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(Chest. 2002;121:513-518.)
© 2002 American College of Chest Physicians

The Prognostic Role of the ECG in Primary Pulmonary Hypertension*

Eduardo Bossone, MD, PhD, FCCP; Giuseppe Paciocco, MD, FCCP; Diana Iarussi, MD; Angelo Agretto, MD, FCCP; Aldo Iacono, MD; Brenda W. Gillespie, PhD and Melvyn Rubenfire, MD, FCCP

* From the Division of Cardiology, Department of Internal Medicine (Drs. Bossone, Paciocco, and Rubenfire), and Center for Statistical Consultation and Research (Dr. Gillespie), University of Michigan, Ann Arbor, MI; and Dipartimento di Cardiologia (Drs. Iarussi, Agretto, and Iacono), II Universita’ degli Studi, Napoli, Italy.

Correspondence to: Melvyn Rubenfire MD, FCCP, University of Michigan, Preventive Cardiology, 24 Frank Lloyd Wright Dr, Ann Arbor, MI 48106-0363; e-mail: mrubenfi{at}umich.edu


   Abstract
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 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
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Background/rationale: Doppler echocardiography and invasive hemodynamic parameters reflective of right ventricular failure are associated with a poor prognosis in patients with primary pulmonary hypertension (PPH). The aims of the present study were to examine whether ECG features in patients with PPH are associated with a decrease in survival, and to determine the value of the ECG in risk stratification.

Methods/results: We analyzed the ECG, New York Heart Association (NYHA) class, and hemodynamic parameters in 51 untreated patients with PPH (88% women; mean age, 41.7 years; 79% NYHA classes III and IV) evaluated between 1992 and 1998. Subsequent treatment included epoprostenol in 37 patients, calcium channel blockers in 10 patients, epoprostenol and atrial septostomy in 2 patients, and lung transplant in 3 patients. As of 1999, 16 patients had died. Based on Kaplan-Meier estimates, median survival was > 6.5 years and estimated survival at 1 year, 3 years, and 5 years was 86%, 71%, and 57%, respectively. Significant predictors of decreased survival by Cox regression analysis include pulmonary vascular resistance (PVR; hazard ratio [HR], 1.11 per Wood unit), cardiac index (HR, 0.22 per L/min/m2), p wave amplitude in lead II (HR, 3.06 per mm), p >= 0.25 mV in lead II (HR, 2.77), qR in V1 (HR, 3.55), and World Health Organization criteria for right ventricular hypertrophy (HR, 4.26). After controlling for PVR, the HRs attributable to the ECG criteria were only slightly diminished. NYHA class and pulmonary artery pressures did not correlate with a decrease in survival.

Conclusions: ECG parameters reflective of physiologic and anatomic abnormalities in the right ventricle are associated with decreased survival in patients with PPH, and may be useful for deciding therapeutic choices including the timing for lung transplantation listing.

Key Words: ECG • primary pulmonary hypertension • prognosis


   Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Primary pulmonary hypertension (PPH) is a progressive disease of the pulmonary vasculature characterized by a poor prognosis, which is mainly attributable to progressive right-heart failure.1 2 Recent advances in treatment have altered the course in patients with PPH, but the prognosis remains relatively poor and unpredictable.3 4 5 In selected patients, atrial septostomy6 and lung and heart-lung transplant7 can be effective options for patients with unsuccessful therapy, but an uncertain natural history2 5 8 and an 18-month to 24-month waiting list for transplant adds to the difficulty of therapeutic decisions.9 10

Hemodynamic11 and Doppler echocardiographic12 indexes of impaired right ventricular function, New York Heart Association (NYHA) clinical class,11 and the absence of pulmonary vasodilator reserve13 have been associated with a poor outcome, but these parameters are not predictive of treatment failure and early mortality in epoprostenol-treated subjects.5 10 Miyamoto et al14 recently reported that the distance achieved on the 6-min walk test has a strong independent association with mortality in patients treated with inhaled and IV prostacyclin. We have also found the 6-min walk test predictive of outcome in a similar population with PPH, in particular the degree of arterial desaturation occurring at peak distance.15

ECG evidence for left ventricular hypertrophy is an independent predictor of myocardial infarction, heart failure, and death in patients with hypertension.16 ECG criteria for left ventricular hypertrophy as well as right ventricular hypertrophy (RVH) are reflective of both anatomic and physiologic changes in the atria and ventricles. ECG criteria for RVH have been shown to correlate with mortality in patients with PPH.17 18 However, these studies were performed prior to the use of treatment with vasodilators and epoprostenol. The aim of the present study was to examine whether pretreatment ECG parameters are associated with a decreased survival in the "epoprostenol era."


