To the Editor,
We read with interest the Martín García et al.1 paper. The authors analyzed negative deflection of the P wave in precordial lead V1 (NTDV1) which is, in fact, one of the possible patterns of “P-wave terminal force V1” introduced in 1964 by Morris et al.2 He did not study patients with atrial fibrillation (AF) but since his cohort had rheumatic heart disease one can assume that many of them experienced AF. His results showed that P-wave terminal force in V1, ie, NTDV1, “may be abnormal even in the face of normal mean left atrial pressure and normal left atrial size by x-ray examination.” He called it “left atrial involvement” to stress that this electrocardiographic sign is independent of structural or pressure changes of left atrium. Those observations were confirmed later by Robitaille et al.,3 who studied patients with lone AF and found significant differences in NDTV1 between patients with lone AF and the control group.
The report by Martín García et al.1 gives more evidence that NTDV1 is independent of the size of left atrium, a predictor of AF recurrence. Interestingly, NTDV1 can be “positively” modified with pulmonary vein antrum isolation.4 Striated myocardial sleeves of left atrium extend a variable distance into the pulmonary veins. They constitute the arrhythmogenic substrate and triggers implicated in AF.5, 6 Additionally, patients with AF have significantly larger diameters of pulmonary vein.7, 8 In that way NTDV1 may reflect not only retrograde activation of left atrium but enlarged pulmonary veins, most of which are posteriorly activated areas.4
According to Coumel′s triangle of arrhythmogenesis,9 three cornerstones are required for the onset of clinical arrhythmia: the arrhythmogenic substrate, the trigger factor, and the modulation factors such as autonomic nervous system or inflammation. When analyzing NTDV1 we analyze the arrhythmogenic substrate, which could be electrical or structure remodeling of left atrium or both. Electrical remodeling (completely reversible after restoration of sinus rhythm), the result of alterations in ionic changes, eg, L-type Ca2+ current down-regulation, leads to decreases in action potential duration and in conduction velocity. Structural remodeling (a far less reversible process of myocyte loss, diffuse and patchy fibrosis, scarring) leads to nonhomogeneity, slowed conduction and electrical uncoupling in electrical tissue, facilitating AF.10
Restoration of sinus rhythm and continuation with anti-arrhythmic drugs allows us to fight electrical remodeling. In patients with structurally changed atria we need inhibition of angiotensin converting enzyme and angiotensin I receptors (as angiotensin II has a central role in the development of atrial fibrosis) as well as statins and antioxidants. Other substances, including antagonists of the TGF-ß1 pathway and corticosteroids, are under evaluation.10 Pulmonary vein antrum isolation, by eliminating focal triggers, may reverse electrical remodeling but cannot be expected to stop or reverse structural remodeling.
Two groups of patients described by Garcia,1 without and with NTDV1 after cardioversion, most probably had electrical and structural remodeling of left atria, respectively. Modification of NTDV1 with pulmonary vein antrum isolation may be the result of cutting off depolarization of only the most posterior left atrial area.4 In these settings the standard 12-lead ECG tracing with additional evaluation of NTDV1 could appear to be the easiest everyday clinical tool for primary evaluation and further follow-up of patients with AF.
Conflicts of interestMaciej Wojcik was supported by European Heart Rhythm Association (2-year Clinical Electrophysiology Fellowship).
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Corresponding author: m.wojcik@am.lublin.pl