HEART FAILURE DISORDERS Intracardiac (left to right) shunting-Chronic

bradyarrhythmias
Dr. Tamayo Extracardiac shunting-Chronic bradyarrhythmias
February 6, 2017  Preserved ejection fraction (> 40-50%)
Pathologic hypertrophy –Restrictive
Definition cardiomyopathy
 A Clinical syndrome Primary (hypertrophic cardiomyopathies) -
 Inherited or acquired abnormalities of cardiac Infiltrative disorders (amyloidosis,sarcoidosis)
structure Secondary (hypertension)-Storage diseases
 Constellation of Symptoms (hemochromatosis)
- Dyspnea and Fatigue Aging-Fibrosis
 Signs Endomyocardial disorders
- Edema and rales  Pulmonary heart disease
 Frequent hospitalization Cor Pulmonale
Pulmonary vascular disorders
 Poor quality of life
 High-output states
 Shortened life expectancy
Metabolic disorders-Excessive blood-flow
requirements
Epidemiology
Thyrotoxicosis-Systematic arteriovenous shunting
 Burgeoning problem worldwide
Nutritional disorders-Chronic anemia
 20 M affected
 2% in adult population in developed countries
Prognosis of Heart Failure
 Rises with age
 Poor Prognosis
 10% of people over 65 yrs of age
 30-40 % die within 1 year
 Lower in women
 60-70 % die within 5 years
 Women constitute at least one half the cases
 NYHA Class IV- 30-40 % Mortality
 Women with longer expectancy
 NYHA Class II- 5-10 % Mortality
 Overall prevalence increasing
New York Heart Association Classification
2 Broad Categories of Heart Failure
 Heart failure with depressed ejection fraction
Functional Capacity - Objective Assessment
(Systolic Failure)
Class I – Patients with cardiac disease but without
 Heart failure with preserved ejection fraction resulting limitation of physical activity. Ordinary physical
(Diastolic Failure) activity does not cause undue fatigue, palpitations,
dyspnea or anginal pain
Etiologies of Heart Failure Class II – Patients with cardiac disease resulting in slight
 Depressed ejection fraction (< 40%) limitation of physical activity. They are comfortable at rest.
o Coronary artery disease-Nonischemic Ordinary physical activity results in fatigue, palpitations,
dilated cardiomyopathy dyspnea or anginal pain.
Myocardial Infarction Class III – Patients with cardiac disease resulting in
Myocardial Ischemia-Familial/genetic marked limitation of physical activity. Less than ordinary
disorders activity causes fatigue, palpitations, dyspnea or anginal
Infiltrative disorders pain
o Chronic pressure overload-Toxic/drug- Class IV – Patients with cardiac disease resulting in
induced damage inability to carry on any physical activity without
Hypertension-Metabolic disorder discomfort. Symptoms of heart failure or the angina
Obstructive VHD-Viral syndrome may be present even at rest. If any physical
o Chronic volume overload-Chagas’ activity is undertaken, discomfort is increased.
disease
Regurgitant valvular disease-Disorders of
rate and rhythm

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 Overview of Left Ventricular Remodeling
 Alterations in myocyte biology
o Excitation-contraction coupling
o Myocyte heavy chain (fetal) gene
expression
o β-adrenergic desensitization
o Hypertrophy
o Myocytolysis
o Cytoskeletal proteins
 Myocardial changes
o Myocyte loss
 Necrosis
 Apoptosis
 Autophagy
o Alterations in extracellular matrix
Pathogenesis
 Matrix degradation
 A Progressive disorder that is initiated after an
 Myocardial fibrosis
index event that
 Alterations in left ventricular chamber geometry
- damage the heart muscle
o Left ventricular (LV) dilation
- disrupt the ability of the myocardium to
o Increased LV sphericity
generate force
o LV wall thinning
 Compensatory mechanisms that becomes
o Mitral valve incompetence
activated
in HF Clinical Manifestations
> Renin- Angiotensin- Aldosterone System
 Fatigue and shortness of breath
> Adrenergic Nervous system
 Orthopnea
 Activated Vasodilatory Molecules in HF
 Paroxysmal Nocturnal Dyspnea
> Atrial Natriureticpeptide
 Cheyne-stokes respiration
> Brain Natriureticpeptide
 Other symptoms
> Prostaglandin
> Nitric Oxide
Physical examinations
 General appearance and vital signs
 Jugular veins
 Pulmonary examination
 Cardiac examination
 Abdomen and extremities
 Cardiac cachexia

Diagnosis
 Straight forward  when patient presents with
classic signs and symptoms of HF
 High index of suspicion
 Laboratory testing
o Routine lab testing
o ECG
Basic Mechanisms of Heart Failure o Chest x-ray
 Systolic dysfunction o Assessment of LV function
 Diastolic dysfunction o Biomarkers
 Left ventricular remodeling o Exercise testing