   Materials and Methods
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 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Population
Consecutive patients evaluated in a pulmonary hypertension program between September 1992 and July 1998 with newly diagnosed PPH (criteria per the National Institutes of Health registry)1 were enrolled in a study designed to determine factors associated with mortality in patients with PPH. Patients with PPH associated with HIV were excluded. The standard protocol for all patients included a clinical examination, 6-min walk test, chest radiography, ECG, and echocardiography. Symptoms (type and duration), effort tolerance, and NYHA class were recorded at the initial visit. A right-heart catheterization and acute challenge to assess pulmonary vasoreactivity was performed with IV adenosine,19 inhaled nitric oxide,20 and or nifedipine.21

Treatment Strategy and Follow-up
A standardized treatment regimen was followed in all patients. Patients with edema or receiving epoprostenol were contacted regularly by a nurse for diuretic or epoprostenol dose adjustment (average, 2 to 3 weeks). In the event of death outside our institution, the date and circumstances of death were obtained from attending physicians and family members.

Treatment options were determined by assessing pulmonary vasodilator reserve as previously reported.19 20 21 Patients with at least a 20% reduction in mean pulmonary artery pressure (mPAP) and or pulmonary vascular resistance (PVR) during the acute challenge underwent a dose-titration response with short-acting nifedipine or diltiazem to determine the optimal daily dose prescribed as a sustained release preparation.21 From 1992 to 1995, IV epoprostenol therapy or lung transplant when feasible were utilized in patients unsuccessfully treated with nifedipine. After 1995, epoprostenol was administered to all patients in NYHA class IV, to all patients in NYHA class III with less than a 20% reduction in PVR, or when nifedipine was contraindicated. Digoxin and anticoagulation with warfarin were prescribed in the absence of contraindications. Patients < 60 years of age were referred for lung or heart-lung transplant evaluation and listing. Those listed who maintained an improved NYHA class and functional capacity as determined by 6-min walk testing and improved hemodynamic indexes were placed on transplant hold.

ECG
Standard 12-lead ECGs were performed in the supine position by certified ECG technicians (Muse Network Series; Marquette Electronics; Milwaukee, WI) [paper speed, 25 mm/s; sensitivity of 1 mV = 10 mm]. The ECG parameters evaluated included rate and rhythm, PR or PQ and QRS duration, mean frontal plane axis of the P and QRS, and ST-segments, and T wave vectors. RVH was assessed with the following sets of published ECG criteria: World Health Organization (WHO), Heikkila, Louridas, Butler, and Lehtonen et al.22

ECG variables were measured with and without a magnifying lens and divider and analyzed with standard ECG nomenclature and definitions23 24 by two investigators blinded to clinical and hemodynamic data and outcome. The first investigator performed the initial measurements and entered the results on a case report form. The second investigator reviewed these determinations prior to computer data entry. Any discrepancies between investigators were resolved by joint re-review.

Statistical Analysis
Where applicable, variables are described using a mean ± SD and range. Length of survival after initial ECG (at the time of diagnosis) is described using Kaplan-Meier survival estimates. Hemodynamic and ECG variables and NYHA functional class were examined as possible predictors of survival time using the Cox proportional-hazards model. Hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) are presented. Initially, all variables were entered individually in the models. The ECG parameters were reanalyzed after controlling for the strongest non-ECG predictors.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Demographic, clinical, and hemodynamic data are presented in Table 1 . Forty-five of the 51 patients were female, and 79% were classified to NYHA functional class III or IV. The initial dominant symptom was dyspnea on exertion in 92%. Syncope occurred in 20% and chest pain in 16%. The mean time from onset of symptoms to diagnosis was 20.6 ± 20.2 months (median, 12 months; range, 1 to 84 months). Long-term IV epoprostenol was administered in 37 patients, calcium channel blockers were administered in 10 patients, and 3 patients underwent lung transplantation. Two patients died within a month of the diagnosis in spite of treatment with IV epoprostenol, an atrial septostomy, and extracorporeal membrane oxygenation.


