pathophysiology of coronary artery disease

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Pathophysiology of Coronary Artery Disease (CAD) From: Dr. A.P.Netraranjn

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Page 1: Pathophysiology of Coronary Artery Disease

Pathophysiology of Coronary Artery Disease (CAD)

From: Dr. A.P.Netraranjn

Page 2: Pathophysiology of Coronary Artery Disease

Cardiac Anatomy

Page 3: Pathophysiology of Coronary Artery Disease

Coronary Arteries

Coronary blood supplyArises from the ascending aortaEmpties into the coronary sinus

Page 4: Pathophysiology of Coronary Artery Disease

Coronary Arteries

Right Coronary Artery

• Acute Marginals • Posterior Descending

Artery (PDA)• Posteriolateral Artery (PLA)

Left Coronary Artery

• Left Main

• Left Anterior Descending (LAD)

– Diagonals

– Septals

• Left Circumflex (LCx)

– Obtuse Marginals (OM)

Page 5: Pathophysiology of Coronary Artery Disease

Coronary Artery Disease (CAD)

An imbalance in the myocardial oxygen supply:

• Impaired blood flow• Increased oxygen demand • Decreased supply

Page 6: Pathophysiology of Coronary Artery Disease

CAD - Etiology

• Subintimal deposition of atheromas in large and medium-sized coronary arteries (atherosclerosis).

• Less common - Coronary spasm.

• Rare - Coronary artery embolism, dissection, aneurysm (eg, in Kawasaki disease), and vasculitis (eg, in SLE, syphilis).

Page 7: Pathophysiology of Coronary Artery Disease

Myocardial Oxygen Supply and Demand

Factors that Impair Myocardial Oxygen Supply

• Atherosclerosis– Plaque rupture

• Thrombosis• Embolism• Spasm

Factors that Increase Myocardial Oxygen Demand

• Physical exertion• Stress

– Emotional – Physical

Page 8: Pathophysiology of Coronary Artery Disease

Progression of Atherosclerosis

Page 9: Pathophysiology of Coronary Artery Disease

Progression of Atherosclerosis

Page 10: Pathophysiology of Coronary Artery Disease

Progression of Atherosclerosis

Plaque

Page 11: Pathophysiology of Coronary Artery Disease

Progression of Atherosclerosis

Angina pectoris

Page 12: Pathophysiology of Coronary Artery Disease

Progression of Atherosclerosis

Plaque rupture reasons: unclear but probably related to

• Plaque morphology,• Plaque Ca content, and• Plaque softening due to an inflammatory process

Page 13: Pathophysiology of Coronary Artery Disease

Risk Factors

• Hypertension

• Elevated LDL/decreased HDL

• Smoking

• Obesity

• Diabetes

• Physical inactivity

• Advanced age

• Gender (Male >Female)

Page 14: Pathophysiology of Coronary Artery Disease

CAD – Clinical Presentation

Chest PainCommon non cardiac causes of chest pain

Angina pectoris

Atypical angina

Acute coronary syndrome

Other cardiac or vascular causes: pericarditis, Aortic dissection, pulmonary embolism

No Chest Pain = Silent Ischemia

Cardiac or non cardiac

MusculoskeletalRespiratory diseaseGastrointestinalAnxiety/Emotional

Page 15: Pathophysiology of Coronary Artery Disease

Angina Pectoris - Symptoms

• Angina may be a vague, barely troublesome ache or may rapidly become a severe, intense precordial crushing sensation. It is rarely described as pain.

• Discomfort is most commonly felt beneath the sternum, although location varies.

• Radiate to: – left shoulder and down the inside of the left arm, even to the fingers; straight

through to the back; – into the throat, jaws, and teeth; and, – occasionally, down the inside of the right arm. It may also be felt in the upper

abdomen.

• The discomfort of angina is never above the ears or below the umbilicus.

