ORIGINAL PAPER
The Etiology-Filling Pattern-Pulmonary Artery Pressure Score: A Simple
Tool for Risk Stratification of Patients with Systolic Heart Failure
Alessandro Vallebona, MD; Guido Gigli, MD; Sandro Orlandi, MD; Davide Orlandi, MD; Lorenzo Gigli, PhD;
Giorgio Reggiardo, PhD
From the Department of Cardiology, Rapallo Hospital, Rapallo, Italy
Heart failure (HF) is a leading cause of morbidity and mor-
tality. The detection of patients at high risk for death is a
major challenge in HF management. The authors com-
pared the prognostic value of 23 clinical Doppler echocar-
diography and cardiopulmonary exercise indexes in a
stable, moderately symptomatic, systolic HF outpatient
population receiving optimal medical therapy. The end
point was the incidence of overall mortality. Between Janu-
ary 2002 and December 2008, a total of 146 patients with
left ventricular (LV) ejection fraction 0.310.8 and New
York Heart Association functional class II or III were
enrolled. The prognostic power of single variables was
assessed using chi-square test for categoric variables and
t test for continuous variables. Variables associated with
the prespecified end point were included as predictors in a
binary logistic regression multivariate model. At multivari-
Heart failure (HF) is a leading cause of morbidity and
mortality in Western society and a growing public health
problem. Almost 30 million people all over the world
have HF, with 5 million in the United States, and an inci-
dence of 550,000 new cases each year.1 It is likely that
the number of cases will rise in the coming years due to
better survival of ischemic heart disease and expansion
of the elderly population.2 Despite advances in manage-
ment and treatment, survival with HF continues to be
poor and the mortality rate is comparable to that of
many forms of cancer.3–5 The detection of patients at
high risk for death is a major challenge in the evaluation
and management process. Several clinical, functional,
and laboratory variables have been recognized to be
predictive of mortality.6–17 We compared the prognostic
value of 23 classical clinical Doppler echocardiography
and cardiopulmonary exercise (CPX) indexes in a stable,
moderately symptomatic, systolic HF outpatient popu-
lation receiving optimal medical therapy.
METHODS
Study Population
Consecutive HF outpatients who underwent their first
ambulatory visit between January 2002 and December
Address for correspondence: Alessandro Vallebona, Department of
Cardiology, Rapallo Hospital, via S Pietro 8, Rapallo, Genova 16035, Italy
E-mail: avallebona@asl4.liguria.it
Manuscript received: December 12, 2011; revised: February 6, 2012;
accepted: February 17, 2012
DOI: 10.1111/j.1751-7133.2012.00294.x
Congest Heart Fail. 2013;19:39–43
ate analysis, ‘‘restrictive’’ LV filling pattern (P=.004), ische-
mic etiology (P=.022), pulmonary artery systolic pressure
(PASP) 50 mm Hg (P=.027), and peak oxygen uptake
(VO2) <15.9 mL ⁄ kg ⁄ min (P=.046) resulted independent pre-
dictors of the outcome. A simple risk score was then
obtained using these significant independent variables,
excluding peak VO2 because of only borderline signifi-
cance. Patients with ischemic etiology, restrictive LV filling
pattern, and PASP 50 mm Hg have a very high risk of
death (odds ratio, 33.77; 95% confidence interval, 5.74–
198.8; P<.001, compared with patients with no risk fac-
tors). In this high-risk group, evaluation of peak VO2 could
be superfluous. A very simple clinical echocardiographic
model based on etiology-LV filling and pulmonary pressure
is a powerful tool for risk stratification of systolic HF in
ambulatory patients. 2012 Wiley Periodicals, Inc.
2008 were recruited. Inclusion criteria were chronic
symptomatic HF and New York Heart Association
functional class II or III, left ventricular (LV) ejection
fraction 0.40, and clinical stability while taking opti-
mized medical therapy for at least 3 months. Patients
with angina or silent ischemia, myocardial infarction or
heart surgery during the past 6 months, HF due to
primitive valvular disease, anemia (hemoglobin
<11 g ⁄ dL), neoplasia, and contraindication to exercise
testing for cardiac or noncardiac reasons were excluded.
Enrolled patients performed clinical examination, elec-
trocardiography, Doppler echocardiographic study, and
CPX. The etiology of HF was defined as ischemic in
patients with previous myocardial infarction and ⁄ or
surgical or percutaneous revascularization and ⁄ or previ-
ous coronary angiography showing at least one critical
coronary stenosis (>50% luminal narrowing).
Echocardiography
The Hewlett-Packard Sonos 5500 echograph (Philips,
Amsterdam, The Netherlands) was used. Ejection frac-
tion was calculated by means of the modified Simp-
son’s rule.18 LV mass was calculated using the
American Society of Echocardiography19 formula. LV
filling was obtained by pulsed wave Doppler mitral
velocity profile from the 4-chamber apical view by
positioning a sample volume between the tips of the
mitral valve leaflets in diastole. LV filling pattern was
classified as ‘‘restrictive’’ (E ⁄ A ratio >2 or from 1 to 2
with E-wave deceleration time 140 ms) or
‘‘nonrestrictive’’ in the other cases. In case of atrial
Vol. 19 | No. 1 | January . February 2013 39
a simple tool for risk stratification in systolic heart failure
fibrillation, only E-wave deceleration time was used to
discriminate the restrictive pattern. Five beats were
measured and the mean value was utilized. Mitral
regurgitation was evaluated from the apical view and
graded as mild, moderate, or severe on the basis of the
