P-wave Terminal Force In Lead V1 Research Articles

Relation of Electrocardiographic Left Atrial Abnormalities to Risk of Stroke in Patients with Atrial Fibrillation

The P-wave terminal force in lead V1 (PTFV1) on the 12-lead electrocardiogram (ECG) quantifies left atrial (LA) structural and electrophysiologic abnormalities. We aimed to evaluate the association between PTFV1 and cerebrovascular accident (CVA) as well as LA structure and function in patients with atrial fibrillation (AF). We conducted a cross-sectional study of 229 patients with AF (60 ± 10years, 72% men) with (n = 21) and without (n = 208) a history of CVA, who underwent preablation ECG and cardiac magnetic resonance in sinus rhythm. PTFV1 was defined as the duration (in milliseconds) of the downward deflection of the P wave in lead V1 multiplied by the absolute value of its amplitude (in microvolts) on ECG. PTFV1 is associated with LA minimum volume (Vmin) and left ventricular ejection fraction but not associated with the extent of LA fibrosis quantified by cardiac magnetic resonance late gadolinium enhancement. In addition, PTFV1 is associated with CVA independent of the CHA2DS2-VASc score and LA Vmin (odds ratio 1.23; 95% confidence interval 1.08 to 1.40; p = 0.002). Furthermore, PTFV1 has an incremental value over the CHA2DS2-VASc score as a marker of CVA (p <0.001). In conclusion, ECG-defined PTFV1 is independent marker of stroke in patients with AF and reflects the underlying LA remodeling. Our findings suggest that evaluation of PTFV1 can improve the current risk stratification of stroke.

Diagnostic value of electrocardiographic P-wave characteristics in atrial fibrillation recurrence and tachycardia-induced cardiomyopathy after catheter ablation.

Abnormal P-wave characteristics were reportedly associated with left ventricular interstitial fibrosis as defined by cardiac magnetic resonance images. The objective of this study is to investigate the utility of P-wave characteristics to predict atrial fibrillation (AF) recurrence and the recovery of left ventricular systolic dysfunction (LVSD) after catheter ablation (CA) for AF. Two hundred and five AF patients (109 paroxysmal and 96 persistent) who underwent CA were enrolled. We measured maximum P-wave duration (max PWD) and P-wave terminal force in lead V1 (PTFV1) calculated as a product of P-wave terminal amplitude (PTaV1) and duration (PTdV1) in lead V1 during sinus rhythm. AF recurrence was noted in 50 patients at 12months after CA. Patients with AF recurrence had a higher prevalence of persistent AF, a larger left atrial volume, and a longer max PWD than those without. We divided the patients into 2 groups: 156 patients with left ventricular ejection fraction (LVEF) > 45% and 49 patients with LVEF ≤ 45% (Low-EF group). In Low-EF group, tachycardia-induced cardiomyopathy (TIC) was defined as improvement in LVEF ≥ 15% or LVEF ≥ 50% at 5months after CA. TIC and non-TIC groups consisted of 37 and 12 patients, respectively. Max PWD, PTFV1, PTdV1, and PTaV1 were significantly greater in non-TIC-group than in TIC-group. PTFV1 had the highest diagnostic accuracy to discriminate between TIC and no-TIC-groups; cut-off value for PTFV1 was determined as 56.7mVms (area under the ROC curve = 0.80; 75% sensitivity; and 76% specificity). Max PWD was a useful predictor of AF recurrence and the complete recovery of LVSD after CA. PTFV1 had the highest diagnostic accuracy to discriminate between TIC and no-TIC-groups.

Usefulness of Electrocardiographic Left Atrial Abnormality to Predict Response to Cardiac Resynchronization Therapy in Patients With Mild Heart Failure and Left Bundle Branch Block (a Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy Substudy)