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  		Table 1.. Demographic, Clinical, and Hemodynamic Data*

 
ECG Findings
Sinus rhythm was present in 48 of the 51 patients (94%). Two patients had sinus bradycardia, five patients had sinus tachycardia, six patients had a first-degree AV block, one patient had an AV sequential pacemaker, one patient had a junctional rhythm, and one patient had an ectopic atrial rhythm. The measured ECG parameters are summarized in Table 2 . The mean frontal plane p wave axis was 58.1 ± 19.4° (range, - 21° clockwise to + 117°) and > 70° in 8 of the 48 patients (17%) in sinus rhythm. Excluding the patient with a pacemaker, the mean frontal plane QRS axis (aQRS) was 103.1 ± 52.3° (range, - 111° clockwise to + 175°) and > 90° in 78%; in the horizontal plane, electrical clockwise rotation was seen in 76% and counterclockwise rotation in 10%. The most common QRS patterns in V1 were rSR' (20%) and qR in 18%, which are characteristic of RVH. Complete right bundle branch block was present in only 4%.


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  		Table 2.. Summary of ECG Data*

 
ECG criteria for RVH was present using the criteria of Lehtonen et al in 96%, Heikkila in 90%, Louridas in 60%, the WHO in 48%, and by Butler in 38%. ST-T depression (>= 1 mm) and T wave inversions suggestive of ischemia or strain were very common in the inferolateral leads (II, III, aVF, V4, V5, V6) and right precordial leads (Table 3 ).22


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  		Table 3.. Distribution of T Wave Inversion and ST-T Depression >= 1 mm in 50 Subjects*

 
Follow-up Data
As of March 1999, sixteen patients died, 31 patients were alive, 3 patients underwent lung transplantation, and 1 was unavailable for follow-up. For the latter four patients, survival times were considered censored (time end point for survival) at the time of last visit or transplant. Median survival time was > 6.5 years. The estimated percentages of patients surviving at 1 year, 3 years, and 5 years were 86% (95% CI, 77 to 96%), 71% (95% CI, 58 to 84%), and 57% (95% CI, 34 to 81%; Fig 1 ). All 16 deaths were attributable to progressive right-heart failure.



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  		Figure 1.. Estimated percentage of patients surviving over time from date of ECG by Kaplan-Meier analysis. Tick marks show total follow-up time for patients still alive when the study ended (n = 31); one patient was unavailable for follow-up, and three patients received a lung transplant. Median survival is > 6.5 years. Estimated percentages of patients surviving at 1 year, 3 years, and 5 years are 86%, 69%, and 57%, respectively.

 
Variables Associated With Survival Duration
The variables associated with survival time based on Cox regression analysis are listed in Table 4 . Subjects in NYHA functional classes III and IV were compared to subjects in class II. While patients with greater pretreatment disability had shorter survival times (HR, 2.04), this relationship was not significant (p = 0.347).


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  		Table 4.. Predictors of Survival Time in Cox Regression Analysis*

 
Cardiac index was a significant predictor of mortality. An increasing cardiac index was associated with a decrease in mortality (HR, 0.22 per L/min/m2; 95% CI, 0.05 to 0.98; p = 0.047). The mortality increased with increasing PVR (HR, 1.11 per Wood unit; 95% CI, 1.02 to 1.21; p = 0.017) and increasing right atrial pressure (HR, 1.08 per mm Hg; 95% CI, 1.00 to 1.16; p = 0.05). Systolic, diastolic, and mPAPs were not significantly associated with survival time.

Of the ECG variables examined individually (Table 4) , p wave amplitude in leads II and III and in aVF, p >= 0.25 MV in lead II, qR in V1, and WHO RVH criteria were each significantly associated with increasing mortality. The risk of death increased 31% for each additional 10-beat/min increase in heart rate (HR, 1.31; 95% CI, 1.00 to 1.72; p = 0.064).

An additional mm of p wave amplitude in lead III corresponded with a 4.5-fold increase in risk of death (HR, 4.54; 95% CI, 1.40 to 14.79; p = 0.012). Among survivors, the average p wave amplitude in lead II at diagnosis was 1.7 ± 0.5 mm, as compared to 2.2 ± 0.8 mm in those who died. Whether measured by sight or calipers, a p >= 0.25 mV in lead II was associated with a 2.8-times greater risk of death (HR, 2.77; 95% CI, 1.03 to 7.45; p = 0.04).

The WHO criteria for RVH (not others) and several QRS morphologies were associated with decreased survival. A qR pattern in V1 increased the hazard of death by 3.6 times (HR, 3.55; 95% CI, 1.28 to 9.82; p = 0.015), and patients with RVH by the WHO criteria were 4.3 times more likely to die at any given time (HR, 4.26; 95% CI, 1.35 to 13.38; p = 0.013).

We analyzed the association of the ECG parameters with survival after controlling individually for PVR, right atrial pressure, and cardiac index and found most to still be significant. After controlling for PVR, the p wave amplitude in lead II, a qR in V1, and the WHO RVH criteria remained significantly predictive of an increased risk of death (Table 4) .


