diastolic dyssynchrony parameters as predictors of favorable outcomes in responders and super-responder patients with fusion CRT pacing. These findings may have important implications in patient selection and follow-up.

Monoamine oxidase is a source of cardiac oxidative stress in obese rats: the beneficial role of metformin.

Diet-induced metabolic diseases, such as obesity, metabolic syndrome, and type 2 diabetes (T2DM) are the global threatening epidemics that share cardiovascular oxidative stress as common denominator. Monoamine oxidase (MAO) has recently emerged as a constant source of reactive oxygen species (ROS) in DM. Metformin, the first-line drug in T2DM, elicits cardiovascular protection via pleiotropic effects. The present study was aimed to assess the contribution of MAO to the early cardiac oxidative stress in a rat model of high-calorie junk food (HCJF) diet-induced obesity and prediabetes and whether metformin can alleviate it. After 6 months of HCJF, rats developed obesity and hyperglycemia. Hearts were isolated and used for the evaluation of MAO expression and ROS production. Experiments were performed in the presence vs absence of metformin (10 µM) and MAO-A and B inhibitors (clorgyline and selegiline, 10 µM), respectively. Both MAO isoforms were overexpressed and led to increased ROS generation in cardiac samples harvested from the obese animals. Acute treatment with metformin and MAO inhibitors was able to mitigate oxidative stress. More important, metformin downregulated MAO expression in the diseased samples. In conclusion, MAO contributes to oxidative stress in experimental obesity and can be targeted with metformin.

Update in LV Only Fusion CRT Pacing: Annals and Future Perspectives.

Triple-chamber cardiac devices are utilized for cardiac resynchronization therapy (CRT) and is the standard-of-care therapy for heart failure (HF) patients in the current guidelines. In the setting of biventricular (BIV) pacing it involves a mandatory implantation of right ventricular (RV) lead that allows simultaneous BIV pacing with 0 ms VV (ventricular to ventricular) interval. Nevertheless, it seems that response to CRT is not related to RV lead position. RV pacing is known for deleterious effects on RV/Left Ventricle (LV) function and should not be used in persons with normal atrioventricular conduction (AV) and sinus rhythm. As it compensates for the additional asynchrony induced by unnecessary stimulation of RV pacing, only pacing the left ventricle (LV) may result in improved cardiac resynchronization therapy (CRT) outcomes and a decrease in the number of individuals who do not respond to the procedure. Furthermore, leadless LV fusion CRT pacing without RV lead could be a potential CRT therapy alternative to BIV pacing in nonischemic heart failure patients with preserved AV conduction. The aim of our study is to made an update in cardiac resynchronization therapy with LV only fusion pacing.

Factors Associated with Stroke in Atrial Fibrillation. A Retrospective Study.

AIM: The aim of our study was to retrospectively evaluate known factors such as CHA2DS2-VASc, but, also, new factors (such as left atrial remodeling), associated with the development of stroke in patients with atrial fibrillation (AFi). MATERIAL AND METHODS: We performed a retrospective study in which 251 patients with AFi were included. 47 patients had an ischemic stroke before the diagnosis of AFi, at the time of diagnosis or after AFi was diagnosed. The CHA2DS2-VASc score was analyzed for all patients together with other left atrial remodeling parameters. RESULTS: We observed that among the patients with ischemic stroke approximately 61.70% were over 72.5 years old compared to those without stroke who presented this age in a proportion of only 44.61% (OR=2.001, P=0.0367). The CHA2DS2-VASc score had the greatest statistical impact for stroke, as expected. Patients with a CHA2DS2-VASc score >4.5 presented stroke in a proportion of 87.23% compared to CHA2DS2-VASc <4.5 who had stroke only in a proportion of 12.77% (OR=11.51, P=<0.0001). Regarding left atrial remodeling parameters, low LA ejection fraction was associated with a high percentage of stroke among patients (61.70%) compared to those with LA EF>34.5% who had stroke only in a percentage of 38.30% (OR= 2.124, P=0.0238). CONCLUSIONS: Although the CHA2DS2-VASc score remains a good factor for predicting the association of AFi with ischemic stroke, echocardiographic parameters for the evaluation of the left atrium can be used as new risk factors for predicting the occurrence of ischemic stroke in patients with AFi.

