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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

Definition: atherosclerosis of the intima of the coronary arteries

Statistics:
- #1 cause of death in the US*
- Men > women; after age 70 -> same risk for both genders
- estrogen protection stops after menopause
-18.2 million adults
- MI every 40 seconds

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2
Q

Atherosclerosis and progression

A

Atherosclerosis: accumulation of plaque in the intima of any artery
1) Lipid deposition (LDL)
2) fibrosis
3) calcification
4) plaque formation
- eventually plaque ruptures

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3
Q

Cardiovascular disease and its subbranches

A

Cardiovascular disease: atherosclerosis of the arterial circulation

  • Peripheral arterial disease (PAD)
  • Carotid artery disease
  • Cerebral artery disease:
    CVA, TIA
  • Coronary artery disease (CAD) -> Ischemic heart disease: same ds and can lead to MI
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4
Q

Coronary Artery Disease
Risk Factors:

A

Tobacco use**
Diabetes mellitus *
Metabolic syndrome
- Three of more of the following:
- 1) Triglycerides > 150 mg/dL
- 2) HDL cholesterol < 40 mg/dL men, <50 mg/dL women
- 3) Fasting blood glucose > 110mg/dL
- 4) Abdominal obesity
- 5) HTN

Hypertension
Hyperlipidemia
Family hx of CAD
Obesity

“HDL = happy lipids; LDL = loser lipids”

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5
Q

Hyperlipidemia def + types

A

Definition: increased levels of lipids (triglycerides + cholesterol) in the blood

Types:
- Mixed hyperlipidemia: cholesterol and triglycerides
- Hypercholesterolemia: high cholesterol
- Hypertriglyceridemia: high triglycerides

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6
Q

Hyperlipidemia: risk factors

A

Risk factors:
- Diet: alcohol + saturated fats
- Age
- Sedentary lifestyle
- Family history
- Men > Women
- Genetic mutations: Familial hypercholesterolemia

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7
Q

Hyperlipidemia: clinical features

A
  • Asymptomatic
  • Xanthoma = hard yellowish plaque/nodule of tendons and skin-> Severe hyperlipidemia
  • Pancreatitis with hypertriglyceridemia
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8
Q

Hyperlipidemia: Fasting lipid panel goals:

A

Cholesterol < 200 mg/dL

LDL (MOST IMPORTANT FOR CAD RISK) **
- < 100 mg/dL
- < 70 for patient with DM, CAD

HDL : Protective factor; happy!!!
- > 40 mg/dL men
- > 50 mg/dL women

Triglycerides:
- < 150 mg/dL

“LDL is double HDL and men less than women bc they more at risk”

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9
Q

Statins (HMG-CoA reductase inhibitors): what is their use, MOA

A
  • Most potent to lower LDLs***
  • put atherosclerotic pts on statins even if they dont have high cholesterol -> stabilizes plaque

MOA:
- Inhibit cholesterol synthesis by inhibiting the enzyme HMG-CoA reductase
- Increase LDL receptors -> promotes LDL clearance
-Reduce PROGRESSION of plaque and reduce MORTALITY rates from cardiovascular disease
- stabilizes plaque, lowers cholesterol

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10
Q

Statins: ADR, drug names

A

ADR:**
- Myalgia, arthralgia (common)
- rhabdomyolysis: muscle injury that releases myoglobin into bloodstream
- elevated ALT/AST - need routine lfts

Examples: “-statins”
- Rosuvastatin (Crestor)
- atorvastatin (Lipitor)
- simvastatin (Zocor)
- pravastatin (Pravachol)

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11
Q

PSK9 inhibitors: MOA, indications, ADR, drug names

A

MOA:
- Inhibit DEGRADATION of LDL receptors -> increase LDL clearance

Indications:
-Familial hypercholesterolemia
- CAD

ADR:
-Headaches
- diarrhea
- URI symptoms

Drugs: “-CUmab”
- Alirocumab (Praluent)
- evolocumab (Repatha)

“Saiki K - CUsuo -> CUmab”
- saiki taking this med because hes sick with URI, diarrhea, headache

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12
Q

Hyperlipidemia all medication tx

A

-statins: most potent to lower LDL
- PSK9 inhibitors: lowers LDL
- Niacin: lowers triglycerides, increases HDL
- Fenofibrates(ex: gemfibrozil): lowers triglycerides
- bile acid binding resins (rarely used): lowers LDL

