Card - Path (Part 3: Ischemic Heart Disease & MI)

Question 1

What defines angina? Include what causes it and whether angina causes myocyte necrosis.

Answer 1

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necrosis

Question 2

What are 3 types of angina?

Answer 2

(1) Stable (2) Variant angina (Prinzmetal) (3) Unstable/Crescendo

Question 3

To what is stable angina usually secondary?

Answer 3

Usually secondary to atherosclerosis

Question 4

Characterize the pain and ECG findings of stable angina.

Answer 4

Exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest

Question 5

What is another name for Variant angina? When does it occur, and to what is it secondary?

Answer 5

Occurs at rest secondary to coronary artery spasm

Question 6

What ECG finding characterizes Variant angina (Prinzmetal)?

Answer 6

Transient ST elevation on ECG

Question 7

What are 3 known triggers of Variant angina (Prinzmetal)? What is often the case in terms of the trigger?

Answer 7

Known triggers include tobacco, cocaine, and triptans, but trigger is often often

Question 8

How can Variant angina (Prinzmetal) be treated?

Answer 8

Treat with calcium channel blockers, nitrates, and smoking cessation (if applicable).

Question 9

What defines Unstable/Crescendo angina?

Answer 9

Thrombosis with incomplete coronary artery occlusion

Question 10

Describe the chest pain and ECG finding of Unstable/Crescendo angina.

Answer 10

ST depression on ECG (increase in frequency or intensity of chest pain; any chest pain at rest).

Question 11

What are 5 types of ischemic heart disease manifestations?

Answer 11

(1) Angina (2) Coronary steal syndrome (3) Myocardial infarction (4) Sudden cardiac death (5) Chronic ischemic heart disease

Question 12

What defines Coronary steal syndrome? Give 2 examples of the type of substance involved. What is an important clinical correlation for this?

Answer 12

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas => decreased flow and ischemia in the poststenotic region; Principle behind pharmacologic stress

Question 13

What most often defines and causes myocardial infarction?

Answer 13

Most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis

Question 14

What will the ECG show in transmural versus subendocardial myocardial infarction?

Answer 14

If transmural, ECG will show ST elevation; if subendocardial, ECG may show ST depressions.

Question 15

What is used to diagnose myocardial infarction?

Answer 15

Cardiac biomarkers are diagnostic

Question 16

What defines sudden cardiac death, and what most commonly causes it?

Answer 16

Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (e.g., ventricular fibrillation).

Question 17

What are 3 conditions associated with sudden cardiac death, and what is important to relate to each?

Answer 17

Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (e.g., long QT syndrome).

Question 18

What defines chronic ischemic heart disease?

Answer 18

Progressive onset of CHF over many years due to chronic ischemic myocardial damage.

Question 19

What are the 3 most commonly occluded arteries leading to MI? List them in order of most to least common.

Answer 19

LAD > RCA > Circumflex

Question 20

What 7 symptoms characterize MI?

Answer 20

Symptoms: (1) diaphoresis (2) nausea (3) vomiting (4) severe retrosternal pain (5) pain in left arm and/or jaw (6) shortness of breath (7) fatigue

Question 21

What gross myocardial changes occur at the following time periods after an MI: (1) 0-4 hr (2) 4-12 hr (3) 12-24 hr (4) 1-3 days (5) 3-14 days (6) 2 weeks to several months?

Answer 21

(1) None (2) & (3) [Occluded artery]; Infarct, Dark mottling; Pale with tetrazolium stain (4) Hyperemia (5) Hyperemic border; central yellow-brown softening - maximally yellow and soft by 10 days (6) [Recanalized artery], Gray-white (scar)

Question 22

What changes can be seen under light microscope at the following time periods after an MI: (1) 0-4 hr (2) 4-12 hr (3) 12-24 hr (4) 1-3 days (5) 3-14 days (6) 2 weeks to several months?

Answer 22

(1) None (2) Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers (3) Neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage) (4) Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils. (5) Macrophages, then granulation tissue at margins (6) Contracted scar complete

Question 23

Again, what microscopic change(s) occur(s) 0-4 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

Answer 23

None; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an MI

Question 24

Again, what microscopic change(s) occur(s) 4-12 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

Answer 24

Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an MI

Question 25

Again, what microscopic change(s) occur(s) 12-24 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

Answer 25

Neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage).; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an M

Question 26

Again, what microscopic change(s) occur(s) 1 to 3 days after onset of an MI? What are is a complication that may occur in this time frame?

Answer 26

Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils.; Fibrinous pericarditis

Question 27

Again, what microscopic change(s) occur(s) 3-14 days after onset of an MI? What are 4 complications that may occur in this time frame?

