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P-wave amplitude and pulmonary artery pressure in scleroderma
Journal of Electrocardiology 39 (2006) 385 – 388 www.elsevier.com/locate/jelectrocard
P-wave amplitude and pulmonary artery pressure in scleroderma Nina Wokhlu, MD,a Vivien M. Hsu, MD,b Alan Wilson, PhD,a Abel E. Moreyra, MD,a Daniel Shindler, MD a,4 a Division of Cardiology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA Division of Rheumatology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA Received 11 October 2005; accepted 24 January 2006
b
Abstract
Background and Purpose: Scleroderma is an immune-mediated disease characterized by excess deposition of collagen leading to microvascular occlusion. Morbidity and mortality are often secondary to pulmonary hypertension from injury to pulmonary microvasculature and interstitial lung disease. This study correlated P-wave findings on the 12-lead electrocardiogram (ECG) with mean pulmonary artery pressure (mPAP) measured by right heart catheterization in patients with scleroderma. Methods: A retrospective review of 12-lead ECGs in 23 patients referred to a rheumatology clinic with the diagnosis of scleroderma was performed. Right heart catheterization was performed within 1 month of the resting ECG. Results: Linear regression related P-wave amplitude in lead II with mPAP (r = 0.52, P = .011) This model was 73% sensitive and 67% specific for the presence or absence of elevated mPAP. Conclusions: P-wave amplitude analysis on the ECG may be helpful in the assessment of pulmonary hypertension in patients with scleroderma. D 2006 Elsevier Inc. All rights reserved.
Keywords:
P-wave amplitude; Electrocardiogram; Scleroderma
Introduction Scleroderma is an immune-mediated disease characterized by excess production and deposition of collagen. This results in progressive microvascular constriction and eventual luminal obliteration. Pulmonary hypertension is observed in patients with scleroderma with a prevalence of 4% to 38%.1,2 Major causes of mortality in this population are injury to the pulmonary microvasculature and interstitial lung disease with the typical manifestations of cor pulmonale. Prognosis in patients with scleroderma and pulmonary hypertension is significantly worse than in patients with other causes of pulmonary hypertension, that is, congenital heart disease, idiopathic pulmonary arterial hypertension, portopulmonary hypertension, and early HIV.3 Electrocardiographic (ECG) findings have been investigated in idiopathic pulmonary arterial hypertension and, to a lesser extent, in pulmonary hypertension of other etiolo-
4 Corresponding author. Tel.: +1 732 235 7855; fax: +1 732 235 8722. E-mail address: [email protected] (D. Shindler). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.01.004
gies.1,3-5 Scleroderma studies address overall prevalence of ECG manifestations rather than significance of individual ECG findings.6 Morelli and colleagues7 have compared ECG findings in 72 patients with echocardiographic findings in patients with scleroderma. Right heart catheterization, however, was not performed. We measured P-wave amplitude on 12-lead ECGs in patients with scleroderma using a high-resolution optical magnifier capable of 0.01-mV precision.8,9 The objective of this study was to determine the strength of correlation between P-wave amplitude on the 12-lead ECG and the degree of elevation of mean pulmonary artery pressure (mPAP) in a population of patients with scleroderma.
