Force In Lead V1 Research Articles

Factors influencing P terminal force in lead V1 of the ECG in hemodialysis patients.

IntroductionAtrial fibrillation (AF) is a highly prevalent arrhythmia in hemodialysis (HD) patients, and an HD session may be a trigger for AF episodes. An abnormal P-terminal force in lead V1 (PTFV1) may predict new-onset AF in HD patients. The aim of the study was to assess the influence of the HD process on PTFV1 and to evaluate possible factors influencing PTFV1 in a group of selected HD patients.Material and methodsOne hundred and fifty-three selected HD patients entered the study. Blood chemistry, electrocardiography, and impedance cardiography were evaluated before and after HD. Echocardiography was performed on the morning after dialysis. Abnormal PTFV1 was defined as PTFV1 > 40 mm × ms.ResultsAbnormal PTFV1 was found in 35.3% of patients before dialysis and in 48.4% of patients after dialysis. The results of multiple regression analysis revealed that the independent predictors of pre-dialysis abnormal PTFV1 were: left atrial volume index (p = 0.002), left ventricular mass index (p = 0.014), and pre-dialysis thoracic fluid content (p = 0.021) values. The independent predictors of HD-induced abnormal PTFV1 values were larger differences between pre-dialysis and post-dialysis values of serum potassium (p < 0.001) and mean arterial pressure (p = 0.008).ConclusionsAbnormal PTFV1 is prevalent in HD patients. The HD process adversely affects PTFV1 values. Pre-dialysis abnormal PTFV1 is mainly associated with structural heart abnormalities and hydration status. HD-induced abnormal PTFV1 is associated predominantly with serum potassium changes as well as HD-induced hypotension. Our results suggest possible risk factors for AF; however, their clinical significance needs to be confirmed in follow-up studies.

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.

Electrocardiographic left atrial abnormality and stroke subtype in the atherosclerosis risk in communities study.

The aim of this study was to assess the relationship between abnormally increased P-wave terminal force in lead V1 , an electrocardiographic (ECG) marker of left atrial abnormality, and incident ischemic stroke subtypes. We hypothesized that associations would be stronger with nonlacunar stroke, given that we expected left atrial abnormality to reflect the risk of thromboembolism rather than in situ cerebral small-vessel occlusion. Our cohort comprised 14,542 participants 45 to 64 years of age prospectively enrolled in the Atherosclerosis Risk in Communities study and free of clinically apparent atrial fibrillation (AF) at baseline. Left atrial abnormality was defined as PTFV1 >4,000μV*ms. Outcomes were adjudicated ischemic stroke, nonlacunar (including cardioembolic) ischemic stroke, and lacunar stroke. During a median follow-up period of 22 years (interquartile range, 19-23 years), 904 participants (6.2%) experienced a definite or probable ischemic stroke. A higher incidence of stroke occurred in those with baseline left atrial abnormality (incidence rate per 1,000 person-years, 6.3; 95% confidence interval [CI]: 5.4-7.4) than in those without (incidence rate per 1,000 person-years, 2.9; 95% CI: 2.7-3.1; p < 0.001). In Cox regression models adjusted for potential confounders and incident AF, left atrial abnormality was associated with incident ischemic stroke (hazard ratio [HR]: 1.33; 95% CI: 1.11-1.59). This association was limited to nonlacunar stroke (HR, 1.49; 95% CI: 1.07-2.07) as opposed to lacunar stroke (HR, 0.89; 95% CI: 0.57-1.40). We found an association between ECG-defined left atrial abnormality and subsequent nonlacunar ischemic stroke. Our findings suggest that an underlying atrial cardiopathy may cause left atrial thromboembolism in the absence of recognized AF.

P-wave indices in emphysema. What do we actually know?

