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Dexmedetomidine (DEX) is a commonly used sedative agent with no or minimal effects on breathing. DEX may also be beneficial in myocardial protection. Since the mechanisms of cardiac effects are not well known, we carried out a descriptive review and examined the effects of DEX on myocardial electrical conduction in a prospective and controlled manner. For the review, clinical studies exploring DEX in myocardial protection published between 2020-2022 were explored. A case study included 11 consecutive patients at a median (range) age of 48 (38-59), scheduled for elective radiofrequency ablation of paroxysmal atrial fibrillation. A bolus dose of DEX 1 µg/kg given in 15 min was followed by a continuous infusion of 0.2-0.7 µg/kg/h. Direct intracardiac electrophysiologic measurements, hemodynamics and oxygenation were measured before and after the DEX bolus. Experimental studies show that DEX protects the heart both via stabilizing cardiac electrophysiology and reducing apoptosis and autophagy after cell injury. The clinical evidence shows that DEX provides cardiac protection during different surgeries. In a clinical study, DEX increased the corrected sinus node recovery time, prolongated the atrioventricular (AV) nodal refractory period and cycle length producing AV nodal Wenckebach retrograde conduction block. DEX has a putative role in organ protection against hypoxic, oxidative and reperfusion injury. DEX slows down the firing of the sinus node and prolongs AV refractoriness.

Aims: LMNA- cardiomyopathy is often associated with pathology in the cardiac conduction system necessitating device implantations. The aim was to study the timing and types of device implantations and need for re-implantations in LMNA mutation carriers., Methods: We studied the hospital records of 60 LMNA mutation carriers concerning device implantations and re-implantations and their indications. Data were collected until April 2019., Results: The median follow-up time from the first ECG recording to the last clinical follow-up, transplantation, or death was 7.7 (IQR=9.1) years. Altogether 61.7% (n=37) of the LMNA mutation carriers received a pacemaker or an implantable cardioverter defibrillator (ICD), and of them 27.0% (n=10) needed a device upgrade. Notably, in some patients the upgrade took place very soon after the first implantation. The first device was implanted at an average age of 47.9 years (SD=9.5), whereas the upgrade took place at an average age of 50.3 years (SD=8.1). Most upgrades were ICD implantations. Male patients underwent device upgrade more often and at a younger age than women. By the end of follow-up, 35.0% (n=21) of the patients fulfilled echocardiographic criteria for dilated cardiomyopathy, and 90.5% of them (n=19) needed pacemaker implantation., Conclusion: Most LMNA mutation carriers underwent pacemaker implantation in this study. Due to the progressive nature of LMNA -cardiomyopathy, device upgrades are quite common. An ICD should be considered when the initial device implantation is planned in an LMNA mutation carrier., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Aims: Alteration in conduction from right to left atrium (LA) is linked to susceptibility to atrial fibrillation (AF). We examined whether different inter-atrial conduction pathways can be identified non-invasively by magnetocardiographic mapping (MCG)., Methods and Results: In 27 patients undergoing catheter ablation of paroxysmal AF, LA activation sequence was determined during sinus rhythm using invasive electroanatomic mapping. Before this, 99-channel magnetocardiography was recorded over anterior chest. The orientation of the magnetic fields during the early (40-70 ms from P onset) and later part (last 50%) of LA depolarization was determined using pseudocurrent conversion. Breakthrough of electrical activation to LA occurred through Bachmann bundle (BB) in 14, margin of fossa ovalis (FO) in 3, coronary sinus ostial region (CS) in 2, and their combinations in 10 cases by invasive reference in total of 29 different P-waves. Based on the combination of pseudocurrent angles over early and late parts of LA activation, the MCG maps were divided to three types. These types correctly identified the LA breakthrough sites to BB, CS, FO, or their combinations in 27 of 29 (93%) cases., Conclusion: Magnetocardiographic mapping seems capable of distinguishing inter-atrial conduction pathways. Recognizing the inter-atrial conduction pattern may assist in understanding the pathogenesis of AF and identifying the subgroups for patient-tailored therapy.

Background: Plasma B-type natriuretic peptide (BNP), as well as the N-terminal part of the prohormone (Nt-BNP), are frequently elevated in aortic valve stenosis (AS). Yet, their release from the heart into the circulation has never been directly studied in AS., Aim: To assess the release of Nt-BNP in AS with focus on the identification of its main determinants., Methods: We studied 49 adult patients undergoing preoperative cardiac catheterization for isolated AS. Blood was sampled from the aortic root and the coronary sinus for Nt-BNP determination by immunoassay., Results: The mean (+/-S.E.) transcardiac Nt-BNP step-up averaged 79+/-53 pmol/l in 11 control patients free of structural heart disease, 75+/-32 pmol/l in 31 AS patients free of heart failure (HF), 236+/-62 pmol/l in 8 AS patients with diastolic HF (ejection fraction > or = 50%, pulmonary wedge pressure > 14 mm Hg) and 469+/-66 pmol/l in 7 AS patients with systolic HF (ejection fraction < 50%, wedge pressure > 14 mm Hg) (p<0.001). The transcardiac Nt-BNP gradient was independently associated with left ventricular (LV) end-diastolic pressure (beta=0.47, p<0.001) and ejection fraction (beta=-0.29, p<0.019) and with co-existent coronary artery disease (beta=0.23, p=0.050)., Conclusion: LV diastolic and systolic dysfunction along with coronary artery disease are likely to be the key determinants of cardiac Nt-BNP release in AS. The transcardiac Nt-BNP gradient increases on average three-fold with the development of diastolic HF and six-fold in systolic HF.

Objectives: The study aimed to assess the hemodynamic and neuroendocrine effects of candoxatril and frusemide compared with placebo in patients with mild chronic heart failure., Background: Candoxatril is an atriopeptidase inhibitor. It increases circulating levels of atrial natriuretic peptide leading to natriuresis and diuresis, which alleviate the symptoms of a failing heart., Methods: This was a multicenter, randomized, double-blind study. Forty-seven patients with mild stable chronic heart failure received candoxatril 400 mg/day, frusemide 40 mg/day or placebo for up to six weeks. Cardiac indices were determined at rest and during exercise, and blood samples were taken for laboratory analysis. Assessments were performed at baseline (day 0) and after six weeks (day 42)., Results: In comparison with placebo, both drugs significantly reduced mean pulmonary capillary wedge pressure following the first dose administration. Only candoxatril significantly reduced pulmonary capillary wedge pressure during exercise on day 0, while both drugs significantly reduced this parameter on day 42. Changes in the remaining hemodynamic parameters were comparable for both drugs relative to placebo. Frusemide significantly increased mean plasma renin activity (days 0 and 42), and the mean aldosterone concentration (day 42) in comparison with placebo, whereas candoxatril caused no significant changes in any of the hormonal parameters assessed., Conclusions: These results show that candoxatril, 400 mg/day, has a similar hemodynamic profile to frusemide, 40 mg/day, but it does not induce adverse neuroendocrine effects. Candoxatril therefore appears to offer a clinically significant advantage over frusemide, providing an alternative therapeutic approach to the treatment of patients with mild stable chronic heart failure.