Ischemic Heart Disease Flashcards

1
Q

What is Ischemic Heart Disease?

A

imbalance between the myocardial blood flow and the metabolic demand of the myocardium

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2
Q

Coronary artery perfusion depends upon

A

ostia (aortic diastolic pressure) Minus coronary sinus (right atrial pressure).

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3
Q

Coronary blood flow is reduced during systole because of

A

Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction.

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4
Q

Factors reducing coronary blood flow include:

A
  1. Decreased aortic diastolic pressure
  2. Increased intraventricular pressure and myocardial contraction
  3. Coronary artery stenosis
  4. Aortic valve stenosis and regurgitation
  5. Increased RA pressure
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5
Q

collateral vessels are present in all hearts that measure ?

A

40 microns

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6
Q

the cross-sectional area of the coronary artery lumen must be reduced by _____ to significantly affect perfusion.

A

> 75%

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7
Q

“Thrombolytic therapy” with agents such as streptokinase or tissue plasminogen activatorS (TPA) such as atelpase is often used within

A

first 12 hours following onset of symptoms and with ST-segment elevation to try and lyse a recently formed thrombus.

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8
Q

there is no ST-segment change and there is not sufficient myocardial damage for for release of a biomarker such as the troponins or CK-MB. There is one or more of the following:

(1) rest angina,
(2) new-onset severe angina, &
(3) a crescendo pattern of occurrence

A
  1. Unstable angina:
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9
Q

there is no ST-segment change but there is myocardial necrosis for release of a biomarker such as the troponins or CK-MB.

A
  1. Non-ST-segment Elevation Myocardial Infarction (NSTEMI)
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10
Q

there is ST-segment elevation and myocardial necrosis with release of a biomarker such as the troponins or CK-MB.

A
  1. ST-segment Elevation Myocardial Infarction (STEMI)
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11
Q

In 2000, the European Society of Cardiology and the American College of Cardiology Consensus group redefined myocardial infarction, with the definition being based on

A

myocyte necrosis as determined by troponins in the clinical setting of ischaemia

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12
Q

The molecular events during MI relate to the initial ischemic event, reperfusion, and subsequent inflammatory response. Up to 6 hours following the initial ischemic event, most cell loss occur via

A

apoptosis. After that, necrosis predominates

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13
Q

Transmural infarct involves

A

the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%.

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14
Q

Subendocardial infarct involves

A

multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall

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15
Q

Ischemic Cardiomyopathy

A

disease results from severe coronary atherosclerosis involving all major branches. The result is an inadequate vascular supply which leads to myocyte loss. The myocyte loss coupled with fibrosis in the form of interstitial collagen deposition results in decreased compliance, which along with the accompanying cardiac dilation, results in overload of remaining myocytes. This keeps the process going, with compensation by continuing myocyte hypertrophy. There may even be compensation through hyperplasia as well as hypertrophy, which can explain the enormous size (2 to 3 times normal size) of the resulting heart. Eventually, the heart can no longer compensate, and cardiac failure ensues with arrhythmias and/or ischemic events.

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16
Q

B-type natriuretic peptide (BNP)

A

released from ventricular myocardium. BNP release can be stimulated by systolic and diastolic left ventricular dysfunction, acute coronary syndromes, stable coronary heart disease, valvular heart disease, acute and chronic right ventricular failure, and left and right ventricular hypertrophy secondary to arterial or pulmonary hypertension. BNP is a marker for heart failure.

17
Q

C-reactive protein (CRP)

A

is an acute phase protein elevated when inflammation is present. Since inflammation is part of atheroma formation, then CRP may reflect the extent of atheromatous plaque formation and predict risk for acute coronary events. However, CRP lacks specificity for vascular events.