Professional Documents
Culture Documents
DISEASE
Pages 374-385
https://www.facebook.com/pages/Human-Pathology/169869373198364
VARIANTS
STABLE OR TYPICAL ANGINA
Episodic chest pain due to exertion, emotional excitement or any cause leading to
increased cardiac workload (> 70% stenosis), relieved by rest and nitroglycerine
(vasodilator)
Percent of Population
80 73.3 72.6
70
Estrogen
40
30
20 15.9
7.8
10
0
20-39 40-59 60-79 80+
Men Women
LAD
RCA
Infarction of the Right Ventricle is rare, because the right side has far less
demand for oxygen. Right Ventricular infarcts are usually extensions of
posterior septal infarcts caused by occlusion of the Right Coronary Artery.
GRADES
Coronary atherosclerosis or stenosis is graded as follows.
Unstable Stable
Lack of
Inflammatory inflammatory
cells cells
Thin Thick
Few fibrous cap More fibrous cap
SMCs SMCs
Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells
Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with permission from Cannon CP.
Atherothrombosis slide compendium. Available at: www.theheart.org.
Coronary Atherosclerosis
TRANSMURAL INFARCT
Infarct extending from epicardium to endocardium (full or nearly full
thickness of ventricular wall,
(caused by occlusion of major coronary epicardial trunk or major secondary epicardial
branches- shows ST segment elevation, negative Q wave with loss of R wave amplitude in ECG-
STEMIs)
SUBENDOCARDIAL INFARCT
Diffuse, circumferential infarct, around the subendocardium limited to inner 1/3 of
ventricular wall
(caused by shock, CHF, hypotension, tachycardia, hypertensionor anything that results in
inadequate blood supply to the coronary arteries or lysed coronary thrombus No ST segment
elevation or negative Q wave in ECG- Non-STEMIs)
MICROSCOPIC INFARCTS
(Occur in small vessel occlusion and may not show any diagnostic ECG changes seen in vasculitis,
embolization of valve vegetations or vessel spasm due to elevated catecholamines.
RECOGNITION OF ACUTE MYOCARDIAL INFARCTION
BY PATHOLOGIC METHODS
ECG FINDINGS
Transmural infarction shows Q waves or loss of R waves
Non transmural infarction shows transient ST -segment & T wave changes
CARDIAC IMMAGING
Chest x-ray, Echocardiogram, CT, MRI, Nuclear imaging, Coronary
angiography
Common serum markers used to detect AMI
Marker Initial Mean time to Time to return to
elevation peak elevation baseline after AMI
after AMI after AMI
Myoglobin 1-4h 6h 18 - 24 h
CK-MB 2-4h 10 - 24 h 48 - 72 h
cTnI 2-4h 24 - 48 h 5 - 10 days
cTnT 2-4h 24 - 48 h 5 - 14 days
Treatment of Coronary Thrombosis
IN HOSPITAL
Uncomplicated cases (10-20%)
Complicated cases (80-90%)
Cardiac arrhythmia (75-95%)
LVF & Mild to moderate pulmonary edema (60%)
Cardiogenic Shock (10%)
Rupture of free wall, septum or papillary muscles (4-8%)
Thromboembolism (15-49%)
OTHER COMPLICATIONS
PERICARDITIS
Fibrinous or fibrino-hemorrhagic type is encountered in patient with acute
transmural MI on 2 nd or 3 rd day, responds to aspirin
DRESSLER SYNDROME (postmyocardial syndrome)
It is a delayed autoimmune pericarditis, pleuritis and/or pneumonitis that
occurs following cardiac surgery or myocardial infarction. It is
characterized by pleuro-pericardial chest pain and fever. Develops within
few days to 6 weeks. Respond to aspirin
THROMBOEMBOLISM
Observed in15-49% of cases, occur in association with large infarct, hear
failure and left ventricular thrombosis. Results due to abnormality in the
contractility with endocardial damage.
Treatment: systemic anticoagulant
INFARCT EXPANSION
It is disproportionate stretching, thinning and dilatation of the infarcted region
(especially with anteroseptal infarcts), which is often associated with mural
thrombosis. Early MI expansion likely provides the substrate for scar thinning
and late aneurysm formation.
Large transmural infarcts lead to cardiogenic shock, arrhythmia and late congestive
heart failure
Anterior infarcts are commonly complicated by regional dilatation, mural thrombi &
rupture
Posterior/inferior infarcts are accompanied by serious conduction blocks
Subendocardial infarcts are rarely complicated by pericarditis, rupture and ventricular
aneurysm
Right ventricular infarction is characterized by jugular venous distension, Kassmaul s
sign & hepatomegaly (with or without hypotension).
VENTRICULAR REMODELING
Noninfarcted regions undergo hypertrophy and dilation; in combination with the scarring and
thinning of the infarcted zones
Morphology
Moderate to severe coronary atherosclerosis
Cardiomegaly
Myocardial hypertrophy
Dilation of all cardiac chambers
Myocardial fibrosis
Myocytolysis
Cause of Death
Arrhythmia, CHF,MI
SUDDEN CARDIAC DEATH