Atherosclerosis

- Chronic vascular disease which targets large and medium-sized elastic and
muscular arteries. It is characterized by the accumulation within the intima of
inflammatory cells, smooth muscle cells, lipid, and connective tissue
- A condition in which plaque builds up inside the arteries. Plaque is made of
cholesterol, fatty substances, cellular waste products, calcium and fibrin (a
clotting material in the blood).
- Rupture plaques may cause a blood clot to form that can totally block blood
flow in the artery. If a clot blocks a blood vessel that feeds the heart, it causes a
heart attack. If it blocks a blood vessel that feeds the brain, it causes a stroke.
Independent risk factors: Hypertension, Hyperlipidemia, Cigarette smoking, Obesity,
Diabetes mellitus, Sedentary lifestyle Family history of premature atherosclerosis

Coronary artery disease (CAD)

A result of plaque buildup in your coronary arteries -- a condition
called atherosclerosis -- that leads to blockages. The arteries, which start out smooth
and elastic, become narrow and rigid, restricting blood flow to the heart. The heart
becomes starved of oxygen and the vital nutrients it needs to pump properly.
5 Types of CAD
1. Asymptomatic state (subclinical phase)
2. Angina pectoris
3. Acute MI
4. Chronic ischemic cardiomyopathy
5. Sudden cardiac arrest
Cause
- High blood cholesterol
- High blood pressure
- Smoking
- Obesity
- Lack of physical activity
Symptoms and signs of CAD, including chest pain(angina pectoris), heart
attack (myocardial infarction), and sudden death.
Treatment for CAD includes bypass surgery, balloon angioplasty, and the use of stents.

Angina pectoris
- An uncomfortable sensation such as pressure, tightness, heaviness, burning,
squeezing, or choking in the retrosternal area.
- A perceived symptom resulting from a mismatch of myocardial supply & demand.
- The compromised myocardial blood flow due to obstructive coronary artery
disease is not able to meet the metabolic demands of the myocardial tissue.
- Angina pectoris typically initially occurs with exertion or emotional stress, and it
subsides within a few minutes with rest or after a coronary artery vasodilator
such as sublingual nitroglycerin is administered.

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Stable angina
- Angina pectoris is said to be stable when the pattern of its frequency, intensity,
ease of provocation, or duration does not change over a several-week period.
- Identification of activities that provoke angina and the amount of sublingual
nitroglycerin required to relieve symptoms are helpful indicators of stability.
Unstable angina
- angina pectoris (or equivalent type of ischemic discomfort) with at least one of
three features:
1. It occurs at rest (or with minimal exertion) usually lasting more than 15 min.
2. It is severe and described as frank pain and of new onset (i.e., within 1 month)
3. It occurs with a crescendo pattern (i.e., more severe, prolonged, or frequent
than previously).
- Unstable angina pectoris occurs when the pattern of chest pain changes
abruptly.
- ST segment changes and ventricular arrhythmias often precursor of myocardial
infarction.
- Caused by: Transient formation of platelet aggregates in a coronary artery
region narrowed atherosclerosis; This decreases further oxygen supply to the
myocardium

Dx CAD : Hx + PE + ECG
Hx : Chest pain, Shortness of breath, Weakness, tiredness, reduced exertional
capacity, Dizziness, palpitations, Leg swelling, weight gain
ECG : ST-segment changes, T-wave changes, Conduction abnormalities such as
complete left bundle branch block
- normal in approximately 50% of patients with chronic stable angina, and
can remain normal during an episode of chest discomfort
Treatment : 3 most common therapeutic options
1. Medical therapy
Antiplatelet
- Aspirin : inhibits both cyclo-oxygenase and the synthesis of thromboxaneA2
- Clopidogrel(Plavix), a thienopyridinederivative, blocks adenosine
diphosphate-induced platelet activation.
Anti-anginals
- Beta-blockers : first-line therapy for stable angina
- Calcium channel blockers : the treatment of angina or ischemia in
symptomatic patients with CAD
- Nitrates : nitroglycerin
ACEI
Statin
2. Percutaneous coronary intervention (PCI)
3. Coronary artery bypass grafting (CABG).

