Long-term effects of beta blocker therapy on P-wave duration and dispersion in congestive heart failure patients: A new effect?

Prevalence of P wave dispersion and interatrial block in patients with systolic heart failure and their relationship with functional status, hospitalization and one year mortality

“…Similarly, it was reported that patients with low LVEF had PWD, and that the use of beta blockers improved HF and PWD 13 . It was reported that IAB is common even in hospitalized patients regardless the etiology (41.1%), especially in patients >60 years 14 …”

The Effects of Trimetazidine on P‐Wave Duration and Dispersion in Heart Failure Patients

“…Camsari et al 13 have also reported that PWD and Pmax were decreased significantly 6 months after addition of beta‐blocker therapy in 42 congestive heart failure patients. There were significant correlations between LVEF and Pmax and PWD 13 .…”

“…Camsari et al 13 have also reported that PWD and Pmax were decreased significantly 6 months after addition of beta‐blocker therapy in 42 congestive heart failure patients. There were significant correlations between LVEF and Pmax and PWD 13 . Senen et al 4 evaluated 72 patients with dilated cardiomyopathy and found significantly higher Pmax and PWD in patients with dilated cardiomyopathy than those of healthy subjects.…”

The Resting Electrocardiogram in the Management of Patients with Congestive Heart Failure: Established Applications and New Insights

“…(8) persistent ST elevation in association with predominantly positive QRS complexes (usually V5 and V6) in the presence of LBBB suggestive of ventricular aneurysm and DCM, 11 (9) persistent ST elevation in association with predominantly positive QRS complexes (usually V1‐V3) in the presence of RBBB suggestive of ventricular aneurysm and DCM, 12 (10) low amplitude QRS complexes suggestive of mutual electrical cancellation of large myocardial zones of infarction opposite each other, 13,14 although this feature is also found in some patients with chronic nonischemic DCM, 15,16 and acute myocarditis, with transient cardiac dilatation and CHF 17 (it is a misconception that low amplitude QRS complexes is a specific feature of restrictive or infiltrative cardiomyopathy without cardiac dilatation), (11) low amplitude of the limb leads, with high voltage of the precordial leads, and an R/S ratio <1.0 in lead V4, which has been described to be associated with CHF, 18 (12) the “strain pattern” in hypertensive patients with ECG LVH, receiving aggressive blood pressure lowering, which was found to be predictive of new onset of, and dying from, CHF, 19 although it was not independently predictive of those patients with more severe diastolic dysfunction 20 . The ECG, in general, has not been implemented prospectively as a predictor for the development of CHF; this will require studies with long follow‐up and serial ECGs, in patients at risk, (13) an LBBB‐like ECG pattern, found in patients with CHF and pacemakers or implantable cardioverter/defibrillators (ICD), (14) an intraventricular conduction delay ECG pattern, seen in patients with CHF and implanted CRT systems, (15) a widened P wave in limb and precordial leads, an increase in P‐wave dispersion, and an accentuated negative component of the P wave in lead V1, found in patients with CHF, and which indicate intra‐atrial block, 21 left atrial hypertrophy, hypertension, or dilatation (not specific for any of the four), which predict emergence of atrial fibrillation in patients with CHF, and show dynamic changes with therapy 22,23 . Studies on short‐term and long‐term changes of the accentuated negative component of the P wave in V1 in response to therapy of CHF are needed, similar to the ones carried out in the follow‐up of patients with mitral stenosis, post balloon commissurotomy, (16) increase in the QRS duration, which reflects the severity of CHF, and which shows lengthening or shortening when patients with CHF decompensate, or improve 24,25 .…”

“…20 The ECG, in general, has not been implemented prospectively as a predictor for the development of CHF; this will require studies with long follow-up and serial ECGs, in patients at risk, (13) an LBBB-like ECG pattern, found in patients with CHF and pacemakers or implantable cardioverter/defibrillators (ICD), (14) an intraventricular conduction delay ECG pattern, seen in patients with CHF and implanted CRT systems, (15) a widened P wave in limb and precordial leads, an increase in P-wave dispersion, and an accentuated negative component of the P wave in lead V1, found in patients with CHF, and which indicate intra-atrial block, 21 left atrial hypertrophy, hypertension, or dilatation (not specific for any of the four), which predict emergence of atrial fibrillation in patients with CHF, and show dynamic changes with therapy. 22,23 Studies on short-term and long-term changes of the accentuated negative component of the P wave in V1 in response to therapy of CHF are needed, similar to the ones carried out in the follow-up of patients with mitral stenosis, post balloon commissurotomy, (16) increase in the QRS duration, which reflects the severity of CHF, and which shows lengthening or shortening when patients with CHF decompensate, or improve. 24,25 The QRS duration at baseline is not predictive of response to CRT, and although significant reduction in QRS duration after such therapy is noted in responders, the individual response varies highly, not allowing the decrease of the QRS postimplantation to be employed as a predictor of eventual response, 9 (17) prolongation of the QTc interval, noted in patients with CHF, 26,27 (18) a wide frontal QRS/T angle, ST-segment depression in lead V5, and high T-wave amplitude in V1, which are prognostic of incident CHF in postmenopausal women, 28 (19) a QTc ≥ 487 ms, a QRS dispersion ≥ 42.7 ms, voltage criteria for LVH, two ambulatory ECGs, and three non-ECG parameters, which stratified outpatients with CHF into subgroups with high and low mortality risk.…”