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13
Q

Bile acid binding resins

A

Other hyperlipidemia tx: rarely used

Bile acid binding resins:
- lowers LDL
- no change on triglycerides
- ADR: GI side effects
- drugs: Cholestyramine, Colestipol, Colesevelam (Welchol)

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14
Q

Niacin

A

Niacin: Other hyperlipidemia tx
- lowers triglycerides
- increases HDL
- ADR: flushing, pruritis, nausea/vomiting

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15
Q

Fenofibrates

A

Other hyperlipidemia tx
Fenofibrates (ex: gemfibrozil)
- lowers triglycerides
- ADR: nausea vomiting, ab pain

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16
Q

Differential Diagnosis of Chest Pain: cardiac

A

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

“AAAA- HPV-M”
“Always Ask About Aches, Heart Problems Vary Much”

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17
Q

Differential Diagnosis of Chest Pain: non-cardiac

A

Anxiety
Cholecystitis
Costochondritis
GERD
PUD
PE
Pneumothorax
Musculoskeletal disease

“A- CCG-PPP- M”

“Anxious Cats Craft Great Plans, Pondering Pneumatic Mysteries” -> MOCHA HAD ATYPIC CHEST PAIN

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18
Q

Angina Pectoris

A

Definition:
- chest pain caused by inadequate tissue perfusion of the myocardium (heart muscle)
- Imbalance in cardiac demand and tissue perfusion
- MC cause: CAD*

Sx:
- Chest pain that originates from the heart
- Can have typical and atypical chest pain

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19
Q

typical chest pain

A

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

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20
Q

atypical chest pain

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
- pain: jaw, right shoulder; may not be in chest
- Radiation:
- Right or bilateral arms
- Back

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21
Q

Prinzmetal Angina

A
  • Vasospasm of coronary artery at REST
  • MC in females
  • 75% w/ atherosclerotic lesion (+/-)
  • Early morning
  • Exercise capacity is preserved
  • Can be induced via cocaine

Tx: calcium channel blockers

“elderly female in early morning hours presents with chest pain who is addicted to exercise and cocaine”

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22
Q

Stable Angina

A

Predictable chest pain:
- ex: i walk 2 blocks, 5 sec it goes away consistently
- always 2 blocks
Lasts <3 mins

Exacerbated by:
- activity
- emotion

Relieved by:
- rest
- sublingual nitroglycerin (immediate)

first line tx: beta blockers

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23
Q

Unstable Angina

A

Grouped w/ acute coronary syndrome
Angina that WORSENS (not consistent, not typical or predictable)

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

Less responsive to sublingual nitroglycerin
Indicates stenosis that has enlarged

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24
Q

Angina Pectoris
Causes:

A

CAD: MC **

Embolus
Arteritis
Dissection
Congenital abnormality
Vasospasm
- Cocaine
- Prinzmetals

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25
Q

Coronary Artery Disease
Diagnosis: EKG

A

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

26
Q

Coronary Artery Disease
Diagnosis: what are all the dx tests

A
  • CARDIAC CATHETERIZATION/coronary angiography: definitive dx**
  • EKG
  • exercise stress test
  • echocardiogram

“CEEE u got CAD”

27
Q

Coronary Artery Disease
Diagnosis: Exercise stress testing

A
  • 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
28
Q

Coronary Artery Disease
Diagnosis: Echocardiogram

A

Echocardiogram:
- Wall motion abnormalities
- Decreased LVEF

29
Q

Coronary Artery Disease
Diagnosis: Cardiac catheterization

A

Cardiac catheterization (coronary angiography) is the DEFINITITE DIAGNOSIS
- Selective due to invasiveness
- can be dx and tx

30
Q

Coronary Artery Disease
Treatment:
Risk factor modification

A

STOP SMOKING!!*

Treat comorbidities:
- Hypertension
- Hyperlipidemia
- Diabetes

Lifestyle changes:
- Exercise and dietary modification
- Weight reduction
- quit smoking!!!

