pathophysiology of acs

Question 1

acs with st elevatoon?

Answer 1

troponin & ck elevated

Question 2

nonstemi?

Answer 2

troponin elevated or not

Question 3

coronary artery disease?

Answer 3

Most commonly due to coronary artery atheroma
Other coronary artery diseases:
Coronary artery spasm
Arteritis
Embolism
Congenital anomaly
Coronary artery dissecting aneurysm
Syphilitic aortitis

Question 4

aha type 1?

Answer 4

non specific intimal thickening

Question 5

aha type 2. fatty streaks

Question 6

ulcerated complicated plaque?

Answer 6

thrombosis of plaque, involvement of media, thrombus

Question 7

3 mechhanisms of atheroma occlusion?

Answer 7

1. Thrombosis on complicated atheroma
2. Haemorrhage into plaque
3. Rupture of “vulnerable plaque”

Question 8

recanalised thrombus?

Answer 8

Recanalized thrombus
End-stage of a thrombus. The blood clot (thrombus) is replaced by connective tissue with many newly formed channels. If these channels reestablish the continuity of the original vessel, blood may flow at a rate adequate to maintain perfusion. Note calcification

Question 9

haemorrhage into plaque?

Answer 9

bleeding in the moddle of a plaque

Question 10

ruptureof vulnerable plaque?

Answer 10

Stable plaque
Vulnerable plaque

Concept of remodelling

Question 11

stable plaque?

Answer 11

thick fibrous collagen cap, few inflammatory cells

Question 12

vulnerable plaque?

Answer 12

Loss of collagen and smooth muscle= thin fibrous cap Inflammation-

matrix degrading proteases
Weaken fibrous cap

Question 13

glagov phenomenon?

Answer 13

Positive remodelling outward = compensatory remodeling : Glagov phenomenon
lumen diameter retained. no angina. thin fibrous cap

Question 14

negative remodelling?

Answer 14

negative remodelling no dilatation

Question 15

angina?

Answer 15

more than 70% narrowing

Question 16

Stary Fuster classification

Answer 16

Question 17

growing of arterial brnaches in atherosclerosis to accomodate?

Answer 17

adventitial vasa-vasorum

Question 18

macrophage quantification score

Answer 18

score 0 - <5 macs

Score 1 - 6-25 macs

Score 2 - >25 macs

Question 19

signs of intra plaque hemorraheg?

Answer 19

lipid core hemorrhage

re blood cells and fibrin

erythrocytes

inflammation

Question 20

intraplaque hemorraheg?

Answer 20

Conversion of a stable, asymptomatic lesion to an unstable, ruptured plaque involves many processes, the most studied of which is inflammation, cellular breakdown, and expansion of the acellular, lipid rich, necrotic core.
Commonly believed that death of macrophages and SM foam cells, in addition to the aggregation of lipoproteins, contribute to the accumulation of extracellular free cholesterol within unstable plaques.
Intraplaque hemorrhage plays a role in the expansion of core of plaques though the relative importance of this vs. other mechanisms by which plaque burden increases is uncertain

Question 21

how does the vessel respond to a plaque formation?

Answer 21

As plaque accumulates, the arterial wall often reacts by remodeling. As atherosclerosis progresses toward the more severe stages pictured on the right, the lumen remains constant because of compensatory expansion of the arterial wall. Eventually, however, in more severe stages of the disease, the artery is unable to expand further and the lumen begins to narrow.
The same process may work in reverse with disease regression. That is, plaque can be removed from the arterial wall with little change in lumen size. Therefore, the mildly narrowed lumen may be a less sensitive marker for the progression or regression of disease than direct estimates of plaque size.

Question 22

postivie remodelling?

Answer 22

EEM and contour increases and allows the plaque to push against the walls and keep the luemn enlarged. I.E. plaque isn’t a [problem.

Question 23

negative remodeling?

Answer 23

as he plaque grows the walls cave in and the lumen narows. looks like a christmas cracker (narrowing of arterial wall in places

Question 24

remodeling properties?

Answer 24

Plaques with Remodeling
More Macrophages
More Lipid-rich Atheroma
Less Collagen
Less Smooth Muscle Cells
More Metalloproteinases (MMP 2 and MMP-9)

Question 25

unstabe and stable

Answer 25

more positive remodeling in unstable, and more negative remodeling in stable

Question 26

ruptue

Answer 26

The Thin Cap Fibroatheroma (TCFA) has been identified as being often the atheromatous lesion responsible for an acute coronary event

Question 27

components of thin-cap atheroma?

Question 28

types of plaques?

