Differences in Echocardiographic Indices Between Patients With Partial and Advanced Interatrial Conduction Delay

Authors

  • Vignendra Ariyarajah MD,

    1. From the Department of Medicine, Division of Cardiology, St Boniface General Hospital/University of Manitoba, Winnipeg, Manitoba;1the Department of Medicine, Division of Cardiology, St Vincent Hospital/University of Massachusetts Medical School, Worcester, MA;2 and the Department of Medicine, Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY3
    Search for more papers by this author
  • 1 Jaxon Fernandes MD,

    1. From the Department of Medicine, Division of Cardiology, St Boniface General Hospital/University of Manitoba, Winnipeg, Manitoba;1the Department of Medicine, Division of Cardiology, St Vincent Hospital/University of Massachusetts Medical School, Worcester, MA;2 and the Department of Medicine, Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY3
    Search for more papers by this author
  • 2 Sirin Apiyasawat MD,

    1. From the Department of Medicine, Division of Cardiology, St Boniface General Hospital/University of Manitoba, Winnipeg, Manitoba;1the Department of Medicine, Division of Cardiology, St Vincent Hospital/University of Massachusetts Medical School, Worcester, MA;2 and the Department of Medicine, Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY3
    Search for more papers by this author
  • and 3 David H. Spodick MD, DSc 2

    1. From the Department of Medicine, Division of Cardiology, St Boniface General Hospital/University of Manitoba, Winnipeg, Manitoba;1the Department of Medicine, Division of Cardiology, St Vincent Hospital/University of Massachusetts Medical School, Worcester, MA;2 and the Department of Medicine, Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY3
    Search for more papers by this author

Vignendra Ariyarajah, MD, Y3 Cardiology, Bergen Cardiac Center, St Boniface General Hospital, 409 Tache Avenue, Winnipeg, Manitoba R2H 2A6, Canada; e-mail: vignendra@hotmail.com

Abstract

Partial interatrial block (IAB) (P wave ≥110 ms) is a marker of left atrial abnormality. A similar association among patients with advanced IAB (biphasic P waves ≥110 ms in leads II, III, and aVF) is unknown. The authors screened 27 consecutive patients for advanced IAB with transthoracic echocardiograms (TTEs). Of those, 19 who had repeat TTEs after 2 years formed our study cohort. The authors used 44 consecutive controls with partial IAB who had been similarly screened and had follow-up TTEs 2 years apart. TTE parameters were comparable at baseline between groups but were expectedly different on follow-up. When change (delta value) in these indices was compared, however, only left atrial dimension remained significant (advanced 0.07±0.06 mm vs partial IAB 0.03±0.06 mm; P=.03). Further study over a longer duration is warranted to ascertain if advanced IAB patients would benefit from follow-up noninvasive cardiac imaging for appropriate risk stratification.

Delay in interatrial conduction (P waves ≥110 ms) is manifested as partial or advanced interatrial block (IAB).1 While both conduction abnormalities are thought to be associated with myocardial ischemia2 and atrial tachyarrhythmias,3 precise associations with the latter electrocardiographic (ECG) abnormality, which is considerably uncommon, is less well-known. Indeed, partial IAB could progress to its advanced counterpart when interatrial conducting pathways become increasingly encumbered4; impulses are forced inferiorly toward the atrioventricular node before being caudocranially reflected into the left atrium (biphasic P waves ≥110 ms in the inferior ECG leads) (Figure 1).1,5 Moreover, while partial IAB is often considered a potent marker of echocardiographic left atrial dilatation,1,6 there remains a paucity of data on a similar association with advanced IAB.

Figure 1.

Comparison for change in left ventricular hypertrophy (size) among patients during the study period.

Methods

Study Sample and Design. Between January 2003 and June 2004, we identified 27 consecutive patients at a tertiary care hospital (St Vincent Hospital, Worcester, MA) who had advanced IAB on routine 12-lead ECGs. None of the patients had been admitted for severe illnesses or myocardial infarction, underwent a surgical procedure, or required intensive care during hospital admission. Each patient's medical record was then reviewed in detail for reports of transthoracic echocardiograms (TTEs) performed within 90 days of their respective ECGs. Of those, 19 patients who had undergone follow-up TTE assessment in June 2006 formed our study cohort. For direct comparison, we used 44 consecutive patients with partial IAB who had been initially screened between January 2003 and June 2004 and had now undergone similar follow-up TTE assessment after June 2006. Patients from both groups were then appraised for baseline clinical data that had been documented in their medical records by physicians involved directly in their care, consistent with current classifications and guidelines for disease definition and diagnosis outlined by American College of Cardiology/American Heart Association/American College of Physicians-American Society of Internal Medicine Task Force on Practice Guidelines.

