Ischemic heart disease (IHD) Flashcards

1
Q

what is IHD

A

IHD – group of related syndromes resulting from myocardial ischemia (imbalance between perfusion and demand of the heart for oxygenated blood)

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2
Q

why is IHD known as coronary artery disease

A

IHD is also known as coronary artery disease (as in over 90% of the cases of IHD are caused by atherosclerotic coronary artery disease)

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3
Q

what are the Clinical manifestations of IHD- 4 syndromes

A

Myocardial infarction
Angina pectoris
Chronic IHD with heart failure
Sudden cardiac death (due to arrhythmias originating in ischemic myocardium)

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4
Q

what are the clinical manifestations of acute coronary syndromes

A

1.Unstable angina (periinfarction angina)
2.Acute myocardial infarction and
3.Sudden cardiac death

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5
Q

what is the mechanism of IHD

A

Mechanism – change of stable atherosclerotic plaque into an unstable atherothrombotic lesion

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6
Q

what is the pathogenesis of IHD

A

Interaction of many factors lead to diminished perfusion of myocardium resulting in IHD syndromes; these are

Atherosclerotic narrowing of the coronary artery, (dominant factor)
Disruption of plaque (acute plaque changes )
Intraluminal thrombosis overlying the plaque and
Coronary vasospasm .

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7
Q

what is the role of fixed coronory obstruction in IHD

A

More than 75% reduction in the cross –sectional area of the lumen (critical stenosis) of one or more of the major coronary arteries lead to symptomatic IHD

Chronic fixed obstruction –90% stenosis of lumen can lead to ischemia even at rest

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8
Q

what epicardial coronary artery is obstructed in IHD

A

Usually, one epicardial coronary artery is obstructed; sometimes 2 or all three are affected; left anterior descending artery (LAD), left circumflex artery (LCX), Right coronary artery RCA

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9
Q

what is the role of acute plaque changes in IHD

A

Disruption of a partially stenosing plaque precipitate acute coronary syndromes in many patients; The event may be:

Rupture or fissuring, erosion or ulceration –followed by thrombosis,
Hemorrhage into the plaque with enlargement of the plaque

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10
Q

what is the role of coronary thrombosis in IHD

A

Thrombosis of a disrupted plaque may lead to total /incomplete occlusion of the lumen.
Transmural acute MI –total occlusion
Unstable angina, acute subendocardial infarction and sudden death- incomplete occlusion

Embolization of thrombus- microinfarcts

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11
Q

what is the role of vasoconstriction in IHD

A

Reduces the lumen size, increases mechanical stress on the plaque

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12
Q

what is vasoconstriction in IHD stimulated by

A

It is stimulated by:
1.Circulating adrenergic agonists
2. Platelet contents
3.Endothelial dysfunction
4.Mediators from inflammatory cells.

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13
Q

what is angina pectoris

A

Characterized by paroxysmal and recurrent attacks of substernal or precordial chest pain caused by transient myocardial ischemia (15 seconds-15 minutes).

[note: The duration of ischemia is not sufficient to cause cellular necrosis (infarction)]

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14
Q

what are the three patterns of angina pectoris

A

stable angina
prinzmetal angina
unstable or preinfraction angina

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15
Q

what is stable angina

A

Stable angina-occurs with physical activity or emotional excitement and is relieved by rest, caused by chronic stenosing atherosclerosis without plaque disruption

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16
Q

what is prinzmetal angina

A

Prinzmetal angina- occurs at rest, caused by coronary artery spasm; responds to vasodilators

17
Q

what is unstable or pre infraction angina

A

Unstable or pre infarction angina- induced by disruption of plaque with incomplete occlusion of lumen and embolization or vasospasm (or both) ; is usually the prodrome of subsequent MI

18
Q

what is the leading cause of death in industralized nations

A

MI ( heart attack)

19
Q

what are the three patterns of infraction

A

Transmural/regional-full thickness
subendocardial/circumferential
microscopic infracts

20
Q

what is the transmural/regional full thickness pattern of infraction

A

Transmural/ regional-full thickness caused by epicardial vessel occlusion through a combination of chronic atherosclerosis and acute thrombosis; such transmural MIs typically yield ST segment elevations on the electrocardiogram (ECG) (STEMI)

21
Q

what is the subendocardial/circumferential pattern of infraction

A

Subendocardial/ circumferential -necrosis limited to inner one third or one half of the ventricular wall in global ischemia as in hypotension (“non–ST elevation infarct”(NSTEMI); ST depression)

22
Q

what is the microscopic infract pattern of infraction

A

Microscopic infarcts occur in the setting of small vessel occlusions and may not show any diagnostic ECG changes as in case of vasculitis

23
Q

what is the pathogenesis of myocardial infraction

A

Coronary artery occlusion –dynamic interaction among the factors

Atherosclerois, plaque changes, thrombosis and vasospasm in over 90% of MI patients

Other less common causes of myocardial ischemia (in less than 10% of MI patients ) : Emboli, vasculitis, coronary artery aneurysms, hypoxemia, shock and left-sided failure
Myocardial response-irreversible myocyte damage occurs with ischemia lasting at least 20-40 minutes, however typical MI occurs only when severe ischemia lasts for hours, hence early restoration of perfusion may prevent cell death.

24
Q

whats is the myocardial response to ischemia

A

Functional alterations-
Rapid loss of contractility, which occurs within a minute or so of the onset of ischemia

Biochemical changes
Within seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in adenosine triphosphate (ATP) and accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes.

25
what are the ultrastrucutal changes to myocardium in response to ischemia
Ultrastructural changes (including myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling) also become rapidly apparent. These early changes are potentially reversible. Only severe ischemia lasting at least 20 to 40 minutes causes irreversible damage and myocyte death leading to coagulation necrosis With longer periods of ischemia, vessel injury occurs, leading to microvascular thrombosis.
26
whats the form of necrosis caused by irreversible damage and myocyte death in response to severe ischemia
coagulation necrosis
27
what are the gross examination findings of a myocradial infraction
Gross examination findings Myocardial infarcts less than 12 hours old usually are not grossly apparent. By 12 to 24 hours after MI, an infarct usually can be grossly identified by a red-blue discoloration caused by stagnated, trapped blood Thereafter, infarcts become progressively better delineated as soft, yellow-tan areas; by 10 to 14 days, infarcts are rimmed by hyperemic (highly vascularized) granulation tissue. Over the succeeding weeks, the infarcted tissue evolves to a fibrous scar.
28
how can we visualize infracts more than 3 hours old
infarcts more than 3 hours old can be visualized by exposing myocardium to vital stains, such as tri phenyl tetra zolium chloride, a substrate for lactate dehydrogenase.
29
what is the morphology of myocardial infraction after 24-72 hours
pallor gross appearance. complete coagulation necrosis of myofibers, heavy neutrophilic infiltrate with early fragmentation of neutrophil nuclei