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Acute Coronary Syndrome (ACS)
- Patients with ischemic discomfort may present with or without ST segment
elevation on the ECG.
- The majority of patients with ST segment elevation ultimately develop a Q-wave
acute myocardial infarction (QwMI)
- The minority develops a non-Q-wave AMI (NQMI).
- Patients who present without ST segment elevation are either experiencing
unstable angina or a non-ST segment elevation MI (NSTEMI)
Non-ST-Segment Elevation MI : ST depression +/- T wave inversion on EKG

Acute myocardial infarction (AMI) : death or necrosis of myocardial cells

It is a diagnosis at the end of the spectrum of myocardial ischemia or acute
coronary syndromes.
Myocardial ischemia occurs when there is an imbalance between the supply of
oxygen and the myocardial demand.
Cause of AMI
1. Decrease supply: Atheroma, Thrombosis, Spasm, Embolus, Arteritis, Anemia
Hypotension causing decreased coronary perfusion pressure
2. Increase demand: High cardiac output eg. Thyrotoxicosis, pregnancy, exercise
Myocardial hypertrophy
Pathophysiology
- Most MIs are caused by a disruption in the vascular endothelium associated
with an unstable atherosclerotic plaque that stimulates the formation of an
intracoronary thrombus, which results in coronary artery blood flow occlusion.
- If such an occlusion persists long enough (20 to 40 min), irreversible
myocardial cell damage and cell death will occur.
The severity of an MI is dependent on three factors:
1. The level of the occlusion in the coronary artery,
2. The length of time of the occlusion, and
3. The presence or absence of collateral circulation
Sign & Symptoms
- Chest pain, may radiated to jaw, teeth, shoulder, arm arm/or back
- Dyspnea
- Epigastric discomfort
- Disphoresis or sweating
- Syncope or near syncope
Treatment : MONA immediately after the patient arrives in the hospital.
M = Morphine
O = Oxygen
N = Nitrates
A = Aspirin
Complications of MI
1. Early: Thromboembolism
2. Delayed:
- Ventricular aneurysm
- Dresslers syndrome (Pericarditis, pericardial effusion, pyrexia)
- Shoulder hand syndrome

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Infective Endocarditis (IE)
The microbial infection(usually Bacteria or Fungus) within the endocardial surface
of the heart which may include one or more heart valves, the mural endocardium, or a
septal defect
Characteristics:
- The vegetation is the hallmark of endocarditis.
- Its characteristic lesion is a variably sized amorphous mass of platelets and fibrin
in which abundant microorganisms and scant inflammatory cell are enmeshed.

Acute IE
- A fulminant illness over days to weeks
- More likely due to staphylococcus aureus
Subacute IE
- A mild to moderate illness which progresses over weeks and months
- Often due to streptococci

Current Criteria for Classification

1. Native Valve Endocarditis (NVE) :
Mitral Valve Prolapse 30 - 50%
Rheumatic Heart Disease 20 - 40%
Streptococci 50 - 70% Viridans Streptococci (50% of all Strep)
Staphylococci ~ 25% Mostly Coagulase +ve Staph. Aureus
Enterococci ~ 10%
Characteristics
1. Viridans Streptococci
Infect primarily abnormal valves
Indolent clinical course
Common with oropharynx, ingival crevice, therapy or trauma
Highly sensitive to Penicillins
2. Staph. Aureus
- Infect normal and abnormal valves
- Fulminant course with rapid destruction of valves and multiple metastatic
abscesses
- Common with soft tissue infections, and infected IV catheters
- Mostly resistant to Penicillins and sensitive to penicillinase resistant -lactams
3. Staph. Epidermidis
Indolent Course
Affects abnormal valves
4. Enterococci
- Normally affects damaged valves
- Recent history of genitourinary (GU) or gastrointestinal (GI) manipulation,
disease or trauma
- Usually sensitive to Penicllin+Gentamicin
- Resistant strains prevalent

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2. Prosthetic valve endocarditis (PVE)
happened after implanted artificial valve
Risk of PVE peaks at 15 days postop. , then rapidly declines by 150 days
Classification and Characteristics
1. Early ( < 60 days )
Reflects perioperative contamination
Staph (45 - 50%) : Staph. Epiderm (~ 30%), Staph. Aureus (~ 20%)
Gram -ve aerobes (~20%)
Fungi (~ 10%)
Strep and Entero (5-10%)
2. Late ( > 60 days)
- After endothelialization
- Transient bacteraemia from dental, GI or GU
- Microbiology resembles native valve endocarditis
~ Streptococci :Viridans Streptococci
~ Staphylococci :Mostly Coagulase +ve Staph. Aureus, Staph. Epidermidis
Enterococci
3. IE in IV Drug Abusers
Right sided predilection (usually affect right side heart valves)
- Tricuspid Valve ~ 55%, Aortic Valve ~ 25%
Characteristic :
Skin most predominant source of infection
Also contamination of drugs and paraphernalia (eg: needles)
70 - 100% of Rt. sided IE results in pneumonia and septic emboli
Staph aureus ~60%
4. IE in adults with congenital heart disease
Common defects
- VSD (Septal defect
- PDA (Patent Ductus Arteriosus)
- Bicuspid AV
- PS (pulmonary stenosis )
- Coarctation (narrowing) of Aorta