Electrocardiography. Resting ECGs had been recorded from an electrocardiograph (Marquette Electronics Incorporated, Milwaukee, WI) at 25 mm/s and 10 mm/mV. ECGs had been evaluated on a single, separate-read for IAB by investigators (V.A., D.H.S.) with blinded, independent measurements using the greatest duration of P waves on every lead as measured with a calibrated magnifying graticule (reproducibility and interobserver concordance >92%). To increase specificity and because 1 mm represents 40 ms on ECGs with such standardization, 120 ms (which is also the mode P-wave duration in IAB) was used as our diagnostic criterion for IAB. The onset of the P wave was defined as the junction between the isoelectric T-P baseline and the beginning of the P deflection, while the terminal point was defined as the junction between the end of the P deflection and the PR segment. Advanced IAB was defined as biphasic P waves ≥120 ms in leads II, III, and aVF and, as such, P-wave measurements were restricted to these leads in these patients.1

Echocardiography. Two-dimensional TTEs had been performed on each study participant in the left lateral recumbent position for parasternal long and short axes and apical 4- and 2-chamber views as well as in the supine position for subcostal views using an ATI HDL 5000W imaging system with a P4–2 scan head and 2.6-MHz transducer (Phillips Medical Systems Company, Bothell, WA) consistent with American Society of Echocardiography (ASE) guidelines. Left atrial dilatation was considered when anteroposterior measurement from leading edge to leading edge during end-systolic frames exceeded 40 mm in men and 38 mm in women. End-systolic frames were defined as the frame depicting the cardiac systolic event just before separation of the mitral valve tips. All echocardiograms were recorded and analyzed by experienced, board-certified echocardiographers who were blinded to both clinical presentation and ECG findings.

Statistical Analyses. Data are expressed as mean ± SD for continuous variables and frequencies for categoric variables. Differences between groups were assessed using chi-square statistics for categoric variables and analysis of variance for continuous variables. A P value <.05 was considered significant. Statistical analyses were performed using SPSS version 13.0 statistical software (SPSS Inc, Chicago, IL).

Results

Coronary artery disease and hypertension were prevalent between groups but did not reveal significant differences statistically (Table I). β-Adrenergic blocker use was common among patients (P=.42) (Table I). TTE parameters were statistically comparable between groups at baseline. About half of the patients had some degree of left ventricular hypertrophy, but this was not statistically significant between groups (P=.88) (Table I).

Table I.  Comparison Between Patients With Partial and Advanced Interatrial Block (n=63)
Interatrial Block
VariablePartial (n=44)Advanced (n=19)P Value
Age, y75.9±7.778.5±10.2.29
Female23 (52)11 (58).48
Coronary artery disease21 (48)12 (63).26
Hypertension34 (77)16 (84).53
Hyperlipidemia16 (36)7 (37).97
Diabetes mellitus8 (18)6 (32).24
Cardiomyopathy5 (11)5 (26).14
Preexisting atrial fibrillation history11 (25)3 (16).42
Preexisting atrial flutter history00 
Chronic obstructive pulmonary disease8 (18)6 (32).24
Atrioventricular valvular disease4 (9)5 (26).07
Angiotensin-converting enzyme inhibitor use14 (32)11 (58).05
Angiotensin receptor blocker use2 (5)2 (11).37
β-Adrenergic blocker use23 (52)12 (63).42
Hydrochlorothiazide use10 (23)4 (21).88
Furosemide, spironolactone, or other diuretic use17 (39)4 (21).17
Statina use14 (32)6 (32).99
Left atrial dimension,b mm41.9±443.4±7.29
Ventricular septal thickness, mm9.2±29.9±2.24
Posterior wall thickness, mm9.6±210.3±2.24
Left ventricular hypertrophy
 None23 (52.3)9 (47.4).88
 Mild14 (31.8)6 (31.6) 
 Moderate7 (15.9)4 (21.1) 
 Severe00 
Left ventricular end-systolic volume, mL44.2±743.3±6.59
Left ventricular end-diastolic volume, mL100.1±1199.4±10.79
Left ventricular ejection fraction, %48.3±1045.3±9.26
Data are presented as mean ± SD or No. (%). a3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. bAnteroposterior linear dimension on transthoracic echocardiogram.

