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
NSTEMI
Characteristic of VULNERABLE PLAQUE responsible for ACS
LIPID RICH CORE with a THIN fibrous cap
coronary angiography - ECCENTRIC stenosis with SCALLOPED or overhanging edges and a narrow neck
HEART
History
ECG
Age
Risk Factors
Troponin
Figure 274-3
TIMI Risk Score
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
Characteristic chest pain of NSTEMI
SEVERE CHEST DISCOMFORT and has at least 1 of 3 features:
VASODILATORS with peripheral and coronary vascular effects
↓ preload (by venodilation) and afterload (arterial dilation)
NITRATES
↓ HR, contractility and BP –> MVO2
Beta Blockers
target HR - 50-60
Contraindications of Beta blockers
presence of ACUTE or SEVERE heart failure
LOW cardiac output
PR interval ≥ 0.24 s (high degree AV block)
HYPOtension
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
Calcium Channel Blockers
Shown to ↓ periprocedural MI and recurrences of ACS
STATINS (HIGH DOSE)
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)
EZETIMIBE
shown to ↓ future cardiovascular events
10 mg daily to reduce further the LDL-C
Cyclooxygenase inhibitor –> blocks synthesis and release of thromboxane A2 (platelet activator) –> ⬇️ platelet aggregation and thrombus formation
Aspirin
INITIAL TREATMENT
Thienopyridine - an inactive prodrug that is converted into an active metabolite that causes IRREVERSIBLE blockade of the platelet P2Y12 receptor
Clopidogrel
loading dose - 600 or 300 mg
maintenance dose - 75 mg daily
Thienopyridine - achieves a more rapid onset and higher level of platelet inhibition than clopidogrel
Prasugrel
approved for ACS patients following angiography when PCI is planned
Potent, REVERSIBLE platelet P2Y12 inhibitor
↓ the risk of cardiovascular death, total mortality or MI compared to clopidogrel across a broad-spectrum patient with ACS
Ticagrelor
Should be considered in patients with NSTE-ACS who DEVELOP a NEW coronary event while receiving clopidogrel and aspirin
P2Y 12 blockers (PRASUGREL or TICAGRELOR)
Anticoagulants
UFH - mainstay of therapy
LMWH - Enoxaparin
DTI - Bivalirudin
Indirect Factor XA inhibitor - Fondaparinux
Carried out within ~48 h of presentation, followed by coronary revascularization (PCI or coronary artery bypass grafting) depending on the coronary anatomy
Coronary arteriography
VERY HIGH –> VERY HIGH
immediate transfer to PCI center
intermediate invasive (<2 hr)
HIGH –> HIGH
same day transfer
early invasive <24 hr
INTERMEDIATE –> INTERMEDIATE
transfer
invasive <72 hr
LOW –> LOW
transfer optional
invasive <72 hr
non invasive testing if appropriate
LONG TERM MANAGEMENT
beta blockers
intensive lipid lowering therapies - LDL<55
ACE (-) or ARBs
SGLT2 or GLP1 agonists - DM Type 2
antiplatelet therapy
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
continuation of DAPT to 3 years has been shown to be beneficial