I was very pleased to read the article by Kowgli and Chhabra [ [1] Kowlgi N.G. Chhabra L. The role of P-wave indices in the diagnosis of emphysema. Int. J. Cardiol. 2015; 199: 264-273 Abstract Full Text Full Text PDF PubMed Google Scholar ] in response to our recent paper [ [2] Goudis C.A. Konstantinidis A.K. Ntalas I.V. et al. Electrocardiographic abnormalities and cardiac arrhythmias in chronic obstructive pulmonary disease. Int. J. Cardiol. 2015; 199: 264-273 Abstract Full Text Full Text PDF PubMed Scopus (41) Google Scholar ]. The authors underline that specific P-wave indices such as P-wave terminal force in lead V1 (P-tf), amplitude of initial positive component of P-wave in V1 (i-PV1) and interatrial block (IAB), may confer additional diagnostic value to the accuracy of electrocardiogram interpretation in patients with emphysema [ [1] Kowlgi N.G. Chhabra L. The role of P-wave indices in the diagnosis of emphysema. Int. J. Cardiol. 2015; 199: 264-273 Abstract Full Text Full Text PDF PubMed Google Scholar ].

A Predictive Study of the Dynamic Development of the P-Wave Terminal Force in Lead V1 in the Electrocardiogram in Relation to Long-Term Prognosis in Non-ST-Segment Elevation Acute Coronary Syndrome Patients during Hospitalization.

Changes in the ECG indicator PtfV1 reflect left atrial pressure and left ventricular diastolic function in NSTE-ACS patients during hospitalization. The value of PtfV1 in the evaluation of long-term prognosis in NSTE-ACS is still not clear. The purpose of this study was to investigate the relationship between the dynamic changes in P-wave terminal force in lead V1(PtfV1) in the ECG of non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients during hospitalization and the long-term major adverse cardiovascular events (MACEs) of patients. A total of 595 patients who received coronary angiography and were confirmed as NSTE-ACS in the coronary heart disease database of Department of Cardiology of West China Hospital were continuously included. The PtfV1 and other clinical data at admission and discharge were collected and dynamically observed. The end events of follow-up observation were MACEs. Follow-up was performed on 595 patients for 24.71 ± 1.95 months. There were 127 PtfV1(+) and 468 PtfV1(-) at admission, and the incidences of MACEs were 14.2% and 11.1%, respectively (P = 0.731). Compared with patients with persistent PtfV1(-) ECG at admission and discharge, 53 patients with persistent PtfV1(+) ECG at admission and discharge had increased risk for MACEs (HR: 2.221, 95% CI: 1.072-4.601, P = 0.032); 94 patients with new PtfV1(+) ECG at discharge also had significantly increased risk for MACEs (HR: 2.993, 95% CI: 1.660-5.397, P = 0.000). NSTE-ACS patients with persistent PtfV1(+) ECG indicators at admission and discharge and new PtfV1(+) at discharge had significantly increased risk of MACEs.

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

Associations of electrocardiographic P-wave characteristics with left atrial function, and diffuse left ventricular fibrosis defined by cardiac magnetic resonance: The PRIMERI Study.

Abnormal P-terminal force in lead V1 (PTFV1) is associated with an increased risk of heart failure, stroke, atrial fibrillation, and death. Our goal was to explore associations of left ventricular (LV) diffuse fibrosis with left atrial (LA) function and electrocardiographic (ECG) measures of LA electrical activity. Patients without atrial fibrillation (n = 91; mean age 59.5 years; 61.5% men; 65.9% white) with structural heart disease (spatial QRS-T angle ≥105° and/or Selvester QRS score ≥5 on ECG) but LV ejection fraction >35% underwent clinical evaluation, cardiac magnetic resonance, and resting ECG. LA function indices were obtained by multimodality tissue tracking using 2- and 4-chamber long-axis images. T1 mapping and late gadolinium enhancement were used to assess diffuse LV fibrosis and presence of scar. P-prime in V1 amplitude (PPaV1) and duration (PPdV1), averaged P-wave-duration, PR interval, and P-wave axis were automatically measured using 12 SLTM algorithm. PTFV1 was calculated as a product of PPaV1 and PPdV1. In linear regression after adjustment for demographic characteristics, body mass index, maximum LA volume index, presence of scar, and LV mass index, each decile increase in LV interstitial fibrosis was associated with 0.76 mV*ms increase in negative abnormal PTFV1 (95% confidence interval [CI] -1.42 to -0.09; P = .025), 15.3 ms prolongation of PPdV1 (95% CI 6.9 to 23.8; P = .001) and 5.4 ms prolongation of averaged P-duration (95% CI 0.9-10.0; P = .020). LV fibrosis did not affect LA function. PPaV1 and PTFV1 were associated with an increase in LA volumes and decrease in LA emptying fraction and LA reservoir function. LV interstitial fibrosis is associated with abnormal PTFV1, prolonged PPdV1, and P-duration, but does not affect LA function.

