MI 12/04 Flashcards
(275 cards)
1
Q
How many proc. is considered as significant stenosis?
A
> 50 proc.
2
Q
What happens in distal part of vessel in coronary stenosis?
A
Reduced distal perfusion pressure –» decreased distal blood flow –> myocardial ischemia
3
Q
When there is decreased blood flow distal to stenosis, how myocardium responses to maintain blood flow?
A
Myocardium triggers the release of vasodilators = NO, adenosine –> vasodilation = reduced downstream vascular resistance
4
Q
The reduced vascular resistance distal to coronary stenosis due to vasodilators effect on blood flow?
A
Corrective increase in blood flow at the new, reduced perfusion pressure
5
Q
Distal to coronary stenosis increases blood flow. What is perfusion pressure? why?
A
Blood flow increased at lower perfusion pressure - because of vasodilation ie decreased vascular resistance
6
Q
The effects of coronary autoregulation are limited in ……………
A
The effects of coronary autoregulation are limited in the setting of extreme changes in perfusion pressure.
7
Q
Compensation to coronary stenosis –>->->Arterioles reach the point of maximal vasodilation. What effect on blood flow?
A
Once arterioles reach the point of maximal vasodilation, vascular resistance cannot be further reduced, and a further decrease in perfusion pressure results in a precipitous drop in blood flow.
8
Q
Early biochemical changes in myocardial ischemia. What glycolysis?
A
Cessation of aerobic glycolysis and initiation of anaerobic glycolysis.
9
Q
Aerobic to anaerobic glycolysis. When this transition occurs in myocardial ischemia?
A
Within seconds
10
Q
Transition from aerobic to anaerobic glycolysis results in ……………………..
A
Inadequate production of high-energy phosphates (eg, ATP and creatine phosphate) and the accumulation of deleterious metabolites, including lactate.
11
Q
What deleterious metabolite accumulates in ischemic myocardium?
A
Lactate
12
Q
In which myocardium areas rapidly decreases ATP when ischemia occurs?
A
ATP is rapidly depleted from areas of the cell with high metabolic demand, such as the cytosol surrounding the contraction fibers and electrolyte transport pumps.
13
Q
What 2 cells levels mechanisms are the reason of rapid decrease of ATP in metabolic active regions in myocardium?
A
High metabolic demand: cytosol surrounding contraction fibers and electrolyte transport pumps
14
Q
Depletion of ATP and accumulation of toxic metabolites –> effect on contractility? Time frame?
A
LOSS OF CONTRACTILITY WITHING 60 seconds (1 minute) of total myocardial ischemia
15
Q
When ischemia lasts less than 30 minutes, loss of contractile function is ………………………..
A
Reversible
16
Q
How is called phase when blood flow is restored to myocardium but still contractility function is not full?
A
Myocardial stunning - prolonged contractility dysfunction, ie contractility returns gradually
17
Q
How long it takes to return to full contractility after ischemia when blood flow is restored?
A
Several hours to days
18
Q
How correlates duration of ischemia and function recovery time?
A
Increasing duration of ischemia prolong the time that myocardium is stunned
19
Q
Main factor maintaining vasodilation in ischemia?
A
Adenosine
20
Q
ATP is consumed for …… production
A
ATP –> ADP and AMP –> Adenosine
21
Q
When about half of the cellular adenine stores are lost?
A
After 30 min of total myocardial ischemia
22
Q
Under what conditions ATP is degraded to ADP and AMP?
A
Hypoxic
23
Q
At what point ischemic injury becomes irreversible?
A
After 30 min, when about half of the cellular adenine stores are lost
24
Q
What mitochondrial changes indicate reversible cell injury?
A
Simple swelling
25
What mitochondrial changes indicate irreversible cell injury?
The appearance of vacuoles and phospholipid-containing amorphous densities within mitochondria.
26
When mitochondria have changes that indicate irreversible damage, what reaction/function is impaired?
Generation of ATP via oxidative phosphorylation.
27
Myofibril relaxation is an early sign of ................. which occurs ............ (time frame)
Reversible injury; within 30 min
28
Myofibril relaxation corresponds ............ (2 processes)
Intracellular ATP depletion and lactate accumulation
29
Disaggregation of polysomes results in ...........................
Impaired protein synthesis
30
In ischemia impaired protein synthesis occurs due to ......................
