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82 Cards in this Set
- Front
- Back
What are the contents of the atheroma (atherosclerotic plaque)?
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- Necrotic core
- Fibrous cap - Variable degrees of inflammation - Several cellular types: collagen, elastin, proteoglycans, debris, cholesterol, crystals, calcium |
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What causes atherosclerosis?
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Continuous vessel wall injury and inflammation, develops slowly over decades
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What are the steps of atherosclerosis?
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1. Chronic endothelial "injury"
2. Endothelial dysfunction (increased permeability, leukocyte adhesion), monocyte adhesion, and emigration 3. Macrophage activation, smooth muscle recruitment 4. Macrophages and smooth muscle cells engulf lipid 5. Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid |
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What are the characteristics of a stable atheroma?
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- Thick fibrous cap
- Small lipid core - Minimal inflammation |
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What are the characteristics of a unstable atheroma?
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- Thin fibrous cap
- Large lipid core - High content of inflammatory cells |
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What can happen if a vulnerable plaque ruptures?
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- Exposes blood to thrombogenic components of plaque such as tissue factor
- Leads to adhesion, activation, and aggregation of platelets and activation of coagulation cascade - Ultimately results in thrombus formation w/ variable degrees of coronary artery lumen occlusion - Leads to Acute Coronary Syndrome |
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What precipitates an acute coronary syndrome?
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- Disruption of a vulnerable (unstable) plaque
- Subsequent intravascular thrombus formation - Thrombus results in partial or complete vessel occlusion, reduced coronary flow, ischemic symptoms, characteristic ECG changes, and elevated serum cardiac biomarkers |
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What are the three Acute Coronary Syndromes?
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- Unstable Angina (UA)
- Non-ST Segment Elevated MI (NSTEMI) - ST Segment Elevated MI (STEMI) |
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What is the clinical presentation of Acute Coronary Syndrome?
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- Chest discomfort (tightness, pressure, squeezing)
- Dyspnea - Nausea - Diaphoresis - Sx related to arrhythmias (palpitations, syncope) |
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What are the ECG changes for STEMI?
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- ST-segment elevation (d/t complete occlusion of vessel) = blue arrows
- Pathologic Q wave formation in leads overlying infarcted area = yellow arrows |
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What is the most specific protein marker diagnostic of MI? How soon does it appear? How long does it last?
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Cardiac Troponin I (appears after 4 hours and remains elevated for 7-10 days)
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What are the types of infarcts?
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- Transmural infarcts (entire wall)
- Subendocardial infarcts (<50% of ventricle wall) |
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What are the features of transmural infarcts?
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- ↑ Necrosis
- Affects entire wall - ST elevation on ECG - Pathological Q waves |
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What are the features of subendocardial infarcts?
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- Due to ischemic necrosis, <50% of ventricle wall affected
- Subendocardium especially vulnerable to ischemia - D/t fewer collaterals, higher pressure - ST depression on ECG |
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What leads will have Q waves for an infarct of the anterior wall (LAD)?
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V1-V4
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What leads will have Q waves for an infarct of the anteroseptal wall (LAD)?
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V1-V2
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What leads will have Q waves for an infarct of the anterolateral wall (LCX)?
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V4-V6
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What leads will have Q waves for an infarct of the lateral wall (LCX)?
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I, aVL
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What leads will have Q waves for an infarct of the inferior wall (RCA)?
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II, III, aVF
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What are the potential complications of MI?
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- Cardiac arrhythmia
- LV failure - Pulmonary edema - Cardiogenic shock - Ventricular free wall rupture → tamponade; papillary muscle rupture → mitral regurg.; interventricular septal rupture → VSD - Aneurysm - Post-infarction fibrinous pericarditis - Dressler's syndrome (autoimmune) |
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How should you treat a STEMI?
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- Reperfusion therapy to re-establish flow (thrombolysis or percutaneous coronary intervention, PCI)
- Tx for ACS: antiplatelet/antithrombotic agents, statin, aspirin, β-blockers, nitrates |
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What are the ECG changes for UA or NSTEMI?
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- ST-segment depression
- ± T-wave inversion (blue arrows) - Do not distinguish UA from NSTEMI |
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How do you distinguish UA from NSTEMI when they have identical ECG changes?
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Based on presence of absence (UA) or abnormal (NSTEMI) serum cardiac biomarkers
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How should you treat a UA or NSTEMI?
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- Tx for ACS: antiplatelet/antithrombotic agents, statin, aspirin, β-blockers, nitrates
- Coronary angiography should be performed w/in 24-48 hours for evaluation of coronary anatomy and need for re-vascularization by stent or CABG |
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What are the types of anti-platelet agents for ACS?
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- COX-inhibitors
- ADP receptor inhibitors - Glycoprotein IIb/IIIa inhibitors |
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What are the COX inhibitors? What are they used for?
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- Aspirin
- Anti-platelet agent for management of ACS |
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What are the ADP Receptor inhibitors? What are they used for?
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- Clopidogrel
- Prasugrel - Ticagrelor - Anti-platelet agent for management of ACS |
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What are the Glycoprotein IIb/IIIa inhibitors? What are they used for?
