Block I: CAD Flashcards
epicardial vessel atherosclerosis can lead to []
coronary heart disease/ Coronary artery disease
what are some presentations of CAD?
- acute coronary syndrome
- chronic stable exertional angina pectoris
- ischemia w/o clinical symptoms
- heart failure
- arrythmias
- cerebrovascular disease
- periperal vascular disease
squeezing, pressure, heaviness, tightness, pain in chest are signs of []
angina
[] is a type of angina with a fixed stenosis
chronic stable
[] is a type of angina that involves vasospasm of coronary arteries
variant (printzmetal’s sign assoc.)
what are some precipitating factors for variant angina?
- pregnancy
- drugs (cocaine)
- cold weather
- emotional stress
[] is a type of angina involving a fixed stenosis rupture
untable angina
what is L main/ L main equivalent CAD
blocking entire L coronary artery
what is the 12 yr. survival rate for 0 occluded vessels
88%
what is the 12 yr. survival rate for 2 occluded vessels
59%
what is the 12 yr survival rate for one occluded vessel
74%
what is the 12 yr survival rate for three occluded vessels
40%
- pressure/bruning near sternum
- chest tightness, SOA
- visceral pain lasting 0.5-30 minutes
- precipitated by exercise, cold, anger, coitus, freight
this describes symptoms of []
stable angina
deep, poorly localized chest/arm discomfort
-rarely described as pain
that is producable (brought about by exercise, freight, emotional distress)
usually relieved in 5-10 minutes with rest or NTG
describes []
stable angina
angina or ischemic discomfort while
- at rest
- lasts > 10 minutes
- severe pain
- occurring in a crescendo pattern
this describes []
unstable angina
dull discomfort brought about by exrtion that lass under 10 minutes is likely []
stable angina
sharp pain lasting more than 10 minutes in a crescendo pattern is []
unstable angina
what are some ekg changes you may expect to see in an acute coronary patient
- St depression
- ST elevation
- T wave inversion
exertional hypotension and reduced exercise tolerance indicate [] ischemia
significant
what are 2 signs significant ischemia
- hypotenion on exertion
2. reduced exercise tolerance
what is the gold standard to evaluating coronary anatomy to quantify the presence and severity of atherosclerotic disease
coronary angiography (AKA cardiac catherterization)
when are good times to order coronary angiography
- markedly positive stress test
- suspected non-arthersclerotic cause ischemia (congenital abrnom.)
- recurrent chest pain despite aggressive medical therapy for angina
what is a treatment goal for stable ischemic heart disease
reduce/prevent angina symptoms that limit exercise capability & impair QOL
prevent CHD event (mi, arrythmia, heart failure)
exten pt. life
what is a class 1 rec. immediate relief pain asoc. with stable ischemic heart disease?
NTG
what is the initial therapy that should be rx’ed for relief of symptoms for stable ischemic heart disease (class 1 guideline)
BB
what is a second line for symptom relief of stable ischemic heart disease if BB is contrainindicated or not tolerated (class 1 guideline)
CCB/ long acting nitrate
what can be added to treatment of stable ischemic heart disease if BB alone are not efficacious (class 1 guideline)
CCB/long acting nitrate
what is a class 2a rec. for symptomatic relief of stable ischemic heart disease for symptom relief
- long acting non-DHP (dipine drugz)
* instead of BB as initial therapy for relief of symptoms
what are substitutes for BB in SIHD?
class 1a:
- CCB
- long acting nitrate
class 2a:
- non-DHP CCB
- ronolazine
what 2 drugs can be used as sdjuvant therapy when BB alone are innefective in SIHD?
class 1a:
- CCB
- long acting nitrate
Class 2a:
-ronolazine
if a patient with SIHD has high lipids (try > 150, LDL > 100)
what should be added to their therapy?
moderate-high dose statin
whats the BP goal for SIHD pts.
= 140/90
whats the A1C goal in SIHD pts.
< 7%
whats a good physical activity goal for SIHD pts.