area covered by the regurgitant signals visualized with
color Doppler flow.20 Pulmonary artery systolic pres-
sure (PASP) was estimated from the 4-chamber apical
or parasternal short-axis view, using continuous-wave
Doppler between the tricuspid valve leaflets, applying
the modified Bernoulli equation and adding right atrial
pressure to systolic gradient across the tricuspid
valve.21 Right atrial pressure was assumed to vary
from 5 mm Hg to 20 mm Hg and was clinically rated
from the height of jugular vein with the patient lying
at a 45 angle.22 Doppler-derived PASP was catego-
rized as <50 mm Hg or 50 mm Hg.20
Cardiopulmonary Exercise Testing
All tests were performed in the morning immediately
after echocardiographic examination using a bicycle
ergometer with the physician unaware of the result of
the previous echocardiogram. One to 7 days before
CPX, all patients performed a preliminary test in order
to become familiar with it. After a 1-minute warm-up
period at 0 W, a 10-W ⁄ minute incremental protocol
was started. Ventilation (VE), oxygen uptake (VO2),
and carbon dioxide production (VCO2) were monitored
online (OXYCONDELTA; Jaeger, Wurzburg, Ger-
many). Calibration with reference gases was performed
immediately before each test. A standard 12-lead elec-
trocardiogram was continuously recorded. Ventilatory
anaerobic threshold was determined by the ventilatory
equivalent for VO2 or by the V slope method.23 Peak
VO2 was defined as the highest O2 consumption
obtained during the test and peak VE ⁄ VCO2 was
defined as the value of the ventilatory equivalent for
VCO2 at the time of the peak VO2. Resting heart rate
was defined as the lowest recorded in the upright posi-
tion before exercising and peak heart rate as the highest
obtained during exercise. The heart rate response to
exercise was assessed by the chronotropic index calcu-
lated by the formula suggested by Robbins and col-
leagues11: peak heart rate-rest heart rate ⁄ 220-age-rest
heart rate 100. Patients were encouraged to exercise
until limiting dyspnea or fatigue.
Follow-Up
Follow-up was obtained through clinic visit or phone
call after 1 year and then every 6 months. The end
point was mortality for any cause. In all cases, the
events were confirmed by review of clinical record
and ⁄ or death certificate. Minimum follow-up lasted
23 days and the longest was 3740 days.
Statistical Analysis
Numeric values were expressed as meanstandard
deviations. Prognostic power of single variables was
assessed using the chi-square test for categoric variables
40 Congest Heart Fail Vol. 19 | No. 1 | January . February 2013
| Vallebona et al.
and the t test for continuous variables. All variables
that were significantly associated with the prespecified
end point were included in a binary logistic regression
multivariate model. Cumulative lifetime survival rates
were generated with the Kaplan-Meier method and
compared using the log-rank test. Hazard ratios (HRs)
with 95% confidence intervals (CI) were estimated. A
P value <.05 was considered significant. All calcula-
tions were performed with SAS software release 8.2 for
Microsoft Windows (SAS Institute Inc, Cary, NC).
RESULTS
Twenty patients were unable to perform CPX and were
therefore excluded. Thereafter, of the initially screened
166 patients, 146 were evaluated. The characteristics of
the patient population are listed in Table I and pharma-
cologic therapy in Table II. All continuous variables
had an approximate normal distribution. No patient
was lost during follow-up. After 4.802.62 years, there
were 43 deaths (29.5%). On univariate analysis, vari-
ables significantly associated with mortality were peak
VO2, LV filling pattern, pulmonary artery hypertension,
heart rate, and blood pressure response to exercise
(Table III). Heart rate response to exercise, as expressed
by chronotropic index, was significantly lower in
patients taking b-blockers (0.54 vs 0.67, P<.05); how-
ever, the risk did not differ according to b-blocking sta-
tus. Of the clinical and therapeutic variables, ischemic
etiology, treatment with amiodarone or digoxin and
exclusion from therapy with renin-angiotensin system
(RAS) inhibitors were significantly related to mortality.
Patients with a contraindication to RAS inhibitors (8 of
147 patients) were significantly older (age 744 years
vs 655 years; P<.01) and had more impaired func-
tional capacity (peak VO2 11.64 mL ⁄ kg ⁄ min vs
16.23 mL ⁄ kg ⁄ min; P<.05). On multivariate analysis,
only restrictive LV filling pattern (B: )1.30, P=.004;
Exp(B): 0.27; 95% CI, 0.11–0.66), ischemic etiology (B:
)1.01, P=.022; Exp(B): 0.36; 95% CI, 0.15–0.86), and
PASP 50 mm Hg (B: )1.11, P=.027; Exp(B): 0.32;
95% CI, 0.12–0.88) maintained an independent predic-
tive value. Peak VO2 <15.9 mL ⁄ kg ⁄ min showed a
weaker association with mortality (B: 0.124, P=.046;
Exp(B): 0.88; 95% CI, 0.78–0.99). Using the three most
potent independent risk factors (etiology, LV filling pat-
tern, and PASP), a simple risk score was obtained. Peak
VO2 was excluded because of only borderline signifi-
cance. Patients with no risk factors (score 0) were
assumed as the reference. Different levels of risk were
identified by the presence of 1, 2. or 3 variables
(Table IV). Patients with ischemic etiology, restrictive
LV filling pattern, and PASP 50 mm Hg (score 3)
showed an incidence of death of 100% at 72 months
(Figure).
DISCUSSION
The annual mortality rate for patients with HF can
range from 10% to 50%.3–6 Many studies have
addressed the question of prognostic stratification of
 a simple tool for risk stratification in systolic heart failure | Vallebona et al.

