Inflammatory Heart Disease (IHD)

Marye G.

May, 2021

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 OUTLINES
• Definition

• Etiology and risk factors

• Pathophysiology

• Clinical manifestation

• Diagnostic modalities

• Management and prevention

• Complications
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 Objectives
At the end of this presentation, we will be able to:

Define pericarditis, myocarditis and endocarditis

Identify cause and risk factors

 Describe common clinical manifestations

 List differential diagnosis

Explain medical and nursing managements

 Inflammatory Heart Diseases
• The inflammation of the heart muscles, the membrane
sac which surrounds the heart, or the inner lining of the
heart is known as inflammatory heart diseases. These
includes:

o Infective Endocarditis

o Myocarditis

o Pericarditis
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 INFECTIVE ENDOCARDITIS

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 Definition
• Endocarditis is an inflammation of the inner layer of the
heart, the endocardium.

• It usually involves the valves and other structures like the

intraventricular and the septum.

• IE is an infection of the endocardial surface of the heart.

• The intracardiac effects of this infection include severe

valvular insufficiency, which may lead to intractable
congestive heart failure and myocardial abscesses.
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 Etiologies
• Although bacteria remain the most common etiology,
virtually all organisms (including viruses, fungi, and

rickettsia) can cause endocarditis.

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 Risk factors
• Advanced age • Heart surgery
• Acute rheumatic fever • Intubations
• Congenital heart disease
• Procedures involving GI &
• Previous heart damage GU

• Dental procedures • Reproductive conditions

like delivery of new babies,
abortions and PID

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 Pathophysiology
• Pathogens gain access to the bloodstream  Pathogens adhere
to an area of abnormal cardiac valve surface  Pathogens,
such as S. aureus, obtain intracellular access to the valve
endothelium  The infected vegetation is created by burying
of the proliferating organism within a protective matrix of
serum molecules  Vegetation particles can detach and
disseminate to form emboli  These may lead to
complications such as ischemic stroke, mycotic aneurysms
and infarcts or abscesses at remote sites. 
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 Classification
• Depending on the type of valve affected
1. Native valve endocarditis (NVE)

 The commonest type of Infective endocarditis in

Ethiopia and other developing countries.

 Endocarditis that may develop on natural valve.

 The affected valve may be damaged.

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2. Prosthetic valve endocarditis
Is when the endocarditis develops on prosthetic/’artificial’ valve.

There is a marked rise in cases of prosthetic valve endocarditis and

endocarditis in IV drug abusers in different parts of the world.

3. Endocarditis in intravenous drug abuser (IVDA)

Intravenous (IV) drug users are at very high risk of acute
endocarditis, because numerous needle punctures give aggressive Staph
bacteria many opportunities to enter the blood through broken skin.

Dirty drug administering equipments increases the risk.

If untreated, this form of endocarditis can be fatal in < 6 weeks.

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• Depending on the clinical course
A. Acute Infective endocarditis:

Frequently involves healthy valves.

It is a rapidly progressive illness with destruction of

valvular structures.

B. Subacute Infective endocarditis:

Typically affects only previously damaged valves.

The course is insidious even in untreated cases which may

extend over many months.
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Etiologic agent of Infective endocarditis
• Streptococcus viridans: is a normal flora of the oral cavity.

It accounts for 50-60% of cases of subacute infective

endocarditis.

• Group D streptococci: found in the gastrointestinal or

genitourinary tract.

Most cases infective endocarditis due to this organism is

subacute.

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 Cont…
• S. aureus: is the leading cause of Prosthetic valve
endocarditis (PVE), acute infective endocarditis and
endocarditis in IV drug abusers.

• Approximately 35-60.5% of staphylococcal bacteremia is

complicated by infective endocarditis.

In more than half of cases endocarditis due to S. aureus

occurs in the absence of underlying valvular disease.

 Mortality rate may range 40-50%.

