Ischemic Heart Disease Flashcards
1
Q
What is ischemic heart disease?
A
narrowing of one or more coronary arteries due to atherosclerosis
2
Q
What are the many names for ischemic heart disease?
A
coronary artery disease (CAD)
coronary heart disease (CHD)
atherosclerotic cardiovascular disease (ASCVD)
3
Q
What is the most well known outcome of ischemic heart disease?
A
heart attack
4
Q
What is the epidemiology of ischemic heart disease?
A
2nd leading cause of death (after cancer)
leading cause of hospitalization
#1 cause of life-years lost due to premature mortality
5
Q
What are the main types of cardiovascular diseases caused by atherosclerosis?
A
ischemic heart disease
cerebrovascular disease
peripheral arterial disease
6
Q
What is atherosclerosis called when it is present in the following: coronary artery, cerebral arteries, arteries of limbs
A
coronary artery disease
-major cause of myocardial infarction (heart attack)
cerebrovascular disease
-major cause of cerebrovascular accident (stroke)
peripheral arterial disease
-poor circulation, pain, numbness
7
Q
What are the three presentations of coronary atherosclerosis?
A
silent (asymptomatic) disease=most patients
chronic, stable (exertional) angina
acute coronary syndromes (ACS)
-includes: unstable angina, NSTEMI, STEMI
8
Q
Describe the symptoms of angina.
A
dull, retrosternal discomfort/ache/heaviness
may or may not radiate to jaw, neck, shoulders, arms
9
Q
What are the two types of angina?
A
stable angina: problem of demand exceeding supply
unstable angina: inadequate supply regardless of demand
10
Q
Describe fixed obstruction angina (stable angina).
A
an increase in demand that cannot be accommodated with increased supply
“demand” for oxygen increases when cardiac myocytes increase energy expenditure
angina pain that is NOT associated with plaque rupture
11
Q
What will cause an increased demand for blood?
A
heart rate
blood pressure
venous return
contractility
exertion, emotion, stress
12
Q
What are real world examples for triggers of stable angina?
A
SNS activity: physical exertion, emotion, stress
exertion after a heavy meal (SNS and metabolic demands)
metabolic demands imposed by:
-chills, fever, hyperthyroidism, tachycardia, exposure to cold,
and hypoglycemia
anemia
13
Q
Which arteries are supplied during diastole?
A
coronary arteries
14
Q
When will endocardial vessels be fully dilated under resting conditions?
A
if epicardial vessels are obstructed over 70-75%
15
Q
True or false: for a vessel with epicardial vessel plaque that is dilated at rest, it can dilate further during exercise
A
false
its maximally dilated at rest, thus exercise creates ischemia and thus the symptoms of angina appear
16
Q
What are some additional issues in fixed obstruction angina?
A
endothelial dysfunction (decreased NO production)
microvascular dysfunction (poor response to NO)
17
Q
What is a rare form of angina that is due to vasospasm?
A
Prinzmetals angina/variant angina
18
Q
When does the pain occur from stable angina?
A
during conditions of increased demand
19
Q
How is stable angina relieved?
A
rest and nitroglycerin
20
Q
Describe nitrates.
A
a class of medications that cause vasodilation
all are prodrugs (not active when administered)
converted to NO
21
Q
What is nitric oxide?
A
a paracrine hormone synthesized by endothelial cells to signal to smooth muscle cells next door
relaxes smooth muscle in blood vessel walls
22
Q
What does nitroglycerin target?
A
veins
23
Q
What is preload?
A
the degree to which the myocardium is stretched before it contracts
increased preload=increased work of the heart
24
Q
Describe the grading of angina.
A
class I: ordinary physical activity does not cause angina,
strenuous or prolonged exertion causes angina
class II: slight limitation of ordinary activity, angina occurs on
walking or climbing stairs rapidly
class III: marked limitations of ordinary physical activity
class IV: inability to carry on any physical activity, symptoms
may be present at rest
25
What is exercise stress testing?
occurs on a treadmill or stationary bike
patient hooked up on a ECG, heart rate and bp monitor
exercise is initiated slowly and slowly builds
it is stopped if chest pain, ST changes, decrease in bp>=10mmHG
26
What is a classic sign of cardiac ischemia?
