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1 STEP Uworld cardio > MI 12/04 > Flashcards

MI 12/04 Flashcards

1
Q

How many proc. is considered as significant stenosis?

A

> 50 proc.

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2
Q

What happens in distal part of vessel in coronary stenosis?

A

Reduced distal perfusion pressure –» decreased distal blood flow –> myocardial ischemia

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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

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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

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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

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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.

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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.

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8
Q

Early biochemical changes in myocardial ischemia. What glycolysis?

A

Cessation of aerobic glycolysis and initiation of anaerobic glycolysis.

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9
Q

Aerobic to anaerobic glycolysis. When this transition occurs in myocardial ischemia?

A

Within seconds

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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.

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11
Q

What deleterious metabolite accumulates in ischemic myocardium?

A

Lactate

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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.

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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

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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

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15
Q

When ischemia lasts less than 30 minutes, loss of contractile function is ………………………..

A

Reversible

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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

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17
Q

How long it takes to return to full contractility after ischemia when blood flow is restored?

A

Several hours to days

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18
Q

How correlates duration of ischemia and function recovery time?

A

Increasing duration of ischemia prolong the time that myocardium is stunned

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19
Q

Main factor maintaining vasodilation in ischemia?

A

Adenosine

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20
Q

ATP is consumed for …… production

A

ATP –> ADP and AMP –> Adenosine

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21
Q

When about half of the cellular adenine stores are lost?

A

After 30 min of total myocardial ischemia

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22
Q

Under what conditions ATP is degraded to ADP and AMP?

A

Hypoxic

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23
Q

At what point ischemic injury becomes irreversible?

A

After 30 min, when about half of the cellular adenine stores are lost

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24
Q

What mitochondrial changes indicate reversible cell injury?

A

Simple swelling

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25
Q

What mitochondrial changes indicate irreversible cell injury?

A

The appearance of vacuoles and phospholipid-containing amorphous densities within mitochondria.

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26
Q

When mitochondria have changes that indicate irreversible damage, what reaction/function is impaired?

A

Generation of ATP via oxidative phosphorylation.

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27
Q

Myofibril relaxation is an early sign of …………….. which occurs ………… (time frame)

A

Reversible injury; within 30 min

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28
Q

Myofibril relaxation corresponds ………… (2 processes)

A

Intracellular ATP depletion and lactate accumulation

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29
Q

Disaggregation of polysomes results in ………………………

A

Impaired protein synthesis

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30
Q

In ischemia impaired protein synthesis occurs due to ………………….

A

Disaggregation of polysomes

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31
Q

Disaggregation of polysomes denotes the dissociation of …………………………… reversible ischemic/hypoxic injury.

A

rRNA from mRNA

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32
Q

What promotes the dissolution of polysomes into monosomes as well as the detachment of ribosomes from the rough endoplasmic reticulum?

A

Depletion of intracellular ATP

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33
Q

What effect of ATP depletion for ribosomes and polysomes?

A

Ribosomes detachment from RER and polysomes dissolute into monosomes

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34
Q

Disaggregation of granular and fibrillar elements of the nucleus is associated with ……………………. cell injury.

A

Reversible

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35
Q

Disaggregation of …….. and ……………….. elements of the nucleus is associated with reversible cell injury.

A

Granular and fibrillar

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36
Q

Apart from disaggregation of granular and fibrilar elements in the nucleus, what other changes are seen in reversible damage? Why?

A

Clumping of nuclear chromatin, perhaps secondary to a decrease in intracellular pH

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37
Q

Triglycerides accumulation indicates ……………. cell injury. In what cells?

A

Reversible. In hepatocytes, renal and striated muscle cells.

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38
Q

Glycogen loss is ……….. cellular response to injury.

A

Reversible

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39
Q

The time frame when glycogen depletes in severe ischemia?

A

Within 30 min

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40
Q

The physiologic effect of cocaine on sympathetic stimulation? (2)

A

Hypertension and tachycardia;

Coronary vasoconstriction

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41
Q

Clinical manifestation (complications) of cocaine? (3)

A

Myocardial ischemia or infarction;
Aortic dissection;
Neurologic ischemia or stroke

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42
Q

What 2 medications are used in cocaine intoxication?

A

Benzodiazepines and nitroglycerin

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43
Q

What medication group is contraindicated in cocaine intoxication?

