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Magdy El-Masry
Prof. of Cardiology
Tanta University
We have no conflict of interest to declare.
Acta Clin Croat 2017; 56:269-276
Let's get close
closer than close
closer than you
could ever
imagine us
CHF patients
COPD
COPD patients
CHF
 The prevalence of heart failure in COPD patients is estimated at 20 %.
 For the converse situation in heart failure, COPD prevalence has been quoted as 33%.
prevalence
The Heart is Not Always
in Good Hands
Have a lung disease?
Your heart’s in trouble
Chest. 1990, Feb;97(2):453-60.
Recently there have been
considerable advances in
our understanding of the
role of the “hands that
hold the heart” —the
lungs which form the
cardiac fossa in which the
heart lies in the chest —in
affecting cardiovascular
function in health and in
disease1 (Fig 1).
I shall try to use this new
knowledge to clarify some
of the clinical problems of
cardiopulmonary
interactions that have
puzzled physicians dealing
with chest diseases.
Association of Cardiovascular Disease With Respiratory Disease
Journal of the American College of Cardiology, March 2019
Association
Smoking
Ageing
COPD HF
Association is not the same as causation
(or Correlation does not equal causation)
The presence of each
increase morbidity and
mortality of the other
COPD HF
COPD and HF "DOUBLE TROUBLE"
The presence of untreated or unrecognised (i.e. silent) CVD may
contribute to mortality in COPD and may also be an underlying
causative factor in exacerbations, which can be difficult to separate
from respiratory aetiologies
It is also possible, if not likely, that the burden of CVD may be
underrated by pulmonologists when treating COPD patients
because symptoms are presumed to be primarily driven by airflow
obstruction, especially during exacerbations.
CVD potentially under-detected in patients with COPD
An atypical presentation of myocardial infarction (MI) should be considered in every patient presenting with COPD exacerbation with
the understanding that MI may coexist with another acute illness in these patients. Patients with COPD and MI should be urgently
assessed for revascularisation via percutaneous coronary intervention and started on guideline-based therapy. Any hospitalisation in a
patient with COPD, even in the absence of an MI, should be considered an opportunity to assess and optimise the coronary risk factors.
The recommended approach to patients with COPD presenting with dyspnea
Why COPD and Heart Failure Go Hand-in-Hand
Studies suggest that COPD and heart failure
frequently coexist.
Is this because having one places you at greater
risk for the other?
Or could it be that they share a common risk
factor?
Here's how COPD and heart failure are linked
Biological pathways and mechanisms linking COPD and CVD.
Cardiovascular and pulmonary disease in the context of inflammation
(“CardioPulmonary Continuum”) J. Clin. Med. 2019, 8, 69
Today’s talk will include: COPD and HF
Diagnostic
Challenges
Therapeutic
Challenges
Cardiologist
Pulmonologist
“It's a Matter of
Breath and Death”
Top causes of death in hospitals
This patient is not breathing properly :
is this COPD , heart failure ,both ,or neither?
COPD HF
Diagnostic and therapeutic challenges for both
emergency department and outpatient physicians
COPD and HF : Diagnostic and Therapeutic Challenges
Acute heart failure is the most common disease underlying acute dyspnea
Acute heart failure (AHF) is responsible for about 50 % of all cases and therefore requires particular
attention . Pneumonia, exacerbated COPD and asthma, pulmonary embolism and anemia are also common
(AE-COPD)
?The accuracy of bedside
diagnosis in dyspnea
Has the
stethoscope
had its day?
The stethoscope is
having a crossroads
moment.
“All That Wheezes Is Not Asthma” (or COPD)!
Clinical Question: Can bronchodilators improve wheeze in heart failure?
HF itself can cause a non-asthmatic bronchial obstruction that can be variable and which can respond to
bronchodilators( because they constrict bronchial vessels and reduce the epithelial wall edema that is
thought to be implicated ).The important feature is that this form of reversible airway narrowing is not a
contraindication to beta-blockers which severe classic asthma is.
