Hearth failure

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Hearth failure

• Doc.Dr Emir Fazlibegovic,ESC,FESC
• Prof.Dr Mustafa Hadžiomerovic, ESC,FESC
• 5th International Congress of cardiologysts and
  angyologysts of Bosnia and Herzegovina,Sarajevo
  2010.

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WHAT IS HEART FAILURE?

• HF is a complex clinical syndrome that can
  result from any structural or functional cardiac
  disorder that impairs the ability of the
  ventricle to fill with or eject blood. The
  cardinal manifestations of HF are dyspnea and
  fatigue, which may limit exercise tolerance, and
  fluid retention, which may lead to pulmonary and
  peripheral edema.
• Both abnormalities can impair the functional
  capacity and quality of life of affected
  individuals, but they may not necessarily
  dominate the clinical picture at the same time.
• Evaluation and Management of Chronic Heart
  Failure in the Adult
• A Report of the ACC/AHA Task Force on Practice
  Guidelines
• February 2002
• Supply is less then demand
• Failure of the heart as a pump

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Systolic/Diastolic does it matter?

• Systolic
• heart cannot contract normally and cannot
  pump enough blood into the arteries (EFlt40)
• Diastolic
• heart cannot relax and fill normally and cannot
  pump enough blood into the arteries (EFgt40)

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Left, right, or both?

• Right Heart Failure
• Results in increased, systemic venous congestion
  and peripheral oedema
• Left Heart Failure
• Results in pulmonary congestion

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Different etiology so what?

• Many causes but clinical manifestations similar
• Coronary artery disease is the underlying cause
  of HF in approximately two thirds of patients
  with ischemic left ventricular systolic
  dysfunction.
• The remainder have nonischemic causes, e.g.
  hypertension, valvular disease, myocardial
  toxins, or myocarditis
• or may have no discernible cause (e.g.,
  idiopathic dilated cardiomyopathy).

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PHASE

• Compensated phase
• Supply temporarily meets the altered demand, no
  or very mild symtoms and signs
• Decompensated heart failure
• new or worsening symptoms/signs of dyspnoea,
  fatigue or oedema leading to hospitalisation or
  unscheduled medical care

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Terminology or just semantics?

• Congestive Heart Failure (CHF)
• Heart failure with extra fluid in vessels and
  tissues
• Acute heart failure (AHF)
• sudden initial episode of HF, severe symptoms
  frequent pulmonary edema
• Chronic heart failure (CHF) (chronic HF)
• Slow process of myocardium destruction, often
  unnoticed, mild to moderate symptoms frequent
  peripheral edema, may follow acute insult
• Acute exacerbation of chronic heart failure
• Immediate and massive decompensation of the
  previously existing chronic heart

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Current indication
Acutely Decompensated Severe Low-output Chronic
Pre-existing
Symptomatic
-24 hours? -Abruptly -Suddenly
NYHA III-IV
Cardiac -EFlt40 -CIlt2.0 l/min/m2 -Cold
Congestive Heart Failure (CHF)
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ONSET

• Acute heart failure
• sudden onset of symptoms or signs of heart
  failure in a patient with no history of heart
  failure and previously normal cardiac function

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ONSET

• Exacerbation of chronic heart failure
• patient with established diagnosis of heart
  failure who develops increasing signs or symptoms
  of the disease after a period of relative
  stability

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Conceptual differences between acute and chronic
heart failure

• Chronic heart failure
• neurohumoral disease that responds to
  neurohumoral intervention
• Remodeling, RAAS, cateholamines, PDE
• Acute heart failure
• haemodynamic disease that responds to
  haemodynamic interventions

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Classification and causes of heart failure

• Acute de novo heart failure
• Myocardial infarction
• Arrhythmias
• Valve destruction
• Myocarditis
• Hypertensive crisis
• Cardiac surgery

• Decompensated chronic heart failure
• Myocardial ischaemia
• Arrhythmias
• Malcompliance
• Infections
• Salt overload
• Hypertension

Pulmonary oedema Low output heart failure
(congestion) Cardiogenic shock
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Differences between acute heart failure and
decompensated Chronic HF

• Haemodynamics
• AHF RV /- LV, normovolaemic
• Decompensation of Chronic HF both RV and LV,
  increased EDV, hypervolaemic
• Prognosis
• AHF potentially reversible, stunning, sepsis
• Decompensation of Chronic HF chronic disease

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DIAGNOSISFramingham Criteria

• Major Criteria
• Parox. Nocturnal dyspnea
• Orthopnea
• ? JVP
• Pulmonary rales
• Third heart sound
• Cardiomegaly
• Pulmonary edema

