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in

Heart Failure
Basics to Recent Advances
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Definition, Etiology
Epidemiology and
Pathophysiology
 Floor Plan of This Talk

Introduction Etiology Diagnosis

Patho Prognosis
Definitions
Physiology Risk Scoring

Clinical Treatment &

Epidemiology
features Prevention
www.drsarma.in

“The very essence of cardiovascular

practice is early detection of Heart
Failure”
 HF is a ‘BIG’ Subject
• It afflicts millions of people worldwide
• Has many diverse causes and risk factors
• Large number of Mega trials and literature
• High mortality; Several drugs and devices
• A paradigm shift in understanding & Rx.
• Extremely costly – huge no. of bed days
• Complicated by many co morbidities
• Truly multidisciplinary in its management
 Floor Plan of This Talk

Introduction Etiology Diagnosis

Patho Prognosis
Definitions
Physiology Risk Scoring

Clinical Treatment &

Epidemiology
Features Prevention
Definitions of Heart Failure
Heart failure is a clinical syndrome characterized
by decreased systemic perfusion, inadequate to
meet the body's metabolic demands as a result of
impaired cardiac pump function - Cleveland Clinic

A pathophysiologic state in which an abnormality

of cardiac function is responsible for failure of the
heart to pump blood at a rate commensurate with
metabolic requirements of the tissues -E Braunwald
 Definition of HF
Physiological:
Inability of the heart to pump sufficient
oxygenated blood to the metabolizing tissues
despite an adequate filling pressure.
Working Clinical Definition:
Clinical syndrome consisting of symptoms such
as breathlessness, fatigue, and swelling of ankle
caused by cardiac dysfunction.
 Types of Heart Failure
• Chronic Heart Failure (CHF)
• Acute Heart Failure (Cardiogenic Shock)
• Systolic Failure (LVSD) – Reduced EFHF
• Diastolic Heart Failure (LVDD) – NEFHF
• Left Heart Failure (LVF)
• Right Heart Failure (Congestive CCF)
• Forward Failure and Backward Failure
• High output failure -Thyrotoxic, Paget's,
Anemia, Pregnancy, A-V fistula
• Low output failure – 95% of HF is this
 Floor Plan of This Talk

Introduction Etiology Diagnosis

Patho Prognosis
Definitions
Physiology Risk Scoring

Clinical Treatment &

Epidemiology
Features Prevention
Heart Failure – Some Statistics
• Affects 10% of people over 65 years
• Affects over 50% of people with 85+ years
• Approx 10% of patients with HF die each yr.
• It is the most common condition for which
patients 65 + require admission to hospital
• It is NOT a single disease – A syndrome
• Results from any cardiac disorder that impairs
the ability of the ventricles to fill with or eject
blood
Epidemiology of Heart Failure
Clinical criteria – Prevalence 1-2 %

Males > Females; in 65+ Prevalence 7%

50% of LVSD is asymptomatic

NEF HF varies from 15 to 50%

Incidence 0.2 to 0.3 %;  with age

Epidemiology of Heart Failure
• Age Men Women
• 5059 8 8
• 8089 66 79
Prevalence • All ages 7.4 7.7

• Age Men Women

• 5059 3 2
• 8089 27 22
Incidence • All ages 2.3 1.4

Data from Framingham Heart Study per 1000 population

 Incidence of Heart Failure

McKee PA et al. Framingham study; N Eng J Med 1971; 285: 1441-6

Age, MI and Heart Failure
 Systolic Heart Failure
• LVSD – Left Ventricular Systolic Dysfunction
• Most common type of Heart Failure; 60-70%
• LV is usually dilated & enlarged.
• Fails to contract normally due to WMA, Ischemia
• Cannot pump sufficient blood to meet needs
• Normal ejection fraction (EF) is at least 50-55%
• In LVSD heart failure the EF is <40 -45%
• This carries a 10% mortality per annum
 Diastolic Heart Failure
• Accounts for 20-40% of patients
• Ventricles are normal-sized with normal emptying
• But there is an impairment in the ability of the
ventricles to fill with blood during diastole.
• Because of stiff myocardium due to hypertrophy
• The heart fails to relax normally (relaxation poor)
• Generally older women
• Hypertension is the commonest cause
• This carries a 5-8% mortality per annum
 Floor Plan of This Talk