Disaggregation of polysomes
31
Disaggregation of polysomes denotes the dissociation of ................................. reversible ischemic/hypoxic injury.
rRNA from mRNA
32
What promotes the dissolution of polysomes into monosomes as well as the detachment of ribosomes from the rough endoplasmic reticulum?
Depletion of intracellular ATP
33
What effect of ATP depletion for ribosomes and polysomes?
Ribosomes detachment from RER and polysomes dissolute into monosomes
34
Disaggregation of granular and fibrillar elements of the nucleus is associated with ......................... cell injury.
Reversible
35
Disaggregation of ........ and .................... elements of the nucleus is associated with reversible cell injury.
Granular and fibrillar
36
Apart from disaggregation of granular and fibrilar elements in the nucleus, what other changes are seen in reversible damage? Why?
Clumping of nuclear chromatin, perhaps secondary to a decrease in intracellular pH
37
Triglycerides accumulation indicates ................ cell injury. In what cells?
Reversible. In hepatocytes, renal and striated muscle cells.
38
Glycogen loss is ........... cellular response to injury.
Reversible
39
The time frame when glycogen depletes in severe ischemia?
Within 30 min
40
The physiologic effect of cocaine on sympathetic stimulation? (2)
Hypertension and tachycardia;
| Coronary vasoconstriction
41
Clinical manifestation (complications) of cocaine? (3)
Myocardial ischemia or infarction;
Aortic dissection;
Neurologic ischemia or stroke
42
What 2 medications are used in cocaine intoxication?
Benzodiazepines and nitroglycerin
43
What medication group is contraindicated in cocaine intoxication?
Beta blockers
44
What is clinical manifestation of CNS stimulation in cocaine intoxication?
Agitation, dilated pupil
45
Why there is incr. HR, BP and myocardial contractility in cocaine intoxication?
Overstimulation of adrenergic receptors (alpha-1, beta-1)
alpha-1 --> BP
beta-1 --> HR and contractility
46
What is the effect on O2 demand in heart in cocaine intoxication? Why?
Increased. Due to overstimulation of adrenergic receptors --> incr. HR, contractility and BP
47
Why there is decreased coronary oxygen supply in cocaine intoxication?
Coronary vasoconstriction due to alpha-1 --> decreased oxygen supply
48
What causes retrosternal chest pain and ST depression in cocaine intoxication?
MYOCARDIAL OXYGEN SUPPLY-DEMAND MISMATCH
49
Why there may be low grade fever in cocaine intoxication?
Peripheral vasoconstriction --> impaired heat loss
50
Why cocaine intoxication is treated with nitroglycerin?
Reduces cardiac preload
51
Why cocaine intoxication is treated with benzodiazepines?
Reduces sympathetic outflow --> alleviated tachycardia/hypertension;
also, calms agitation --> decr. myocardial O2 demand
52
Can cocaine intoxication cause coronary artery thrombosis?
Rarely
53
What is difference between MI and PATE chest pain?
MI - oxygen supply-demand mismatch.
PATE - pleuritic chest pain - pleural effusion seen on xrayn - doesnt resolve without medication - eg in angina relax resolve pain
54
Transient myocardial ischemia. How cells look?
Increase in size
55
What ions accumulate intracellulary due to decr. ATP?
Ca2+ and Na+
56
What component function of cell membrane is impaired in ATP deficiency?
Ion pump failure
57
What happens to cell when solutes accumulate in the cell?
Water moves to the cell --> mitochondrial and cell swelling
58
Impaired Na/K ATPase due to decr. ATP. What result?
Increased intracellular Na and Ca
59
Sarcoplasmic reticulum Ca2+-ATPases fails to function due to decr. ATP. Result?
Incr. intramitochondrial Ca
60
Why there is cessation of contraction within ischemic zones of myocardium?
Failure of the sarcoplasmic reticulum to resequester Ca2+
61
What happens due to failure of the sarcoplasmic reticulum to resequester Ca2+?
Cessation of contraction within ischemic zones of myocardium.
62
What is K concentration in cell in ischemia?
Decreased, Na/K ATPase: Na incresed, K decreased intracellularly
63
Levels of cellular HCO3- in cardiac ischemia? Why?
Not elevated.
| Lactatic acidosis --> decr. pH. Tissue CO2, a conjugate acid of HCO3-, is thus elevated in ischemic myocardium.