Study population and methods A retrospective review of 12-lead ECGs in 23 patients with the diagnosis of scleroderma referred to a rheumatology clinic at a university hospital was performed. The diagnosis of scleroderma was based on one major criterion or two minor criteriac from the guidelines defined by the
386
N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385 – 388
3 Wood units. During exercise, patients performed at least 3 minutes of arm exercise with 5-lb dumbbells until fatigued. Prior to discontinuing exercise, pulmonary artery pressure, cardiac output, and pulmonary capillary wedge pressure were recorded. Patients with pulmonary hypertension from causes other than scleroderma, including pulmonary venous hypertension and other factors that could contribute to increased left atrial pressure, were excluded from the study. Statistical analysis Correlation was made by linear regression between 12-lead ECG P-wave amplitude and pulmonary artery pressures obtained during right heart catheterization. Where applicable, variables were presented as mean F SD. Data were analyzed with SAS Version 8.2 (SAS Institute Inc, Cary, NC).11 Using linear regression, P-wave amplitude in lead II (mV) was plotted as a function of mPAP (mm Hg) and PVR (Wood units). Sensitivity and specificity were analyzed using the LOGISTIC procedure function of SAS. Results
Fig. 1. Manual loop magnifier. It is a cylindrical structure with a triplet viewing lens and a surface lens on the opposite side with an imprinted 20-mm grid that is placed directly on ECG paper to avoid parallax error. The loop provides a 1-in field of view and 6 magnification. Reprinted with permission.9
10
American College of Rheumatology. Onset of symptoms was defined as the first presenting symptom other than Raynaud phenomenon. P-wave amplitude was measured in lead II on standard 12-lead ECGs. Measurements were performed using a magnified measuring loop device (Fig. 1).8 The loop magnifier was used to obtain precise P-wave amplitude measurements on each 12-lead ECG to the nearest 0.1 mm (0.01 mV). The measurement of P-wave amplitude was recorded based on the technique described in the Minnesota Code Manual of Electrocardiographic Findings.9 Complexes that contained excessive artifact were not included in the analysis. Right heart catheterization was performed within 1 month of the ECG. Cardiac output was measured by the thermodilution technique. Pulmonary artery pressure was measured by right heart catheterization. Elevated mPAP was defined as greater than 25 mm Hg at rest or greater than 30 mm Hg with exercise. Elevated pulmonary vascular resistance (PVR) was defined as greater than c Major criteria include symmetrical skin thickening, tightening, and induration proximal to the metacarpophalangeal or metatarsophalangeal joints. Minor criteria include sclerodactyly (skin thickening limited to fingers or toes), digital pitting scars or loss of finger pad substance, and bibasilar pulmonary fibrosis.
Table 1 shows the demographic and study variables. Mean age was 53 F 14 years. The group (n = 23) consisted of 20 (87%) women. Twelve patients (52%) were diagnosed Table 1 Patient variables Age at Sex Type of Symptom Pulmonary P-wave ECG scleroderma duration at hypertension amplitude (y) ECGa (y) (WHO class) on ECG (mV)
Mean PA Pressure on RVC (mm Hg)
66 79 20 69 58 45 34 54 36 43 46 53 41 44 77 64 58 51 57 53 59 60 54
24 12 12 18 18 42 10 24 28 34 15 47 11 12 33 56 30 37 22 37 23 43 54
F F F F F M M F M F F F F F F F F F F F F F F
Limited Limited Undiff CTD Limited Diffuse Limited Limited Limited Diffuse Diffuse Diffuse Limited Limited Diffuse Limited Diffuse Diffuse Diffuse Overlap Limited Diffuse Limited Limited
15 18 27 4 6 1 11 4 1 2 6 4 20 5 1 6 4 4 3 12 16 12 15
II II 0 0 0 IV 0 II 0 III 0 III 0 II IV IV III 0 II IV II II IV
0.06 0.07 0.09 0.09 0.09 0.09 0.1 0.1 0.1 0.1 0.11 0.13 0.14 0.14 0.14 0.14 0.15 0.15 0.16 0.17 0.21 0.24 0.32
WHO, World Health Organization; PA, pulmonary artery; RVC, right ventricular catheterization; Undiff CTD, undifferentiated connective tissue disorder. a Onset of symptoms is defined as first presenting symptom other than Raynaud phenomenon.
N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385–388
Fig. 2. Plot of P-wave amplitude in ECG lead II vs mPAP as determined by right ventricular catheterization. Linear regression analysis generated the regression line equation PAMP lead II = 0.022 mPAP + 0.731. Dotted lines represent the 95% confidence limits around the mean predicted values.
