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30 Cards in this Set
- Front
- Back
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Risk Factors for CHD: |
-DM and Patient Age are two of the strongest risk factors
-PVD and CRF are also strongly associated w/ CHD
-Additionally, low activity level, low intake fruits and veggies, lack of moderate etoh intake, and an elevated homocysteine level or elevated inflammatory markers such as CRP all appear to confer add'l risk for CHD |
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The typical manifestation of symptomatic CHD is: |
Angina Pectoris:
-Characterized as a substernal pressure, heaviness, burning, squeezing, or choking
-The discomfort is rarely well localized or described as sharp pain
-Radiation to the jaw, shoulder, back or arms can occur |
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Clinical Manifestation of Stable Angina: |
-Attacks brought on by exertion or emotional stress
-Pain increases over several minutes and is relieved by rest in several minutes |
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Clinical Manifestation of Unstable Angina: |
-Defined as angina that occurs at rest or as a significant change in the pattern of existing chronic angina |
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How is angina classified? |
Angina is classified by the amount of exertion needed to reproduce symptoms:
-Class I (strenuous activity)
-Class II (walking several blocks or up an incline)
-Class III (mild activity, such as walking short distances)
-Class IV (any activity, or at rest)
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Clinical Manifestation of Atypical Angina: |
Not all patients describe typical anginal pain during periods of myocardial ischemia:
-With atypical angina, may have isolated sxs such as jaw pain or dyspnea
*This is particularly true in patients w/ underlying DM
**Pts w/ silent angina can be completely asymptomatic
*** In some pts w/ angina who have underlying compromise of ventricular fxn or severe widespread ischemia, angina can be accompanied by sxs of heart failure (dyspnea, orthopnea)
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Physical Exam -
CHD patients often have a normal PE, particularly if they are not symptomatic at the time of examination.
They may however have findings of predisposing conditions or from atherosclerosis outside of the coronary arteries including.... |
-Retinal Vascular Changes (e.g., arteriovenous nicking and/or "copper wire" changes caused by HTN)
-Third Heart Sound (CHF)
-Fourth Heart Sound (HTN)
-Arterial Bruits (peripheral atherosclerosis)
-Absent or diminished peripheral pulses (peripheral atherosclerosis)
-Xanthomas - skin lesions caused by the accumulation of fat in macrophage immune cells in the skin and more rarely in the layer of fat under the skin (Hyperlipidemia) |
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Examination during an Anginal Attack can reveal: |
-A fourth heart sound (b/c of decreased compliance of the ischemic myocardium)
-Signs of Left Ventricular Failure (third heart sound, single S2, rales, elevated JVP)
*The PE should also look for findings that would prohibit safe exercise testing (e.g., critical aortic stenosis) |
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Differential Diagnosis -
The probability that a patient w/ chest pain has significant CHD is estimated by considering the following: |
-Characteristics of pain -Patient age and gender -Patient risk factors (esp. DM, CRF, or the presence of known peripheral or cerebrovascular disease) -Echocardiogram |
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Diagnostic Evaluation - The Framingham Prediction Model: |
-Remains the most widely accepted prediction model
-Tallies points for the major known cardiac risk factors: age, gender, DM, smoking, LDL, HDL, and BP |
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Diagnostic Evaluation - The Electrocardiogram (ECG): |
-The resting ECG is normal in about half of patients w/ angina pectoris. Some may have evidence of old MI (Q waves, inverted T waves)
-The typical ECG change seen during acute ischemia is ST-segment depression, defined as depression of the ST segment from baseline greater than 1 mm in at least two contiguous leads |
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Confirming a suspected diagnosis of CHD... |
-Confirm a suspected diagnosis of CHD w/ an exercise stress test |
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The Exercise Stress Test: |
-During a stress test, the pt exercises on a treadmill or bicycle ergometer.
-The workload is increased in a standardized progressive manner, and symptoms, vital signs, and ECG are monitored
-Exercise is continued to achieve 85% maximal heart rate (max HR = 220 bpm - pt age)
-Reasons for stopping test include: moderate to severe chest pain or dyspnea, dizziness, > 2 mm ST-segment depression, fall in SBP of > 10 mm Hg when assoc. w/ ischemia, or sustained V-tach
-Development of diagnostic ST-segment depression (> 1 mm downsloping or horizontal) is considered to be a positive test
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Sensitivity of the Exercise Stress Test: |
-The sensitivity of exercise testing in detecting significant CHD (> 70% stenosis of at least one artery) is approx. 60%.
