Myocardial ischemia occurs when blood flow to the heart muscle is reduced, depriving it of oxygen. It can be caused by conditions like atherosclerosis and coronary artery disease. Treatment aims to improve blood flow and may include medications, angioplasty, or bypass surgery. Left untreated, prolonged ischemia can lead to a myocardial infarction (heart attack).
2. Clinical pathology/Heart diseases 2
Ischemia
• Ischemia is an absolute or relative shortage of the blood supply to an
organ, i.e. a shortage of oxygen, glucose and other blood-borne fuels.
• Ischemia results in tissue damage due to shortage of oxygen and
nutrients.
• Cardiac ischemia may be asymptomatic or may cause chest pain, known
as angina pectoris.
• Ischemia most frequently results from atherosclerosis, which is the long-
term accumulation of cholesterol-rich plaques in the coronary arteries.
3. Clinical pathology/Heart diseases 3
Myocardial ischemia: pathophysiology
• Myocardial ischemia occurs when the blood flow through one or more of the
coronary arteries is decreased which ultimately leads to a decreased
oxygen supply to the myocardium.
• The pathogenesis of myocardial ischemia includes:
√ Coronary artery disease (atherosclerosis)
√ Blood clotting from the rupture of atherosclerotic plaque
√ Coronary spasm resulting in decrease of blood flow to a part of the
heart muscle
√ Severe illnesses causing failure to meet the metabolic demand of the
heart
5. Clinical pathology/Heart diseases 5
Myocardial Ischemia: Treatment
• Treatment of myocardial ischemia is directed at improving blood flow to
the heart muscle.
• Depending on the severity of the condition, the patient may be treated
with medications, undergo a surgical procedure or both.
• Medications
√ Nitroglycerin
√ Cholesterol-lowering medications
√ Aspirin
√ Beta blockers
√ Calcium channel blockers
√ Angiotensin-converting enzyme (ACE) inhibitors
√ Ranolazine (MI that doesn't respond to other medications)
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Clinical pathology/Heart diseases 6
Carditis
• Carditis is the inflammation of the heart or its surroundings.
• Carditis may be classified as:
√ Pericarditis: inflammation of the pericardium (from infection or trauma)
√ Myocarditis: inflammation of the myocardium (from infection or
autoimmune reaction)
√ Endocarditis: inflammation of the endocardium, usually involving the
heart valves (infection or non-infection)
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Clinical pathology/Heart diseases 7
Pericarditis
• Pericarditis is an inflammation of the
pericardium.
• A characteristic chest pain is often
present.
• Fluid may build up in the pericardial
sac.
• Most often occurs after some type of
respiratory infection.
• It can also occur after heart surgery
or during bacteremia.
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Clinical pathology/Heart diseases 8
Pericarditis: pathophysiology
• Microorganisms reach the pericardium from pulmonary or myocardial
infection, or direct inoculation during surgery, other invasive procedures,
or penetrating trauma.
• The most common bacteria causing pericarditis: Haemophilus influenza
(also called H. flu), Meningococci, Pneumococci, Staphylococci,
Streptococci.
• The tissue damage is the result of:
√ Toxin and enzyme production by the bacteria
√ Myocardial damage
√ Rapid build up blood/fluid in the pericardium
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Clinical pathology/Heart diseases 9
Pericarditis: treatment
• Bed rest
• Control of pain with NSAIDs
• Anti-microbial therapy based on the species of the infecting
agent and its sensitivity pattern.
• Diuretics to remove excess fluid
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Clinical pathology/Heart diseases 10
Myocarditis
• Myocarditis is inflammation the
myocardium.
• It resembles a heart attack but coronary
arteries are not blocked.
• It is an uncommon disorder caused by
√ Virus (Coxsackie, Cytomegalovirus,
Hepatitis C, Herpes, HIV)
√ Bacteria (Chlamydia, Mycoplasma,
Streptococcus, Treponema)
√ Fungus (Candida, Histoplasma)
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Clinical pathology/Heart diseases 11
Myocarditis: pathophysiology
• Myocarditis is most often due to infection or as a hypersensitivity
response to drugs. It is often an autoimmune reaction.
• The products from infection (Streptococcal M protein and Coxsackievirus B)
are immunologically similar to cardiac myosin. As a result the immune
system may attack cardiac myosin.
• Myocardial cell damage occurs in several ways:
√ Direct damage (from Streptococcal M protein or Coxsackie B virus).
√ Inhibition of humoral and macrophage-mediated immunity early in the
infection.
√ T-cell mediated cell lysis late in the disease.
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Clinical pathology/Heart diseases 12
Myocarditis: treatment
• Bed rest
• Control of pain with NSAIDs
• Anti-microbial therapy based on the species of the
infecting agent and its sensitivity pattern.
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Clinical pathology/Heart diseases 13
Endocarditis
• Endocarditis is an inflammation
of the endocardium.
• It usually involves the heart
valves.