A

Beta blockers

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44
Q

What is clinical manifestation of CNS stimulation in cocaine intoxication?

A

Agitation, dilated pupil

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45
Q

Why there is incr. HR, BP and myocardial contractility in cocaine intoxication?

A

Overstimulation of adrenergic receptors (alpha-1, beta-1)
alpha-1 –> BP
beta-1 –> HR and contractility

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46
Q

What is the effect on O2 demand in heart in cocaine intoxication? Why?

A

Increased. Due to overstimulation of adrenergic receptors –> incr. HR, contractility and BP

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47
Q

Why there is decreased coronary oxygen supply in cocaine intoxication?

A

Coronary vasoconstriction due to alpha-1 –> decreased oxygen supply

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48
Q

What causes retrosternal chest pain and ST depression in cocaine intoxication?

A

MYOCARDIAL OXYGEN SUPPLY-DEMAND MISMATCH

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49
Q

Why there may be low grade fever in cocaine intoxication?

A

Peripheral vasoconstriction –> impaired heat loss

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50
Q

Why cocaine intoxication is treated with nitroglycerin?

A

Reduces cardiac preload

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51
Q

Why cocaine intoxication is treated with benzodiazepines?

A

Reduces sympathetic outflow –> alleviated tachycardia/hypertension;
also, calms agitation –> decr. myocardial O2 demand

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52
Q

Can cocaine intoxication cause coronary artery thrombosis?

A

Rarely

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53
Q

What is difference between MI and PATE chest pain?

A

MI - oxygen supply-demand mismatch.
PATE - pleuritic chest pain - pleural effusion seen on xrayn - doesnt resolve without medication - eg in angina relax resolve pain

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54
Q

Transient myocardial ischemia. How cells look?

A

Increase in size

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55
Q

What ions accumulate intracellulary due to decr. ATP?

A

Ca2+ and Na+

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56
Q

What component function of cell membrane is impaired in ATP deficiency?

A

Ion pump failure

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57
Q

What happens to cell when solutes accumulate in the cell?

A

Water moves to the cell –> mitochondrial and cell swelling

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58
Q

Impaired Na/K ATPase due to decr. ATP. What result?

A

Increased intracellular Na and Ca

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59
Q

Sarcoplasmic reticulum Ca2+-ATPases fails to function due to decr. ATP. Result?

A

Incr. intramitochondrial Ca

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60
Q

Why there is cessation of contraction within ischemic zones of myocardium?

A

Failure of the sarcoplasmic reticulum to resequester Ca2+

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61
Q

What happens due to failure of the sarcoplasmic reticulum to resequester Ca2+?

A

Cessation of contraction within ischemic zones of myocardium.

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62
Q

What is K concentration in cell in ischemia?

A

Decreased, Na/K ATPase: Na incresed, K decreased intracellularly

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63
Q

Levels of cellular HCO3- in cardiac ischemia? Why?

A

Not elevated.

Lactatic acidosis –> decr. pH. Tissue CO2, a conjugate acid of HCO3-, is thus elevated in ischemic myocardium.

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64
Q

Cardiac ischemia effect on protein phosphorylation?

A

The cell’s response to ischemia does involve initiating certain metabolic processes through protein phosphorylation, but this does not cause cell swelling.

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65
Q

Stable angina results from …………………….

A

Fixed coronary artery stenosis in the setting of atherosclerotic coronary artery disease (CAD).

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66
Q

When fixed coronary artery stenosis cause mismatch of oxygen supply and demand? Why?

A

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

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67
Q

What medication can be used in stress test? What effect on the heart?

A

Dobutamine - beta 1 agonist. It increases HR and contractility –> incr. O2 demand

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68
Q

Myocardium that is unable to obtain sufficient blood flow to meet the increased oxygen demand typically demonstrates a ……………

A

Transient decrease in contractility ie wall motion defect

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69
Q

Transient decrease in contractility due to insufficient blood flow in stable angina affects what heart function feature?

A

Reduced ejection fraction

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70
Q

How long lasts wall motion defect in stable angina when used dopamine?

A

When increased oxygen demand due to incr. HR and contractility

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71
Q

How long lasts wall motion defect in MI when used dopamine?

A

Persistent wall motion defect - before, during and after dobutamine infusion

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72
Q

Vasospastic angina. Use dopamine in stress test. Result?

