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Cardiology > Coronary Artery Disease and Acute Coronary Syndrome > Flashcards

Coronary Artery Disease and Acute Coronary Syndrome Flashcards

1
Q

coronary artery disease

A

-atherosclerosis of the intima of the coronary arteries
-Atherosclerosis is an accumulation of plaque in the intima of any artery
-Lipid deposition -> fibrosis -> calcification -> plaque formation
-Men > women
-Age 70 1:1 ratio
-Number one cause of death in the United States
-18.2 million adults
-MI every 40 seconds

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2
Q

coronary artery disease: where

A

-Cardiovascular disease: atherosclerosis of the arterial circulation
-Peripheral arterial disease (PAD)
-Carotid artery disease - can cause stroke
-Cerebral artery disease -CVA, TIA
-Coronary artery disease (CAD)- Ischemic heart disease

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3
Q

risk factors

A

-tobacco use*
-Diabetes mellitus *
-Hypertension
-Hyperlipidemia
-Hypertension

-Metabolic syndrome*
-3 of more of the following!!!:
-Triglycerides > 150 mg/dL
-HDL < 40 mg/dL men, <50 mg/dL women
-Fasting blood glucose > 110mg/dL
-Abdominal obesity
-HTN
-Family history of coronary artery disease
-Obesity

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4
Q

picture of artery

A
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5
Q

hyperlipidemia types and causes

A

-increased levels of lipids (fats) in the blood
-Types:
-Mixed hyperlipidemia
-Hypercholesterolemia
-Hypertriglyceridemia

-Risk factors:
-Diet- Alcohol, saturated fats
-Age
-Sedentary lifestyle
-Family history
-Gender- Men > Women -> until menopause
-Genetic mutations- Familial hypercholesterolemia

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6
Q

hyperlipidemia features

A

-Asymptomatic
-Xanthoma = hard yellowish plaque/nodule of tendons and skin -> Severe hyperlipidemia
-Pancreatitis with hypertriglyceridemia

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7
Q

hyperlipidemia: fasting lipid panel goals

A

-Cholesterol < 200 mg/dL
-LDL < 100 mg/dL:
-< 70 for patient with DM, CAD
-Most important for CAD risk*

-HDL > 40 mg/dL men, > 50 mg/dL women -> Protective factor

-Triglycerides < 150 mg/dL - more short term

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8
Q

hyperlipidemia tx: Statins (HMG-CoA reductase inhibitor)

A

-Rosuvastatin (Crestor), atorvastatin (Lipitor), simvastatin (Zocor) pravastatin (Pravachol)
-Inhibits cholesterol synthesis by inhibiting enzyme HMG-CoA reductase
-Increases LDL receptors which promotes LDL clearance

-Have been found to reduce progression of plaque (smooths) and reduce mortality rates from cardiovascular disease
-anyone with CAD needs a STATIN
-MOST POTENT TO LOWER LDLs

-Side effects/adverse reactions*:
-Rhabdomyolysis
-Myalgia, arthralgia
-Elevated ALT/AST - check every 3 months

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9
Q

hyperlipidemia tx: PSK9 inhibitors

A

-Alirocumab (Praluent), avolocumab (Repatha)
-Inhibits degradation of LDL receptors and increases LDL clearance

-Indications:
-Familial hypercholesterolemia
-Coronary artery disease

-Side effects: headaches, diarrhea, URI symptoms

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10
Q

hyperlipidemia tx: niaotinic acid

A

-Niacin
-Lowers Triglycerides
-Can increase HDL
-Side effects:
-Facial flushing
-Pruritus
-Nausea and vomiting
-skin on fire

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11
Q

hyperlipidemia tx: fenofibrates

A

-Gemfibrozil
-Lowers triglycerides
-Side effects:
-Nausea and vomiting
-Abdominal pain

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12
Q

hyperlipidemia tx: bile acid binding resins

A

-Cholestyramine Colestipol
-Colesevelam (Welchol)
-Lowers LDL
-Does not change triglycerides
-GI side effects
-Rarely used- last resort

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13
Q

diff dx of chest pain

A

CARDIAC
-Angina pectoris
-Acute MI
-Pericarditis
-Myocarditis
-Aortic dissection
-Heart failure
-Valvular heart disease
-Arrythmias

NONCARDIAC
-PE
-Pneumothorax
-GERD
-Peptic ulcer disease
-Cholecystitis
-Costochondritis
-Musculoskeletal disease
-Anxiety

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14
Q

angina pectoris

A

-inadequate tissue perfusion of the myocardium
-Imbalance in cardiac demand and tissue perfusion
-Chest pain that originates from the heart
-Most commonly from coronary artery disease
-Can have typical and atypical chest pain

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15
Q

angina pectoris: typical and atypical

A

TYPICAL
-Men
-Mid-sternal or left sided
-Squeezing, tightness, pressure- “sitting on chest”
-Levine sign – clenches fist over sternum
-Radiation- Left arm