ST depression
-common way to establish stable angina
-does NOT indicate if myocardial cell death has occurred
27
True or false: stable angina is not a medical emergency
true
28
What is commonly performed to evaluate coronary artery blood flow?
cardiac catherterization and angiography
-identify locations of narrowed vessels due to atherosclerosis
29
Name the core medication therapy for patients with CAD.
ABCKDE
antiplatelets
blood pressure medications (not necessarily for bp)
cholesterol-lowering medications
K-CKD (CKD often present with CAD)
diabetes medications
exercise/diet/lifestyle changes (stress, alcohol, tobacco)
30
What is an agent (aside from nitrates) that should be considered in all patients with stable ischemic heart disease?
ACEI
*ARBs used in patients with intolerance to ACEI*
31
What are the drugs that have an indication to prevent or reduce the frequency/intensity of stable angina episodes?
beta blockers
non-DHP CCBs
DHP CCBs
nitrates
ranolazine
32
How do beta blockers work for angina?
prevents angina by reducing contractility to decrease demand
33
When should beta blockers be used first line for stable angina?
first-line for stable angina in people with another indication for beta blockers:
-systolic heart failure
-post MI
evidence for the above has made it first line in almost all cases of SIHD
34
How is the dose titrated for beta blockers in stable angina?
dose titrated to a resting heart rate of 55-60bpm
35
Which beta blockers are used in stable angina?
all BB are effective equally to prevent angina
B1 selective agents preferred due to lower risk of:
-erectile dysfunction (B2-blockade)
-peripheral circulation problems (esp in pts with PAD)
-interaction with B2 agonists
36
Which beta blockers should be avoided for stable angina?
BB with ISA (e.g., acebutolol)
37
Describe the monitoring of beta blockers.
decreased heart rate and bp-->AV block or low HR
signs of poor cardiac output-->exercise tolerance or decreased renal perfusion (RAAS/edema etc)
reduced circulation-->caution in Raynaud's/PAD (esp B2)
respiratory disease (asthma)-->generally safe
*diabetes-->can mask hypoglycemia*
38
What are the non-selective beta and alpha blockers?
carvedilol and labetalol
*not typically used for stable angina (unless complications exist)*
39
What is the main difference between non-DHP CCBs and beta blockers?
intensity of action
40
What can non-DHP CCBs inhibit?
3A4 (its also a substrate)
41
When should non-DHP CCBs be avoided?
systolic dysfunction
already using a beta blocker
bradycardia or AV block
42
What is the difference between a 1st degree, 2nd degree, and 3rd degree AV block?
1st degree: P-R interval delay
2nd degree: intermittently dropped QRS
3rd degree: P and QRS are independent
43
What is a 2nd or 3rd degree AV block a contraindication for?
beta blockers and non-DHP CCB
*UNLESS A PACEMAKER IS PRESENT*
44
True or false: bradycardia or first degree heart block can occur from non-DHP CCB or BB
true
45
When are DHP CCBs used for stable angina?
can be safely combined with BB if symptoms persist
good alternative as monotherapy for patients with bradycardia or intolerance to BB
46
How can nitrates be used for angina?
prn use (treatment): sprays or tablets
prevention: NTG patch
47
Why are nitrate-free intervals required?
to prevent tolerance
unknown mechanism
48
What is the nitrate-free interval to prevent tolerance from occurring?