TABLE I. Data for 146 Study Patients TABLE II. Pharmacologic Therapy in 146 Patients
Clinical Drugs Patients, No. Daily Dosage, mg
Age, y 6610
RAS inhibitors
Men ⁄ women 121 ⁄ 25
ACE inhibitors
NYHA functional class II or III 105 ⁄ 41
Ramipril 66 3.91.6
Coronary artery disease 81 (55%)
Enalapril 51 12.57.3
Chronic atrial fibrillation 25 (17%)
Lisinopril 5 14.25.2
Left bundle branch block 24 (16%)
ARBs
CRT and ⁄ or AICD 41 (28%)
Losartan 7 68.327
Echocardiographic
Valsartan 6 98.853
Left atrial, mm 456.6
Olmesartan 2 200
LVEF 0.310.8
Telmisartan 1 800
Mitral regurgitation, mean 1.460.9
138 (94%)
‘‘Restrictive’’ LVFP 50 (34%)
b-Blockers
PASP 50 mm Hg 31 (21%)
Carvedilol 47 21.310.2
LVMI, g ⁄ mq 16742
Bisoprolol 25 3.22.2
CPX
Nebivolol 12 3.30.7
Peak VO2, mL ⁄ kg ⁄ min 15.94.2
Sotalol 1 120
Peak VE ⁄ VCO2 35.27.0
85 (58%)
Peak SBP 130 mm Hg 21 (14%)
Diuretics
Peak SBP fall 20 mm Hg 7 (5%)
Furosemide 102 46.828.1
Chronotropic index 0.5929
Torasemide 25 10.07.6
Abbreviations: AICD, automatic implantable cardioverter-defibrillator; Chlorthalidone 4 15.63.1
chronotropic index, peak heart rate-rest heart rate ⁄ 220-age-rest 131 (90%)
heart rate; normal value >0.80; CPX, cardiopulmonary exercise test-
ing; CRT, cardiac resynchronization therapy; left bundle branch Aldosterone inhibitors
block, QRS >120 ms; LVEF, left ventricular ejection fraction; LVMI, Spironolactone 90 28.941.1
left ventricular mass index; LVFP, left ventricular filling pattern; Canrenone 5 5532
mitral regurgitation: 1, mild; 2, moderate; 3, severe; NYHA, New York
95 (65%)
Heart Association functional class; PASP, pulmonary artery systolic
pressure; SBP, systolic blood pressure; VE ⁄ VCO2, ventilation ⁄ Other
carbon dioxide output; VO2, oxygen uptake. Amiodarone 23 (16%)
Digitalis 19 (13%)