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- Abciximab
- Eptifibatide - Anti-platelet agent for management of ACS |
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What are the types of anti-thrombotic agents for ACS?
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- Unfractionated Heparin
- Low Molecular Weight Heparin (LMWH) - Direct Thrombin Inhibitors |
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What is the action of β-blockers in ACS?
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- ↓ Myocardial O2 demand
- ↓ Contractility, ↓ HR, ↓ Systemic BP - Prevent action of catecholamines |
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What is the action of Nitrates in ACS?
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- ↓ Preload and afterload
- Coronary vasodilation |
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What is the action of HMG-CoA Reductase Inhibitors (Statins) in ACS?
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- ↓ Serum LDL
- Atheromatous plaque stabilization - Improve endothelial function - Anti-inflammatory effect |
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What kind of patients should get thrombolytic therapy?
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- Patients w/ STEMI in absence of contraindications
- Contraindicated in UA and NSTEMI |
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What is the thrombolytic treatment of choice for STEMI?
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Emergency percutaneous coronary intervention and stenting of infarct related artery
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What causes chronic ischemic heart disease (IHD)?
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- Most commonly by obstruction of coronary arteries by atheromatous plaque
- Congenital abnormalities of coronaries - Vasculitis - Radiation-induced |
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What is the clinical presentation of chronic ischemic heart disease?
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- Chronic chest discomfort (stable angina)
- Heart failure - Cardiac arrhythmias - Sudden death |
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How does Ischemic Heart Disease compare to acute MI in terms of symptoms?
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- Similar presentation
- Time course is of more chronic nature for IHD - MI associated w/ unstable/accelerating angina, whereas IHD is more stable and relieved w/ rest or Nitroglycerin - Both dyspnea - Also, lower extremity edema, orthopnea, paroxysmal nocturnal dyspnea |
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How do you diagnose Ischemic Heart Disease?
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** Coronary angiography to determine if there is obstructed coronary blood flow; lesions >70% are considered significant
- EKG may demonstrate Q-waves in areas of old MI - Treadmill stress testing looks for EKG changes (t-wave inversions, ST-depression or elevation) during exercise - Imaging (echo, MRI, nuclear) to look for wall motion abnormalities or perfusion defects during exercise |
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What can you do for a patient who can't do treadmill stress testing?
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- Dobutamine stress testing - causes increase in HR and contractility to simulate exercise
- Adenosine - causes arterial dilation, normal coronary arteries will dilate in response to adenosine, but diseased vessels will not dilate as much (detected on nuclear or MRI) |
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What are the goals of treating stable angina? What drugs are used? Any other therapies?
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- Improve O2 demand and supply mismatch
- β-blockers, CCB, Nitrates, Anti-platelet drugs, Statins, ACE-I's - Revascularization (PCI, CABG) |
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What drugs are used to treat unstable angina or NSTEMI? Any other therapies?
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- Anti-platelets: Aspirin, Clopidogrel
- β-blockers, CCB, Heparin, Nitrates, GPIIb/IIIa inhibitors - Revascularization (PCI, CABG) |
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What drugs are used to treat STEMI? Any other therapies?
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- Fibrinolytics
- Aspirin, Clopidogrel - Heparin, nitrates, GPIIb/IIIa inhibitors - Revascularization (PCI, CABG) |
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What drugs are used to secondarily prevent Acute Coronary Syndrome? Any other therapies?
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- Aspirin, Clopidogrel
- β-blockers, ACE-I, Statins - ICD if EF <35% - Revascularization (PCI, CABG) |
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What is the lifetime risk of developing symptomatic CAD after age 40 for men and women?
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- Men: 49%
- Women: 32% |
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When does demand angina occur?
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O2 requirements of myocardium increase but coronary flow cannot compensate d/t obstructions, eg:
- Exertion - Fever - Tachycardia |
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What is the location of angina?
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- Retrosternal region
- Radiates to or occasionally isolated to neck, jaw, shoulders, arms (usually L), or epigastrium |
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WWhat is the quality of angina?
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- Pressure
- Squeezing - Tightness - Heaviness - Burning - Indigestion |
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What is the duration of angina?
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<2-10 minutes
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What are the aggravating or alleviating factors of angina?
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- Precipitated by exertion, cold weather, emotional stress
- Relieved by rest or nitroglycerin - Variant (Prinzmetal) angina may be unrelated to exertion, often in the morning |
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What are the associated symptoms or signs of angina?
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- Dyspnea
- S3, S4, or murmur of papillary dysfunction during pain |
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What EKG change is associated with immediately before the actual MI starts? Implication?
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T-wave inversion - cardiac tissue is ischemic
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What does this EKG finding indicate?
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- T-wave inversion - cardiac tissue is ischemic
- Immediately before actual MI starts |
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What EKG change occurs within hours after an MI starts? Implication?
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- Marked ST elevation
- Upright T wave - Acute MI has begun, starting w/ MI injury |
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What does this EKG finding indicate?
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- Marked ST elevation
- Upright T wave - Acute MI has begun, starting w/ MI injury - Occurs within hours after MI starts |
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What EKG change occurs hours after an MI starts? Implications?