64
Cardiac ischemia effect on protein phosphorylation?
The cell's response to ischemia does involve initiating certain metabolic processes through protein phosphorylation, but this does not cause cell swelling.
65
Stable angina results from .........................
Fixed coronary artery stenosis in the setting of atherosclerotic coronary artery disease (CAD).
66
When fixed coronary artery stenosis cause mismatch of oxygen supply and demand? Why?
During periods of increased myocardial oxygen demand (eg, exercise) because it limits blood supply to the downstream myocardium. Then manifest symptoms eg chest pain, shortness of breath
67
What medication can be used in stress test? What effect on the heart?
Dobutamine - beta 1 agonist. It increases HR and contractility --> incr. O2 demand
68
Myocardium that is unable to obtain sufficient blood flow to meet the increased oxygen demand typically demonstrates a ...............
Transient decrease in contractility ie wall motion defect
69
Transient decrease in contractility due to insufficient blood flow in stable angina affects what heart function feature?
Reduced ejection fraction
70
How long lasts wall motion defect in stable angina when used dopamine?
When increased oxygen demand due to incr. HR and contractility
71
How long lasts wall motion defect in MI when used dopamine?
Persistent wall motion defect - before, during and after dobutamine infusion
72
Vasospastic angina. Use dopamine in stress test. Result?
Vasospastic - due to coronary spasm. Dobutamine - Beta 1 agonist. To cause vasoconstriction need alpha 1 agonist. Therefore dobutamine unlikely to trigger coronary vasospasm
73
How long last wall motion defect in focal myocardial fibrosis?
Persistent - wall motion defect is similar to defect in MI. Furthermore, fibrosis typically results from previous MI
74
What is EF after dopamine infusion in normal patients?
Transient increase in EF due to increased HR and contractility
75
What pathophysiological mechanism cause vasospastic angina?
Coronary endothelial dysfunction and autonomic imbalance
76
Age of vasospastic angina patients?
Younger than 50 y/o
77
What are and are no risk factor for vasospastic angina?
Smoking.
| Patients lack of typical risk factor for CAD (hypertension, DM)
78
Symptoms of vasospastic angina are thought to be triggered by .............., and they occur most commonly ..................
Excess vagal tone; at night
79
How vasospastic angina is diagnosed?
ECG: ST elevation during episode of chest dicomfort.
+
Angiography: abscence of CAD
80
What 2 pharm provoke symptoms of vasospastic angina?
Acetylcholine and ergot alkaloids.
81
How acetylcholine causes vasospastic angina symptoms?
Acetylcholine normally stimulates vasodilation via endothelial induced mechanism: NO causes vasodilation.
In affected patients ie with endothelial dysfunction there is no release of NO and only increased vagal tone --> vasoconstriction
82
How ergot alkaloids cause symptoms?
They activate 5HT2 serotonergic receptors --> vasoconstriction. Normally, released prostaglandins from endothelium overcomes it and causes vasodilation, but in patients with impaired endothelium lack of response --> vasoconstriction occurs
83
In patients with vasospastic angina peripheral endothelial function is .....
Intact
84
Acetylcholine effect on peripheral vessels in patients with vasospastic angina.
Acetylcholine causes vasospastic angina, because endothelium is impaired in coronary arteries. Endothelium in periphery is intact, therefore ACh would cause peripheral vasodilation: decreased preload and afterload
85
What drug prevents vasospastic angina?
calcium channel blockers (diltiazem, amlodipine)
86
What drug is used in vasospastic angina episode?
Sublingual nitroglycerin
87
Endothelin-1 effect on vessels?
Vasoconstriction
88
Prostacyclin effect on vessels?
Vasodilator
89
In what pathology increased HR can exacerbate angina due to increased myocardial oxygen demand?
In CAD. If there is no CAD, it unlikely that myocardial ischemia will manifest
90
Stable angina is exacerbated by ............. and relieved by ............
exertion; rest
91
Why does stable angina manifest as chest pain?
Due to temporary myocardial ischemia from demand-supply mismatch of oxygen rich blood to the myocardium
92
What causes restricted coronary blood flow in stable angina?
Atherosclerotic lesion that obstructs > 70 proc. of lumen.
93
Clinical manifestation of stable angina?