Answer 27

Macrophages, then granulation tissue at margins; (1) Free wall rupture => tamponade; (2) Papillary muscle rupture => mitral regurgitation; (3) Interventricular septal rupture due to macrophage-mediated structural degradation (4) LV pseudoaneurysm (mural thrombus “plugs” hole in myocardium => “time bomb”)

Question 28

Again, what microscopic change(s) occur(s) 2 weeks to several months after onset of an MI? What are 4 complications that may occur in this time frame?

Answer 28

Contracted scar complete; (1) Dressler syndrome, (2) HF, (3) arrhythmias, (4) true ventricular aneurysm (outward bulge during contraction, “dyskinesia”)

Question 29

What is the gold standard for diagnosis of MI in the first 6 hours?

Answer 29

In the first 6 hours, ECG is the gold standard

Question 30

Give 2 cardiac biomarkers used for diagnosis of MI and their timelines and advantages/limitations.

Answer 30

CARDIAC TROPONIN I rises after 4 hours and is increased for 7-10 days; more specific than other protein markers. CK-MB is predominately found in myocardium but can also be released from skeletal muscle. Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours.

Question 31

What are 3 ECG changes that may be seen with MI, and what causes each?

Answer 31

ECG changes can include (1) ST elevation (STEMI, acute transmural infarct), (2) ST depression (subendocardial infarct), and pathologic Q waves (evolving or old transmural infarct).

Question 32

What are the 2 major types of infarcts?

Answer 32

(1) Transmural infarcts (2) Subendocardial infarcts

Question 33

Distinguish between transmural infarcts and subendocardial infarcts in terms of the degree of necrosis caused.

Answer 33

TRANSMURAL INFARCTS: Increased necrosis; SUBENDOCARDIAL INFARCTS: Due to ischemic necrosis of < 50% of ventricle wall

Question 34

Distinguish between transmural infarcts and subendocardial infarcts in terms of the extent of area affected.

Answer 34

TRANSMURAL INFARCTS: Affects entire wall; SUBENDOCARDIAL INFARCTS: Subendocardium especially vulnerable to ischemia

Question 35

Distinguish between transmural infarcts and subendocardial infarcts in terms of their ECG findings.

Answer 35

TRANSMURAL INFARCTS: ST elevation on ECG, Q waves; SUBENDOCARDIAL INFARCTS: ST depression on ECG

Question 36

For each of the following infarct locations, give the ECG leads with (patholologic) Q waves that could be used to diagnose MI: (1) Anterior wall (LAD) (2) Anteroseptal (LAD) (3) Anterolateral (LAD or LCX) (4) Lateral wall (LXC) (5) Inferior wall (RCA).

Answer 36

(1) V1-V4 (2) V1-V2 (3) V4-V6 (5) I, aVL (6) II, III, aVF; Think: “Lateral wall (LCX) = I, aVL” & “inFerior wall (RCA) = II, III, aVF”

Question 37

What are 7 kinds of MI complications?

Answer 37

(1) Cardiac arrhythmia (2) LV failure and pulmonary edema (3) Cardiogenic shock (4) Rupture (e.g., ventricular free wall, papillary muscle, or interventricular septum) (5) Ventricular pseudoaneurysm formation (6) Postinfarction fibrinous pericarditis (7) Dressler syndrome

Question 38

What is an important cause of death in MI patients before reaching the hospital? When is it common?

Answer 38

Cardiac arrhythmia - important cause of death before reaching hospital; common in first few days

Question 39

What kind of infarct is associated with cardiogenic shock as a complication of MI? What risk does this complication increase?

Answer 39

Cardiogenic shock (large infarct - high risk of mortality)

Question 40

What are 3 types of ruptures that can occur as complications of MI? What effect can/does each rupture have?

Answer 40

(1) Ventricular free wall rupture => cardiac tamponade (2) Papillary muscle rupture => severe mitral regurgitation (3) Interventricular septum rupture => VSD

Question 41

When is the greatest risk for rupture (e.g., ventricular free wall, papillary muscle, interventricular septum) as a complication of MI?

Answer 41

Greatest risk 6-14 days postinfarct

Question 42

What hemodynamic change, risk, and pathology are associated with ventricular pseudoaneursym formation as a complication of MI? When is the greatest risk for this post-MI?

Answer 42

Decreased CO, Risk of arrhythmia, Embolus from mural thrombus; Greatest risk approximately 1 week post-MI

Question 43

What is a sign of postinfarction fibrinous pericarditis as a complication of MI? When does it occur?

Answer 43

Friction rub (1-3 days post-MI)

Question 44

What is Dressler syndrome? When does it occur as a post-MI complication?

Answer 44

Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI)