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Ischemic Heart Disease. William J Hunter MD. Types of Heart Disease. Acquired Heart Disease Congenital Heart Disease. Acquired Heart Disease. Ischemic Heart Disease Hypertensive Heart Disease Valvular Heart Disease Myocardial Heart Disease. Ischemic Heart Disease.

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ischemic heart disease
Ischemic Heart Disease

William J Hunter MD

types of heart disease
Types of Heart Disease
  • Acquired Heart Disease
  • Congenital Heart Disease
acquired heart disease
Acquired Heart Disease
  • Ischemic Heart Disease
  • Hypertensive Heart Disease
  • Valvular Heart Disease
  • Myocardial Heart Disease
ischemic heart disease1
Ischemic Heart Disease
  • Supply of oxygen in the coronary arterial blood is inadequate to provide for the oxygen demands of the heart.
epidemiology of ischemic heart disease
Epidemiology of ischemic heart disease
  • 500,000 die
  • Overall rate has fallen since 1980
    • Prevention - working on risk factors: smoking, hypertension, cholesterol, better diabetic control, aspirin prophylaxis
    • Therapeutic advances- new medications, coronary care units, thrombolysis, angioplasty, stents and coronary bypass surgery
results of ischemic hd
Results of Ischemic HD
  • Angina Pectoris - ASVD
    • Stable angina
    • Prinzmetal’s angina - spasm
    • Preinfarction (unstable) angina - MI
  • Myocardial Infarct- myocardial necrosis
  • Sudden cardiac death
  • Chronic ischemic HD with heart failure- ‘focal fibrosis’ or presbycardia
acute coronary syndromes
Acute Coronary Syndromes
  • The new ‘in’ word- TV ads
  • A spectrum -from unstable angina to acute myocardial infarct
  • Atherosclerotic plaque disruption and associated platelet-fibrin thrombus formation
  • Sudden death
etiology of ischemic hd
Etiology of Ischemic HD
  • 95-98% Atherosclerotic Narrowing with plaques
  • Coronary embolism (rare)
  • Dissecting aneurysm (rare)
  • Arteritis (polyarteritis, rheumatoid, Kawasaki Disease) (rare)
  • Syphilis (rare)
  • Cocaine abuse
coronary atherosclerosis
Coronary Atherosclerosis
  • 90% have at least one 75% occlusion- the key is acute change of the plaque
    • Hemorrhage into the atheroma
    • Rupture of the plaque with thrombosis
    • Erosion or ulceration of the plaque with thrombosis
  • Most have two arteries involved
  • Most blocks are in the epicardial arteries
myocardial infarct
Myocardial Infarct
  • Most have
      • >75% occlusion of coronary by plaque
      • multi-vessel disease
      • 80% have recent thrombus
      • LAD most commonly involved
typical mi
Typical MI
  • Most have multivessel disease
  • Ulcerative stenotic plaque or hemorrhage into the plaque
  • Platelets aggregate
  • Tissue thromboplastin released
  • Vasoactive amines released
  • Thrombosis and spasm occur
  • Ischemic necrosis
arteries involved
Arteries involved
  • LAD (40 - 50%) Anterior wall, apex, Anterior 2/3 septum
  • RCA (30- 40%) Post wall, post 1/3 septum
  • LCA (15- 20%) Lateral wall
role of hemodynamic changes
Role of Hemodynamic Changes
  • Sudden drop in BP
  • Must be difference in pressure between coronary ostia and coronary sinus
role of vasospasm
Role of Vasospasm
  • Vasospasm documented in angina
  • Spasm can cause rupture of plaques
  • Rare cases of MI after spasm
role of platelet
Role of Platelet
  • Rupture of Plaques > adherence
  • The aggregation contributes to blockage
  • Thromboxane, histamine, serotonin => vasospasm
  • ASA helps
supply of o2 in the blood
Supply of O2 in the Blood
  • Anemia
  • CO and cyanide
  • O2 demand
  • Hypertension
  • Valvular disease
  • Hyperthyroidism
  • Fever
  • Catecholamines
  • (? personality types)
role of acute plaque change in mi
Role of acute Plaque Change in MI
  • Hemorrhage into the atheroma - expanding its volume
  • Rupture or fissuring, exposing the highly thrombogenic plaque constituent
  • Erosion or ulceration
  • Note that the original plaque may not have been a significant lesion (no critical stenosis
time of day
Time of Day
  • Peak incidence of MI: 6am to noon
  • Adrenergic stimulation of awakening can put more stress on the plaque
  • Surge of blood pressure at same time frame
gross changes of mi
Gross Changes of MI
  • Up to 5 hours- no changes
  • 6-24 hour- pallor
  • 24-48 hours- central pallor - hyperemia at margins
  • 2-5 days - hyperemic border, yellow band, soft dull center
  • 5-10 days- broader yellow border and thin new pink border
  • 10 days-3 wks - islands of red brown tissue surrounded by red-purple granulation tissue
  • 3-6 weeks - fibrosis
histology of mi
Histology of MI
  • 0-6 hours - none (? waviness)
  • 6-24 hours- eosinophilia, loss of cross striation
  • 24-48 hours- coagulative necrosis, PMN
  • 2-5 days- phagocytosis, granulation tissue
  • 10 days - 3weeks increasing fibrosis, PMN’s disappear
  • 3-6 weeks - maturing fibrosis
complications of mi
Complications of MI
  • Arrhythmias (90%)
  • CHF 60%
  • Cardiogenic shock 10%
  • Rupture (wall, septum, PAP M.) 5-10%
  • Mural thrombus and embolism
  • Pericarditis
  • Ventricular Aneurysms
  • Papillary muscle dysfunction
slide45

Area of infarct

Rupture of myocardial infarct

hemopericardium

slide48

Rupture of ventricular

septum– giving rise to

Acute right heart failure

diagnosis of mi
Diagnosis of MI
  • Symptoms and signs
  • 1/2 may be silent
  • EKG- New Q-wave, S-T segment and T-wave changes
  • Enzymes, CK, (CKMB) , Troponins
  • Drs. Lynch & Baltaro will talk more about this
subendocardial infarct non q wave infarct
Subendocardial Infarct- non Q wave infarct
  • severe ASCD
  • no critical stenosis
  • Multifocal or bridges arterial zones
  • diabetes
  • Dangerous
infarct modification after reperfusion
Infarct Modification After Reperfusion
  • Reperfusion early- may prevent most necrosis
  • Hemorrhage - leaky damaged vessels
  • Necrosis with contraction bands
  • Increased oxygen free radicals