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CCD
discharged after ACS or coronary revascularization
LV systolic dysfunction with known/suspected CAD or those with established ischemic cardiomyopathy
angina symptoms medically managed without positive results of imaging test
diagnosis based on screening study (stress test) and concluded to have coronary disease
CAD
coronary artery disease
build up of plaque coronary arteries that may lead to ischemia
Ischemia
lack of oxygen and decreased/no blood flow in myocardium
mismatch between O2 supply/demand
Ischemic heart disease (IHD)
primarily caused by atherosclerosis → coronary heart disease
process begins early in life, manifests in middle years
Angina pectoris
chest pain due to decreased oxygen supply to myocardial tissue
Stable CAD
microvascular angina
stable angina pectoris
vasospastic angina
Pathophys of decreased myocardial O2 supply
coronary flow (perfusion pressure, resistance)
arterial O2 content
myocardial O2 content
Pathophys of increased myocardial O2 demand
heart rate
contractility
wall tension
Clinical presentation of CCD
may be silent
angina → chronic or variant
acute coronary syndrome= unstable angina, nstemi, stemi
other manifestations: HF, arrhythmias, stroke, PAD/PVD
Chest Pain
one of most common reasons people seek medical care
50% have non-cardiac cause
important to determine if chest pain is related to myocardial ischemia
High probability of ischemic chest pain
central
pressure
squeezing/gripping/heaviness/tightness
extertional/stress-related
restrosternal
left-sided
dull, aching
Low probability of ischemic chest pain
sharp
fleeting, shifting
pleuritic
positional
right-sided
tearing/ripping
burning
Acute chest pain
new onset or involves change in pattern, intensity, or duration
Stable chest pain
symptoms are chronic and associated with consistent precipitants
Chest Pain Initial Eval
PQRST
Precipitating factors
Palliative measures (relieved by rest w/wo SL nitro)
Quality of pain (squeezing, heaviness, tightness)
region (substernal)
radiation
severity
temporal pattern (pain less than 20 min, usually relived in 5-10)
CCD in Women
less likely to have timely/appropriate care
present with different sx: nausea, fatigue, SOB
CCD in geriatrics
> 75
can have SOB, syncope, or acute delirium
possibly unexplained fall
Clinical Chest pain eval
substernal chest discomfort with characteristic quality/duration
provoked by exertion or emotional stress
relieved by rest or nitroglycerin
cardiac → meets all 3
possible → meets 2
noncardiac → meets 1 or less
Cardiac Testing
ECG (all)
Stress testing (if symptoms)
Echo (TTE, TEE)
Coronary angiography (gold standard)
ECG
oldest diagnostic tool used
map of electrical activity across heart
critical step in eval
may be normal in CCD
Exercise Stress Testing
resting ECG may be normal for CCD pts
physical excertion → increased HR, contractility, and BP →increased myocardial O2 demand → abnormalities on ECG
treadmill with bruce protocol (continuous ECG, BP every 3 min, assess chest pain sx)
must achieve 85% of age-predicted max HR to be diagnostic
Pharmacological Stress Testing
alt for pts unable to exercise or cannot achieve target HR
2 methods:
agent that increases myocardial O2 deman (dobutamine ± atropine)
agent that dilates coronary arteries → regional perfusion abnormalities (adenosine, dipyridamole, regadenoson)
ECHO
most common modality for cardiac function and presence of CVD
use of emission of ultrasound waves to construct image
Coronary angiography
may be preformed with cardiac catherization
use of contrast and imaging to determine blood flow through coronary arteries
does not provide info on arterial walls or implication of lesion
Cardiac catherization
catheter inserted into large blood vessel and advanced to heart
may be used to perform therapeutic interventions
may be left or right sided depending on insertion site/info needed
left more common
right → acute decompensated HF, PAH, surveillance, shock
General management of CCD