10-14 hours every day
49
Describe nitrates based on the following: efficacy, safety, drug interactions, convenience, contraindications (table from first slide deck on IHD)
efficacy:
-primary is to decrease preload through venodilation
-some effect on coronary artery dilation (supply) possible
-PRN NTG can be used BEFORE activities known to cause
angina (take 2-5min before, should last 30min)
-nitrate free interval (10-14hrs/day) required or anti-angina
effects will often be lost within 24hrs
-for immediate (prn) effects, s/l rout bypasses GI absorption
and 1st pass
-NOT to be used to prevent heart attacks
safety:
-headache most common se, tolerance develops within 2 wks
-low bp/orthostatic hypotension possible but uncommon
-patches may cause skin irritation, redness, etc (rotate site
every day)
drug interactions:
-PDE5 inhibitors (24hrs for sildenafil/vardenafil; 48hrs for
tadalafil)
-caution with bp lowering drugs
convenience:
-spray may have to be replaced due to expiry date
contraindications:
-PDE5 concurrently
50
Which drug would you add onto a beta blocker for stable angina for the following scenarios: low bp, high bp, high HR
low bp: nitro
high bp: amlodipine
high HR: increase beta blocker dose
51
Describe ranolazine.
not commonly used, indicated as add on therapy for people inadequately controlled or intolerant to 1st line agents
inhibits the late sodium current
-leads to decreased Ca in cardiac cell and possibly lower
diastolic tone
no impact on bp or hr
cautions: 3A4 inhibitors, QT prolongation, renal dysfunction
52
What are the most common options to treat coronary atherosclerosis?
medical therapy: continue with drugs
revascularization:
-coronary artery bypass grafting (CABG)
-percutaneous coronary intervention (stent)
-fibrinolytic medications (only for acute emergencies such as
MI)
53
Describe coronary artery bypass grafting.
invasive-->requires open heart surgery
take a vein from elsewhere in the body and stick it on the aorta to bypass the blocked area
54
Describe percutaneous coronary intervention.
balloon blown up and then stent placed to keep artery open
most common+effective treatment for stable angina
-increasing supply
-expected to cure angina
55
What is a therapy that must be given for someone with a stent?
dual antiplatelet therapy (DABT)
ASA + ADP inhibitor
56
What types of stent were originally used? What kind of stents do we use now?
bare metal stents (BMS)
drug eluting stents (DES)
-drug coating is usually an immunosuppressant to decrease
inflammatory cytokines and cell proliferation following stent
implantation
57
Longer DAPT has an ____ for ____. Shorter DAPT has a ____ for ____.
longer DAPT has increased risk of bleeding
shorter DAPT has increased risk of events
58
Describe elective PCI if the patient is not at risk of bleeding. (flow chart)
DAPT for 6 months ASA+clopidogrel
high-risk clinical or angiographic feature for thrombotic CV events and not at high risk of bleeding:
-YES: extend DAPT up to 3 years (ASA 81mg OD + clopidogrel
75mg OD)
-NO: SAPT (ASA 81mg OD or clopidogrel 75mg OD)
59
Describe elective PCI if the patient is at high risk of bleeding. (flow chart)
DAPT for 1 month if BMS, or 3 months if DES-->SAPT ASA 81mg OD or clopidogrel 75mg OD
60
True or false: in the setting of stable ischemic heart disease, DAPT is recommended after PCI
true
61
What is all the DAPT evidence based on in the context of ISHD?
clopidogrel + ASA
62
Describe DAPT monitoring.
clinical signs of bleeding:
-bloody stools (bleed that is distal)
-melena (dark stools=ulcer in stomach)
-hematemesis
-bruising
-oozing from injuries
general tolerability:
-GI upset
laboratory testing:
-RBC
-Hb
-platelet count (q6 months)
63
What is presentation of coronary atherosclerosis?
silent (asymptomatic) disease-->most patients
chronic, stable angina
acute coronary syndromes (ACS)
-includes: unstable angina, NSTEMI, STEMI
64
Describe the categorization of ACS.