A

Vasospastic - due to coronary spasm. Dobutamine - Beta 1 agonist. To cause vasoconstriction need alpha 1 agonist. Therefore dobutamine unlikely to trigger coronary vasospasm

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73
Q

How long last wall motion defect in focal myocardial fibrosis?

A

Persistent - wall motion defect is similar to defect in MI. Furthermore, fibrosis typically results from previous MI

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74
Q

What is EF after dopamine infusion in normal patients?

A

Transient increase in EF due to increased HR and contractility

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75
Q

What pathophysiological mechanism cause vasospastic angina?

A

Coronary endothelial dysfunction and autonomic imbalance

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76
Q

Age of vasospastic angina patients?

A

Younger than 50 y/o

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77
Q

What are and are no risk factor for vasospastic angina?

A

Smoking.

Patients lack of typical risk factor for CAD (hypertension, DM)

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78
Q

Symptoms of vasospastic angina are thought to be triggered by ………….., and they occur most commonly ………………

A

Excess vagal tone; at night

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79
Q

How vasospastic angina is diagnosed?

A

ECG: ST elevation during episode of chest dicomfort.
+
Angiography: abscence of CAD

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80
Q

What 2 pharm provoke symptoms of vasospastic angina?

A

Acetylcholine and ergot alkaloids.

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81
Q

How acetylcholine causes vasospastic angina symptoms?

A

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

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82
Q

How ergot alkaloids cause symptoms?

A

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

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83
Q

In patients with vasospastic angina peripheral endothelial function is …..

A

Intact

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84
Q

Acetylcholine effect on peripheral vessels in patients with vasospastic angina.

A

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

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85
Q

What drug prevents vasospastic angina?

A

calcium channel blockers (diltiazem, amlodipine)

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86
Q

What drug is used in vasospastic angina episode?

A

Sublingual nitroglycerin

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87
Q

Endothelin-1 effect on vessels?

A

Vasoconstriction

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88
Q

Prostacyclin effect on vessels?

A

Vasodilator

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89
Q

In what pathology increased HR can exacerbate angina due to increased myocardial oxygen demand?

A

In CAD. If there is no CAD, it unlikely that myocardial ischemia will manifest

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90
Q

Stable angina is exacerbated by …………. and relieved by …………

A

exertion; rest

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91
Q

Why does stable angina manifest as chest pain?

A

Due to temporary myocardial ischemia from demand-supply mismatch of oxygen rich blood to the myocardium

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92
Q

What causes restricted coronary blood flow in stable angina?

A

Atherosclerotic lesion that obstructs > 70 proc. of lumen.

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93
Q

Clinical manifestation of stable angina?

A

Substernal or left-sided chest pressure, tightness or pain

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94
Q

Myocardial oxygen DEMAND is determined by …….. (4)

A

HR, BP (afterload), LVEDV (preload), cardiac contractility

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95
Q

Myocardial oxygen SUPPLY is determined by ………….. (1)

A

Coronary blood flow

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96
Q

Atherosclerotic plaque obstructing 50proc. of the lumen. Symptoms?

A

No symptoms. They occur when lumen is obstructed more than 70proc.

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97
Q

Effect of exertion and rest on vasospastic angina.

A

None. Not precipitated by exertion and not relieved by rest

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98
Q

Acute coronary syndrome usually occurs due to ………………….

A

Plaque rupture –> superimposed thrombosis –> vessel occlusion

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99
Q

The likelihood of plaque rupture is typically related to ……………….

A

Plaque stability rather than plaque size or degree of luminal narrowing.

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100
Q

Plaque stability depends on the mechanical strength of the ……………………….

A

fibrous cap

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101
Q

…………….. fibroatheromas are generally unstable and more vulnerable to rupture.

A

Thin-cap

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102
Q

Thin-cap fibroatheromas are generally …………….. and more vulnerable to rupture.

A

Unstable

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103
Q

During the chronic inflammatory progression of an atheroma, the fibrous cap is continually being …………………

A

Remodeled

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104
Q

What determined the strength of the fibrous cap?

A

The balance of collagen synthesis and degradation

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105
Q

Thin-cap fibroatheromas are characterized by ………….(1) + (1)

A

Large necrotic core covered by a thin fibrous cap

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106
Q

What macrophages in atheromas secreting to break down a collagen?

