931 research outputs found

    Catheter Based Simultaneous Mapping of Cardiac Activation and Motion: A Review

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    Heart failure as a result of a variety of cardiac diseases is an ever growing, challenging condition that demands profound insight in the electrical and mechanical state of the myocardium. Assessment of cardiac function has largely relied on evaluation of cardiac motion by multiple imaging techniques. In recent years electrical properties have gained attention as heart failure could be improved by biventricular resynchronization therapy. In contrast to early belief, QRS widening as a result of left bundle branch block could not be identified as a surrogate for asynchronous contraction

    Rationale and design of BERLIN VT study: a multicenter randomised trial comparing preventive versus deferred ablation of ventricular tachycardia

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    Introduction Catheter ablation ( CA) has shown to effectively reduce the burden of ventricular tachycardia in patients with implanted cardioverter-defibrillator (ICD). However, in patients with ICD implantation for secondary prevention of ventricular tachycardia (VT), the appropriate time point of CA and its effect on mortality and heart failure progression remains a matter of debate. Methods and analysis We present the design of the ongoing preventive aBlation of vEntriculartachycaRdia in patients with myocardiaLINfarction (BERLIN VT) study that aims to prospectively enrol 208 patients with a stable ischaemic cardiomyopathy, a left ventricular ejection fraction of 30% to 50% and documented ventricular tachycardia. Patients will be 1: 1 randomised to undergo CA at the time of ICD implantation or CA after the third appropriate ICD shock for ventricular tachycardia. ICD implantation will be performed in all patients. The primary endpoint is defined as the time to first event comprising all-cause mortality and unplanned hospital admission for congestive heart failure or for symptomatic VT/ventricular fibrillation. The patients will be followed until study termination according to the event driven design. Completion of enrolment is expected for mid of 2019. Ethics and dissemination The study had been approved by the "Ethik-kommission der Landesarztekammer Hamburg" as well as the local institutional review boards for each of the participation sites. The results of the trial will be published in peer-reviewed journal

    Low myocardial energetic efficiency is associated with increased mortality in aortic stenosis

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    Objectives In hypertension, low myocardial energetic efficiency (MEEi) has been documented as an integrated marker of metabolic and left ventricular (LV) myocardial dysfunction. We tested the predictive performance of MEEi in initially asymptomatic aortic stenosis (AS) patients free from diabetes and known cardiovascular disease. Methods Data from 1703 patients with mostly moderate AS enrolled in the Simvastatin and Ezetimibe in Aortic Stenosis study followed for 4.3 years was used. MEE was calculated from Doppler stroke volume/([heart rate/60]) and indexed to LV mass (MEEi). The threshold value for MEEi associated with increased mortality was identified in generalised additive model with smoothing splines. Covariables of MEEi were identified in logistic regression analysis. Outcome was assessed in Cox regression analysis and reported as HR and 95% CI. Results MEEi <0.34 mL/s per gram was associated with increased cardiovascular mortality (n=80) (HR 2.53 (95% CI 1.50 to 4.28)) and all-cause mortality (n=155) (HR 1.74 (95% CI 1.20 to 2.52)) (both p<0.01). The association was independent of confounders of low MEEI (<0.34 mL/s per gram) identified in multivariable logistic regression analysis, including more severe AS, higher body mass index, lower LV midwall shortening and ejection fraction and presence of hypertension. Comparison of the Cox models with and without MEEi among the covariables demonstrated that MEEi significantly improved the prognostic yield (both p<0.01). Conclusions In patients with initially asymptomatic AS, low MEEi was associated with clustering of cardiometabolic risk factors, lower LV myocardial function and subsequent increased mortality during 4.3 years follow-up, independent of known prognosticators.publishedVersio

    Prospective measurement of the width of cerebrospinal fluid spaces by cranial ultrasound in neurologically healthy children aged 0-19 months

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    BACKGROUND Ultrasound (US) is often the first method used to look for brain or cerebrospinal fluid (CSF) space pathologies. Knowledge of normal CSF width values is essential. Most of the available US normative values were established over 20 years ago, were obtained with older equipment, and cover only part of the age spectrum that can be examined by cranial US. This prospective study aimed to determine the normative values of the widths of the subarachnoid and internal CSF spaces (craniocortical, minimal and maximal interhemispheric, interventricular, and frontal horn) for high-resolution linear US probes in neurologically healthy infants and children aged 0-19 months and assess whether subdural fluid collections can be delineated. METHODS Two radiologists measured the width of the CSF spaces with a conventional linear probe and an ultralight hockey-stick probe in neurologically healthy children not referred for cranial or spinal US. RESULTS This study included 359 neurologically healthy children (nboys_{boys} = 178, 49.6%; ngirls_{girls} = 181, 50.4%) with a median age of 46.0 days and a range of 1-599 days. We constructed prediction plots, including the 5th, 50th, and 95th percentiles, and an interactive spreadsheet to calculate normative values for individual patients. The measurements of the two probes and the left and right sides did not differ, eliminating the need for separate normative values. No subdural fluid collection was detected. CONCLUSION Normative values for the widths of the subarachnoid space and the internal CSF spaces are useful for evaluating intracranial pathology, especially when determining whether an increase in the subarachnoid space width is abnormal

    Atrial Fibrillation Begets Atrial Fibrillation in the Pulmonary Veins On the Impact of Atrial Fibrillation on the Electrophysiological Properties of the Pulmonary Veins in Humans

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    ObjectivesOur purpose was to investigate the impact of short-lasting atrial fibrillation (AF) on the electrophysiological properties of the atria and pulmonary veins (PVs) in patients devoid of AF.BackgroundThe presence of AF is associated with electrical remodeling processes that promote a substrate for arrhythmia maintenance in the atria, which has been termed “AF begets AF.” However, it is unclear whether those electrical alterations also occur in the PVs.MethodsThirty-five patients with a left-sided accessory pathway and without a prior history of AF were included. After successful ablation, the effective refractory periods (ERPs) and conduction times of the right atrium (RA), left atrium (LA), and the PVs were determined. Afterwards, AF was induced and maintained for a period of 15 min. Thereafter, the stimulation protocol was repeated.ResultsAt baseline, the PVs had significantly longer ERPs than the atria. After exposure to AF, the ERPs of both the atria and the PVs decreased significantly. The ERPs of the PVs, however, decreased by a significantly greater extent than the ERPs of the atria (PVs: 248 ± 27 ms vs. 211 ± 40 ms, p < 0.001; LA: 233 ± 23 ms vs. 214 ± 20 ms, p = 0.004; RA: 226 ± 29 ms vs. 188 ± 20 ms; p = 0.003). After AF exposure, the PVs demonstrated a significant conduction slowing whereas the atria did not (PVs: 125 ± 33 ms vs. 159 ± 37 ms, p < 0.001; LA: 129 ± 26 ms vs. 130 ± 24 ms, p = NS; RA: 192 ± 36 ms vs. 196 ± 32 ms, p = NS). Finally, AF was more frequently induced after the presence of AF, particularly by pacing in the PVs (14% vs. 49%, p = 0.001).ConclusionsNew-onset, short-lasting AF creates electrical characteristics similar to those of patients with AF. However, these alterations are pronounced in the PVs compared with the atria, indicating that “AF begets AF in the PVs” (Electrophysiological Properties of the Pulmonary Veins; NCT00530608)
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