cvs lab dxami-csbrp
TRANSCRIPT
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v1-NOV-2014-CSBRP
Lab Diagnosis of AMI
CSBR.Prasad, MD.,
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PM angiogram: Posterior aspect of the heart of a patient who died of AMI.
Total occlusion of the distal right coronary artery by an acute thrombus (arrow)
and
Large zone of myocardial hypoperfusion involving the posterior left and right ventricles, as indicated by arrowheads.
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v1-NOV-2014-CSBRP
Temporal sequence of early biochemical findings and progression of necrosis after
onset of severe myocardial ischemia.
A, Early changes include loss of adenosine triphosphate (ATP) and accumulation of lactate.
B, For approximately 30 minutes after the onset of even the most severe ischemia, myocardial injury is
potentially reversible.
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v1-NOV-2014-CSBRP
Progression of myocardial necrosis after coronary artery occlusion
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v1-NOV-2014-CSBRP
Distribution of myocardial ischemic necrosis correlates with the location and nature of decreased perfusion
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v1-NOV-2014-CSBRP
Patterns of Infarction• Transmural infarction
– Necrosis involves the full thickness of the ventricular wall
• Subendocardial (nontransmural) infarction– Necrosis involving inner third of the ventricular wall
• Multifocal microinfarction– pathology involving only smaller intramural vessels– occur in the setting of microembolization, vasculitis, or
vascular spasm– Eg: Takotsubo cardiomyopathy (“broken heart
syndrome” )
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v1-NOV-2014-CSBRP
Patterns of Infarction - ECG
Owing to the characteristic ECG changes resulting from myocardial ischemia or necrosis in various distributions:
• Transmural infarct is referred to as an “ST elevation myocardial infarct” (STEMI) and
• Subendocardial infarct as a “non–ST elevation infarct” (NSTEMI)
• Microinfarctions show nonspecific changes or can even be electrocardiographically silent
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v1-NOV-2014-CSBRP
Infarct Modification by Reperfusion“time is myocardium”
• Reperfusion: is the restoration of blood flow to ischemic myocardium threatened by infarction
• The goal: is to salvage cardiac muscle at risk and limit infarct size– Prompt reperfusion is the preeminent objective for treatment of
patients with AMI– This can be accomplished by a host of coronary interventions:
• Thrombolysis• Angioplasty• Stent placement or • CABG
The first 3 to 4 hours following obstruction are critical
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v1-NOV-2014-CSBRP
Typical appearance of reperfused myocardium:Large, densely hemorrhagic, anterior wall acute myocardial infarction treated with streptokinase,
(triphenyl tetrazolium chloride - stained heart slice)
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v1-NOV-2014-CSBRP
Microscopic features of MI and its repair One-day-old infarct
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v1-NOV-2014-CSBRP
Microscopic features of MI and its repair MI 3-4 days old
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v1-NOV-2014-CSBRP
Microscopic features of MI and its repairMI 7-10 days old
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v1-NOV-2014-CSBRP
Microscopic features of MI and its repairGranulation tissue
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v1-NOV-2014-CSBRP
Microscopic features of MI and its repairHealed myocardial infarct
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v1-NOV-2014-CSBRP
Effects of reperfusion on myocardial viability and function
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v1-NOV-2014-CSBRP
Reperfusion
• Reperfusion not only salvages reversibly injured cells but also alters the morphology of lethally injured cells
• The effects of reperfusion on myocardial viability and function:
• Clearly beneficial• Can trigger deleterious complications:
– Arrhythmias– Reperfusion injury– Endothelial swelling that occludes capillaries (no-reflow)– Biochemical abnormalities may also persist for days to weeks in
reperfused myocytes• Stunned myocardium• Hibernation
