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Diagnosis and Management of Chronic Heart Failure: What is the Standard of Care and What Will Become Standard. Philip B. Adamson MD, MSc, FACC Director, Oklahoma Foundation for Cardiovascular Research Director, Heart Failure Institute at Oklahoma Heart Hospital

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slide1

Diagnosis and Management of Chronic Heart Failure: What is the Standard of Care and What Will Become Standard

Philip B. Adamson MD, MSc, FACC

Director, Oklahoma Foundation for Cardiovascular Research

Director, Heart Failure Institute at Oklahoma Heart Hospital

Associate Professor of Physiology, University of Oklahoma Health Sciences Center

Oklahoma City, OK

initial diagnosis and evaluation
Initial Diagnosis and Evaluation
  • Symptoms of left heart failure
    • Dyspnea on exertion or at rest
    • Orthopnea, Paroxysmal Nocturnal Dyspnea
    • Lung Crackles, S3
  • Symptoms of right heart failure
    • Swelling
    • Ascites, liver congestion
    • Anorexia
    • Elevated JVP, Hepatomegaly, AJR, edema
initial diagnosis and evaluation1
Initial Diagnosis and Evaluation
  • Evaluation of ventricular structure and function (estimate LVEF)
    • Echocardiogram, NVG, Chest X-Ray, ECG
  • Heart Failure with:
    • Preserved ejection fraction
    • Reduced ejection fraction
  • Renal function, potassium, magnesium, TSH
  • WHY, WHY, WHY, WHY is this ventricle damaged?!?!?!
left ventricular ejection fraction
Left Ventricular Ejection Fraction

Left ventricular Ejection Fraction =

(LVEDV – LVESV)/LVEDV x 100

Normal is 55-70%

Systolic Heart Failure <40%

heart failure causes

Ao

PA

120/80

24/12

LA

12

RA

6

120/12

24/6

LV

RV

Heart Failure Causes

Left Heart Failure

1.Myocardial Infarction

2. Hypertension

3. Valvular failure

4. Viral

5. Genetic

6. Idiopathic

Right Heart Failure

1. Left heart failure

2. Pulmonary Hypertension

3. RV infarction

4.Sleep apnea

5. Left to right shunts

nyha class vs stage
NYHA Class vs. Stage

NYHA Classification

  • I – no symptoms
  • II – symptoms with significant exertion
  • III – symptoms with mild exertion
  • IV – symptoms at rest

ACC/AHA Stages

  • A – at risk for heart failure
  • B – LV dysfunction never had symptoms
  • C – LV dysfunction with symptoms
  • D – Refractory heart failure
goals of heart failure management
Goals of Heart Failure Management
  • Relieve Symptoms
    • “Make you feel better”
  • Prevent Progression of Disease
    • “Help your heart get better”
  • Prolong life
    • Obvious
two sides of pathophysiology
Two Sides of Pathophysiology
  • Hemodynamic Mechanisms
    • Increased left ventricular end-diastolic pressure
    • “Backline pressures” increase
  • Symptoms of heart failure
  • Neurohormonal Mechanisms
    • Sympathetic and parasympathetic responses
    • Renin-angiotensin and aldosterone responses
  • Fibrosis
  • Genetic control
  • Worsening systolic and diastolic function
heart failure symptoms

Ao

PA

120/80

24/12

LA

12

RA

6

120/12

24/6

LV

RV

Heart Failure Symptoms

Left Ventricular Failure

Lung Congestion

Dyspnea

Orthopnea

Paroxysmal Nocturnal Dyspnea

Right Ventricular Failure

Liver Congestion

Ascites

Gut edema

Leg edema

evaluating jugular venous pressure

Evaluating Jugular Venous Pressure

Photo Courtesy of Dr. J. Thomas Heywood

slide11

Neural

Hormonal

Activation

Neural

Hormonal

Activation

↓SV

↑LVEDP

example of adverse remodeling

Acute MI

(hours)

Infarct expansion

(hours to days)

Global remodeling

(days to months)

Example of Adverse Remodeling
  • Apical infarction from total occlusion LAD,remainder of coronaries without obstruction
pathologic progression of cv disease
Pathologic Progression of CV Disease

Electrical

Remodeling

Sudden

Death

Coronary artery disease

Left ventricularinjury

Hypertension

Ventricular

Dysfunction

Pathologicremodeling

Death

Diabetes

Cardiomyopathy

Pump failure

Valvular disease

Symptoms:DyspneaFatigueEdema

Chronicheartfailure

Sympathetic Activation

Parasympathetic withdrawal

Renin Angiotensin Activation

Aldosterone Activation

Renal Reabsorption

  • Neurohormonalstimulation
  • Endothelial dysfunction
  • Myocardial toxicity

Adapted from Cohn JN. N Engl J Med. 1996;335:490–498.

