Ischemic Heart Disease

Front 1

Describe the atherosclerosis process

Back 1

-Chronic inflammatory process resulting in arterial narrowing that starts early in life
-Endothelial injury-->Oxidized LDL-->Inflammatory cells & mediators-->Smooth muscle migration

Front 2

Role of endothelial dysfunction in pathogenesis of CAD

Back 2

Endothelial damage leads to endothelial dysfunction and ultimately allows lipids and toxins to penetrate the endothelial layer and enter the smooth muscle cells. This results in the initiation of an oxidative and inflammatory cascade that culminates in the development of plaque deposits

Front 3

Epidemiology of CAD

Back 3

-Leading cause of death in US
-50% of M & 63% of W died of CAD w/ no previous Sx
-Women have atypical Sx
->50% of W have no obstruction upon cath

Front 4

CAD Risk Factors

Back 4

-Dyslipidemia
-Smoking
-HTN
-DM
-FH
-Obesity
-Age: M <45, W <55

Front 5

Clinical presentation of Stable Angina

Back 5

A supply & demand problem:
-P
-Radiation to jaw or arm
-Reproducible w/ exertion
-Relieved w/ rest

Front 6

Management of Stable Angina

Back 6

Tx Angina w/
-Nitrates
-CCB
Risk reduction secondary to MI w/:
-Statins
-ASA
-Plavix
Add:
-BB
-ACEI

Front 7

Clinical presentation of Unstable Angina Pectoris/NSTEMI

Back 7

-CP @ rest, new onset, or crescendo
-Often w/ >20min duration
-Elevated creatine kinase & troponin

Front 8

Management of USA/NSTEMI

Back 8

-O2
-ASA (decreases thrombus formation & inflammation)
-Heparin (break thrombus)
-BB (decrease workload of heart)
-Nitrates (vasodilation)
-Plavix
+/- Cath depending on risk

Front 9

Prognosis of USA/NSTEMI

Back 9

-Better than STEMI

Front 10

Clinical presentation of STEMI

Back 10

-Complete arterial occlusion w/ cell death
-ST elevation
-Q wave
-Elevated creatine kinase & troponin

Front 11

Prognosis of STEMI

Back 11

-Mortality 25-30%
-Pts w/ MI have 3-5 fold incresed risk of CV death or MI
-25% of M, 38% of W will die within 1 yr
-W/in 6 yrs of MI: 18% of M, 35% of W will have another MI & 22% of M, 46% of W will be disabled from CHF

Front 12

Management of STEMI

Back 12

Reperfusion 'time is muscle'
-Thrombolytics if no access to Cath lab
-Cath lab
-ASA, Heparin, BB, ACEI, Clopidogrel, O2, Morphine, Nitrates
-F/U w/ stress tests, exercise, & cardiac rehab

Front 13

Variant Angina

Back 13

-Transient coronary A spasm accompanied by fixed atherosclerotic lesion
-Can occur at rest & ass'd w/ V dysrhythmias
-Hallmark=transient ST elevation during CP-transmural ischemia
-Dx test=angiography w/ ergonovine
-Tx w/ CCB & Nitrates

Front 14

Diagnostic studies for evaluating Angina

Back 14

-Exercise treadmill test: Dx for ischemia is ST depression
-Exercise capacity
-Nuclear perfusion imaging
-Stress echo provides functional info
-Noninvasive stress test
-Coronary Angiography: 1:1000 risk of death, stroke, MI

Front 15

EKG findings

Back 15

In Stable Angina:
-Usually normal
In USA/NSTEMI:
-ST depression
-Inverted T waves
In STEMI:
-Peaked T waves (occur early)
-ST segment elevation (larger, transmural, & acute infarct)
-Q waves (indicate necrosis)
-T wave inversion
-ST segment depression (subendocardial injury)

Front 16

Diagnostic studies for Stable Angina

Back 16

-EKG
-Stress Echo; if pt cannot tolerate stress echo, perform Pharmacologic stress echo
-Holter monitoring
-Cath lab

Front 17

Diagnostic studies for USA/NSTEMI

Back 17

Same as in Stable Angina but must stabilize before stress echo or consider Cath lab initially

Front 18

Diagnostic studies for STEMI

Back 18

-EKG
-Cardiac enzymes

Front 19

Diagnostic studies for Variant Angina

Back 19

-EKG
-Angiography

Front 20

Acute plaque rupture

Back 20

-the cause of acute coronary syndromes; it causes a thrombus in the middle of the ruptured plaque which occludes the vessel

Front 21

Indications for:
-Thrombolytics
-Angioplasty
-Stent placement

Back 21

-re-establish coronary A perfusion
-salvage myocardium
-improve survival