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Dr. Pearl Myers

Path

Fall 2011

With acknowledgement to Dr SA

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Ischemic Heart Disease

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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)

Elevated by

Peak Returns to normal by

Total CK 4-6 hrs 12-24 hrs 3-4 days

CK-MB 2-4 hrs 24 hrs 2-3 days

Troponin I and T

2-4 hrs 48 hrs 7-10 days

LDH 24 hrs 3-6 days 8-14 days

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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.

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Angina Pectoris

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

ECG

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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

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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

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 (sub-

endocardial ischemia)

Coronary arteriography Severe, fixed CAD

atherosclerosis with >75% narrowing

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Variant Angina

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Prinzmetal’s 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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Cause1. 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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SyndromeStenose

s

PlaqueDisruptio

nPlaque-asso.

thrombus

Stable angina

>75% No No

Unstableangina

Variable Frequent Non-occlusive, with thrombo-

emboli

Suddendeath

UsuallySevere

Frequent Small plateletaggregates/thrombi&/or thromboemboli

Another handy chart

Note

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

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

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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Confirmatory test after a positive ECG stress test

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MI

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

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How an occlusion forms

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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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POSTERIOR

ANTERIOR

LV

RV LA

D

RCA

LCA

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Important Slide!!!

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((V1-3)

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ECG anterior infarct

Leads V1, V2, V3

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Lateral infarct ECGLeads I, aVF, V4-V6

Better lead I lateral infarct

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Inferior or Posterior Infarct ECGLeads II, III and aVF

Gross changes

Survival time Predominant finding

<6-12 hrs No gross change

18-24 hrs Discrete pale to cyanotic areas

1-7 days Yellow and soft

7-10 days Central pallor with a red border

> 6 weeks White, fibrous scar

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EM changes ( Make Millette happy)

Reversible 0-½ hr

Glycogen depletion; mitochondrialSwelling; relaxation of myofibrils

Irreversible ½-4 hrs

Sarcolemmal disruption;Mitochondrial Amorphous densities

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