30-60 minutes of mod intensity aerobic activity at least 5-7 days per weak
how should pts. sith SIHD cut saturated fat?
< 7% calories sat fat
whats a systolic BP goal for SIHD
< 130 mmHG
whats a LDL goal for SIHD pts.
< 70 (< 100 good)
whats a BMI goal for SIHD pts.
< 25
what are mainstays of ischemic heart disease optimal therapy?
- aspirin daily
2. statin: max tolerated dose
what statins are most rec?
Rosuvastatin 20-40mg
atorvastatin 40-80mg
a IHD pt. with hypertension or requires waht regimen?
- ASA
- Statin (max)
- ACEI/ARB
a IHD pt. with DM requires what regimen
- ASA
- Statin (max)
- ACEI/ARB
a IHD pt. with LVEF < 40 % requires what regimen
- ASA
- Statin (max)
- ACEI/ARB
a IHD pt with eGFR < 60 requires what regimen
- ASA
- Statin (max)
- ACEI/ARB
what is optimal therapy for a IHD pt. with MI or LVEF < 40%
- ASA
- Statin
- BB
what can be added to a pt. where ASA in contraindicated or who need an adjuvant to ASA?
- P2Y12 receptor agonists
if a patient is unable to reach LDL goal with max statin, what can be added?
ezetimibe
what can be added to a statin and exetimibe if pt. still is not at LDL goal?
evolcumab, alicromab
monoclonal ab for LDL receptors (to keep high numbers of them active to less LDL is stuck in blood)
what should be recomended anually for SIHD pts
flu vax
what is the MOA for nitrates
potent vasodilatory (primarly venous) and diminish platelet aggregation
nitrate primarily vasodilate [] vessels
venous
[] is essential exogenous NO
nitrates
what is the role of NO
released from endothelial cells to increase cyclic guanosine monophosphate (cGMP) levels through activation of guanylate cyclase
platelet agreggation diminished, vasodilation
what are some indications nitrates
- terminate acute anginal attacks
- prevent effort/stress-induced attacks (prophylactically before exercise)
- can be used for long-term prophylaxis
- usually in combo with BB< CCB
what are some AE nitrates
- postural hypotension
- HA
- nausea
- reflex tachycardia
- rash
what happens when beta receptors are activated by NE
- AV node conduction accelerated
- increase HR and contractility
- increased myocardial oxygen demand
during MI [] receptors become activated which exacerbate the MI how?
- beta receptors
- increase contractility and HR thereby increasing myocardial oxygen demand
the whole reason they are having an MI is because they dont have o2!
what are the effects of blocking beta receptors?
- decrease HR/contractility
- decrease AV node conduction
- decrease O2 demand
- decreased angina both at rest and exercise
what is the first line in chronic angina that requires daily maintenance therapy
BB
what is the benefit of BB in angina
- reduce MI, CAD. mortality
- can be used prophylactically in pts. with multiple anginas a day
- reduce need for revascularization surgery
[] can decrease anti-anginal effects of BB
smoking
what are some AE or BB
- hypotension
- bradycardia
- bronchospasm
- altered glucose metabolism
- fatigue
- malaise
- depression
what should you counsel your patient on about abruptly stoping BB?
- assoc. with increased severity and number of pain episodes if stopped abruptly
MOA CCB
improve coronary blood flow through coronary atery vasodilatoin to decrease myocardial oxygen demand
blocks long Ca2+ channels in myocytes
who are good candidates for CCB?