Page 16: Pathophysiology of Coronary Artery Disease

Angina Pectoris

Class Activities Triggering Chest Pain 1

 

Strenuous, rapid, or prolonged exertionNot usual physical activities (eg, walking, climbing stairs)

2

 

 

 

 

 

 

Walking rapidlyWalking uphillClimbing stairs rapidlyWalking or climbing stairs after mealsColdWindEmotional stress

3

 

Walking, even 1 or 2 blocks at usual pace and on level groundClimbing stairs, even 1 flight

4

 

Any physical activitySometimes occurring at rest

Symptom severity is often classified by the degree of exertion resulting in angina Canadian Cardiovascular Classification System of (Stable) Angina Pectoris.

Page 17: Pathophysiology of Coronary Artery Disease

Acute Coronary Syndrome

• Acute coronary syndromes result from acute obstruction of a coronary artery.

• Consequences depend on degree and location of obstruction and range from

– Unstable angina

– Non-ST-segment elevation MI (NSTEMI)

– ST-segment elevation MI (STEMI)

– Sudden cardiac death.

Page 18: Pathophysiology of Coronary Artery Disease

Myocardial Infarction

Blocked Blood Supply

OccludedCoronary

Artery

DamagedHeart Muscle

Page 19: Pathophysiology of Coronary Artery Disease

Myocardial Infarction

Stages of myocardial cell death due

to prolonged lack of oxygen • Ischemia - insufficient oxygen supply• Inflammation• Infarction - necrosis

Page 20: Pathophysiology of Coronary Artery Disease

Myocardial Infarction

Extent of Infarction• Subendocardial infarct- isolated in the subendocardial layer• Transmural infarct - involves

the full thickness of a portion of myocardium

Page 21: Pathophysiology of Coronary Artery Disease

MI Classification

Classification is based on ECG changes and presence of cardiac markers in blood.

• Non-ST-segment elevation MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or T and CPK will be elevated) without acute ST-segment elevation or Q waves.

• ST-segment elevation MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin or showing new left bundle branch block Q waves

may be present. Both troponin and CPK are elevated.

Page 22: Pathophysiology of Coronary Artery Disease

Acute Coronary Syndrome - symptoms

Unstable angina

Similar to angina pectoris except that the pain is

• more intense

• lasts longer

• is precipitated by less exertion

• occurs spontaneously at rest

• is progressive in nature

• or involves any combination of these features.

Page 23: Pathophysiology of Coronary Artery Disease

Unstable Angina

Classification Description Designation Severity

I New onset of severe angina or increasing† angina

No angina during rest

II Angina during rest within past month but not within preceding 48 h

Subacute angina at rest

III Angina during rest within 48 h Acute angina at restClinical situation

A Develops secondary to an extracardiac condition that worsens myocardial ischemia

Secondary UA

B Develops when no contributory extracardiac condition is present

Primary UA

C Develops within 2 wk of acute MI Post-MI UA

Unstable angina is classified based on severity and clinical situation

Braunwald Classification of Unstable Angina :

Page 24: Pathophysiology of Coronary Artery Disease

Acute Coronary Syndrome - symptoms

NSTEMI and STEMI

• Usually - deep, substernal, visceral pain described as aching or

pressure, often radiating to the back, jaw, left arm, shoulders, or all

of these areas.

• The pain is similar to angina pectoris but is usually more severe and

long-lasting; more often accompanied by dyspnoea, diaphoresis,

nausea, and vomiting; and relieved little or only temporarily by rest

or nitroglycerin.

Page 25: Pathophysiology of Coronary Artery Disease

Acute Coronary Syndrome - Investigations

• Serial ECGs

• Stress testing with ECG

• Serial cardiac markers

• Coronary angiography

Page 26: Pathophysiology of Coronary Artery Disease

ECG - Limb leads

• Three electrodes attached to the left arm, the right arm, and the left leg, respectively.

• The three bipolar limb leads:– lead I: right arm–left arm– lead II: right arm–left leg– lead III: left leg–left arm

• The unipolar leads: – aVR lead: right arm– aVL lead: left arm– aVF lead: left leg

Page 27: Pathophysiology of Coronary Artery Disease

ECG - Chest leads

• Another six electrodes, placed in standard positions on the chest wall, give rise to a further six unipolar leads –

• the chest leads (also known as precordial leads), V1–V6.