A

Metalloproteinases

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107
Q

What cells participate in fibrous cap remodeling?

A

Macrophages

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108
Q

What process in atheroma can destabilize the mechanical integrity of the plaque? How?

A

Ongoing intimal inflammation. Due to release of metalloproteinases

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109
Q

Lysyl oxidase strengthens extracellular collagen fibers by mediating cross-link formation between ……….. and ………….

A

Mediating cross-link formation between lysine and hydroxylysine residues (requires copper).

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110
Q

What ion is required for lysyl oxidase?

A

Copper

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111
Q

High activity of lysyl oxidase effect on atheroma formation?

A

Favor atheroma stabilization, because strengthens collagen fibers

112
Q

Function of procollagen peptidase?

A

Procollagen –> insoluble tropocollagen

113
Q

Function of tropocollagen?

A

Aggregates to form collagen fibrils

114
Q

What cells (2) exocytoses procollagen?

A

Fibroblasts or smooth muscle cells

115
Q

What enzyme participates in collagen formation and requires copper?

A

Lysyl oxidase

116
Q

What vitamin requires prolyl hydroxylase?

A

vit. C

117
Q

What enzyme participating in collagen formation requires vit C?

A

Prolyl hydroxylase

118
Q

Prolyl hydroxylase is responsible for the ………………….. of proline on procollagen chains?

A

Hydroxylation

119
Q

Prolyl hydroxylase hydroxylases ………………… on …………………….

A

Proline on procollagen chains

120
Q

What step is necessary for the formation of a stable collagen triple helix?

A

Hydroxylation of proline on procollagen chains

121
Q

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

A stable collagen triple helix

122
Q

Unstable angina pathophysiology?

A

Artery partially occluded by ruptured atherosclerotic plaque. Tissue beyond in ischemic, but not injured (no infarction)

123
Q

NSTEMI pathophysiology?

A

Artery partially occluded, but tissue beyond is injured (infarction). Subendocardial

124
Q

STEMI pathophysiology?

A

Artery is fully occluded and tissue beyond is injured (infarction). Transmural

125
Q

STEMI symptoms?

A

Persistent chest pain which is not relieved by rest

126
Q

Why does thrombus develop overlying ruptured atherosclerotic plaque?

A

Rupture of plaque –> release of thrombogenic factors into the blood stream –> formation of thrombus

127
Q

What thrombogenic factors are released into the bloodstream when atheroslerotic plaque ruptures?

A

Lipids, collagen, tissue factors

128
Q

What symptoms may accompany STEMI?

A

Nausea, diaphoresis, dyspnea

129
Q

NSTEMI ECG?

A

ST depression and T waves inversion

130
Q

STEMI ECG?

A

Peak T waves –> ST elevation (minutes)–> Q waves (hours/days)

131
Q

2 patho changes seen in autopsy in MI?

A
  1. Atherosclerotic plaque rupture

2. Occlusive thrombus

132
Q

What is common cause of sudden cardiac death (SCD)?

A

Acute MI

133
Q

What is SCD?

A

Abrupt cessation of organized cardiac activity leading to hemodynamic collapse and inadequate tissue perfusion

134
Q

Abrupt cessation of organized cardiac activity leads to ……….. and ………

A

Hemodynamic collapse and inadequate tissue perfusion

135
Q

SCD due to MI usually results from ……………….

A

Malignant ventricular arrhythmia

136
Q

What are types of malignant ventricular arrhythmia?

A

ventricular fibrillation of ventricullar tachycardia degenerating to ventricular fibrillation

137
Q

What triggers malignant ventricular arrhythmia in acute MI?

A

Electric instability in the ischemic myocardium

138
Q

Where forms mural thrombus eg in LV?

A

In the area of infarcted and akinetic myocardium

139
Q

How long it takes to form a thrombus in LV post MI?

A

Several days

140
Q

If more than 50proc of myocardium is infarcted, what complications? (2)

A

Ventricular failure

Cardiogenic shock

141
Q

Ventricular failure and cardiogenic shock in MI. Manifestation? (2)

A

Hypotension and respiratory distress

142
Q

The pathogenesis of atherosclerosis likely begins with …………………

A

Endothelial cell injury

143
Q

Chronic endothelial cell injury may result from … (4)

A

Hypertension (and related hemodynamic factors), hyperlipidemia, smoking, and DM.

