Heart Failure and Cardiomyopathies

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Heart Failure and

Cardiomyopathies
Francis Kiweewa, MBChB, MMED, MPH
Notes to heart physiology
• Essential functions of the heart
• to cover metabolic needs of body tissue (oxygen, substrates) by
adequate blood supply
• receive all blood comming back from the tissue
• Essential conditions for fulfilling these functions
• normal structure and functions of the heart
· normal structure and function of tissue surrounding heart
· adequate filling of the heart by blood
Essential functions of the heart are secured by
integration of its electrical and mechanical
functions
Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)
• changes of the heart rate
• changes of stroke volume
•Control of HR:
• autonomic nervous system
• Hormonal (humoral) control

Control of SV:
• preload, contractility, afterload, number and
size of myocytes, heart architecture,
synchronisation of function of the atrias and
ventricles
Definition of Heart Failure
• Heart failure can be defined as an abnormality of cardiac structure
or function leading to failure of the heart to deliver oxygen at a
rate commensurate with the requirements of the metabolizing
tissues, despite normal filling pressures (or only at the expense of
increased filling pressures)
• HF is a complex clinical syndrome identified by presence of current
or prior characteristic symptoms, such as dyspnea and fatigue, and
evidence of cardiac dysfunction as a cause of these symptoms
• The clinical diagnosis of HF is limited to patients with current or
prior symptoms of HF
TERMINOLOGY USED TO DESCRIBE
HF
• Related to EF*:
• HFrEF (reduced ejection fraction: EF<40%) aka Systolic HF
• HFmEF (mildly impaired EF: EF 40-49%
• HFpEF (preserved ejection fraction: EF ≥50%)* aka Diastolic HF
• Related to time-course:
• New onset, transient, chronic
• Related to progression:
• Acute, stable, worsening
• Related to location:
• Left heart, right heart, combined
• Related to cardiac output
• High output HF
• Low output HF
TERMINOLOGY USED TO DESCRIBE
HF
• HF is often referred to as left-sided failure when caused
primarily by left heart pathologies
• HF is called right-sided when caused by right heart conditions
• Left HF and right HF may each occur separately or
concurrently
• Left HF is a common cause of right HF, and most patients
with right HF have some element of left HF
Aetiology of HF
VALVULAR HEART DISEASE MYOCARDIAL DISEASE
• Coronary artery disease
• Mitral
• Hypertension
• Aortic
• Cardiomyopathy
• Trisuspid
• Pulmonary
ENDOCARDIAL DISEASE
PERICARDIAL DISEASE • With/without hypereosinophilia
• Constrictive pericarditis • Endocardial fibroelastosis
• Pericardial effusion
HEART
ARRHYTHMIA
HIGH OUTPUT STATES FAILURE • Tachyarrhythmia
• Anaemia • Atrial
• Sepsis • Ventricular
• Thyrotoxicosis • Bradyarrhythmia
• Paget‘s disease • Sinus node dysfunction
• Arteriovenous fistula CONDUCTION DISORDERS
• Atrioventricular block
VOLUME OVERLOAD
• Renal failure
• Iatrogenic (e.g. post-operative
CONGENITAL
fluid infusion HEART DISEASE McMurray et al. Eur Heart J 2012;33:1787–847
HFrEF vs HFpEF
• HFrEF patients show up more often with:
• Coronary heart disease (myocardial infarction)
• Valvular disease (aortic stenosis, mitral regurgitation)
• Uncontrolled hypertension
• Eccentric remodeling accompanied with chamber dilatation
• Volume overload leading to forward failure
• Patients with HFpEF are:
• More often older
• Female,
• Obese
• History of hypertension
• +/- atrial fibrillation
• Concentric remodeling and/or ventricular hypertrophy
• Pressure overload and often backward failure
Predominant clinical situations for left-
sided and right-sided heart failure
Left-sided heart failure Right-sided heart failure
Coronary artery disease Coronary artery disease (right ventricle
MI)
Hypertension COPD
Myocarditis Pulmonary hypertension
Heart valve disease Pulmonary valve stenosis
Tachycardiomyopathy Pulmonary embolism
Tricuspid regurgitation
Pneumothorax
Pericardial effusion
High output vs Low output HF
• High out put Failure: characterized by high cardiac index but low
systemic vascular resistance
• Common causes:
• severe anemia
• vascular shunting
• hyperthyroidism
• vitamin B1 deficiency
• Low output failure: characterized by insufficient forward cardiac output
• Common causes:
• large MI,
• acute pulmonary embolus
• biventricular dysfunction
The Stages of Heart Failure
The Stages of Heart Failure
The Stages of Heart Failure

ACC/AHA Stage Symptoms

A At high risk for heart failure but without structural heart


disease or symptoms of heart failure.