-The test is more sensitive for three-vessel disease |
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Specificity of the Exercise Stress Test: |
-The specificity of the test ranges from 77% to 90%
-B/c of this fairly low specificity, pts w/ low pretest probability for heart disease (estimated risk of < 10%) are not generally assessed w/ simple exercise stress testing; a positive result would be more likely to be a false positive than a true positive
-Stress testing is therefore reserved for patients w/ intermediate (10% to 90%) pretest probability
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With Exercise Testing, which conditions are associated with False-Positive ST Depressions? |
-Left BBB -LVH -Pre-excitation (Wolff-Parkinson-White) syndrome, and -Digoxin use
*Pt's with these conditions or other ECG abnormalities should have imaging studies done along w/ the exercise test |
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Prognostic Information obtainable through exercise testing includes... |
-In patients who complete an exercise study (> 10 minutes) w/o chest pain or ST depressions, annual mortality from CHD is very low (< 1% annually) |
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The sensitivity and specificity of exercise testing can be improved by the use of what? |
-Radiolabeled tracers (e.g., technetium, sestamibi, or tetrofosmin) to determine regional myocardial perfusion.
-Images are recorded immediately after exercise, and then after a several hour rest period, to identify ischemic areas that have decreased blood flow after exercise but normal or increased flow after rest.
-Infarcted areas of myocardium lack perfusion at both time points
-This technique is semi-quantitative, estimating the amount of ischemic or infarcted myocardium by the size of the defect seen on the images |
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Pharmacological stress testing: |
-Used for patients who are unable to exercise b/c of orthopedic problems or severe deconditioning.
- Agents used = dipyridamole or adenosine
-Dipyridamole and adenosine act as vasodilators of normal but not atherosclerotic coronary vessels and thus can cause shunting of blood flow away from diseased vessels, resulting in ischemia
-They may cause bronchospasm and should be used w/ caution in pts w/ COPD or asthma
-Theophylline w/in 72 hours and Caffeine w/in 24 hours can both reduce the sensitivity of the vessel to these medications |
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Echocardiography: |
-May be used as an alternative to radiologic imaging
-Dobutamine stress echocardiography, which looks for wall motion abnormalities w/ increasing myocardial demand, has similar test characteristics to pharmacologic imaging studies
-It can be safely performed in patients w/ asthma as well as in the presence of recent caffeine use
-Exercise echocardiography is slightly less sensitive than perfusion imaging, but it is more specific --> this makes it a popular option for pts w/ lower pretest probabilities of CHD |
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The GOLD STANDARD to diagnose CHD is: |
-Coronary Angiography
-Angiography is indicated when non-invasive testing is inconclusive or when clincal parameters suggest severe (i.e., three-vessel) coronary artery disease.
-The parameters include: severe (class III or IV) angina despite medical therapy, angina assoc. w/ CHF, EF < 35%, or large perfusion defect on stress testing |
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Treatment of CHD - Goals: |
-Initial tx of confirmed, chronic stable angina pectoris is usually medical.
-The goals of tx are to (a) prevent MI and death from CHD and (b) decrease angina and improve QoL
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Treatment of CHD -
AHA Mnemonic for the important elements in treatment of Stable Angina |
A: Aspirin, ACEIs, and Anti-Anginals
B: B-blocker and BP
C: Cholesterol and Cigarettes
D: Diet and Diabetes
E: Education and Exercise |
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Treatment of CHD -
Prevention of Myocardial Infarction and Death from Coronary Artery Disease |
-Aspirin (75 to 325 mg daily) limits platelet aggregation by inhibiting platelet thromboxane A2.