Only 6% of cardiologists and 12% of pulmonologists had certified or
ruled out COPD in patients with CHF, or vice versa
6% of
Cardiologists
R/O
COPD
12% of
Pulmonologists
R/O
CHF
Concurrent COPD may play part of the missing puzzle in
the complex pathophysiology of HF, and vice versa.
Considering the high prevalence of
ventricular dysfunction in COPD,
routine assessment with either BNP or
echocardiography should be
considered in COPD patients
On the other hand,
pulmonary function tests
should be performed in
all HF patients.
Clinical Utility of BNP
Cardiologist Pulmonologist
Therefore, closer collaboration
between pulmonologists and
cardiologists should be warranted
in the future.
Schematic representation of the diagnostic
flow chart in chronic obstructive pulmonary
disease (COPD) and heart failure (HF).
COPD and HF require a careful assessment of
patient symptoms and signs (i.e., of clinical
presentation) coupled with diagnostic tests.
The top blue box presents the symptoms
suggesting COPD, and the top red box shows
those suggesting HF. As some symptoms are
common in both diseases, they are presented in
the center (purple) and should warrant further
diagnostic assessment for both COPD and HF.
The second part of the figure summarizes the
minimum requirements for the diagnosis of
COPD and/or HF.
*Positive history of CAD or other cardiac
disorders, hypertension, and exposure to
cardiotoxic drugs, increase the likelihood of HF,
as well as signs of congestion and overload
(e.g., rales, jugular venous dilatation).
$ Spirometry is required to make the diagnosis
in the appropriate clinical context and must
show a post-bronchodilator fixed ratio of
FEV1/FVC , 70%. # An objective cardiac cause
must be identified.
American Journal of Respiratory and Critical Care Medicine Volume 194 Number 11 | December 1 2016
Schematic representation of the diagnostic flow chart in COPD and HF
Cardiovascular effects of respiratory drugs
Respiratory effects of cardiovascular drugs
The cornerstones of therapy are beta-blockers and beta-agonists ,which as
their modes of action suggest oppose each other’s action
Stepwise approach to pharmacologic management based on severity of COPD
COPD = chronic obstructive pulmonary disease; ICS = inhaled corticosteroid; LABA = long-acting beta2-agonist; LAMA =
long-acting antimuscarinic antagonist; SABA = short-acting beta2-agonist; SAMA = short-acting muscarinic antagonist.
Mechanism of action of LAMAs (long-acting muscarinic antagonists)
Mechanism of action of LABAs ( long-acting β2 agonists).
Journal of Food and Drug Analysis, Available online 7 January 2019
LAMAs & LABAs → ? Adverse CV events
Highlights
 Inhaled long-acting β2 agonists (LABA) and muscarinic antagonists (LAMA) are
concerned about the cardiovascular (CV) risk.
 Randomized trials did not find CV risk with LABAs and LAMAs despite insufficient
power and exclusion of high-risk patients.
 Most observational studies, however, tied CV risk with LABAs and LAMAs, though
they may be subject to confounding and bias.
Frequently used medication in COPD
Inhaled steroids Good safety profile
Systemic steroids Pro-arrhythmic potential
Short acting beta agonists (SABAs) Pro-arrhythmic potential (high doses)
Long acting beta agonists (LABAs) Acceptable safety profile
Short acting muscarinic antagonists(SAMAs) Pro-arrhythmic potential (high doses)
Long acting muscarinic antagonists(LAMAs) Acceptable safety profile
PDE inhibitors : roflumilast Reduction of cardiovascular events
PDE inhibitors : theophylline Narrow therapeutic range and
considerable pro-arrhythmic potential
The Beta-Blocker Controversy
YES
NO
Patients with HF and
concomitant COPD
can be safely treated
with a combination
LABA and a LAMA
when on a baseline
beta-blocker.
