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faster man,
VARIANTS
STABLE OR TYPICAL ANGINA
Exertional, emotional excitement or any cause leading to increased
cardiac workload (> 75% stenosis)
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
Blood clot: mass of coagulated blood formed in vitro or in stagnant column of blood
Hematoma: extravasular accumulation of blood clot into tissues.
Hemostatic plugs: simplest form of thrombus formed in healthy individuals at the site
of bleeding
COMPOSITION OF THROMBUS
LOCATION OF THROMBI
Arteries, veins, heart chambers, heart valves
TYPES OF THROMBI
Arterial vs. venous;
bland vs. septic
PATHOGENESIS OF THROMBOSIS
(Predisposing Factors)
Virchows Triad
Endothelial injury (in atherosclerosis)
Stasis or turbulence of blood flow
Blood hypercoagulability
MYOCARDIAL RESPONS
Early biochemical changes (CPK & ATP) within seconds loss of contractility within
60 Sec.
Irreversible cell injury20-40 min
Microvascular injury>1 hr
Permanent damage to the heart occurs when the perfusion of the myocardium is
severely reduced for an extended interval (usually at least 2 to 4 hours)
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)
SUBENDOCARDIAL INFARCT
Diffuse, circumferential infarct, around the subendocardium
limited to inner 1/3 or at most of ventricular wall
(caused by shock, CHF, hypotension, or anything that results in inadequate blood
supply to the coronary arteries or lysed coronary thrombus )
RECOGNITION OF ACUTE MYOCARDIAL INFARCTION
BY PATHOLOGIC METHODS
Reperfusion injury by generation of O2 free radicals , infiltrating WBC & calcium overload can
cause some small amount of new cellular damage due to prominent apoptosis, and can induce
microvascular injury can cause hemorrhage & endothelial cell swelling that occludes capillaries
& prevent local reperfusion to areas of critically injured myocardium. It may induce arrhythmia
& hibernation.
Salvaged part may show stunned myocardium (prolonged postischemic ventricular dysfunction)
In any moment of decision the best thing you
can do is the right thing, the next best thing is
the wrong thing, and the worst thing you can
do is nothing.
CLINICAL PRESENTATION
SYMPTOMS
PAIN
(deep, visceral) heavy squeezing, crushing, stabbing or burning, more severe than
angina pectoris and lasts longer, typically it is in central portion of chest and/or
epigastrium and on occasion it radiates to arm, neck, jaw & shoulder, not relieved by
NTG.
(D/D acute pericarditis, pulmonary embolism, acute aortic dissection,
costochondritis etc.)
Painless infarction is seen in elderly and in patients with diabetes mellitus-(Silent or
asymptomatic infarction- 10-15%)
DYSPNEA
ANXIETY
NAUSEA & VOMITING
WEAKNESS
COLLAPSE & SYNCOPE
SUDDEN DEATH
SIGNS
SYMPATHETIC ACTIVATION
Tachycardia, hypertension, sweating, pallor
PARASYMPATHETIC ACTIVATION
Bradycardia, hypotension, nausea, vomiting.
ECG
SERUM CARDIAC MARKERS
CARDIAC IMMAGING
NON-SPECIFIC INDICES OF TISSUE NECROSIS &
INFLAMMATION
ECG
Acute inferior myocardial infarction: ST elevation in the inferior leads II, III
and aVF reciprocal ST depression in the anterior leads
Chest x-ray
Echocardiogram
Computed tomography (CT) scan
Magnetic resonance imaging (MRI)
Magnetic resonance angiography (MRA)
Nuclear imaging (MUGA scan, Thallium stress test, SPECT & PET test)
Other imaging tests
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.
VENTRICULAR REMODELING
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
Morphology
Marked Coronary atherosclerosis: one or more 3 coronaries > 75% occlusion is present in
80-90%
50% show acute placque disruption & 25% show MI
Most die of ischemic malignant Ventricular Arrhythmia
(channelopathies, long QT syndrome, short QT syndrome, WPW syndrome, Sick sinus syndrome )
PERICARDITIS
INFECTIOUS AGENTS
ACUTE Viruses
<6 WEEKS Pyogenic becteria
Tuberculosis
Fungi
Other parasites
MISCELLANEOUS
Myocardial infarction
Uremia
Following cardiac surgery
CHRONIC Neoplasia
>6 MONTHS Trauma
Radiation