Substernal or left-sided chest pressure, tightness or pain
94
Myocardial oxygen DEMAND is determined by ........ (4)
HR, BP (afterload), LVEDV (preload), cardiac contractility
95
Myocardial oxygen SUPPLY is determined by .............. (1)
Coronary blood flow
96
Atherosclerotic plaque obstructing 50proc. of the lumen. Symptoms?
No symptoms. They occur when lumen is obstructed more than 70proc.
97
Effect of exertion and rest on vasospastic angina.
None. Not precipitated by exertion and not relieved by rest
98
Acute coronary syndrome usually occurs due to ......................
Plaque rupture --> superimposed thrombosis --> vessel occlusion
99
The likelihood of plaque rupture is typically related to ...................
Plaque stability rather than plaque size or degree of luminal narrowing.
100
Plaque stability depends on the mechanical strength of the ............................
fibrous cap
101
................. fibroatheromas are generally unstable and more vulnerable to rupture.
Thin-cap
102
Thin-cap fibroatheromas are generally ................. and more vulnerable to rupture.
Unstable
103
During the chronic inflammatory progression of an atheroma, the fibrous cap is continually being .....................
Remodeled
104
What determined the strength of the fibrous cap?
The balance of collagen synthesis and degradation
105
Thin-cap fibroatheromas are characterized by .............(1) + (1)
Large necrotic core covered by a thin fibrous cap
106
What macrophages in atheromas secreting to break down a collagen?
Metalloproteinases
107
What cells participate in fibrous cap remodeling?
Macrophages
108
What process in atheroma can destabilize the mechanical integrity of the plaque? How?
Ongoing intimal inflammation. Due to release of metalloproteinases
109
Lysyl oxidase strengthens extracellular collagen fibers by mediating cross-link formation between ........... and .............
Mediating cross-link formation between lysine and hydroxylysine residues (requires copper).
110
What ion is required for lysyl oxidase?
Copper
111
High activity of lysyl oxidase effect on atheroma formation?
Favor atheroma stabilization, because strengthens collagen fibers
112
Function of procollagen peptidase?
Procollagen --> insoluble tropocollagen
113
Function of tropocollagen?
Aggregates to form collagen fibrils
114
What cells (2) exocytoses procollagen?
Fibroblasts or smooth muscle cells
115
What enzyme participates in collagen formation and requires copper?
Lysyl oxidase
116
What vitamin requires prolyl hydroxylase?
vit. C
117
What enzyme participating in collagen formation requires vit C?
Prolyl hydroxylase
118
Prolyl hydroxylase is responsible for the ....................... of proline on procollagen chains?
Hydroxylation
119
Prolyl hydroxylase hydroxylases ..................... on .........................
Proline on procollagen chains
120
What step is necessary for the formation of a stable collagen triple helix?
Hydroxylation of proline on procollagen chains
121
Prolyl hydroxylase is responsible for the hydroxylation of proline on procollagen chains (requires vitamin C), which is a necessary step in the formation of .........................
A stable collagen triple helix
122
Unstable angina pathophysiology?
Artery partially occluded by ruptured atherosclerotic plaque. Tissue beyond in ischemic, but not injured (no infarction)
123
NSTEMI pathophysiology?
Artery partially occluded, but tissue beyond is injured (infarction). Subendocardial
124
STEMI pathophysiology?
Artery is fully occluded and tissue beyond is injured (infarction). Transmural
125
STEMI symptoms?
Persistent chest pain which is not relieved by rest
126
Why does thrombus develop overlying ruptured atherosclerotic plaque?
Rupture of plaque --> release of thrombogenic factors into the blood stream --> formation of thrombus
127
What thrombogenic factors are released into the bloodstream when atheroslerotic plaque ruptures?
Lipids, collagen, tissue factors
128
What symptoms may accompany STEMI?
Nausea, diaphoresis, dyspnea
129
NSTEMI ECG?
ST depression and T waves inversion
130
STEMI ECG?
Peak T waves --> ST elevation (minutes)--> Q waves (hours/days)
131
2 patho changes seen in autopsy in MI?
1. Atherosclerotic plaque rupture
| 2. Occlusive thrombus
132
What is common cause of sudden cardiac death (SCD)?
Acute MI
133
What is SCD?
Abrupt cessation of organized cardiac activity leading to hemodynamic collapse and inadequate tissue perfusion
134
Abrupt cessation of organized cardiac activity leads to ........... and .........