- cont/intolerance BB
- printzmetal angina
- peripheral vascular disease
- concurrent uncontrolled HTN
printzmetal angina is best treated with []
CCB
peripheral vascular disease is best treated with []
CCB
what CCBS can be used to treat arrythmias
non DHP
what CCBs can be used to vasodilate and cause reduction in BP?
all of them, DHP and non DHP
what is the moa of ronalozine
reduce CA2+ overload in ischemic myocye through selective inhibition of late NA_ current (lna)
what drug has an MOA that
reduced Ca2+ overload in ischemic myocyte through selective inhibition of late Na current
ronalozine
what drug has an MOA that improves coronary blood flow through coronary artery vasodilation by decreasing oxygen demant, wby blocking Ca2+ long channels in myocytes
CCB
what drug has an MOA that
is a potent vasodilator and diminished platelet aggregation
nitrate
what drug does NO affect HR, inotropic state, hemodynamic state or increase coronary blood flow?
ronolazine
what are some indications for ronolazine
- chronic angina treatment
- reserved for pts. who have no achieved adequate response with other antianginal agents (BB,CCB)
what drugs can cause bradycardia
- non DHP
2. BB
what drug causes prolonged QT interval
ronolazine
what drug can cause HA
nitrates
what drug can cause depression
BB
what is an adverse effect of ronalazine?
prolonged QT interval
what are some contraindications for ronalazine?
- pre-existing QT interval prolongation
2. hepatic impairment
what re drug interactions for ronalazine?
- other QT prolongating drugs
2. cytochrome P450 3A decrease ranalazine clearance and will cause torsades des points
prior to undergoing revascularization surgery for stable exertional angina pectoris what should you do?
- max 2-3 anti-anginal therapies
[] is generally recommended to improve survival in patients with DM and CAD for which revascularization can improve survival
CABG (pref. over PCI)
patients shold [] taking ASA before their CABG
continue
a patient on clopidogrel or ticagrelor should [] treatment before CABG
d/c for 24 hrs
ticagrelor should be help for [] days in elective CBG
3
clopidogrel should be held for [] days in elective CBG
5
prasurgrel should be held for [] days in elective CBG
7
what pharm should be dispensed post op CABG
- ASA within 6 hours post-op
- continued indefinitley
all PCI pts. receive [] to take indef. post procedure
ASA
how long should clopidogrel be given after drug eluting PCI placed?
6 months (3 if bleeding risk)
how long should clopidogrel be given post bare metal stint placing?
1 month
[] plays a key role in arhterosclerosis
inflammation
what factors can lead to endothelial dysfunction? (which can lead to atherosclerotic plaques)
- HTN
- smoking
- dyslipidemia
- male
- age
- tobacco
- obesity
[] results from myocardial ischemia due to imbalance between myocardial O2 demans and supply
ACS (acute coronary syndrome)
exposure of collagen & tissue factor from plaque leads to platelet activatoin and adhesion and the release of what vasoactive substances?
- adenosine diphosphate
2. thromboxane 2
[] is defined as changes in shize, shape, and function of L ventricle
ventricular remodleing
ventricular remodeling can lead to []
heart failure
what 4 drugs can slow down or reverse ventricular remodeling to improve change of survival
- ACEI
- ARB
- BB
- aldosterine agonists
what are three examples of acute coronary asyndromes
- STEMI
- NSTEMI
- unstable angina
what complication of ACS do you want to avoid at all costs?
