PATH - Myocardial Infarction Flashcards
Myocardial infarction
Most often acute thrombosis due to rupture of coronary artery atherosclerotic plaque.
Commonly occluded coronary arteries: LAD > RCA > circumflex.
SX
diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw,
shortness of breath, fatigue
cardiac biomarkers (CK-MB, troponins) are diagnostic
-Cardiac troponin I rises after 4 hours (peaks at 24 hr) and is for 7–10 days; more specific
than other protein markers
-CK-MB rises after 6–12 hours (peaks at 16–24 hr)Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours.
ST-segment elevation MI (STEMI)
Transmural infarcts
Full thickness of myocardial wall involved
ST *elevation
*Q waves
Non–ST-segment elevation MI (NSTEMI)
Subendocardial infarcts
Subendocardium (inner 1⁄3) especially vulnerable to ischemia
ST *depression
0–24 hr
GROSS
Dark mottling; pale with
tetrazolium stain
LIGHT MICROSCOPE
- Early coagulative necrosis, release of necrotic cell contents into blood
- edema, hemorrhage, wavy fibers.
- Neutrophils appear.
- Reperfusion injury, associated with generation of free radicals, leads to hypercontraction of myofibrils
COMPLICATIONS
Ventricular arrhythmia
HF
cardiogenic shock
1–3 days
GROSS
Hyperemia
LIGHT MICROSCOPE
- Extensive coagulative necrosis.
- Tissue surrounding infarct shows acute inflammation with neutrophils.
COMPLICATIONS
Postinfarction fibrinous pericarditis
3–14 days
GROSS
Hyperemic border; central yellow-brown softening maximally yellow and soft by 10 days
LIGHT MICROSCOPE
Macrophages, then granulation
tissue at margins
COMPLICATIONS -Free wall rupture-->tamponade -papillary muscle rupture-->mitral regurgitation -interventricular septal rupture due to macrophage-mediated structural degradation. -LV pseudoaneurysm
2 weeks to several months
GROSS
- Recanalized artery
- Gray-white
LIGHT MICROSCOPE
Contracted scar complete
COMPLICATIONS
Dressler syndrome, HF, arrhythmias, true ventricular
aneurysm (risk of mural
thrombus).