-Multiple studies have demonstrated that ASA reduces the risk of subsequent MI as primary prevention, in pts w/ CHD, and for Post-MI
**Pts who are allergic to ASA should be placed on Clopidogrel (75 mg daily), which prevents adenosine diphosphate(ADP)-Mediated platelet aggregation |
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Treatment of CHD -
Prevention of Myocardial Infarction and Death from Coronary Artery Disease (CONTINUED) |
HMG-CoA reductase inhibitors (Statins) have demonstrated convincing benefit (25% to 35% relative risk reductions) in pts w/ established CHD, even when cholesterol levels are normal
-A target LDL cholesterol level < 70 to 80 mg/dL is recommended for people who have CVD and have multiple major risk factors (eg, people with diabetes or who smoke)
-ACEIs or ARBs have shown to provide benefit for higher risk pts w/ CHD, even when BP is optimal (goal BP is < 140/90 for general hypertensive pop < 60 yrs (< 150/90 for > 60 yrs) and for pts w/ DM
-A target LDL cholesterol level less than 100 mg/dL is recommended for people who have CVD but do not have many additional risk factors. Lifestyle changes as well as non-statin medications may be recommended when LDL cholesterol levels are higher than 100 mg/dL |
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Treatment of CHD-
Antianginal Treatment: Beta-adrenergic blocking agents |
- Beta-adrenergic blocking agents reduce myocardial workload by limiting adrenergic increases [from stress or exercise] in HR and contractility
-Data suggesting that b-blockers decrease the risk of MI or death in stable angina are limited (or non-existent), many physicians extrapolate the benefits from post-MI pts or elderly patients w/ HTN.
-B-Blockers are clearly effective at reducing anginal sxs.
C/I's include: -Severe bradycardia -high degree AV block -Decompensated CHF
*Dose should be titrated to a goal HR of 50-60 bpm
S/E's include: -fatigue -impotence -bradycardia -development of, or worsening, heart failure |
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Treatment of CHD-
Antianginal Treatment: Calcium Channel Blockers (CCBs) |
-Decrease myocardial contractility and increase coronary blood flow.
-Equivalent antianginals compared w/ BB's and tend to cause fewer side effects...
-However, studies have demonstrated increased cardiac risk w/ short-acting dihydropyridine CCBs (Nifedipine)...
-Therefore, only long-acting dihydropyridines or non-dihydropyridines (verapamil, diltiazem) are recommended.
-Second Generation dihydropyridines (amlodipine, nicardipine) have fewer inotropic effects than the other options, so can be used in the setting of reduced EF
C/I's: the same as beta-blockers - -Severe bradycardia -high degree AV block -Decompensated CHF
S/E's: -peripheral edema -reflex tachycardia -Constipation
*When reflex tachycardia is a concern, CCBs can be combined with BBs |
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Treatment of CHD-
Antianginal Treatment: Nitates |
-Nitroglycerin, isosorbide mononitrate, or dinitrate
-Are endothelium-independent vasodilators that reduce myocardial wall stress through venous pooling (decreased prelaod).
-They also produce coronary vasodilation , increasing myocardial blood flow.
-Used in sublingual form for relief of acute ischemia
-Used in long-acting forms (via transdermal patches or slow-release oral formations) for limiting frequency and severity of attacks.
S/Es: (Most prominent with sublingual administration) are: -hypotension -lightheadedness -Headache
-Constant use results in nitrate tolerance, which is prevented by an adequate (8-hr) nitrate-free interval |
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Surgical Treatment of CHD -
General situations where surgical therapy is superior to medical therapy include:
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Some patients w/ CAD benefit from surgical revascularization with coronary artery bypass grafting (CABG).
Each patient must be assessed individually, but general situations where surgical therapy is superior to medical therapy include:
-Left main coronary disease or left main equivalent (proximal left anterior descending [LAD] stenosis plus proximal left circumflex artery stenosis)
-Three-vessel disease, especially w/ decreased Ejection Fraction
-Severe proximal LAD stenosis w/ "myocardium at risk" on noninvasive testing
-Survivors of sudden cardiac death or sustained ventricular tachycardia/fibrillation
**Percutaneous coronary intervention (PCI) can be used to relieve sxs in pts who fail medical therapy but who do not have significant enough disease to require CABG.
Most patients w/ single- or double-vessel disease will fall in this group.
The routine use of drug-coated coronary stents has led to decreased risk of restenosis in the treated vessel
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CHD - Key Points: |
-The risk for underlying CHD is determined by patient age, gender, cardiac risk factors, and characteristics of chest pain
-Exercise stress testing is insufficiently specific for assessment of patients w/ low (<10%) pre-test probability of CHD. Exercise testing is best reserved for pts w/ intermediate pre-test probability. Sensitivity and specificity can be increased with imaging studies such as radionuclide imaging or echocardiography
-For patients w/ a baseline abnormal ECG, the stress test should include either radionuclide or echocardiographic imaging
-Aspirin and Statins decrease mortality from CAD
-B-Blockers are the first-line antianginal drugs. ACEIs, CCBs, and nitrates may be used as well.
-Severe multi-vessel disease, stenosis of the left main coronary artery, or equivalent lesions (proximal lesions in LAD and left circumflex artery) require CABG for survival benefit |