cardiogenic shock, high mortality rate
[] is a rare complication of MI and occurs when the heart is not able to pump enough blood to meet body’s demand
cardiogenic shock
[]% STEMI pts. will exerpience cardiogenic shock
5-6
[]% non stemi pts with experience cardiogenic shock
2
what is the morality rate of cardiogenic shock
60
- middle anterior anginal chest pain
- severe new onset angina
- increasing angina duration > 20 min
- radiating pain
- N/V
- diaphoresis
- SIA
these are signs of []
ACS
- unstable angina
- MI
- STEMI
- NSTEMI
what populations may present with abnormal/minimal ACS symptoms
- women
- elderly
- diabetics
if you suspect ACS, an ECG needs done [] amount of time
10 minutes of arrival,
every 15-30 minute intervals during first houe
what are key findings on ECG of ACs
- ST segment elevatoin
- ST segment depression
- T wave inversion
what biomarker can you order if you suspect ACS
troponin
released when myocardial cells die
order
- at presentation
- 3-6 hrs after symptom reset
- after 6 hrs in patient with initial normal troponins with ECG change and/or intermediate high risk clinical features
[] is the best predictor of mortality after an MI
left ventricular function
LVEF of [] has a high risk of death
< 40%
infarction in [] has worse outcomes
hyperglycemia
what is the best treatment for STEMI
- coronary reperfusion via primary PCI, fibrinolysis or emergent CABG to restore coronary blood flor
what non=pharm revascularization is preferred in STEMIpts
PCI
high risk NSTEMI may be candidates for []
PCI, CABG
early invasive therapy
what is pharmacotherapy
ptotocol for ACS
- Morphine
- oxygen (when sat < 90%)
- NTG
- aspirin
- BB
- within first 24 hours in absence of acute HF exacerbation, low output state, risk coardiogenic shock or con. BB
MONA B
when should o2 be admin in ACS
< 90% sat, respiratory distresss
how often should NTG be given in ACS
every 5 minutes
what should be discharged after ACS
- NTG SL
- ASA
- BB
- High intensity statin
- ACEI/ARB
- *HrfEF patients with aldosterone antagonist
what is the MOA ASA
irreversible inhibition of platelet cyclooxygenase-1
-may have antiinflammatory effects
what are contraindications ASA
- hypersensitivity
- active bleeding
- severe bleeding irsk
what should NOT be administered with ASA
NSAID
what kind of drug is ticagrelor
cyclopentyltriazolopyrimide P2Y12 inhibitor
what is the MOA ticagrelo
binds REVERSIBLY to P2Y12 ADP receptor
to reduce rate of combined endpoint CV death, MI, stroke
what drugs MOA is
binding reversible to P2Y12
ticagrelor
what is the indication for ticagrelor
indicated to reduce CV thrombotic events in patients with ACD
ticagrelor vs. clopidogrel
which is more efficacious
ticagrelor
what are contraindications ticagrelor
- hepatic impairment
- intracranial hemorrhage hx
- active bleeding
- ASA > 100
what are AE of ticagrelor
- bleeding
- dyspnea
- bradyarrythmia
- elevated uric acid
- elevated Scr
what kind of drug of clopidogrel
thienopyridine
P2Y12 inhib.
moa clopidogrel
irreversible bind to P2Y12 reveptor, prevent firbinr clots
contra. clopidogrel
- hypersensitivity
- active bleeding
- severe bleeding risk
AE clopidogrel
- bleeding
2. N/V/D
important drug interaction clopidogrel
PPIs may lower effectivement
-omeprazole and esomeprazole esp.
what kind of drug is prasugrel
thienopyridine
P2Y12 inhib.
MOA prasugrel
irreversibly block P2Y12 in paltelets
which of the thienopyridines acts quicker?
prasugrel
which thienopyridine is more efficacious in patients undergoing PCI
prasugrel
which thienopyridine is NOT affected by PPI
prasugrel
which thienopyridine is affected by PPI
clopidogrel (esp. omeprazole and esomeprazole)
which thienopyridine is assoc with increased CABG bleeding rates in clinical trials
prasugrel
P2Y12 should be given to patients undergoin PCI
prsugrel
what P2Y12 should be given to patients undergoind CABG
clopidogrel
when is really the only time to use prasugrel
pt. undergoing PCI
what are contraindications prasugrel
- active bleeding
2. prior stroke
what precautions should you take with prasugrel
age >/= 75
body weight < 60
what are AE prasugrel
- bleeding
2. TTP
stent thrombosis usually present as []
MI, STEMI
what are components of drug eluting stint
platform
- stainless steel
- cobalt chrome
- platinum
polymer coating
1. controlled release drug carriers
antiproliferative agent
- lipophilic
- immunsuppressive
what medications should a pt be on to prevent secondary MI
- ASA
- BB
- CCB
- ACEI
- high intensity statin
- NTG if ischemic chest pain
- Antiplatelet for at leas 12 months
- ticagrelor
- clopidogrel
- prasugrel - annual flu vax
- glycemic control