Download 2- Unstable Angina

Ischemic Heart
Disease
BY
Ragab Abdelsalam.(MD)
Prof. of cardiology
* Clinical
Presentations :
The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.
• Presentation & Mechanism
1-Stable Angina
exertion .
2- Unstable Angina:
-Transient myocardial
- ischemia on
- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .
5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .
6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.
Angina Pectoris
Definition:
It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply
* Types:
A) It is either :
1- Stable
2- Unstable
• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina
c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.
Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.
*Risk
Factors:
Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•
Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity
• *Precipitating Factors:
•
•
•
•
•
•
Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.
*Clinical
data:
A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.
B - Autonomic effects: sweating, irritability,
diaphoresis
C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)
Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.
Other systems >> Comorbidity
* Investigation:
A Basic Investigations :
Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.
B) Specialized Investigations :
> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.
C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography
* Summary Of Treatment
> Initial:
Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin
Then:
> Risk Stratification 
> Control risk factors 
Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.
• *Revascularization
:
–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery
Bypass Grafting).
Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management
* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.
*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:
>> Rupture of an unstable plaque leads to
Coronary artery occlusion:
> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI
The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.
• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain
Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.
Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.
Pain is severe but serum markers
are not yet released .
Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.
* Electrocardiogram (ECG)
• a-Ischemia:
•
- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.
b) (20 – 40 min)
>> ST
– segment elevation.
c) Infraction:
.
.
- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead
*Clinical
data :
• 1) Symptoms:
– Chest pain:
• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.)
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.
• Silent – painless myocardial infarction
Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:
•
•
In diabetics.
In elderly.
* Signs :
•
•
•
•
•
•
Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.
> Pulse: Arrhythmias may be detected.
> Low grade fever
** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs
> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.
** However, auscultation may reveal no
abnormality.
Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.
Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.
B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.
- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.
Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.
2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>
Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).
3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.
>Thrombolytic agents: (door – to –
needle time < 30 min).
> Primary PTCA: (door – to – dilation
time < 60 min
Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.
Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-
- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.
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