pathologic progression of cv disease1
Pathologic Progression of CV Disease

Electrical

Remodeling

Sudden

Death

Coronary artery disease

Left ventricularinjury

Hypertension

Ventricular

Dysfunction

Pathologicremodeling

Death

Diabetes

Cardiomyopathy

Pump failure

Valvular disease

Symptoms:DyspneaFatigueEdema

Chronicheartfailure

Sympathetic Activation

Parasympathetic withdrawal

Renin Angiotensin Activation

Aldosterone Activation

Renal Reabsorption

  • Neurohormonalstimulation
  • Endothelial dysfunction
  • Myocardial toxicity

Adapted from Cohn JN. N Engl J Med. 1996;335:490–498.

ace inhibitors
ACE Inhibitors
  • Block conversion of Angiotensin I to Angiotensin II (among other things)
  • Prevent adverse remodeling
  • ~21% mortality risk reduction
  • Protect renal function in diabetics
  • High dose (lisinopril 40 mg) may be better than low dose
  • Class effect (NYHA Class I-IV, Stage A-D)
  • Complications: Hyperkalemia, worsening renal function, hypotension, cough
angiotensin receptor blockers
Angiotensin Receptor Blockers
  • As the name implies
  • Same expectations as ACE inhibitors except no cough
  • Class effect (NYHA Class I-IV, Stage A-D)
  • Complications: Hypotension, hyperkalemia, worsening renal function
beta blockers
Beta-Blockers
  • Antagonize beta-receptors
  • Reduce fibrosis, adverse remodeling
  • 34% mortality risk reduction
  • Improvement in LV function (NYHA Class I-IV, Stage A-D)
  • NOT a class effect
    • Carvedilol 6.25 mg BID to 25 mg BID
    • Metoprolol SUCCINATE 25 mg qD to 200 mg qD
    • Bisoprolol 2.5 mg daily to 10 mg daily
  • Complications: bradycardia, hypotension
aldosterone antagonists
Aldosterone Antagonists
  • Block the hormone Aldosterone
  • Decrease fibrosis and remodeling
  • ~34% mortality risk reduction
  • Eplerenone and spironolactone 25-50 mg qD
  • NYHA Class II-IV, Stage C-D
  • COMPLICATIONS: HYPERKALEMIA!
  • MUST check potassium at baseline, day 1, day 7 and day 30.
device therapies
Device Therapies
  • Sudden Cardiac Death (due to ventricular fibrillation)
    • Risk increases as LVEF declines (<35%)
    • Beta-blockers effective
    • Implantable Cardioverter Defibrillators
  • Ventricular Dyssynchrony
    • Wide QRS on ECG
    • Increases risk for sudden death and adverse remodeling
    • Cardiac Resynchronization (biventricular pacing)
slide21

Is there a relationship between LV diastolic volume and LV diastolic pressure?

1. Yes, it is linear:

as volume increases pressure increases, Pressure = A x volume + B.

2. Yes, it is exponential:

as volume increases pressure increases,

Pressure = A e volume B + C.

3. No, there is no relationship:

volume Δ is independent of pressure Δ.

4. I’m looking forward to a long weekend:

and frankly Scarlette I don’t care.

slide22

14

10

LV Diastolic Pressure (mmHg)

Pres x 3

6

(3)

Vol

2

ΔPressure

(7)

2

(1)

ΔVolume

(15)

50

82

89

65

70

40

100

LV Diastolic Volume (ml)

slide24

Acutely Decompensated Heart Failure

PAD

PCWP

Intravascular Pressure

>>>

Extravascular Pressure

Diastolic Pressures

slide25

Acutely Decompensated Heart Failure

Diastolic Volume

Diastolic Pressures

Hemodynamic Mechanism ?

slide26

Acutely Decompensated Heart Failure

Relationship

Diastolic Volume

vs.

Diastolic Pressure

slide27

Acutely Decompensated Heart Failure

↑ Intravascular

Diastolic Volume

↑ Intravascular

Diastolic Pressure

Hyper “VOL” emia

Hyper “PRESS” emia

Hemodynamic Mechanisms ?

slide28

What is the mechanism (s) causing acutely decompensated heart failure in

SHF vs. DHF ?

1. In SHF there is a dominant ↑ in LV Volume.

2. In DHF there is a dominant ↑ in LV Pressure.

3. The mechanism is the same in SHF vs. DHF.

4. I refuse to answer any more questions until you explain the differences between DHF and SHF.

slide29

 Diastolic

Distensibility

Circulation 2006; 113: 296-304

 Diastolic

Distensibility

slide30

DHF

SHF

slide32

Hospitalization

Intrathoracic

Impedance

Changes

Symptoms

Filling pressures

Increase

Weights

Change

Autonomic

Adaptation

Pathophysiology of Congestion

-30

-20

0

Days

- 10

Adamson PB: Current Heart Fail Reports 2009;287-292

slide33

Close monitoring of Heart Failure Patients

Avoiding Clinical Events

Averted

Heart Failure Event

Medical Intervention

Reducing High Filling Pressures

Days

-21

-14

- 7

0

Proactive

Adamson PB Curr Heart Fail Reports 2009;6:287

33

status of hemodynamic monitors
Status of Hemodynamic Monitors
  • 3 sensors tested in prospective trials, one trial ongoing (LAPTOP-HF).
  • 1 sensor being evaluated by FDA
  • None currently have FDA approval for use in the US. CE mark is in place for one.