Cardiac resynchronization therapy (CRT) has proven prognostic benefits in patients with heart failure (HF) with left bundle branch block (LBBB) QRS morphology. Electrocardiographic left atrial (LA) abnormality has been proposed as a noninvasive marker of atrial remodeling. We aimed to assess the impact of electrocardiographic LA abnormality for prognosis in patients with HF treated with CRT. Baseline resting 12-lead electrocardiograms recorded from 941 patients enrolled in the CRT arm of the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy was processed automatically using Glasgow algorithm, which included automated assessment of P-wave terminal force in lead V1 (PTF-V1) as a marker of LA abnormality. A PTF-V1 of ≥0.04 mm⋅s was considered abnormal. The primary end point was HF event and/or death. Total mortality and appropriate defibrillator therapies were the secondary end points. At baseline 550, patients treated with CRT with a defibrillator had LBBB QRS morphology and normal PTF-V1. Normal PTF-V1 was associated with significant risk reduction for all assessed end points and for the primary end point comprised a hazard ratio of 0.55 (95% confidence interval 0.36 to 0.84) compared with patients with LBBB with abnormal PTF-V1 (n = 120), and a hazard ratio of 0.42 (95% confidence interval 0.32 to 0.55) compared with patients with implanted defibrillator (n = 729). In CRT-treated patients with HF, electrocardiographic LA abnormality appears to be an electrocardiographic indicator of poor long-term outcome in patients with LBBB. In conclusion, our data suggest that PTF-V1 bears additive prognostic information in the context of CRT, thus further strengthening the role of electrocardiographic diagnostics in risk stratification of patients with HF.

The association between acute mental stress and abnormal left atrial electrophysiology.

Acute stress may trigger atrial fibrillation (AF), but the underlying mechanisms are unclear. We examined if acute mental stress results in abnormal left atrial electrophysiology as detected by more negative deflection of P-wave terminal force in lead V1 (PTFV1 ), a well-known marker of AF risk. We examined this hypothesis in 422 patients (mean age =56 ± 10 years; 61% men; 44% white) with stable coronary heart disease who underwent mental (speech task) stress testing. PTFV1 was defined as the duration (milliseconds) times the value of the depth (μV) of the downward deflection (terminal portion) of the P-wave in lead V1 measured on digital electrocardiograms (ECG). Electrocardiographic left atrial abnormality was defined as PTFV1 ≤ -4000 μV*ms. Mean PTFV1 values during stress and recovery were compared with rest. The percentage of participants who developed left atrial abnormality during stress and recovery was compared with the percentage at rest. Compared with rest, PTFV1 became more negative during mental stress (mean change = -348, 95% CI = [-515, -182]; P<0.001) and no change was observed at recovery (mean change =12, 95%CI = [-148, 172]; P=0.89). A larger percentage of participants showed left atrial abnormality on ECGs obtained at stress (n=163, 39%) and recovery (n=142, 34%) compared with rest (n=127, 30%). Acute mental stress alters left atrial electrophysiology, suggesting that stressful situations promote adverse transient electrical changes to provide the necessary substrate for AF.

P-Wave Terminal Force in Lead V1 Predicts Paroxysmal Atrial Fibrillation in Acute Ischemic Stroke

Detection of paroxysmal atrial fibrillation (PAF) in cryptogenic stroke is critical to selecting an antithrombotic therapy for preventing recurrent stroke. However, the predictor of PAF in patients with acute ischemic stroke is not well elucidated. P-wave terminal force in lead V1 (PTFV1) is a standard electrocardiogram marker of left atrial abnormality. In this study, we aimed to investigate the utility of PTFV1 for the prediction of PAF in patients with acute ischemic stroke. The study included 295 consecutive patients who had acute ischemic stroke and were admitted to the hospital between September 2014 and August 2016. Patients with a known history of PAF, persistent atrial fibrillation, or cardiac pacemaker were excluded from the study. The clinical characteristics of patients with or without PAF were compared, and multiple logistic regression analysis was performed to assess the independent contribution of each variable. Among 226 patients eligible for our analysis, 16 (7.1%) were diagnosed with PAF after admission. PTFV1 was significantly higher in patients with PAF than those without PAF (.051 versus .027 mm⋅s; P < .001). Multivariate analysis showed that PTFV1 per .01 mm⋅s increase was strongly associated with PAF (odds ratio, 1.61; 95% confidence interval, 1.24-2.09; P < .001). The optimal cutoff value of PTFV1 for the prediction of PAF was .04 mm⋅s. PTFV1 is a strong predictor of PAF detection in acute ischemic stroke.

Association between electrocardiographic and echocardiographic markers of stage B heart failure and cardiovascular outcome.

