ACS - NSTEMI Flashcards

(32 cards)

1
Q

Caused by an IMBALANCE between myocardial oxygen supply and demand resulting from one or more of the following 3 processes –> coronary arterial thrombosis

1. plaque fissure w/ inflammation - inflammatory response reflected by an increased activity of effector T cells as part of an adaptive immunity dysregulation
2. plaque fissure w/o inflammation
3. plaque erosion - (+) in at least ⅓ of ACS; recognized w/ increasing frequency

A

NSTEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Characteristic of VULNERABLE PLAQUE responsible for ACS

A

LIPID RICH CORE with a THIN fibrous cap

coronary angiography - ECCENTRIC stenosis with SCALLOPED or overhanging edges and a narrow neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HEART

A

History
ECG
Age
Risk Factors
Troponin

Figure 274-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TIMI Risk Score

A

Age >65
Known CAD >50% stenosis
ST deviation >0.5 mm on ECG
⬆️cardiac markers
>2 original episodes in prior 24 h
prior angina
>3 CAD risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Characteristic chest pain of NSTEMI

A

SEVERE CHEST DISCOMFORT and has at least 1 of 3 features:

  • occurrence at rest (or with minimal exertion), lasting >10 min
  • relatively recent onset (i.e., within the prior 2 weeks)
  • CRESCENDO pattern - distinctly more severe, prolonged, or frequent than previous episodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

VASODILATORS with peripheral and coronary vascular effects

↓ preload (by venodilation) and afterload (arterial dilation)

A

NITRATES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

↓ HR, contractility and BP –> MVO2

A

Beta Blockers

target HR - 50-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contraindications of Beta blockers

A

presence of ACUTE or SEVERE heart failure

LOW cardiac output

PR interval ≥ 0.24 s (high degree AV block)

HYPOtension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Recommended for patients who have persistent symptoms or ECG signs of ischemia AFTER treatment with FULL DOSE NITRATES and BETA BLOCKERS and in patients with contraindications to either class of these agents

A

Calcium Channel Blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Shown to ↓ periprocedural MI and recurrences of ACS

A

STATINS (HIGH DOSE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

For patients who do not have an adequate response to maximally tolerated statin (i.e., <50% ↓ in LDL-C from untreated baseline or LDL-C on treatment >70 mg/dL)

A

EZETIMIBE

shown to ↓ future cardiovascular events

10 mg daily to reduce further the LDL-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cyclooxygenase inhibitor –> blocks synthesis and release of thromboxane A2 (platelet activator) –> ⬇️ platelet aggregation and thrombus formation

A

Aspirin

INITIAL TREATMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Thienopyridine - an inactive prodrug that is converted into an active metabolite that causes IRREVERSIBLE blockade of the platelet P2Y12 receptor

A

Clopidogrel

loading dose - 600 or 300 mg

maintenance dose - 75 mg daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thienopyridine - achieves a more rapid onset and higher level of platelet inhibition than clopidogrel

A

Prasugrel

approved for ACS patients following angiography when PCI is planned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Potent, REVERSIBLE platelet P2Y12 inhibitor

↓ the risk of cardiovascular death, total mortality or MI compared to clopidogrel across a broad-spectrum patient with ACS

A

Ticagrelor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Should be considered in patients with NSTE-ACS who DEVELOP a NEW coronary event while receiving clopidogrel and aspirin

A

P2Y 12 blockers (PRASUGREL or TICAGRELOR)

17
Q

Anticoagulants

A

UFH - mainstay of therapy
LMWH - Enoxaparin
DTI - Bivalirudin
Indirect Factor XA inhibitor - Fondaparinux

18
Q

Carried out within ~48 h of presentation, followed by coronary revascularization (PCI or coronary artery bypass grafting) depending on the coronary anatomy

A

Coronary arteriography

19
Q

VERY HIGH –> VERY HIGH

A

immediate transfer to PCI center
intermediate invasive (<2 hr)

20
Q

HIGH –> HIGH

A

same day transfer
early invasive <24 hr

21
Q

INTERMEDIATE –> INTERMEDIATE

A

transfer
invasive <72 hr

22
Q

LOW –> LOW

A

transfer optional
invasive <72 hr
non invasive testing if appropriate

23
Q

LONG TERM MANAGEMENT

A

beta blockers
intensive lipid lowering therapies - LDL<55
ACE (-) or ARBs
SGLT2 or GLP1 agonists - DM Type 2
antiplatelet therapy

24
Q

Patients at HIGH ISCHEMIC RISK (e.g., those with prior MI, diabetes mellitus, coronary vein graft, heart failure) who are also at low risk of bleeding and not on an anticoagulant

A

continuation of DAPT to 3 years has been shown to be beneficial

25
**Syndrome of severe ischemic pain that usually occurs at rest** Associated with **ST segment elevation**
**PRINZMETAL ANGINA** ## Footnote minority of patients have a **generalized vasospastic disorder associated with migraine and/or Raynaud’s phenomenon**
26
**Pathophysiology of Prinzmetal Angina**
**FOCAL SPASM of an EPICARDIAL CORONARY ARTERY with resultant transmural ischemia and abnormalities in left ventricular function -- acute MI, ventricular tachycardia or fibrillation, and sudden cardiac death**
27
**Diagnostic hallmark of Prinzmetal Angina**
**coronary angiography - TRANSIENT coronary spasm**
28
**The main therapeutic agents of PVA**
**NITRATES and CCB**
29
**Patients with PVA who have had ischemia-associated ventricular fibrillation despite maximal medical therapy should receive**
**implantable cardioverter-defibrillator (ICD)**
30
**Mechanism contributing to the pathophysiology of NSTE-ACS**
**Coronary plaque fissure with ⬆️ T cell activity causing obstructive thrombosis**
31
**Elevations of cTn >99th percentile WITHOUT a clear clinical history of ECG features of acute myocardial ischemia**
**Myocardial INJURY** Table 274-2
32
Have been used to **provoke focal coronary stenosis** on angiography or to **provoke rest angina with ST-segment elevation to establish the diagnosis of Prinzmetal Angina**
**hyperventilation and intracoronary acetylcholine**