ATYPICAL
-Females, elderly, diabetes*, immunocompromised
-Jaw, back of right shoulder pain
-Radiation-Right or bilateral arms AND Back

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15
Q

causes of angina pectoris

A

-Coronary Artery Disease – most common ***
-Embolus
-Arteritis
-Dissection
-Congenital abnormality
-Vasospasm:
-Cocaine
-Prinzmetals

16
Q

stable angina

A

-Exacerbated with activity and relieved at rest
-Predictable
-Last less than 3 mins
-Exacerbating factors- Exercise, emotion
-Relieved with sublingual nitroglycerin
-MUST BE CAUSED BY ACTIVITY AND DO AWAY WITH REST

17
Q

unstable angina

A

-Grouped with acute coronary syndrome
-Angina that worsens

-One of the following:
-Angina at rest
-New onset of angina symptoms
-Increasing pain in stable patients

-Less responsive to sublingual nitroglycerin
-Indicates stenosis that has enlarged
-

18
Q

prinzmetal angina

A

-Vasospasm at rest
-More common in females*
-75% with atherosclerotic lesion*
-Early morning
-Exercise capacity is preserved
-Cocaine use

19
Q

coronary artery disease dx

A

-EKG:
-Normal in 25% of patients
-Horizontal or down sloping depression ST-segments
-Non-specific changes:
-Flattening or inversions of T-waves -> T-wave changes can in Lead III can be diaphragmatic

-Exercise stress testing:
-Non-invasive testing
-ST depressions of 1mm in two leads = positive test
-More specific with single-photon emission computed topography (SPECT)
-Nuclear exercise stress testing allows imaging for extent and location of disease
-Can use pharmacologic stress testing if patient is unable to exercise

-Echocardiogram:
-Wall motion abnormalities
-Decreased LVEF

-Cardiac catheterization (coronary angiography) is the definitive diagnosis!!!!!!!!!!
-Selective due to invasiveness

20
Q

coronary artery disease tx: Risk factor modification

A

-Hypertension
-Hyperlipidemia
-Diabetes
-Exercise and dietary modification
-Smoking cessation**
-Weight reduction

21
Q

coronary artery disease: medical therapy

A

-3 classes of Antianginals:
-1) Beta blockers – first line for patient with stable angina **
-Increase oxygenation by decreasing heart rate which prolong diastole
-Prevents reinfarction
-DO NOT USE FOR VASOSPASTIC ANGINA

-2) Calcium channel blocks (diltiazem, verapamil)
-Second-line if beta-blockers fail or contraindicated
-Vasodilation
-First-line for Prinzmetal’s angina!
-dont give to HF

-3) Nitrates (nitroglycerin, isosorbide, hydralazine)
-Increases oxygenation by vasodilation
-Angina that persists with monotherapy
-Sublingual nitroglycerin immediate effective - episodic tx
-Long acting: isosorbride, hydralazine
-Side effects: headache, fascial flushing, orthostatic hypotension, syncope
-cant give to patient with ED meds

-Additional therapy:
-Ranolazine (Ranexa): late sodium channel blocker

22
Q

coronary artery disease tx: revascularization

A

-Percutaneous coronary intervention:
-Balloon angioplasty

-Percutaneous coronary intervention:
-Drug eluding stents:
-need Dual antiplatelet therapy for 12 months
->Aspirin 81 mg
->Clopidogrel 75 mg (Plavix) - antiplatelet
-Bare metal stents -> 1 month of dual antiplatelet therapy

-Coronary artery bypass grafting (CABG)
-Indication:
-Triple-vessel disease with >70% stenosis of each vessel
-Left main coronary disease > 50% stenosis
-YOU CAN NEVER PUT A STENT IN A LEFT MAIN CORONARY unless someone is having VF episodes on the table and would otherwise die

23
Q

acute coronary syndrome

A

-Umbrella term that includes:
-1) Unstable angina
-2) Non-ST segment myocardial infarction (NSTEMI)
-Partial thickness necrosis (endocardial muscle)

-3) ST segment myocardial infarction (STEMI)
-full thickness necrosis

24
Q

Acute Coronary Syndrome: Myocardial Infarction: necrosis of the myocardium due to interruption of blood supply to the myocardium

A

-Most common cause is thrombosis*
-Ruptured plaque -> thrombus formation -> occlusion
-1 in 5 of MIs are silent
-MC of pt with atypical symptoms:
-Atypical chest pain
-Fatigue
-Weakness
-Abdominal pain

25
Q

acute coronary syndrome: symptoms

A

-Typical or atypical chest pain
-Diaphoresis
-Shortness of breath/dyspnea
-Nausea/vomiting
-Dizziness/lightheadedness
-Syncope
-Anxiety