• Staphylococcus aureus is the
primary pathogen of endocarditis.
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Clinical pathology/Heart diseases 14
Endocarditis: pathophysiology
• All cases of infective endocarditis develop from a commonly shared
process, as follows:
√ Bacteremia (nosocomial or spontaneous) that delivers the
organisms to the surface of the valve
√ Adherence of the organisms
√ Eventual invasion of the valvular leaflets
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Clinical pathology/Heart diseases 15
Endocarditis: pathophysiology
• As bacteria colonizes the endocardium and form vegetations from tiny
bodies to masses large enough to occlude valve orifices.
• There are four consequences to the formation of this vegetation:
√ a. Organisms within the vegetation are protected from antibodies,
complement, and leukocytes
√ b. Organisms within the vegetation are metabolically inactive, replicating
at an unusually slow rate, rendering them relatively resistant to the action
of many antimicrobials.
√ c. Healing is slow because endothelial cells grow over the surface.
√ d. Emboli are generated when vegetations break off; these cause
infarcts.
• Abscesses may develop by direct invasion of the valve rings of the heart
near the vegetations.
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Clinical pathology/Heart diseases 16
Endocarditis: treatment
• Antibiotics are the mainstay of treatment for infective endocarditis.
• Most commonly used antibiotics:
Penicillin G, Oxacillin, Ampicillin, Ceftriaxone, Ceftazidim, Cefazolin,
Cefipime Vancomycin, Gentamycin, Streptomycin etc.
• A combination of antibiotics, rather than a single antibiotic, is always
used.
• The recommended therapy is: Ampicillin + Gentamycin.
• If antibiotic therapy is not successful surgical removal of infected
endocardium may be necessary.
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Clinical pathology/Heart diseases 17
Congestive cardiac failure
• Congestive heart failure (CHF) is generally defined as the inability of the
heart to supply sufficient blood flow to meet the needs of the body.
• CHF may be caused by myocardial failure but may also occur in the
presence of near-normal cardiac function under conditions of high
demand.
• To maintain the pumping function of the heart, compensatory
mechanisms increase blood volume, cardiac filling pressure, heart rate,
and cardiac muscle mass.
• However, despite these mechanisms, there is progressive decline in the
ability of the heart to contract and relax, resulting in worsening heart
failure.
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Clinical pathology/Heart diseases 18
Stages of CCF
According to the guideline of the American Heart Association, there are
four stages of heart failure:
Stage A: Patients at high risk for developing HF in the future but no
functional or structural heart disorder
Stage B: a structural heart disorder but no symptoms at any stage
Stage C: previous or current symptoms of heart failure in the context of
an underlying structural heart problem, but managed with medical
treatment;
Stage D: advanced disease requiring hospital-based support, a heart
transplant or palliative care.
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Clinical pathology/Heart diseases 19
Sing and symptoms of CCF
-shortness of breath
-tiredness
-persistent coughing/wheezing
-pulmonary edema (excess fluid in lungs)
-pleural effusion (excess fluid around lungs)
-swelling in abdomen (ascites)
-swelling in ankles and legs
-pumping action of the heart grows weaker
-lack of appetite/nausea
-confusion/impaired thinking
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Clinical pathology/Heart diseases 23
Treatment of CCF
Surgery:
• Coronary bypass surgery (if
the disease results from
arteriosclerosis)
• Heart valve repair or
replacement (if there is valve
disease)
• Heart transplant
• Myectomy (removal a part of the
overgrown septal muscle)
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Clinical pathology/Heart diseases 26
Angina pectoris
• Angina pectoris:
severe chest pain due to
ischemia of the heart muscle,
generally due to obstruction or
spasm of the coronary arteries.
• Angina isn't a disease; usually
is a symptom of CHD.
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Clinical pathology/Heart diseases 27
Types of angina
Stable Angina
Stable angina is the most common type of angina.
It occurs when the heart is working harder than usual.
The pain usually goes away a few minutes after taking rest or angina
medicine.
Stable angina suggests that a heart attack is more likely to happen in
the future.
Unstable Angina
It may occur more often and be more severe than stable angina.
It also can occur with or without physical exertion, and rest or medicine
may not relieve the pain.
It is very dangerous and requires emergency treatment.
This type of angina is a sign that a heart attack may happen soon.
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Clinical pathology/Heart diseases 28
Types of angina
Variant Angina
A spasm in a coronary artery causes this type of angina.
It usually happens between midnight and early morning.
It usually occurs even at rest, and the pain can be severe.
Medicine can relieve this type of angina.
Variant angina is rare.
Microvascular angina
Also known as Angina Syndrome X
It is characterized by angina-like chest pain, but have different causes.
Since microvascular angina isn't characterized by arterial blockages, it's
harder to recognize and diagnose, but its prognosis is excellent.
The cause is unknown, but it appears to be the result of poor function in
the tiny blood vessels of the heart.