AimsThe detection of non‐ischaemic (mainly hypertension, diabetes, and obesity) stage B heart failure (SBHF) may facilitate the recognition of those at risk of progression to overt HF and HF prevention. We sought the relationship of specific electrocardiographic (ECG) markers of SBHF to echocardiographic features of SBHF and their prognostic value for development of HF. The ECG markers were Cornell product (Cornell‐P), P‐wave terminal force in lead V1 (PTFV1), ST depression in lead V5 V6 (minSTmV5V6), and increased heart rate. Echocardiographic assessment of SBHF included left ventricular hypertrophy (LVH), impaired global longitudinal strain (GLS), and diastolic dysfunction (DD).Method and resultsAsymptomatic subjects ≥65 years without prior cardiac history, but with HF risks, were recruited from the local community. At baseline, they underwent clinical assessment, 12‐lead ECG, and comprehensive echocardiography. New HF was assessed clinically at mean follow‐up of 14 ± 4 months, and echocardiography was repeated in subjects with HF. Of the 447 study subjects (age 71 ± 5, 47% men) with SBHF, 13% had LVH, 32% impaired GLS, and 65% ≥grade I DD (10% ≥grade II DD). Forty were lost to follow‐up. Clinical HF developed in 47 of 407, of whom 20% had echocardiographic LVH, 51% abnormal GLS, and 76% DD at baseline. Baseline LVH and abnormal GLS (not grade I DD) were independently associated with outcomes (clinical HF and cardiovascular death). Cornell‐P and heart rate (not minSTmV5V6 nor PTFV1) were independently associated with LVH, impaired GLS, and DD. Cornell‐P and minSTV5V6 (not heart rate nor PTFV1) were independently associated with outcomes. More ECG abnormalities improved sensitivity, but ECG‐markers were not independent of or incremental to echocardiographic markers to predict HF in SBHF.ConclusionsIn this elderly study population, ECG markers showed low diagnostic sensitivity for non‐ischaemic SBHF and low prognostic value for outcomes. Cornell‐P and minSTmV5V6 had predictive value for outcomes in non‐ischaemic SBHF independent of age, gender, and common comorbidities but were not incremental to echocardiography.

Abstract 46: The Association between Acute Mental Stress and Changes in Left Atrial Electrophysiology

Background: Acute stress may trigger atrial fibrillation, but the mechanisms are not clear. We hypothesized that acute mental stress results in abnormal atrial remodeling via electrophysiologic effects. Methods: We examined our hypothesis in 168 patients (mean age=63±8.7 years; 74% men; 65% Caucasian) with stable coronary heart disease who underwent mental (speech task) stress testing. PTFV 1 duration (ms) times the value of the depth (μV) of the downward deflection (terminal portion) of the median P-wave in lead V 1 , and was automatically measured on digital electrocardiograms (ECG) at rest, stress, recovery. Electrocardiographic left atrial abnormality was defined as P-wave terminal force in lead V1 (PTFV1) ≤ -4000 μV*ms. The mean values of PTFV 1 during stress and recovery were compared with rest. Additionally, the percentage of participants who had left atrial abnormality during stress and recovery was compared with those at rest. Results: The mean PTFV 1 at rest was -2857±2459 μV*ms. There were 51 (30%) participants who had baseline left atrial abnormality. Compared with rest, PTFV 1 became more negative with stress [mean change=-474, 95%CI=(-103, -845); p=0.013] and during recovery [mean change=-420, 95%CI=(-79, -761); p=0.016]. A larger percentage of participants showed left atrial abnormality during stress (n=63, 38%) and recovery (n=67, 40%) compared with rest. Similar changes in PTFV 1 with stress [mean change=-833, 95%CI=(-372, -1295); p&lt;0.001] and recovery [mean change=-796, 95%CI=(-389, -1204); p&lt;0.001] were observed when we excluded those with baseline left atrial abnormality. No differences were noted in the PTFV 1 response based on age, gender, race, or hemodynamic response to stress. Conclusion: Acute mental stress alters left atrial electrophysiology, as measured by PTFV 1 , suggesting that stressful situations promote adverse atrial remodeling. This possibly explains the poor cardiovascular outcomes associated with acute mental stress that are triggered by left atrial abnormalities such as atrial arrhythmias and stroke.

