pulmonary hypertension in left heart...
TRANSCRIPT
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Stephan Rosenkranz
Klinik III für Innere Medizin
Zentrum für Molekulare Medizin (ZMMK)
Herzzentrum der Universität zu Köln
Pulmonary Hypertension in
Left Heart Disorders
European Society of Cardiology (ESC)
Zürich Heart House
Cardiology Update 2011ESC Update Programme
Davos, Switzerland, February 16, 2011
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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Cardio-Pulmonary Interaction
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Cardio-Pulmonary Interaction
heterogeneous
poorly defined
highly variable
condition
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Who are these patients?
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Updated Clinical Classification of
Pulmonary Hypertension (Dana Point, 2009)
4th World Symposium PAH; Dana Point, CA Feb 11-14, 2008
Simonneau-G et al.; JACC 2009; 54(Suppl. S): S43-S54
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Cologne Consensus Conference 2010:
Classification of PH due to Left Heart Disease
Rosenkranz et al., DMW 2010;135(Suppl3): S102-S114; Int J Cardiol 2011 (in press)
Heart Failure with reduced left ventricular Ejection Fraction (EF ≤50%)*
Ischemic Cardiomyopathy (ICM)
Dilative Cardiomyopathy (DCM)
Heart Failure with preserved left ventricular Ejection Fraction (EF >50%)*
Valvular Left Heart Disease
Hypertensive Heart Disease
Coronary Heart Disease
Diabetic Cardiomyopathy
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
Constrictive Pericarditis
Aortic Valve Stenosis
Aortic Valve Insufficiency
Mitral Valve Stenosis
Mitral Valve Insufficiency
Persistent / residual PH after correction of valular heart disease
Atrial fibrillation
Other rhythm disorders
Cor triatriatum
Myxoma or left atrial thrombus
Other causes
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LVEF ≥40% LVEF <40%
Moller et al. Am J Cardiol 2005; 96: 199-203
Survival of Patients After Acute Myocardial
Infarction Stratified by RVSP
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Überleben bei Herzinsuffizienz:
Bedeutung von PH und RV-Funktion
Normal PAP (PAPm <20 mm Hg)
High PAP (PAPm >20 mmHg)Low RVEF (<35%)
n=379
Months402010 50 60
–0.2
0.0
0.2
0.4
0.6
Cu
mu
lati
ve p
rop
ort
ion
su
rviv
ing
0.8
1.0
0 30 70
Low RVEF (<35%)
Ghio S, et al. J Am Coll Cardiol 2001;37:183–188
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Epidemiology and Prognostic Impact
of PH in Diastolic Heart Failure
Lam et al., JACC 2009; 53: 1119-1126
HFpEF: PASP > 35 mmHg present in 83% (median PASP 48 mmHg)
PVH does not fully account for the severity of PH in HFpEF
Prevalence Survival
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LV Diastolic Dysfunction in Elderly Hypertensives:
Results of the APROS-diadys Study
Zanchetti A et al, J Hypertens, 2007
Prevalence of Diastolic Heart Failure
25.8 %
ECHO
2545 Patients > 65 Years with Systemic
Hypertension without Systolic HF
(LVEF > 45 %)
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LV Diastolic Dysfunction in Elderly Hypertensives:
Results of the APROS-diadys Study
2545 Patients > 65 Years with Systemic
Hypertension without Systolic HF
(LVEF > 45 %)
Zanchetti A et al, J Hypertens, 2007
Prävalenz der diastolischen Herzinsuffizienz
25.8 %
ECHO
Prevalence of left ventricular diastolic dysfunction
in a general population
Kuznetsova T et al. Circ Heart Fail 2009; 2: 105-112
(n = 539, mean age 52,5 years)
27.3%
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How to Diagnose Diastolic Heart Failure
(HFNEF)
Paulus et al., ESC Consensus Statement, Eur Heart J 2007
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Pre- versus postcapillary PH
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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PAH vs. PVH: PCWP vs. LVEDP
3.926 Patienten
Halpern-SC, Taichman-DB, Chest 2009; 136: 37-43
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RHC: Pressure Curves
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The PCWP Controversy
The technical quality of PCWP tracing
should be perfect
(31% technically inadequate)
Morris A et al. Crit Care Med 1984
The correct interpretation mandatory
(50% misinterpreted). Crit Care Med 1997;25:213 and 2002;30:1197
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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Threshold of PCWP - Normal LVEDP
