Kardionevroablacija pri zdravljenju refleksne nevrokardiogene sinkope - Prikaz primera

Izvleček Refleksna nevrokardiogena sinkopa je ena izmed najbolj pogostih oblik izgube zavesti, pri kateri prekomeren odziv parasimpatičnega živčnega sistema vodi do padca krvnega pritiska preko vazodilatacije in/ali znižanja srčnega utripa. Gre za sinkopo, ki praviloma ni povezana z organsko boleznijo, zato je njena prognoza dobra in umrljivost ni povečana, lahko pa vpliva na kvaliteto življenja. Z novo metodo zdravljenja - kardionevroablacijo - želimo doseči izboljšanje kvalitete življenja pri pacientih s pogostimi epizodami refleksne nevrokardiogene sinkope s prevladujočo kardioinhibitorno komponento, pri katerih nefarmakološki in farmakološki načini zdravljenja niso učinkoviti, vstavitev srčnega spodbujevalnika pa zaradi mladosti odsvetovana. Gre za perkutani elektrofiziološki poseg, kjer z radiofrekvenčno ablacijo z endokardialne strani uničimo specifične parasimpatične ganglije epikardialno na srcu. Na ta način dosežemo delno parasimpatično denervacijo srca in s tem zmanjšamo ali odpravimo prekomeren vpliv parasimpatičnega živčevja na srce in posledično tudi kardioinhibitorno komponentno refleksne nevrokardiogene sinkope

Pulse wave analysis during supine rest may identify subjects with recurrent vasovagal syncope A B S T R A C T

In the present study, we studied whether analysis of the FAP (finger arterial pressure) waveform during supine rest discriminates subjects with recurrent VVS (vasovagal syncope) from healthy controls. Signal-averaged FAP waveforms (Finapres) were obtained in 32 head-up tilt-test-positive subjects with recurrent VVS (35 + − 13 years) and in 32 sex-and age-matched healthy controls. The DT (time delay) between the systolic and diastolic peaks of the FAP waveform was measured and large artery SI (stiffness index) was calculated as a ratio of body height and DT. VVS patients had significantly shorter DT compared with controls (303 + − 31 compared with 329 + − 18 ms; P < 0.001) and higher SI (5.79 + − 0.70 compared with 5.20 + − 0.36 m/s; P < 0.001). The differences were independent of heart rate and blood pressure. SI > 5.45 m/s identified subjects with syncope with a sensitivity of 72 % and a specificity of 84 %. Age-corrected DT (cDT = DT + age − 350) identified subjects with syncope with a sensitivity of 75 % and a specificity of 84 %. Combined use of cDT < 0 ms and SI > 5.45 m/s increased sensitivity and specificity to 81 % and 96 % respectively. The discriminative power of FAP descriptors improved further when younger subjects were excluded. In subjects aged > 30 years (median age), the combination of cDT and SI identified subjects with syncope with a sensitivity of 93 % and a specificity of 100 %. These results suggest that FAP descriptors during supine rest might be useful in the diagnosis of VVS in middle-aged subjects

Anticoagulation with edoxaban in patients with long Atrial High-Rate Episodes ≥24 hours

BACKGROUND AND AIMS: Patients with long atrial high-rate episodes (AHRE) ≥ 24 hours and stroke risk factors are often treated with anticoagulation for stroke prevention. Anticoagulation has never been compared to no anticoagulation in these patients.METHODS: This secondary prespecified analysis of NOAH-AFNET 6 examined interactions between AHRE duration at baseline and anticoagulation with edoxaban compared to placebo in patients with AHRE and stroke risk factors. The primary efficacy outcome was a composite of stroke, systemic embolism, or cardiovascular death. The safety outcome was a composite of major bleeding and death. Key secondary outcomes were components of these outcomes and ECG-diagnosed atrial fibrillation.RESULTS: AHRE ≥24 hours were present at baseline in 259/2389 patients enrolled in NOAH-AFNET 6 (11%, 78 ± 7 years old, 28% women, CHA2DS2-VASc score 4). Clinical characteristics were not different from patients with shorter AHRE. During a median follow-up of 1.8 years, the primary outcome occurred in 9/132 patients with AHRE ≥24 hours (4.3%/patient-year, 2 strokes) treated with anticoagulation and in 14/127 patients treated with placebo (6.9%/patient-year, 2 strokes). AHRE duration did not interact with the efficacy (p-interaction = 0.65) or safety (p-interaction = 0.98) of anticoagulation. Analyses including AHRE as a continuous parameter confirmed this. Patients with AHRE ≥24 hours developed more ECG-diagnosed atrial fibrillation (17.0%/patient-year) than patients with shorter AHRE (8.2%/patient-year; p &lt; 0.001).CONCLUSIONS: This hypothesis-generating analysis does not find an interaction between AHRE duration and anticoagulation therapy in patients with device-detected AHRE and stroke risk factors. Further research is needed to identify patients with long AHRE at high stroke risk.</p

