MI Flashcards
(58 cards)
1
Q
Risks for Atherosclerosis
A
- Age, sex (male), total cholesterol, HDL cholesterol, smoking, DM, HTN, family history of premature CVD (Framingham heart study)
- inter heart study then added: abdominal obesity, psychosocial index, Apo A/B ratio, exercise, alcohol (which actually seen to be protective)
- newer risks: CRP, lipoprotein A (inherited risk factor, elevated in 20% of the population), chronic loud noise exposure, sedentarism
- inflammation is a risk! SLE, RA, psoriasis, IBD, COPD, HIV, etc.
2
Q
CVD in developing countries
A
- low education has greater impact on CVD risk in low income countries
- majority of CVD deaths are in lower income countries
3
Q
Framingham risk score
A
Low - <10% 10 year risk
Intermediate - 10-20% 10 year risk
High - >20%10 year risk
4
Q
Who can benefit from statins?
A
- LDL over 5, DM, CKD, ASCVD
- people with increased systemic inflammation but normal cholesterol
5
Q
How does stress affect CVD?
A
- increases SNS/ HPA axis/ HTN/ insulin resistance
6
Q
Cholesterol
A
- made by all cells except mature RBCs
- major constituent of plaque
- component of cell membranes, steroid and bile acid synthesis
input: diet and synthesis
output: bile acids and biliary cholesterol
7
Q
Triglycerides
A
- main dietary and endogenous fat
- main source of immediate and stored energy
- carried by chylomicrons and VLDLs
- water insoluble lipid that must be solubilized and transported by lipoproteins (along with cholesterol)
8
Q
Size of lipoproteins and their respective compositions
A
- chylomicrons < VLDLs < LDLs < HDLs
- smaller are more triglycerides, larger are more cholesterol/ phospholipids/ proteins
9
Q
Journey of fat through the body
Different methods of entry into SI?
A
- Emulsified fats are digested by lipase/ co-lipase
- Cholesterol esters are digested by pancreatic lipase/ co-lipase into cholesterol and FFAs
- monoglycerides and FFAs diffuse into SI
- cholesterol enters via NPC1L1 transporter
- these products are re-combined to form chylomicrons, which travel through the body via lymph
10
Q
Role of lipoprotein lipase (LPL)
A
- sits on capillaries to digest TGs and deliver FAs to issues for energy (similar role in VLDL catabolism)
11
Q
Role of VLDL
A
- body’s means of delivering FAs to tissues for energy, even when fasting
- synthesized by the liver using MTP
12
Q
How is LDL broken down?
A
- binds to LDL receptors and internalized
- hydrolyzed in a lysosome into cholesterol and amino acids
- results in decreased HMG CoA reductase, decreased LDL receptors, and increased ACAT (produces cholesterol oleate with excess cholesterol)
13
Q
Definition of dyslipidemia
Primary vs secondary
A
- increased cholesterol and/or triglycerides and/or low HDL-C
- Primary - genetic, often severe lipid elevations (cholesterol over 6.5 and LDL-C over 4.5 and TG over 3)
- Secondary - diet/ obesity/ DM/ etc, often minor elevations
14
Q
Signs of genetic hyperlipidemia?
A
- tendon/ palmar/ eruptive xanthomas
- xanthelasma
- corneal arcus
15
Q
Examples of genetic dyslipidemia
A
- Familial hypercholesterolemia - mutations in LDL receptor/apoB, increased function of PCSK9
- Dysbetalipoprotenemia - apoE2:E2 and overproduction of VLDL
- Lipoprotein lipase deficiency - no LPL activity
- Tangier disease - no ABCA1 activity (responsible for HDL formation)
16
Q
Fat targets if low/ med/ high risk?
A
Low risk - LDL under 2.5, ApoB under 0.85, non HDL under 3.2
Med risk - LDL under 2, ApoB under 0.8, non HDL under 2.6
High risk - LDL under 1.8, ApoB under 0.7, non HDL under 2.4
17
Q
Preferred fuel of heart when fasting?
What does the myocardium depend on?
A
- FFAs
- totally relies on aerobic metabolism (need enough ATP for cross bridge cycling in sarcomeres, can only be achieved if O2 is present)
18
Q
What does the LMCA supply?
(originates from L sinus of valsalva)
A
- L anterior descending supplies anterior wall of the L ventricle and most of the inter ventricular septum
- Circumflex supplies the lateral wall of the L ventricle
19
Q
What does the RCA supply?
(originates from the R sinus of valsalva)
A
- SA and AV nodes
- RV and posterior inter ventricular septum
20
Q
What are the conductance vs resistance vessels of the heart?