Braunwald E: Heart Diseases, 2005
O´Rourke RA: Hurst´s The heart, 2008
Harrison´s principles of internal medicine, 2008
Lapp H, Krakau I: Das Herzkatheterbuch, 2008
Standard Textbooks of Cardiology
LVEDP 6 – 12 mmHg
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Normal Values for LVEDP (Cardiology World)
and PCWP (PAH World)
Rosenkranz et al., DMW 2010; 135(Suppl 3): S102-S114
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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Right Heart Catheter (RHC)
PCWP PAP
TPG
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Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
PAPm LAP
15
8
normal
TPG = 7 mmHg
25
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PAPm LAP
15
8
normal
TPG = 7 mmHg
40
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
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PAPm LAP
15
8
normal
TPG = 7 mmHg
precapillary PH
TPG = 32 mmHg
40
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
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PAPm LAP
15
8
normal
TPG = 7 mmHg
elevated
filling pressure20
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
30„passive“
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
postcapillary PH
LAP > 15 mmHg
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
Protective
Pulmonary Vasoconstriction
30„passive“
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
postcapillary PH
LAP > 15 mmHg
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
30
55
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
postcapillary PH
LAP > 15 mmHg
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
30
55
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
postcapillary PH
LAP > 15 mmHg
Precapillary
Component
TPG = 35 mmHg
„reactive“
„out of proportion“
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PH in Left Heart Failure:
Pathophysiology
Rosenkranz et al., DMW 2010; 135(Suppl 3): S102-S114
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Delgado, Rev Esp Cardiol 2010; 63: 334-345
LHI + PH LHI - PH
PH in Left Heart Failure:
Pathophysiology
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
30
55
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
postcapillary PH
LAP > 15 mmHg
Precapillary
Component
TPG = 35 mmHg
„reactive“
„out of proportion“
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PAPm LAP
15
8
normal
TPG = 7 mmHg
20
30
55 VARIABLE
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
Volume load
Heart Failure Treatment
Correction of Valvular Disease
postcapillary PH
LAP > 15 mmHg
Precapillary
Component
TPG = 35 mmHg
„reactive“
„out of proportion“
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PAPm LAP
15
8
normal
TPG = 7 mmHg
postcapillary PH
LAP > 15 mmHg20
30
Precapillary
Component
TPG = 35 mmHg
55 VARIABLEVolume load
Heart Failure Treatment
Correction of Valvular Disease
„reactive“
„out of proportion“
Pulmonary Hemodynamics in Left Heart Disease:
Pulmonary Circulation
elevated
filling pressure
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Pulmonary Hemodynamics in Left Heart Disease
Impact of Volume Load
70 year-old patient
Diastolic Heart Failure
Body weight 80 kg
70 year-old patient
6 days later
Body weight now 73 kg
PAPm 51 mmHg
PAPm
mmHg
10
20
30
40
50
60
30
21
PAPm 24 mmHg
PAPm
mmHg
10
20
30
40
50
60
13
11
PCWP TPG PCWP TPG
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Redfield M, Mayo Clinic, 2007
Hemodynamic Monitoring during Physical Exercise
and Sexual Intercourse in Patients with CHF and PH
Chronical Device, IHM, Medtronic Inc.
Cremers B et al, Am J Med, 2002
53-y.o. patient; ICM; EF 25%
20
40
60
80
100
120
140
11:50 PM 11:52 PM 11:54 PM 11:56 PM 11:58 PM 12:00 AM 12:02 AM
0
5
10
15
20
25HEART RATE (bpm) ACTIVITY (counts)
20
40
60
80
100
120
140
12:57 PM 12:58 PM 12:59 PM 1:00 PM 1:00 PM 1:01 PM 1:02 PM
0
5
10
15
20
25
HEART RATE (bpm) ACTIVITY (counts)
Exercise (brisk walking)
Sexual Intercourse
11:50 PM 11:52 PM 11:54 PM 11:56 PM 11:58 PM 12:00 AM 12:02 AM
0
20
40
60
80
100
120
PRESSURE (mmHg)
ePADP
RVSP
RVDP
0
20
40
60
80
100
120
12:57 PM 12:58 PM 12:59 PM 1:00 PM 1:00 PM 1:01 PM 1:02 PM
RVSP
ePADPRVDP
0
20
40
60
80
0
20
40
60
80
100
67-y.o. patient; DHF
40 Watt
PAP = 85/40/55 mmHg
RAP = 28 mmHg
Baseline
0
20
40
60
80
0
20
40
60
80
100
PAP = 45/20/28 mmHg
RAP = 9 mmHg
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Diagnostic Tests in PH Group 2 ?
