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Abstract: Introduction: Although macroreentrant atrial tachycardia (MRAT) and focal atrial tachycardia (FAT) can be successfully cured by catheter ablation, the proper diagnosis and treatment of these arrhythmias can still be challenging. Aim: The objective of this study is to develop an algorithm allowing rapid diagnosis of the mechanism and the chamber of origin of atrial tachycardia based on intracardiac catheter recordings from the right atrium and the coronary sinus (CS). Methods: A 2-stepped algorithm was designed: (1) The time of biatrial activation expressed as a percentage of the tachycardia cycle length served to discriminate FAT from MRAT. (2) In FAT, the direction of activation of the CS catheter and the earliest atrial activation were used to define the chamber of origin. In MRAT, the time of right atrium activation was determined or entrainment was used at different sites. Thirty-two intracardiac recordings were reviewed off-line after the algorithm by 4 electrophysiologists blinded to the mechanism and the chamber of origin. The results of their analysis were compared with the intraoperative diagnosis. Results: The algorithm correctly identified 11 (100%) of 11 FATs and 19 (90.4%) of 21 MRATs. The site of origin was correctly identified in 8 (72.7%) of 11 FATs and in 20 of 21 (95.2%) MRATs. The site of origin was misidentified in 3 FATs, all arising from the CS ostium. Conclusions: This algorithm allows rapid discrimination between FAT and MRAT. The chamber of origin is detected with a high accuracy in MRAT. However, the earliest atrial activation taken as an isolated event is not a good predictor for the chamber of origin in FAT arising from the ostium of the CS. [Copyright &y& Elsevier]

Abstract: Objective: β-Adrenergic stimulation modulates cardiac contractility through protein kinase A (PKA), which phosphorylates proteins such as troponin I (cTnI) and C-protein (cMyBP-C). The relative contributions of cTnI and cMyBP-C to the regulation of myofilament Ca2+ sensitivity are still controversial because of difficulty in targeting specific protein phosphorylation. Recently, impaired relaxation was found in cMyBP-C-deficient mice (KO) in vivo under basal conditions and after β-adrenergic stimulation. The goal of this study was to analyse the length-dependent and PKA-dependent modulations of the cardiac contractile machinery in a mouse model lacking cMyBP-C. Methods: In the present work, we studied the PKA effect on myofilament Ca2+ sensitivity of left ventricular skinned myocytes isolated from 5-week- and 55-week-old wild-type (WT) and cMyBP-C knockout (KO) mice at 1.9 and 2.3 μm sarcomere lengths (SL). The cTnI content and phosphorylation status were examined by Western blot analysis. Results: Without PKA stimulation and at the shorter SL, Ca2+ sensitivity was higher in KO compared to WT. The difference disappeared at the longer SL. No difference in passive tension or maximal active tension was observed. PKA stimulation induced a desensitization of WT myofilaments at both SL but had almost no effect in KO myofilaments despite similar levels of cTnI phosphorylation. We also observed expression of slow skeletal TnI in KO animals that was not correlated with the PKA effects. Conclusion: The results suggest that cMyBP-C contributes to the regulation of cardiac contraction at short sarcomere length and that myofilament desensitization induced by PKA requires the presence of cMyBP-C and does not depend only upon TnI phosphorylation. [Copyright &y& Elsevier]

Presents a study that examined the physiological and pathological stretch-dependent regulation of cardiac contractility using rat isolated skinned cardiomyocytes from normal and diseased hearts. Passive properties of control and PMI cardiomyocytes; Transmural gradient of stretch-dependent contractile properties; Conclusions and significance.