cvs lab dxami-csbrp

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v1-NOV-2014-CSBRP Lab Diagnosis of AMI CSBR.Prasad, MD.,

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Page 1: Cvs lab dxami-csbrp

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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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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Progression of myocardial necrosis after coronary artery occlusion

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Distribution of myocardial ischemic necrosis correlates with the location and nature of decreased perfusion

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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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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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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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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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Microscopic features of MI and its repair One-day-old infarct

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Microscopic features of MI and its repair MI 3-4 days old

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Microscopic features of MI and its repairMI 7-10 days old

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Microscopic features of MI and its repairGranulation tissue

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Microscopic features of MI and its repairHealed myocardial infarct

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Effects of reperfusion on myocardial viability and function

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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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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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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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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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Laboratory diagnosis of AMI

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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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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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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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Complications of AMIAnterior myocardial rupture in an acute infarct (arrow)

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Complications of AMIComplete rupture of a necrotic papillary muscle

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Complications of AMI Fibrinous pericarditis - Dressler syndrome

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Complications of AMI Mural thrombus

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Complications of AMI Large apical left ventricular aneurysm

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Causes and outcomes

of IHD

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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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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