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- Significant Q wave
- ST elevation - Upright T wave - Some of injured myocardial tissue has died, while other tissues remain injured |
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What does this EKG finding indicate?
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- Significant Q wave
- ST elevation - Upright T wave - Some of injured myocardial tissue has died, while other tissues remain injured - Occurs hours after MI starts |
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What EKG change occurs hours to 1-2 day after an MI starts? Implications?
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- Significant Q wave
- Less ST elevation - Marked T inversion - Infarction is almost complete - Some injury and ischemia persist at infarct edges |
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What does this EKG finding indicate?
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- Significant Q wave
- Less ST elevation - Marked T inversion - Infarction is almost complete - Some injury and ischemia persist at infarct edges |
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What EKG change occurs days to weeks later (in some cases up to a year) after an MI? Implications?
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- Significant Q wave
- T wave inversion - No ST elevation - Infarction is complete, but T wave persists - No more ischemic tissue (it has either recovered or died) |
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What does this EKG finding indicate?
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- Significant Q wave
- T wave inversion - No ST elevation - Infarction is complete, but T wave persists - No more ischemic tissue (it has either recovered or died) - Occurs days to weeks after an MI (sometimes up to a year) |
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What are the long-term EKG change that occur weeks, months, years after an MI? Implications?
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- Significant Q wave only
- Signifies permanent tissue death |
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What does this EKG finding indicate?
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- Significant Q wave only
- Signifies permanent tissue death - Long-term EKG findings weeks/months/years after MI |
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If you are trying to determine if someone had an MI in the past, what should you do?
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EKG - look for significant Q wave (deep and wide) - indicates permanent tissue death
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What is coronary angiography used for? What is a significant finding?
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Diagnose whether there is obstructed coronary blood flow; lesions >70% are considered significant
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What lifestyle modifications are helpful for coronary artery disease?
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- Smoking cessation
- Low-fat diet (LDL reduction) - Exercise (HDL increase) - Glycemic control - HTN control - Stress management |
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How useful is Aspirin (75-162 mg) in treating Coronary Artery Disease?
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Reduces future events by 25%
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How useful are β-blockers in treating Coronary Artery Disease?
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- Reduces risk of mortality after MI by 23%
- Reduces remodeling and improves LV hemodynamic function - Improves LV diastolic function w/ less restrictive filling pattern - Slows yearly progression of coronary atherosclerosis |
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How useful are Ca2+ Channel Blockers in treating Coronary Artery Disease?
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- No significant mortality benefit
- Used for symptom relief |
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How useful are ACE-Inhibitors in treating Coronary Artery Disease?
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- After MI, reduces mortality by 7-22%
- If LV ejection fraction is low after MI, the benefit is even higher (26%) |
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How useful are Nitrates in treating Coronary Artery Disease?
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- Relax vascular smooth muscle (especially venous system)
- Reduces ventricular preload, decreasing wall tension and O2 requirements |
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What are the goals for lipids?
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- LDL <100 (ideally <70 in CAD)
- HDL >40 - TG <200 |
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How useful is estrogen in treating Coronary Artery Disease?
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No benefit and may present possible risk to patients
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When is re-vascularization used for Coronary Artery Disease? What are the treatment options?
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- Electively for symptomatic chronic coronary lesions (>90% blockage that causes lots of pain and to prevent future MI)
- Should not be initial management strategy for chronic angina (before trying/optimizing medical therapy) - Percutaneous Coronary Interventions (balloon or stent), CABG |
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What factors make CABG a preferable treatment over Percutaneous Coronary Intervention?
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- Left Main
- Triple Vessel - Double vessel w/ proximal LAD and LVEF <50% - Diabetics |
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What are the consequences of chronic coronary artery disease besides UA/NSTEMI/STEMI?
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- Cardiomyopathy (heart failure)
- LV Aneurysms - Ventricular Arrhythmias / Sudden Death |
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What are the types of LV aneurysms in coronary artery disease?
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- Anatomical: True and False
- Functional |
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What is the difference between a True and False Anatomical LV aneurysm?
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- True: mouth of aneurysm is wide / part of LV (covered by wall of ventricle)
- False: mouth of aneurysm is narrow and through wall of LV (only covered by parietal pericardium) |
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What is a Functional LV aneurysm?
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- Mouth of aneurysm is wide / part of LV
- Wall of aneurysm is a scar |
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How does cardiac arrest risk differ after an MI? What can be done to mediate this?
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- Risk is higher, especially if LVEF is depressed
- Implantable Cardiac Defibrillator if LVEF <35% more than 40 days post MI (or 3 months post re-vascularization) |
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What drugs should all patients w/ chronic ischemic heart disease be on?
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- Statin
- β-blocker (↓HR and ↓BP) - Nitrates (unless contraindicated) |
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What causes chronic ischemic heart disease to progress to acute coronary syndrome?
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- Plaque rupturs
- Activates platelet adhesion and aggregation as well as coagulation factors - Leads to thrombus = ACS |
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What mechanical complication of STEMI will result in an acute L→R shunt?
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Interventricular septum rupture
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