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 Clinical manifestations
 Fever and Shortness of breath
Murmurs
 Clubbing of fingers
Splinter Hemorrhage
Osler’s nodes
Janeway’s lesions
 Shock
 Finger clubbing
 Weight loss, Malaise, Chills, Night sweats
 Chest and abdominal pain
 Anorexia
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 Splinter Hemorrhage

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 Diagnostic evaluations
 History and physical examination

 Blood culture and white blood cell count: leukocytosis

 Urinalysis: microscopic hematuria

 Computerized tomography rule out heart damage

 BUN and creatinine levels to evaluate renal function

 Echocardiography: for valvular and ventricular function

 Chest x-ray
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 Differential Diagnosis
• Lyme Disease-an acute inflammation of joints with fever

• Systemic Lupus Erythematosus

• Polymyalgia Rheumatica

• Primary Cardiac Neoplasms

• Reactive Arthritis

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 Medical management
• Administer oxygen therapy

• Administer antibiotic treatment like ampicillin +

flucloxacillin +gentamicin

• Administer paracetamole 1g po as analgesic

• Administer inotropic drugs like digoxin

• Morphine to decrease anxiety

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Specific Antibiotics treatment
Native valve endocarditis (NVE)
•Crystalline penicillin 3-4 million IU IV every 4 hours for 4- 6 weeks plus

Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks for synergistic coverage of

streptococci.

Prosthetic valve endocarditis (PVE); due to MRSA

•Vancomycin 1gm IV BID for 6 weeks Plus

Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks plus

Refampicin 300 mg PO /TID for 6 weeks

Patients with a history of IV drug use

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 Complications

Chronic heart failure

Shock

 Stroke

Embolism

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 Myocarditis

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 Definition
• Myocarditis is inflammation of the myocardium often
resulting from infectious process, which subsequently leads
to myocardial destruction and a dilated cardiomyopathy.

• Can be produced by a variety of different disorders, many of

which are infectious.

• Viral infection is the most frequently identified cause of

myocarditis.

• Myocarditis may be acute or chronic.

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 Etiologies of Myocarditis
1. Infectious causes
Viral infections : is the most common cause, enterovirus
(Coxsackie virus B), HIV myocarditis (10 % of HIV pts).

Bacterial, Fungal and Protozoal infections

Rickettsia: associated with Typhus

Spirochetes: associated with Relapsing fever.

2. Immune mediated: Hypersensitivity and autoantigens

3. Toxic substances: Heavy metals, ethanol and Radiation

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 Classification
• Fulminant myocarditis - presents with acute heart failure
up to 2 weeks after a distinct viral infection.

Patients have severe cardiovascular compromise with

ventricular dysfunction.

Multiple foci of active myocarditis are typical; either

resolves spontaneously or results in death.

• Acute myocarditis - Less distinct onset of illness, with

established ventricular dysfunction; may progress to dilated
cardiomyopathy
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 Pathophysiology

• Virus invades the muscle cause local inflammation

• Body's immune system inflict inflammatory damage

• Myocyte degeneration or necrosis

• Cardiomegaly and diminished systolic function occur

due to myocardial damage.

• CHF, shock, arrythmias and sudden death.

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 Clinical Presentations
History
• The clinical presentation of myocarditis is variable.

• The typical time interval between the onset of the viral illness and
cardiac involvement is 2 weeks.

• Fever is present in 20% of cases.

• Chest pain (pleuritic, squeezing, sharp stabbing) is reported in 35% of
cases.

• Dyspnea, fatigue, sweating, chills

• Palpitations and syncope are common.

• Sudden cardiac death
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 Physical Examination
• Tachycardia, gallop, mitral regurgitation, edema

• Acute rheumatic fever - Usually affects heart in 50-90%;

associated signs, such as erythema marginatum,
polyarthralgia, chorea, subcutaneous nodules (Jones
criteria)

• Hypersensitive myocarditis - Pruritic maculopapular rash

and history of using offending drug

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 Diagnostic modalities
Laboratory Studies:
• CBC - Leukocytosis is present in 25% of cases.