P-wave morphology and the risk of incident ischemic stroke in the Multi-Ethnic Study of Atherosclerosis.

Emerging data suggest that left atrial disease may cause ischemic stroke in the absence of atrial fibrillation or flutter (AF). If true, this condition may provide a cause for many strokes currently classified as cryptogenic. Among 6741 participants in the Multi-Ethnic Study of Atherosclerosis who were free of clinically apparent cerebrovascular or cardiovascular disease (including AF) at baseline, we examined the association between markers of left atrial abnormality on a standard 12-lead ECG-specifically P-wave area, duration, and terminal force in lead V1-and the subsequent risk of ischemic stroke while accounting for incident AF. During a median follow-up of 8.5 years, 121 participants (1.8%) had a stroke and 541 participants (8.0%) were diagnosed with AF. In Cox proportional hazards models adjusting for potential baseline confounders, P-wave terminal force in lead V1 was more strongly associated with incident stroke (hazard ratio per 1 SD increase, 1.21; 95% confidence interval, 1.02-1.44) than with incident AF (hazard ratio per 1 SD, 1.11; 95% confidence interval, 1.03-1.21). The association between P-wave terminal force in lead V1 and stroke was robust in numerous sensitivity analyses accounting for AF, including analyses that excluded those with any incident AF or modeled any incident AF as having been present from baseline. We found an association between baseline P-wave morphology and incident stroke even after accounting for AF. This association may reflect an atrial cardiopathy that leads to stroke in the absence of AF.

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.

Risk Stratification for Recurrent Heart Failure in Patients Post-Myocardial Infarction With Electrocardiographic and Echocardiographic Left Atrial Abnormality

Left atrial enlargement is predictive of cardiovascular events. The predictive power, however, of the combination of electrocardiographic (LAE-ECG) and echocardiographic left atrial enlargement (LAE-Echo) has not been extensively evaluated. We prospectively identified patients admitted with non-ST-segment elevation myocardial infarction (NSTEMI) who developed new-onset heart failure during admission. Baseline electrocardiograms obtained < or =12 months before admission were evaluated for LAE-ECG, such as prolonged P-wave duration or positive P-wave terminal force in lead V1, and in-hospital echocardiographic reports obtained < or =1 month after admission were assessed for linear, anteroposterior LAE-Echo. Follow-up was directed toward pertinent cardiovascular events and death. Of the 462 patients with NSTEMI, 108 developed new-onset heart failure (23%); 71 patients had LAE-Echo. Follow-up was 23.2 months (mean 22.1 months). Although in-hospital (early) cardiovascular complications (other than heart failure) were not significantly higher in patients with LAE-Echo, these patients demonstrated more postdischarge (late) cardiovascular complications, predominantly recurrent heart failure. In addition, those with a combination of LAE-Echo and LAE-ECG demonstrated significantly higher recurrence of heart failure (hazard ratio 1.52, 95% confidence interval 1.12 to 4.35; p = 0.02 for interatrial conduction delay, and hazard ratio 1.07, 95% confidence interval 1.01 to 3.27 for P-wave terminal force in lead V1; p = 0.03) and increased mortality compared with those with LAE-Echo alone. In conclusion, our data suggest that a combination of electrical and mechanical left atrial dysfunction is significantly more predictive of increased cardiovascular events and mortality compared with left atrial mechanical dysfunction alone.