Metformin Acutely Mitigates Oxidative Stress in Human Atrial Tissue: A Pilot Study in Overweight Non-Diabetic Cardiac Patients.

Metformin, the first-line drug in type 2 diabetes mellitus, elicits cardiovascular protection also in obese patients via pleiotropic effects, among which the anti-oxidant is one of the most investigated. The aim of the present study was to assess whether metformin can acutely mitigate oxidative stress in atrial tissue harvested from overweight non-diabetic patients. Right atrial appendage samples were harvested during open-heart surgery and used for the evaluation of reactive oxygen species (ROS) production by means of confocal microscopy (superoxide anion) and spectrophotometry (hydrogen peroxide). Experiments were performed after acute incubation with metformin (10 µM) in the presence vs. absence of angiotensin II (AII, 100 nM), lipopolysaccharide (LPS, 1 µg/mL), and high glucose (Gluc, 400 mg/dL). Stimulation with AII, LPS, and high Gluc increased ROS production. The magnitude of oxidative stress correlated with several echocardiographic parameters. Metformin applied in the lowest therapeutic concentration (10 µM) was able to decrease ROS generation in stimulated but also non-stimulated atrial samples. In conclusion, in a pilot group of overweight non-diabetic cardiac patients, acute incubation with metformin at a clinically relevant dose alleviated oxidative stress both in basal conditions and conditions that mimicked the activation of the renin-angiotensin-aldosterone system, acute inflammation, and uncontrolled hyperglycemia.

Monoamine Oxidase (MAO) Is Expressed at the Level of Mitral Valve with Severe Regurgitation in Hypertrophic Obstructive Cardiomyopathy: A Case Report.

Hypertrophic obstructive cardiomyopathy (HOCM) is one of the most common hereditary heart diseases. The severely hypertrophied interventricular septum combined with the systolic anterior movement (SAM) of the mitral valve (MV) frequently cause a significant pressure gradient in the left ventricular outflow tract associated with varying degrees of mitral regurgitation (MR). We present the case of a 64-year-old female patient who was diagnosed with HOCM two years ago and was admitted to the Institute of Cardiovascular Disease with exertion dyspnea and fatigue. Transthoracic echocardiography revealed concentric, asymmetrical left ventricular hypertrophy, an elongated anterior mitral leaflet (AML) and a significant SAM causing severe regurgitation, with indication for valvular replacement Monoamine oxidase (MAO), a mitochondrial enzyme, with 2 isoforms, MAO-A and B, has emerged as an important source of reactive oxygen species (ROS) in the cardiovascular system, but literature data on its expression in valvular tissue is scarce. Therefore, we assessed MAO-A and B gene (qPCR) and protein (immune fluorescence) expression as well as ROS production (spectrophotometry and confocal microscopy) and in the explanted MV harvested during replacement surgery. MAO expression and ROS production (assessed by both methods) were further augmented following ex vivo incubation with angiotensin II, an effect that was reversed in the presence of either MAO-A (clorgyline) or B (selegiline) inhibitor, respectively. In conclusion, MAO isoforms are expressed at the level of severely impaired mitral valve in the setting of HOCM and can be induced in conditions that mimic the activation of renin-angiotensin-aldosterone system. The observation that the enzyme can be modulated by MAO inhibitors warrants further investigation in a patient cohort.

Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.

Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature.

Nonischemic Super-Responders in Fusion CRT Pacing with Normal Atrioventricular Conduction.

