Utility and Limitations of the Surface ECG: Present and Future

Abstract Background Advanced interatrial block (IAB), prolonged and bimodal P waves in surface ECG inferior leads, is an unrecognized surrogate of atrial dysfunction and a trigger of atrial dysrhythmias, mainly atrial fibrillation (AF). Our aim was to prospectively assess whether advanced IAB in sinus rhythm precedes AF and stroke in elderly outpatients with structural heart disease, a group not previously studied. Methods Prospective observational registry that included outpatients aged ≥70 years with structural heart disease and no previous diagnosis of AF. Patients were divided into three groups according to P-wave characteristics. Results Among 556 individuals, 223 had normal P-wave (40.1%), 196 partial IAB (35.3%), and 137 advanced IAB (24.6%). After a median follow-up of 694 days; 93 patients (16.7%) developed AF, 30 stroke (5.4%), and 34 died (6.1%). Advanced IAB was independently associated with AF (hazard ratio [HR] 2.9, 95% confidence interval [CI] 1.7–5.1, p<0.001), stroke (HR 3.8, 95% CI 1.4–10.7, p=0.010), and AF/stroke (HR 2.6, 95% CI 1.5–4.4, p=0.001). P-wave duration (ms) was independently associated with AF (HR 1.05, 95% CI 1.03–1.07, p<0.001), AF/stroke (HR 1.04, 95% CI 1.02–1.06, p<0.001), and mortality (HR 1.04, 95% CI 1.00–1.08, p=0.021). Conclusions The presence of advanced IAB in sinus rhythm is a risk factor for AF and stroke in an elderly population with structural heart disease and no previous diagnosis of AF. P-wave duration was also associated with all-cause mortality. Figure. Age- and sex-adjusted linear and non-linear association between P-wave duration (msec) and atrial fibrillation (A), stroke (B), and atrial fibrillation or stroke (C) risk. Results of a generalized additive model with spline smoothing functions and 4 degrees of freedom. Figure 1. Kaplan-Meyer curves of survival free of atrial fibrillation (A), stroke (B) and atrial fibrillation or stroke (C) in patients with normal P-wave, partial interatrial block (IAB) and advanced IAB. Funding Acknowledgement Type of funding source: None

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Interatrial block is related to atrial dysfunction in hypertensive subjects

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jeaa356.110 ◽

2021 ◽

Vol 22 (Supplement_1) ◽

Author(s):

L Tirapu Sola ◽

F Loncaric ◽

M Mimbrero ◽

LG Mendieta ◽

L Nunno ◽

...

Keyword(s):