with limited scleroderma. Fifteen patients (65%) had functional class II or greater pulmonary hypertension on evaluation as defined by World Health Organization criteria. The duration of symptoms ranged from 1 to 27 years, with a mean duration of 8.3 years at presentation. Mean pulmonary artery pressure by right heart catheterization was 28 F 14 mm Hg. Eleven patients (48%) had mPAP greater than 25 mm Hg. P-wave amplitude in lead II ranged from 0.06 to 0.32 mV (median, 0.13 mV). An increase in mPAP was associated with an increase in P-wave amplitude in lead II (r = 0.52, P = .011) (Fig. 2). Mean pulmonary artery pressure predicted by linear regression analysis from P-wave amplitude on the ECGs was 28 F 27 mm Hg. A P-wave amplitude of 0.12 mV corresponded to mPAP of 25 mm Hg on the regression line. This calculated upperlimit-of-normal lead II P-wave amplitude value had a sensitivity of 73% and a specificity of 67% for detecting mPAP greater than 25 mm Hg. The model was similar when lead II P-wave amplitude was plotted as a function of PVR. This had a sensitivity of 58% and a specificity of 82%. Discussion Increased PVR initiates a sequence of right ventricular pressure overload, elevated tricuspid regurgitant velocity, enlargement of the right atrium, and distension of the inferior vena cava. Elevated right atrial pressure triggers right atrial enlargement and associated increases in P-wave amplitude on the inferior leads of the ECG. Increased Pwave amplitude greater than 0.25 mV in lead II of the ECG has been independently correlated with reduced survival in patients with idiopathic pulmonary arterial hypertension.12 In addition, a dynamic decrease in P-wave amplitude has been noted in patients with chronic obstructive pulmonary disease after recovery from acute exacerbation.13 Although ECG criteria for pulmonary hypertension are well defined, this study explores a linear regression model relating P-wave amplitude and mPAP. Pulmonary vascular
387
resistance is related to mPAP by the equation PVR = (mPAP PCW)/CO where PCW is pulmonary capillary wedge pressure (mm Hg) and CO is cardiac output (L/min). As expected, there was an excellent correlation between PVR and mPAP with r = 0.91. Although PVR, a gold standard for assessing pulmonary hypertension, showed greater specificity with ECG criteria, mPAP showed better overall correlation with the data. Mean pulmonary artery pressure has been validated as a factor in predicting the likelihood of survival in patients with pulmonary arterial hypertension.5,14 In addition, assessment of pulmonary artery pressures is in widespread use in most clinical settings. Right heart catheterization remains the gold standard in the assessment of pulmonary hypertension.15 The application of P-wave amplitude in a linear regression analysis is noninvasive and straightforward. In addition, automated programs could be used to directly and accurately calculate P-wave amplitude on the 12-lead ECG and perform simple mathematical analysis to derive projected pulmonary arterial pressures. This is preferable to the tedious manual process we used to precisely measure P-wave amplitude. The signal-averaged ECG has been used to assess right atrial dimensions in the setting of delayed atrial conduction secondary to right atrial enlargement.16 In addition, imaging methods including tricuspid regurgitant velocity by echocardiography, pulmonary artery dilation, pulmonary artery velocity by cardiac magnetic resonance imaging, and Doppler tissue imaging have been investigated.15 Limitations of this study include small sample size. In addition, only 3 (13%) of the 23 patients were men. Of the 23 patients, 12 (52%) had limited scleroderma, which may have a different prevalence of pulmonary hypertension compared with systemic sclerosis. Furthermore, these results may not be applicable to patients with pulmonary hypertension of other etiologies.17,18 Although useful in the identification of pulmonary hypertension in patients with scleroderma, P-wave amplitude on the 12-lead ECG lacks adequate sensitivity and specificity for definitive detection and treatment. However, our findings could be integrated into a larger analysis to gain further knowledge of P-wave utility in screening and diagnosis of pulmonary hypertension in patients with scleroderma.
References 1. Rolla G, Colagrande P, Scappaticci E, et al. Exhaled nitric oxide in systemic sclerosis: relationships with lung involvement and pulmonary hypertension. J Rheumatol 2000;27:1693. 2. Stupi A, Steen VD, Owens GR, Barnes EL, Rodnan GP, Medsger Jr TA. Pulmonary hypertension in the CREST syndrome variant of systemic sclerosis. Arthritis Rheum 1986;4:515. 3. McLaughlin VV, Presber KW, Doyle RL, et al. Prognosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004;126(1 Suppl):78S. 4. Sandoval J, Bauerle O, Palomar A, et al. Survival in primary pulmonary hypertension. Validation of a prognostic equation. Circulation 1994;89:1733.