A
Conductance - epi/myocardial penetrating vessels
Resistance - arterioles and pre-capillary sphincters
21
Q
How is coronary flow affected by diastole? With ischemia, which part of the heart suffers first?
A
- coronary flow to the LV is almost ALL diastolic
- in systole, aortic root pressure is equal to LV pressure, thus almost no coronary flow
- diastolic root pressure is higher than diastolic LV pressure, and so duration of diastole is important
- endocardial ischemia will occur earlier and more severely
*Coronary perfusion gradient = aortic root pressure - LV pressure
22
Q
Methods of Coronary resistance?
A
1 metabolic - ischemia increases adenosine, H/K/CO2/ decreased O2 that all lead to vasodilation
- endothelial - production of NO/ prostacyclin (dilates) and endothelin (constricts)
- neurogenic - SNS (constricts) and PNS (dilates)
- myogenic - pressure/ flow sensitive smooth muscle in arteriolar walls
23
Q
What can cause an increase in O2 demand?
A
- bigger radius (preload)
- bigger intraventricular pressure (impedence)
- increased HR
- increased contractility
*interestingly, a thicker wall requires less O2
24
Q
What is the law of LaPlace?
A
Force in ventricular wall = (pressure x radius)/ 2x wall thickness
25
What is coronary reserve?
difference between resting coronary flow and maximum coronary flow
26
What leads to the chest discomfort experienced in angina?
Adenosine --> vasodilation
27
When is flow reduced in atherosclerosis?
70% - reduction of flow
75% - angina
90% - cannot increase flow to meet demands
28
What is an example of an acute rise of demand vs chronic?
Acute reduction of supply vs chronic?
Acute demand - exercise
Chronic demand - anemia, respiratory failure, CHF, shunt, HTN
Acute supply - MI
Chronic supply - atherosclerosis
29
Where does atherogenesis most commonly occur?
- occurs in the arterial intima (superficial to media and adventitia)
- bends and branches w low shear forces/ turbulence and non-laminar flow (i.e. lesser curve of aorta)
30
Role of endothelial cells
- tight junctions act as a barrier to protect sub endothelial space
- make mediators that maintain a non-thrombotic lumen, maintain sm cell relaxed state
31
ECM composition
- fibrillar collagen (strength), proteoglycans and elastin (flexibility)
32
Process of artherogenesis
- loss of endothelial cell alignment results in increased permeability and increased leukocyte adhesion molecules (ICAM/ VCAM/ P-selectin)
- sub endothelial chemokine promote diapedesis of WBCs into sub endothelial space
- monocytes retain lipids, resulting in macrophage foam cells
- macrophages express scavenger proteins that uptake mLDL to the point of destruction, resulting in cholesterol/ crystal spillage and inflammation
33
How are smooth muscle cells affected in atherosclerosis?
- increased endothelin and angiotensin II and decreased prostacyclin/NO results in constriction
- more IL-6, TNF-A, PAI-1 and tissue factor (inflammation)
- proliferate and migrate to sub endothelial space, produce free radicals, synthesize excess ECM, fibrous cap formation
34
Vulnerable vs. Stable plaque
Vulnerable - large lipid/ necrotic core, few sm cells, thin fibrous cap, little ECM, many foam cells esp. in shoulder, proteases, big plaque
Stable - thick fibrous cap, less lipids, fewer inflamm cells, dense ECM
*can be achieved by decreased LDL/BP/ATII and increasing HDL
35
Optimal therapy for atherosclerosis
- ASA (decrease platelet activity)
- statins/ezetimibe/PCSK9 inhibitors (reduce cholesterol)
- no smoking (reduces oxidized LDL, platelets, sm constriction)
- DM therapy (reduces irritating glycated products)
- exercise (increases laminar shear)
- anti-hypertensives (reduces barotrauma and ox radicals)
36
Chest pain criteria for angina
1. Substernal chest discomfort with characteristic quality and duration
2. Provoked by exertion/ emotional distress
3. Relieved promptly by rest or nitroglycerin
*consider other causes if males under 40 and females under 60 with few risks, but test anyway if over these ages or severe/ multiple risks
37
Ischemic symptoms
- chest pain, dyspnea, shoulder/arm/hand/jaw/neck pain, nausea/ vomiting, diaphoresis, presyncope, arrhythmia
38
Prognostic factors for stable CAD
- anatomical distribution/ burden
- ischemic burden
- LVEF and wall motion abnormalities
39
Criteria for myocardial injury (i.e. HF, myocarditis) vs. acute MI?
