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Best wishes to YOU. Heart Failure Basics to Recent Advances. Dr. R.V.S.N. Sarma., M.D., M.Sc.(Canada), FIMSA Consultant Physician and Cardiometabolic Specialist. Definition, Etiology Epidemiology and Pathophysiology. Floor Plan of This Talk.

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Best wishes to YOU

Heart Failure Basics to Recent Advances

Dr. R.V.S.N. Sarma., M.D., M.Sc.(Canada), FIMSA

Consultant Physician and Cardiometabolic Specialist

Definition, Etiology Epidemiology and Pathophysiology

Floor Plan of This Talk

“The very essence of cardiovascular practice is early detection of Heart Failure”

Sir Thomas Lewis, 1933

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

Detection of Heart Failure

About half of the patients with left ventricular dysfunction had no symptoms and therefore would be difficult to identify at this early stage by clinical examination alone – underscoring the need for echocardiography.

Framingham Heart Study has been the most important longitudinal source of data on the epidemiology of heart failure.

Why HF is increasing ?

  • Almost any disease of heart can cause it

  • More of HT, DM, MS, Obesity - ASCVD

  • CAD - which is its commonest cause

  • Better tools for diagnosis and availability

  • Better detection and treatment of causes

  • Better Rx. of RF, CAD, MI - PTCA, CABG

  • Increasing longevity of the population

  • HF is an aging process – longer life span

Important Points

  • Chronic Heart Failure (CHF) can be caused by any type of cardiac dysfunction

  • Most commonly attributable to LV Dysfunction

  • Rarely HF is due to isolated RV dysfunction

  • Most common and best studied cause of CHF is LV Systolic Dysfunction (LVSD)

  • Normal Ejection Fraction Heart Failure (NEFHF) is due to LV Diastolic Dysfunction – (HFPSF)

  • It is difficult to diagnose and quantify.

Floor Plan of This Talk

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


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

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

Epidemiology of Heart Failure

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

Ethnic Differences in HF

Sosin MD, et al. Eur J Heart Fail 2004;6:669-72

Age, MI and Heart Failure

Prevalence of Chronic AF in HF

181 92 9970 11062 11016No in study

Cleland JG, et al. Heart Fail Rev 2002;7:229-42

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

Population Differences in DHF

McMurray JJ, et al. Lancet 2005;365:1877

Floor Plan of This Talk

Causes of Heart Failure

  • Coronary Artery Disease (MI, IHD) (2/3 of cases)

  • Hypertension(common fore runner of LVSD, LVDD)

  • 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

Major Risk Factors

Ethnicity – Etiological factors

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


Floor Plan of This Talk

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 LVend diastolic volume). This is in turn dependent on LV end diastolic pressureand 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

LV Diastolic Volume

X 100

LV EF% =

(140 ml – 70 ml) = 70 ml

140 ml

X 100

LV-EF% = 50% (Normal 50 to 70%)

May go up to 90% with exercise

Mechanisms of Heart failure

Frank-Starling Curves

Sustained LVDF Leads to

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)

Understanding RAAS

Globular protein

Deca (10 AA)


Octa (8 AA)


Angiotensin II Receptors







AT II – Major Effector Hormone

AT-I (1- 7,9)


 Sympathetic

 Aldosterone

Non ACE pathways

Pathological Effects of RAAS

AT II and Aldosterone Havoc

AT II is the key hormone

  • Increased AT II

  • Vasoconstriction

  • Myocyte hypertrophy

  • Myofibril fibrosis

  •  Aldosterone release

  • Activation of NA

  • Activation of ETH

  • ED – NO,  Inflam.

Aldosterone Excess imp.

  • Na and H2O retention

  • Hypokalemia

  • Volume over load

  • Pulmonary edema

  • Peripheral edema

  • Myocardial apoptosis

  • Myocardial fibrosis

  • Increased after load

Harmful Effects of Angiotensin II

Adverse Effects of Aldosterone



Interstitial Fibrosis


Renal Failure


Cardiac Fibrosis

LV Dysfunction

Heart Failure




Oxidative Stress

MRA – Eplerenone

Brand name: Eplirestat

RAAS Axis and its Blockade

RAAS Blockade


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

Effect of Norepinephrine in HF

Circulating Paracrine Effects

  •  Production of Endothelin (ETH)

    • A potent vasoconstrictor through ET1R

  •  in Vasopressin (ADH) from pituitary

    • Excess water retention and vasoconstriction

  • Excess of Cytokines – TNF, IL-1 & IL-6

    • Myocyte apoptosis and cardiac cachexia

  •  in circulating Steroids and GH

Counter Regulatory System

Natriuretic Peptides in HF

B-Natriuretic Peptide (BNP)

Endothelium – The Endocrine Organ


  • NO, Bradykinin, Prostacyclin, EDHF, Serotonin, Histamine CNP, Substance P

    Inhibitors of SMCG

  • NO, Prostacyclin, Bradykinin, Heparin, CNP, TGF-

    Inflammation inhibitors - NO

    Thrombolytic factors- t-tPA


  • AT-II, Endothelin, TXA2 AA, PGH2,

    Promoters of SMCG

  • PDGF, BFGF, ILGF Endothelin, AT-II

    Promoters of Inflammation

  • Superoxide, TNF- ELCAM, ICAM, VCAM

    Thrombotic Factors - PAI-1

Vaso Activity of Endothelins


Endothelin Antagonists: Darusentan, Sitaxsentan, Tezosentan & Bosentan



Endothelium, Heart, Renal Tubule, VSMC

AT-II, Catacholamines, Insulin, LDL, GF, Stress

Other Changes in HF

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

Cardiac Remodeling

Na and H2O retention,  Performance

Myocyte hypertrophy, death, fibrosis

Dilated and spherical ventricle, thinned

The Cardiovascular Continuum



Important Events after MI

“Stunning” and “Hibernation”

  • Myocardial “Stunning”

    • Post ischemic dysfunction

    • Delayed recovery of the myocardial function despite restoration of coronary blood flow

    • In the absence of irreversible damage

  • Myocardial “Hibernation”

    • Persistent myocardial dysfunction at rest

    • Secondary to reduced myocardial perfusion

    • Function improves with revascularization

    • Cardiac myocytes remain viable in hibernation

“Stunning” and “Hibernation”

  • Myocardial “Stunning” and “Hibernation”

    • Viable myocardium retains responsiveness to inotropic stimulation

    • Can be identified by resting and stress echo, thallium scintigraphy, PET, MR Imaging with gadolinium

    • Revascularization may improve the over all ventricular function with beneficial effects on symptoms and prognosis.

Thank You All

Clinical Features, StagingInvestigations, Scoring

will follow

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