31
Q

Antiangina meds:

A

1) Beta blockers – first line for patient with stable angina *
- NOT FOR VASOSPASTIC ANGINA (prinzmetal angina)

2) Calcium channel blocks (diltiazem, verapamil)
- Second-line if beta-blockers fail or contraindicated
- first line tx: prinzmetal angina
3) Nitrates (nitroglycerin, isosorbide, hydralazine)
- Angina that persists with monotherapy
- first line tx: acute MI

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

32
Q

Beta blockers - angina tx; indication and MOA

A

Beta blockers =first line tx for pt with STABLE ANGINA
- DO NOT USE FOR VASOSPASTIC ANGINA*

MOA:
- Increase oxygenation by decreasing heart rate -> prolongs diastole
- Prevents reinfarction

33
Q

Calcium channel blockers: antiangina tx; indication, MOA, drug names

A

Indication:
- Second-line tx: use if beta-blockers fail or contraindicated
- First-line tx: Prinzmetal’s angina

MOA:
- Vasodilation

Drug names:
- diltiazem
- verapamil

34
Q

Nitrates - antiangina tx; indication, MOA, drug names

A

Indication:
- angina that persists with monotherapy

MOA:
- vasodilation

Immediately effective:
- Sublingual nitroglycerin

Long acting:
- isosorbride
- hydralazine

35
Q

Nitrates - antiangina; ADR

A

ADR: ***
- headache
- fascial flushing
- orthostatic hypotension
- syncope

36
Q

Coronary Artery Disease: Treatment - Percutaneous coronary intervention

A

1) Balloon angioplasty
- small balloon at the tip of the catheter that is inflated to compress plaque against artery walls

2) Drug eluding stents: slowly releases meds that prevent blocakge
- requires dual antiplatelet therapy for 12 months to prevent clots forming in stent
- Aspirin 81 mg
- Clopidogrel 75 mg (Plavix)

3) Bare metal stents: 1 month of dual antiplatelet therapy; no med release

37
Q

Coronary Artery Disease: Treatment - Coronary artery bypass grafting (CABG)

A

Indication:
- 1) 3 vessel disease with >70% stenosis of each vessel
- 2) Left main coronary disease > 50% stenosis

surgery to bypasses stenosis

38
Q

Acute Coronary Syndrome
Symptoms:

A

Typical or atypical chest pain*
Diaphoresis: excess sweating *
Shortness of breath/dyspnea
Nausea/vomiting
Dizziness/lightheadedness
Syncope
Anxiety

39
Q

Acute Coronary Syndrome - Signs

A

Hypertension
Hypotension
Tachycardia
Bradycardia/heart block
- inferior wall MI
Murmur

Lungs:
Friction rub (pericardial effusion)
Bibasilar rales

“both hypo/hyper; tachy/brady + heart murmurs + block”

40
Q

Acute Coronary Syndrome:
Definition

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

“basically acute coronary syndrome = any unstable angina, NSTEMI, STEMI”

41
Q

Myocardial Infarction: definition and important facts

A

Definition:
- necrosis of the myocardium due to interruption of blood supply to the myocardium
- 1 in 5 of MIs are silent**
- MCC: thrombosis - plaque ruptures -> thrombus -> occlusion

42
Q

Myocardial Infarction: MC cause + typical presentation

A

MC cause: thrombosis
- Ruptured atherosclerotic plaque → thrombus formation (clot) → occlusion (artery blocked)

MC: pts present w atypical sx (right arm, back, odd age)
- Atypical chest pain**
- Fatigue
- Weakness
- Abdominal pain
- they will often think they have a stomach bug

43
Q

Acute Coronary Syndrome
Diagnosis

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

44
Q

Cardiac Enzymes

A

cardiac enzymes = Gold standard diagnosis for NSTEMI!!!
- Release with necrosis of myocardial tissue
- serve as markers for diagnosing myocardial injury
- Three 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

Others:
- CK-MB: normalizes faster (2-3 days)
- Myoglobin: increases (4h), peaks(4h), normalizes faster (1 day)

45
Q

Acute Coronary Syndrome: MI
Treatment

A

“MONAB”

*Morphine: use when pain is not adequately controlled by NTG
*Oxygen
*Nitroglycerin (NTG):
*Aspirin
*Beta Blocker

*Statins:
- reduce risk of further coronary events
*Unfractionated heparin or low molecular weight heparin (LMWH)
- both: reduce clot formation
- unfractionated heparin: inactivate thrombin (factor 2) -> no clot formation/activation of fibrin (factor 1)
- LMWH: inactivates factor Xa by potentiating anti-thrombin III

46
Q

Aspirin allergy alternative

A

Adenosine diphosphate receptor inhibitors
*Inhibits ADP mediated platelet aggregation -> anti-platelet agent
*Caution if bleeding of planned CABG within seven days

Drugs: “-grel”
-Clopidogrel (Plavix)
- Prasugrel (Effient)
- Ticlopidine (Ticlid)

47
Q

Inferior MI: what EKG leads and corresponding artery?