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N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385 – 388
5. D’Alonzo GE, Barst RJ, Ayres SM, et al. Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. Ann Intern Med 1991;115:343. 6. Targa L, Cardin G, Cozzi F, Glorioso S, Rossi L, Todesco S. Electrocardiographic disorders in diverse clinical variations of scleroderma. G Clin Med 1990;71:17 [Italian]. 7. Morelli S, Sgreccia A, Ferrante L, et al. Relationships between electrocardiographic and echocardiographic findings in systemic sclerosis (scleroderma). Int J Cardiol 1996;57:151. 8. Edmundoptics.com [homepage on the Internet] Barrington, NJ: Edmund Optics, Inc. c2005. Available from: http://www.edmundoptics.com/. 9. Prineas RJ, Crow RS, Blackburn H. The Minnesota Code Manual of Electrocardiographic Findings. Standards and Procedures for Measurement and Classification. Boston7 John Wright PSG Inc; 1982. 10. American Rheumatism Association Diagnostic and Therapeutic Criteria Committee. Preliminary criteria for the classification of systemic sclerosis (scleroderma). Subcommittee for scleroderma criteria of the American Rheumatism Association Diagnostic and Therapeutic Criteria Committee. Arthritis Rheum 1980;23:581. 11. SAS Procedures Guide, Version 8. Cary (NC): SAS Institute, Inc; 1999. p. 1643.
12. Bossone E, Paciocco G, Iarussi D, et al. The prognostic role of the ECG in primary pulmonary hypertension. Chest 2002; 121:513. 13. Asad N, Johnson VM, Spodick D. Acute right atrial strain: regression in normal as well as abnormal P-wave amplitudes with treatment of obstructive pulmonary disease. Chest 2003;124:560. 14. Galie N, Torbicki A, Barst R, et al. ESC Guidelines on diagnosis and treatment of pulmonary arterial hypertension. Eur Heart J 2004; 25:2243. 15. Hsu VM, Shinnar M, Moreyra A, et al. Assessment of pulmonary hypertension (PH) in systemic sclerosis(SSc): a comparison of Doppler echocardiography, cardiac MRI, and right heart catheterization. Arthritis Rheum 2004;50:S424 [Abstract #1059]. 16. Dixen U, Joens C, Rasmussen BV, Parner J, Jensen GB. Signalaveraged P wave duration and the dimensions of the atria. Ann Noninvasive Electrocardiol 2004;9:309. 17. Jobsis MM, Crow JW, Long W. Echocardiographic predictors of adverse outcomes in primary pulmonary hypertension. J Am Coll Cardiol 2002;39:1214. 18. Gaine SP, Rubin LJ. Primary pulmonary hypertension. Lancet 1998; 352:719.
P-wave amplitude and pulmonary artery pressure in scleroderma Nina Wokhlu, MD,a Vivien M. Hsu, MD,b Alan Wilson, PhD,a Abel E. Moreyra, MD,a Daniel Shindler, MD a,4 a Division of Cardiology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA Division of Rheumatology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA Received 11 October 2005; accepted 24 January 2006
b
Abstract
Background and Purpose: Scleroderma is an immune-mediated disease characterized by excess deposition of collagen leading to microvascular occlusion. Morbidity and mortality are often secondary to pulmonary hypertension from injury to pulmonary microvasculature and interstitial lung disease. This study correlated P-wave findings on the 12-lead electrocardiogram (ECG) with mean pulmonary artery pressure (mPAP) measured by right heart catheterization in patients with scleroderma. Methods: A retrospective review of 12-lead ECGs in 23 patients referred to a rheumatology clinic with the diagnosis of scleroderma was performed. Right heart catheterization was performed within 1 month of the resting ECG. Results: Linear regression related P-wave amplitude in lead II with mPAP (r = 0.52, P = .011) This model was 73% sensitive and 67% specific for the presence or absence of elevated mPAP. Conclusions: P-wave amplitude analysis on the ECG may be helpful in the assessment of pulmonary hypertension in patients with scleroderma. D 2006 Elsevier Inc. All rights reserved.