Oral anticoagulation in device-detected atrial fibrillation: effects of age, sex, cardiovascular comorbidities, and kidney function on outcomes in the NOAH-AFNET 6 trial.

Implanted pacemakers, defibrillators, and loop recorders detect short and rare episodes of device-detected atrial fibrillation [DDAF, previously also called atrial high-rate episodes or subclinical atrial fibrillation (AF)] in ∼30% of patients. Device-detected atrial fibrillation rarely has therapeutic consequences in patients with ECG-documented AF. Device-detected atrial fibrillation without ECG-documented AF can lead to consideration of oral anticoagulation in clinical practice, especially in older patients with multiple stroke risk factors and/or very long DDAF episodes, largely based on observational data. Two recent controlled trials, NOAH-AFNET 6 and ARTESiA, observed a low rate of ischaemic stroke without anticoagulation (1.1%–1.2%/patient-year) in patients with DDAF and stroke risk factors, including in patients with very long DDAF episodes in NOAH-AFNET 6. Current guidelines leave the decision to anticoagulate to clinical judgement, balancing the expected stroke risk, typically estimated by using stroke risk scores developed in patients with ECG-documented AF, and the stroke risk reduction induced by anticoagulation, with the increase in bleeding associated with anticoagulation therapy

Fyziologické mechanismy turbulence srdeční frekvence

Our papers on HRT physiology covered several electrophysiological phenomena associated with turbulent behaviour of sinus nodal discharge after isolated premature beat. Some observations were fairly novel (AV nodal turbulence, QT-turbulence, and HRT after atrial premature complexes), others were confirmative or complementary to the findings of other authors (impact of left ventricular ejection fraction and coupling interval). All of them were helpful for even deeper understanding the fundamental principles involved in HRT that, consequently, may offer an explanation of why HRT is such a potent postinfarction risk stratifier. From the very beginning we tried to suggest that late deceleration phase of HRT does not simply reflect the vagal function but originates from a complex interplay of both sympathetic and parasympathetic systems. Our paper on HRT hemodynamics (Wichterle et al. 2006) together with the article by Segersen et al. (2007) added perhaps &quot;the last piece to the heart turbulence puzzle&quot;, as appreciated in Heart Rhythm editorial by Munich working group (Bauer et al. 2007).Institute for Clinical and Experimental MedicineInstitut klinické a experimentální medicínyFirst Faculty of Medicine1. lékařská fakult

Physiological Mechanisms of Heart Rate Turbulence

Our papers on HRT physiology covered several electrophysiological phenomena associated with turbulent behaviour of sinus nodal discharge after isolated premature beat. Some observations were fairly novel (AV nodal turbulence, QT-turbulence, and HRT after atrial premature complexes), others were confirmative or complementary to the findings of other authors (impact of left ventricular ejection fraction and coupling interval). All of them were helpful for even deeper understanding the fundamental principles involved in HRT that, consequently, may offer an explanation of why HRT is such a potent postinfarction risk stratifier. From the very beginning we tried to suggest that late deceleration phase of HRT does not simply reflect the vagal function but originates from a complex interplay of both sympathetic and parasympathetic systems. Our paper on HRT hemodynamics (Wichterle et al. 2006) together with the article by Segersen et al. (2007) added perhaps "the last piece to the heart turbulence puzzle", as appreciated in Heart Rhythm editorial by Munich working group (Bauer et al. 2007)