A

II,III, aVF
Right Coronary Artery

48
Q

Posterior MI: what EKG leads and corresponding artery?

A

V1, V2, V3
Posterior descending artery

49
Q

Septal MI: what EKG leads and corresponding artery?

A

V1, V2
Left anterior descending

50
Q

Anterior MI: what EKG leads and corresponding artery?

A

V3, V4
Left anterior descending

51
Q

Lateral MI: what EKG leads and corresponding artery?

A

I, avL,V5,V6
Left anterior descending or circumflex

52
Q

Acute Coronary Syndrome: STEMI reperfusion

A

STEMIs need IMMEDIATE REPERFUSION

First line: percutaneous transluminal coronary angioplasty (PCI) -> better than thrombolysis
- can be performed fast: DOOR TO CATH TIME = 90 min!!!
- wantto treat pts asap, less than 90 minutes

1) Drug eluding stents (DES): release meds to help prevent artery from becoming blocked again
- require dual anti-platelet therapy x 12 months
2) Bare metal stents: dual anti-platelet therapy x 1 month

53
Q

Acute Coronary Syndrome: STEMI reperfusion - thrombolytic therapy

A

Used when PCI cannot be performed within recommended time; not as good tx
- goal door to cath time: 30 min
- reduces mortality and infarction by using meds to dissolve clots

TPA Agents (-“plase”: activate tissue plasminogen to dissolve clots
- alteplase
- reteplase
- tenecteplase

54
Q

Absolute contraindications to thrombolytic therapy

A

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

Thrombolytic -> A (big) IMPACT:
- AORTIC DISSECTION
- intracranial hemorrhage
- major surgery 2 wks
- previous CVA HEMORRHAGIC
- active internal bleeding
-CVA in the last year
- trauma 2 wks

55
Q

Relative contraindications to thrombolytic therapy - weight risk vs benefit

A

“2 BP DR PANda + CPR” need to consider risk vs benefit of thrombolytic therapy

2 wks: trauma + surgery
Bleeding Diathesis: unusual susceptibility to bleeding- platelet disorders, coagulation factor deficiencies, etc.
Pressure: BP over 180/110
Diabetic retinopathy
Recent internal bleed
PUD + Pregnant
Anticoagulation use
Noncompressible vascular puncture
+
CPR (prolonged or traumatic)

56
Q

Acute Coronary Syndrome: MI
Complications

A

Ventricular tachycardia
Ventricular fibrillation
Ventricular aneurysm/rupture
Cardiogenic shock
Sudden death
Heart failure

Pericarditis
Papillary muscle rupture
Dressler syndrome

57
Q

Acute Coronary Syndrome
Unstable angina - tx

A

Unstable angina needs management strategy !!!

Risk stratification scales:
- TIMI scale – identifying the likelihood of death, new or recurrent MI
- GRACE: Global Registry of Acute Coronary Events

GRACE:
- Low score = conservative treatment
- Antiplatelet therapy
- Anticoagulation therapy
- High score = invasive treatment
- Cardiac angiogram/angioplasty

Low risk pts:
- conservative tx
- antiplatelet therapy
- anticoagulation therapy

High score:
- invasive tx
- cardiac angiogram/angioplasty

58
Q

Cocaine Induced Myocardial Infraction definition

A

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

59
Q

Cocaine Induced Myocardial Infraction dx, tx, contraindication

A

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

Contraindication:
- beta- blockers: risk of vasospasm

60
Q

TIMI Risk Score

A
  • score calculates risk of death and ischemic events in patients with unstable angina or NSTEMI

Points:
- Age ≥ 65: 1 point
- ≥ 3 CAD risk factors (such as family history, hypertension, high cholesterol, diabetes, and being a smoker): 1 point
- Known CAD with stenosis ≥ 50%: 1 point
- ASA use in the past 7 days: 1 point
- Recent (≤24h) severe angina: 1 point
- Elevated cardiac markers (such as troponins): 1 point
- ST deviation ≥ 0.5 mm: 1 point

Cardiology (6 decks)

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