B Structural heart disease but without signs or symptoms


of heart failure.

C Structural heart disease with prior or current symptoms


of heart failure.

D Refractory heart failure requiring specialized


interventions.
The Stages of Heart Failure
Implication of staging HF
Signs and symptoms of HF
• Shortness of breath (SOB)/dyspnea (sensitivity of 84%–100%)
• Orthopnea/SOB on lying own (sensitivity of 22%–50%)
• Paroxysmal nocturnal dyspnea (sensitivity 39%–41%)
• Fatigue/weakness/lethargy
• Edema,
• Abdominal distention
• Right hypochondrial pain (sensitivity 23%)
• Tachycardia
• Increased jugular venous pressure (JVP)
• Abnormal lung sounds (crackles)
• S3 gallop
• Hepatojugular reflux
• Ascites
Diagnosis
• The Framingham criteria for the diagnosis of heart failure
• Concurrent presence of either two major criteria or one major and two minor
criteria
Major criteria comprise the following: Minor criteria (accepted only if they
 Paroxysmal nocturnal dyspnea cannot be attributed to another medical
 Weight loss of 4.5 kg in 5 days in response condition) are as follows:
to treatment
 Nocturnal cough
 Neck vein distention
 Rales  Dyspnea on ordinary exertion
 Acute pulmonary edema  A decrease in vital capacity by one
 Hepatojugular reflux third the maximal value recorded
 S 3 gallop  Pleural effusion
 Central venous pressure greater than 16  Tachycardia (rate of 120 bpm)
cm water  Hepatomegaly
 Circulation time of 25 seconds or longer  Bilateral ankle edema
 Radiographic cardiomegaly
 Pulmonary edema, visceral congestion, or
cardiomegaly at autopsy
2022 ACC/AHA/HFSA guidelines
recommend
• Levels of: B-type natriuretic peptide/N-terminal BNP (BNP/NT-proBNP),
urea and electrolytes, fasting glucose and HbA1c, lipids
• 12-Lead electrocardiography (ECG)
• Transthoracic echocardiography (TTE)
• Chest radiography
• Complete blood cell (CBC) count
• Thyroid function tests
• Iron studies (transferrin saturation and ferritin)
There are many treatment objectives for chronic HF
Objectives of treatment for chronic HF
1. Prognosis • reduce mortality
2. Morbidity • relieve symptoms and signs
• improve QoL
• eliminate edema and fluid retention
• increase exercise capacity
• reduce fatigue and breathlessness
• reduce the need for hospitalization
• provide end of life care

3. Prevention • occurrence of myocardial damage


• progression of myocardial damage
• remodelling of the myocardium
• reoccurrence of symptoms and fluid
accumulation
• hospitalization

• Dickstein et al. Eur Heart J 2008;29:2388–442

• McMurray et al. Eur Heart J 2012;33:1787–847


ACC/AHA Guidelines recommend incremental
addition of treatments as HF progresses
STAGE A
STAGE B
At high risk for HF, STAGE C STAGE D
but without Structural heart
Structural heart disease Refractory HF
structural heart disease, but without
with prior or current requiring specialized
disease or signs or symptoms or
symptoms of HF interventions
symptoms of HF HF
Therapy goals Therapy goals Therapy goals Therapy goals
 Treat hypertension  All measures under  All measures under Stages  Appropriate measures
 Encourage smoking Stage A A and B under Stages A, B, C

Refractory symptoms of HF at rest


Development of symptoms of HF
 Dietary salt restriction
cessation  Decision re: appropriate
Drugs

Structural heart disease


 Treat lipid disorders Drugs for routine use level of care
 ACEIs or ARBs in  Diuretics for fluid retention
 Encourage regular appropriate Options
 ACEIs
exercise patients  Compassionate end-of-
 β-blockers
 Discourage alcohol  β-blockers in appropriate life care/hospice
intake, Drugs in selected patients
patients  Extraordinary measures
illicit drug use  Aldosterone antagonists
Devices in selected  ARBs  Heart transplant
 Control metabolic
patients  Digitalis  Chronic inotropes
syndrome
 Implantable defibrillators  Hydralazine/nitrates  Permanent mechanical
Drugs support
Devices in selected patients
 ACEIs or ARBs in  Biventricular pacing  Experimental surgery or
appropriate patients for  Implantable defibrillators drugs
vascular disease or
diabetes
HFpEF and HFrEF respond differently to pharmacological treatment
options
Treatment option HFpEF HFrEF
Diuretics YES YES