Hemodynamic collapse and inadequate tissue perfusion
135
SCD due to MI usually results from ...................
Malignant ventricular arrhythmia
136
What are types of malignant ventricular arrhythmia?
ventricular fibrillation of ventricullar tachycardia degenerating to ventricular fibrillation
137
What triggers malignant ventricular arrhythmia in acute MI?
Electric instability in the ischemic myocardium
138
Where forms mural thrombus eg in LV?
In the area of infarcted and akinetic myocardium
139
How long it takes to form a thrombus in LV post MI?
Several days
140
If more than 50proc of myocardium is infarcted, what complications? (2)
Ventricular failure
| Cardiogenic shock
141
Ventricular failure and cardiogenic shock in MI. Manifestation? (2)
Hypotension and respiratory distress
142
The pathogenesis of atherosclerosis likely begins with .....................
Endothelial cell injury
143
Chronic endothelial cell injury may result from ... (4)
Hypertension (and related hemodynamic factors), hyperlipidemia, smoking, and DM.
144
Endothelial injury by CAD risk factors leads to ............ and/or ............
Endothelial cell dysfunction and/or exposure of subendothelial collagen
145
How is called process when occur exposed subendothelial collagen?
Endothelial cell denudation
146
Endothelial cell dysfunction results in .................. (2) + (2)
Monocyte and lymphocyte adhesion and migration into the intima
147
Exposure of subendothelial collagen promotes ...............
Platelet adhesion
148
In atheroma formation growth factors are produced by .......... (2)
Monocytes and platelets
149
What is a function of the growth factors in atheroma formation?
Stimulate medial smooth muscle cell (SMC) migration into the intima
150
What facilitate/allows LDL cholesterol to spread into the intima?
Increased vascular permeability
151
What phagocytose LDL cholesterol in the intima? What is the result?
Accumulating macrophages and SMCs. Lipid-laden foam cells (fatty streak)
152
Chronic inflammatory state in the intima --> deposition of LDL and SMC proliferation --> increased production of ..... (2)
Increased production of collagen and proteoglycans
153
Necrosis of foam cells results in ............... to the .............
Release of toxic oxidized LDL into the extracellular matrix --> perpetuates cycle of injury
154
Fibrofatty atheroma consists of .........
Core lipid of debris surrounded by monocytes and lymphocytes covered by a fibrous cap with intermixed SMCs
155
Core of lipid debris surrounded by .......... (2)
Monocytes and lymphocytes
156
The fibrous cap, of atheromas is synthesized by ...........
SMCs
157
Fibroblasts significance in formation of atheroma?
None. Fibrous cap is synthesized by SMCs
158
What is role of pericytes in atherosclerosis? Why?
None. Pericytes surround the smallest blood vessels. Atherosclerosis - in large elastic and large/medium muscular arteries.
159
What arteries are affected by atherosclerosis?
Large elastic;
| Large/medium muscular
160
When does atherosclerosis begin? Result?
Childhood. Fatty streaks
161
What happens to fatty streaks in advanced age?
Fatty streaks transitions into atherosclerotic plaques ie fibrous cap atheromas and fibrous plaques.
162
Turbulent blood flow also leads to ............................... on the vascular walls and prolonged endothelial contact with ................
Decreased shear stress;
Cholesterol particles.
163
What are 2 most susceptible vascular regions for atherosclerosis?
Bends and branch points
164
Atherosclerosis in bends and branch points cause .......... which ................ and leads to ...............
Turbulent blood flow;
Disrupts vascular wall integrity;
Leads to endothelial cell dysfunction
165
What 2 vessels most susceptible to atherosclerosis? Why?
Lower abdominal aorta and coronary arteries. Due to hemodynamics
166
When intimal thickening/fatty streaks start to develop?
As early as the second decade of life
167
Expression of what molecules increase monocytes and T lymphocytes adhesion in hemodynamic stress?
VCAM
168
What growth factors participate in atheroma formation?
Platelet derived growth factor (PDGF)
| Fibroblast growth factor (FGF)
169
What cytokines participate in atheroma formation?
Endothelin-1
| IL-1
170
What cells release growth factors and cytokines?
Activated platelets, activated macrophages and dysfunctional endothelial cells
171
What is the effect of growth factors and cytokines in atheroma formation?
It triggers vascular smooth muscle cells (VSMCs) migration and proliferation in the intima.