Pathogenesis of IE : Vegetation
- The common lesion seen is a vegetation situated usually on the valve leaflets
and less often on the endocardium of the atria or ventricles.
- The vegetation consists mainly of platelet-fibrin thrombi containing colonies of
bacteria

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Pathology of IE
1. Primary heart disease and new heart damage
2. Embolization of fragment of vegetation
3. An immunologic response to the infection in form of immune complex vasculitis
Clinical Features : Onset usually within 2 weeks of infection
Indolent course : Malaise, Fatigue, Night sweats, Weight loss, Anorexia
Explosive course : S/o severe systemic sepsis, CCF
Signs
Fever
Heart murmur
Nonspecific signs petechiae, subungual or splinter hemorrhages, clubbing,
splenomegaly, neurologic changes
More specific signs - Oslers Nodes, Janeway lesions, and Roth Spots
Complications :
1. Congestive Cardiac Failure
2. Embolism : MI
3. Local spread of infection : Paravalvular abscess (30-40%) Most common in
aortic valve, IVDA, and S. aureus
4. Metastatic spread of infection : Kidneys, spleen, brain, soft tissues
5. Formation of immune complexes glomerulonephritis and arthritis
Laboratory Test
Routine examination
- ESR - this is always elevated.
- Anaemia - is present in approximately 80% of patients when first seen.
- WBC - the white cell count is usually elevated.
- Urine - hematuria, proteinuria
Blood culture: every 1hour*3 times
immunologic test
X-ray
Electrocardiogram
Echocardiography
Dx
- positive blood cultures in the presence of a new or changing heart murmur
- persistent fever in the presence of heart disease
Modified Duke Criteria
Possible IE
2 major
1 major and 3 minor
5 minor
Rejected IE
Resolution of illness with four days or less of antibiotics
Diagnosis is based upon:
Major criteria
Positive blood culture
Evidence of endocardial involvement
- Positive echocardiogram (vegetation, or intracardiac abscess )
- New valvular regurgitation
Minor criteriaPredisposition; Fever; Vascular phenomena; Microbiological evidence;
Echocardiogram

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Treatment
General principles
- To eradicate the infecting organism as soon as possible
- To operate with correct time if required
- To treat complications
- Long enough treatment to ensure thatrelapse will not occur
1. Parenteral antibiotics
High serum concentrations to penetrate vegetations
Prolonged treatment to kill dormant bacteria clustered in vegetations
Antibiotics
Streptococcus Viridans -for 4 weeks
- Pennicillin G: If renal function is okay, then add gentamycin or amilacin
- Pen allergic then Vancomycin or Ceftriaxone
Enterococcus - for 4-6 weeks
- can use Pennicillin G or Vancomycin/Gentamycin Usually
Staph. Aures - for 6 weeks
- Nafcillin with gentamycin for first 3-5days,
2. Surgery : Valve replacement in severe heart failure, valvular obstruction
3. Surveillance of blood cultures

In conclusion
1. IE is the microbial infection within the endocardial surface of the heart.
2. Causative organism is usually Bacteria or Fungus, including :
Streptococci (Viridans Streptococci),
Staphylococci (Aureus, Epidermidis ),
3. Enterococci The vegetation is the hallmark of endocarditis, is a variably sized
mass of platelets and fibrin, microorganisms and scant inflammatory cell.
4. Requires interaction between:
Damage to host vascular endothelium (acquired or congenital heart disease),
Exterior circulating organisms (disease or trauma);
Host Immune system (HIV, drug abusers)
5. Clinical featrues:
Primary heart disease and new heart damage;
Embolization of fragments of the vegetation
Immunologic response
The infection itself: fever
Complications : abscesses, septic infarcts, and bacterial aneurysms
6. Diagnosis is based upon:
Major criteria
Positive blood culture
Evidence of endocardial involvement
- Positive echocardiogram (vegetation, or intracardiac abscess )
- New valvular regurgitation
Minor criteriaPredisposition; Fever; Vascular phenomena; Microbiological
evidence; Echocardiogram
7. Principles of Treatment:
Medical Management (Antibiotics): prolonged, high dose, bactericidal;
Surgical treatment (Valve replacement): in severe heart failure, valvular
obstruction.