Some physicians
may still hesitate
to give beta-
blockers to
patients with
COPD, despite
the numerous
proven benefits
of beta-blockers
in HF
and evidence
that supports
their safety and
lack of
detrimental
effects on
pulmonary
function.
Theoretical risks and benefits for those with HF and COPD treated with β-blockers
(over and above the known cardiovascular benefits)
Beneficial and unfavorable effects of beta-blockers on HF and COPD.
What is Evidence?
Conclusion
Treatment with β-blockers may reduce the risk of
exacerbations and improve survival in patients
with COPD, possibly as a result of dual
cardiopulmonary protective properties.
CHEST 2018; 153(6):1315-1325
CONCLUSIONS:
 Lung function, overall respiratory status, and safety of
tiotropium (LAMA) /olodaterol (LABA) were not
influenced by baseline β-blocker treatment in patients
with moderate to very severe COPD.
 Results from this large patient cohort support the
cautious and appropriate use of β-blockers in patients
with COPD and cardiovascular comorbidity.
Implications of all available evidence
Results from this study advocates changes in the present
hesitation of treatment of hypertension with β-blockers
in patients at risk of or with concomitant COPD
2019
The study by Nielsen et al. comes as close as possible to reassure us
not to be scared of the “wolf” ,
as β-blockers (even older non-β1-selective ones) do prove quite safe
to be chronically administered to cardiac patients with COPD.
2019
The GOLD was launched in 1997
Not All ß-blockers Are Equal
Safety of Beta-Blockers in COPD
propranolol
• Beta-1 selective antagonists such as bisoprolol, nebivolol and metoprolol are preferred to
the nonselective carvedilol as they are less likely to produce bronchoconstriction in COPD.
• Long-acting muscarinic antagonists, which are commonly used in COPD, protect against the
potential for bronchoconstriction due to dose related beta-2 receptor antagonism.
Differential Selectivity of ß-Blockers for ß-Receptor Subtypes
In conclusion, cardioselectivity is paramount, and therefore metoprolol, bisoprolol
and in particular nebivolol should be the first choice treatment.
Carvedilol is the only non-cardioselective ß-blocker approved for treating HF.
it should be avoided when possible in patients with COPD, especially during acute
exacerbations.
Evidence-based doses of beta blockers
in key randomized trials in HFrEF (or after MI)
Starting dose (mg) Target dose (mg)
Be Systematic !
COPD and HF : Dangerous Liaisons?
“ Thank you
for your
kind attention ”
When we share something with someone else it is equal to caring him

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Chronic Obstructive Pulmonary Disease and Heart Failure The challenges facing cardiologists and pulmonologists& hf final

  • 1. Magdy El-Masry Prof. of Cardiology Tanta University
  • 2. We have no conflict of interest to declare.
  • 3.
  • 4. Acta Clin Croat 2017; 56:269-276 Let's get close closer than close closer than you could ever imagine us
  • 5. CHF patients COPD COPD patients CHF  The prevalence of heart failure in COPD patients is estimated at 20 %.  For the converse situation in heart failure, COPD prevalence has been quoted as 33%. prevalence
  • 6.
  • 7. The Heart is Not Always in Good Hands Have a lung disease? Your heart’s in trouble
  • 8. Chest. 1990, Feb;97(2):453-60. Recently there have been considerable advances in our understanding of the role of the “hands that hold the heart” —the lungs which form the cardiac fossa in which the heart lies in the chest —in affecting cardiovascular function in health and in disease1 (Fig 1). I shall try to use this new knowledge to clarify some of the clinical problems of cardiopulmonary interactions that have puzzled physicians dealing with chest diseases.