Introduction Etiology Diagnosis

Patho Prognosis
Definitions
Physiology Risk Scoring

Clinical Treatment &

Epidemiology
Features Prevention
 Causes of Heart Failure
1. Coronary Artery Disease (MI, IHD) (2/3 of cases)
2. Hypertension (common fore runner of LVSD, LVDD)
3. Diabetes Mellitus (via IHD, direct cardiomyopathy)
• Cardiomyopathy (DCM, HOCM, OCM, RCM)
• Valvular Heart Disease (MS, MR, AS, AR)
• Congenital Heart Disease (ASD, VSD)
• Arrhythmias (AF, Brady, Tachy, Heart Block, SSS)
• ‘High output’ failures (Anemia, hyperthyroidism, AV-F)
• Pericardial Disease (Constrictive, Effusion)
• Right Heart Failure (PHT, PE, Cor Pulmonale)
 Drugs and Heart Failure
Many drugs may precipitate HF or cause its deteriorate
Sodium and water retention agents
• Glucocorticoids, androgens, estrogens, NSAIDs (dose
dependent), Aspirins, Alginates
Negative Inotropic agents
• Anti arrhythmics, NDHP CCBS-Diltiazem & Verapamil
• Non selective beta blockers especially in NYHA class IV
particularly when used in large doses
Cardio toxins: Anthracyclines – Anti tumour- doxorubicin
Decongestants, High sodium containing drugs
 Precipitating Causes of HF
• Arrhythmias, especially atrial fibrillation
• Infections (especially pneumonia)
• AMI, Angina pectoris or recurrent MI
• Anemia, Alcohol excess, Pregnancy
• Iatrogenic - postoperative fluid replacement or
• Poor drug compliance in pts on treatment for HT
• Thyroid disorders—Thyrotoxicosis
• Use of steroids or NSAIDs
• Pulmonary embolism
BMJ Vol . 320, 22 Jan 2000
 Changing Pattern of Etiology

McMurray J J, Stewart S Heart 2000;83:596-602

 Ethnicity – Etiological factors
Etiological Factor White European Black South Asian

Ischemic Heart Disease +++ + +++

Diabetes Mellitus ++ +++ +++
Hypertension ++ +++ +
Atrial Fibrillation ++ + +
Dilated Myopathy + ++ No data

Increasing age +++ ++ ++

Access to care NA + +

Sosin MD, et al. Eur J Heart Fail 2004;6:831-43

 Floor Plan of This Talk

Introduction Etiology Diagnosis

Patho Prognosis
Definitions
Physiology Risk Scoring

Clinical Treatment &

Epidemiology
Features Prevention
Pathophysiology of Heart Failure
Developments in our understanding of the
Pathophysiology of heart failure have been
essential for recent therapeutic advances

After MI, plasma concentration of norepinephrine

is of prognostic value in the early phase after MI

Natriuretic peptides are also shown to predict

outcome after MI – “The Leukocyte Count of HF”
 Cardiac Output
CO = SV x HR
CO is cardiac output expressed in L/min
Normal Cardiac Output is 5 L/min
SV ( Stroke Volume) is volume of blood put out/beat
Pre load, After load and Contractility determine the SV
HR (Heart rate) - number of beats/minute (Chronotrop)
Normally SV = 70 ml/beat. HR = 70/mt; so
CO = 70 x 70 = 4,900 ml/mt or 5 L approximately
 Important Concepts
• Contractility: Contractility is the intrinsic ability of
cardiac muscle to develop force for a given muscle
length. It is also referred to as inotropism.
• Pre load: Preload is the muscle (stretch) length prior to
contractility, and it is dependent of ventricular filling (or
LV end diastolic volume). This is in turn dependent on LV
end diastolic pressure and LA pressure. The most important
determining factor for pre load is venous return.
• After load: It is the tension (or the arterial pressure)
against which the ventricle must contract. After load for
the left ventricle is determined by aortic pressure which
in turn is dependent on peripheral arterial resistance.
 LV Ejection Fraction (EF%)
LV EF% =
LV Diastolic Volume – LV Systolic Volume
X 100
LV Diastolic Volume
LV EF% =
(140 ml – 70 ml) = 70 ml
X 100
140 ml
LV-EF% = 50% (Normal 50 to 70%)
May go up to 90% with exercise
 Mechanisms of Heart failure
Restricted Filling: MS, Restrict CM, Constr Pericarditis

