Cardio c reactive protein crp h nonspecific marker of

–
• Cardio C-reactive protein (CRP-h)
Nonspecific marker of inflammation C-reactive protein ( CRP ) is an annular (ring-
shaped), pentameric protein found in blood plasma, whose levels rise in response to
inflammation. It is an acute-phase protein of hepatic origin that increases following
interleukin-6 secretion by macrophages and T cells.
–
– Increased in many patients with CAD
– Chronic exposure to CRP triggers the rupture of plaques
• Endothelial alteration ®
– Platelets are activated
– Growth factor stimulates smooth muscle proliferation
– Cell proliferation entraps lipids, which are calcified over time and form an irritant
to the endothelium on which platelets adhere and aggregate
– Thrombin is generated
– Fibrin formation and thrombi occur
Developmental Stages
• Fatty streak
– Earliest lesions
– Characterized by lipid-filled smooth muscle cells
– Yellow tinge appears
– Reversible
• Raised fibrous plaque
– Beginning of progressive changes in the arterial wall
– Initiated by chronic endothelial injury
• Complicated lesion
– Final stage in development
– The most dangerous
– Plaque consists of a core of lipid materials within an area of dead tissue
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DYSRYTHMIAS/VALVULAR HEART DISEASE/CHEST PAIN
– With the incorporation of lipids, thrombi, damaged tissue, and accumulation of
calcium, the growing lesion becomes complex
Collateral Circulation
• Normally some arterial branching, termed collateral circulation, exists within the
coronary circulation
• When occlusion of the coronary arteries occurs slowly over a long period, there is a
greater chance of adequate collateral circulation developing
• Growth of collateral circulation is attributed to two factors:
– The inherited predisposition to develop new vessels
– The presence of chronic ischemia
• Collateral Circulation
•
Acute Coronary Syndrome
• Unstable Angina
• Non ST elevation MI
• ST elevation MI
Unstable angina:
• Classifications of Unstable Angina:
ACC/AHA Guidelines:
• NSTEMI is an acute process of myocardial ischemia with sufficient severity and duration
to result in myocardial necrosis.
• The initial ECG in patients with NSTEMI does not show ST-segment elevation.
• NSTEMI is distinguished from UA by the detection of cardiac markers indicative of
myocardial necrosis in NSTEMI and the absence of abnormal elevation of such
biomarkers in patients with UA.
• Myocardial infarction: acute, evolving, recent
• Typical rise and gradual fall (troponin) or more rapid rise and
fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the
following:
• a) ischemic symptoms;
• b) development of pathologic Q waves on the ECG;
• c) ECG changes indicative of ischemia (ST segment elevation
or depression); or
• d) coronary artery intervention (e.g., coronary angioplasty).
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DYSRYTHMIAS/VALVULAR HEART DISEASE/CHEST PAIN
•
Recommended Treatment:
• Class I: MONA
• Aspirin, Nitrate, B-blockers, morphine, O2 (prn).