• Minor Criteria
• Peripheral edema
• Night cough
• Dyspnea on exertion
• Hepatomegaly
• Pleural effusion
• Heart rategt120/min
• Wight loss gt 4.5 kg in 5 days

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Classification
ONSET ETIOLOGY PATOPHYSIOLOGY LOCATION NYHA DIAGNOSIS
ACUTE CHRONIC ISCHEMIC TOXIC INFALMATORY REUMATOID IDIOPATIC SYSTOLIC DIASTOLIC LEFT RIGHT I II III IV HEART FAILURE Cardiac insufficiency CARDIOMIOPATHY Cardiac dysfunction
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Treatment of Decompensated CHF
67
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5
8
Decompensated HF Patient Edema () or (-) Cold
Extremities SBP lt 90 mm Hg
Decompensated HF Patient Edema () Warm
Extremities SBP gt 90 mm Hg
Decompensated HF Patient Edema () Cold
Extremities SBP gt 90 mm Hg
Decompensated HF Patient Edema (-) Cold
Extremities SBP gt 90 mm Hg
Low-output HF
Cardio shock
High output
Dobutamine/ Dopamine/ Norepinephrine

• Optimization of therapy
• Increase ACEI doses
• IV diuretics
• Other PO or IV vasodilators (nitroprusside)

Levosimendan
Add Levo?

• Inadequate response
• Increasing BUN
• Persisting edema
• Persisting dyspnea

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Calcium-Induced Conformational Changes in
Troponin Complex

Ca2
cTnC
TnI
Myosin head
TnT
Ca2
Actin
Actin
Tm
TnT
Tm
Myosin head
Tm
cTnC
TnI
TnI
Actin
Actin
Tm
cTnC
TnT
Myosin head
Tm
Tm
Myosin head
TnT
Ca2
TnI
cTnC
Ca2
Myofilament length
Myofilament length
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Levosimendan

• Calcium sensitisation through bindingto troponin
  C
• increases cardiac contractility and efficiency
• Opening of ATP-sensitive potassium channels in
  vascular smooth muscles
• pulmonary, coronary, systemic vasodilation

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Calcium Sensitization by Levosimendan

• No increase in cAMP
• No increase in i/c calcium
• No increase in energy consumption
• No arrhythmogenicity
• No impairment in relaxation
• Anti-stunning effect
• No antagonism by ?-blockers

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Heart Failure

• LIDO study
• 203 patients with severe HF, levo vs. dobut
• CASINO study
• 299 patients low-output HF, levo vs. dobut vs.
  placebo.
• REVIVE-2 study
• 600 patients. Levo vs placebo. Higher early
  mortality, but no difference at 90 days.
• SURVIVE trial
• 1327 patients, levo vs. dobutamine No mortality
  difference at 180 days.

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IHD and Cardiac surgery

• RUSSLAN study
• 504 patients with recent MI, levo vs. placebo.
  Trend to lower mortality at 180 days.
• Small studies in cardiac surgery show
  levosimendan increases cardiac output and lowers
  SVR

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Mostar study in 20 patients NYHA III-IV

• aged 43-84, average 69
• All patients treated with ACE inhibitors,
  diuretic, beta blockers, aldosterone blockers,
  statins, and cardiotonics (digoxin chronically
  and dobutamin, dopamine in the shortly crisis
  period).
• on follow-up 1-3 day after infusion and 3 and 6
  month, and 1-2-3 year after.

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Levosimendan and NYHA
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Levosimendan and NYHA

• Mean-1.0000 Std Dev0.6124 Plt 0.0001

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EFLV in patients with levosimendan
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Levosimendan and EFLV

• Mean15.7059
  Std Dev14.3952 P 0.0004

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Levosimendan and ENDLV
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Levosimendan and FS
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Distrubtion of FS with levosimendan

• Med0.0818 SD0.0915 P
  0.002

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Conclusion 1

• Experience from our practice shows that single
  dose of Levosimendan in patients with
  decompensated advanced heart failure produces
  significant improvement, which reflects in
  extension of life.

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Conclusion 2

• Use of Levosimendan seams to be beneficial
  demonstrated by great benefit in the quality of
  life with better systolic function without any
  arrythmogenic effect.

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Conclusion 3

• There are probably other benefits masked by
  uknown lusitropic and pleotropic influences of
  Levosimendan in the physiology and
  pathophysiology of heart and others systems of
  body.

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Conclusion 4

• Almost all cases of death are results of
  co-morbidity disease, and are not related to
  levosimendan effect
• In the future
• ICD device
• Cardiac surgery
• Transplantation