risk factor modification
angina management
Modifiable risk factors of CCD
smoking
HTN
dyslipidemia
obesity
sedentary lifestyle
psychosocial factors
certain drugs
General Tx approach
team-based
individualized education on sx management, lifestyle, SDOH, med adherence
routine assessment for SDOH
diet emphasizes veggies, fruit, legumes, nuts
exercise 150+ min/week of moderate intensity
Smoking approach CCD
tobacco use assessed at every health care visit
advise quitting every visit
behavioral interventions with pharmacotherapy
routinely asked and counseled about substance use to reduce ASCVD events
Lipid approach to CCD
high intensity statin
goa: 50+% reduction in LDL
adherence measured by fasting lipids in 4-12 weeks after initiation/adjustment, ever 3-12 mo after
BP management in CCD
non-pharm first-line in elevated BP
Target < 130/80
GDMT ACEi/ARB/BB firstline for compelling indications with additional anti-HTN meds added as needed
SGLT2 inhibitors and GLP-1 agonists
CCD + T2DM → use with proven CV benefit is recommended to reudduce risk of MACE
CCD and HFrEF → reduce CV death and HF hospitalization and improve QOL
SGLT2 inhibtiros don’t appear to primarily reduce atherosclerosis vs HR
GLP-1 inhibitors appear to primary reduce risk of atheroscleotic (some inconstanstinsy)
CCD with no inidcation for oral anticoag
low dose aspirin 81 mg
CCD treated with PCI
DAPT with aspirin and clopidogrel → 6 months post
SAPT initated at 6 months to reduce MACE and bleeding
CCD with no PCI or ACS in 1 year
aspirin indefinitely
Prior ACS with/without PCI
DAPT for 1 year
post PCI with low bleeding risk
DES DAPT for 6 months
SAPT after 1 year
past PCI with high bleed risk
DES DAPT 1-3 mo
P2Y12 3-12 mo
SAPT after 1 year
PCI with low bleed risk
DOAC/clopidogrel/aspirin for 1 month
DOAC and clopidogrel 6 months
DOAC alone for around 6 months
OAC use without PCI
doac alone
Beta Blockers
CCD and LVEF 40% or less → reduce MACE
< 50% → metoprolol succinate, carvedilol, or bisoprolol with tiration to target doses
Renin-Angiotensin-Aldosterone inhibitors
ARBS/ACEi recommended to reduce CV events in CCD+ HTN or DM
Medical therapy for angina relief
BB, CCB, or long-acting nitrate
pts who remain symptomatic after initial can add 2nd antianginal
ranolazine → for pts who remain symptomatic symptomatic
SL/spray NTG rec for immediate short term believe
Agents that decrease myocardial O2 deman
decrease contractility, HR, or both
beta blockers (1st line, pref for LV dysfunction)
non-DHPs
can depress LV function, do not use with signifcant LV dysfunction
Agents that increase myocardial O2 supply
nitrates
DHP CCBs
Long acting nitrates
isosornbide mononitrate and isosorbide dinitreate
for sx uncontrolled with BB or CCD
Short acting nitrate
SL NTG, NTG spray, buccal tablets
for anginal attacks or prophylaxis
Nitrate counseling points
10-12 hour nitrate free interval to avoid tolerance
keep in original container
replace every 3-6 months
store away from heat, light, moisture
sit down during use
do not use with PDE-5 inhibits due to risk of hypotension
can take 3 doses in 15 min or 5-10 min prior to activites that may provoke angina
Nitroglycerin ointment counseling
apply ½ inch upon rising and another ½ inch 6 H later
max freq is 2 doses/day
include nitrate free interval
Nitroglycerin patch
0.2-/0.4 mg/hour; increase as needed
max 0,8 mg/hour
patch on for 12-14 H/day, then patch off period
notify or remove before MRI
Ranolazine
MOA: reduce Ca overload in ischemic myoctes through selective inhibition of late sodium current
do not depend on reductions in HR/BP
indicated in chronic angina for pts who remian symptomatic despite maximally tolerated stnadard antiangial therapy
risk of QTx prolongation
PCI
use of balloon angioplasty with stent placement
catheter guided through femoral or radial access into coronary arteries
deflated balloon slide along guidewire and infalted at site of plaque
Coronaray Artery Bypass Graft
CABG
sternotomy
vascular conduits harvested
used to bypass plaque