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Scompenso cardiaco e sindromi correlate: non trascuriamo lo “sleep disorder”. Michele Emdin, Claudio Passino U.O. Medicina Cardiovascolare Fondazione Toscana Gabriele Monasterio Istituto di Fisiologia Clinica CNR, Pisa Scuola Superiore Sant’Anna. Congresso tosco-umbro FIC

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slide1

Scompenso cardiaco e sindromi correlate:non trascuriamo lo “sleep disorder”

Michele Emdin,Claudio Passino

U.O. Medicina Cardiovascolare

Fondazione Toscana Gabriele Monasterio

Istituto di Fisiologia Clinica CNR, Pisa

Scuola Superiore Sant’Anna

Congresso tosco-umbro FIC

Montecatini Terme, 14 novembre 2007

slide2

60 sec.

30 sec.

…of a patient with probable cardiac asthma:

I have little doubt that this was a case of weakened and probably fatty heart, with disease of the aorta…”

0

1

2

3

4

5

6

7

8

9

1

0

Cheyne, J. “A case of Apoplexy, in Which the Fleshy Part of the Heart Was Converted into Fat.”Dublin Hospital Reports, 1818, II, 216.“…For several days his breathing was irregular; it would entirely cease for a quarter of minute, then it would become perceptible, though very low, then by degrees it became heaving and quick, and then it would gradually cease again: this revolution in the state of his breathing occupied about a minute during which there were about thirty acts of respiration...”

Stokes, W. “Observations on some Cases of permanently slow Pulse.” Dublin Quart. Jour. Med. Sc.,1846,II,83.“…Then a very feeble, indeed barely perceptible inspiration would take place, followed by another somewhat stronger, until at length high heaving, and even violent breathing was established, which would then subside till the next period of suspension… This was frequently a quarter of minute in duration .

slide4

Chronic heart failure:PREVALENCE

of Cheyne-Stokes Respiration and Obstructive Apneas

%

20*

75 *

450#

100*

34 *

NB

OA

CSR

Creteil 1994

Toronto 1999

Grenoble 1999

Cincinnati 2005

Melbourne 1999

* prospective

# retrospective

slide5

Chronic heart failure: PREVALENCE

of Cheyne-Stokes Respiration and Obstructive Apneas

679 patients

5 studies

44%

NB

AB

OA

56%

CSR

16%

40%

slide6

Sleep characteristics - 81 HF patients

Minutes

*

*

*

Javaheri S Ital. Circulation 1998-97: 2154

slide7

Sleep characteristics - 81 HF patients

Sleep efficiency

Arousal/h

Javaheri S Ital. Circulation 1998-97: 2154

slide8

Andamento temporale su un’epoca di 12 min della potenza dell’EEG nelle bande caratteristiche in un soggetto con scompenso cardiaco senza respiro di Cheyne-Stokes.

Andamento temporale su un’epoca di 12 min della potenza dell’EEG nelle bande caratteristiche in un soggetto con scompenso cardiaco con respiro di Cheyne-Stokes.

analisi tramite algoritmo gstft
Analisi tramite algoritmo GSTFT

Rappresentazione tempo-frequenza del segnale EEG (C4 –A1) in un soggetto con scompenso cardiaco e respiro di Cheyne-Stokes

metodi
METODI

REGISTRAZIONE CARDIORESPIRATORIA BREVE

CHF

patient

slide11

CSR/PB -

85 pts

CSR/PB +

65 pts

Prevalence of day-time CSR/PB: Pisa

57%

43%

Prevalence in previous studies:

- Mortara et al, Circulation 1997: CSR/PB - 64% pts

- Ponikowski et al, Circulation 1999: CSR/PB - 66% pts

metodi12
METODI

REGISTRAZIONE CARDIORESPIRATORIA AMBULATORIALE

effetti clinici del respiro di cs
Effetti clinici del respiro di CS
  • Cicli di desaturazione arteriosa
          • Ipossia  disfunzione d’organo/danno endoteliale, vasocostrizione polmonare
  • Iperattivazione simpatica
          • Diretta
          • Indiretta in risposta all’ipossia
  • Effetti emodinamici (prevalentemente indiretti)
          •  FC, vasocostrizione

 Aumento del post-carico e

del lavoro cardiaco

  • Effetti sulla variabilità della FC e PA
slide19

 baroreflex

 ergo-chemoreflex

BNP

-

ANP

system

activation

>>>

Sympathetic

-

RAA

activation

Na

-

H20

retention

vasoconstriction

arrhythmogenesis

tissue ischaemia

arrhythmias

dyspnoea

fatigue

sudden death

oedema

NEURO-HORMONAL IMBALANCE IN HEART FAILURE

LV

DYSFUNCTION

slide20

Cheyne-Stokes e Mortalità nello SCC

16 pazienti con SCC severo in fase di stabilità clinica

età media 64 aa, FE < 35%

CSR 9/16 (AHI 41± 17 vs 6 ± 5)

Hanly PJ, Am J Resp Crit C M 1996;153:272

slide21

Valore prognostico del CS notturno nello SCC

62 pz con FE < 35%, NYHA II-III

P Lanfranchi et al, Circulation 1999; 99:1435

slide22

Valore prognostico RP/CS durante la veglia

MT LA Rovere et al., Eur Heart J 2003;

slide23

60 sec.