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Clinical pathology/Heart diseases 29
Symptoms of angina pectoris
Angina symptoms include:
• Chest pain or discomfort
• Pain in your arms, neck, jaw, shoulder or back accompanying chest pain
• Nausea
• Fatigue
• Shortness of breath
• Anxiety
• Sweating
• Dizziness
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Clinical pathology/Heart diseases 30
Angina: pathophysiology
• Angina is a symptom of coronary artery disease, in which the vessels that
supply blood to the heart become narrow or blocked.
• Coronary artery disease is usually caused by atherosclerosis, a condition in
which fatty deposits (called plaque) build up along the inside walls of blood
vessels.
• The plaque of the coronary block the blood flow to the heart muscle and fails to
meet myocardial oxygen demand.
• This causes myocardial cells to switch from aerobic to anaerobic metabolism,
with a progressive impairment of metabolic, mechanical, and electrical
functions.
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Clinical pathology/Heart diseases 31
Angina: pathophysiology
• Studies have shown that adenosine may be the main chemical mediator
of anginal pain.
• During ischemia, ATP is degraded to adenosine, which, after diffusion to
the extracellular space, causes arteriolar dilation and anginal pain.
• Angina is closely related with myocardial infarction (MI). The continuum
of events between the development of stable angina and the occurrence of
MI is termed acute coronary syndromes (ACS), which also includes
unstable angina.
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Clinical pathology/Heart diseases 33
Treatment of angina
Medications
• Nitrates
• Aspirin
• Betablockers
• Calcium channel blockers
• Angiotensin-converting enzyme (ACE) inhibitors
• Statins
Medical procedures and surgery
• Angioplasty and stenting
• Coronary artery bypass surgery
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Clinical pathology/Heart diseases 34
Myocardial infarction (MI)
• Myocardial infarction is the
irreversible necrosis of heart
muscle secondary to prolonged
ischemia.
• It is commonly known as a heart
attack.
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Clinical pathology/Heart diseases 35
Symptoms of MI
• Approximately one fourth of all myocardial infarctions are silent,
without chest pain or other symptoms.
• Chest pain/angina is the most common symptom
• Sensation of tightness, pressure, or squeezing
• Shortness of breath (dyspnea)
• Pulmonary edema
• Diaphoresis (an excessive form of sweating)
• Loss of consciousness and sudden death
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Clinical pathology/Heart diseases 36
Pathophysiology of MI
The most common triggering event of MI is the disruption of an
atherosclerotic plaque in a coronary artery, which leads to a clotting
cascade, sometimes resulting in total occlusion of the artery.
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Clinical pathology/Heart diseases 41
Congenital heart disease
• Congenital heart disease refers to a problem with the heart's structure
and function due to abnormal heart development before birth.
• It is the most common type of birth defect.
• They can be a part of various genetic and chromosomal syndromes.
• Drugs and toxicants during pregnancy can contribute to some congenital
heart problems.
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Clinical pathology/Heart diseases 43
Rheumatic heart disease
• Rheumatic heart disease is a condition in which permanent damage to
heart valves is caused by rheumatic fever.
• The disease process generally begins with a strep throat caused by
bacteria Streptococcus, and may eventually cause rheumatic fever.
• This infection may damage all the heart valves, but it affects the mitral valve
most often.
• The rheumatic heart disease caused by childhood rheumatic fever usually
doesn't cause symptoms until early or mid-adulthood.
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Clinical pathology/Heart diseases 44
Symptoms of rheumatic heart disease
Rheumatic heart disease does not always cause symptoms.
Common symptoms may include:
• Chest pain
• Heart palpitations
• Breathlessness on exertion
• Breathing problems when lying down (orthopnoea)
• Swelling (oedema)
• Fainting (syncope)
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Clinical pathology/Heart diseases 45
Pathophysiology of RHD
• Rheumatic heart disease arises from rheumatic fever if it is left untreated.
• Rheumatic fever occurs after an untreated Group A Beta hemolytic
streptococcal pharyngeal infection.
• Group A streptococcus pyogenes contain M protein that are highly
antigenic.
• The antibodies against the M protein may cross react with cardiac
myofiber protein myosin, heart muscle glycogen and smooth muscle cells
of arteries, inducing cytokine release and tissue destruction.
• The infection causes stenosis of the heart valves.
• Stenosis of the valve prevents the valve from opening normally.
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Clinical pathology/Heart diseases 47
Treatment of RHD
According to the American Heart Association
• Patients with rheumatic fever without carditis receive prophylactic
antibiotics for 5 years or until aged 21 years.
• Patients with rheumatic fever and carditis but no valve disease should
receive prophylactic antibiotics for 10 years or well into adulthood.
48. Clinical pathology/Heart diseases 48
Treatment of RHD
According to the American Heart Association
• Finally, patients with rheumatic fever with carditis and valve disease should
receive antibiotics for at least 10 years or until age 40 years.
• Often the valve can be repaired with surgery, may also need valve
replacement surgery.