Abbreviations: ACE, angiotensin-converting enzyme; ARBs, angio-

HF and many risk factors for death or acute decom-
pensation have been identified, although most did not
have independent prognostic power.24 Moreover, often
the real patient is different from those of the study
population from which the marker was deduced. The
timing of patient evaluation in relation to therapy
optimization and physical deconditioning is not consis-
tently defined, nor is the effect of contemporary use of
different evidence-based treatments, including b-block-
ers and cardiac resynchronization therapy-automatic
implantable cardioverter-defibrillator devices. Finally,
prognostic stratification based on a single risk factor
has limited predictive value.25 For these reasons, sev-
eral models integrating different variables have been
proposed.26–30 However, many of these prognostic
models cannot be easily utilized in ambulatory patients
due to their complexity and the need for additional
noninvasive as well as invasive measurements. Our
study compared the prognostic power of 23 easy-to-
obtain variables for predicting death in stable systolic
HF outpatients, moderately symptomatic and treated
with the best medical therapy available today. Univari-
ate analysis confirmed previous evidence that peak
VO2, LV restrictive filling pattern, PASP 50 mm Hg,
blood pressure, and heart rate response to exercise are
most significantly associated with prognosis. Regard-
ing therapy, patients taking amiodarone or digoxin or
tensin II type 1 receptor blockers; RAS, renin-angiotensin system.
with contraindication to RAS inhibitors are identified
with a worse prognosis. On multivariate analysis, only
ischemic etiology, LV restrictive filling pattern, and
PASP 50 retained an independent risk predictive
power, whereas peak VO2 achieved only borderline
statistical significance. We therefore suggest a simple
method based on the integration of these three inde-
pendent risk factors that are extremely simple to use
and powerful for stratification of systolic HF progno-
sis. Patients with ischemic etiology, LV restrictive pat-
tern, and PASP 50 mm Hg (score 3) are at extremely
high risk for death and should be aggressively treated
and closely monitored. In this very high-risk group the
measurement of peak VO2 could be superfluous,
whereas CPX can attain the most important adjunctive
value in patients with a moderately adverse prognosis
(risk score 1 and 2). Finally, because HF is a dynamic
condition, it is important to stress that prognostic
stratification must be performed when the patient is
stable and on optimal medical therapy.
Limitations
The main limitation of this study is a small sample
size. Moreover, this etiology-filling pulmonary pressure

Congest Heart Fail Vol. 19 | No. 1 | January . February 2013 41

a simple tool for risk stratification in systolic heart failure | Vallebona et al.

