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Arrhythmias

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Transmural ablation of all the pulmonary veins: Is it the Holy Grail for atrial fibrillation cure? - Figure 1

Eur. Heart J. (2010), 31 (22), 2708-2711; 10.1093/eurheartj/ehq241 - Click here to view abstract

Schematic of the anatomo-functional arrhythmic mechanism and common ablation strategies in paroxysmal and long-standing/persistent AF. (A) Active triggers arising from the atrial myocardium within the PVs and other thoracic veins (CS, vein/ligament of Marshall, and the SVC) are shown in green. Autonomic ganglia and nerves are shown in yellow. Abrupt changes of fibre orientation along the PV antrum and posterior LA wall favouring anatomic re-entry or high frequency rotors are also shown. (B) The two most common approaches for paroxysmal AF: segmental PV isolation for electric disconnection of triggers within the veins; and circumferential ostial PV isolation (one-by-one linear ablation of the PVs). (C) Simultaneous isolation of the ipsilateral PVs, encircling the antrum and additional linear lesions between the superior and inferior PVs. (D) Combinations of more than two techniques are usually necessary for a successful outcome in long-standing or persistent AF. These approaches include (i) PV isolation; (ii) isolation of the thoracic veins and non-PV triggers; (iii) additional linear lesions such as the ‘mitral isthmus’ line connecting the mitral valve and the lesion encircling the LIPV, a ‘roof’ line connecting the lesions encircling the left and right PVs, a ‘right atrial isthmus’ line, and an ‘anterior’ line connecting the roof line to the mitral annulus anteriorly; (iv) ablation of complex fractionated activity; and (v) ablation of autonomic plexuses. CS, coronary sinus; LAA, left atrial appendage; LIPV, left inferior PV; LSPV, left superior PV; RIPV, right inferior PV; RSPV, right superior PV; SVC, superior vena cava.

Tilt testing and neurally mediated syncope: too many protocols for one condition or specific protocols for different situations? - Figure 1

Eur. Heart J. (2009), 30 (18), 2174-2176; 10.1093/eurheartj/ehp290 - Click here to view the abstract

This figure shows very schematically the different possible afferent pathways of neurally mediated syncope and how tilt testing and the different drugs can act on these different triggers. Tilt testing and nitroglycerin provoke central hypovolaemia by increasing venous pooling; isoproterenol, increases the adrenergic nerve tone, as happens in those cases triggered by fear or pain; clomipramine enhances central serotonergic activity as probably happens in some syncopal centrally induced syncopal episodes.

Psychosis, depression, and high risk for sudden cardiac death: time for co-operation between psychiatrists and cardiologists - Figure 1

Eur. Heart J. (2011) 33 (6), 687; 10.1093/eurheartj/ehr405 - Click here to view the abstract

The triangle of sudden death in psychiatric patients.

Risk stratification for sudden cardiac death: current status and challenges for the future - Figure 1

Eur Heart J (2014) 35 (25): 1642-1651; 10.1093/eurheartj/ehu176 - Click here to view the abstract

Illustration of the potential impact on outcome (survival vs. sudden death) of the interaction between two arrhythmogenic substrates (acute myocardial infarction or heart failure, and mutations causing arrhythmogenic diseases) and predominantly protecting or damaging clusters of common genetic variants (SNPs). As the cluster of SNPs of a given individual reflects the inheritance by the parents, this interaction is clearly governed by chance.

Novel mechanisms in the pathogenesis of atrial fibrillation: practical applications

Eur. Heart J. (2015), Fig 3; 10.1093/eurheartj/ehv375 - click here to view abstract

Individualized mechanistic-based atrial fibrillation management. Various non-invasive substrate based atrial mapping can help to improve phenotyping of AF patients. These may include: (A) atrial pericardial adipose tissue assessment using CMR from Mahajan et al.60; (B) atrial fibrosis detection using LGE-CMR from Daccarett et al.46; (C) non-invasive mapping of AF rotors from Haissaguerre et al.130; (D) assessment of pro-coagulation state; (E) assessment of sympathetic tone from measurement of subcutaneous nerve activity from Robinson et al.123

Another jigsaw piece in the complex picture of hormonal regulation of cardiac repolarization

Eur. Heart J. (),  (), -, Fig 1; 10.1093/eurheartj/ehv475 - click here to view abstract

Oestradiol effects on cardiac ion channels/currents and action potential duration. Illustration of oestradiol effects on KCNH2/HERG (IKr) and Cav1.2α channels (ICa,L) that are mediated either via oestradiol receptors or in a receptor-independent manner (information based on1,6,12,13). Consecutive changes in action potential duration (APD) are depicted in insets. E2, oestradiol; E2 receptor, oestradiol receptor α; HRE, hormone responsive element; Hsp90, heat-shock protein 90; ICa,L, L-type Ca2+ current; IK1, inward rectifier current; IKr, rapid delayed rectifier K+ current; IKs, slow delayed rectifier K+ current; INa, depolarizing Na+ current; Ito, transient outward K+ current; +, increase; –, decrease/blockade; →, prolongation of APD; ←, shortening of APD.

Genetic screening in acquired long QT syndrome? CAUTION: proceed carefully

Eur. Heart J. (2016) 37(18) doi: 10.1093/eurheartj/ehv620 - Click here to view the abstract

The molecular mechanism underlying congenital (cLQTS) and acquired long QT syndrome (aLQTS). The lower panel shows the distribution of QTc duration in health (green line), aLQTS (orange), and cLQTS (red line). The circles display the genetic architecture of the QTc duration, consisting of rare variants (mutations) with a large effect on QTc (red circles), common variants with an intermediate effect on QTc (orange circles), and very common variants with a small effect on QTc. The middle panels show that in aLQTS relatively fewer pathogenic mutations (e.g. mutations in non-pore regions of cardiac ion channels) or multiple common variants may cause mild QT prolongation at baseline and facilitate further QT prolongation upon exposure to acquired triggers. In comparison, in cLQTS, a disease-causing mutation in a transmembrane region of a cardiac ion channel may lead to clinically manifest QT prolongation at baseline, which is further prolonged upon exposure to acquired triggers.

Genetic variants and disease: correlate or cause?

Eur. Heart J. (2016) 37(18) doi: 10.1093/eurheartj/ehv516 - Click here to view the abstract

(A) Expression pattern of Irx3 and connexins in the ventricular conduction system (VCS). Irx3 is expressed in the mature His-Purkinje system. Connexin 40 (Cx40) is co-expressed with Irx3 in the VCS. In the distal Purkinje fibres, Cx43 expression overlaps with that of Cx40. Cx43 is the only significantly expressed connexin in the working myocardium. (B) Schematic illustration of the Iroquois protein structure and the variants reported by Koizumi et al. All Iroquois proteins possess a highly conserved TALE-homeobox domain (TALE-HD) and an Iro motif. Both of the variants found in the probands with idiopathic ventricular fibrillation reside in the C-terminus within a region of unknown function.

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