2013-09-17 Acute Coronary Syndromes

Question 1

What is the clinical presentation of unstable angina?

Answer 1

Dx based on combo of characteristic history, ECG findings, and positive biomarkers

[Similar to NSTEMI]
Increasing CP or CP at rest
ECG changes: None or ST-depression
**Normal biomarkers**
^distinguishing characteristic

Question 2

Describe management of unstable angina.

Answer 2

[Same as NSTEMI]

1. Anti-ischemic
   - -beta-blockers
   - -nitrates
   - -Ca2+ channel blockers (less important)
2. Anti-thrombic
   - -Platelet inhib: ASA, clopodigrel, glycoprotein IIb/IIIa inhibitors (e.g. abciximab)
   - -Anti-coag: heparin
   * *FIBRINOLYSIS NOT INDICATED

**PCI may be indicated based on severity/ability for med mgmt to ctrl sx

Question 3

What is the clinical presentation of NSTEMI?

Answer 3

Dx based on combo of characteristic history, ECG findings, and positive biomarkers

[Similar to UA]
Increasing CP or CP at rest
ECG changes: None or ST-depression
**ELEVATED biomarkers**
^distinguishing characteristic

Question 4

Describe management of NSTEMI.

Answer 4

[Same as UA]

1. Anti-ischemic
   - -beta-blockers
   - -nitrates
   - -Ca2+ channel blockers (less important)
2. Anti-thrombic
   - -Platelet inhib: ASA, clopodigrel, glycoprotein IIb/IIIa inhibitors (e.g. abciximab)
   - -Anti-coag: heparin
   * *FIBRINOLYSIS NOT INDICATED

**PCI may be indicated based on severity/ability for med mgmt to ctrl sx

Question 5

What is the clinical presentation of STEMI?

Answer 5

Dx based for the most part on the CP hx, ECG, and serum biomarkers:
CP at rest
ST-elevation
Elevated biomarkers

Question 6

Describe management of STEMI.

Answer 6

1. General measures: bedrest, oxygen, anxiolytics, morphine PPA
2. Anti-ischemic: Same as UA/NSTEMI
   - -beta-blockers
   - -nitrates
   - -Ca2+ channel blockers (less important)
   * Beta-blockers are usually administered intravenously, in part for their acute anti-arrhythmic activity, as well as their long-term benefits on post-MI survival.
3. Adjunctive therapies:
   - -ACE-inhibitors and statins decrease mortality. ACE-inhibitors appear to prevent remodeling. Statins appear to have effects > their lipid lowering activity; possibly stabilize unstable plaque.
4. Anti-thrombotic: Aspirin, clopidogrel, and heparin have all been shown to improve outcomes in patients with STEMI.
5. Revascularization: decision to intervene must typically be based on the chest pain story and ECG, before the diagnosis of infarction can be confirmed by serum biomarkers (i.e. don’t wait for enzymes!).
   a. tPA: accelerates nl fibrinolytic pathway; clot lysis in roughly 70-80% of STEMI pts. signaled by pain relief, resolution of the ST-elevation, and the earlier and higher peaking of CK-MB and troponin levels.
   b. Primary: The preferred revasc technique, primary PCI can achieve opening of the occluded artery > 90-95% of STEMI pts.

Question 7

What are the complications of MI?

Answer 7

1. Power failure
   a. LV fail
   b. cardiogenic shock
2. pericarditis
   a. acute: typically 1-2 days s/p
   b. Dresslers (autoimm): typically 1-2 wks s/p
3. RV infarct
4. arrhythmias
   a. ventricular
   b. Heart block A-V block (Wenkebach) His-Purkinje (Mobitz II)
5. Myocardial rupture
   a. LV free wall
   b. VSD
   c. papillary muscle –> mitral regurg

Question 8

Explain the pathophysiology of ACS.

Answer 8

Plaque formation
Plaque rupture (not fully understood shear stress, degen of ECM and inflamm)
Thrombogenic subendothelial layers now exposed
1° hemostasis–Platelet activation
2° hemostasis: Activation of clotting cascade
Fibrinolysis

Question 9

How do you perform risk stratification in the setting of ACS?

Answer 9

Use TIMI Score

Efforts to risk stratify post-MI patients are based on the theory that interventions (e.g., elective PCI or CABG) are most likely to benefit patients at greatest risk. The four important independent risk determinants:
a. Severity of LV dysfunction (e.g., LVEF by echocardiography) b. Number of diseased coronary arteries (e.g., coronary angiography, various imaging techniques) c. Ventricular arrhythmias (e.g., Holter monitor) -possibly more as a marker for LV dysfunction) d. Extent of residual territory at risk of ischemia (e.g., nuclear stress-testing)

Question 10

Define ACS

Answer 10

“a clinical syndrome, usually associated with new or increasing chest pain, compatible with acute myocardial ischemia.” can have other causes but “the ACS term is commonly restricted to conditions caused by acute coronary lesions.”

Question 11

Define unstable angina

Answer 11

acute ischemic syndrome

• -NON-occlusive plaque rupture
• -infarction does NOT occur
• -may present with ECG abnormalities similar to those seen in NSTEMI.

Question 12

Define NSTEMI

Answer 12

acute ischemic syndrome

• -NON-occlusive plaque rupture
• -myocardial infarction DOES occur
• -may present with ECG abnormalities, e.g., ST-segment depression, but NOT with ST-elevation.

Question 13

Define STEMI

Answer 13

acute ischemic syndrome

• -plaque rupture that DOES leads to acute thrombotic occlusion
• -myocardial infarction DOES occur
• -These patients present with ST-segment elevation and are classified as “ST-Elevation MI.”

Question 14

What is the typical presentation of stable angina?

Answer 14

Exertional CP
ST depression with CP
Normal biomarkers

Question 15

Post-STEMI 2° Prevention

Answer 15

BASIC:

Beta-blockers
Anti-platlet drugs: ASA and clopidogrel
Statins
Inhibitors of ACE
Correction of risk factors (smoking, exercise, diet, HTN ctrl)