1

AHI < 30 / hour

0.8

EOV

0.6

AHI > 30 / hour

0.4

proportion surviving

AHI > 30 / hour + EOV

0.2

p=0.0001

6

7

8

9

1

0

AHI = apnea-hypopnea index

0

0

10

20

30

months

Exercise

Recovery

Corrà, Circulation 2006

Cheyne-Stokes Respiration during exercise in CHF:

impact on PROGNOSIS

.

slide24

Pathogenesis of CSR in CHF: hypotheses

  • Central (?)
    • Hypocapnic (?!)
      • “Instability loop” (!)
        • - increased chemosensitivity
        • - prolonged circulation time
slide25

Ipotesi periferica- ipersensibilità chemocettoriale

Variazioni di PaCO2

Risposta ventilatoria eccessiva

 PaCO2 sotto la soglia apneica

Apnea

 PaCO2

Ripresa ventilazione

slide26

16

HVR slope

15

14

R= -0.87, p<0.001

Slope = -0.378

13

12

VE/MIN (L/min)

11

10

9

8

7

6

5

SaO2 (%)

80

82

84

86

88

90

92

94

96

98

100

Hypoxic Ventilatory Response

1050

RR interval

ms

700

30

Minute Ventilation

L/min

0

90

PET CO2

mmHg

0

SaO2

100

%

65

0

6

TIME (min)

slide27

20

HCVR slope

18

R = 0.93, p<0.001

Slope = 1.001

16

VE/MIN (L/min)

14

12

10

8

6

36

38

40

42

44

46

48

50

52

Pet CO2

HypercapnicVentilatory Response

1050

RR interval

ms

700

Minute Ventilation

30

L/min

0

90

PET CO2

mmHg

0

100

SaO2

%

65

0

6

TIME (min)

slide28

*

20

15

Prevalence of diurnal CSR (%)

Nocturnal apnea-hypopnea index

10

5

Normal

chemoreflex

Increased

HVR

Increased

HCVR

Increased

HVR+HCVR

Giannoni A, Emdin M, Poletti R, Bramanti F, Prontera C, Piepoli M, Passino C.

Clinical significance of chemosensitivity in chronic heart failure: influence on neurohormonal derangement, Cheyne-Stokes respiration and arrhythmias. Clin Sci (Lond). 2007 Oct 26; [Epub ahead of print]

slide29

VE/VCO2 slope

peakVO2

**

ml/min/kg

*

NB

CS

NB

CS

* p<0.05, ** p<0.01

Giannoni A, Emdin M, et al.. Clin Sci (Lond). 2007 Oct 26; [Epub ahead of print]

slide30

NT-proBNP

NorEPI

BNP

pg/ml

**

***

***

NB

CS

NB

CS

NB

CS

** p<0.01, *** p<0.001

Giannoni A, Emdin M, et al.. Clin Sci (Lond). 2007 Oct 26; [Epub ahead of print]

multivariate analysis
Multivariate Analysis
  • CO2-sensitivity and BNP level are independent predictors of CSR

(also considering O2-sensitivity, peak VO2, VE-VCO2 slope, norepinephrine, NT-proBNP from univariate analysis)

slide32

CO2-sensitivity andBNP aspredictors of CSR

HCVR slope

Sensitivity

AUC 0.93

P<0.001

BNP

AUC 0.89

P<0.001

Specificity

slide33

chemoceptors

 Norepi

 BNP, ANP

CSR

hypoxia

LV dysfunction

altered

haemodynamics

slide34

 baroreflex

 ergo-chemoreflex

BNP

-

ANP

system

activation

>>>

Sympathetic

-

RAA

activation

Na

-

H20

retention

vasoconstriction

arrhythmogenesis

tissue ischaemia

arrhythmias

dyspnoea

fatigue

sudden death

oedema

NEURO-HORMONAL IMBALANCE IN HEART FAILURE

LV

DYSFUNCTION

slide35

60 sec.

CSR in CHF: therapeutical target?

  • Why?
  • To improve respiratory pattern
  • To improve sleep quality/QOL
  • To improve cardiac performance
  • To improve prognosis (?)
  • When?
  • Which patient?
  • Which marker (daytime abnormalities, PSG-AHI, BNP, …)?
  • How?
slide36

60 sec.

Diagramma del trattamento del respiro di Cheyne Stokes nello scompenso cardiaco

Scompenso cardiaco con respiro di Cheyne-Stokes

Ottimizzare la terapia per CHF.

