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CARDIO HARRISONS > C274: NSTEMI > Flashcards

C274: NSTEMI Flashcards

1
Q

Parameters (7) involved in TIMI Risk Markers

A
  • Age ≥ 65
  • Known CAD ( ≥ 50% stenosis)
  • ST deviation > 0.5mm on presenting ECG
  • increased cardiac markers
  • ≥ 2 original episodes in prior 24hrs
  • prior angina
  • ≥ 3 CAD risk factors
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2
Q

Difference between myocardial injury vs myocardial necrosis

A
  • Myocardial injury - elevations of cTN >99th percentile of the upper reference limit in patients WITHOUT a clear clinical histoy or ECG features of acute myocardial ischemia
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3
Q

3 RISK STRATIFICATION EME used in NSTEMI

A
  • TIMI - Thrombolysis in Myocardial Infarction
  • GRACE - Global Registry of Acute Coronary Event
  • HEART - History, ECG, Age, Risk fx, Troponin
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4
Q

What does HEART risk stratification stand for in NSTEMI

A

History, ECG, Age, Risk fx, Troponin

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5
Q

When is AMBULATION allowed in NSTEMI

A
  • if with no recurrence of ischemia for 24hrs
  • and if no development of elevation of cTn for 24 hrs
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6
Q

How should Nitrates be given in NSTEMI

A
  • given sublingually or by buccal spray (0.3 to 0.6mg ) up to 3 doses , 5 mins apart
  • if still with chest pain, may give IV nitroglycerin (5-10ug/min)
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7
Q

ABSOLUTE CONTRAINDICATION FOR USE OF NITRATES

A
  • hypotension
  • Sildenafil / Vardenafil (within 24hrs)
  • Taladafil (within 48 hrs )
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8
Q

Target heart rate in NSTEMI patients on BETA BLOCKERS

A

Target heart rate in NSTEMI patients on BETA BLOCKERS —> 50-60 bpm

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9
Q

CCBs for NSTEMI

A
  • Verapamil or Diltiazem
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10
Q

Patients who have persistent severe chest pain despite maximal anti-ischemic therapy may be given ________

A

MORPHINE IV 1-5mg every 5-30 mins

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11
Q

High dose statins should be given in NSTEMI. If patients who still failed to have adequate response to statins, the other drugs that can be given are: ( 2 DRUGS)

A
  • Ezetimibe 10mg OD
  • PCSK9 inhibitor - Alirocumab, Evolocumab
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12
Q

Two other P2Y12 inhibitors that are superior to Clopidogrel in preventing recurrent cardiac ischemic events both both increase bleeding

A
  • Prasugrel
  • Ticagrelor - REVERSIBLE
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13
Q

Gene involved why some have inadequate response to Clopidogrel

A
  • genetic variant of CYP450 —> 2C19 gene that leads to reduced conversion of clopidgorel into its active metabolite
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14
Q

DAPT should continue at least _______months and preferably _______months in NSTEMI patients

A

DAPT should continue at least 3 months and preferably 12 months in NSTEMI patients

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15
Q

The only intravenous P2Y12 inhibitor

A

Cangrelor

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16
Q

LOADING DOSE and MAINTENANCE DOSE OF Aspirin vs Clopidogrel vs Prasugrel vs Ticagrelor

A

Aspirin - 150-325mg then 75-100mg OD

Clopidogrel - 600mg if for PCI vs 300mg if not for PCI THEN 75mg OD

Prasugrel - 60mg (PCI) then 10mg OD

Ticagrelor - 180mg then 90mg OD

17
Q

Anticoagulant that is mainstay of therapy in NSTEMI

A
  • Unfractionated heparin
18
Q

LMWH that is superior to UFH in reducing recurrent cardiac events

A
  • Enoxaparin
19
Q

Direct thrombin inhibitor that has same efficacy w/ LMWH and UFH and is used just prior and /or during PCI

A
  • Bivalirudin
20
Q

Synthetic factor Xa inhibitor that is same efficay with Enoxaparin but has lower risk of major bleeding

A
  • Fondaparinux
21
Q

Difference in timing among intermediate invasive, early invasive, and invasive strategy:

A
  • intermediate invasive - less than 2 hrs
  • early invasive - less than 24hrs
  • invasive - less than 72 hrs
22
Q

If an early invasive strategy is indicated, _____ artery access is recommended to reduce the risk of bleeding

A
  • radial artery
23
Q

Recommended anti thrombotic regimen for patients with Afib and NSTEMI who underwent PCI

A
  • duration of DAPT should be shortened
    • ( ex: Stop aspirin after hospital discharge or up to 4 weeks post PCI except for patients at very high risk of ischemic events)
  • then continue P2Y12 inhibitor plus DOAC for 1 year
  • then after 1 year, DOAC monotherapy na laaaaang
24
Q

Difference between invasive VS selective invasive approach

A
  • In an invasive strategy, following initiation of anti-ischemic and antithrombotic agents as described above, coronary arteriography is carried out within ~48 h of presentation, followed by coronary revascularization (PCI or coronary artery bypass grafting), depending on the coronary anatomy
  • consists of anti-ischemic and antithrombotic therapy followed by a “selective invasive approach,” in which the patient is observed closely and coronary arteriography is carried out if coronary computed angiography shows the presence of epicardial coronary stenosis, rest pain or ST-segment changes recur, a biomarker of necrosis becomes positive, or there is evidence of severe ischemia on a stress test.
25
Q

Recommended antiplatelet regimen for NSTEMI:

A
  • low-dose (75–100 mg/d) aspirin PLUS
  • P2Y 12inhibitor (clopidogrel, prasugrel, or ticagrelor)

.
.

  • Duration: for 12 months, unless there is a high risk of bleeding. Antiplatelet monotherapy should be continued thereafter,
    - unless long-term full-dose anticoagulation is indicated, in which case anticoagulant without antiplatelet therapy is recommended after 1 year
26
Q

What is Prinzmental’s variant angina

A

Prinzmental’s variant angina is syndrome of severe ischemic pain that usually occurs at rest and is associated with STsegment elevation.

27
Q

Cause of Prinzmetal’s variant angina (PVA)

A

Prinzmetal’s variant angina (PVA) is caused by focal spasm of an epicardial coronary artery with resultant transmural ischemia and abnormalities in left ventricular function that may lead to acute MI, ventricular tachycardia or fibrillation, and sudden cardiac death.

28
Q

clinical diagnosis of PVA

A

made by the detection of transient ST-segment elevation with rest pain, although many patients may also exhibit episodes of silent ischemia

29
Q

diagnostic hallmark of PVA.

A

Coronary angiography demonstrates transient coronary spasm as the diagnostic hallmark of PVA.

30
Q

2 ways provoke transient coronary spasm for establishing diagnosis of PVA

A
  • Hyperventilation
  • intracoronary acetylcholine
31
Q

main therapeutic agents for PVA (2)

A

Nitrates
calcium channel blockers

32
Q

Effect of Aspirin on PVA

A

Aspirin may actually increase the severity of ischemic episodes, possibly as a result of the sensitivity of coronary tone to modest changes in the synthesis of prostacyclin

33
Q

Statin is useful in PVA. How?

A
  • Statin therapy has been shown to reduce the risk of major adverse events, although the precise mechanism is not established
34
Q

Duration of acute active phase of PVA

A

first 6 months after initial presentation
.
.
- after which, the symptoms and cardiac events may diminish over time

CARDIO HARRISONS (7 decks)

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