   Discussion
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
There is a strong association between ECG QRS and p wave features reflective of right ventricular and right atrial anatomy and physiology22 25 and mortality in patients with PPH. The ECG parameters remain predictive of outcome independent of hemodynamic parameters, NYHA class, and treatment including epoprostenol, and atrial septostomy. We have confirmed that the risk of death in PPH patients increases as resting heart rate increases.12 The tachycardia likely represents the neurohumoral response to a decreasing stroke volume and elevated circulating catecholamines present in PPH patients with impaired right ventricular function.12 26

The presence of a qR pattern in V1 and the magnitude of the p wave amplitude in the inferior leads (particularly lead II) were highly predictive of an adverse outcome. In 1980, Kanemoto17 reported that in 86 patients with PPH (pre-epoprostenol and treatment not specified), a qR was present in V1 in 21.6% of survivors and 42.1% of the deceased (p < 0.05), which is similar to the HR of > 3 in our study. In a separate report in 41 patients, Kanemoto27 reported the p wave amplitude in lead II was significantly greater in PPH patients who died suddenly (n = 12) or with right-heart failure (n = 19) than the 10 long-term survivors, again similar to our findings in patients treated with an aggressive and standardized protocol.

Each of the ECG parameters may reflect the severity of impairment of the right atrial and right ventricular function, and in particular the p wave morphology may be reflective of RVH and right ventricular diastolic parameters.28 29 30 RVH and right ventricular enlargement are consistently found on ECG and echocardiography in patients with PPH, and each has been demonstrated to correlate with the pulmonary pressures and cardiac index.12 31 32 The criteria of Lehtonen et al22 for RVH were fulfilled in 96% of our patients, but because of the very high prevalence had no prognostic value. In contrast, while considerably fewer fulfilled the WHO criteria for RVH, when present it was associated with a substantial increased risk of mortality independent of therapy.

The echocardiogram has decreased our dependency on the ECG and on catheterization to make the diagnosis of PPH. Yet, ECG criteria for RVH, right atrial enlargement, and heart rate still deliver valuable independent prognostic data for this disease, which may be used with other information for deciding therapeutic choices, including the timing for lung transplantation listing.


   Footnotes
 
Abbreviations: CI = confidence interval; HR = hazard ratio; mPAP = mean pulmonary artery pressure; NYHA = New York Heart Association; PPH = primary pulmonary hypertension; PVR = pulmonary vascular resistance; RVH = right ventricular hypertrophy; WHO = World Health Organization

Received for publication February 21, 2001. Accepted for publication June 1, 2001.