144
Q

Endothelial injury by CAD risk factors leads to ………… and/or …………

A

Endothelial cell dysfunction and/or exposure of subendothelial collagen

145
Q

How is called process when occur exposed subendothelial collagen?

A

Endothelial cell denudation

146
Q

Endothelial cell dysfunction results in ……………… (2) + (2)

A

Monocyte and lymphocyte adhesion and migration into the intima

147
Q

Exposure of subendothelial collagen promotes ……………

A

Platelet adhesion

148
Q

In atheroma formation growth factors are produced by ………. (2)

A

Monocytes and platelets

149
Q

What is a function of the growth factors in atheroma formation?

A

Stimulate medial smooth muscle cell (SMC) migration into the intima

150
Q

What facilitate/allows LDL cholesterol to spread into the intima?

A

Increased vascular permeability

151
Q

What phagocytose LDL cholesterol in the intima? What is the result?

A

Accumulating macrophages and SMCs. Lipid-laden foam cells (fatty streak)

152
Q

Chronic inflammatory state in the intima –> deposition of LDL and SMC proliferation –> increased production of ….. (2)

A

Increased production of collagen and proteoglycans

153
Q

Necrosis of foam cells results in …………… to the ………….

A

Release of toxic oxidized LDL into the extracellular matrix –> perpetuates cycle of injury

154
Q

Fibrofatty atheroma consists of ………

A

Core lipid of debris surrounded by monocytes and lymphocytes covered by a fibrous cap with intermixed SMCs

155
Q

Core of lipid debris surrounded by ………. (2)

A

Monocytes and lymphocytes

156
Q

The fibrous cap, of atheromas is synthesized by ………..

A

SMCs

157
Q

Fibroblasts significance in formation of atheroma?

A

None. Fibrous cap is synthesized by SMCs

158
Q

What is role of pericytes in atherosclerosis? Why?

A

None. Pericytes surround the smallest blood vessels. Atherosclerosis - in large elastic and large/medium muscular arteries.

159
Q

What arteries are affected by atherosclerosis?

A

Large elastic;

Large/medium muscular

160
Q

When does atherosclerosis begin? Result?

A

Childhood. Fatty streaks

161
Q

What happens to fatty streaks in advanced age?

A

Fatty streaks transitions into atherosclerotic plaques ie fibrous cap atheromas and fibrous plaques.

162
Q

Turbulent blood flow also leads to …………………………. on the vascular walls and prolonged endothelial contact with …………….

A

Decreased shear stress;

Cholesterol particles.

163
Q

What are 2 most susceptible vascular regions for atherosclerosis?

A

Bends and branch points

164
Q

Atherosclerosis in bends and branch points cause ………. which ……………. and leads to ……………

A

Turbulent blood flow;
Disrupts vascular wall integrity;
Leads to endothelial cell dysfunction

165
Q

What 2 vessels most susceptible to atherosclerosis? Why?

A

Lower abdominal aorta and coronary arteries. Due to hemodynamics

166
Q

When intimal thickening/fatty streaks start to develop?

A

As early as the second decade of life

167
Q

Expression of what molecules increase monocytes and T lymphocytes adhesion in hemodynamic stress?

A

VCAM

168
Q

What growth factors participate in atheroma formation?

A

Platelet derived growth factor (PDGF)

Fibroblast growth factor (FGF)

169
Q

What cytokines participate in atheroma formation?

A

Endothelin-1

IL-1

170
Q

What cells release growth factors and cytokines?

A

Activated platelets, activated macrophages and dysfunctional endothelial cells

171
Q

What is the effect of growth factors and cytokines in atheroma formation?

A

It triggers vascular smooth muscle cells (VSMCs) migration and proliferation in the intima.

172
Q

What do VSMCs in atheroma formation?

A

synthesize extracellular matrix proteins (collagen, elastin, proteoglycans) that form the fibrous cap.

173
Q

What cells induce fibrous cap formation?

A

VSMCs

174
Q

Necrotic debris in atheroma consists of ….

A

macrophage/foam cell and SMC death

175
Q

What encourage plaque stability?

A

SMCs by synthesizing collagen

176
Q

What induces plaque instability?

A

Activated inflammatory cells break down collagen

177
Q

HDL effect on atheroma?

A

Extracts lipids from the intima back into the bloodstream thus helps to slow atheroma development

178
Q

What in atheroma formation directly responsible for collagen formation?