Abstract WMP64: Utility of Left Atrial Abnormality on Admission Electrocardiography in Acute Ischemic Stroke

Introduction and Hypothesis: Clinical categorization of ischemic stroke is very important to select the antithrombotic therapy for preventing the recurrent stokes. However, about 25% of ischemic stroke is the stroke for undetermined cause, termed as cryptogenic stroke. Recently, proactive detecting of paroxysmal atrial fibrillation (PAF) in cryptogenic stroke has gained attention. P-wave terminal force in lead V1 (PTFV1) of electrocardiography (ECG) is a specific indicator of left atrial abnormality. In this study, we tested PTFV1 for the utility of PAF detection and further clinical categorization in acute ischemic stroke. Methods: One hundred forty eight consecutive acute ischemic stroke patients were admitted to our hospital from September 2014 to March 2016. We included 105 patients (mean age 72.8±13.4 years), who had sinus rhythm on admission 12-lead ECG without atrial fibrillation, or cardiac pacing. PTFV1 (mmхsec) of participants was assessed, and had analyzed the association with PAF detection in a 24-hour ECG monitoring and clinical categories of ischemic stroke. Results: PTFV1 was significantly higher in the patients with PAF (n=11) than in those without PAF (0.049±0.024 vs 0.031±0.027; p&lt;0.05). Multiple logistic regression analysis revealed that PTFV1 was an independent predictor for PAF detection (odds ratio, 1.46; 95% confidence interval, 1.02-2.08; p&lt;0.05). According to the clinical categorization, PTFV1 of cardioembolic stroke (0.061±0.022) was significantly higher, compared to lacunar stroke (0.018±0.019; p&lt;0.01), atherothrombotic stroke (0.035±0.026; p&lt;0.05), and cryptogenic stroke (0.031±0.029; p&lt;0.05). The proportion of patients with left atrial abnormality defined by PTFV1 (≧0.04), was 10 out of 11 (91%) for cardioembolic stroke, and 10 out of 27 (37%) for cryptogenic stroke. Conclusions: PTFV1 on admission ECG in acute ischemic stroke was a strong predictor for PAF detection and cardioembolic stroke diagnosis. Extended ECG monitoring may be useful in cryptogenic stroke with left atrial abnormality defined by PTFV1.

The P-wave terminal force in embolic strokes of undetermined source

BackgroundThe Embolic Stroke of Undetermined Source (ESUS) is a recently developed clinical construct which describes stroke patients for whom the embolic source remains undetermined despite recommended investigations. The aim of the study was to characterize the ESUS population according to the abnormality in the P-wave terminal force in lead V1 (PTFV1). MethodsWe retrospectively identified consecutive patients hospitalized for acute ischemic stroke who met the ESUS diagnostic criteria. The PTFV1 was obtained from the admission 12-lead ECG. Increased PTFV1 was defined a value >5000μV·ms. Baseline and diagnostic work-up findings were compared between the PTFV1 patient groups. ResultsAmong 109 patients with ESUS, 31 (28.4%) had evidence of increased PTFV1. The patients with the ECG-defined left atrial abnormality had higher rates of hypertension (77.4% versus 55.1%; p=0.031), history of prior stroke or TIA (35.5% versus 16.7%; p=0.032), and moderate to severe left atrial enlargement (29.0% versus 7.7%; p=0.004) and ventricular hypertrophy (35.5% versus 16.7%; p=0.032), whereas they were less likely to have patent foramen ovale (9.7% versus 28.2%, p=0.038) and unstable sub-stenotic atherosclerosis of aortic arch and cranial arteries (12.9% versus 32.1%, p=0.041). ConclusionsThe abnormally increased PTFV1 was observed in about one third of patients with ESUS and it was inversely associated with artery-to artery and paradoxical potential sources of stroke. Left atrial cardiopathy could be involved in the ESUS pathogenesis and the ECG-defined abnormality could point towards the risk of cardiac embolism.

Electrocardiographic left atrial abnormalities and risk of incident stroke in hypertensive patients with electrocardiographic left ventricular hypertrophy.

