C reactive protein
marker for inflammation
levels of 1-3 - moderate risk for coronary heart disease
atherosclerotic plaques - cause sustained chronic inflammation
prinzmetal angina
sustained vasospasm causing angina
cardiac raynaud
cold or emotion induced cardiac vasospasm
-> 20 mins - can lead to MI
takotsubo cardiomyopathy
dilated cardiomyopathy - secondary to emotional or physical stress with normal coronary angiogram
repeated bouts of vasospasm
cocaine
can cause vasospasm
sudden cardiac death
unexpected death from cardiac cause early after onset of symptoms (1-24 hours)
or sudden death from cardiac cause without acute symptoms
normally - lethal arrhythmia - V-fib
caused by IHD
channelopathies
K, Na, Ca channel problems
-most autosomal dominant
brugada syndrome
ST elevation and RBBB
syncope or sudden cardiac death during rest, sleep, after large meals
CPVT syndrome
childhood life threatening arrhythmias
-stress induced
no EKG changes
change in diastolic Ca release
non-ischemic SCD
people < 40yo
majority hypertrophic cardiomyopathy
commotio cordis
set off arrhythmia by poking individual in chest
chronic IHD
CHF in pt with previous MIs and angina
LVH and dilation
myocardial fibrosis - past MI
arrhythmia, CHF, MI develop
myocyte hibernation
chronic ischemia that does not cause necrosis - hypokinetic myocardium
angina pectoris
recurrent substernal discombort
ischemia falling short of inducing necrosis
stable angina
with exertion
goes away with rest
unstable angina
crescendo
- acute plaque change
- may occur at rest
prinzmetal angina
coronary vasospasm
-relieved with rest, nitro, and CCBs
longer than 20 minutes
kill myocytes
MI
death of cardiac muscle from ischemia
more in men
> 65 yo higher risk
stain for MI
triphenyltetrazolium chloride
- viable - red
- non-viable - pale
transmural infarct
more than half - around 75%
subendo infarct
less than half
balloon angioplasty
do within 6 hours
-after this time - unsalvagable necrosis
gross changes with MI
dark mottling by 12 hours
1-3 days yellow-tan infarct center
1 week hyperemic border with yellow-tan softening
10 days yellow-tan/soft depressed red-tan margins
2 weeks red-gray borders
2 months - white scar
micro changes with MI
waviness - earliest change - 4 hours or so 4-12 hrs - coaguative necrosis 12-24 hours - neutrophils 1-3 days - lots of neutrophils 3-7 days early phagocytosis 7-10 days granulation tissue forms at margins 10-14 days lots of granulation tissue 2-8 weeks - collagen deposition 2 months - dense collagen scar
MI with neutrophils
1-3 days old
MI with no neutrophils
less than 1 day old
MI with macrophages
1 week old
MI with granulation tissue and collagen
2 weeks old
MI with pure scar
months old
occluded LAD
most common
widowmaker
occluded RCA
arrhythmias
MI reperfusion techniques
lysis - tPA, streptokinase, urokinase
bypass graft
-balloon angioplasty
with thrombolytic drugs - cannot do procedure until drugs are gone**
reperfusion after 6 hours
does not reduce MI size
stunning
viable tissue but non-functional after MI
-is reversible
reperfusion 2-4 hours after MI
pathology of reperfusion
arrhythmias
hemorrhage with contraction bands
no-reflow (capillary closure)
-stunning
MI clinical Sx
chest pain, radiate left arm, neck, jaw
weak pulse rapid
sweating
nausea
dyspnea
STEMI
transmural
NSTEMI
subendocardial
troponins for heart
I and T
slower rise and fall
5 to 10 days to fall
CK for heart
CK-MB
quick rise and fall
decreased by 2-3 days
myoglobin
used to exclude MI
-no myoglobin - no MI
yes myoglobin - could be lots of reasons
quick rise and fall - decreased by 24 hours
serial cardiac enzymes
taken every 2 hours or so
CK-MB low and troponin high
more than 3 days ago
CK-MB high and troponin high
current MI
complications of MI
myocardial rupture - VSD, papillary (regurg), cardiac tamponade
pericarditis
right ventricular infarction
infarct extension and expansion (dilation and thinning of heart)
mural thrombus
ventricular aneurysm