A

VSMCs

179
Q

Function of metalloproteinases? Result?

A

degrade extracellular matrix –> large, soft lipid-rich core with thinning of the fibrous cap.

180
Q

The earliest pathophysiologic change that precedes the formation of atherosclerotic lesions?

A

Endothelial cell dysfunction

181
Q

Right ventricular infarction –> right-sided HF. Presentation? (3)

A

Hypotension, DJV, clear lungs

182
Q

Why there is hypotension in right ventricular infarction?

A

Decreased RV output –> decr. LV filling –> decr. CO –> hypotension and shock

183
Q

PCWP in right ventricular infarction?

A

Decreased - because decreased RV output

184
Q

decr. PCWP, CVP and CO in …………….

A

Distributive shock due to sepsis

185
Q

Which LV infarct more likely to cause LV systolic dysfunction?

A

Anterior wall than inferior

186
Q

The inferior wall of the left ventricle (LV) is supplied by the ………………. which arises off the …………………

A

Supplied by the posterior descending artery (PDA), which arises off the dominant right coronary artery (RCA).

187
Q

Inferior wall myocardial infarction is often associated with ……………. Why?

A

Right ventricular infarction.

Because RCA gives rise to branches that supply most of the right ventricle.

188
Q

Myocardial hibernation refers to a state of ………..

A

Chronic myocardial ischemia

189
Q

What 2 processes are altered in myocardial hibernation?

A

Myocardial metabolism and function

190
Q

What level of stenosis induces myocardial hibernation?

A

Moderate/severe flow-limiting stenosis

191
Q

What process is prevented by myocardial hibernation?

A

Myocardial necrosis

192
Q

Chronically hibernating myocardium demonstrates: (3)

A

Decreased expression and disorganization of contractile and cytoskeletal proteins;
Altered adrenergic control;
Reduced calcium responsivness

193
Q

3 main changes in hibernating myocardium lead to…… (2)

A

Decreased contractility and LV systolic dysfunction

194
Q

Does myocardial hibernation is permanent?

A

No, when blood flow is restored eg in revascularization contractility and LV function restore

195
Q

What is ischemic preconditioning?

A

Repetitive episodes of myocardial ischemia, followed by reperfusion, protect the myocardium from subsequent prolonged episodes of ischemia

196
Q

Reperfusion injury complications?

A

Arrhythmias, microvascular dysfunction with myocardial stunning, and myocyte injury and death.

197
Q

Atheroembolic disease typically occurs after ………..

A

Invasive vascular procedure in arteries with atherosclerotic plaques

198
Q

What patho usually develop patients with atheroembolism? What arteries affected?

A

Acute kidney injury.

Complete occlusion of the arcuate or interlobular arteries.

199
Q

What other organs apart from kidney are affected in atheroembolism?

A

Skin, Gi, CNS

200
Q

Mechanical dislodgement in invasive procedures in vessels affected by atherosclerosis leads to ……………….. –> leads to kidney, CNS, skin, GI injury

A

Showering of cholesterol-rich microemboli into the circulation –> obstruction of distal arterioles and tissue ischemia

201
Q

Fibrinolysis or …………………are used to achieve …………… in acute MI patients

A

percutaneous coronary intervention (PCI); myocardial reperfusion

202
Q

Why PCI is prefered over fibrinolytic therapy?

A

Due to lower rates of ICH and reccurent MI

203
Q

Alteplase converts ……… to ………….

A

plasminogen to plasmin

204
Q

Alteplase binds …………. which is in …………..

A

fibrin; thrombus (clot)

205
Q

Plasmin …………….. (name of reaction) key bonds in the …………… causing clot lysis –> restoration of coronary arterial blood flow.

A

hydrolyzes;

fibrin matrix

206
Q

Fibrinolytic therapy for acute STEMI is a reasonable reperfusion technique for patients with …………………..

A

No contraindications to thrombolysis.

207
Q

MI microscopic changes 0-4h?

A

NONE. May be seen waviness of myofibrils at the border of the infarct (due to myofibril relaxation)

208
Q

MI microscopic changes 4-12h?

A

Early coagulative necrosis - cytoplasmic hepereosinophilia + edema, puctuate hemorrhage, wavy fibers, nuclear pyknosis

209
Q

MI microscopic changes 12-24h?