TABLE III. Univariate Predictors of Death

Variable Source P Value HR 95% CI

Peak VO2 <15.9 mL ⁄ kg ⁄ min Mean <.001

‘‘Restrictive’’ LVFP Previous <.001 5.03 2.35–10.80
studies
Chronotropic index <0.59 Mean <.001
PASP 50 mm Hg Previous <.001 4.16 1.81–9.55
studies
Double product <21,200 Mean <.001
Ischemic etiology Previous <.01 2.74 1.27–5.92
studies
Peak SBP fall 20 mm Hg <.05 6.64 1.24–35.71
Peak SBP <130 mm Hg <.05 3.20 1.24–8.23
Therapy with RAS inhibitors <.05 0.23 0.05–0.98
FIGURE. Score 0: no risk factors; Score 1: 1 risk factor; Score 2:
2 risk factors; Score 3: 3 risk factors. For risk factors see Table IV.
Therapy with amiodarone <.05 2.61 1.05–6.49
Therapy with digoxin <.05 2.14 1.04–4.41
VE ⁄ VCO2 >35 Mean .06 patients were treated with b-blockers and we could
Therapy with b-blockers NS 0.58 0.28–1.20 speculate that b-blocking therapy affects blood pres-
Age NS
sure, heart rate, and exertional ventilation and could
NYHA functional NS 2.10 0.84–5.24
change the prognostic value of some exercise variables.
class II or III
Finally, the small number of women involved and the
Chronic atrial fibrillation NS 2.19 0.90–5.31
absence of populations different from Caucasians indi-
Left bundle branch block NS 0.91 0.42–1.97
CRT-AICD NS 0.95 0.28–3.23
cates that the results cannot be extended to women
Left atrial size NS
and to non-Caucasian races.
LV mass index NS
LVEF NS Clinical Implications
Mitral regurgitation NS Our findings suggest that a very simple clinical echo-
Inclusion in training NS 1.34 0.58–3.09 cardiography risk score based on etiology, LV filling
programs pattern, and pulmonary pressure is a powerful tool for
risk stratification of systolic HF ambulatory patients.
Abbreviations: CI, confidence interval; CRT-AICD, cardiac resyn-
chronization therapy-automatic implantable cardioverter-defibrillator; The score does not require additional invasive or non-
HR, heart rate; left bundle branch block, QRS >120 ms; LV, left invasive measurements and, after the completion of a
ventricular; LVEF, left ventricular ejection fraction; LVFP, left validation study, can be proposed in everyday clinical
ventricular filling pattern; NS, not significant; NYHA, New York Heart
Association; PASP, pulmonary artery systolic pressure; RAS, practice.
renin-angiotensin system; SBP, systolic blood pressure; VE ⁄ VCO2,
ventilation ⁄ carbon dioxide output; VO2, oxygen uptake. Disclosures: No grants and other support received for this article.

References
1 Cleland JG, Khand A, Clark A. The heart failure epidemic: exactly
how big is it? Eur Heart J. 2001;22:623–626.
TABLE IV. The Etiology-Filling Pulmonary Pressure 2 Najafi F, Jamrozik K, Dobson AJ. Understanding the epidemic of
Risk Score heart failure: a systematic review of trends in determinants of heart
failure. Eur J Heart Fail. 2009;11:472–479.
95% Incidence 3 Deedwania PC. The key to unraveling the mystery of mortality in
heart failure. Circulation. 2003;107:1719–1721.
Odds Confidence P of 4 Saxon LA, Stevenson WG, Middlekauff HR, et al. Predicting death
Score Patients Ratio Interval Value Death, % from progressive heart failure secondary to ischemic or idiopathic
dilated cardiomyopathy. Am J Cardiol. 1993;72:62–65.
0 (no risk factors) 41 – 13 5 Shafazand M, Schaufelberger M, Lappas G, et al. Survival trends in
1 (1 risk factor) 59 3.94 1.05–14.75 .032 38 men and women with heart failure of ischaemic and non-ischaemic
2 (2 risk factors) 35 13.41 3.48–51.71 <.001 72
origin: data for the period 1987–2003 from the Swedish Hospital
Discharge Registry. Eur Heart J. 2009;30:671–678.
3 (3 risk factors) 11 33.77 5.74–198.8 <.001 100 6 Wikstrom G, Blomstrom-Lundqvist C, Andren B, et al; on behalf of
the CARE-HF Study Investigators. The effects of aetiology on out-
Risk factors include ischemic etiology, restrictive left ventricular come in patients treated with cardiac resynchronization therapy in
filling pressure, and pulmonary artery systolic pressure 50 mm Hg. the CARE-HF trial. Eur Heart J. 2009;30:782–788.
7 Pinamonti B, Di Lenarda A, Sinagra GF, et al. Restrictive left ven-
tricular filling pattern in dilated cardiomyopathy assessed by Doppler
echocardiography: clinical, echocardiographic and hemodynamic
correlations and prognostic implications. J Am Coll Cardiol. 1993;
risk score has not yet been validated in an independent 22:808–815.
validation group. The score is derived from a stable 8 Morales FJ, Asencio MC, Oneto J, et al. Deceleration time of early
HF population eligible for exercise testing. Indeed, our filling in patients with left ventricular dysfunction: functional and
prognostic independent value. Am Heart J. 2002;143:1101–1106.
results cannot be extended to patients unable to per- 9 Hansen A, Haass M, Zugck C, et al. Prognostic value of Doppler
form CPX for cardiac or noncardiac reasons. Many echocardiographic mitral inflow patterns: implications for risk