Proper
classification
pre- vs. postcapillary
PH
VOLUME
CHALLENGE
Differentiation
vasoconstriction /
vascular
remodeling
VASOREACTIVITY
TESTING
Costard-Jackle A, Fowler MB, JACC 1992Oudiz RJ, Clin Chest Med 2007
Pulmonary
hemodynamics
during
exercise
EXERCISE
TEST
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Treatment of PH in
Left Heart Disease?
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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ESC/ERS Guidelines 2009
Galiè et al., Eur Heart J 2009; 30: 2493-2537
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Systolic HF: Standard Treatment
Medical Treatment:
• ACE-Inhibitors / AT1R-Blockers / Beta-Blockers
• Diuretics
• Digitalis
• Aldosterone Antagonists
Interventional / surgical Treatment:
• CRT (may reduce PH, but PH ↓ effectiveness)
– QRS > 120 ms (50% SHF)
• LVAD (Bridge-to-Transplant)
• HTX (limited)
Heart Failure Treatment may improve PH
But: PH frequent despite maximal Treatment
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Targeted PAH Therapies in Heart Failure
• Calcium Channel Blockers
– SHF – No Benefit
– DHF – Potential Benefit – “Need for RCT”
• PDE 5-Inhibitors
– Small RCT and Experimental Data – efficacious?
– Potential Benefit in SHF and DHF – “Need for RCT”
– RELAX Trial ongoing (Sildenafil)
• Endothelin-Receptor-Antagonists
– SHF – No Benefit in multiple Studies
– Potential Benefit in DHF – “Need for RCT”
– Sitaxsentan – DHF Trial stopped
• Epoprostenol
– SHF – Increased Mortality !! (FIRST Trial)
– DHF – No Data
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PAH/PH in Left Heart Disease:
Transpulmonary Gradient (TPG)
Volume loadinitial Sildenafil Mean change p value*
Hemodynamics
PAPsyst (mmHg) 84.3 ± 5.7 60.2 ± 11.5 -24.1 ± 7.1 <0.05
PAPmean (mmHg) 52.5 ± 2.5 37.2 ± 5.5 -15.3 ± 4.4 <0.05
PCWP# (mmHg) 27.5 ± 2.4 21.3 ± 3.6 -6.2 ± 4.4 n.s.
TPG (mmHg) 25.2 ± 3.2 15.8 ± 4.2 -9.4 ± 2.2 <0.05
HZV (ml/min) 3.4 ± 0.6 3.7 ± 0.4 +0.3 ± 0.1 n.s.
PVR (Wood units) 10.2 ± 3.0 3.9 ± 0.7 -6.3 ± 2.8 <0.05
RAP (mmHg) 17.0 ± 1.2 13.5 ± 1.8 -3.5 ± 1.9 n.s.
Echocardiography
RVEDD (mm) 41.0 ± 2.4 41.3 ± 3.9 +0.3 ± 3.6 n.s.
RA area (cm2) 30.5 ± 4.1 28.3 ± 4.0 -2.2 ± 2.3 n.s.
LVEF (%) 36.8 ± 5.3 40.6 ± 8.8 + 3.8 ± 5.6 n.s.
TAPSE (mm) 12.7 ± 1.5 15.8 ± 0.9 +3.2 ± 1.4 <0.05
Serum markers
NTproBNP (ng/dl) 7123 ± 1835 3201 ± 504 -3922 ± 2099 <0.05
Exercise tolerance
6MWD (m) 212 ± 75 336 ± 62 +124 ± 65 <0.05
Dumitrescu & Rosenkranz, 2010 (submitted)
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Volume loadinitial Sildenafil Mean change p value*
Hemodynamics
PAPsyst (mmHg) 84.3 ± 5.7 60.2 ± 11.5 -24.1 ± 7.1 <0.05
PAPmean (mmHg) 52.5 ± 2.5 37.2 ± 5.5 -15.3 ± 4.4 <0.05
PCWP# (mmHg) 27.5 ± 2.4 21.3 ± 3.6 -6.2 ± 4.4 n.s.
