HEART OR CARDIAC FAILURE�Clinical presentation, Diagnosis and Management

PROF S S DANBAUCHI

Objectives

• For the student to learn about Cardiac failure- Definition, Epidemiology, Pathophysiology, Presentation and diagnosis

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• For the student to learn about investigations and treatment of Cardiac failure

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• To learn about prevention of Cardiac failure

Heart failure

Definition

It is the pathophysiological process in which

the heart as a pump is unable to meet

the metabolic requirements of the tissue for

oxygen and substrates despite the venous

return to heart is either normal or increased

It also mean depressed EF, FS and diastolic dysfunction

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Definition Heart Failure

• Heart failure is a global term for the physiological state in which cardiac output is insufficient for the body's needs.
• Heart Failure is a condition in which a problem with the structure and or function of the heart impairs its ability to supply sufficient blood flow to meet the body's needs.

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⁎ Heart Failure Guideline Updates 2019 ACC

Definition of the terms

• Myocardial failure = abnormalities reside in the myocardium and lead

to inability of myocardium to fulfill its function

• Circulatory failure = any abnormality of the circulation

responsible for the inadequacy in body tissue

perfusion, e.g. decreased blood volume, changes

of vascular tone, heart function disorders

• Congestive heart failure = clinical syndrome which is developed

due to accumulation of the blood in front

of the left or right parts of the heart

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GLOBAL MORTALITY

cardiovascular diseases

( Three quarters of the burden in LMIC)

Cancer

All other Non communicable diseases

Communicable

maternal

infant

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Diabetes

(17 million)

30%

13%

30%

25%

2%

EPIDEMIOLOGY

• Syndrome that is increasing in incidence
• Primarily a disease of aging
• About 75% or more in those > 65 years
• Prevalence goes from 1% in < 65 years and 10% in age >65 years
• Approximately 5 million in the US
• 500, 000 new cases every year

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EPIDEMIOLOGY IN NIGERIA

• Incidence and prevalence not known (but constitute good percentage of admissions)

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• Hypertension is the most common cause

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• Seen in all age ranges

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• Aetiology differ with age

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• Prognosis also not determined in Nigeria

About Cardiovascular Risk Factors:

• Traditional: Well documented, understood risk factors -The big “9”
• Emerging: Evidence is mounting linking these factors to CVD/CAD
• Markers: Other characteristics linked to CAD – perhaps indicating a genetic “cluster” of characteristics

A Closer Look at the �Traditional Risk Factors:

• Know the “Big 9”
• Know the 6 Modifiable Factors

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• Know the acceptable levels for PRIMARY , SECONDARY AND TERTIARY PREVENTION

Non-Modifiable Risk Factors

• Family History
• Twice the risk of MI if one first-degree relative with MI, similar to DM and hypertension are heriditary
• Triple the risk of MI if 2+ first-degree relatives with MI
• Risk is strongest if MI occurred at age ≤ 55
• Advancing Age
• Risk of CAD Increases as we get older, hypertension also follow age
• Gender
• Men are at risk at an earlier age than women
• Women’s risk of heart disease increases after menopause and soon equals or over shoots men’s

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Modifiable Risk Factors

• Tobacco Smoking
• Dyslipidemia
• Hypertension
• Obesity
• Sedentary Lifestyle
• Diabetes
• Emerging Risk Factors

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Covid and Heart failure

Management of Heart failure

Heart Failure Pathophysiology

Heart failure is caused by any condition which reduces the efficiency of the myocardium leading to overload on the myocardium. Over time the increased workload will produce changes to the heart:

• • Reduced contractility, or force of contraction, due to overloading of the ventricle.
• • A reduced stroke volume, as a result of a failure of systole, diastole or both.
• • Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output.
• • Hypertrophy of the myocardium, caused by the terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility.
• • Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart.

