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 & 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.

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:

>> Decrease blood flow >> Hypoxia accumulation of metabolites (Lactic acid, pyruvic, histamine ….) stimulate the never endings via upper 4 thoracic segments to the

Brain>>>>>pain. >>

*Risk Factors: Major Minor

• Hypertension. - Type A personality.

• Diabetes mellitus. - Inactive (Sedentary) life.

• Dyslipidemia. - Stress.

• Family History. - Male Sex.

Smoking - 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.

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.

* 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 >> Morphine = pain killer 2-4mg / 5-10 min.

O >> Oxygen : 4L / min.

N >> Nitroglycerin : SL or I.V.

A >> 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.

THANK YOU