Keywords:
P-wave amplitude; Electrocardiogram; Scleroderma
Introduction Scleroderma is an immune-mediated disease characterized by excess production and deposition of collagen. This results in progressive microvascular constriction and eventual luminal obliteration. Pulmonary hypertension is observed in patients with scleroderma with a prevalence of 4% to 38%.1,2 Major causes of mortality in this population are injury to the pulmonary microvasculature and interstitial lung disease with the typical manifestations of cor pulmonale. Prognosis in patients with scleroderma and pulmonary hypertension is significantly worse than in patients with other causes of pulmonary hypertension, that is, congenital heart disease, idiopathic pulmonary arterial hypertension, portopulmonary hypertension, and early HIV.3 Electrocardiographic (ECG) findings have been investigated in idiopathic pulmonary arterial hypertension and, to a lesser extent, in pulmonary hypertension of other etiolo-
4 Corresponding author. Tel.: +1 732 235 7855; fax: +1 732 235 8722. E-mail address: [email protected] (D. Shindler). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.01.004
gies.1,3-5 Scleroderma studies address overall prevalence of ECG manifestations rather than significance of individual ECG findings.6 Morelli and colleagues7 have compared ECG findings in 72 patients with echocardiographic findings in patients with scleroderma. Right heart catheterization, however, was not performed. We measured P-wave amplitude on 12-lead ECGs in patients with scleroderma using a high-resolution optical magnifier capable of 0.01-mV precision.8,9 The objective of this study was to determine the strength of correlation between P-wave amplitude on the 12-lead ECG and the degree of elevation of mean pulmonary artery pressure (mPAP) in a population of patients with scleroderma.
Study population and methods A retrospective review of 12-lead ECGs in 23 patients with the diagnosis of scleroderma referred to a rheumatology clinic at a university hospital was performed. The diagnosis of scleroderma was based on one major criterion or two minor criteriac from the guidelines defined by the
386
N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385 – 388
3 Wood units. During exercise, patients performed at least 3 minutes of arm exercise with 5-lb dumbbells until fatigued. Prior to discontinuing exercise, pulmonary artery pressure, cardiac output, and pulmonary capillary wedge pressure were recorded. Patients with pulmonary hypertension from causes other than scleroderma, including pulmonary venous hypertension and other factors that could contribute to increased left atrial pressure, were excluded from the study. Statistical analysis Correlation was made by linear regression between 12-lead ECG P-wave amplitude and pulmonary artery pressures obtained during right heart catheterization. Where applicable, variables were presented as mean F SD. Data were analyzed with SAS Version 8.2 (SAS Institute Inc, Cary, NC).11 Using linear regression, P-wave amplitude in lead II (mV) was plotted as a function of mPAP (mm Hg) and PVR (Wood units). Sensitivity and specificity were analyzed using the LOGISTIC procedure function of SAS. Results
Fig. 1. Manual loop magnifier. It is a cylindrical structure with a triplet viewing lens and a surface lens on the opposite side with an imprinted 20-mm grid that is placed directly on ECG paper to avoid parallax error. The loop provides a 1-in field of view and 6 magnification. Reprinted with permission.9
10
American College of Rheumatology. Onset of symptoms was defined as the first presenting symptom other than Raynaud phenomenon. P-wave amplitude was measured in lead II on standard 12-lead ECGs. Measurements were performed using a magnified measuring loop device (Fig. 1).8 The loop magnifier was used to obtain precise P-wave amplitude measurements on each 12-lead ECG to the nearest 0.1 mm (0.01 mV). The measurement of P-wave amplitude was recorded based on the technique described in the Minnesota Code Manual of Electrocardiographic Findings.9 Complexes that contained excessive artifact were not included in the analysis. Right heart catheterization was performed within 1 month of the ECG. Cardiac output was measured by the thermodilution technique. Pulmonary artery pressure was measured by right heart catheterization. Elevated mPAP was defined as greater than 25 mm Hg at rest or greater than 30 mm Hg with exercise. Elevated pulmonary vascular resistance (PVR) was defined as greater than c Major criteria include symmetrical skin thickening, tightening, and induration proximal to the metacarpophalangeal or metatarsophalangeal joints. Minor criteria include sclerodactyly (skin thickening limited to fingers or toes), digital pitting scars or loss of finger pad substance, and bibasilar pulmonary fibrosis.