A

Coagulation necrosis and marginal contraction band necrosis

210
Q

MI microscopic changes 1-3d/5days?

A

Extensive coagulation necrosis and neutrophils infiltrate. Acute inflammation in tissue surrounding infarct

211
Q

MI microscopic changes 5-10d.?

A

Extensive macrophages phagocytosis of the dead cells. Most prominent 7-10d.
Also, at 7th day starts fibrovascular granulation tissue formation and neovascularization.

212
Q

MI microscopic changes 10-14d.?

A

Prominent fibrovascular granulation tissue formation and neovascularization. It starts 7d, but prominent 10-14.

213
Q

MI microscopic changes 2 weeks - months?

A

Fibrosis. Increased collagen deposition and dcecreased cellularity in inforcted zone. Dense collagenous scar - by 2 months post-MI

214
Q

What cells release cytokines and growth factors in MI? What is the purpose?

A

Neutrophils and macrophages.

Initiate tissue proliferation.

215
Q

What growth factors plays important role in post-MI?

A

TGF-beta

216
Q

What is the function of TGF-beta in MI?

A

Downregulate inflammation and stimulate fibrobrasts migration and proliferation –> extensive type I and III collagen depositions.

217
Q

What collage types are is proliferation stage post-MI?

A

Type I and III

218
Q

When happens proliferation phase post-MI?

A

Days to weeks

219
Q

When happens remodeling post-MI?

A

Weeks to months

220
Q

What component, stimulated by TGF-beta facilitate collagen remodeling?

A

Activation of metalloproteinases

221
Q

What enzymes play important role in scar formation?

A

Metalloproteinases

222
Q

What is the function of metalloproteinases?

A

Facilitate collagen remodeling and crosslinking to form dense scar tissue

223
Q

Patients with large scars from previous MI are at high risk to die due to ……………

A

Arrythmia

224
Q

What are levels of NO post-MI?

A

Increased –> reperfusion. No effect on fibrous scar formation

225
Q

IFN-beta effect post-MI?

A

anti-inflammatory cytokine –> reduces the formation of fibrotic tissue

226
Q

IL-8 and TNF-α effect in post-MI?

A

Proinflammatory cytokines that stimulate the recruitment and activation of other immune cells (eg, neutrophils). However, neither directly promotes fibrosis in a healing wound

227
Q

Papillary muscle rupture, when?

A

Acute or 3-5 days

228
Q

Papillary muscle rupture clinical findings? (3)

A

Severe mitral regurgitation with flail leaflet
New holosystolic murmur
Severe pulmonary edema

229
Q

Interventricular septal rupture, when?

A

Acute or 3-5 days

230
Q

Interventricular septal rupture clinical findings?

A

Chest pain
New holosystolic murmur
biventricular failure, shock
Set up in O2 level from RA to RV

231
Q

Ventricular free-wall rupture, when?

A

5 days - 2 weeks

232
Q

Ventricular free-wall rupture, symptoms?

A

Chest pain, tamponade, shock, distant heart sound (tamponade beck triad: hypotension, JVD, distant heart sound)

233
Q

Left ventricular aneurysm, when?

A

within several months

234
Q

Left ventricular aneurysm clinical findings?

A

Subacute HF, stable angina

235
Q

How called ventricular septal defect in septum rupture post-MI?

A

Shunt

236
Q

What resolves newly occurred systolic murmur in mitral regurgitation due to muscle dysfunction?

A

Revascularization

237
Q

What is a difference of cause between papillary muscle displacement and rupture?

A

Displacement: ischemia –> hypokinesis and outward displacement of the muscle –> increased tension on the chordae tendineae –> prevented complete clossure of mitral valve

238
Q

Papillary muscle displacement can be resolved by …………

A

Coronary revascularization –> restored papillary muscle and LV wall motion –> resolution of the mitral regurgitation

239
Q

Papillary muscle rupture can be resolved by …………

A

It does not resolve with coronary revascularization and typically requires surgical repair.

240
Q

Rupture of the interventricular septum can be resolved by …………..

A

The condition does not resolve with coronary revascularization and typically requires surgical repair

241
Q

What effect of MI ischemia can have on aortic root, aortic valve leaflet, mitral valve chordae tendineae?

A

Those structures are not directly affected by my myocardial ischemia

242
Q

What infarction can cause LV free-wall rupture?

