Coronary Artery Disease Flashcards
1
Q
Non-classic sx of CAD
A
- Dyspnea
- Dizziness
- Syncope
- Pulmonary edema
2
Q
Gold standard dx test for CAD
A
Coronary angioraphy
3
Q
- 75% reduction in coronary artery cross-sectional area results in _
- 90% reductino in coronary artery cross-sectional area resutls in _
A
- 50% loss of arterial diamter (anginia with activity)
- 75-80% doss of diamter (angina with rest)
4
Q
Presenting clinical scenarios for CAD
A
- Chronic, stable angina
- Acute coronary syndrome (ACS)
- ST elevation MI (STEMI)
- myocardial necrosis with elevated biomarks and ST changes on EKG
- Non-ST elevatin MI (NSTEMI)
- myocardial necrosis with elevated biomarkers without ST changes on EKG
- Unstable angina
- ST elevation MI (STEMI)
5
Q
Etiology of STEMI
A
Rupture of atherosclerotic plauqe with acute mural thrombus formation and CA obstruction
6
Q
Etiology of NSTEMI
A
- Atherosclerotic plaque rupture and thrombosis (MC)
- Coronary spasm (Prinzmetal’s angina)
- Progressive coronary obstruction
- Increased oxygen demand (demand ischemia, tachycardia)
- Decreased oxygen supply (anemia)
7
Q
3 primary mechanisms through which CAD results in LV dysfunction
A
- MI (irreversible) with loss of myocardium
- Hybernating myocardium
- Myocardial dysfunction at rest due to CAD that partially resolves after revascularization
- Stunned myocardium
- Transient myocardial dysfunction after reperfusion
8
Q
AHA/ACC Guidelines for Medical Management of CAD
A
- Smoking cessation
- Hypertension (goal < 140/90, or < 130/80 if DM or CKD)
- Hypercholesterolemia (goal LDL < 100; if TG > 200, then non-HDL < 130)
- Obesity (BMI 18.5-24.9)
- DM (goal HgbA1c < 7%)
- Anticoagulation
- ASA 81 mg (all patients)
- ASA 81 + Plavix 75 (ACS or PCI)
- ACE-I (EF < 40%)
- ARB if intolerant to ACE-I
- Beta-blocker (all pts with MI, ACS, LV dysfunction)
- Aldosterone inhibitor (large MI in patient with low EF, no renal dysfunction)
9
Q
Summary of SYNTAX Trial
A
NEJM (2009)
- PCI vs. CABG
- Non-inferiority (LM or 3v CAD)
- Primary results:
- Composite adverse events + cerebrovasc events higher in PCI vs. CABG
- Primarily driven by higher repeat revascularization in PCI
- Simlar MI and death rates
- Stroke rates higher in CABG
- Composite adverse events + cerebrovasc events higher in PCI vs. CABG
10
Q
General repeat revascularizaton rates for PCI and CABG
A
- PCI (30% at 1 year and 55% at 5 years)
- CABG (3-15%)
11
Q
AHA/ACC Guidelines for CABG
A
- LM disease (>50% stenosis)
- LM equivalent diease (pLAD >70% + pCx stenosis)
- 3v CAD (especially if EF < 50%)
- 2v CAD with EF < 50%
- pLAD + 1-2v CAD
- Disabling angina refractory to medical managment
- Failed PCI
- Anatomy not suitable for PCI
- Total occlusion
- Circumferential calcification
- Bifurcation involvment
- Diffuse or distal lesions
- Concomitant cardiac lesions requiring surgery
12
Q
Tx STEMI
A
Non-surgical, usually medical, unless ongoing ischemia or cardiogenic shock despite maximal medical therapy
13
Q
Hemodynamic instability during OPCAB often due to:
A
- RV compression (exposure of lateral LV wall)
- Diastolic dysfunction from excessive downward pressure from coronary stabilizer
- Intraoperative ischemia from native CAD or coronary snaring
14
Q
Results of OPCAB versus On pump-CAB
A
- Surgical outcomes similar
- OPCAB:
- Less blood loss and tranfusions
- Less myocardial enzyme release in 24 hrs
- Less neurocognitive dysfunction
- Less renal insufficiency
- On-pump CABG
- Higher number of total bypass grafts (more complete revascularization)
- Easier grafts to posterior (Cx) targets
- ? better long-term graft patency
15
Q
A