  • 9. Association of Cardiovascular Disease With Respiratory Disease Journal of the American College of Cardiology, March 2019
  • 10. Association Smoking Ageing COPD HF Association is not the same as causation (or Correlation does not equal causation)
  • 11. The presence of each increase morbidity and mortality of the other COPD HF COPD and HF "DOUBLE TROUBLE"
  • 12. The presence of untreated or unrecognised (i.e. silent) CVD may contribute to mortality in COPD and may also be an underlying causative factor in exacerbations, which can be difficult to separate from respiratory aetiologies It is also possible, if not likely, that the burden of CVD may be underrated by pulmonologists when treating COPD patients because symptoms are presumed to be primarily driven by airflow obstruction, especially during exacerbations. CVD potentially under-detected in patients with COPD
  • 13. An atypical presentation of myocardial infarction (MI) should be considered in every patient presenting with COPD exacerbation with the understanding that MI may coexist with another acute illness in these patients. Patients with COPD and MI should be urgently assessed for revascularisation via percutaneous coronary intervention and started on guideline-based therapy. Any hospitalisation in a patient with COPD, even in the absence of an MI, should be considered an opportunity to assess and optimise the coronary risk factors. The recommended approach to patients with COPD presenting with dyspnea
  • 14. Why COPD and Heart Failure Go Hand-in-Hand Studies suggest that COPD and heart failure frequently coexist. Is this because having one places you at greater risk for the other? Or could it be that they share a common risk factor? Here's how COPD and heart failure are linked
  • 15. Biological pathways and mechanisms linking COPD and CVD.
  • 16. Cardiovascular and pulmonary disease in the context of inflammation (“CardioPulmonary Continuum”) J. Clin. Med. 2019, 8, 69
  • 17. Today’s talk will include: COPD and HF Diagnostic Challenges Therapeutic Challenges Cardiologist Pulmonologist
  • 18. “It's a Matter of Breath and Death”
  • 19. Top causes of death in hospitals
  • 20. This patient is not breathing properly : is this COPD , heart failure ,both ,or neither? COPD HF
  • 21. Diagnostic and therapeutic challenges for both emergency department and outpatient physicians COPD and HF : Diagnostic and Therapeutic Challenges
  • 22. Acute heart failure is the most common disease underlying acute dyspnea Acute heart failure (AHF) is responsible for about 50 % of all cases and therefore requires particular attention . Pneumonia, exacerbated COPD and asthma, pulmonary embolism and anemia are also common (AE-COPD)
  • 23. ?The accuracy of bedside diagnosis in dyspnea Has the stethoscope had its day? The stethoscope is having a crossroads moment.
  • 24. “All That Wheezes Is Not Asthma” (or COPD)! Clinical Question: Can bronchodilators improve wheeze in heart failure? HF itself can cause a non-asthmatic bronchial obstruction that can be variable and which can respond to bronchodilators( because they constrict bronchial vessels and reduce the epithelial wall edema that is thought to be implicated ).The important feature is that this form of reversible airway narrowing is not a contraindication to beta-blockers which severe classic asthma is.
  • 25. Only 6% of cardiologists and 12% of pulmonologists had certified or ruled out COPD in patients with CHF, or vice versa 6% of Cardiologists R/O COPD 12% of Pulmonologists R/O CHF
  • 26. Concurrent COPD may play part of the missing puzzle in the complex pathophysiology of HF, and vice versa.
  • 27.
  • 28. Considering the high prevalence of ventricular dysfunction in COPD, routine assessment with either BNP or echocardiography should be considered in COPD patients On the other hand, pulmonary function tests should be performed in all HF patients. Clinical Utility of BNP
  • 29. Cardiologist Pulmonologist Therefore, closer collaboration between pulmonologists and cardiologists should be warranted in the future.