172
What do VSMCs in atheroma formation?
synthesize extracellular matrix proteins (collagen, elastin, proteoglycans) that form the fibrous cap.
173
What cells induce fibrous cap formation?
VSMCs
174
Necrotic debris in atheroma consists of ....
macrophage/foam cell and SMC death
175
What encourage plaque stability?
SMCs by synthesizing collagen
176
What induces plaque instability?
Activated inflammatory cells break down collagen
177
HDL effect on atheroma?
Extracts lipids from the intima back into the bloodstream thus helps to slow atheroma development
178
What in atheroma formation directly responsible for collagen formation?
VSMCs
179
Function of metalloproteinases? Result?
degrade extracellular matrix --> large, soft lipid-rich core with thinning of the fibrous cap.
180
The earliest pathophysiologic change that precedes the formation of atherosclerotic lesions?
Endothelial cell dysfunction
181
Right ventricular infarction --> right-sided HF. Presentation? (3)
Hypotension, DJV, clear lungs
182
Why there is hypotension in right ventricular infarction?
Decreased RV output --> decr. LV filling --> decr. CO --> hypotension and shock
183
PCWP in right ventricular infarction?
Decreased - because decreased RV output
184
decr. PCWP, CVP and CO in ................
Distributive shock due to sepsis
185
Which LV infarct more likely to cause LV systolic dysfunction?
Anterior wall than inferior
186
The inferior wall of the left ventricle (LV) is supplied by the ................... which arises off the .....................
Supplied by the posterior descending artery (PDA), which arises off the dominant right coronary artery (RCA).
187
Inferior wall myocardial infarction is often associated with ................ Why?
Right ventricular infarction.
| Because RCA gives rise to branches that supply most of the right ventricle.
188
Myocardial hibernation refers to a state of ...........
Chronic myocardial ischemia
189
What 2 processes are altered in myocardial hibernation?
Myocardial metabolism and function
190
What level of stenosis induces myocardial hibernation?
Moderate/severe flow-limiting stenosis
191
What process is prevented by myocardial hibernation?
Myocardial necrosis
192
Chronically hibernating myocardium demonstrates: (3)
Decreased expression and disorganization of contractile and cytoskeletal proteins;
Altered adrenergic control;
Reduced calcium responsivness
193
3 main changes in hibernating myocardium lead to...... (2)
Decreased contractility and LV systolic dysfunction
194
Does myocardial hibernation is permanent?
No, when blood flow is restored eg in revascularization contractility and LV function restore
195
What is ischemic preconditioning?
Repetitive episodes of myocardial ischemia, followed by reperfusion, protect the myocardium from subsequent prolonged episodes of ischemia
196
Reperfusion injury complications?
Arrhythmias, microvascular dysfunction with myocardial stunning, and myocyte injury and death.
197
Atheroembolic disease typically occurs after ...........
Invasive vascular procedure in arteries with atherosclerotic plaques
198
What patho usually develop patients with atheroembolism? What arteries affected?
Acute kidney injury.
| Complete occlusion of the arcuate or interlobular arteries.
199
What other organs apart from kidney are affected in atheroembolism?
Skin, Gi, CNS
200
Mechanical dislodgement in invasive procedures in vessels affected by atherosclerosis leads to .................... --> leads to kidney, CNS, skin, GI injury
Showering of cholesterol-rich microemboli into the circulation --> obstruction of distal arterioles and tissue ischemia
201
Fibrinolysis or .....................are used to achieve ............... in acute MI patients
percutaneous coronary intervention (PCI); myocardial reperfusion
202
Why PCI is prefered over fibrinolytic therapy?
Due to lower rates of ICH and reccurent MI
203
Alteplase converts ......... to .............
plasminogen to plasmin
204
Alteplase binds ............. which is in ..............
fibrin; thrombus (clot)
205
Plasmin ................. (name of reaction) key bonds in the ............... causing clot lysis --> restoration of coronary arterial blood flow.
hydrolyzes;
| fibrin matrix
206
Fibrinolytic therapy for acute STEMI is a reasonable reperfusion technique for patients with .......................
No contraindications to thrombolysis.
207
MI microscopic changes 0-4h?
NONE. May be seen waviness of myofibrils at the border of the infarct (due to myofibril relaxation)
208
MI microscopic changes 4-12h?