Background: Fusion CRT pacing (FCRT) is noninferior to biventricular pacing, according to the current data. The aim of this study is to assess the response to FCRT and to identify predictors of super-responders (SRs) in a nonischemic population with normal AV conduction. Methods: LV-only CRT patients (pts) with a right atrium/left ventricle pacing system implanted in two CRT centers in Romania were included. Device interrogation, exercise tests, echocardiography, and individualized drug optimization were performed every 6 months during close follow-up. SRs pts were defined as those with left ventricular end-systolic volume (LVESV) improvement ≥30% and stable ejection fraction (LVEF) ≥45%. Results: A total of 25 out of 83 pts (31%) were SRs, with nonischemic LBBB low EF cardiomyopathy (50 male, 62 ± 9 y.o.) initially included. Mean follow-up was 5 years ± 27 months. Patients were divided in two groups: SRs and non-SRs (52 responders/6 hypo-responders). Two predictors were found in the SRs group: a higher baseline LVEF (SRs 29 ± 5% vs. non-SRs 26 ± 5%, p = 0.02) and a lower pulmonary arterial systolic pressure (SRs 38 ± 11 mm Hg vs. non-SRs 50 ± 15 mmHg, p = 0.003). Baseline severe mitral regurgitation was found in 11% of SRs vs. 64% in the non-SRs group. Conclusions: SRs in the selected NICM-FCRT group are significative high. Higher baseline LVEF and mild pulmonary arterial hypertension were independently associated with super-response.

Potential role for pentoxifylline as an anti-inflammatory drug for patients with acute coronary syndrome.

The link between inflammation and acute coronary syndrome (ACS) remains to be sufficiently elucidated. It has been previously suggested that there is an inflammatory process associated with ACS. Pentoxifylline, a methylxanthine derivate, is known to delay the progression of atherosclerosis and reduce the risk of vascular events, especially by modulating the systemic inflammatory response. The present study is a single-blind, randomized, prospective study of pentoxifylline 400 mg three times a day (TID) added to standard therapy vs. standard therapy plus placebo in ACS patients with non-ST elevation myocardial infarction (NSTEMI). Patients with ACS were randomized to receive standard therapy plus placebo in one arm (group A; aspirin, clopidogrel or ticagrelor, statin) and in the other arm (group B) pentoxifylline 400 mg TID was added to standard therapy. The primary outcome was the rate of major adverse cardiovascular events (MACEs) at 1 year. A total of 500 patients underwent randomization (with 250 assigned to group A and 250 to group B) and were followed-up for a median of 20 months. The mean age of the patients was 62.3±10.3 years, 80.4% were male, 20.8% had diabetes, 49.4% had hypertension, and 42% were currently smoking. The statistical analysis was performed for 209 patients in group A and 210 patients in group B (after dropouts due to study drug discontinuation). A primary endpoint occurred in 12.38% (n=26) of patients in group B, as compared with 15.78% (n=33) of those in group A [relative risk (RR), 0.78; 95% confidence interval (CI), 0.486-0.1.263; P=0.40], including cardiovascular death (RR, 0.93; 95% CI, 0.48-1.80, P=0.84), non-fatal myocardial infarction (RR, 1.1; 95% CI, 0.39-3.39, P=0.78), stroke (RR, 0.99; 95% CI, 0.14-6.99, P=0.99) and coronary revascularization (RR, 0.12; 95% CI, 0.015-0.985, P=0.048). Thus, adding pentoxifylline to standard treatment in patients with ACS did not improve MACE at 1 year but had some benefit on the need for coronary revascularization.

An Up-to-Date Article Regarding Particularities of Drug Treatment in Patients with Chronic Heart Failure.

Since the prevalence of heart failure (HF) increases with age, HF is now one of the most common reasons for the hospitalization of elderly people. Although the treatment strategies and overall outcomes of HF patients have improved over time, hospitalization and mortality rates remain elevated, especially in developed countries where populations are aging. Therefore, this paper is intended to be a valuable multidisciplinary source of information for both doctors (cardiologists and general physicians) and pharmacists in order to decrease the morbidity and mortality of heart failure patients. We address several aspects regarding pharmacological treatment (including new approaches in HF treatment strategies [sacubitril/valsartan combination and sodium glucose co-transporter-2 inhibitors]), as well as the particularities of patients (age-induced changes and sex differences) and treatment (pharmacokinetic and pharmacodynamic changes in drugs; cardiorenal syndrome). The article also highlights several drugs and food supplements that may worsen the prognosis of HF patients and discusses some potential drug-drug interactions, their consequences and recommendations for health care providers, as well as the risks of adverse drug reactions and treatment discontinuation, as an interdisciplinary approach to treatment is essential for HF patients.