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.

Correlation study of PtfV1 with Heart-Qi deficiency syndrome in patients with hypertensive left ventricular hypertrophy

It is generally believed that the change of p-wave terminal force in lead V1 (PtfV1) is associated with the inner diameter of left atrium, left ventricular compliance,and ventricular diastolic function. The increase of negative value of PtfV1 in essential hypertensive (EH) patients with left ventricular hypertrophy (LVH) indicates the cardiac function may be damaged. In order to explore the relationship between Heart-Qi Deficiency Syndrome (HQDS) of TCM and PtfV1 level in hypertensive LVH patients, correlation analysis of scores of Heart-Qi Deficiency Syndrome and negative value of PtfV1 was made by the authors.

Abnormalities of electrocardiographic P wave morphology and their relation to electrophysiological parameters of the atrium in patients with sick sinus syndrome.

We examined the incidence of long P wave duration in lead II and increased P terminal force in lead V1 (PTFV1), and their relationship to electrophysiological findings of atrial muscle in 34 patients with sick sinus syndrome (SSS). Patients were divided into three groups: Group I, consisting of 20 patients with various cardiac arrhythmias other than SSS and paroxysmal atrial fibrillation (PAF) who served as controls; Group II, consisting of 18 patients with SSS but without PAF; and Group III consisted of 16 patients with SSS and PAF. P wave duration was significantly longer in Group III (122 +/- 11 ms, mean +/- SD, P < 0.0001) and Group II (111 +/- 15 ms, P < 0.002) than in Group I (98 +/- 10 ms). PTFV1 was greater in Group III (0.052 +/- 0.025 ms) than in Group I (0.028 +/- 0.011 ms, P < 0.05). P wave duration and PTFV1 had significantly and/or borderline correlations with longest duration of right atrial electrograms (r = 0.84, P < 0.0001 and 0.47, P < 0.02, respectively), maximal number of fragmented deflections of atrial electrograms (r = 0.69, P < 0.0001 and r = 0.51, P < 0.02, respectively), repetitive atrial firing zone (RAFZ) (r = 0.81, P < 0.0001 and 0.48, P < 0.05, respectively) and fragmented atrial activity zone (FAAZ)(r = 0.53, P < 0.01 and r = 0.45, P = 0.06, respectively). We concluded that long P wave duration and increased PTFV1 are electrocardiographic indicators for coexistence of electrophysiological abnormalities in the atria in SSS without recognizable heart disease.

Signal averaged P wave compared with standard electrocardiography or echocardiography for prediction of atrial fibrillation after coronary bypass grafting.

OBJECTIVE: To define the clinical value of the signal averaged P wave (SAPW) and to compare it with the standard electrocardiogram (ECG), echocardiogram, and clinical assessment for the prediction of...

P-Wave changes in obstructive and restrictive lung diseases

To evaluate the P wave changes in the electrocardiogram (ECG) in chronic lung diseases, we examined ECGs from twenty patients with interstitial pulmonary fibrosis (the FLD group) and twenty patients with chronic obstructive lung disease (fifteen with pulmonary emphysema and five with bronchial asthma, the COLD group). In the COLD group, the amplitude of P waves in leads II and III increased and the axis of the P wave shifted rightward. In the FLD group, however, these changes were not observed. Furthermore, the axis of the P wave exceeded +70 degrees in all the patients in the COLD group, and was less than +70 degrees for all the patients in the FLD group. The increased P wave terminal force in lead V1 was found in nine patients (45%) of the FLD group and in ten patients (50%) in the COLD group. We concluded that the rightward shift of the axis of the P wave was a characteristic of obstructive lung disease and that it was mainly caused by the overinflation of the lung. This P wave change was not observed in interstitial pulmonary fibrosis.