Early coagulative necrosis - cytoplasmic hepereosinophilia + edema, puctuate hemorrhage, wavy fibers, nuclear pyknosis
209
MI microscopic changes 12-24h?
Coagulation necrosis and marginal contraction band necrosis
210
MI microscopic changes 1-3d/5days?
Extensive coagulation necrosis and neutrophils infiltrate. Acute inflammation in tissue surrounding infarct
211
MI microscopic changes 5-10d.?
Extensive macrophages phagocytosis of the dead cells. Most prominent 7-10d.
Also, at 7th day starts fibrovascular granulation tissue formation and neovascularization.
212
MI microscopic changes 10-14d.?
Prominent fibrovascular granulation tissue formation and neovascularization. It starts 7d, but prominent 10-14.
213
MI microscopic changes 2 weeks - months?
Fibrosis. Increased collagen deposition and dcecreased cellularity in inforcted zone. Dense collagenous scar - by 2 months post-MI
214
What cells release cytokines and growth factors in MI? What is the purpose?
Neutrophils and macrophages.
| Initiate tissue proliferation.
215
What growth factors plays important role in post-MI?
TGF-beta
216
What is the function of TGF-beta in MI?
Downregulate inflammation and stimulate fibrobrasts migration and proliferation --> extensive type I and III collagen depositions.
217
What collage types are is proliferation stage post-MI?
Type I and III
218
When happens proliferation phase post-MI?
Days to weeks
219
When happens remodeling post-MI?
Weeks to months
220
What component, stimulated by TGF-beta facilitate collagen remodeling?
Activation of metalloproteinases
221
What enzymes play important role in scar formation?
Metalloproteinases
222
What is the function of metalloproteinases?
Facilitate collagen remodeling and crosslinking to form dense scar tissue
223
Patients with large scars from previous MI are at high risk to die due to ...............
Arrythmia
224
What are levels of NO post-MI?
Increased --> reperfusion. No effect on fibrous scar formation
225
IFN-beta effect post-MI?
anti-inflammatory cytokine --> reduces the formation of fibrotic tissue
226
IL-8 and TNF-α effect in post-MI?
Proinflammatory cytokines that stimulate the recruitment and activation of other immune cells (eg, neutrophils). However, neither directly promotes fibrosis in a healing wound
227
Papillary muscle rupture, when?
Acute or 3-5 days
228
Papillary muscle rupture clinical findings? (3)
Severe mitral regurgitation with flail leaflet
New holosystolic murmur
Severe pulmonary edema
229
Interventricular septal rupture, when?
Acute or 3-5 days
230
Interventricular septal rupture clinical findings?
Chest pain
New holosystolic murmur
biventricular failure, shock
Set up in O2 level from RA to RV
231
Ventricular free-wall rupture, when?
5 days - 2 weeks
232
Ventricular free-wall rupture, symptoms?
Chest pain, tamponade, shock, distant heart sound (tamponade beck triad: hypotension, JVD, distant heart sound)
233
Left ventricular aneurysm, when?
within several months
234
Left ventricular aneurysm clinical findings?
Subacute HF, stable angina
235
How called ventricular septal defect in septum rupture post-MI?
Shunt
236
What resolves newly occurred systolic murmur in mitral regurgitation due to muscle dysfunction?
Revascularization
237
What is a difference of cause between papillary muscle displacement and rupture?
Displacement: ischemia --> hypokinesis and outward displacement of the muscle --> increased tension on the chordae tendineae --> prevented complete clossure of mitral valve
238
Papillary muscle displacement can be resolved by ............
Coronary revascularization --> restored papillary muscle and LV wall motion --> resolution of the mitral regurgitation
239
Papillary muscle rupture can be resolved by ............
It does not resolve with coronary revascularization and typically requires surgical repair.
240
Rupture of the interventricular septum can be resolved by ..............
The condition does not resolve with coronary revascularization and typically requires surgical repair
241
What effect of MI ischemia can have on aortic root, aortic valve leaflet, mitral valve chordae tendineae?
Those structures are not directly affected by my myocardial ischemia
242
What infarction can cause LV free-wall rupture?
Transmural
243
Gross presentation of heart of LV free-wall rupture?
Slitlike tear in the anterior LV wall
244
The infarcted myocardium becomes ................. and does not move with the remaining healthy myocardium, creating ........................
Akinetic;
| Creating additional shear stress on the myocardial wall.