Follow-up TTE was 2.7±0.8 years among advanced IAB patients and 2.2±0.4 years among partial IAB patients after initial TTE assessment. Reported TTE parameters were expectedly different on followup assessment. When changes (delta value) in these TTE indices were compared between groups, however, only left atrial dimension remained significantly changed (Figure 2). Patients with advanced IAB had a significantly greater increase in left atrial size compared with those with partial IAB (P=.03) (Table II; Figure 2).

Figure 2.

Comparison for change in left atrial dimension (size) among patients during study period. (A) Patients with partial interatrial delay or block. (B) Patients with advanced interatrial delay or block.

Table II.  Factors Related to Change in Left Atrial Linear Dimension from Baseline to Present (n=63)a
Categoric Variables
Exposure VariableChange in Left Atrial Dimension, mmP Value
Age
 Older than 75 y (n=39)0.04±0.07.91
 75 y and younger (n=24)0.04±0.07 
IAB type
 pIAB (n=44)0.03±0.06.03b
 aIAB (n=19)0.07±0.06 
Coronary artery disease
 Present (n=33)0.05±0.06.39
 Absent (n=30)0.04±0.07 
Hypertension
 Present (n=50)0.05±0.06.49
 Absent (n=13)0.03±0.06 
Diabetes mellitus
 Present (n=14)0.04±0.05.91
 Absent (n=49)0.04±0.07 
Hyperlipidemia
 Present (n=23)0.05±0.07.31
 Absent (n=40)0.04±0.06 
Preexisting history of atrial fibrillation
 Present (n=14)0.03±0.06.6
 Absent (n=49)0.04±0.07 
Cardiomyopathy
 Present (n=10)0.04±0.07.51
 Absent (n=53)0.05±0.06 
Chronic obstructive pulmonary disease
 Present (n=14)0.05±0.07.47
 Absent (n=49)0.04±0.06 
Atrioventricular valvular disease
 Present (n=9)0.08±0.05.09
 Absent (n=54)0.04±0.07 
Angiotensin-converting enzyme inhibitor use
 Yes (n=25)0.04±0.06.98
 No (n=38)0.04±.0.07 
Angiotensin receptor blocker use
 Yes (n=4)0.07±0.06.4
 No (n=59)0.04±0.06 
β-Adrenergic blocker use
 Yes (n=36)0.04±0.06.93
 No (n=27)0.04±0.07 
Statinc use
 Yes (n=20)0.04±0.07.98
 No (n=43)0.04±0.06 
Continuous Variables and Change in Left Atrial Dimension
Exposure VariableRP Value
Any age, y−0.15.24
Baseline left ventricular ejection fraction, %−0.22.07
Baseline posterior wall thickness, mm0.07.55
Baseline ventricular septal thickness, mm0.14.27
Baseline left ventricular end-systolic volume, mL−0.11.41
Baseline left ventricular end-diastolic volume, mL−0.02.89
Abbreviations: aIAB, advanced interatrial block; pIAB, partial interatrial block. Data are presented as mean ± SD. aOverall mean change in left atrial linear dimension = 0.04±0.06 mm; range for change = −0.1 to 0.17 mm. bStatistically significant. c3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.

Discussion

Advanced IAB is perhaps perceived as a progressive worsening of already prolonged interatrial conduction.1,4 We had previously demonstrated that the duration of progression from normal conduction (P wave <110 ms) to advanced IAB is approximately one and a half times longer (66 months; mean ± SD = 64.2±25.6 months) than that of partial to advanced IAB (42 months; mean ± SD = 39.2±30.5).4 In this regard, angiotensin-converting enzyme inhibitors could perhaps play a role in slowing progression times (50.1±28.3 vs 10.0±10.4 months; P=.04).4 The exact mechanisms and substrates that directly affect interatrial conducting pathways remain largely unknown, however. Atrial fibrosis,5,7 myocardial ischemia,2,8 impaired renal function,9 and common cardiovascular risk factors10 such as hypertension, hyperlipidemia, and diabetes mellitus among others have been cited as potential inciting factors.

