Coronary Artery Disease and Acute Coronary Syndrome Flashcards
coronary artery disease
-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
coronary artery disease: where
-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
risk factors
-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
picture of artery
hyperlipidemia types and causes
-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
hyperlipidemia features
-Asymptomatic
-Xanthoma = hard yellowish plaque/nodule of tendons and skin -> Severe hyperlipidemia
-Pancreatitis with hypertriglyceridemia
hyperlipidemia: fasting lipid panel goals
-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
hyperlipidemia tx: Statins (HMG-CoA reductase inhibitor)
-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
hyperlipidemia tx: PSK9 inhibitors
-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
hyperlipidemia tx: niaotinic acid
-Niacin
-Lowers Triglycerides
-Can increase HDL
-Side effects:
-Facial flushing
-Pruritus
-Nausea and vomiting
-skin on fire
hyperlipidemia tx: fenofibrates
-Gemfibrozil
-Lowers triglycerides
-Side effects:
-Nausea and vomiting
-Abdominal pain
hyperlipidemia tx: bile acid binding resins
-Cholestyramine Colestipol
-Colesevelam (Welchol)
-Lowers LDL
-Does not change triglycerides
-GI side effects
-Rarely used- last resort
diff dx of chest pain
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
angina pectoris
-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
angina pectoris: typical and atypical
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
causes of angina pectoris
-Coronary Artery Disease – most common ***
-Embolus
-Arteritis
-Dissection
-Congenital abnormality
-Vasospasm:
-Cocaine
-Prinzmetals
stable angina
-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
unstable angina
-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
-
prinzmetal angina
-Vasospasm at rest
-More common in females*
-75% with atherosclerotic lesion*
-Early morning
-Exercise capacity is preserved
-Cocaine use
coronary artery disease dx
-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
coronary artery disease tx: Risk factor modification
-Hypertension
-Hyperlipidemia
-Diabetes
-Exercise and dietary modification
-Smoking cessation**
-Weight reduction
coronary artery disease: medical therapy
-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
coronary artery disease tx: revascularization
-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
acute coronary syndrome
-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
Acute Coronary Syndrome: Myocardial Infarction: necrosis of the myocardium due to interruption of blood supply to the myocardium
-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
acute coronary syndrome: symptoms
-Typical or atypical chest pain
-Diaphoresis
-Shortness of breath/dyspnea
-Nausea/vomiting
-Dizziness/lightheadedness
-Syncope
-Anxiety
acute coronary syndrome: signs
-Hypertension
-Hypotension
-Tachycardia
-Bradycardia/heart block- Inferior wall MI
-Murmur
-Friction rub
-Bibasilar rales
acute coronary syndrome: dx
-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
acute coronary syndrome: cardiac enzymes
-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
t wave inversion
acute coronary syndrome: myocardial infarct with corresponding artery
-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
acute coronary syndrome: MONAB tx
-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
acute coronary syndrome: reperfusion
-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
thrombolytic therapy: absolute contraindications
-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
thrombolytic therapy: relative contraindications
-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
acute coronary syndrome: MI complications
-Ventricular tachycardia
-Ventricular fibrillation
-Cardiogenic shock
-Ventricular aneurysm/rupture
-Papillary muscle rupture
-Heart failure
-Pericarditis
-Dressler syndrome- pericarditis post MI
-Sudden death
acute coronary syndrome: unstable angina needs management strategy
-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
time/risk score for UA/NSTEMI
cocaine induced myocardial infarction: definition, dx and tx
-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
