ACS Flashcards
Coronary angiography
We access the arterial artery through peripheral artery could be initially femoral Nowdays standard is radial artery , we place against the blood flow catheters that are tubes that we are able to inject contrast.
We place this catheters at the origin of the aorta and into the coronary artery Ostia and we inject contrast and we look different radiological incidents ,contrast means radio opaque substance and try to characterise the anatomy of coronary arteries and associated anomalies
Acute coronary syndrome
Suspicion acute ischaemia with or without infarction
Atherothrombosis
UA,Stroke,SCD,AMI,Peripheral Ischaemia
Criteria for type 1 MI due to atherothrombosis
- Symptoms AMI
- New ischemic ECG changes
- > severe degree 02 supply decrease - increased troponin
- Path.Q waves
- Image : loss myoc
- Thrombus identification
Type 2 MI
Secondary to illness e.g. Anemia,hypotension,shock
Due to atherosclerosis,vasospasm,02 supply decreased , increased O2 demand
so 02 supply is not the main mechanism
Type 3 MI
SCD
Died before blood sample
When autopsy reveals MI -
Type 4A MI
- coronary intervention
- new ischemic changes
Type 4B MI
- stent thrombosis
Type 4C MI
-Interstent re stenosis
Troponin rise/fall
With ischemia-> acute MI -> ATS / thrombosis
W/o ischemia -> AMI
ACS W/o ST elevation
NSTEMI,UA
ACS With ST elevation
STEMI , NON Q,Q-AMI
AMI vs US
Increased biomarkers myoc.necrosis (Tn)
NSTEMI vs STEMI
Incomplete +/- intermittent coronary occlusion
AMI
- Acute chest discomfort, retrosternal
- Radiates to left arm, neck, Jaw
- Sweating ,dyspnea, nausea syncope
- Cardiac arrest
- Electric instability : VAS,Bradyarrhythmia,SVT
- Pneumodynamic shock(cardiogenic)
- Systemic embolism due to LV thrombi ( UA < AMI)
ECG
- ST changes: persistent: STEMI , new LBBB
- T wave inversion or flat
- new q wave or loss R wave ( STEMI vs NSTEMI )
- pseudonormalisation of T wave
NSTEMI
ST segment depression ,transient ST elevation ,
Isolated T wave inversion
Biomarkers
-Troponin: N <0.4 μg/L-> Tachyarrh,HF,HTN,Myoc.
- LV dysfunction: BNP/NT -pro-BNP
-CRP
OTHERS: CBC , HbAic,eGFR: Creatinine, lipids ,chol
Persistent occlusion
Release enzymes slow
Rule out
Angiography,stress test,CCTA
Echo
-Can be normal
-New ventricle wall motion a anomalies
Effect on LVEF
- Complications:MR, left ventricle wall rapture, tamponade coma left ventricle thrombus
-Additional : Contrast echo -> decreased perfusion,stress test ,XRay,CCTA,SPECT,CMRI
Culprit lesion
Not a logical features suggestive of acute plaque rupture)
- Intraluminal filling defects consistent with thrombus
- Plaque ulceration
- Plaque irregularly
Type UA
De novo < 3M,class II,III At rest (esp. > 20”)-> MI CRESCENDO( class III) Early postAMI noctural Prinzmetal
Positive Tall R waves in V1,V2 or early R wave transition
WPW syndrome for left accessory pathway
If it is a transient occlusion the release of enzyme will be
earlier and the peak will be earlier and the persistence will be shorter
Additional Imaging Methods
Useful for differential diagnosis and/or unraveling latent myocardial ischemia - Chest X-RaY - CT CCTA -SPECT -cMRI ( stress)