Ischemic Heart disease

Dr. Pearl Myers

Path

Fall 2011
With acknowledgement to Dr SA
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Ischemic Heart Disease

Def
Cardiac ischemia sec. to atherosclerotic coronary artery disease

Most common cause of death in US Age

25% of all deaths

Middle-age men Post-menopausal women

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Etiology
Coronary artery disease (80%) Hypertrophic cardiomyopathy Mitral valve prolapse Aortic valve stenosis Congenital heart abnormalities Myocarditis

Autopsy findings
Severe, fixed atherosclerotic CAD No acute changes in myocardium (coagulation necrosis) No grossly obvious coronary thrombosis
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Labs to measure heart ischemia

LDH
CK Troponin ANP

LDH

LDH (lactate dehydrogenase)

LDH has been supplanted by other tests.
rises in 12 to 24 hours following MI, peaks in 2 to 3 days, gradually dissipating in

5 to 14 days.

CK

Creatine Kinase - Total:

The total CK is a simple and inexpensive test that is readily available using many laboratory instruments. An elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible

from a variety of non-cardiac conditions.

Creatine Kinase
Three isoenzymes
CK MM (heart & skeletal muscle) CK BB (brain, lung & other tissues) CK MB (Principally myocardium, variable

amounts in skeletal muscle)

CK MB rises within 4 8 hours of MI, peaks

at 18 hours and disappears by 48 to 72 hours

CK-MB
is a very good marker for acute myocardial injury, because of its

excellent specificity, and it rises in serum within 2 to 8 hours of onset of acute myocardial infarction.
Serial measurements every 2 to 4 hours for a period of 9 to 12

hours after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury.
The CK-MB is also useful for diagnosis of reinfarction or

extensive of an MI because it begins to fall after a day, dissipating in 1 to 3 days, so subsequent elevations are indicative of another event.

Troponins

Troponin I and T
Troponin I and T are structural components of cardiac muscle.
They are highly specific for myocardial injury

more so than CK-MB and help to exclude elevations of CK with skeletal muscle trauma. Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB but they last longer.

Troponins
Troponins will remain elevated longer than CK--up to 5

to 9 days for troponin I and up to 2 weeks for troponin T. makes troponins a superior marker for diagnosing myocardial infarction in the recent past--better than lactate dehydrogenase (LDH) which appears after 24 hrs. Continued elevation has the disadvantage of making it more difficult to diagnose reinfarction or extension of infarction in a patient who has already suffered an initial MI. (CK is better for reinfarction)

Serum markers (handy chart)

Elevated by Peak Returns to normal by 3-4 days 2-3 days 7-10 days 8-14 days
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Total CK
CK-MB Troponin I and T LDH

4-6 hrs
2-4 hrs 2-4 hrs 24 hrs

12-24 hrs
24 hrs 48 hrs 3-6 days

Myocardial infarction (MI) Angina pectoris Chronic IHD Sudden cardiac death

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Angina Pectoris

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Angina pectoris
A symptom complex of IHD

characterized by paroxysmal (sudden) attacks of chest pain, usually substernal or precordial (front of heart), caused by myocardial ischemia that falls short of inducing infarction.

Angina Pectoris
Most common clinical manifestation of occlusive atherosclerotic CAD

Recurrent episodes of chest pain (constricting/ squeezing/ choking/ knifelike)

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Since usually hearts are not biopsied, what test to differentiate between anginas?

ECG

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Classic ECG evolution

Peaked (hyperacute) T waves
Area of ischemia

ST segment elevation
Area of injury, loss of normal myocardial cell

membrane ion pumps

Symmetric T wave inversion

Area of ischemia

Q wave
Area of infarction with cell death

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Hyper peaked T waves

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Inverted T waves

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Types of Angina

Stable angina (Exertional or Classical angina) Prinzmetal variant angina Unstable angina (crescendo angina)

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Stable Angina

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Stable Angina
Stable angina (typical) - paroxysms of pain

related to exertion and relieved by rest or vasodilators. Subendocardial ischemia with ST-segment depression on ECG

ECG S-T depression

Stable angina (Exertional or Classical angina)

Sudden chest pain due to an

increased cardiac demand (exertional or emotional)

Lasts for 1-15 min Relieved by rest or nitroglygerin

ECG

ST depression (subendocardial ischemia)

Coronary arteriography

Severe, fixed CAD atherosclerosis with >75% narrowing

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Variant Angina

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Prinzmetals Angina
Variant or Prinzmetal's angina - is caused by reversible

spasm in normal to severely atherosclerotic coronary arteries

Clinical Symptoms
Episodic chest pain at rest Relieved by nitroglycerin (vasodilatation)

ST-segment elevation or depression on ECG maybe

seen during attacks.