TPG (mmHg) 25.2 ± 3.2 15.8 ± 4.2 -9.4 ± 2.2 <0.05
HZV (ml/min) 3.4 ± 0.6 3.7 ± 0.4 +0.3 ± 0.1 n.s.
PVR (Wood units) 10.2 ± 3.0 3.9 ± 0.7 -6.3 ± 2.8 <0.05
RAP (mmHg) 17.0 ± 1.2 13.5 ± 1.8 -3.5 ± 1.9 n.s.
Echocardiography
RVEDD (mm) 41.0 ± 2.4 41.3 ± 3.9 +0.3 ± 3.6 n.s.
RA area (cm2) 30.5 ± 4.1 28.3 ± 4.0 -2.2 ± 2.3 n.s.
LVEF (%) 36.8 ± 5.3 40.6 ± 8.8 + 3.8 ± 5.6 n.s.
TAPSE (mm) 12.7 ± 1.5 15.8 ± 0.9 +3.2 ± 1.4 <0.05
Serum markers
NTproBNP (ng/dl) 7123 ± 1835 3201 ± 504 -3922 ± 2099 <0.05
Exercise tolerance
6MWD (m) 212 ± 75 336 ± 62 +124 ± 65 <0.05
Dumitrescu & Rosenkranz, 2010 (submitted)
PAH/PH in Left Heart Disease:
Transpulmonary Gradient (TPG)
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Abraham et al., Lancet 2011; published on-line February 10, 2011
CHAMPION Trial: Wireless Pulmonary Artery
Hemodynamic Monitoring in Heart Failure
Randomized, controlled trial (Left HF, NYHA III; n=550)
HF-related hospitalizations @ 6 monthsWireless implantable hemodynamic
monitoring system (W-IHM)
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Specific Recommendations of the Working Group regarding Treatment of PH
associated with Left Heart Disease:
Potential Use of Targeted PAH Therapies in PH and elevated PCWP:
- pronounced precapillary component foregrounded to the disease
- Requirement: complete diagnostics including RHC and LHC.
Patients must fullfill the following criteria:
1. Invasively confirmed PH, which markedly exceeds the extent usual seen in left
heart disease (markedly elevated TPG / PVR);
2. no treatable cause of heart failure (CAD, valvular disease);
3. Guideline-based, evidence-based treatment for heart failure for a reasonable
period of time (> 3-6 months) and at the anticipated target doses;
4. Exclusion of other causes of PH and of CTEPH.
Primary Goal: Inclusion in clinical trials (e.g., LEPHT, CAESAR)
Cologne Consensus Conference 2010
Rosenkranz et al., DMW 2010; 135(Suppl 3): S102-S114
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….. a long way to go
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Thank you!
PH in Left Heart Disorders
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Doppler / Gewebe-Doppler
IVCT IVRT
Systole
E„ A„
RV LV
St
Tissue Doppler Imaging (TDI)
MK: E/E´
LAP/PCP
TK: E/E´
RAP
TDI-MPI
RV-Fkt.
STK
MK: E/ADT
LA-Größe
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Olmsted County, MI
EFFECT data base,
Ontario, Canada
Survival in Systolic versus
Diastolic Heart Failure
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Diastolic HF: Ready for Treatment?
1990 2010
Diuretics X X
BP Control X X
Revascularization X X
BB/ACEI/ARB/CCB (?) X X
HR in A-Fib X X
Guidelines only Expert Opinion
ESC HF Guidelines, Eur Heart J, 2008
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Diastolic HF: Clinical Trials
AT1-Antagonist (Candesartan):
CHARM-Preserved: Yusuf et al., Lancet 2003
ACE Inhibitor (Perindopril):
PEP-CHF: Cleland et al., Eur Heart J 2006
I-Preserve: Massie et al., NEJM 2008
AT1-Antagonist (Irbesartan):
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Diastolic HF: Ready for Treatment?