Global Longitudinal Strain ◽

Female Gender ◽

Left Ventricular ◽

P Wave ◽

P Value ◽

Atrial Remodeling ◽

Maximal Volume ◽

Surface Ecg ◽

Interatrial Block ◽

And Function

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): La Marató TV3 Background Interatrial block (IAB), a delay of conduction of the sinus stimulus from right to left atria (LA), is defined as surface ECG P-wave duration ≥120 ms. Arterial hypertension (AH) and IAB have been related to development of atrial fibrillation. Aim To investigate the IAB prevalence in a cohort of AH patients and relate it to LA function. Methods 162 patients with well-regulated AT were included. 12-lead ECG were performed and analysed with a digital caliper. 2D and 3D echocardiography were performed, and LA function assessed with speckle-tracking deformation imaging. Results The median age was 56 ± 6 years, 54% were males. Average duration of AH was 10 ± 6 years. IAB was seen in 25% of AH patients. The comparison between groups is shown in Table 1. There were no differences in demographic characteristics, QRS complex duration (p = 0.179) or left ventricular (LV) size and function between subgroups. LA was enlarged in IAB patients, which was coupled with impairment of the LA reservoir strain. Conclusion Our results show considerable prevalence of IAB in AH patients. The demonstrated LA enlargement and function impairment is not associated with LV dysfunction, therefore suggesting an independent role of IAB in atrial remodeling. Table 1 Interatrial block P value Yes (n= 40) No (n= 142) Age 59 (54-62) 57 (53-61) 0.157 Female gender 16 (40%) 58 (48%) 0.467 Duration of Hypertension (years) 10 (6-12) 8 (5-15) 0.421 Systolic blood pressure (mmHg) 136 (125-150) 136 (127-147) 0.799 Diabetes 3 (8%) 16 (13%) 0.410 LVEDV (mL) 73 (63-91) 71 (57-87) 0.424 E/A 0.98 (0.84-1.25) 0.94 (0.79-1.11) 0.230 E/e’ 7.0 (4.9-8.9) 6.6 (5.2-8.4) 0.779 LVEF (%) 63 ± 7 64 ± 6 0.864 LV global longitudinal strain (%) 21.22 ± 2.63 21.19 ± 2.30 0.932 3D LA maximal volume (mL/m2) 36 (30-39) 30 (26-37) 0.028 3D LA minimal volume (mL/m2) 16 (12-18) 14 (11-17) 0.050 LA reservoir strain (%) 27.64 (24.90-31.23) 29.55 (26.17-32.81) 0.032 LA conduit strain (%) 13.91 (10.71-15.47) 14.37 (11.75-16.72) 0.192 LA contractile strain (%) 14.46 (11.86-16.59) 15.52 (13.66-16.96) 0.079 LVEDV Left Ventricular End Dyastolic Volume

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Inducibility, but not stability, of atrial fibrillation is increased by NOX2 overexpression in mice

Cardiovascular Research ◽

10.1093/cvr/cvab019 ◽

2021 ◽

Author(s):

Alexandra S Mighiu ◽

Alice Recalde ◽

Klemen Ziberna ◽

Ricardo Carnicer ◽

Jakub Tomek ◽

...

Keyword(s):

Atrial Fibrillation ◽

Superoxide Production ◽

Right Atrial ◽

Burst Stimulation ◽

Lv Mass ◽

Surface Ecg ◽

Tissue Homogenates ◽

Genotype Difference ◽

Left And Right

Abstract Aims Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling in animal models and predicts incident AF in humans; however, a direct causal role for NOX2 in AF has not been demonstrated. Accordingly, we investigated whether myocardial NOX2 overexpression in mice (NOX2-Tg) is sufficient to generate a favourable substrate for AF and further assessed the effects of atorvastatin, an inhibitor of NOX2, on atrial superoxide production and AF susceptibility. Methods and results NOX2-Tg mice showed a 2- to 2.5-fold higher atrial protein content of NOX2 compared with wild-type (WT) controls, which was associated with a significant (twofold) increase in NADPH-stimulated superoxide production (2-hydroxyethidium by HPLC) in left and right atrial tissue homogenates (P = 0.004 and P = 0.019, respectively). AF susceptibility assessed in vivo by transoesophageal atrial burst stimulation was modestly increased in NOX2-Tg compared with WT (probability of AF induction: 88% vs. 69%, respectively; P = 0.037), in the absence of significant alterations in AF duration, surface ECG parameters, and LV mass or function. Mechanistic studies did not support a role for NOX2 in promoting electrical or structural remodelling, as high-resolution optical mapping of atrial tissues showed no differences in action potential duration and conduction velocity between genotypes. In addition, we did not observe any genotype difference in markers of fibrosis and inflammation, including atrial collagen content and Col1a1, Il-1β, Il-6, and Mcp-1 mRNA. Similarly, NOX2 overexpression did not have consistent effects on RyR2 Ca2+ leak nor did it affect PKA or CaMKII-mediated RyR2 phosphorylation. Finally, treatment with atorvastatin significantly inhibited atrial superoxide production in NOX2-Tg but had no effect on AF induction in either genotype. Conclusion Together, these data indicate that while atrial NOX2 overexpression may contribute to atrial arrhythmogenesis, NOX2-derived superoxide production does not affect the electrical and structural properties of the atrial myocardium.

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