Recent findings in population-based studies suggest that abnormal P wave terminal force in lead V1 (PTFV1), a marker of left atrial abnormalities such as fibrosis, dilatation and elevated filling pressures, is associated with incident ischemic stroke, even in the absence of atrial fibrillation. However, whether PTFV1 predicts incident stroke in hypertensive patients during blood pressure lowering has not been examined. Risk of incident stroke was examined in relation to abnormal PTFV1 on a baseline ECG in 7778 hypertensive patients with ECG left ventricular hypertrophy, no history of atrial fibrillation, in sinus rhythm on their baseline ECG with no incident atrial fibrillation during follow-up, who were randomly assigned to losartan-based or atenolol-based treatment. Results focused on the subset of patients between 55 and 60 years old (n = 1879) because of a significant interaction between PTFV1 and age in Cox analyses. Abnormal PTFV1 was defined by the presence of a negative terminal P wave in lead V1 with amplitude × duration ≥ 4000 μV ms. During mean follow-up of 4.8 ± 0.9 years, 364 patients (4.7%) of the overall study population and 45 patients (2.4%) in the subset of patients aged 60 years or less experienced a definite stroke. In the overall population, abnormal PTFV1 was not a significant predictor of incident stroke [hazard ratio 1.12, 95% confidence interval (CI) 0.91-1.38, P = 0.301], but there was a highly significant interaction of PTFV1 with age stratified at 60 (P = 0.009, hazard ratio 2.30, 95% CI 1.27-4.13, P = 0.006 for abnormal PTFV1 in the interaction model). Further analyses in the subset of patients aged 60 years or less revealed a higher incidence of stroke occurred in those with abnormal than normal baseline PTFV1: incidence rate per 1000 person-years, 7.8 (95% CI 5.2-11.4) vs 3.4 (95% CI 2.2-5.2; P = 0.004); a greater than two-fold increased risk of incident stroke (hazard ratio 2.31, 95% CI 1.28-4.16, P = 0.005) in univariate Cox analysis; and in multivariable Cox regression models that adjusted for other significant predictors of incident stroke in this population (sex, history of stroke or transient ischemic attack, ischemic heart disease or diabetes, baseline creatinine and in-treatment SBP), that abnormal PTFV1 remained associated with a greater than two-fold increased risk of incident stroke (hazard ratio 2.06; 95% CI 1.14-3.74, P = 0.017). Abnormal PTFV1, a marker of left atrial abnormality, was strongly associated with incident stroke in hypertensive patients, independent of in-treatment SBP and other predictors of incident stroke. This association, in the absence of detectable atrial fibrillation, suggests that an underlying atrial cardiopathy may cause left atrial thrombus formation and a subsequent stroke without intervening clinically recognized atrial fibrillation.

Relationship between abnormal P-wave terminal force in lead V1 and left ventricular diastolic dysfunction in hypertensive patients: the LIFE study

Background: Abnormal P-wave terminal force in lead V1 (PTF-V1) is an ECG marker of increased left atrial (LA) volume, elevated LA filling pressures and/or LA systolic dysfunction. Because left ventricular (LV) diastolic dysfunction is one of the potential mechanisms driving LA remodelling, we hypothesized that PTF-V1 might be an additional ECG marker of diastolic dysfunction.Methods: LV diastolic function after 3 years’ systematic antihypertensive treatment was examined in relation to baseline PTF-V1 in 431 hypertensive patients undergoing protocol-driven blood pressure reduction who had baseline and year-3 ECG and echocardiographic data and a preserved LV ejection fraction (EF >45%) at year-3. Abnormal diastolic function was defined by the tenth or 90th percentile values from 405 normotensive, non-obese and non-diabetic adults without overt cardiovascular disease. Abnormal PTF-V1, defined by the presence of a negative terminal P-wave in lead V1 ≥ 4000 μV·ms, was present in 167 patients (38.7%).Results: Abnormal PTF-V1 was associated with worse year-3 mean diastolic first third filling time (0.43 ± 0.08 vs 0.40 ± 0.07 sec, p = 0.039), first half filling time (0.55 ± 0.07 vs 0.53 ± 0.07 sec, p = 0.041), mitral valve A velocity (86 ± 27 vs 76 ± 19 cm/sec, p = 0.009) and mitral valve E/A ratio (0.85 ± 0.22 vs 0.94 ± 0.27, p = 0.007) after adjusting for other potential predictors of diastolic dysfunction including race, and heart rate, systolic blood pressure and severity of ECG LVH by Cornell product criteria at baseline. In parallel multivariate logistic regression analysis, abnormal PTF-V1 was associated with significantly increased odds of abnormal mitral valve E/A ratio (OR 1.55, 95%CI 1.04–2.32 p = 0.032), and a trend toward higher odds of abnormal half filling time (OR 1.42, 95%CI 0.94–2.15, p = 0.098) at year-3 of follow-up.Conclusions: Abnormal P-wave terminal force in lead V1 is associated with worse diastolic function and predicts abnormal LV diastolic behaviour in patients with preserved EF after 3 years of blood pressure reductive therapy.