ECG S-T elevation

Unstable Angina

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Unstable or crescendo angina

Cause
1. Disrupted atherosclerotic plaques with

superimposed non-occlusive/mural thrombus 2. Vasospasm

Symptoms
Frequent bouts of chest pain at rest with increasing intensity, and duration of episodes ST-segment depression (usually) and ST-segment elevation. High risk for myocardial infarction
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Unstable angina pathogensis

Occlusive intracoronary thrombus - a thrombus

overlying an ulcerated or fissured stenotic plaque which causes 90% of transmural acute myocardial infarctions. Vasospasm - with or without coronary atherosclerosis and possible association with platelet aggregation. Emboli - from left sided heart mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale.

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Another handy chart

Plaque Stenoses Disruption Plaque-asso. thrombus >75% No No Variable Usually Severe Frequent Frequent Non-occlusive, with thrombo-emboli Small platelet aggregates/thrombi &/or thromboemboli

Syndrome Stable angina Unstable angina Sudden death

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Note
Aspirin inhibits formation of platelet thrombi and may prevent ischemic heart disease

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Microscopic Findings

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Microscopic findings
Prinzmetal angina and stable angina
No pathologic changes in myocardium

Unstable angina
Fibrosis of myocardium--- replaces dead myocytes

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Unstable angina fibrosis microscopic

Stress ECG
Screening test of choice for determining type of angina Positive test
ST depression Subendocardial ischemia; stable exertional angina ST elevation Transmural ischemia, Prinzmetal angina

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Coronary arteriography/angiography

Confirmatory test after a positive ECG stress test

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Myocardial infarction

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Myocardial infarction
Definition
Localized area of cardiac muscle necrosis due to ischemia

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MI
Usually caused by total occlusion of a coronary artery
By thrombus

By spasm

Mechanism
Coronary artery atherosclerosis with plaque rupture and superimposed thrombus Coronary artery spasm

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How an occlusion forms

Sudden change in morphology of an atheromatous plaque
Role of platelets Exposure to subendothelial collagen and necrotic plaque contents Platelets undergo adhesion, aggregation, activation, and release of potent aggregators Thromboxane A2 Serotonin Platelet factors 3 and 4 50

Intra-plaque hemorrhage Erosion Ulceration Rupture / fissuring

Vasospasm

Due to platelet aggregation, release of mediators Activate extrinsic coagulation pathway

Other mediators

Within minutes, thrombus evolves to completely occlude vessel lumen

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ECG
ECG will show specific infarct changes 6-8

hrs after infarction Transmural infarcts

Q wave changes (myocardial necrosis)

Subendocardial infarcts
No Q wave changes

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Q-waves ECG

Distribution

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Distribution of coronary artery thrombosis

Left anterior descending (LAD)= 40-50%
Right coronary artery (RCA)= 30-40% Left circumflex coronary artery (LCA)= 15-20%
POSTERIOR

Posterior wall of LV, posterior part of septum, RV

RCA LV LCA

Lateral wall of LV
LAD- Most common

RV

LAD

RCA- Intermediate
LCA- Less common

Anterior wall of LV, anterior part of septum

ANTERIOR

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Left circumflex coronary

Right coronary artery

Postero-inferior wall of LV, posterior 1/3rd of IV septum, RV, AV node

Lateral free wall of LV Left anterior descending coronary (LAD)

Anterior wall of LV, anterior 2/3rd of IV septum

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Important Slide!!!

((V1-3)

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Anterior infarct
LAD Occlusion of anterior descending branch (left anterior descending,) of left coronary artery; in anterior wall and adjacent 2/3rds of septum; involves entire circumference of wall near apex
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ECG anterior infarct

Leads V1, V2, V3

Postero-lateral infarct Occlusion of left circumflex artery Present in postero-lateral wall.

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Lateral infarct ECG

Leads I, aVF, V4-V6

Better lead I lateral infarct

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Posterior (inferior or diaphragmatic) infarct

Occlusion of right coronary artery; involves posterior wall, including posterior 1/3rd of inter-ventricular septum and posterior papillary muscle in basal half of ventricle

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Inferior or Posterior Infarct ECG

Leads II, III and aVF

Gross changes
Survival time <6-12 hrs Predominant finding No gross change

18-24 hrs
1-7 days 7-10 days > 6 weeks

Discrete pale to cyanotic areas Yellow and soft

Central pallor with a red border White, fibrous scar
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EM changes ( Make Millette happy)

Reversible 0- hr Irreversible -4 hrs Glycogen depletion; mitochondrial Swelling; relaxation of myofibrils Sarcolemmal disruption; Mitochondrial Amorphous densities

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