Used with Permission from Systolic and Diastolic Heart

Notes to heart physiology

• Essential functions of the heart

• to cover metabolic needs of body tissue

(oxygen, substrates) by adequate blood supply

• to receive all blood comming back from

the tissue (metabolic waste and CO2

• Essential conditions for fulfilling these functions

• normal structure and functions of the heart

• adequate filling of the heart by blood

• normal structure and function of tissue

surrounding the heart

PATHO-PHYSIOLOGICALLY

• CF is characterized by increased venous filling pressure
• Inadequate peripheral oxygen delivery during stress or at rest or caused by cardiac dysfunction

Pathologic Progression of CV Disease

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

Pathologic�remodeling

Low ejection�fraction

Death

Symptoms:�Dyspnea�Fatigue�Edema

Chronic�heart�failure

• Neurohormonal�stimulation
• Myocardial toxicity

Sudden

Death

Pump failure

Coronary artery disease

Hypertension

Cardiomyopathy

Valvular disease

Myocardial�injury

Diabetes

MECHANISM OF CARDIAC FAILURE

• Myocardial contractility/relaxation dysfunction
• Obstruction
• High out put
• Volume overload
• Restriction
• Arrhythmias

PATHOPHYSIOLOGY�

• Systolic function of the heart is governed by

four determinants:

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# contractile state of the myocardium

# preload of the ventricle (EDV)

# after load

# heart rate

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The normal heart is able to tolerate wide variation in HR, preload, after load but a diseased heart cannot.......

PATHOPHYSIOLOGY

• Diastolic function is determined by rate of relaxation of the heart

▹IVRT (determines 70% of LV or RV filling)

▹Late diastole the atrial kick (30% filling of LV or RV)

• Contractility may well be preserved or supra normal
• Diastolic RV or LV pressures are raised

MYOCARDIAL REMODELLING

• Pathologic myocardial hypertrophy and dilatation in response to increased stress on the myocardium
• Accompanied by changes in the interstitium (fibrosis/apoptosis)
• Myocardial remodelling is a progressive process

Heart Failure -hypothesis

Adaptive mechanisms of the heart

to increased load

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• Frank - Starling mechanism; to increase force of contraction

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• Ventricular hypertrophy

– increased mass of contractile elements → ↑strength

of contraction

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• Increased sympathetic adrenergic activity

– increased HR, increased contractility

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• Incresed activity of R–A–A system- Salt and water retention, vasoconstriction, thirst to enhance volume

Compensatory Mechanisms:�Renin-Angiotensin-Aldosterone System

Renin + Angiotensinogen

Angiotensin I

Angiotensin II

Peripheral Vasoconstriction

• Afterload

• Cardiac Output

Heart Failure

• Cardiac Workload

• Preload

• Plasma Volume

Salt & Water Retention

Edema

Aldosterone Secretion

ACE

Kaliuresis

Beta

Stimulation

• CO
• Na⁺

Fibrosis

Pathophysiology of Heart Failure

NEUROHOMORAL RESPONSE IN HF

• Tachycardia
• Increase venous filling pressure
• Salt and water retention
• Sympathetic activity/ beta agonist amines
• Atrial natriuretic peptides (ANP) and BNP
• Cortisol
• Renin-angiotensin -aldosterone axis

GENERAL CHARACTERIZATION OF HF

• Myocardial muscle dysfunction or loss
• Left ventricular hypertrophy or dilatation
• Left untreated will progress in worsening cardiac function and symptoms
• Clinical symptoms might vary substantially in the course of illness with little bearing to cardiac function

Categorization of Heart Failure

There are many different ways to categorize heart failure, including:

• ▪ Which side of the heart involved (left heart failure versus right heart failure)
• ▪ Whether the abnormality is due to contraction (systolic dysfunction) or relaxation of the heart (diastolic)
• ▪ Degree of functional impairment conferred by the abnormality (as in the NYHA functional classification)
• ▪ Whether the problem is primarily increased venous back pressure (behind) the heart, or failure to supply adequate arterial perfusion (in front of) the heart (backward vs. forward failure)
• ▪ Whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure) U

Types of Heart Failure

Classification of heart failure is based on which heart function or which side of the heart is most affected by the condition.

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• • Systolic heart failure (HFrEF) – failure of contraction to pump blood out of the chambers. This is measured by ejection fraction (EF) or the percentage of blood that is ejected out of the ventricle. Normal is 50% or higher.