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Differential Diagnosis - active infection
 Circulatory congestion secondary to abnormal - covert pulmonary embolism
salt and water retention - arrhythmia
 Non-cardiac causes of pulmonary edema - ischemia
 Chronic lung disease Predictors of worse outcomes:
 Obesity 1. BUN of > 43mg/dl
2. SBP < 115mmHg
Management 3. CREA > 2.75mg/dl
4 Phenotypes of Presentation: 4. ↑Troponin
1. Chronic heart failure with reduced EF (HF & EF)
2. Heart failure with preserved EF (HP & EF) Volume Management:
3. Acute decompensated heart failure - IV diuretic agents
4. Advanced heart failure - Addition of Thiazide diuretic agent such as metolazone
synergistic effect with loop diuretic
Heart failure with preserved EF
General principles The Cardiorenal Syndrome
1. Therapeutic Targets - an interplay between abnormalities of heart and kidney
a. Control of congestion function with deteriorating function of one organ while
b. Stabilization of heart rate and BP therapy is administered to preserve the other
c. Improving exercise tolerance
*lowering BP alleviate symptoms more effectively Ultrafiltration
- an invasive fluid removal technique that may
Clinical Trials in HF and EF supplement the need for diuretic therapy.
1. Charm preserved (candesartan in heart failure)
- assessment of mortality and morbidity Vascular Therapy
- reduction in hospitalizations but not in Vasodilators including
all cause mortality 1. IV Nitrates
2. I- preserved (irbesartan in HF with preserved 2. Nitroprusside
systolic function 3. Nesiritide
- no differences in meaningful end points
3. DIG trial (digitalis investigation group) Inotropic Therapy
- no role for digitalis in HF & EF - pharmacologic agents that increases intracellular cyclic
4. Seniors ( study of effects nebivolol intervention AMP
on outcomes and rehospitalization in seniors with > Sympathomimetic amines (dobutamine)
HF) > Phosphodiesterase-3 inhibitors (micronons)
- no effect on all cause mortality Inotropic Therapy
- Leads to ↑ cytoplasmic calcium(+) inotropic agent
Acute decompensated heart failure - Augments cardiac output
General Principles - Improves perfusion
- A heterogenous clinical syndrome Hospitalization due - Relieves congestion
to confluence of - Acts as bridge therapy prior to VAD or transplant
a. ↓Cardiac performance - Prolong use lead to increased arrhythmia, hypotension
b. Renal dysfunction and no beneficial effect on hard outcomes.
c. alteration in vascular compliance
- Associated with excessive morbidity and mortality Heart failure with reduced EF
50% readmitted in 6mos Whereas Before:
20% mortality in 1 year -renocentric (diuretics)
First Principle of management Identify and tackle down - hemodynamic tx (digoxin, inotropic)
pricipitants of decompensation Now:
- non adherence to RX medicines - Neurohormonal
- use of non- RX medicines
NSAID , cold and flu preparations, herbal
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Neurohormonal Antagonism  Fish Oil
23% ↓ in mortality  Micronutrients
35% ↓ in mortality and hospitalization
35% ↓ further reduction on top of that provided by ACE Treatment
inhibitors those given beta blockers STAGE A – high risk for developing HF, no
structural heart disease, or symptoms
Class effect and sequence of administration of HF (e.g. DM or HPN)
ACE inhibitors- exert beneficial effect as A class
Beta Blockers- limited to specific class
- carvedilol STAGE B – have structural heart disease, no
- bisoprolol symptoms of HF (e.g. Previous MI and
- metoprolol succinate asymptomatic LV dysfunction)
Mineralocorticoid Antagonists
Aldosterone antagonism ↑ survivor STAGE C – have structural heart disease and
- NA retention developed symptoms of HF (e.g. previous
- Electrolyte imbalance MI with dyspnea and fatigue
- endothelial dysfunction myocardial fibrosis