injury --> elevated cardiac tropnin
acute MI --> evidence of ischemia on ECG, rise and fall of troponin, pathological Q waves, loss of myocardium or wall motion abnormalities
40
Unstable angina vs. non ST elevation MI vs. ST elevation MI
unstable angina --> transient acute ischemia not resulting in myocardial injury
- typical sx, negative biomarkers, +/- ischemia on ECG
Non-ST MI --> subendocardial ischemia resulting in myocardial injury
- typical sx, positive biomarkers, +/- ischemia on ECG
ST MI --> acute transmural ischemia (occlusive thrombus) resulting in MI and ECG changes
- typical sx, ECG changes, +/- imaging of ischemia
- do not need biomarkers for initial diagnosis
41
What are ischemic biomarkers? when do they peak?
- troponin I - cardiac myocytes
- troponin T - cardiac myocytes and some skeletal muscle
- creatine kinase - cytosol of most myocytes
- creatine kinase-MB isoenzyme - specific to cardiac myocytes
- myoglobin (muscle cells)
- AST (myocytes and hepatocytes)
- LDH (erythrocytes, muscle, kidneys, brain)
*linear peak at 1-2 days post AMI
42
Type I MI vs. Type II
1 - plaque rupture/ erosion
2 - severe HTN/ sustained tachyarrythmis
43
Stable vs unstable CAD?
Stable - predictable and low mortality, at least 70% lesion
Unstable - higher mortality, can be any size
44
How does an MI kill you?
- Mechanical VSD - short term, prevent with B-blocker and treat w surgery
- Heart failure - long term, prevent with LV enhancers, treat with transplant
Recurrent MI - long term, prevent via risk factors, treat w revascularization
Ventricular arrythmias - prevent with B-blockers and LVEF preservation, treat with ICD
45
Ways to help supply/demand/ cardioprotection?
Supply - antithrombotics and antiplatelets (prevent re-occlusion)
Demand - anti-ischemics
Cardioprotection - anti-arrythmics and anti-inflammatories
46
Examples of antiplatelets and antithrombins used to prevent MI?
antiplatelet - ASA (aspirin) - inhibits TXA2 which activates platelets
- ticagrelor (collagen), voraxapar (thrombin), clopidogrel, prasugrel
antithrombin - unfractionated heparin - prevents conversion of fibrinogen to fibrin
- LMWH, fondaparinux (factor X),
* DOACs (rivaroxaban, apixaban, dabigatran are NOT used as they bleed you out!)
47
Treatment if PI due to STEMI
- dual antiplatelet therapy for 1 year (ASA and clopidogrel)
- if after 1 year high risk of bleed -> SAPT or clopidorel
- if low risk of bleed -> DAPT up to 3 years
48
When should angiography be done?
- only if medium risk (DM, CKD, EF <40%, PCI in last 6 months)
- urgent only if high risk (elevated troponin, ST depression, T wave inversion, refractory angina, sx of heart failure, arrythmias)
49
What should the initial anticoagulant given be?
IV heparin in invasive, fondaparinux if conservative (though avoid if PCI in the next 7 days)
50
Medications to:
- lower afterload
- lower contractility
- lower HR
- lower preload
- increase fibrillatory threshold
afterload - Ca blocker, B-blocker, RAS antagonists
contractility and HR - Ca blocker, B-blocker
preload - diuretic, nitroglycerin
fibrillary threshold - B--blocker
51
Sx of acute MI
- chest pain radiating to both arms, 3rd heart sound, hypotension
- women and elderly can present with R-sided chest pain, abnormal T waves, normal physical exam and troponin (always do serial troponins)
52
Sx of acute thoracic aortic dissection
- acute chest/ back pain and pulse differential in upper extremities, wide mediastinum, sinus tach
53
Heart healthy diet
- avoid saturated fats (ideally under 9%)
- mediterranean diet, DASH diet (lowers both systolic and diastolic BP), portfolio diet
54
Signs of a STEMI on ECG?
- ST elevation in leads that overlie the affected tissue
- often reciprocal ST depression in opposite leads
- if a patient has had an MI before, they will have a pathological Q wave (inverted)
55
Signs of ischemia on ECG?
- ST depression or T wave flattening/ inversion
- changes do not localize to an anatomical location
56
Signs of pericarditis on ECG?
- see diffuse ST elevation, diffuse PR depression, and PR elevation in aVR
57
Which leads correspond to which anatomical region of the heart?
Inferior - II, III, aVF
Anteroseptal - V1, V2
Anterior - V3, V4
Lateral - V5, V6
58
Consequences of an inferior STEMI?
- hypotension, mitral regurgitation, complete heart block