  • 30. Schematic representation of the diagnostic flow chart in chronic obstructive pulmonary disease (COPD) and heart failure (HF). COPD and HF require a careful assessment of patient symptoms and signs (i.e., of clinical presentation) coupled with diagnostic tests. The top blue box presents the symptoms suggesting COPD, and the top red box shows those suggesting HF. As some symptoms are common in both diseases, they are presented in the center (purple) and should warrant further diagnostic assessment for both COPD and HF. The second part of the figure summarizes the minimum requirements for the diagnosis of COPD and/or HF. *Positive history of CAD or other cardiac disorders, hypertension, and exposure to cardiotoxic drugs, increase the likelihood of HF, as well as signs of congestion and overload (e.g., rales, jugular venous dilatation). $ Spirometry is required to make the diagnosis in the appropriate clinical context and must show a post-bronchodilator fixed ratio of FEV1/FVC , 70%. # An objective cardiac cause must be identified. American Journal of Respiratory and Critical Care Medicine Volume 194 Number 11 | December 1 2016
  • 31. Schematic representation of the diagnostic flow chart in COPD and HF
  • 32.
  • 33. Cardiovascular effects of respiratory drugs Respiratory effects of cardiovascular drugs
  • 34. The cornerstones of therapy are beta-blockers and beta-agonists ,which as their modes of action suggest oppose each other’s action
  • 35. Stepwise approach to pharmacologic management based on severity of COPD COPD = chronic obstructive pulmonary disease; ICS = inhaled corticosteroid; LABA = long-acting beta2-agonist; LAMA = long-acting antimuscarinic antagonist; SABA = short-acting beta2-agonist; SAMA = short-acting muscarinic antagonist.
  • 36. Mechanism of action of LAMAs (long-acting muscarinic antagonists)
  • 37. Mechanism of action of LABAs ( long-acting β2 agonists).
  • 38. Journal of Food and Drug Analysis, Available online 7 January 2019 LAMAs & LABAs → ? Adverse CV events
  • 39. Highlights  Inhaled long-acting β2 agonists (LABA) and muscarinic antagonists (LAMA) are concerned about the cardiovascular (CV) risk.  Randomized trials did not find CV risk with LABAs and LAMAs despite insufficient power and exclusion of high-risk patients.  Most observational studies, however, tied CV risk with LABAs and LAMAs, though they may be subject to confounding and bias.
  • 40. Frequently used medication in COPD Inhaled steroids Good safety profile Systemic steroids Pro-arrhythmic potential Short acting beta agonists (SABAs) Pro-arrhythmic potential (high doses) Long acting beta agonists (LABAs) Acceptable safety profile Short acting muscarinic antagonists(SAMAs) Pro-arrhythmic potential (high doses) Long acting muscarinic antagonists(LAMAs) Acceptable safety profile PDE inhibitors : roflumilast Reduction of cardiovascular events PDE inhibitors : theophylline Narrow therapeutic range and considerable pro-arrhythmic potential
  • 41. The Beta-Blocker Controversy YES NO Patients with HF and concomitant COPD can be safely treated with a combination LABA and a LAMA when on a baseline beta-blocker. Some physicians may still hesitate to give beta- blockers to patients with COPD, despite the numerous proven benefits of beta-blockers in HF and evidence that supports their safety and lack of detrimental effects on pulmonary function.
  • 42. Theoretical risks and benefits for those with HF and COPD treated with β-blockers (over and above the known cardiovascular benefits)
  • 43. Beneficial and unfavorable effects of beta-blockers on HF and COPD.
  • 44.
  • 46.
  • 47. Conclusion Treatment with β-blockers may reduce the risk of exacerbations and improve survival in patients with COPD, possibly as a result of dual cardiopulmonary protective properties.
  • 48. CHEST 2018; 153(6):1315-1325 CONCLUSIONS:  Lung function, overall respiratory status, and safety of tiotropium (LAMA) /olodaterol (LABA) were not influenced by baseline β-blocker treatment in patients with moderate to very severe COPD.  Results from this large patient cohort support the cautious and appropriate use of β-blockers in patients with COPD and cardiovascular comorbidity.