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• • Diastolic heart failure (HFpEF) – failure of relaxation to fill the chambers with blood

Classification of heart failure

HF WITH REDUCED LVEF

• Clinical syndrome characterized symptoms and signs of HF and reduced LVEF
• Most commonly associated with LV dilatation

Characteristic features of systolic dysfunction

(systolic failure)

• ventricular dilatation

• reducing ventricular contractility (either generalized

or localized)

• diminished ejection fraction (i.e. that fraction of end-diastolic

blood volume ejected from the ventricle during each systolic

contraction – less then 45%)

• in failing hearts, the LV end-diastolic volume (or pressure)

may increse as the stroke volume (or CO) decreases

Characteristic features of diastolic dysfunctions

(diastolic failure)

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• ventricular cavity size is normal or smaller than normal

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• myocardial contractility is normal or hyperdynamic

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• ejection fraction is normal (>50%) or supranormal

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• ventricle is usually hypertrophied

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• ventricle is filling slowly in early diastole (during the period

of passive filling)

∙ end-diastolic ventricular pressure is increased

CLINICAL PRESENTATION

• Three different subtypes of the syndrome

Left ventricular failure(LVF)

Right Ventricular failure (RVF)

Biventricular cardiac failure

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It can also present Acute syndromes ALVF or ARVF OR Chronic heart failure

LEFT VENTRICULAR FAILURE

• Symptoms refer to LV- SOB on exertion,

PND, othopnoea, cough productive of frothy white sputum sometimes pink depending of severity of pulmonary oedema

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• Signs of left ventricular dysfunction- S3, S4, rhales or crepitations, sometimes rhonchi depending severity of pulmonary oedema

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RIGHT VENTRICULAR FAILURE

• Symptoms related right ventricular dysfunction
• The lungs are usually protected because back flow to systemic veins leading to- SOB on exertion, leg and abdominal swelling, right upper quadrant
• Signs are those of venous congestion- pedal pitting swelling, hepatomegaly, ascites

BIVENTRICULAR CARDIAC FAILURE�

• Most common form of the syndrome seen in clinical practice
• It is usually seen in chronic cardiac failure
• Both symptoms and signs of LVF and RVF are seen

NYHA classification of cardiac failure

• NYHA I- asymptomatic
• NYHA II- symptomatic with moderate activity
• NYHA III- symptomatic with mild activity
• NYHA IV- symptomatic at rest

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• The classification has flows, symptom reporting is subjective and it varies from day to day. It is difficult for predict outcome

Major criteria comprise the following. Modified Framingham Criteria

• Paroxysmal nocturnal dyspnea
• Weight loss of 4.5 kg in 5 days in response to treatment (diuretics)
• Neck vein distention
• Rales
• Acute pulmonary edema
• Hepatojugular reflux
• S ₃ gallop
• Central venous pressure greater than 16 cm water
• Circulation time of 25 seconds or longer
• Radiographic cardiomegaly
• Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
• Diagnosis (CF = 2 major criteria or 1 major + 2 or more minor criteria)

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Minor criteria (accepted only if they cannot be attributed to another medical condition) are as follows

• Nocturnal cough
• Dyspnea on ordinary exertion
• A decrease in vital capacity by one third the maximal value recorded
• Pleural effusion
• Tachycardia (rate of 120 bpm)
• Hepatomegaly
• Bilateral ankle edema

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ACUTE LVF

• Sudden shortness of breath with probably cough
• Its caused by aetiologies like hypertension, acute coronary syndromes like AMI, myocarditis, acute valvular leak due to endocarditis
• Pulmonary oedema is hall mark

ACUTE RVF

• Symptoms are sytemic venous based
• It is caused by AMI- Right ventricular involvement, pulmonary embolism
• Patient is free of pulmonary edema

Management of Cardiac failure

• Good medical history

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• Good physical examination

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• Investigations

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• Treatment

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• Prevention

INVESTIGATIONS�

• FBC and differentials, ESR
• Serum electrolyte (U&E), Creat, Uric acid
• Blood glucose, FBS and 2 hours pp
• Lipid profile
• CXR, CT, MRI
• ECG, Holter or event monitoring
• Echocardiography
• Urine microanalysis

Biomarkers

Specific

• CPK- CKM- MB
• Troponins
• ANP-BNP�

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Non- specific

• ALT
• AST
• LDH
• CRP

Specific Investigations

• Chest x-ray
• Electrocardiography
• Exercise Electrocardiography (TMT)
• Ultrasound/Echocardiography (TTE)
• Exercise echocardiography
• Trans-esophageal echocardiography(TEE)

