CVPR Week 4: CAD Flashcards
Objectives
Case 1 ECG
Case 1 ECG
What does this indicate and why?
Identify
Identify
Identify
Identify
Identify
Identify
Question 2 of ECG 1
Ck levels
came in almost normal around 300 then rose massively
Temporary occlusion with reperfusion
the earlier the reperfusion the better
still viable until around 20 minutes
Atherosclerosis onset
Atherosclerotic plaque cartoon
fibrous cap
composed of collagen and smooth muscle cells
the goal of the fibrous plaque is to wall off the lipid pool from the circulating blood
Atherosis & sclerosis
Factors that predispose a plaque to stability
3 listed
- Dense fibrous cap
- Smooth muscle cell hyperplasia
- Laminar flow
Factors that predispose a plaque to instability
4 listed
- Production of inflammatory cytokines, proteases, vasoactive molecules (breakdown of collagen and causes instability)
- Activated macrophages, mast cells, T cells (inflammatory plaque)
- LArge lipid core/oxidized LDL
- Low levels of NO
blood becomes exposed if the fibrous capsule breaks open and blood meets with the lipids and a clot forms
Segments of coronary artery in different stages of CAD
Atherosis features
4 listed
Sclerosis features
3 listed
Factors predisposing a plaque to stability
3 listed
Factors predisposing a plaque to instability
3 listed
Instability of a plaque results in?
Acute coronary syndrome
Acute coronary syndrome Features
3 listed
Acute coronary syndrome symptoms
3 listed
- can be subclinical/assymptomatic
- can result in unstable angina and NSTEMI
- can result in complete thrombotic occlusion STEMI
Acute coronary syndrome types
4 listed
- Asymptomatic/subclinical
- Unstable angina (NSTEACS)
- NSTEMI (NSTEACS)
- STEMI
Stable ischemic heart disease possibilities
2 listed
- chronic stable angina
- asymptomatic CAD
Acute coronary syndromes vs stable ischemic heart disease
Segments of CAD
in the vulnerable stage - although there is a large atherosclerotic plaque however it doesn’t impinge upon the lumen of the coronary artery (this would be asymptomatic)
When ruptured thrombosis occurs due to tissue factors and thrombogenic factors in the lipid plaque
obstructive is stenosis (could be stable angina or stable ischemic heart disease) This would be considered a stable atherosclerotic plaque)
troponin is a biomarker for?
myocardial injury indicating MI
Case #2
What is the diagnosis?
A. Unstable Angina
B. NSTEMI
C. STEMI
D. Aortic Dissection
E. Anxiety
Correct answer is NSTEMI because the troponin is indicative of myocardial damage and it isn’t a STEMI because there is no ST elevation on the EKG
Case #3
exercise induced chest tightness, stop and rests it goes away, primary care orders stress test
How is typical angina diagnosed?
3 listed
- Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief
- provoked by exertion or emotional stress
- relieved by rest or NTG
A sudden onset and peak intensity immediately is most likely?
Not typical angina
How is atypical angina diagnosed?
- Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief
- provoked by exertion or emotional stress
- relieved by rest or NTG
Meets 2 of the above characteristics
How is non-cardiac chest pain diagnosed?
Meets one or none of the typical angina characteristics shown below
- Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief
- provoked by exertion or emotional stress
- relieved by rest or NTG
Clinical features of Acute MI
Chances of having CAD table
How is CAD clinically classified?
3 listed
- ischemic heart disease
- vs
- STEMI (unstable angina, NSTEMI, STEMI) may not occur with exertion or emotional stress and may not resolve with NO or rest
Case #3 Stress test
Which of the following would not be useful to reduce this patient’s angina burden?
A. Start metoprolol 25 mg BID
B. increased Nifedipine 30 to 60 mg
C. start isosorbide mononitrate 30 mg daily
D. increase aspirin from 81 to 325 mg daily
E. All of the above would be useful
metoprolo will help his angina by reducing HR and contractility
nifedipine Ca blocker will reduce contractility
isosorbide yes by dilation
aspirin no
Statin no doesn’t decrease the burden of angina, howerver would help prevent future events
Anti-anginal therapy
6 listed
top 3 the most important Rxs
Angina basic pathophysiology
myocardial O2 demand > supply
Non-cardioselective β-blockers: effect on vascular tone
↑
Atenolol vs placebo for angina
3 listdd
- weekly angina attack rate goes down and weekly consumption of Nitroglycerine goes down
- exercise ability increases
- ST depression degree of ST-segment depression decreases
Treadmill time on Ca2+ blockers
Exercise duration on nitrates
Case #4
Case #4
Complications after AMI
6 listed
lab levels hours after MI
Lab value typically used to Dx MI
Troponin i
Identify
Case #5
Which of the following has been shown to reduce future CV events?
A. Aspirin 81mg/day
B. Atorvastatin 80mg/daily
C. Regular aerobic exercise
D. Smoking Cessation
E. All of the above
All of the above
Question
What are the major players in MI?
platelets stick to the lipid core after a rupture and promote thrombus formation
Platelets in MI
5 listed
- platelets stick
- Expression of adhesions molecules result in the ability to “stick”
- As a consequence of adherence, platelets become activated and aggregate
- Release of cytokines and growth factors consequent to platelet activation (along with thrombin)
- Platelet membrane facilitates thrombin activation and propagation of thrombosis
Statins and pleitropism
statins do a lot
- reduced lipid levels
- lower oxidized LDL
- lower macrophages
- lower T cell count
- lower apoptotic cells (TUNEL)
- Increased Smooth muscle cells
Lipid levels and CVA
lower LDL or closer to 70 the lower the clinical event rate
Targeting therapy for a beneficial balance
Conclusion