*Hyperkalemia ; worsening renal functions are concerns STAGE D – with refractory HF requiring
special interventions (e.g. with
RAAS therapy and Neurohormonal escape refractory HF for cardiac
- circulating levels of angiotensin II to pretreatment level transplantation)
with long term ACE therapy
- ARB blunt this phenomenon  Defining an appropriate therapeutic strategy for
chronic HF
Arteriovenous Vasodilation  Management of HF with depressed ejection
- Combination of Nitrates and Hydralazine fraction ( < 40 % )
- Hydralazine > General Measures
> decrease systemic vascular resistance > Activity
> induces arterial vasodilation > Diet
- Nitrate > Diuretics
> transformed in sm cellnitric oxideincrease C-
AMParterial veno dilatation Factors that may precipitate acute decompensation
in patients with chronic heart failure
Heart rate modification  Dietary indiscretion
 IVABRADINE – an inhibitor of the I current in the  Myocardial ischemia/infarction
S-A node slows the heart rate without negative  Arrhythmias (tachycardia or bradycardia)
inotropic effect  Discontinuation of HF therapy
DIGOXIN
 Infection
- mild inotropic
 Anemia
- attenuates carotid sinus baroreceptor activity
 Initiation of medications that worsen HF
- symphatoinhibitory
o Calcium antagonists (verapamil, diltiazem)
- ↓ serum epinephrine level
o Beta blockers
- ↓ plasma renin level
o Nonsteroidal anti-inflammatory drugs
- ↓ aldosterone level
o Antiarrhythmic agents [all class I
- DIG trial ↓ in hospitalization but not mortality
agents,sotalol (Class III)]
 Oral diuretics
o Anti-TNF antibodies
 Calcium Antagonists – amlodipine and felodipine
 Alcohol consumption
 Novel Neurohormal Antagonismparadigm shift
 Pregnancy
 Inflammations
 Worsening hypertension
 Statins
 Acute valvular insufficiency
 Anticoagulant and Antiplatelet TX
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Drugs for the treatment of chronic heart failure (EF < Treatment (cont..)
40% )  Preventing Disease Progression
Initiating Maximal  Management of patients who remain
dose dose symptomatic
Angiotensin-Converting  Anticoagulation
Enzyme Inhibitors  Antiplatelet
Captopril 6.25 mg tid 50 mg tid
Enalapril 2.5 mg bid 10 mg bid
Lisinopril 2.5-5 mg 20-35 mg qd
Ramipril 1.25-25 mg 2.5-5 mg bid
bid
Trandolapril 0.5 mg qd 4 mg qd
Diuretics
Furosemide 20-40 mg qd 400 mg/dᵃ
or bid
Torsemide 10-20 mg qd 200 mg/dᵃ
bid
Bumetanide 0.5-1 mg qd 10 mg/dᵃ
or bid
Hydrochlothiazide 25 mg qd 100 mg/dᵃ
Metolazone 2.5-5 mg qd 20 mg/dᵃ
or bid
Angiotensin Receptor
Blockers Treatment (cont…)
Valsartan 40 mg tid 160 mg bid  Management of cardiac arrhythmias
Candesartan 4 mg qd 32 mg qd  Device therapy
Irbesartan 75 mg qd 300 mg qd > Cardiac Resynchronization
Losartan 12.5 mg qd 50 mg qd > Implantable Cardiac Defibrillators
β Receptor Blockers  Management of HF with preserved ejection
Carvedilol 3.125 mg 25-50 mg fraction ( > 40-50 % )
bid bid
 Acute decompensated HF
Bisoprolol 1.25 mg qd 10 mg qd
- Defining an Appropriate Therapeutic
Metoprolol succinate 12.5-25 mg Target dose
Strategy
qd
- Pharmacological Management of Acute
CR 200 mg qd
HF
 Surgical intervention
Fixed dose of 37.5 mg/ 20 75 mg/40
> Intraaortic Balloon Counter Pulsation
hydralazine/Isosorbide mg (one mg (two
> Percutaneous and Surgically Implanted
dinitrate tablet) tid tablets) tid
LV Assist Devices
> Cardiac Transplantation
Digoxin 0.125 mg qd < 0.375
mg/dᵇ
Note: ᵃDose must be titrated to reduce the patient’s
congestive symptoms.
ᵇTarget dose not established.
Additional Therapies
Spironolactone 12.5-25 mg 25-50 mg
bid qd
Eplerenone 25 mg qd 50 mg qd
Combination of 10-25mg/10 75 mg/40
hydralazine/ Isosorbide mg tid mg tid
dinitrate
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Drugs for the Treatment of Acute Heart Failure
Initiating dose Maximal dose
Vasodilators
Nitroglycerin 20 µg/min 40-400 µg/min
Nitroprusside 10 µg/min 30-350 µg/min
Nesiritide Bolus 2 µg/kg 0.01-0.03 µg/kg
per min
Inotropes
Dobutamine 1-2 µg/kg per min 2-10 µg/kg per
min
Milrinone Bolus 50 µg/kg 0.1-0.75 µg/kg
per min
Dopamine 1-2 µg/kg per min 2-4 µg/kg per min
Levosimendan Bolus 12 µg/kg 0.1-0.2 µg/kg per
min
Vasoconstrictors
Dobutamine for 5 µg/kg per min 5-15 µg/kg per
hypotension min
Epinephrine 0.5 µg/kg per min 50 µg/kg per min
Phenylephrine 0.3 µg/kg per min 3 µg/kg per min
Vasopressin 0.05 units/min 0.1-0.4 units/min

“A vigorous 5 mile walk will do more good for an

unhappy but otherwise healthy adult, than all
the medicine and psychology in the world”
-Dr Paul D. White
Founder of Preventive Cardiology

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