Abstract WP176: Electrocardiographic Left Atrial Abnormality and Silent Vascular Brain Injury: The Northern Manhattan Study

Background: Increased P-wave terminal force in lead V1 (PTFV1) of a standard 12-lead electrocardiogram (EKG), a marker of left atrial dilatation and possibly fibrosis, has been associated with stroke risk in the absence of atrial fibrillation (AF), and with subclinical infarcts in some cohorts. We hypothesized that PTFV1 would be associated with an increased prevalence of subclinical infarcts, especially cortical ones, and leukoaraiosis in a population-based, multi-ethnic cohort. Methods: PTFV1 was collected manually from baseline EKGs of participants in the population-based, prospective Northern Manhattan Study (NOMAS) who had remained clinically stroke-free and undergone brain MRI (n=1,290). MRIs were read for superficial and deep infarcts and white matter hyperintensity volume adjusted for head size (WMHV). Logistic regression models were used for the association of PTFV1 with all subclinical infarcts and with cortical infarcts, and linear regression models with logWMHV. Models were adjusted for demographics and risk factors. Results: Among the 1174 participants with PTFV1, mean age was 70 + 9 SD years at the time of MRI, 40.3% were male, and 14.4% were white, 17.6% black, and 65.8% Hispanic. Hypertension was present in 68.0%. Mean PTFV1 was 3587.35 ± 2315.62 μV-ms. MRIs were performed a mean of 6.0 + 3.4 years after EKG. Subclinical infarcts were present in 170 (15.1%) participants, and were cortical in 40 (3.6%). PTFV1 &gt;5000 μV-ms was associated with greater WMHV even after adjusting for demographics and risk factors, including baseline AF (mean difference in logWMHV 0.14, 95% CL 0.01-0.28). There was a trend toward an association of PTFV1 with cortical (unadjusted OR per SD change logPTFV1 1.30, 95% CI 0.94-1.81) but not with all subclinical infarcts (unadjusted OR 1.00, 95% CI 0.85-1.18). Conclusion: EKG evidence of left atrial abnormality was associated with leukoaraiosis, and possibly with subclinical cortical infarcts, though the limited number of outcomes did not permit us to confirm this finding. Left atrial cardiopathy may be a source of emboli, but may also cause cerebral hypoperfusion-related injury. Further studies in large cohorts are needed to determine the relationship of PTFV1 to risk of subclinical cerebrovascular disease.

Abstract 9903: Baseline Left Atrial Abnormality by Electrocardiogram Predicts Incident Stroke in Hypertensive Patients With Electrocardiographic Left Ventricular Hypertrophy

Background: Recent findings in population-based studies suggest that abnormal P-wave terminal force in lead V 1 (PTFV 1 ), a marker of left atrial (LA) abnormalities such as fibrosis, dilatation and elevated filling pressures, is associated with incident ischemic stroke, even in the absence of atrial fibrillation (AF). However, whether PTFV 1 predicts incident stroke in hypertensive patients during aggressive blood pressure (BP) lowering has not been examined. Methods: Risk of incident stroke was examined in relation to abnormal PTFV 1 on a baseline ECG in 1879 hypertensive patients aged 60 or younger with ECG left ventricular hypertrophy (LVH), no history of AF, in sinus rhythm on their baseline ECG with no incident AF during follow-up, who were randomly assigned to losartan- or atenolol-based treatment. Patients &gt;60 years old were not included because of a highly significant interaction between PTFV 1 and age in Cox analyses. Abnormal PTFV 1 was defined by the presence of a negative terminal P wave in lead V 1 with amplitude x duration ≥4000 V*ms. Results: During mean follow-up of 4.8±0.9 years, 45 patients (2.4%) experienced a definite stroke. A higher incidence of stroke occurred in those with abnormal than normal baseline PTFV 1 : incidence rate per 1000 person-years, 7.8, 95% CI, 5.2-11.4 vs 3.4; 95% CI, 2.2-5.2; p=0.004. In univariate Cox models, abnormal PTFV 1 was associated with a &gt; 2-fold increased risk of incident stroke (HR 2.31, 95% CI 1.28-4.16, p=0.005). In multivariable Cox regression models that adjusted for other significant predictors of incident stroke in this population (gender, history of stroke or transient ischemic attack, ischemic heart disease or diabetes, baseline creatinine and in-treatment systolic BP), abnormal PTFV 1 remained associated with a &gt; 2-fold increased risk of incident stroke (HR, 2.06; 95% CI, 1.14-3.74, p=0.017). Conclusions: Abnormal PTFV 1, a marker of LA abnormality, was strongly associated with incident stroke in hypertensive patients, independent of in-treatment systolic BP and other predictors of incident stroke. This association, in the absence of detectable AF, suggests that an underlying atrial cardiopathy may cause LA thromboembolism and a subsequent stroke without necessarily manifesting with AF.