Table 1 shows the demographic and study variables. Mean age was 53 F 14 years. The group (n = 23) consisted of 20 (87%) women. Twelve patients (52%) were diagnosed Table 1 Patient variables Age at Sex Type of Symptom Pulmonary P-wave ECG scleroderma duration at hypertension amplitude (y) ECGa (y) (WHO class) on ECG (mV)
Mean PA Pressure on RVC (mm Hg)
66 79 20 69 58 45 34 54 36 43 46 53 41 44 77 64 58 51 57 53 59 60 54
24 12 12 18 18 42 10 24 28 34 15 47 11 12 33 56 30 37 22 37 23 43 54
F F F F F M M F M F F F F F F F F F F F F F F
Limited Limited Undiff CTD Limited Diffuse Limited Limited Limited Diffuse Diffuse Diffuse Limited Limited Diffuse Limited Diffuse Diffuse Diffuse Overlap Limited Diffuse Limited Limited
15 18 27 4 6 1 11 4 1 2 6 4 20 5 1 6 4 4 3 12 16 12 15
II II 0 0 0 IV 0 II 0 III 0 III 0 II IV IV III 0 II IV II II IV
0.06 0.07 0.09 0.09 0.09 0.09 0.1 0.1 0.1 0.1 0.11 0.13 0.14 0.14 0.14 0.14 0.15 0.15 0.16 0.17 0.21 0.24 0.32
WHO, World Health Organization; PA, pulmonary artery; RVC, right ventricular catheterization; Undiff CTD, undifferentiated connective tissue disorder. a Onset of symptoms is defined as first presenting symptom other than Raynaud phenomenon.
N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385–388
Fig. 2. Plot of P-wave amplitude in ECG lead II vs mPAP as determined by right ventricular catheterization. Linear regression analysis generated the regression line equation PAMP lead II = 0.022 mPAP + 0.731. Dotted lines represent the 95% confidence limits around the mean predicted values.
with limited scleroderma. Fifteen patients (65%) had functional class II or greater pulmonary hypertension on evaluation as defined by World Health Organization criteria. The duration of symptoms ranged from 1 to 27 years, with a mean duration of 8.3 years at presentation. Mean pulmonary artery pressure by right heart catheterization was 28 F 14 mm Hg. Eleven patients (48%) had mPAP greater than 25 mm Hg. P-wave amplitude in lead II ranged from 0.06 to 0.32 mV (median, 0.13 mV). An increase in mPAP was associated with an increase in P-wave amplitude in lead II (r = 0.52, P = .011) (Fig. 2). Mean pulmonary artery pressure predicted by linear regression analysis from P-wave amplitude on the ECGs was 28 F 27 mm Hg. A P-wave amplitude of 0.12 mV corresponded to mPAP of 25 mm Hg on the regression line. This calculated upperlimit-of-normal lead II P-wave amplitude value had a sensitivity of 73% and a specificity of 67% for detecting mPAP greater than 25 mm Hg. The model was similar when lead II P-wave amplitude was plotted as a function of PVR. This had a sensitivity of 58% and a specificity of 82%. Discussion Increased PVR initiates a sequence of right ventricular pressure overload, elevated tricuspid regurgitant velocity, enlargement of the right atrium, and distension of the inferior vena cava. Elevated right atrial pressure triggers right atrial enlargement and associated increases in P-wave amplitude on the inferior leads of the ECG. Increased Pwave amplitude greater than 0.25 mV in lead II of the ECG has been independently correlated with reduced survival in patients with idiopathic pulmonary arterial hypertension.12 In addition, a dynamic decrease in P-wave amplitude has been noted in patients with chronic obstructive pulmonary disease after recovery from acute exacerbation.13 Although ECG criteria for pulmonary hypertension are well defined, this study explores a linear regression model relating P-wave amplitude and mPAP. Pulmonary vascular
387
resistance is related to mPAP by the equation PVR = (mPAP PCW)/CO where PCW is pulmonary capillary wedge pressure (mm Hg) and CO is cardiac output (L/min). As expected, there was an excellent correlation between PVR and mPAP with r = 0.91. Although PVR, a gold standard for assessing pulmonary hypertension, showed greater specificity with ECG criteria, mPAP showed better overall correlation with the data. Mean pulmonary artery pressure has been validated as a factor in predicting the likelihood of survival in patients with pulmonary arterial hypertension.5,14 In addition, assessment of pulmonary artery pressures is in widespread use in most clinical settings. Right heart catheterization remains the gold standard in the assessment of pulmonary hypertension.15 The application of P-wave amplitude in a linear regression analysis is noninvasive and straightforward. In addition, automated programs could be used to directly and accurately calculate P-wave amplitude on the 12-lead ECG and perform simple mathematical analysis to derive projected pulmonary arterial pressures. This is preferable to the tedious manual process we used to precisely measure P-wave amplitude. The signal-averaged ECG has been used to assess right atrial dimensions in the setting of delayed atrial conduction secondary to right atrial enlargement.16 In addition, imaging methods including tricuspid regurgitant velocity by echocardiography, pulmonary artery dilation, pulmonary artery velocity by cardiac magnetic resonance imaging, and Doppler tissue imaging have been investigated.15 Limitations of this study include small sample size. In addition, only 3 (13%) of the 23 patients were men. Of the 23 patients, 12 (52%) had limited scleroderma, which may have a different prevalence of pulmonary hypertension compared with systemic sclerosis. Furthermore, these results may not be applicable to patients with pulmonary hypertension of other etiologies.17,18 Although useful in the identification of pulmonary hypertension in patients with scleroderma, P-wave amplitude on the 12-lead ECG lacks adequate sensitivity and specificity for definitive detection and treatment. However, our findings could be integrated into a larger analysis to gain further knowledge of P-wave utility in screening and diagnosis of pulmonary hypertension in patients with scleroderma.