Estimation of Energy Losses in Nanocrystalline FINEMET Alloys Working at High Frequency.

Soft magnetic materials are at the core of electromagnetic devices. Planar transformers are essential pieces of equipment working at high frequency. Usually, their magnetic core is made of various types of ferrites or iron-based alloys. An upcoming alternative might be the replacement the ferrites with FINEMET-type alloys, of nominal composition of Fe73.5Si13.5B9Cu3Nb1 (at. %). FINEMET is a nanocrystalline material exhibiting excellent magnetic properties at high frequencies, a soft magnetic alloy that has been in the focus of interest in the last years thanks to its high saturation magnetization, high permeability, and low core loss. Here, we present and discuss the measured and modelled properties of this material. Owing to the limits of the experimental set-up, an estimate of the total magnetic losses within this magnetic material is made, for values greater than the measurement limits of the magnetic flux density and frequency, with reasonable results for potential applications of FINMET-type alloys and thin films in high frequency planar transformer cores.

Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Amiodarone Toxicity.

Amiodarone is a potent antiarrhythmic drug and displays substantial liver toxicity in humans. It has previously been demonstrated that amiodarone and its metabolite (desethylamiodarone, DEA) can inhibit mitochondrial function, particularly complexes I (CI) and II (CII) of the electron transport system in various animal tissues and cell types. The present study, performed in human peripheral blood cells, and one liver-derived human cell line, is primarily aimed at assessing the concentration-dependent effects of these drugs on mitochondrial function (respiration and cellular ATP levels). Furthermore, we explore the efficacy of a novel cell-permeable succinate prodrug in alleviating the drug-induced acute mitochondrial dysfunction. Amiodarone and DEA elicit a concentration-dependent impairment of mitochondrial respiration in both intact and permeabilized platelets via the inhibition of both CI- and CII-supported respiration. The inhibitory effect seen in human platelets is also confirmed in mononuclear cells (PBMCs) and HepG2 cells. Additionally, amiodarone elicits a severe concentration-dependent ATP depletion in PBMCs, which cannot be explained solely by mitochondrial inhibition. The succinate prodrug NV118 alleviates the respiratory deficit in platelets and HepG2 cells acutely exposed to amiodarone. In conclusion, amiodarone severely inhibits metabolism in primary human mitochondria, which can be counteracted by increasing mitochondrial function using intracellular delivery of succinate.

Arterial Hypertension: Individual Therapeutic Approaches-From DNA Sequencing to Gender Differentiation and New Therapeutic Targets.

The aim of this paper is to provide an accurate overview regarding the current recommended approach for antihypertensive treatment. The importance of DNA sequencing in understanding the complex implication of genetics in hypertension could represent an important step in understanding antihypertensive treatment as well as in developing new medical strategies. Despite a pool of data from studies regarding cardiovascular risk factors emphasizing a worse prognosis for female patients rather than male patients, there are also results indicating that women are more likely to be predisposed to the use of antihypertensive medication and less likely to develop uncontrolled hypertension. Moreover, lower systolic blood pressure values are associated with increased cardiovascular risk in women compared to men. The prevalence, awareness and, most importantly, treatment of hypertension is variable in male and female patients, since the mechanisms responsible for this pathology may be different and closely related to gender factors such as the renin-angiotensin system, sympathetic nervous activity, endothelin-1, sex hormones, aldosterone, and the immune system. Thus, gender-related antihypertensive treatment individualization may be a valuable tool in improving female patients' prognosis.

Left Ventricular Remodeling Risk Predicted by Two-Dimensional Speckle Tracking Echocardiography in Acute Myocardial Infarction Patients with Midrange or Preserved Ejection Fraction in Western Romania.