Page 28: Pathophysiology of Coronary Artery Disease

ECG

Page 29: Pathophysiology of Coronary Artery Disease

ECG – Normal tracing

Page 30: Pathophysiology of Coronary Artery Disease

ECG – ST Segment Depression

ECG demonstrating ST-segment depression (I, V3–V6). ST depression is diagnostic of ischemia.

Page 31: Pathophysiology of Coronary Artery Disease

ECG – ST Segment Elevation

ECG showing ST elevation on inferior leads (II, III, aVF).

Page 32: Pathophysiology of Coronary Artery Disease

Myocardial Infarction

Page 33: Pathophysiology of Coronary Artery Disease

Exercise Treadmill Test (ETT)

• Myocardial demand is increased by exercise and perfusion to the heart is examined by use of ECG.

• “Exercise” can be done by use of treadmill or bicycle; or by use of drugs that increase heart rate e.g., adenosine, dypiridamole, dobutamine.

• Clinical findings suggestive of ischemia:– BP falls below resting level– Significant arrhythmias– Typical chest pain (>5 on 0-10 scale)– Significant ECG changes.

Page 34: Pathophysiology of Coronary Artery Disease

Cardiac markers

Cardiac markers are cardiac enzymes (eg, CPK-MB) and cell contents (eg, troponin I, troponin T, myoglobin) that are released into the bloodstream after myocardial cell necrosis.

The amount of enzyme release depends on the severity of the injury.

Each enzyme follows a specific pattern of peak levels in blood.

Page 35: Pathophysiology of Coronary Artery Disease

Cardiac markers

Time Course of Cardiac Biomarkers after M.I.

Page 36: Pathophysiology of Coronary Artery Disease

Cardiac markers

Biomarker Range of time to initial

elevation (hrs)

Mean time to Peak

elevation

Time to return to normal

range

Notes

CK-MB 3-12 24 hr 48-72 hrHigh specificity and sensitivity to myocardial necrosis

cTnI 3-12 24 hr 5-10 dNear absolute specificity to myocardial necrosis

cTnT 3-12 12 hr – 2d 5-14 d

High sensitivity to even microscopic areas of necrosis

Not an index of acute injury because of prolonged time to return to normal

Page 37: Pathophysiology of Coronary Artery Disease

Coronary angiography

This diagnostic method outlines the lumina of the coronary arteries and can be used to

detect or exclude serious coronary obstruction.

However, coronary arteriography provides no information regarding the arterial wall, and

severe atherosclerosis that does not encroaches on the lumen may go undetected.

Page 38: Pathophysiology of Coronary Artery Disease

Angiography: Right Coronary Artery (LAO)

Filling defect: Lesion

Page 39: Pathophysiology of Coronary Artery Disease

CAD - Management

• General Measures

• Drugs

• Revascularization

Page 40: Pathophysiology of Coronary Artery Disease

Approach to acute coronary syndromes (ACS).

Page 41: Pathophysiology of Coronary Artery Disease

Revascularization

• Revascularization is the restoration of blood supply to ischemic myocardium

in an effort to limit ongoing damage, reduce ventricular irritability, and

improve short-term and long-term outcomes.

• Modes of revascularization include 1. Thrombolysis with fibrinolytic drugs 2. PCI with or without stent placement 3. CABG.

Page 42: Pathophysiology of Coronary Artery Disease

Percutaneous Coronary Intervention (PCI)

• PTCA, POBA, Angioplasty

• Cutting balloon angioplasty

• Stenting Bare metal stents Drug-eluting stents

• Brachytherapy

• Coronary rotablation and atherectomy

Page 43: Pathophysiology of Coronary Artery Disease

Coronary Artery Bypass Graft (CABG)

CABG is performed for certain groups:

• Patients with three or more blocked arteries

• If the left main artery is narrowed by 50% or more

• When the disease portion of the artery is very long

Page 44: Pathophysiology of Coronary Artery Disease

Thank you

For any feedback, please contact Dr. Netraranjn at [email protected]