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Acute Pericarditis : an inflammation of the pericardium characterized by chest
pain, pericardial friction rub, and serial ECG changes.
Causes
Idiopathic(non-specific idio and pathy) 86%
Infectious: virus, bacterium, fungi, other infectious 7%
Following a myocardial infarction or cardiac surgery (Dresslers syndrome)
Radiation therapy
Neoplastic disease (commonly lung or breast)
Connective tissue disease
Pathology
2 types : fibrinous adhesion pericardial effusion
Symptoms
1. Chest pain : Retrosternal chest pain sharp worse on inspiration and lying flat
- Quality: sharp, or dull, oppressive
- Location: precordium, left trapezius ridge
- Radiation: neck and trapezius ridge, left arm
- Aggravation: lying supine, coughing, deep inspiration, and swallowing; relieve
by sitting up and leaning forward
- Frequently in idiopathic and infectious pericarditis
2. Dyspnea
Most characteristic symptom
Caused by large pericardial effusion:
- compresses adjacent bronchi and pulmonary parenchyma
- pulmonary edema
3. Additional symptoms
Physical Examination
1. Pericardial friction rub : high pitched scratching noise
Scratching, grating, high-pitched sound
Arise from friction between the roughened pericardial and epicardial surface
Detected by deep inspiration, sitting up and leaning forward
Classically have three components: atrial systole, ventricle systole, and ventricle
diastole
2. Pericardial effusion
Ewarts sign : compression of the left lung
Cardiac tamponade:
- Acute cardiac tamponade
- Chronic pericardial effusion withoutcardiac tamponade
Electrocardiogram
Four stages of abnormal of the ST-segment and T-waves:
Stage : ST-segment elevation, T-waves upright
Stage : ST-segment isoelectric, T-waves flat
Stage : T-waves inversion
Stage : T-wave changes to normal
Reduction in QRS voltage, no Q-wave
ECG differential diagnosis - MI
DDx
- Dilated Cardiomyopathy
- Right ventricular heart failure

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Dx : Patient will have 2 or more of the following;
- Characteristic chest pain
- Pericardial friction rub (auscultation)
- ECG showing characteristic ST elevation (caused by epicardial injury)
Clinical signs differential diagnosis pleurisy
Pleuritic pain has similar sharp quality but is usually more specific in location
Pleural rub is heard over the area where the pain occurs
Treatment
Search for the underlying disease
Patients require bed rest
NSAIDs ( aspirin, indomethacin ) are generally accepted as effective for
relieving symptoms of chest pain
Colchicine may be a useful adjunct in those who do not respond to NSAIDs
alone

Pericardial effusion : the presence of an abnormal amount of fluid and/or an

abnormal character to fluid in the pericardial space.
Causes
Major causes are post cardiac surgery and AMI
Neoplastic disease
Tuberculous pericarditis
Hypothyroidism
Connective tissue disease ( SLE )
Pathophysiology
Significantly increased intrapericardial pressure impedes diastolic filling of the
ventricles
Therefore in order for the ventricles to fill the end-diastolic pressure must
exceed the pericardial pressure
Global effusion pericardial pressure is equal around heart
Therefore both ventricles have to increase EDP to same amount for ventricles to
fill
As the pericardial effusion worsens the EDP cannot raise significantly to
maintain cardiac output
Investigations and clinical signs
Clinical examination SOB, orthopnea, tachycardia (varying degrees)
Auscultation may have muffled heart sounds
ECG may show low amplitude QRS complexes
CXR globular appearance to heart and therefore cardiothoracic ratio
Echo size of effusion
Treatment
If persistent problem or life threatening ( Cardiac tamponade), more dramatic
action is called for Pericardiocentesis

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Cardiac tamponade (complication of pericardial effusion)
- It is a medical emergency and must be treated promptly
Acute cardiac tamponade
Beck triad : a decline in systemic arterial pressure; elevation of systemic venous
pressure; a small, quiet heart
Chronic cardiac tamponade
Jugular venous distension, hepatomegaly, ascites, peripheral edema
hypotension
Pulsus paradoxus
Signs and symptoms
- Significant SOB, rapid breathing
- Tachycardia
- Orthopnea
- Cold, clammy extremities because of poor perfusion
- Kussmauls sign
Treatment
Medical emergency intensive care environment needed.
Oxygen
Volume expansion
Bed rest with leg elevation
Inotropic drugs if necessary