1990 2010
Diuretics X X
BP Control X X
Revascularization X X
BB/ACEI/ARB/CCB (?) X X
HR in A-Fib X X
Guidelines only Expert Opinion
Chatterjee K: Western Journal of Medicine: 1990
ESC HF Guidelines, Eur Heart J, 2008
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Olmsted County, MI
EFFECT data base,
Ontario, Canada
Survival in Systolic versus
Diastolic Heart Failure
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Diastolic Dysfunction and Heart Failure
Clinical Signs of Heart Failure
Hypertrophy, Compliance , Relaxation
Preserved LV Ejection Fraction (≥50%)
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Ursache für die Symptomatik bei
diastolischer Herzinsuffizienz
Chattopadhyay-S, et al.
Circ Heart Fail 2009; in press
HFpEF
Kurt-M, et al.
Circ Cardiovasc Imaging 2009; 2: 10-15
Reduzierte LA(S) strain
Erhöhte LA-Steifigkeit
Gestörte LA-FunktionEingeschränkte
Diastolische Reserve
DSE: mitral annular velocity
Reduced Ea, increased E/Ea
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PAH/PH bei Linksherzerkrankungen:
Transpulmonaler Gradient (TPG)
PCWP PAP
PVH PAHP(A)H / LHI
PCWP PAP PCWP PAP
20 41/17/31
TPG 1126 74/40/54
TPG 2811 96/30/53
TPG 42
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Belastungsinduzierte pulmonale Hypertonie
bei Herzinsuffizienz
*Butler JACC 1999; Tumminello Eur Heart J 2007
Systolische versus diastolische Herzinsuffizienz ?PAP unter Belastung in Relation zu PAP in Ruhe ?
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Differenzierung zwischen PAH und
diastolischer Herzinsuffizienz
Diagnosen:
• Hypertensive Herzerkrankung
• Diastolische Herzinsuffizienz
• Pulmonal venöse Hypertonie
Diagnosen:
• Pulmonal arterielle Hypertonie
• Leichte diastolische Dysfunktion des linken Ventrikels
• Arterielle Hypertonie
Leitsymptom „Dyspnoe“
PAH HFpEF
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ESC/ERS-Leitlinien: Therapie der Non-PAH PH?
Was ist „out-of proportion PH“?
Bei Linksherzinsuffizienz TPG > 12 mmHg?
Wann ist die PH „zweite Erkrankung“
Dann PAH bei Herzinsuffizienz?
Galiè N et al; Eur Heart J 2009;30:2493-2537
Indikation Empfehlung
Therapie der PH bei Linksherzerkrankungen
mit PAH-spezifischen Medikamenten?III - C
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PAPm 48 mmHg
PAPm 38 mmHg
0
10
20
30
40
50
Baseline
PCWP TPG
0
10
20
30
40
50
Baseline
PCWP TPG
Pulmonale Hypertonie bei Linksherzerkrankungen:
Patienten mit postkapillärer PH
Patient 1 - NYHA III55 Jahre, DCM, LVEF 25%
6MWD 320 m
Patientin 2 - NYHA III75 J, HPT, VHF, LVEF 55%, NIDDM,
Adipositas, 6MWD 270 m
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PAPm 48 mmHg
PAPm 38 mmHg
0
10
20
30
40
50
Baseline
PCWP TPG
0
10
20
30
40
50
Baseline
PCWP TPG
Pulmonale Hypertonie bei Linksherzerkrankungen:
Patienten mit postkapillärer PH
Patient 1 - NYHA III55 Jahre, DCM, LVEF 25%
6MWD 320 m
Patientin 2 - NYHA III75 J, HPT, VHF, LVEF 55%, NIDDM,
Adipositas, 6MWD 270 m
Optimierte Herzinsuffizienz-
Therapie nach den aktuellen
Leitlinien
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PAPm 48 mmHg
PAPm 38 mmHg
0
10
20
30
40
50
Baseline
PCWP TPG
0
10
20
30
40
50
Baseline
PCWP TPG
Pulmonale Hypertonie bei Linksherzerkrankungen:
Patienten mit postkapillärer PH
Patient 1 - NYHA III55 Jahre, DCM, LVEF 25%