CCBs YES NO

Beta-blockers NO YES

ACEIs NO YES

ARBs NO YES

MR antagonists NO YES

Ivabradine NO YES

Digoxin NO YES
H-ISDN NO YES
ARNIs PARAGON-HF study YES

Raina A and Kanwar M. Curr Heart Fail Rep. 2014: 11(4):374-81


Tschöpe C and Lam CS. Herz 2012: 37(8):875-9
Adding therapies is adding life
24 month mortality

NUMBER of THERAPIES ODDS RATIO


(vs 0 or 1 therapy) (95% confidence interval)

2 therapies 0.63 (0.47-0.85) p=0.0026


3 therapies 0.38 (0.29-0.51) p<0.0001
4 therapies 0.30 (0.23-0.41) p<0.0001
5, 6, or 7 therapies 0.31 (0.23-0.42) p<0.0001

0 0.5 1 1.5 2

This study examined the individual and incremental clinical effectiveness of guideline-recommended therapies for patients with HF and reduced LVEF.
ORs for 24-month mortality associated with the number of guideline-recommended therapies received at baseline.
Analysis includes all patients from the case-control population (N=4128). The number (%) of patients receiving each number of therapies at baseline was as follows: 0 or 1,
238 (5.8%); 2, 712 (17.3%); 3, 1327 (32.2%); 4, 1123 (27.2%); and 5, 6, or 7, 728 (17.6%).

Fonarow GC et al. J Am Heart Assoc 2012;1:16-26


Adding therapies is adding life
Beta-blocker Beta-blocker + Beta-blocker + Beta-blocker + Beta-blocker + Beta-blocker + ACEI/ARB
ACEI/ARB ACEI/ARB + ACEI/ARB + ICD + ACEI/ARB + ICD + HF + ICD + HF education +
ICD HF education education + anticoagulation for AF +
anticoagulation for AF CRT

0%
Series1
-10%
Change in Odds of 24-Month Mortality (%)

-20%

-30%

-40%
-39%
-50%

-60%
-63%
-70%

-80% -76%
-81% -83% -81%
-90%
(-28% to -49%) (-54% to -71%) (-68% to -81%) (-75% to -86%) (-77% to -88%) (-72% to -87%)
P<0.0001 P<0.0001 P<0.0001 P=0.0038 P=0.1388 P=0.1208
Holistic management of HF
ESC Guidelines 2012
Management programmes for patients with HFrEF & HFpEF
Characteristics
• Should employ a multidisciplinary approach
• Should target high-risk symptomatic patients
• Should include competent and professionally educated staff

Components
• Optimized medical and device management
• Adequate patient education, with special emphasis on adherence and self-care
• Patient involvement in symptom monitoring and flexible diuretic use
• Follow-up after discharge
• Increased access to healthcare
• Facilitated access to care during episodes of decompensation
• Assessment of (and appropriate intervention in response to) an unexplained increase in weight,
nutritional status, functional status, quality of life, and laboratory findings
• Access to advanced treatment options
• Provision of psychosocial support to patients and family and/or caregivers McMurray et al. Eur Heart J 2012;33:1787–847

McMurray et al. Eur Heart J 2012;33:1787–847


Summary: HF Guidelines
• ACE-inhibitors, beta-blockers and mineralocorticoid receptor antagonists
form the cornerstone of HF therapy, given their mortality benefit. Incremental
addition of treatments is recommended as HF progresses: Adding therapies
is adding life.

• HFrEF and HFpEF differently respond to treatment. Treatment in HFpEF is


aimed to improve signs and symptoms, as no treatment has yet been shown
to improve prognosis in HFpEF.

• HF care is already somewhat personalised, since management is guided by


traditional biomarkers (echo, ECG, blood pressure, laboratory examinations).
In the future, genetics, pharmacogenomics and gene therapy may yield more
targeted treatment strategies.

• The ESC guidelines also recommend regular aerobic exercise and enrolment
in care-management programmes.

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