CORONARY ARTERY DISEASE

Coronary Artery Disease

o CAD: Heart disease caused by impaired coronary blood flow
o Atherosclerosis most common cause
Pathogenesis of Coronary Artery Disease
o CAD does not produce symptoms until it is advanced because of collateral flow.
Location of significant lesions tend to locate in:
o the first several centimeters of the left anterior descending (LAD) and left circumflex
o the entire length of the right coronary artery (RCA)
Coronary Artery Disease CAD is divided into 2 types of disorders:
Acute coronary syndromes (ACS)
Caused by acute plaque disruption
Range from unstable angina to MI
Chronic ischemic heart disease
Caused by atherosclerotic or vasospastic obstruction of coronary arteries (i.e., stable angina)
Pathogenesis of CAD
Pathophysiology
Stable plaque --> Stable angina
Unstable plaque --> Plaque disruption --> Platelet aggregation -->
Thrombus formation --> Unstable angina and MI
Occlusion of arteries --> contractility stops after several minutes depriving the
myocardial cells of glucose for aerobic metabolism --> Lactic acid accumulates:
myocardial fibres are irritated by the lactic acid --> Pain ensues- angina --> Lead to MI
3 TYPES OF ANGINA
o Stable angina: Pain when heart’s oxygen demand increases
o Variant angina (Printzmetal’s): Pain when coronary arteries spasm
o Silent myocardial ischemia: Myocardial ischemia without pain.
Chronic Stable Angina
o Angina pectoris is a sudden attack of chest pain or pressure due to transient myocardial ischemia.
o Fixed coronary obstruction where coronary blood flow is insufficient to meet the metabolic
demands of the heart.
o Often associated with atherosclerosis
o Triggered by increased work demands of the heart • physical exertion, cold,
or emotional stress.
o Primary Manifestation: PAIN!
o Steady pattern
o Constricting, squeezing or suffocating sensation
o Substernal area;
o may radiate to the left shoulder, jaw, arm or other areas of chest
o Relief after 5 min rest or with nitroglycerine
o If longer than 5-10 min for relief, the pain is likely due to severe ischemia
Diagnosis of Angina
o Detailed pain history, risk factors
o Rule out non-coronary causes
o Noninvasive testing: ECG, Exercise stress testing, Echocardiography, Nuclear imaging studies,
CT, cardiac MRI.
o Definitive diagnosis: Cardiac catheterization, Coronary arteriography
Treatment of Stable Angina
o Treatment aimed at symptom reduction & MI prevention
Nonpharmacologic strategies:
o Risk factor reduction, Symptom control
 Pharmacologic therapy:
o Nitrates, Beta blockers, Calcium channel blockers
Coronary interventions:
o CABG indicated for persons with double or triple vessel disease.
ACUTE CORONARY SYNDROMES (ACS)
o Represent acute ischemic heart diseases like myocardial infarction (MI).
o ACS classified based on presence or absence of ST-segment elevation on
ECG.
o Guides whether a person should be considered for acute reperfusion
therapy.
o Serum biomarkers used to determine whether MI has occurred
Electrocardiogram (ECG)
o Provides an electrical picture of cardiac function.
o Classic changes that occur with ACS include:
• T wave inversion
• ST elevation
• development of an abnormal Q wave.
o Changes in electrical function vary depending on:
• duration of ischemic event,
• extent of damage
• location of damage
Diagnosis of ACS - Serum biomarkers
Serum biomarkers for ACS include;
o troponin I and troponin T
o myoglobin
o creatine kinase MB (CK-MB)
o As myocardial cells die, their intracellular contents begin to diffuse into the
surrounding
interstitium and then the blood.
o Enzymes to degrade the intracellular contents serve as the serum biomarkers.
Serum biomarkers
o Troponin assays
• High specificity for myocardial tissue
• Primary biomarker tests for the diagnosis of MI.
• Troponin complex part of the actin filament, regulates the calcium
mediated actin-myosin contractile process.
o Begins to rise 3 hours after onset of MI
o May stay elevated for 7-10 days (useful for late diagnosis)
CK-MB
o An isoenzyme highly specific for injury to myocardial tissue.
o Become elevated within 4-8hrs after injury
o Return to normal in 2-3 days

MYOCARDIAL INFARCTION
Unstable Angina/NSTEMI
o Unstable angina: pain at rest/new onset of pain in last month/more
frequent pain,
o No serum biomarker changes
o NSTEMI: Sufficient myocardial damage to release detectable quantities
of troponin
 Treatment for Unstable Angina/NSTEMI
o Decrease platelet aggregation and workload of the heart by:
• ASA, Beta-blockers, ACE inhibitors, Nitrates
o Percutaneous coronary intervention (PCI) or
o Coronary artery bypass grafting (CABG)
ST Elevation Myocardial Infarction (STEMI)
o Ischemic death of myocardial tissue ‘
o Size and pattern of infarct depends;
• location and extent of occlusion
• amount of heart tissue supplied by the vessel
• metabolic needs of the affected tissue
• extent of collateral circulation
• heart rate, blood pressure, cardiac rhythm
Unstable Angina/NSTEMI
Unstable angina manifestations:
Characterized by at least one of the following;
o Occurs at rest with minimal exertion
o Severe, frank pain of new onset
o More severe, prolonged and frequent
Pathologic Changes of STEMI
Metabolism changes from aerobic to anaerobic with inadequate energy production
to sustain normal myocardial function --> Striking loss of contractile function within
60 seconds of onset --> Cell structure changes within minutes -->
Ischemic area ceases to function within minutes --> Irreversible myocardial cell death (necrosis)
occurs after 20 to 40 minutes of severe ischemia.
STEMI - Reperfusion
o Re-establish blood flow using fibrinolytic therapy or revascularization procedures.
o Benefits of early reperfusion:
o prevent necrosis, improve myocardial perfusion in the infarct zone, may also prevent
microvascular injury.
o Despite reperfusion, abnormalities in function may persist, causing ventricular dysfunction.
o Recovering area of the heart is called stunned myocardium.
Clinical Manifestations of MI
Chest pain characteristics:
o severe and crushing,
o usually substernal, radiating to left arm, neck or jaw.
o Pain is NOT relieved by rest (whereas it is in angina)
o Women have atypical ischemic type chest pain.
o Elderly complains of shortness of breath.
Other:
o Gastrointestinal complaints common with acute MI.
o Epigastric distress, nausea and vomiting may occur due severity of pain and vagal stimulation.
o Fatigue and weakness.
o Pain and sympathetic stimulation cause tachycardia, anxiety, restlessness, feeling of impending
doom.
o Skin pale, cool and moist