Please enable JavaScript.
Coggle requires JavaScript to display documents.
Acute Coronary Syndromes, Screenshot 2025-02-05 at 8.51.11 PM, Screenshot…
Acute Coronary Syndromes
1. Acute Coronary Syndromes
Risk Factors
non modifiable: age, sex, FHx
lifestyle: smoking, physical inactivity, diet, alcohol, weight
medical conditions: HTN, Diabetes, Dyslipidemia
pathophysiology
2.plaque rupture and thrombosis
rupture exposes the lipid core to the bloodstream
platelets then adhere to the rupture to form a platelet plug and activate the clotting cascade
formation of a fibrin meshwork
formation of a clot (thrombus) is actually bad because it leads to ischemia then myocyte cell death
*stress increases risk of rupture
3.ventricular remodeling after MI
sympathetic nervous system activation
acute changes: increase in contractility, heart rate, peripheral resistance
chronic: desensitization and DOWN regulation of B1 receptors which leads to issues with contractility and cardiac output
RAAS activation
acute changes: slower stimulation, Na retention, peripheral vasocons
chronic: myocardial fibrosis impairs contraction and elasticity, leading to a thinner left wall and development of dilated cardiomyopathy to try to compensate
1.plaque formation
happens first
inflammation contributes to thinning fibre
more cholesterol in the core
potential for rupture to happen
Definitions
ACS
umbrella term for STEMI, NSTE-ACS, NSTEMI, unstable angina
acute
manifestation of coronary artery disease with clinical sx of acute myocardial ischemia
myocardial infarction
any amount of myocardial necrosis (tissue death) caused by ischemia (inadequate blood supply)
STEMI
A
severe, full-thickness
(transmural) myocardial infarction caused by
complete
occlusion of a coronary artery.
NSTE-ACS
An umbrella term that includes NSTEMI and Unstable Angina (UA).
Caused by
partial
occlusion of a coronary artery.
NSTEMI
A type of
heart attack
caused by
partial
occlusion of a coronary artery that results in myocardial necrosis.
unstable angina
Severe chest pain or
discomfort
at rest or with minimal exertion due to
partial
occlusion of a coronary artery.
2. Clinical Presentation and Diagnosis
diagnosis
cardiac troponins: biomarker for myocardial necrosis
STEMI - troponin present
unstable angina: no troponin increase
NSTEMI: troponins present
tests
echocardiography
coronary angiography
oxygen saturation (above 93% is normal)
ECG
STEMI: ST-segment elevation
NSTE-ACS: ST depression, T-wave inversion
to diagnose MI, need to have one positive troponin AND one of these: sx or hx, ischemic ECG changes, imaging evidence of new loss of myocardium
risk stratification
STEMI: highest risk, urgent reperfusion
NSTE-ACS: TIMI, GRACE, and HEART score for risk assessment
first, a person will have sx of SIHD, then a plaque ruptures and forms a clot, leading to ACS
symptoms of ACS
atypical sx: lightheadedness, nausea, dyspnea, syncope
special pops: elderly, women, diabetics may have silent MI
typical sx: chest pain longer than 10 mins, tightness,
discomfort
not pain, radiation to neck/jaw/shoulders/back, squeezing, pressure, rapid acting nitro is INEFFECTIVE
*occur during stress
3. Management of ACS
pre-hospital and initial in-hospital management
ecg and troponin monitoring
reperfusion therapy for STEMI
primary PCI
fibrinolysis
MONA -> morphine, oxygen, nitro, aspirin
NSTE-ACS approach
early invasive vs ischemia driven strategy
parenteral anticoagulation (UFH, enoxaparin, fondaparinux)
revascularization strategies
PCI
stents: drug0eluting stent vs bare-metal stent
complications: stent thrombosis, in-stent restenosis
coronary artery bypass graft (CABG)
indications for CABG over PCI
4. Pharmacotherapy for ACS
ACEi/ARBs
benefits: prevents adverse cardiac remodeling
indications: heart failure, LVEF <40%, HTN, diabetes
aldosterone antagonists (spironolactone, eplerenone)
indications: LVEF <40% with heart failure or diabetes
risk of hyperkalemia
beta blockers
benefits: reduces mortality, MI, arrhythmias
duration: 1-3 years (indefinite if LVEF < 40%)
nitroglycerin
short acting: SL spray or tablet for acute angina relief
long acting: prevention (limited role in ACS)
lipid-lowering therapy
high intensity statins (atorvastatin 80mg, rosuva 40mg)
non statin additions (ezetimibe, PCSK9 inhibitors)
colchicine
potential benefit for reducing inflammation post-ACS
antithrombotic therapy
anticoagulation (hospital setting)
UFH, LMWH (enoxaparin), fondaparinux
DAPT duration
shorter duration: high bleeding risk
extended duration: high ischemic risk
standard: 1 year
dual anti platelet therapy (DAPT)
aspirin
P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel)
5. Long-Term Management + Secondary Prevention
adherence to meds
importance of high-intensity statins
BB, ACEi/ARB for heart failure
pt education on DAPT adherence
cardiac rehab
structured exercise programs
psychosocial support
lifestyle modifications
diet and exercise
BP and Diabetes control
smoking cessation
vaccination
annual flu vaccine recommended for ACS pts
go through slides and do pt case when done reviewing