 Pressure Load on Ventricle: HT, AS, PS, Coarctation

 Volume load on Ventricle: MR, AR, VSD, TR, PR

 Myocardial Contraction: CAD, DCM, Myocarditis

Arrhythmia: Severe Brady or Tachycardia, AF, HB

Frank-Starling Curves
 Complex Mechanisms in HF
• Heart Failure is multi system syndrome
– Abnormalities of cardiac and skeletal muscle
– Abnormal renal function
– Stimulation of sympathetic nervous system
– Complex pattern of neuro humoral changes
• Ventricular Remodeling
– Damage to the myocytes & extracellular matrix
– Changes in size, shape and function of LV
• Electrical instability – causing arrhythmias
• Systemic processes with sequelae in organs
 Pathophysiology of HF
• Decreased cardiac output results in
–  End Diastolic Pressure (LVEDP), LVH, LVD
–  Pulmonary Capillary Wedge Pressure (PCWP)
– The development of pulmonary edema
• Activation of Neurohormonal Mechanism
– Renin-Angiotensin-Aldosterone- System (RAAS)
– Sympathetic Nervous System (SNS)
– Other circulating and paracrine effects
• Counter-regulatory systems
– Natriuretic Peptide System (BNP, pro BNP)
Pathological Effects of RAAS
 AT II and Aldosterone Havoc
AT II is the key hormone Aldosterone Excess imp.
• Increased AT II • Na and H2O retention
• Vasoconstriction • Hypokalemia
• Myocyte hypertrophy • Volume over load
• Myofibril fibrosis • Pulmonary edema
•  Aldosterone release • Peripheral edema
• Activation of NA • Myocardial apoptosis
• Activation of ETH • Myocardial fibrosis
• ED – NO,  Inflam. • Increased after load
Harmful Effects of Angiotensin II
• Myocardial Hypertrophy
Heart • Interstitial Fibrosis; Inotropic Effects

• ED with  NO; Coronary Constriction

Coronaries • Oxidative Stress , Inflammation, Atheroma

• IG pressure , Proteinuria,  Na Reabsorb

Kidneys • Glomerular Growth and Fibrosis,  ADH

• Increased Aldosterone
Adrenals • Augments Sympathetic Nervous System

• Increased Fibrinogen
Coagulation • Increased PAI-1, Platelet Aggregation
 RAAS Blockade

AGTNG AT-I AT-II ALDO

• Renin • ACE • AT1R • Renal

• Aliskiren • ACE-i • ARB • MRA

Bradykinin AT2 AT4 as

Vasoprotection
Sympathetic Nervous System

 CO activates baroreceptors -  SNS

Effects of  Circulating Epinephrine & NE
– Increased Heart Rate
– Increased Blood Pressure
– Increased myocardial oxygen demand
– Toxic effects on myocardium – cell death
– Down regulation of 1 receptors in heart
– Decrease in parasympathetic activity
 Other Changes in HF
Peripheral Changes – Anorexia, IR, TNF, NE
Wasting,  Perfusion, Wt loss Fatigue, Abnorm Metabolism

Atrial Ventricular Arrhythmias - AF

Structural, Neurohumoral Ischemia, Electrolyte abnorm.

Co morbidities cause deterioration

CKD (eGFR<50%), HT, DM Anemia, Valvular Disease, MI
Ventricular Remodeling

McKay RG, et al. Circulation 1986;74:693-702

 Ventricular Remodeling
• After extensive MI - remodeling occurs
– Impaired cardiac contractility
– Neuro humoral activation leads to regional
eccentric and concentric hypertrophy of the
non-infarcted segment
– Regional thinning and dilation of infarct area
• Factors which affect remodeling are
– Large infarct, Anterior infarct, HT, Persistent
occlusion of the artery of the infarct area

McKay RG, et al. Circulation 1986;74:693-702