GW25-e2249 Correlation analysis of P-wave terminal force in lead V1 (PTFV1) with HATCH score

This study assumes that the ECG examination can identify the patients of high-risk progress from paroxysmal atrial fibrillationto persistent atrial fibrillation. By analyzing the correlation of P-wave terminal force in lead V1 (PTFV1) and paroxysmal atrial fibrillation progression risk scoring

Abnormal P-wave terminal force in lead V1 is associated with cardiac death or hospitalization for heart failure in prior myocardial infarction

The aim of this study was to clarify the prognostic significance of P-wave terminal force in lead V1 (PTFV1) in patients with prior myocardial infarction (MI). We retrospectively examined 185 patients with prior MI. The primary end point was cardiac death or hospitalization for heart failure. Abnormal PTFV1 was defined as PTFV1 ≥ 40 mm × ms. During a follow-up period of 6.4 ± 2.9 years, 39 patients developed the primary end point. A Kaplan-Meier analysis showed a lower primary event-free rate in 79 patients with abnormal PTFV1 than in 106 patients with normal PTFV1 (P < 0.001). When we classified 79 patients with abnormal PTFV1 into 31 with a purely negative P wave in lead V1 and 48 with a biphasic negative P wave in lead V1, the primary event-free rate did not differ between the two groups of patients. A multivariate Cox regression analysis selected age (hazard ratio (HR) 1.09, 95 % confidence interval (CI) 1.04-1.14, P < 0.001), multivessel coronary disease (HR 2.33, 95 % CI 1.02-5.28, P = 0.04), and abnormal PTFV1 (HR 2.72, 95 % CI 1.24-5.99, P = 0.01) as independent predictors of the primary end point. In conclusion, abnormal PTFV1 is an independent predictor of cardiac death or hospitalization for heart failure in patients with prior MI. The analysis of P waves in lead V1 should provide useful prognostic information in patients with prior MI.

Association of P‐Wave Duration, Dispersion, and Terminal Force in Relation to P‐Wave Axis among Outpatients

While P-wave duration (P-dur) and dispersion (P-disp) could both reflect fractionated and inhomogeneous propagation of sinus cardiac impulses, and may therefore be associated with each other, a clear relationship has not been extensively studied. We studied these markers as well as the significance of P-wave terminal force in lead V1 (PTFV1) in relation to the P-wave axis (P-axis). We appraised our previously studied sample of 500 consecutively numbered, otherwise unselected, electrocardiograms (ECGs) of outpatients from the University of Massachusetts, Worcester, Massachusetts, for the foregoing P-wave characteristics. P-disp, defined as the difference of the duration between the widest and narrowest P wave, and the greatest P-dur after a 12-lead ECG search, was measured manually to the nearest 10 ms. PTFV1 was considered positive when > or = 40 mm2 terminal deflection was present on biphasic P waves on lead V1. Normal P-axis was considered 0 degrees to +75 degrees by manually constructing the mean frontal plane electrical P-axis from standard limb leads. After excluding those with atrial arrhythmias, paced rhythms, errors in lead placement, P waves with low amplitude or overall technically poor tracing, 428 ECGs formed our final sample. P-dur was strongly associated with P-disp (P < 0.0001), but the correlation remained weak (r = 0.42). Overall, P-dur was not significantly associated with P-axis but when divided into tertiles and quintiles, the significance was evident within the range of the normal P-axis, particularly 0 degrees to +60 degrees (P < 0.0001). In a subanalysis of 380 ECGs that had appreciable biphasic P waves on lead V1, PTFV1 was noted on 178 (47%) ECGs and was significantly associated with P-dur (P < 0.0001), P-disp (P < 0.0001), and P-axis (P = 002). When considering P-axis in tertiles and quintiles, P-dur was greater in patients with a positive PTFV1 and significant within the normal range of the P-axis, especially from 0 degrees to +60 degrees . P-dur, P-disp, and PTFV1 appear to share a significant tripartite association in relation to the normal P-axis, particularly when P-axis ranges 0 degrees to +60 degrees . Therefore, for optimal clinical assessment, these markers should be evaluated in relation to the normal P-axis.