   References
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Rich, S, Dantzker, D, Ayres, S, et al (1987) Primary pulmonary hypertension: a national prospective study. Ann Intern Med 107,216-223
  2. Rubin, L (1997) Current concepts: primary pulmonary hypertension. N Engl J Med 336,111-117[Free Full Text]
  3. Rich, S, Kaufmann, E, Levy, P (1992) Effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. N Engl J Med 327,76-81[Abstract]
  4. Barst, R, Rubin, L, Long, W, et al (1996) Comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Med 334,296-302[Abstract/Free Full Text]
  5. Higenbottam, T, Butt, A, McMahon, A, et al (1998) Long-term intravenous prostaglandin (epoprostenol or iloprost) for treatment of severe pulmonary hypertension. Heart 80,151-155[Abstract/Free Full Text]
  6. Sandoval, J, Gaspar, J, Pulido, T, et al (1998) Graded balloon dilation atrial septostomy in severe primary pulmonary hypertension: a therapeutic alternative for patients nonresponsive to vasodilator treatment. J Am Coll Cardiol 32,297-304[Abstract/Free Full Text]
  7. Hosenpud, J, Bennett, L, Keck, B, et al (1998) The Registry of the International Society for Heart and Lung Transplantation: fifteenth official report–1998. J Heart Lung Transplant 17,656-668[ISI][Medline]
  8. Glanville, A, Burke, C, Theodore, J, et al (1987) Primary pulmonary hypertension: length of survival in patients referred for heart-lung transplantation. Chest 91,675-681[Abstract]
  9. Nootens, M, Freels, S, Kaufmann, E, et al (1994) Timing of single lung transplantation for primary pulmonary hypertension. J Heart Lung Transplant 13,276-281[ISI][Medline]
  10. Conte, J, Gaine, S, Orens, J, et al (1998) The influence of continuous intravenous prostacyclin therapy for primary pulmonary hypertension on the timing and outcome of transplantation. J Heart Lung Transplant 17,679-685[ISI][Medline]
  11. D’Alonzo, G, Barst, R, Ayres, S, et al (1991) Survival in patients with primary pulmonary hypertension: results from a national prospective registry. Ann Intern Med 115,343-349
  12. Eysmann, S, Palevsky, H, Reichek, N, et al (1989) Two-dimensional and Doppler-echocardiographic and cardiac catheterization correlates of survival in primary pulmonary hypertension. Circulation 80,353-360[Abstract/Free Full Text]
  13. Rich, S, Brundage, B, Levy, P (1985) The effect of vasodilator therapy on the clinical outcome of patients with primary pulmonary hypertension. Circulation 71,1191-1196[Abstract/Free Full Text]
  14. Miyamoto, S, Nagaya, N, Satoh, T, et al (2000) Clinical correlates and prognostic significance of six-minute walk test in patients with primary pulmonary hypertension: comparison with cardiopulmonary exercise testing. Am J Respir Crit Care Med 161,487-492[Abstract/Free Full Text]
  15. Paciocco, G, Martinez, F, Bossone, G, et al (2001) Oxygen desaturation during the six-minute walk is associated with mortality in untreated primary pulmonary hypertension. Eur Respir J 17,1-6[Free Full Text]
  16. Verdecchia, P, Schillaci, G, Borgioni, C, et al (1998) Prognostic value of a new electrocardiographic method for diagnosis of left ventricular hypertrophy in essential hypertension. J Am Coll Cardiol 31,383-390[Abstract/Free Full Text]
  17. Kanemoto, N (1981) Electrocardiogram in primary pulmonary hypertension. Eur Respir J 12,181-193
  18. Rozkovec, A, Montanes, P, Oakley, C (1986) Factors that influence the outcome of primary pulmonary hypertension. Br Heart J 55,449-458[Abstract/Free Full Text]
  19. Schrader, B, Inbar, S, Kaufmann, L, et al (1992) Comparison of the effects of adenosine and nifedipine in pulmonary hypertension. J Am Coll Cardiol 19,1060-1064[Abstract]
  20. Ricciardi, M, Knight, B, Martinez, F, et al (1998) Inhaled nitric oxide in primary pulmonary hypertension: a safe and effective agent for predicting response to nifedipine. J Am Coll Cardiol 32,1068-1073[Abstract/Free Full Text]
  21. Rich, S, Kaufmann, E (1991) High dose titration of calcium channel blocking agents for primary pulmonary hypertension: guidelines for short-term drug testing. J Am Coll Cardiol 18,1323-1327[Abstract]
  22. Lehtonen, J, Sutinen, S, Ikaheimo, M, et al (1988) Electrocardiographic criteria for the diagnosis of right ventricular hypertrophy verified at autopsy. Chest 93,839-842[Abstract]
  23. Goldman, M (1986) Principles of clinical electrocardiography 12th ed. Lange Medical Publications Los Altos, CA.
  24. Schamroth, L (1990) Introduction to electrocardiography 7th ed. Blackwell Scientific Publications London, UK.
  25. Roman, G, Walsh, T, Massie, E (1961) Right ventricular hypertrophy: correlation of electrocardiographic and anatomic findings. Am J Cardiol 7,481-487
  26. Rich, S, Seidlitz, M, Dodin, E, et al (1998) The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension. Chest 114,787-792[Abstract/Free Full Text]
  27. Kanemoto, N (1987) Electrocardiogram in primary pulmonary hypertension–with special reference to prognosis. Tokai J Exp Clin Med 12,173-179[Medline]
  28. . World Health Organization. (1953) Chronic cor pulmonale: report of an expert committee. Circulation 27,594-615
  29. Anselmi, G, Munoz-Armas, S, Salazar, A, et al (1968) Electrocardiographic patterns of right atrial overloading in some congenital heart conditions. Am J Cardiol 21,628-638[CrossRef][ISI][Medline]
  30. Sodi-Pallares, D, Bisteni, A, Hermann, G (1952) Some views on the significance of qR and QR type complexes in right precordial leads in the absence of myocardial infarction. Am Heart J 43,716-734
  31. Kanemoto, N (1988) Electrocardiographic and hemodynamic correlations in primary pulmonary hypertension. Angiology 39,781-787
  32. Bossone, E, Duong-Wanger, T, Paciocco, G, et al (1999) Echocardiographic features of primary pulmonary hypertension. J Am Soc Echocardiogr 12,655-662[CrossRef][ISI][Medline]



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