• ESR - is elevated in 60% of patients with acute myocarditis.

• C-reactive protein

• Elevated cardiac enzymes - Creatine kinase or cardiac troponins

• Serum viral antibody titers - For viral myocarditis

Chest x-ray

Echocardiography

ECG
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 Management
• Low sodium diet

• Digoxin: should be given with caution as patients with

myocarditis are sensitive for digitalis toxicities.

• Sympathomimetic and beta-blocker drugs should be

avoided because they increase the extent of myocardial
necrosis and mortality.

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 Cont….
Pharmacotherapy

• Medications used in the management of myocarditis

include the following:
• Penicillin for hemolytic streptococci
• Vasodilators (eg, nitroglycerin, sodium nitroprusside)
• ACE inhibitors (eg, enalapril)
• Angiotensin receptor blocking agents
• Anti inflammatory drugs
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 Complications
• Chronic Heart Failure: due to injured heart muscle

• Pericarditis

• Cardiomyopathy

• Arrhythmia: sudden unexpected, potentially fatal heart

rhythm abnormalities

• Death: myocarditis may cause sudden death in some

patients without medical attention during acute illness.

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 PERICARDITIS

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 Definition
• An inflammation of the pericardium, membranous sac
enveloping the heart.

• It may be a primary illness, or it may develop in the course

of a variety of medical and surgical disorders.

• Pericarditis may be acute ,sub acute and chronic

• Classified by the layers of the pericardium becoming

attached to each other (adhesive) or by what accumulates
in the pericardial sac: serum (serous), pus (purulent),
calcium deposits (calcific), clotting proteins (fibrinous)
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 Etiology

• Idiopathic or viral — 42 to 49 %

• Post cardiac surgery — 11 to 37 %

• Post radiation therapy — 9 to 31 %

• Connective tissue disorder — 3 to 7 %

• Postinfectious (tuberculous or purulent pericarditis) 3

to 6 %

• Miscellaneous causes (malignancy, trauma, drug-

induced, sarcoidosis, uremic (pericarditis) — 1 to 10 %
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Pathologically pericarditis can be classified

1. Effusive pericarditis

2. Effusive constriction pericarditis

3. Constrictive pericarditis

4. Adhesive forms

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 Clinical Manifestations

The most characteristic symptom is chest pain (pleuritic

chest pain)

Sharp, severe substernal pain or to the left of sternum

Pain may be felt in epigastrium and may be referred to

neck, arms, and back and may worsen with deep

inspiration and when lying down.

Pain relieved with a forward leaning or sitting position.

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 Cont…

The most characteristic sign is a friction rub.

Other signs mild fever, increased WBC count and ESR.

Other signs and symptoms of constrictive pericarditis or

cardiac tamponade:-
• Hypotension, and tachycardia
• Pulsus paradoxus
• Raised JVP
• Distant heart sounds
• Ascites, hepatomegaly
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 Diagnostic Modalities
There is no single test that is diagnostic for pericarditis.

The ECG is the most reliable diagnostic tool.

Patient’s history and Signs/symptoms

Physical examination: the hallmark of acute pericarditis is

the pericardial friction rub.

Chest x-ray

Echocardiogram: may detect inflammation and fluid

build-up, as well as indications of heart failure, and help to
confirm the diagnosis.
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 Management
Bed rest until the fever, chest pain, and friction rub have
subsided.

Analgesics and NSAIDs (aspirin/ibuprofen)

Corticosteroids, if the pericarditis is severe or if the patient

does not respond to NSAIDs.

Pericardiocentesis or Pericardiotomy

A pericardial window, a small opening made in the

pericardium, may be performed to allow continuous
drainage into the chest cavity.
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 Rx out come
• The clinical course of pericarditis is variable:

• 60% of patients have complete recovery within 1 week, and

• Almost 80% have complete recovery within 3 weeks.

• Eighteen percent(18%) of patients can have recurrent

pericarditis

Complications

• Cardiac tamponade

• Constrictive pericarditis
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 THANK YOU
questions ???

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