245
What creates additional shear stress on the myocardial wall in post-MI?
Akinetic infarcted myocardium
246
Why myocardial wall may not tolerate additional shear stress caused by akinesis?
Because infarcted myocardium is weakened by coagulative necrosis, leukocyte infiltration, enzymatic lysis of myocardium connective tissue there may be unable withstand the shear stress.
247
What increases the risk of free wall rupture post-MI?
Delayed reperfusion --> therefore weakened LV wall
248
What is the main complication of LV free wall rupture?
Cardiac tamponade and hemopericardium
249
What stimulated collateral vessels formation in myocardium?
Growth factors (eg VEGF)
250
Step by step what induces collateral vessels formation?
Atherosclerosis --> progressive reduction in blood flow --> ischemic myocardium releases growth factors (eg VEGF) --> formation of collateral vessels.
251
Stable atherosclerotic plaque formation in LAD. From what vessel form collaterals? To which area?
From right coronary artery (RCA) collaterals to ischemic myocardium located distal to the LAD occlusion.
252
What facilitates blood flow from RCA collaterals to distal LAD obstruction?
Due to occlusion in the distal area there is low hydrostatic pressure. In collateral RCA normal blood flow and pressure. Gradient facilitates blood flow through the small collateral vessels.
253
In what atherosclerotic plaques do collaterals form and in what not?
In stable - yes, because it's chronic --> causes significant ischemia
In unstable - no, not enough time to form collaterals, because unstable/ruptured probably will result in acute occlusion --> rapid ischemia
254
Unstable atherosclerotic plaque characteristics (3)
Active inflammation, a lipid-rich core and/or a thin fibrous cap
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Why unstable atherosclerotic plaque will not lead to collaterals formation?
It is more likely to rupture before it becomes large enough to cause significant chronic ischemia;
256
High or low calcium in plaque leads to decrease stability?
Low calcium (immature calcification)
257
How correlates coronary artery calcium content with total atherosclerotic plaque burden?
Directly. Calcium scoring can be assessed by cardiac CT scan - estimates severity of coronary artery disease
258
Cardiac CT can estimate severity of what disease?
CAD
259
What are ostial atherosclerotic plaques?
Those located at a branch point of 2 arteries
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What plaques occlude multiple areas of myocardium?
Ostial atherosclerotic plaques
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What plaques limit the availability of nearby well-perfused arteries from which viable collateral vessels can develop?
Ostial atherosclerotic plaques
262
High muscle mass is in ............ ventricle, and low muscle mass is in .............. ventricle.
High - left
| Low - right
263
Resting oxygen extraction is high in ............... and low in ................ ventricle
High - left
| Low - right
264
Coronary perfusion only during diastole is in ..............
Left ventricle
265
Coronary perfusion throughout cardiac cycle is in ................
Right ventricle
266
Right ventricle gets coronary perfusion during ..................
all cardiac cycle
267
In which ventricle collateral circulation is better developed?
Less in left, more in right
268
High ischemic preconditioning is in ...... and low in ....... ventricle
Left - low
| Right - high
269
How changes contractile function in right and left ventricles post-MI?
Left ventricle - scarring and reduction in contractile function
Right ventricle - contractile function almost always returns to normal
270
What protects RV from loss of contractility post-MI? (no pressures in this answer)
Small muscle mass and afterload of RV --> less oxygen demand and necessitate lower oxygen extraction at rest.
271
Systolic pressure in RV relations to protection of RV in MI?
In RV low systolic pressure (=<25mmHg) ---> coronary perfusion throughout the cardiac cycle
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Systolic pressure in LV relations to the protection of LV in MI?
In LV there is high systolic pressure --> block coronary blood flow of the LV walls during systole. THEREFORE IT DOES NOT PROTECTS LV FROM MI DAMAGE AS IN RV, WHERE LOW SYSTOLIC PRESSURE
273
The most robust collateral flow occurs from .................. to the ......................, therefore ............. ventricle is protected better.
From left to right;
| Right - it has more developed collateral circulation
274
Large MI --> decr. CO and contractility ---> activation of what and what is the result?
The aortic and carotid baroreceptors stimulate peripheral vasoconstriction to increased SVR.
Also HR is increased to increased CO (due to these receptors?)
275
Failure to eject blood from the left ventricle increases ...................
LV end-diastolic pressure