26
Q

acute coronary syndrome: signs

A

-Hypertension
-Hypotension
-Tachycardia
-Bradycardia/heart block- Inferior wall MI
-Murmur
-Friction rub
-Bibasilar rales

27
Q

acute coronary syndrome: dx

A

-12 lead EKG
-STEMI: ST segment elevation > 1mm in two contiguous leads
-ST elevation: Ischemia -> “tombstoning”
-Q wave: infarction
-NSTEMI and UA: ST depressions or T wave inversions
-Positive cardiac enzymes = NSTEMI

28
Q

acute coronary syndrome: cardiac enzymes

A

-Release with necrosis of myocardial tissue
-Gold standard diagnosis for myocardial infarction
-3 sets on enzymes every 6 hours

-Troponin T and I most specific*
-Increases 4-8 hours
-Peaks 12-24 hours
-Normalizes 5 to 14 days

-CK-MB:
-Increases 4-6 hours
-Peaks in 12-24 hours
-Normalizes 48-72 hours

-Myoglobin:
-Increases 1-4 hours
-Peaks 4-6 hours
-Normalizes in 24 hours

29
Q

t wave inversion

A
30
Q

acute coronary syndrome: myocardial infarct with corresponding artery

A

-Inferior MI- right coronary artery
-posterior MI- posterior descending artery
-septal MI- left anterior descending
-anterior MI- left anterior descending
-lateral MI- left anterior descending or circumflex

31
Q

acute coronary syndrome: MONAB tx

A

-MONAB:
-Morphine: pain control that is not controlled by nitroglycerin (NTG)
-Oxygen
-Nitroglycerin (NTG)
-Aspirin
-Can use adenosine diphosphate receptor inhibitors if aspirin allergy
-Clopidogrel (Plavix); Ticlopidine (Ticlid); Prasugrel (Effient)
-Inhibits ADP mediated platelet aggregation
-Caution if bleeding of planned CABG within seven days
-Beta-blocker
-Statins - Reduce risk of further coronary events -> Stabilizes plaque, lowers cholesterol
-Unfractionated heparin or low molecular weight heparin (LMWH)
-Unfractionated heparin: inactivates thrombin inhibiting fibrin formation
-LMWH: binds to and potentiates antithrombin III’s ability to inactive Factor Xa

32
Q

acute coronary syndrome: reperfusion

A

-STEMIs need IMMEDIATE reperfusion
-Percutaneous transluminal coronary angioplasty or thrombolytics
-PCI is superior to thrombolysis
-DOOR TO CATH TIME = 90 min
-Drug eluding stent (DES) and Bare mental stents (BMS)
-DES require dual antiplatelet therapy (DAPT) x 12 months
-BMS requires DAPT x 1 month

-Thrombolytic therapy:
-Door to thrombolytics 30 mins -> Reduces mortality and infarction
-Tissue plasminogen activators- alteplase, reteplase, teneceplase -> Dissolves clot by activating tissue plasminogen

33
Q

thrombolytic therapy: absolute contraindications

A

-Previous hemorrhagic CVA
-CVA within the last year
-Intracranial neoplasm
-Active internal bleeding
-Suspected aortic dissection
-Suspected aortic dissection
-Trauma or major surgery < 2 weeks
-Active internal bleeding

34
Q

thrombolytic therapy: relative contraindications

A

-Trauma within the past 2-4 weeks
-Major surgery within the past 3 weeks
-BP > 180/110
-Bleeding diathesis
-Prolonged or traumatic CPR
-Recent internal bleeding
-Noncompressible vascular puncture
-Current use of anticoagulation
-Active diabetic retinopathy
-Pregnancy
-PUD

35
Q

acute coronary syndrome: MI complications

A

-Ventricular tachycardia
-Ventricular fibrillation
-Cardiogenic shock
-Ventricular aneurysm/rupture
-Papillary muscle rupture
-Heart failure
-Pericarditis
-Dressler syndrome- pericarditis post MI
-Sudden death

36
Q

acute coronary syndrome: unstable angina needs management strategy

A

-TIMI scale – Thrombolysis In Myocardial Infarction
-GRACE – Global Registry of Acute Coronary Events

-Low score = conservative treatment
-Antiplatelet therapy
-Anticoagulation therapy

-High score = invasive treatment -> Cardiac angiogram/angioplasty

37
Q

time/risk score for UA/NSTEMI

A
38
Q

cocaine induced myocardial infarction: definition, dx and tx

A

-Coronary artery vasospasm secondary to cocaine activation of sympathetic nervous system and alpha 1 receptors
-Cocaine causes vasoconstriction of coronary arteries

-Diagnosis:
-12 lead EKG: transient diffuse ST elevations
-+ troponins
-+ Utox

-Treatment:
-Calcium channel blockers and nitrates
-ASA and Heparin/LMWH until CAD is rule out
-Beta-blockers contraindicated due to increased risk of vasospasm

Cardiology (11 decks)

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