42 Congest Heart Fail Vol. 19 | No. 1 | January . February 2013

 a simple tool for risk stratification in systolic heart failure
stratification in patients with chronic congestive heart failure. J Am
Coll Cardiol. 2001;37:1049–1055.
10 Mancini DM, Eisen H, Kussmaul W, et al. Value of peak exercise
oxygen consumption for optimal timing of cardiac transplantation in
ambulatory patients with heart failure. Circulation. 1991;83:
778–786.
11 Robbins M, Francis G, Pashkow FJ, et al. Ventilatory and heart rate
responses to exercise: better predictors of heart failure mortality than
peak oxygen consumption. Circulation. 1999;100:2411–2417.
12 Francis DP, Shamin W, Davies LC, et al. Cardiopulmonary exercise
testing for prognosis in chronic heart failure: continuous and inde-
pendent prognostic value from VE ⁄ VCO(2) slope and peak VO(2).
Eur Heart J. 2000;21:154–161.
13 Tabet JY, Logeart D, Geyer C, et al. Comparison of the prognostic
value of left ventricular filling and peak oxygen uptake in patients
with systolic heart failure. Eur Heart J. 2000;21:1864–1871.
14 Arena R, Myers J, Abella J, et al. Development of a ventilatory clas-
sification system in patients with heart failure. Circulation. 2007;
115:2410–2417.
15 Myers J, Arena R, Dewey F, et al. A cardiopulmonary exercise test-
ing score for predicting outcomes in patients with heart failure. Am
Heart J. 2008;156:1177–1183.
16 Russell SD, Miller LW, Pagani FD. Advanced heart failure: a call to
action. Congest Heart Fail. 2008;14:316–321.
17 Corrà U, Mezzani A, Giordano A, et al. Exercise haemodynamic
variables rather than ventilatory efficiency indexes contribute to risk
assessment in chronic heart failure patients treated with carvedilol.
Eur Heart J. 2009;30:3000–3006.
18 American Society of Echocardiography Committee on standards,
subcommittee on quantitation of two-dimensional echocardiograms.
Recommendations for quantitation of the left ventricle by two-
dimensional echocardiography. J Am Soc Echo. 1989;2:358–367.
19 Devereux RB. Detection of left ventricular hypertrophy by M-mode
echocardiography. Anatomic validation, standardization, and com-
parison to other methods. Hypertension. 1987;9(suppl II):19–26.
| Vallebona et al.
20 Dini FL, Michelassi C, Micheli G, et al. Prognostic value of pulmo-
nary venous flow Doppler signal in left ventricular dysfunction. J Am
Coll Cardiol. 2000;36:1295–1302.
21 Currie PJ, Seward JB, Chan KL, et al. Continuous wave Doppler
determination of right ventricular pressure: a simultaneous Doppler-
catheterization study in 127 patients. J Am Coll Cardiol.
1985;6:750–756.
22 Yock PG, Popp RL. Non-invasive estimation of right ventricular sys-
tolic pressure by Doppler ultrasound in patients with tricuspid regur-
gitation. Circulation. 1984;70:657–662.
23 Meyer K, Hajric R, West BrookS, et al. Ventilatory and lactate
threshold determinations in healthy normals and cardiac patients:
methodological problems. Eur J Appl Physiol. 1996;72:387–393.
24 Butler J. More risk factors affecting heart failure outcomes: time for
hope or despair? J Am Coll Cardiol. 2005;46:1027–1028.
25 Ketchum ES, Levy WC. Multivariate risk scores and patient
outcomes in advanced heart failure. Congest Heart Fail. 2011;17:
205–212.
26 Aaronson KD, Schwartz JS, Chen TM, et al. Development and pro-
spective validation of a clinical index to predict survival in ambula-
tory patients referred for cardiac transplant evaluation. Circulation.
1997;95:2660–2667.
27 Brophy JM, Dagenais GR, McSherry F, et al. A multivariate model
for predicting mortality in patients with heart failure and systolic
dysfunction. Am J Med. 2004;116:300–304.
28 Levy W, Mozaffarian D, Linker DT, et al. The Seattle heart failure
model. Circulation. 2006;113:1424–1433.
29 Vazquez R, Bayes-Genis A, Cygankiewicz I, et al. The MUSIC Risk
score: a simple method for predicting mortality in ambulatory
patients with chronic heart failure. Eur Heart J. 2009;30:1088–1096.
30 O’Connor CM, Hasselblad V, Mehta RH, et al. Triage after hospi-
talization with advanced heart failure: the ESCAPE (Evaluation
Study of Congestive Heart Failure and Pulmonary Artery Catheteri-
zation Effectiveness) risk model and discharge score. J Am Coll
Cardiol. 2010;55:872–878.
Congest Heart Fail Vol. 19 | No. 1 | January . February 2013 43