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Specific Investigations

• Blood culture
• Pericardial fluid analysis
• Angiography
• CT scan
• MRI
• Radionuclide studies - Thallium

INVESTIGATIONS

• Thallium scan
• Exercise ECG
• Exercise Echocardiography
• Coronary angiography/ ventriculography
• Myocardial biopsy
• Assay of ANP, BNP, ASO titre, Retroviral antibodies
• EP

CARDIOMYOPATHIES

S S DANBAUCHI

Chest Radiograph

TMT- treadmill exercise ECG

Holter Monitoring

Echocardiography - Long axis parasternal

Coronary Angiography

CT Scan

Thallium Radionuclide studies

Treatment goals for Acute HF

• Improve symptoms, that of congestion and low CO
• Optimize volume status
• Identify etiology
• Identify precipitating factors
• Optimize chronic oral therapy
• Minimize side effects
• Identify patients that benefit from revascularization (rarely in Nigeria)
• Educate patient on the disease and medication

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Admission recommended in acute cardiac failure, HFSA 2006, when

Evidence of severely decompensated HF

• Worsening renal failure
• Altered mentation
• Hypotension

Dyspnoea at rest

‣typically represented by resting tachypnoea

‣less typically represented by oxyg sat < 90%

Haemodynamically significant arrhythmia

‣new onset arrhythmia-rapid AF

Acute coronary syndromes

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Hospitalization should be considered in the presence of

• Worsen congestion

even without dyspnoea

weight gain of > 5 kg

‣ Signs and symptoms of pulmonary or systemic congestion

even in the absence of weight gain

‣ Major electrolyte imbalance

‣ Associated co-mobidities

pulmonary embolism, DKA, pneumonia, stroke or TIA

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Diuretic treatment/monitoring ACF

• Monitor weight, input and output daily ( assess clinical/diuretic efficacy)
• Foley catheter is not recommended for urine volume monitoring.
• Foley is recommended in special cases – altered mentation, special monitoring of urine output or application of condom catheter

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Use of Inotropes in ACF, iv inotropes Milronone or dobutamine

• To improve end organ function in the presence of Dilated LV, reduced LVEF, low peripheral circulation

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• Particularly in marginal systemic blood pressure <90% symptomatic hypotension

unresponsive or intolerant of IV vasodilators

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Evaluating for Precipitating factors in ACF(Acute Cardiac Failure)

• Atrial fibrillation or others like atrial flutter
• Worsening hypertension
• Worsening pulmonary congestion
• Myocardial ischaemia/infarction
• Anaemia or thyroid disease
• Infection
• Electrolyte imbalance
• Drug drug interaction
• Adherence problems
• Drug toxicity

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ACF with preserved LV systolic function

• Difficult clinically to make a diagnosis
• Echocardiography is the gold standard
• Electrocardiography might not give an indication of preserved systolic function.
• Stress imaging- Exercise echocardiography, myocardial perfusion studies

TREATMENT OF CARDIAC FAILURE

• It involves both non pharmacologic and pharmacologic
• Care givers at home need to be educated (family support)
• Societal/NGO/ Government support
• Community surveillance for symptomatic patients

ABC of Heart Failure management

Guidelines 2019 Focused Update of the Guidelines of the Taiwan Society of Cardiology for the Diagnosis and Treatment of Heart Failure�

Guidelines 2019 Focused Update of the Guidelines of the Taiwan Society of Cardiology for the Diagnosis and Treatment of Heart Failure

Non Pharmacologic

• Low salt(sodium) diet 2-3 gm/day
• Caloric constraints in patients with DM, dyslipidemia and obesity
• Low fat diet- dyspilidemia
• Fruits and vegetables
• Fluid restriction to 2- 2.5litres

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Lifestyle Changes �

• Eat a low-sodium, low-fat diet

• Lose weight

• Stay physically active

• Reduce or eliminate alcohol and caffeine

• Quit Smoking

What Why

• Sodium is bad for high blood pressure, causes fluid retention

• Extra weight can put a strain on the heart

• Exercise can help reduce stress and blood pressure

• Alcohol and caffeine can weaken an already damaged heart

• Smoking can damage blood vessels and make the heart beat faster

Care naturoceutical drugs that may contain

• Ephedra (ma haung)
• Drugs that might interact with digoxin, beta blockers, anti arrhythmias and vasodilators
• Sex enhancing drugs should be discussed openly with the patients- phosphodiasterase inhibitors- sildenafil