(farmaci, CRT)

Assenza di

Cheyne-Stokes

Cheyne-Stokes

persiste

Considerare

un trattamento specifico

O2 terapia

CPAP o altri device

(Trapianto Cardiaco)

Metilxantine

slide38

Grazie per l’attenzione!

emdin@ifc.cnr.it

passino@ifc.cnr.it

slide39

NYHA CLASS

LVEF

*

*

%

NB

CS

NB

CS

* p<0.05

Giannoni A, Emdin M, et al.. Clin Sci (Lond). 2007 Oct 26; [Epub ahead of print]

slide40

Effect of Theophylline on Sleep-Disordered Breathing in Heart Failure

S. Javaheri et al. NEJM August 22,1996 n8 335:562-567

Protocollo dello studio: 15 pz con scompenso cardiaco e disturbi della respirazione notturni (AHI > 10/ora). Somministrazione orale di Teofillina o placebo 2 volte die per 5 gg con una settimana di washout fra i due periodi.

Risultati: Significativa riduzione degli episodi di apnea/ipopnea rispetto al placebo:

Placebo 47  37

Teofillina 47  18

Possibili meccanismi della Teofillina:

Competizione a livello centrale con il sito recettoriale dell’Adenosina (depressore respiratorio)

Incremento del deficit ventilatorio polmonare restrittivo associato allo scompenso cardiaco

Effetto inotropo

analisi tramite algoritmo gstft41
Analisi tramite algoritmo GSTFT

Rappresentazione tempo-frequenza del segnale EEG (C4 –A1) in un soggetto con scompenso cardiaco senza respiro di Cheyne-Stokes

slide42

Bi-level PAP may fit the abnormal breathing

pattern of CSR-CSA better than CPAP. Therefore,

bi-level PAP improves an abnormal breathing pattern

more immediately and effectively than CPAP. In a recent

study, it has been reported that 57% of patients showed no

response to CPAP

slide43

Benefit of Atrial Pacing in Sleep Apnea SyndromeNEJM February 7, 2002 n 6, 346: 404-412

Stephane Garrigue, M.D., Philippe Bordier, M.D., Pierre Jaïs, M.D., Dipen C. Shah, M.D., Meleze Hocini, M.D., Chantal Raherison, M.D., Manuel Tunon De Lara, M.D., Michel Haïssaguerre, M.D., and Jacques Clementy, M.D.

15 pz con OSA e PM bicamerale

AHI in ritmo spontaneo: 28

AHI in ritmo elettroindotto 11 (P<0.001)

PRO

CONTRO

slide45

CHF-N

CHF-OSA

CHF-CSA

Increased long-term mortality in heart failure due to sleep apnoea is not yet proven

T. Roebuck1, P. Solin1, D.M. Kaye2,4, P. Bergin2, M. Bailey3 and M.T. Naughton1

Eur Respir J. 2004 May;23:735-40

78 pazienti

LVEF 19.9 ± 7.2%

PCP 16.5 ± 8.3 mmHg

effetti clinici del respiro di cs46
Effetti clinici del respiro di CS
  • Cicli di desaturazione arteriosa
          • Ipossia  disfunzione d’organo/danno endoteliale, vasocostrizione polmonare
  • Iperattivazione simpatica
          • Diretta
          • Indiretta in risposta all’ipossia
  • Effetti emodinamici (prevalentemente indiretti)
          •  FC, vasocostrizione
slide47

Overall CO2 sensitivity

vs

adrenergic activation and ventilatory efficiency

70

10000

R=0.322

P<0.05

R=0.549

P<0.001

60

1000

50

NEPI (pg/ml)

VE-VCO2 SLOPE

40

100

30

20

10

0.5

0.0

1.0

1.5

2.0

2.5

0.0

0.5

1.0

1.5

2.0

2.5

CO2 SENSITIVITY

CO2 SENSITIVITY

slide48

Overall CO2 sensitivity

vs

B-type Natriuretic Peptides

70

10000

R=0.411

P<0.01

R=0.400

P<0.01

R=0.549

P<0.001

R=0.322

P<0.05

60

1000

50

NT-proBNP (pg/ml)

BNP (pg/ml)

40

100

30

20

10

0.0

2.5

0.0

0.5

1.0

1.5

2.0

2.5

0.5

1.0

1.5

2.0

CO2 SENSITIVITY

CO2 SENSITIVITY

slide49

CONCLUSIONS

CSR is associated with:

  • Enhanced chemoceptive sensitivity to O2 and CO2
  • Symptom severity and systolic dysfunction
  • Functional capacity and ventilatory efficiency
  • Adrenergic activation
  • BNP/NT-proBNP levels

CSR is predicted by:

  • Enhanced chemoceptive sensitivity to CO2
  • BNP plasma level