The Obesity Paradox and Discrepancy between O 2 Consumption and Heart Failure Prognosis – It’s...
-
Upload
wesley-goodman -
Category
Documents
-
view
218 -
download
1
Transcript of The Obesity Paradox and Discrepancy between O 2 Consumption and Heart Failure Prognosis – It’s...
The Obesity Paradox and The Obesity Paradox and Discrepancy between ODiscrepancy between O2 2
Consumption and Heart Failure Consumption and Heart Failure
Prognosis – It’s All in the FatPrognosis – It’s All in the Fat
Lorraine S. Evangelista, PhD, RNLorraine S. Evangelista, PhD, RN
Assistant Professor, UCLA School of NursingAssistant Professor, UCLA School of Nursing
ObjectivesObjectives
Demonstrate the paradox between Demonstrate the paradox between obesity and heart failure prognosis.obesity and heart failure prognosis.
Discuss the rationale for correction of Discuss the rationale for correction of cardiopulmonary stress data (used as cardiopulmonary stress data (used as predictors of survival and listing of predictors of survival and listing of cardiac transplantation) for lean weight cardiac transplantation) for lean weight (as opposed to total body weight).(as opposed to total body weight).
Case StudyCase Study 59 y.o. man presented to the HF clinic for evaluation59 y.o. man presented to the HF clinic for evaluation
Dyspnea on exertion, orthopnea, PND, edema Dyspnea on exertion, orthopnea, PND, edema lower extremities (NYHA class II to III status) lower extremities (NYHA class II to III status)
Optimized on diuretics, digitalis, ACE inhibitors, Optimized on diuretics, digitalis, ACE inhibitors, β-blockers, and spironolactone. β-blockers, and spironolactone.
Ht 70’ wt, 217 lb, BMI, 31 kg/m2 ; 33% body fat. Ht 70’ wt, 217 lb, BMI, 31 kg/m2 ; 33% body fat. Resting HR 60 bpm, BP 112/68 mm Hg. Resting HR 60 bpm, BP 112/68 mm Hg. CPX - max peak HR130 bpm, BP 190/90 mm Hg. CPX - max peak HR130 bpm, BP 190/90 mm Hg.
• Peak VOPeak VO2 2 13.4 mL/kg/min, peak O13.4 mL/kg/min, peak O22 pulse (peak pulse (peak
VOVO22 /peak heart rate) 11.8 mL per beat /peak heart rate) 11.8 mL per beat
ObesityObesity Heart FailureHeart Failure
Heart FailureHeart Failure
ObesityObesity
HATEHATE
R E L A T I O N S H I PR E L A T I O N S H I P
LOVELOVE
Obesity is a risk factor for the development of HFObesity is a risk factor for the development of HF1-21-2
Obesity and HF often co-exist Obesity and HF often co-exist 33
15% to 35% of patients with HF are obese15% to 35% of patients with HF are obese30% to 60% of patients with HF are overweight30% to 60% of patients with HF are overweight
Inte
rme
dia
teP
ath
wa
ys
He
mo
dy
na
mic
ch
an
ge
s
PA Pressure
Peripheral Resistance
Preload
Blood volume
RA RV
Plasma viscosity
Sympathetic nervous systemRAAS, Endothelin-1, vasopressinNatriuretic peptides
Suppression of lipolysisImpaired fatty acid metabolismSubstrate competition
Atrial Remodeling
LV Remodeling
Stroke Volume
conduit stiffness
LA LV
Asymptomatic LV systolic & diastolic dysfunction
ObesityIncreased adiposity
Modified from Vasan RS. Heart 2003; 89;1127-29
Afterload
DiabetesGlucose intolerance Insulin sensitivity
Insulin resistanceDyslipidemiaHypertension
HypercoagulabilityF
ac
tors
Ris
k
The Obesity Paradox
Body Mass Index
BMI
All-CauseDeath
All-CauseDeath
Obesity in general is associated with Obesity in general is associated with mortality mortality 4-114-11
Horwich, Fonarow, Hamilton, et al. The relationship between obesity and mortality in patients with heart failure. J Am Coll Cardiol. 2001;38:789–795.
N=1203
Lavie CJ, Osman AF, Milani RV, et al. Am J Cardiol. 2003;91:891–894.