A

Transmural

243
Q

Gross presentation of heart of LV free-wall rupture?

A

Slitlike tear in the anterior LV wall

244
Q

The infarcted myocardium becomes …………….. and does not move with the remaining healthy myocardium, creating ……………………

A

Akinetic;

Creating additional shear stress on the myocardial wall.

245
Q

What creates additional shear stress on the myocardial wall in post-MI?

A

Akinetic infarcted myocardium

246
Q

Why myocardial wall may not tolerate additional shear stress caused by akinesis?

A

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
Q

What increases the risk of free wall rupture post-MI?

A

Delayed reperfusion –> therefore weakened LV wall

248
Q

What is the main complication of LV free wall rupture?

A

Cardiac tamponade and hemopericardium

249
Q

What stimulated collateral vessels formation in myocardium?

A

Growth factors (eg VEGF)

250
Q

Step by step what induces collateral vessels formation?

A

Atherosclerosis –> progressive reduction in blood flow –> ischemic myocardium releases growth factors (eg VEGF) –> formation of collateral vessels.

251
Q

Stable atherosclerotic plaque formation in LAD. From what vessel form collaterals? To which area?

A

From right coronary artery (RCA) collaterals to ischemic myocardium located distal to the LAD occlusion.

252
Q

What facilitates blood flow from RCA collaterals to distal LAD obstruction?

A

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
Q

In what atherosclerotic plaques do collaterals form and in what not?

A

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
Q

Unstable atherosclerotic plaque characteristics (3)

A

Active inflammation, a lipid-rich core and/or a thin fibrous cap

255
Q

Why unstable atherosclerotic plaque will not lead to collaterals formation?

A

It is more likely to rupture before it becomes large enough to cause significant chronic ischemia;

256
Q

High or low calcium in plaque leads to decrease stability?

A

Low calcium (immature calcification)

257
Q

How correlates coronary artery calcium content with total atherosclerotic plaque burden?

A

Directly. Calcium scoring can be assessed by cardiac CT scan - estimates severity of coronary artery disease

258
Q

Cardiac CT can estimate severity of what disease?

A

CAD

259
Q

What are ostial atherosclerotic plaques?

A

Those located at a branch point of 2 arteries

260
Q

What plaques occlude multiple areas of myocardium?

A

Ostial atherosclerotic plaques

261
Q

What plaques limit the availability of nearby well-perfused arteries from which viable collateral vessels can develop?

A

Ostial atherosclerotic plaques

262
Q

High muscle mass is in ………… ventricle, and low muscle mass is in ………….. ventricle.

A

High - left

Low - right

263
Q

Resting oxygen extraction is high in …………… and low in ……………. ventricle

A

High - left

Low - right

264
Q

Coronary perfusion only during diastole is in …………..

A

Left ventricle

265
Q

Coronary perfusion throughout cardiac cycle is in …………….

A

Right ventricle

266
Q

Right ventricle gets coronary perfusion during ………………

A

all cardiac cycle

267
Q

In which ventricle collateral circulation is better developed?

A

Less in left, more in right

268
Q

High ischemic preconditioning is in …… and low in ……. ventricle

A

Left - low

Right - high

269
Q

How changes contractile function in right and left ventricles post-MI?

A

Left ventricle - scarring and reduction in contractile function
Right ventricle - contractile function almost always returns to normal

270
Q

What protects RV from loss of contractility post-MI? (no pressures in this answer)

A

Small muscle mass and afterload of RV –> less oxygen demand and necessitate lower oxygen extraction at rest.

271
Q

Systolic pressure in RV relations to protection of RV in MI?

A

In RV low systolic pressure (=<25mmHg) —> coronary perfusion throughout the cardiac cycle

272
Q

Systolic pressure in LV relations to the protection of LV in MI?

A

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
Q

The most robust collateral flow occurs from ……………… to the …………………., therefore …………. ventricle is protected better.

A

From left to right;

Right - it has more developed collateral circulation

274
Q

Large MI –> decr. CO and contractility —> activation of what and what is the result?

A

The aortic and carotid baroreceptors stimulate peripheral vasoconstriction to increased SVR.
Also HR is increased to increased CO (due to these receptors?)

275
Q

Failure to eject blood from the left ventricle increases ……………….

A

LV end-diastolic pressure

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