6MWD 320 m
Patientin 2 - NYHA III75 J, HPT, VHF, LVEF 55%, NIDDM,
Adipositas, 6MWD 270 m
Optimale Blutdruckeinstellung
Frequenz/Rhythmuskontrolle
Diuretika, Gewichtsreduktion
Optimale Diabetestherapie
Optimierte Herzinsuffizienz-
Therapie nach den aktuellen
Leitlinien
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PAPm 37 mmHg
PAPm 29 mmHg
0
10
20
30
40
50
Baseline 6 Monate
PCWP TPG
0
10
20
30
40
50
Baseline 6 Monate
PCWP TPG
Pulmonale Hypertonie bei Linksherzerkrankungen:
Hämodynamik nach 6 Monaten
Patient 1 - NYHA III55 Jahre, DCM, LVEF 25%
6MWD 320 m
Patientin 2 - NYHA II75 J, HPT, VHF, LVEF 55%, NIDDM,
Adipositas, 6MWD 270 m
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Häufige Diagnosen bei dem Leitsymptom
„Dyspnoe“ in der kardiologischen Praxis
Systolic Heart Failure
Coronary Heart Disease
Diastolic Heart Failure
Valvular Heart Disease
DYSPNEA
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Epidemiologie der PH und der
Linksherzinsuffizienz
Prävalenz PAH: 15-50 / Mio. Einwohner
Prävalenz IPAH: 6-12 / Mio. Einwohner
DCM: 360 / Mio. Einwohner
ICM: 3000-4500 / Mio. Einwohner
Pulmonal arterielle Hypertonie:
Systolische Herzinsuffizienz:
Diastolische Herzinsuffizienz:
~ 250.000-450.000
Prävalenz unklar – hohe Dunkelziffer
Deutschland
~ 1000
~ 4000
???
~ 50.000
ca. 50% aller Patienten mit Herzinsuffizienz
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Epidemiologie der PH bei systolischer
und diastolischer Linksherzinsuffizienz
• Allgemeinbevölkerung (>45 Jahre; n=1417)
2.04% PASP ≥ 40; 0.07% PASP ≥ 60assoziiert mit Alter, PVH (LAvol; E/E’)
• Systolische Herzinsuffizienz (EF<40%; n=1462)
55% PASP ≥ 40; 16% PASP ≥ 60assoziiert mit PVH (LAvol; E/E’) und MI, nicht mit EF
• Diastolische Herzinsuffizienz (EF>50%, n=240)
68% PASP ≥ 40; 20% PASP ≥ 60assoziiert mit PVH (LAvol; E/E’)
Maggie Redfield, JACC 2009; 53: 1119-1126
HFpEF: PASP > 35 mmHg present in 83% (median PASP 48 mmHg)
PVH does not fully account for the severity of PH in HFpEF
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Rechtsherzkatheter-Untersuchung
PCWP PAP
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Diastolische Herzinsuffizienz und PH
M Redfield, Mayo Clinic, 2008
KLINISCH:
• Alter > 65 Jahre
• Adipositas
• Arterielle Hypertonie
• KHK
• Diabetes mellitus
• Vorhofflimmern
ECHOKARDIOGRAPHIE:
• Erhöhter SBP
• LA-Vergrößerung
• LV-Hypertrophie
• Erhöhte Füllungsdrucke
Diastolische Dysfunktion II-III°
FOLLOW-UP:
• Verbesserung durch Diuretika
• Starker SBP-Anstieg bei Belastung
• Rö-Thorax: Zeichen für CHF
KLINISCH:
• Alter < 45 Jahre
• Niedriger SBP
• Keine kardiovaskulären Erkrankungen
– Hypertension
– KHK
– Diabetes mellitus
– Vorhofflimmern
ECHOKARDIOGRAPHIE:
• Kein erhöhter SBP
• Keine LA-Vergrößerung
• Keine LV-Hypertrophie
• Niedrige Füllungsdrucke
Diastolische Dysfunktion ≤ I°
FOLLOW-UP:
• Keine Verbesserung durch Diuretika
• Normaler SBP-Anstieg unter Belastung
• Rö-Thorax: Keine Zeichen für CHF
DHF wahrscheinlich DHF unwahrscheinlich
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Ist die Entstehung einer PH bei
Herzinsuffizienz nur passiv bedingt?
Ghio S, et al. J Am Coll Cardiol 2001;37:183–188
Bei Linksherzinsuffizienz ist die Entstehung einer PH in vielen Fällen durch die Erhöhung des PCWP bedingt……..