BACKGROUND: Patients with acute myocardial infarction (AMI) are at high risk for left ventricular (LV) remodeling and heart failure. We aimed to study whether LV strains (S) and strain rates (SR) could predict cardiac remodeling in patients with AMI having a midrange or preserved LV ejection fraction (EF) following a percutaneous coronary intervention (PCI) within the first 12 hours from the onset of symptoms. PATIENTS AND METHODS: This is a case-control observational study including patients admitted for their first AMI, either with ST-segment elevation (STEMI) or without ST elevation (NSTEMI), with an LVEF > 40% after a successful PCI. Echocardiography was repeated after 6 months, and the patients were divided into two groups, according to whether LV remodeling was determined on echocardiography. RESULTS: Of the 253 AMI patients (mean 66 aged ± 13 years), including 185 males (73%), 61 (24%) presented signs of LV remodeling. In univariate logistic regression analysis, age, male sex, smoking history, hypertension, hypercholesterolemia, Killip class, renal function, peak creatine phosphokinase - MB level, 2- and 3-vessel coronary artery disease (CAD), and several echocardiographic parameters were significantly associated with LV remodeling (P<0.05). In multivariate logistic regression analysis harmed (H) LS and SR, Killip class, 3-vessel CAD, and LV end-diastolic volume were outlined as independent predictors for LV remodeling. Receiver operating characteristic curve analyses showed that HLS and HLSR were the most powerful independent predictors for LV remodeling (P<0.001), with an area under the curve (AUC) of 0.85 (sensitivity 83%; specificity 84%; p <0.001) and 0.77 (sensitivity 93; specificity 61%; p <0.001), respectively. The identified cut-off values for predictor variables were HLS< -11%, and HLSR< -0.65s-1. CONCLUSION: We concluded that 2D-STE was the best method to evaluate LV remodeling in patients with AMI and midrange or preserved LVEF following myocardial revascularization by a PCI.

Three-Dimensional Transesophageal Echocardiography as an Alternative to Multidetector Computed Tomography in Aortic Annular Diameter Measurements for Transcatheter Aortic Valve Implantation.

Background and objectives: Transcatheter aortic valve implantation (TAVI) is a therapeutic choice for high surgical risk patients, serving as an alternative to open-heart surgery. Correct measurement of the aortic annulus, which leads to the selection of a suitable prosthesis and accurate outcome prediction, is essential for the success of TAVI. The objective of this study is to evaluate the accuracy of novel imaging te chniques in measuring the aortic annulus by comparing multi-detector computer tomography (MDCT) and three-dimensional transesophageal echocardiography (3D TEE) for the selection of the optimal prosthesis. Materials and Methods: Measurements of the aortic annulus have been performed on 25 patients using MDCT and TEE, and the correlation and agreement levels between the two measuring techniques were analyzed. MDCT measurements were used for the sizing of the prostheses. Results: MDCT and TEE measurements of aortic annular diameters were significantly correlated, with a mean difference of 0.001 cm. Conclusions: 3D TEE measurements have been in good agreement with MDCT and, therefore, 3D TEE can be used as an alternative in cases where MDCT is contraindicated or not available.

TET2 rs1548483 SNP Associating with Susceptibility to Molecularly Annotated Polycythemia Vera and Primary Myelofibrosis.

BACKGROUND: The complexity of myeloproliferative neoplasms (MPNs) cannot be characterized by acquired somatic mutations alone. Individual genetic background is thought to contribute to the development of MPNs. The aim of our study was to assess the association between the TET2 rs1548483 single nucleotide polymorphism (SNP) and the susceptibility to polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF) or chronic myeloid leukemia (CML). METHODS: We evaluated the TET2 rs1548483 SNP through real-time PCR in 1601 MPN patients out of which 431 with PV, 688 with TE, 233 with PMF, 249 with CML and 197 controls. We included only patients with a molecularly proven driver mutation, such as JAK2 V617F, CALR or BCR-ABL1. RESULTS: Significant association between TET2 rs154843 variant allele and JAK2 V617F-positive PV and PMF (OR = 1.70; 95% CI: 1.01-2.91; p-value = 0.046, and OR = 2.04; 95% CI: 1.10-3.77; p-value = 0.024, respectively), and type 2 CALR-positive PMF (OR = 2.98; 95% CI: 1.12-7.93; p-value = 0.035) was noted. CONCLUSIONS: The TET2 rs1548483 SNP is associated with the susceptibility to molecularly annotated PV and PMF.