Answer 28

fibrous atheroma thin cap hemorrhage ruptur heled rupture

Question 29

morphological change

Answer 29

Question 30

vulnerable plaque, what we do not know

Answer 30

We do not know the length or the circumference of a thin cap nor the volume of the necrotic core that will lead to rupture We do not know the density of macrophages needed to cause a rupture if rupture is mainly determined by macrophage infiltration. We do not know the quantity or the density of vasa vasorum that may predict rupture We do not know the clinical or morphologic or hemodynamic parameters that will lead to rupture ? There are no established laboratory methods of how to recognize a vulnerable lesion and therefore no longitudinal epidemiologic studies are available that identify vulnerable lesion are likely to rupture and at what time. There is no proof today that a thin cap fibroatheroma (as defined today) will definitely rupture Above all no good animal models of vulnerable plaque exist.

Question 31

what we know abot plaques?

Answer 31

Definition (based on ruptured plaques) Frequency is higher in AMI than SCD, males than females Higher prevalence in the presence of high TC, low HDL-C, high TC/HDL-C ration, high hs CRP (\>3.2 mg/dl) Location in SCD, proximal and mid LAD, RCA, and LCX Length 2-22 mm (mean 8 mm) % luminal narrowing (80% of TCFAs occur in lesions \<50% diameter stenosis) % necrotic core is \<25% of plaque area in 70% of TCFAs Calcification is not a marker of TCFA

Question 32

coronary stenosis and risk?

Answer 32

Plaques with \>70% stenosis have a greater numerical probability of causing events than non haemodynamically significant lesions, but since there are vastly more mild, even non angiographically visible plaques than severe lesions, this leads to the observation that a mild lesion is more likely to cause sudden occlusion Acute coronary syndrome more often results from rupture of a vulnerable plaque with thrombosis in mild \<60% stenosis Large lipid core, thin fibrous cap, inflammation Rupture may be precipitated by isometric exertion

Question 33

advanced, obstructive disease: healed plaque rupture?

Question 34

development of athrosclerosis?

Answer 34

Question 35

medical treatet aimed at?

Answer 35

Medical treatment is aimed at reducing lipid (LDL) Stabilise plaque reducing inflammation increasing collagen in fibrous cap

Question 36

distriobution of MI withi the heart?

Answer 36

``` Regional (90% of cases) Diffuse subendocardial (10%) ```

Question 37

regional MI?

Answer 37

Regional (90% of cases) Transmural Wedge-shaped Left ant. descending (LAD) cor. art. 50% Right main cor. art. 30% Circumflex cor.art. 20%

Question 38

diffuse MI?

Answer 38

Diffuse subendocardial (10% of cases) ## Footnote No coronary thrombus Partial stenosis of 2-3 coronary arteries Associated with hypotension & left ventricular hypertrophy

Question 39

left coronary artery occlusion

Answer 39

massive antero-lateral MI

Question 40

left anterior edscending coronary artery

Answer 40

antero-septal MI

Question 41

right coronary artery

Answer 41

postrerior inferiro MI

Question 42

circumflex coronary artery occlusion?

Answer 42

lateral MI

Question 43

sbendocardial MI?

Answer 43

inner 1/3

Question 44

when does a regional subendocardial MI occur?

Answer 44

if flow is restored after occlusion (rest of tissue is saved, only 1/3 of the inner wall affected).

Question 45

massive subendocardial MI around all of te left ventricle endocardium?

Answer 45

Severe stenosis of all arteries Acute (hypotension sudden anaemia/shock)= infarction

Question 46

cronic subendocardial MI?

Question 47

myocardial changes after MI?

Answer 47

Muscle necrosis (SOFTENING) Acute inflammatory response REPAIR of defect in heart wall Demolition of dead tissue by macrophages Organisation of necrotic area Repair by GRANULATION TISSUE END RESULT = HEALING BY SCARRING

Question 48

changes after 0-12hr of MI?

Answer 48

ischemia/necrosis of muscle macro-no macro changes micro - intercellular oedema, subtle change in colour of fibres

Question 49

changes after 6-12 hrs?

Answer 49

muscle fibre eosinophilia oedema

Question 50

chages after I 12-24 hr?

Answer 50

macro- pale with small haemorrhages blotchy micro- oedema, fibre eosinophilia, focal haemorrhage, few neutrophils

Question 51

microscpy 12-24 hr

Answer 51

necrosis, oedema, neutrophils

Question 52

changes after MI 24-72 hr?

Answer 52

necrosis, inflammation maro- soft and plae micro-muscle fibre necrosis, acute inflmmation

Question 53

microscopy 24-72hours?

Answer 53

necrosis, oedema, neutrophils

Question 54

changes after MI - 3-10 days

Answer 54

organisation of infart begins - ingrowth of new vessels macro- pale area with red hyperaemic border micro-necrosis, demolition, granulation tissue at edge

Question 55

chages after MI - 10+ days?

Answer 55

macro- white fibrous scar Micro-vascular collagenous scar later- avascular scar