Should be avoided when patient is on nitrates

‣ Sleep disordered should be addressed- sleep can be aided- benzodiazephines

‣ Exercise is patient capacity tailored

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PHARMACOLOGIC

• Different classes of drugs

Diuretics (NYHAII-IV)

Digoxin (NYHAIII/IV)

ACEI/ARB (NYHA III/IV)

Aldosterone antagonists

Beta blockers (metoprolol, carvidolol)

Inotropes (milrinone, dopamine etc) NYHA IV�Anti-coagulants (warfarin)

Anti-platelets

Nitrates and hydrallazine (NYHA III/IV)

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Heart Failure Treatments: Medication Types

• ACE inhibitor (angiotensin-converting enzyme)

• ARB (angiotensin receptor blockers)

• Beta-blocker

• Digoxin

• Diuretic

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• Aldosterone blockade

Type What it does

• Expands blood vessels which lowers blood pressure, neurohormonal blockade- Reduced PR

• Similar to ACE inhibitor—lowers blood pressure

• Reduces the action of stress hormones and slows the heart rate

• Slows the heart rate and improves the heart’s pumping function (EF)

• Filters sodium and excess fluid from the blood to reduce the heart’s workload
• Blocks neurohormal activation and controls volume

Rational for Medications�

• Improve Symptoms
• Diuretics (water pills)
• digoxin

• Improve Survival
• Betablockers
• ACE-inhibitors
• Aldosterone blockers
• Angiotensin receptor blockers (ARB’s)

Research on treatment of Heart Failure

• Enhancement of current drugs, such as tolvaptan and omecamtiv mecarbil, sheds new light on already-known therapies. Tolvaptan, a vasopressin antagonist, could be adopted in heart failure therapy as it reduces pre- and afterload by decreasing systolic blood pressure and blood volume. Omecamtiv mecarbil, which is a myosin binding peptide, could aid cardiac contractility.
• The next generation vasodilators, serelaxin and ularitide, are based on naturally occurring peptides and they reduce peripheral vascular resistance and increase the cardiac index. In combination with their anti-inflammatory properties, they could turn out to be extremely potent drugs for heart failure treatment.
• Cardiotrophin has exceeded many researchers’ expectations, as evidence suggests that it could cause sarcomere hypertrophy without excessive proliferation of connective tissue.
• Rapid progress in gene therapy has caused it to finally be considered as one of the viable options for the treatment of CVDs. This novel therapeutic approach could restore stable heart function either by restoring depleted membrane proteins or by balancing the intracellular calcium concentration. Although it has been set back by problems concerning its long-term effects, it is still highly likely to succeed.
• SGLT2 related drugs. SGLT2 inhibitors, a class of medications used in the treatment of type 2 diabetes, is now being explored in HFpEF.

SURGICAL TREATMENT

• VR (valve replacement)
• Valve repair
• EP and ablation
• CABG
• Ventricular assisted device
• ICD- CRT, Pacemakers etc
• Cardiac transplant(advanced CF, uncontrolled ventricular arrhythmia and refractory debilitating angina)
• Batista operation(not recommended in non-ischamic CF)

SPECIAL GROUPS

• CF in IHD
• CF in Hypertension
• CF in Diabetes mellitus
• CF in renal failure
• CF in the elderly

PROGNOSIS

• Heart failure carries a poor prognosis
• Five year survival rate is less than 50%
• Mortality varies from <5% in those with less or no symptoms to 30% in those with severe symptoms or refractory
• In men have more poor prognosis than female (more likely to have CAD)
• The wide spread use of ACEI and beta blocker s has improved prognosis

PREVENTION

• Aetiologies associated with CF
• Good hygiene- RF
• Prevention LV dilatation- ACEI
• Good diet
• Comprehensive and accessible ANC
• National nutrition policy
• Health education

In Summary….

• Heart failure is common and has high mortality
• Drug therapy improves survival
• Betablockers, ACE-I, aldosterone antagonists
• Newer device therapies are showing promise for symptom relief and improved survival
• Biventricular pacing, ICD’s
• Transplants remain rare, but technology for mechanical assist devices continues to improve- stay tuned!

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