• Pts in the highest quintile had better event-free survival than pts in the lowest quintile.
• In a logistic regression analysis, a higher % of body fat (X2, 9.1; P=.002) was the strongest independent predictor of event-free survival.
• For every 1% absolute in % of body fat, a in major clinical events exceeding 13% reported.
N=209
Cardiopulmonary Exercise (CPX)Cardiopulmonary Exercise (CPX) CPX has become the accepted standard for HF prognostication & risk CPX has become the accepted standard for HF prognostication & risk
stratification (RS) for transplant; Peak stratification (RS) for transplant; Peak VOVO22 >14 mL/kg/min cut-off value >14 mL/kg/min cut-off value of RSof RS12–1512–15
Peak Peak VOVO22 >18 mL/kg/min have a very good prognosis >18 mL/kg/min have a very good prognosis
Peak Peak VOVO22 <10 ml/kg/min have very poor prognosis <10 ml/kg/min have very poor prognosis
Generally corrected for total wt (opposed to lean wt) despite the fact Generally corrected for total wt (opposed to lean wt) despite the fact that fat is not aerobically active. that fat is not aerobically active. 13, 1513, 15
CPX may lose prognostic power in some sub-groups with CPX may lose prognostic power in some sub-groups with % body fat – % body fat – obese patients and women.obese patients and women.
In an era of In an era of ββ-blockers, adjusted exercise indices may predict better -blockers, adjusted exercise indices may predict better outcome.outcome.
These figures show that adjusted exercise indices (including peak VO2 and peak O2 pulse) predict prognosis better than non-adjusted indices
Osman AF, Mehra MR, Lavie CJ, et al. J Am Coll Cardiol. 2000;36:2126–2131.Lavie CJ, Milani RV, Mehra MR. Am J Cardiol. 2004;93:588–593.
Case Study RevisitedCase Study Revisited
Patient’s peak VOPatient’s peak VO22 & O & O2 2 pulse corrected for pulse corrected for
lean body mass lean body mass
19.7 mL/kg/min & 15.6 mL per beat.19.7 mL/kg/min & 15.6 mL per beat.
These adjusted indices suggest a favorable These adjusted indices suggest a favorable prognosis; thus patient can qualify for a heart prognosis; thus patient can qualify for a heart transplant.transplant.
Recommendations: consistently have the peak Recommendations: consistently have the peak VOVO22 lean lean reported and utilize these values in reported and utilize these values in
evaluating sub-groups of patientsevaluating sub-groups of patients
ReferencesReferences1 Kenchaiah S, Evans JC, Levy D, et al. N Engl J Med. 2002;347:305–313.2 Murphy, MacIntyre, Stewart S, et al. Eur Heart J. 2006;27:96–106.3 Gustafsson F, Kragelund CB, et al, Eur Heart J. 2005;26:58–64. 4 Horwich TB, Fonarow GC, et al. J Am Coll Cardiol. 2001;38:789–795.5 Mosterd A, Cost B, Hoes AW, et al. Eur Heart J. 2001;22:1318–1327.6 Lissin LW, Gauri AJ, Froelicher VF, et al.. J Card Fail. 2002;8:206–215.7 Davos CH, Doehner W, Rauchhaus M, et al. J Card Fail. 2003;9:29–35.8 Lavie CJ, Osman AF, Milani RV, et al. Am J Cardiol. 2003;91:891–894.9 Curtis JP, Selter JG, Wang Y, et al.. Arch Intern Med. 2005;165:55–61.10 Lavie CJ, Milani RV. J Am Coll Cardiol. 2003;42:677–679.11 Lavie CJ, Mehra MR, Milani RV. Eur Heart J. 2005;26:5–7.12 Mancini DM, Eisen H, Kussmaul W, et al. Circulation. 1991;83:778–786.13 Mehra MR, Lavie CJ, Milani RV. Chest. 1996;110:310–312.14 Weber KT, Janicki JS. Am J Cardiol. 1985;55:22A–31A.15 Milani RV, Lavie CJ, Mehra MR, et al. Mayo Clin Proc. 2006;81:1603–1611.16 Osman A, Mehra M, Lavie C, et al. J Am Coll Cardiol. 2000;36:2126–2131.17 Lavie CJ, Milani RV, Mehra MR. Am J Cardiol. 2004;93:588–593.