Our present findings further delineate the association of left atrial dilatation with IAB,6 be it partial or advanced. Given the association of advanced IAB with a progressive impairment in interatrial impulse relay, however, it is perhaps not surprising that patients with advanced IAB in this investigation had a significantly greater increase in left atrial size compared with those with partial IAB. Delayed sinus impulse transmission to the left atrium results in delayed left atrial activation and contraction.11 This scenario predisposes to dyssynchronous atrial activity and sets the stage for mistimed left atrial contraction against a closed or closing mitral valve. The resultant left atrial pressure increase may precipitate increased left atrial wall stress and therefore herald chamber dilatation. Thus, a vicious cycle of progressive left atrial electromechanical dysfunction and added left atrial dilatation ensues.11

The association of left atrial dilatation with cardiovascular events has been described in numerous settings. Often described as a morphophysiologic barometer for diastolic dysfunction,12 increased left atrial dimension, in the context of the already well-described myocardial ischemia cascade,13 could therefore indirectly serve as an early marker for myocardial ischemia. In a population-based study conducted over 7 years, Kizer and colleagues14 demonstrated that echocardiographic evaluation of left atrial diameter independently predicted incident cardiovascular events inclusive of nonfatal stroke, coronary heart disease, congestive heart failure, and fatal cardiovascular disease. Similarly, a prospective population-based study performed in Finland by Laukkanen and colleagues15 also showed that left atrial diameter on TTE was directly related to the risk of cardiovascular death.

In this study, TTE follow-up had expectedly shown change in left atrial dimension from baseline over time in both groups (Figure 2). The rate of increase in left atrial dimension, however, was more pronounced among advanced IAB patients than in partial IAB patients. While this proved to be statistically significant, the true clinical relevance of such a small change remains questionable. Nevertheless, our follow-up was only 24 months, when previous studies that demonstrated cardiovascular complications as a result of left atrial dilatation spanned considerably longer periods.14 Moreover, owing to the already known associated risk of cardiovascular events with increased left atrial dimension,14,15 this change itself could very well be a harbinger of potential morbid events to come, such as atrial tachyarrhythmias, heart failure, embolic strokes, and death. Advanced IAB on the ECG, which denotes a more pronounced conduction abnormality compared with its partial counterpart, may therefore serve as the first sign that clinically heralds the progressive change in echocardiographic left atrial size. It may still be reasonable to follow patients who demonstrate advanced IAB on the ECG with a TTE not only to quantify baseline measurements of the left atrium but also to identify individuals with perhaps significant change in left atrial dimensions for appropriate risk stratification and also for better control of comorbidities such as hypertension, coronary artery disease, or diabetes mellitus. However, further study in this respect, preferably with a larger cohort, is needed before consideration of such clinical strategies.

One limitation in this investigation is that only 19 patients with advanced IAB were investigated. Advanced IAB, however, is relatively uncommon compared with its partial counterpart. It occurs at a very low frequency among inpatients and therefore our sample actually serves as an indirect, large representation of advanced IAB patients in comparable general hospital populations. Conversely, the number of partial IAB patients could therefore be actually too small for optimal comparison and may not be a proportionate representation of such patients in the hospital, where a prevalence of >40% is often noted.1,11 Tsang and colleagues12 have shown that the use of volumes as a measure of left atrial dimension serves as a better quantifier of left atrial chamber size than diameters. Linear measurements, however, although not as accurate as volumes,15,16 also confer increased cardiovascular risk when measurements exceed normal cutoffs.2,14,15 Moreover, although there has been adequate emphasis by the ASE on the importance of left atrial volume measurements, a large number of echocardiogram reports still quantify left atrial size with linear dimension.

Conclusions

In this preliminary 24-month study period, when compared with patients with partial IAB, those with the much less common advanced form of IAB showed a small but statistically significant increase in left atrial size. Further study is required to ascertain whether patients with advanced IAB would benefit from noninvasive cardiovascular imaging such as with TTE not only to quantify baseline measurements of the left atrium but also to identify individuals with significant change in left atrial dimensions for appropriate risk stratification and perhaps better control of precipitating underlying risk factors.

Disclosures:

None of the authors received any funding for this investigation. Any affiliations or financial involvement, within the past 5 years and foreseeable future with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript are completely disclosed. All authors have also disclosed otherwise any potential personal conflict of interest.

Ancillary