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Ischemic Heart Disease
BY
Ragab Abdelsalam.(MD)Prof. of cardiology
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* Clinical Presentations:
The clinical presentation of ischemic heart disease usually depends on the underlying mechanism.
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• Presentation & Mechanism1-Stable Angina -Transient myocardial
- ischemia on exertion.
2- Unstable Angina: - Prolonged ischemia.
- Plaque fissuring > minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary artery occlusion with tissue necrosis.
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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.
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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.
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Angina Pectoris
Definition:
It is a clinical syndrome of a distinctive chest pain due to temporarily insufficient myocardial blood supply
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* Types: A) It is either :
1- Stable
2- Unstable
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• b) Clinical background: • Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina
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c) Specific Forms: - Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.
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Etiology:
*Pathogenesis of pains:
>> Decrease blood flow >> Hypoxia accumulation of metabolites (Lactic acid, pyruvic, histamine ….) stimulate the never endings via upper 4 thoracic segments to the
Brain>>>>>pain. >>
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*Risk Factors: Major Minor
• Hypertension. - Type A personality.
• Diabetes mellitus. - Inactive (Sedentary) life.
• Dyslipidemia. - Stress.
• Family History. - Male Sex.
Smoking - Age
• - Obesity
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• *Precipitating Factors:• Heavily exersion.
• Emotion.
• Cold.
• Digestion (Heavy meals).
• Tachycardia.
• Smoking.
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* 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.
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B - Autonomic effects: sweating, irritability, diaphoresis
C - Physical Examination
Hands > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)
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Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.Or normal findings.
Other systems >> Comorbidity
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* Investigation:
A Basic Investigations:
Electrocardiogram (ECG).
Exercise ECG – Treadmill or Bicycle.
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B) Specialized Investigations:
> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.
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C- Other Imaging Techniques: >Magnetic Resonance Imaging (MRI).
>Ultrafast computed Tomography (UCT).
>Posterior Emission Tomography (PET).
>Colour Kinesis. >Contrast Echocardiography
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*Summary Of Treatment >Initial:
Sublingual nitrate.
Sublingual crushed 75 mg Aspirin
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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.
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• * Revascularization: –PTCA (Percutaneous Transluminal coronary angioplasty).
–CABG (Coronary Artery
Bypass Grafting).
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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
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*The three major syndromes are
1-Unstable angina.
2 -Non – ST elevation
3-myocardial infraction.
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* 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
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The 3 “I” S of coronary artery events, means:
>Ischemia.
> Injury.
> Infraction .
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• 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.
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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.
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Infractionactual 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.
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* Electrocardiogram (ECG)
• a-Ischemia: • - > 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.
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b) (20 – 40 min)
>> ST – segment elevation.
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c) Infraction:> - 1-2 hours
-Abnormal Q – waves.
2 mm wide or.
25 % height of R – wave, in that lead .
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* 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
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Symptoms of complications.
>As , dyspnea PND , irritability , palpitation – Silent – painless myocardial infarction:
• In diabetics.
• In elderly.
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* Signs: • Anxious patient.
• Signs of cardiogenic shock if present:
• Cold sweats.
• Peripheral cyanosis.
• Hypotension, thready pulse.
• Oligurea.
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>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
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>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.
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Investigation: - Electrocardiogram (ECG). -ECG monitoring. -Cardiac enzymes: > Troponins. > Myoglobin. > SGOT. > LDH. > CPK – isoforms. - Echocardiography. - Radionoclide scintigraphy. - Cardiac catheterization.
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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.
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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.
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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.
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2- Initial General Treatment:
** Memory aid “ MONA”M >> Morphine = pain killer 2-4mg / 5-10 min.
O >> Oxygen : 4L / min.
N >> Nitroglycerin : SL or I.V.
A >> Aspirin : 160 – 325 mg (Chew).
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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
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Conjunctive therapy:
combined with thrombolytic agents:
- Aspirin.
- Heparin.
Adjunctive therapies:
Agents given instead of or in addition to thrombolytic agents:
-
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- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.
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