Coronary Artery Disease and Myocardial Infarction

Coronary Artery Disease

• Cardiovascular diseases are the major cause of death in NZ (40% of all deaths)

• Heart attacks are still the leading cause of all cardiovascular deaths and deaths in general

• Maori are disproportionately at risk

• Male deaths twice that of females

Atherosclerosis

• Major cause of CAD• Begins as soft deposits of fat that harden with

age• Referred to as the “hardening of the arteries”• Abnormal accumulation of lipid, or fatty,

substances and fibrous tissue in the vessel wall• Can occur in any artery of the body• Atheromas (fatty deposits) have a preference for

the coronary arteries• Substances create blockages or narrow the

vessel in a way that reduces blood flow

3 Types of Lesions Associated with Atherosclerosis

1. Fatty streaks2. Fibrous atheromatous plaque – basic

lesion- Characterised by accumulation of lipids,

proliferation of smooth muscle cells & formation of scar tissue

3. Complicated lesion – characterised by haemorrhage, ulceration & scar tissue formation

Pathophysiology

• Endothelial lining altered as a result of injuries – hyperlipidaemia & hypertension

• Platelets are activated

• Smooth muscle cell proliferation entraps lipids, which are calcified over time & form an irritant to the endothelium on which platelets adhere & aggregate

• Fibrin formation & thrombi occur

Atherosclerosis

Atherosclerosis

Collateral Circulation

• Normally some arterial branching, termed collateral circulation exists within the coronary circulation

• Growth of collateral circulation is attributed to 2 factors

- The inherited predisposition to develop new vessels

-The presence of chronic ischaemia

Collateral Circulation

• When atherosclerotic plaque occludes the normal flow of blood through a coronary artery & ischaemia is chronic, increased collateral circulation develops

Coronary Artery Disease (CAD)

Other causes of heart disease include:• Vasospasm (sudden constriction or narrowing)

of coronary artery• Myocardial trauma• Structural disease• Congenital abnormalities• Decreased oxygen supply (acute blood loss)• Increased demand for oxygen (e.g.. rapid heart

rate)

Non-modifiable Risk Factors

– Increasing age– Gender (more common in men than

premenopausal women)– Genetic predisposition & family history of

heart didease– Ethnicity (Maori)

Modifiable Risk Factors

Major– Elevated serum lipid levels (serum cholesterol of

more than 5.2mmol/L)– Hypertension– Cigarette smoking– Physical activity– Obesity

Contributing– Diabetes mellitus– Stressful lifestyle– Lack of oestrogen in women

NHF – Risk Tables

• http://www.nhf.org.nz/index.asp?print=true&PageID=2145828662

Clinical Manifestations of CAD

1. Angina pectoris

2. Acute coronary syndrome

3. Sudden cardiac death

They all result from ischaemia (lack of oxygen supply to the heart)

Angina Pectoris

• Episodes or paroxysms of pain or pressure in anterior chest

• Caused by insufficient coronary blood flow• Insufficient flow results in decreased oxygen

supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress

• Usually associated with significant obstruction of a major coronary artery

Types of Angina

1. Stable Angina Pectoris• Pain usually lasts 3-5 minutes• Subsides when precipitating factor is relieved• Pain at rest unusual2. Unstable Angina Pectoris• Occurs at rest• Has a worsening pattern• Unpredictable• Considered to be an acute coronary syndrome

Anginal Pain

• Chest pain or discomfort• Sometimes referred to as a vague sensation,

strange feeling, pressure or ache in chest• Unpleasant feeling – constrictive, squeezing,

heavy, choking, or suffocating sensation• Usually not sharp or stabbing• Does not change with position or breathing• Pain usually located substernally but may occur

in neck or radiate to jaw, shoulders & down arms

Factors associated with Anginal Pain

• Physical exertion ( myocardial oxygen demand)• Exposure to cold (vasoconstriction & BP, with

oxygen demand)• Eating a heavy meal ( blood flow for digestion,

therefore reducing blood supply to heart muscle)• Stress or any emotion-provoking situation

(causes release of adrenaline & BP, increases heart rate & myocardial workload)

Clinical Manifestations of Angina

• Feeling of anxiety or impending doom

• Shortness of breath

• Cold sweat

• Weakness

• Paraesthesia of one or both arms

• Usually relieved by rest

• Doesn’t usually wake pt from rest

Myocardial Infarction (MI)

• Death of heart tissue caused by lack of oxygenated blood flow

• Reduced blood flow in coronary artery usually due to atherosclerosis & occlusion of an artery by an embolus or thrombus

• Area of infarction takes time to develop• As cells are deprived of oxygen, ischaemia develops,

cellular injury occurs, then lack of oxygen results in death of tissue

• Most infarcts involve left ventricle• Location & area of infarct correlate with part of coronary

circulation involved

Myocardial Infarction

• Contractile function of the heart stops in the area of myocardial necrosis

Transmural MIInvolves the entire thickness of the

myocardium

Subendocardial MI The damage has not penetrated through

the entire thickness

Healing Process

• Body’s response to cell death is inflammation. Within 24 hrs, leucocytes infiltrate the area

• Enzymes are released from dead cardiac cells (important indicators of MI)

• Proteolytic enzymes of neutrophils & macrophages remove all necrotic tissue by 2nd or 3rd day

• Development of collateral circulation improves area of poor perfusion

• By 6 weeks after MI, scar tissue has replaced necrotic tissue & area is healed

Clinical Manifestations of MI

• Sudden chest pain, unrelieved by rest & medication• May have no previous symptoms (sudden death)• Increased or decreased BP• ECG may show tachycardia, bradycardia & dysrhythmias• Dyspnoea, tachypnoea• Nausea & vomiting• Cool clammy skin• Anxiety, restlessness, feeling of impending doom

Pain of MI

• Severe & immobilizing• Described as a heaviness, pressure, tightness, burning,

constriction or crushing• Common locations are substernal, retrosternal or

epigastric• May radiate to neck, jaw, arms or back• Occurs while active or at rest, or asleep or awake• Commonly occurs in early morning hrs• Lasts for 20 mins or more & more severe than anginal

pain• Some may not experience pain but may have

‘discomfort’, weakness or shortness of breath

Complications of MI

• Arrhythmias

- present in 80% of MI pts

- common cause of death in pre-hospital period

• Congestive Heart Failure

- pumping power of heart has diminished

• Cardiogenic Shock