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v1-NOV-2014-CSBRP
Clinical Features of AMI• Prolonged chest pain
– > 30 minutes– Crushing, stabbing, or squeezing– Retrosternal – Radiating to left arm along ulnar border– Associated with profuse sweating– Nausea and vomiting (involvement of posterior-inferior
ventricle with secondary vagal stimulation)• No chest pain
– Diabetic neuropathy– Cardiac transplants
• Dyspnea
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v1-NOV-2014-CSBRP
Laboratory diagnosis of AMI
• The laboratory evaluation of MI is based on measuring the blood levels of proteins that leak out of irreversibly damaged myocytes– Cardiacspecific troponins T and I (cTnT and cTnI) – Creatine kinase (CK-MB) – LDH– AST– Myoglobin
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v1-NOV-2014-CSBRP
Laboratory diagnosis of AMI
• Time to elevation of CK-MB, cTnT and cTnI is 3 to 12 hrs
• CK-MB and cTnI peak at 24 hours• CK-MB returns to normal in 48-72 hrs, cTnI
in 5-10 days, and cTnT in 5 to 14 days
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v1-NOV-2014-CSBRP
Laboratory diagnosis of AMI
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v1-NOV-2014-CSBRP
Basic principles of management• Half of the deaths associated with acute MI occur within 1 hour of
onset, most commonly due to a fatal arrhythmia• AMI therapeutic interventions include:
– Morphine to relieve pain and improve dyspneic symptoms– Prompt reperfusion to salvage myocardium– Antiplatelet agents such as aspirin, P2Y12 receptor inhibitors, and
GPIIb/IIIa inhibitors– Anticoagulant therapy with unfractionated heparin, low-molecular-weight
heparin, direct thrombin inhibitors, and/or factor Xa inhibitors to prevent coronary artery clot propagation
– Nitrates to induce vasodilation and reverse vasospasm– Beta blockers to decrease myocardial oxygen demand and to reduce
risk of arrhythmias– Antiarrhythmics to manage arrhythmias– Angiotensin-converting enzyme (ACE) inhibitors to limit ventricular
dilation– Oxygen supplementation to improve blood oxygen saturation
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v1-NOV-2014-CSBRP
Prognostic factors in AMI
Factors associated with a poorer prognosis include:
• Advanced age• Female gender• Diabetes mellitus, and• Previous MI (cumulative effect)
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v1-NOV-2014-CSBRP
Complications of AMI1. Contractile dysfunction
– Cardiogenic shock2. Arrhythmias3. Myocardial rupture4. Ventricular aneurysm5. Pericarditis6. Infarct expansion7. Mural thrombus8. Papillary muscle dysfunction9. Progressive late heart failure (Chronic IHD)
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v1-NOV-2014-CSBRP
Complications of AMIAnterior myocardial rupture in an acute infarct (arrow)
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v1-NOV-2014-CSBRP
Complications of AMIComplete rupture of a necrotic papillary muscle
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v1-NOV-2014-CSBRP
Complications of AMI Fibrinous pericarditis - Dressler syndrome
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v1-NOV-2014-CSBRP
Complications of AMI Mural thrombus
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v1-NOV-2014-CSBRP
Complications of AMI Large apical left ventricular aneurysm
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v1-NOV-2014-CSBRP
Causes and outcomes
of IHD
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v1-NOV-2014-CSBRP
Chronic Ischemic Heart Disease• Def: Progressive congestive heart failure as a
consequence of accumulated ischemic myocardial damage and/or inadequate compensatory responses
Causes:• Chronic IHD usually appears postinfarction due
to the functional decompensation of hypertrophied noninfarcted myocardium
• Severe obstructive coronary artery disease may present as chronic congestive heart failure in the absence of prior infarction
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v1-NOV-2014-CSBRP
Chronic IHD - MorphologyGross:• Cardiomegaly• Stenotic coronary atherosclerosis• Discrete scars representing healed infarcts • Mural endocardium often has patchy fibrous thickenings• Mural thrombi may be presentMicroscopic findings include:• Myocardial hypertrophy• Diffuse subendocardial vacuolization, and • Fibrosis