References 1. Rolla G, Colagrande P, Scappaticci E, et al. Exhaled nitric oxide in systemic sclerosis: relationships with lung involvement and pulmonary hypertension. J Rheumatol 2000;27:1693. 2. Stupi A, Steen VD, Owens GR, Barnes EL, Rodnan GP, Medsger Jr TA. Pulmonary hypertension in the CREST syndrome variant of systemic sclerosis. Arthritis Rheum 1986;4:515. 3. McLaughlin VV, Presber KW, Doyle RL, et al. Prognosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004;126(1 Suppl):78S. 4. Sandoval J, Bauerle O, Palomar A, et al. Survival in primary pulmonary hypertension. Validation of a prognostic equation. Circulation 1994;89:1733.
388
N. Wokhlu et al. / Journal of Electrocardiology 39 (2006) 385 – 388
5. D’Alonzo GE, Barst RJ, Ayres SM, et al. Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. Ann Intern Med 1991;115:343. 6. Targa L, Cardin G, Cozzi F, Glorioso S, Rossi L, Todesco S. Electrocardiographic disorders in diverse clinical variations of scleroderma. G Clin Med 1990;71:17 [Italian]. 7. Morelli S, Sgreccia A, Ferrante L, et al. Relationships between electrocardiographic and echocardiographic findings in systemic sclerosis (scleroderma). Int J Cardiol 1996;57:151. 8. Edmundoptics.com [homepage on the Internet] Barrington, NJ: Edmund Optics, Inc. c2005. Available from: http://www.edmundoptics.com/. 9. Prineas RJ, Crow RS, Blackburn H. The Minnesota Code Manual of Electrocardiographic Findings. Standards and Procedures for Measurement and Classification. Boston7 John Wright PSG Inc; 1982. 10. American Rheumatism Association Diagnostic and Therapeutic Criteria Committee. Preliminary criteria for the classification of systemic sclerosis (scleroderma). Subcommittee for scleroderma criteria of the American Rheumatism Association Diagnostic and Therapeutic Criteria Committee. Arthritis Rheum 1980;23:581. 11. SAS Procedures Guide, Version 8. Cary (NC): SAS Institute, Inc; 1999. p. 1643.
12. Bossone E, Paciocco G, Iarussi D, et al. The prognostic role of the ECG in primary pulmonary hypertension. Chest 2002; 121:513. 13. Asad N, Johnson VM, Spodick D. Acute right atrial strain: regression in normal as well as abnormal P-wave amplitudes with treatment of obstructive pulmonary disease. Chest 2003;124:560. 14. Galie N, Torbicki A, Barst R, et al. ESC Guidelines on diagnosis and treatment of pulmonary arterial hypertension. Eur Heart J 2004; 25:2243. 15. Hsu VM, Shinnar M, Moreyra A, et al. Assessment of pulmonary hypertension (PH) in systemic sclerosis(SSc): a comparison of Doppler echocardiography, cardiac MRI, and right heart catheterization. Arthritis Rheum 2004;50:S424 [Abstract #1059]. 16. Dixen U, Joens C, Rasmussen BV, Parner J, Jensen GB. Signalaveraged P wave duration and the dimensions of the atria. Ann Noninvasive Electrocardiol 2004;9:309. 17. Jobsis MM, Crow JW, Long W. Echocardiographic predictors of adverse outcomes in primary pulmonary hypertension. J Am Coll Cardiol 2002;39:1214. 18. Gaine SP, Rubin LJ. Primary pulmonary hypertension. Lancet 1998; 352:719.