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Ist die Entstehung einer PH bei
Herzinsuffizienz nur passiv bedingt?
Ghio S, et al. J Am Coll Cardiol 2001;37:183–188
Bei Linksherzinsuffizienz ist die Entstehung einer PH in vielen Fällen durch die Erhöhung des PCWP bedingt……..
….aber nicht in allen Fällen
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PH bei Linksherzinsuffizienz:Interaktionen linkes Herz – Lungenstrombahn – rechtes Herz
POSTKAPILLÄRE PH
LVEDP
LAP
PCP
PAP
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PH bei Linksherzinsuffizienz:Interaktionen linkes Herz – Lungenstrombahn – rechtes Herz
LVEDP
LAP
PCP
PAP Vasokonstriktion
Remodeling
POSTKAPILLÄRE PH
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PH bei Linksherzinsuffizienz:Interaktionen linkes Herz – Lungenstrombahn – rechtes Herz
PRÄKAPILLÄRE
KOMPONENTE
LVEDP
LAP
PCP
PAP Vasokonstriktion
Remodeling
POSTKAPILLÄRE PH
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PH bei Linksherzinsuffizienz:Interaktionen linkes Herz – Lungenstrombahn – rechtes Herz
PRÄKAPILLÄRE
KOMPONENTE
LVEDP
LAP
PCP
PAP Vasokonstriktion
Remodeling
POSTKAPILLÄRE PH
RECHTSHERZINSUFFIZIENZ VERMINDERTE FÜLLUNG LINKS
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Zeit (Monate bis Jahre)
CHF
Kra
nk
he
its
pro
gre
ss
ion
PH bei Linksherzinsuffizienz:
Bedeutung der RV-Funktion?
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Zeit (Monate bis Jahre)
CHF
Kra
nk
he
its
pro
gre
ss
ion
PAP
PVR?
PH bei Linksherzinsuffizienz:
Bedeutung der RV-Funktion?
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Zeit (Monate bis Jahre)
CHF
Rechtsherz-
insuffizienz
Kra
nk
he
its
pro
gre
ss
ion
PAP
PVR?
PH bei Linksherzinsuffizienz:
Bedeutung der RV-Funktion?
![Page 82: Pulmonary Hypertension in Left Heart Disordersassets.escardio.org/assets/Presentations/OTHER2011/... · Mitral Valve Stenosis Mitral Valve Insufficiency ... Pulmonary Hemodynamics](https://reader030.vdocuments.pub/reader030/viewer/2022012822/5f463c0636d8164eca3bb0c2/html5/thumbnails/82.jpg)
PH bei Linksherzinsuffizienz:
Bedeutung der RV-Funktion?
Zeit (Monate bis Jahre)
CHF
Rechtsherz-
insuffizienz
Kra
nk
he
its
pro
gre
ss
ion
Jugularvenenstauung
Periphere Ödeme
Hepatomegalie
Ascites
Hypoxie
PAP
PVR?
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Cappola TP et al, Circulation 2002; 105:1663-1668
Pulmonale Hämodynamik und Prognose
• 1134 Pat. mit neu diagnostizierter Kardiomyopathie• PAPmean 25±11, PCWP 17±9, PVR 2,2±1,6
• Follow-up 4,4 Jahre
PH ist bei SHF und DHF mit erhöhter Sterblichkeit assoziiert
Diagnostik und Behandlung der PH bei HF erscheint wichtig
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Therapie der pulmonal arteriellen Hypertonie:
Problematik der Datenlage
Prostanoide ERA PDE5i
Primärer Studienendpunkt: 6-min-Gehstrecke
Kurze Beobachtungsdauer (12-16 Wochen)
BREATHE 1-Studie(Rubin et al., NEJM 2002)
SUPER 1-Studie(Galiè et al., NEJM 2005)
AIR-Studie(Olschewski et al., NEJM 2002)
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E/E‘ lat = 16,8
Echokardiographie:
Diastolische LV-Dysfunktion
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PH in Left Heart Failure:
Pathophysiology
Rosenkranz et al., DMW 2010; 135(Suppl 3): S102-S114
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Cologne Consensus Conference 2010
Rosenkranz et al., DMW 2010;135(Suppl3): S102-S114