Chronic Constrictive Pericarditis

- Chronic constrictive pericarditis is present when a fibrotic, thickened, and
adherent pericardium restricts diastolic filling of the heart.
- Acute pericarditissubacute stage chronic stage consisting of fibrous scarring
and thickening of the pericardium.
- The visceral and parietal layers become completely fused.
- Calcium deposition may contribute to thickening and stiffening of the
pericardium.
Causes
Tuberculous constrictive pericarditis was common cause of constriction pre
1960 decline in incidence.
Post-radiotherapy constriction
Needs to be differentiated from restrictive cardiomyopathy when making
diagnosis.
Clinical manifestation
Acute constrictive: within 1 year
Chronic constrictive: more than 1 year
Symptoms:
- Early stage: palpitation, exertional dyspnea
- Late stage: hepatomegaly, peripheral edema, pleural effusion, ascites
Signs
Jugular venous distention
Kussmauls sign
Hepatomegaly, edema of extremities
SBP, HR
Apical impulse undetected
Heart sound , pericardial knock sound
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Diagnosis and differentiate
Restrictive cardiomyopathy
Superior vena caval obstruction
Hepatic cirrhosis
Nephrotic symdrome
Management
Pericardiectomy as possible as earlier
Internal Medicine 2010
1. Sudden cardiac death (SCD) is an unexpected death due to cardiac causes that
occurs in a short time period (generally within 1 hour of symptom onset) in a person
with known or unknown cardiac disease
2. Rheumatoid arthritis (RA) is a chronic inflammatory multisystemic disease with
the main target being the synovium. The hallmark of RA is inflammatory synovitis that
presents in a symmetric distribution. Symptoms and signs include joint pain in the feet,
hands, and knees, swollen joints, fever, tender joints, loss of joint function, stiff joints,
fatigue, joint redness, rheumatoid nodules, joint warmth, joint deformity.
3. Myelodysplasic Syndrome (MDS) is an idiopathic disorder that is considered pre-
leukemic, in that a number of people go on to develop acute myelogenous leukemia
(AML). MDS is probably from a genetic defect.
4. Myelosarcoma is a malignant tumor derived from bone marrow or from one of its
cellular elements

# Hyperthyroidism is a condition caused by the effects of too much thyroid hormone.

Hyperthyroidism: usu. excess synthesis and secretion of thyroid hormone by the
thyroid gland, also known as thyrotoxicosis.
- free thyroxine (T4), increase free triiodothyronine (T3), or both.
Most common of thyrotoxicosis:
- diffuse toxic goiter (Graves disease, ~50-60%)
- toxic multinodular goiter (Plummer disease, 15-20%)
- toxic adenoma (3-5%).
Common Signs
1. Hyperactivity, Hyper kinesis
2. Sinus tachycardia or atrial arrhythmia, AF, CHF
3. Systolic hypertension, wide pulse pressure
4. Warm, moist, soft and smooth skin- warm handshake
5. Excessive perspiration, palmar erythema, Onycholysis
6. Lid lag and stare (sympathetic over activity)
7. Fine tremor of out stretched hands format's sign
8. Large muscle weakness, Diarrhea, Gynecomastia
Common Symptoms
1. Nervousness
2. Anxiety
3. Increased perspiration
4. Heat intolerance
5. Tremor
6. Hyperactivity
7. Palpitations
8. Weight loss despite increased appetite
9. Reduction in menstrual flow or oligo-menorrhea

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# A diagnosis of COPD should be considered in any patient who has cough, sputum
production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is
confirmed by spirometry.
Symptoms : cough, sputum, exertional dyspnea
Exposure to risk factors : tobacco, occupation , indoor/outdoor pollution
# Lower GI bleeding is defined as bleeding distal to the ligament of Treitz. The most
commonly caused by diverticulosis, angiodysplasia (also know as AVM or vascular
ectasia), hemorrhoids, cancer, and inflammatory bowel disease. The clinical
presentation of LGIB varies with the anatomical source of the bleeding as
- Maroon stools, with LGIB from the right side of the colon
- Bright red blood per rectum with LGIB from the left side of the colon
- Melena with cecal bleeding
# Upper GI bleeding is defined as bleeding from a gastrointestinal source that is
proximal to the ligament of Treitz. The most common causes of upper gastrointestinal
bleeding are ulcer disease,gastritis, Mallory- Weiss syndrome, esophagitis, and gastric
cancer. It usually manifests as hematemesis or melena, and when severe, may even
lead to hematochezia.

# Peptic ulcer is defined as disruption of the mucosal integrity of the stomach and/or
duodenum leading to a local defect or excavation due to active inflammation.
Peptic ulcers include: Gastric ulcers that occur on the inside of the stomach
Duodenal ulcers that occur on the inside of the upper portion of your small intestine
(duodenum)

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