  • 49. Implications of all available evidence Results from this study advocates changes in the present hesitation of treatment of hypertension with β-blockers in patients at risk of or with concomitant COPD 2019
  • 50. The study by Nielsen et al. comes as close as possible to reassure us not to be scared of the “wolf” , as β-blockers (even older non-β1-selective ones) do prove quite safe to be chronically administered to cardiac patients with COPD. 2019
  • 51. The GOLD was launched in 1997
  • 52.
  • 53. Not All ß-blockers Are Equal Safety of Beta-Blockers in COPD
  • 54. propranolol • Beta-1 selective antagonists such as bisoprolol, nebivolol and metoprolol are preferred to the nonselective carvedilol as they are less likely to produce bronchoconstriction in COPD. • Long-acting muscarinic antagonists, which are commonly used in COPD, protect against the potential for bronchoconstriction due to dose related beta-2 receptor antagonism.
  • 55. Differential Selectivity of ß-Blockers for ß-Receptor Subtypes In conclusion, cardioselectivity is paramount, and therefore metoprolol, bisoprolol and in particular nebivolol should be the first choice treatment. Carvedilol is the only non-cardioselective ß-blocker approved for treating HF. it should be avoided when possible in patients with COPD, especially during acute exacerbations.
  • 56. Evidence-based doses of beta blockers in key randomized trials in HFrEF (or after MI) Starting dose (mg) Target dose (mg)
  • 57. Be Systematic ! COPD and HF : Dangerous Liaisons?
  • 58. “ Thank you for your kind attention ” When we share something with someone else it is equal to caring him

Editor's Notes

  1. Schematic representation of the diagnostic flow chart in chronic obstructive pulmonary disease (COPD) and heart failure (HF). COPD and HF require a careful assessment of patient symptoms and signs (i.e., of clinical presentation) coupled with diagnostic tests. The top blue box presents the symptoms suggesting COPD, and the top red box shows those suggesting HF. As some symptoms are common in both diseases, they are presented in the center (purple) and should warrant further diagnostic assessment for both COPD and HF. The second part of the figure summarizes the minimum requirements for the diagnosis of COPD and/or HF (see text for further details). *Positive history of coronary artery disease or other cardiac disorders, hypertension, and exposure to cardiotoxic drugs, increase the likelihood of HF, as well as signs of congestion and overload (e.g., rales, jugular venous dilatation). $ Spirometry is required to make the diagnosis in the appropriate clinical context and must show a post-bronchodilator fixed ratio of FEV1/FVC , 70%. # An objective cardiac cause must be identified (see text). BNP = brain natriuretic peptide; HFmrEF = heart failure with midrange ejection fraction; HFpEF = heart failure with preserved ejection fraction; HFrEF = heart failure with reduced ejection fraction; NT-proBNP = N-terminal prohormone brain natriuretic peptide
  2. Schematic representation of the diagnostic flow chart in chronic obstructive pulmonary disease (COPD) and heart failure (HF). COPD and HF require a careful assessment of patient symptoms and signs (i.e., of clinical presentation) coupled with diagnostic tests. The top blue box presents the symptoms suggesting COPD, and the top red box shows those suggesting HF. As some symptoms are common in both diseases, they are presented in the center (purple) and should warrant further diagnostic assessment for both COPD and HF.
  3. The second part of the figure summarizes the minimum requirements for the diagnosis of COPD and/or HF (see text for further details). *Positive history of coronary artery disease or other cardiac disorders, hypertension, and exposure to cardiotoxic drugs, increase the likelihood of HF, as well as signs of congestion and overload (e.g., rales, jugular venous dilatation). $ Spirometry is required to make the diagnosis in the appropriate clinical context and must show a post-bronchodilator fixed ratio of FEV1/FVC , 70%. # An objective cardiac cause must be identified (see text). BNP = brain natriuretic peptide; HFmrEF = heart failure with midrange ejection fraction; HFpEF = heart failure with preserved ejection fraction; HFrEF = heart failure with reduced ejection fraction; NT-proBNP = N-terminal prohormone brain natriuretic peptide.