ACS is further categorized into unstable angina and myocardial infarction
myocardial infarction is categorized into STEMI or NSTEMI
65
What is the average age of first ACS?
late 60's
66
What are the three main assessments used to determine treatment when someone presents to the ER with what they believe to be a heart attack?
the story and the patient (young, old, etc)
12 lead ECG
blood tests for biomarkers of cardiac cell death
67
What is a strong finding in the ER to rule out ACS?
normal ECG
*physicians will investigate other possible causes of symptoms*
68
What does ST segment depression tell us?
strong evidence for coronary ischemia
however, ST depression is often associated with stable angina, further investigations will be needed to determine severity
69
What does ST segment elevation tell us?
a marker of complete coronary obstruction causing cardiac myocyte death
suggests a serious MI requiring urgent revascularization in most cases
if blood flow is not restored quickly, the person is at high risk for major consequences such as heart failure, arrythmias, or even death
70
What are ST segment elevations referred to as?
STEMI (ST elevation MI)
71
What is usually absent from the QRS in a normal ECG?
Q-waves
72
When do Q-waves appear in an ECG?
following (or during) a STEMI
73
What do Q-waves indicate?
extensive damage (transmural) to the heart wall
74
True or false: Q-waves often remain in the ECG for life
true
75
How is a STEMI confirmed?
evidence of cell death is observed
-increased troponins in the blood within hrs of MI and remain
elevated for several days
76
What is the most sensitive and specific biomarker in the context of ACS?
cardiac troponins
-troponins mainly in cardiac muscle cells, not many other cells
-elevated troponins indicate ruptured cardiac cells
77
Aside from MI, what are other possible causes of increased troponins?
tachyarrythmias
hypotension or hypertension
cardiac trauma
acute HF
myocarditis/pericarditis
pulmonary embolism
severe non-cardiac conditions (burns, sepsis, etc)
78
True or false: ST depression is a classic presentation of a major MI
false
ST elevation is classic presentation of a major MI
79
What is an ECG finding considered equivalent to ST elevation?
Left Bundle Branch Block (LBBB)
-can also remain after the MI resolves
-may complicate future diagnostic decisions in ACS
80
What is a Left Bundle Branch Block?
conduction in the left Bundle of His is slow
results in delayed depolarization of the left ventricle
features:
-QRS is delayed (>0.12s)
-broad monomorphic R waves in I and V6 with no Q waves
-broad monomorphic S waves in V2, may have a small r wave
81
What are the tests administered in ER for a STEMI?
ECG
cardiac troponins (3-6 hrs after symptom onset)
natriuretic peptides (B-type or pro-B type)
chest x-ray
risk stratification tools to assess risk
82
What is the standard treatment in the ER for STEMI?
oxygen (if O2 sat <90% or respiratory distress)
ASA +/- ADP inhibitor
S/L NTG (IV NTG should be used if pain continues)
-ask about PDE5 inhibitor use
beta-blocker may be considered but onset slow and dangerous in acute setting if evidence of reduced CO, HF, or bradycardia
IV anticoagulation-recommended for all patients with suspected MI regardless of initial treatment strategy (UFH, enoxaparin, bivalirudin)
83
What are the recommendations for beta-blockers in the acute phase of STEMI?
should be initiated in the first 24 hrs in patients with STEMI who do not have any of the following:
-signs of HF
-evidence of low CO
-increased risk for cardiogenic shock
-other CI (PR interval more than 0.24s, 2nd-3rd degree heart
block, asthma)
84
Why is post-MI risk generally lower today?
due to the frequency of mechanical revascularization and medication use
people experiencing MIs are less likely to have damaged myocardium (or less myocardium is damaged)
85
Why are beta blockers used post-MI?
beta-blockers are highly protective in people who have experienced damage to myocardial cells
more damage=higher SNS=more likely to benefit from BB
less damage=lower SNS=less likely to benefit from BB
*STEMI is associated with high risk of damage, so routine BB is expected*
86
What is the first goal with STEMI?
all patients presenting with STEMI with symptom onset within past 12 hours should receive reperfusion therapy
primary PCI is the preferred method of reperfusion when done in a timely fashion
if PCI cannot be performed within 2hrs after first medical contact, fibrinolytic medications should be administered
87
When are fibrinolytic drugs used in patients with MI?
patients who cannot access a tertiary hospital quickly
88
What are the advantages of reperfusion therapy as quickly as possible after a STEMI?
great potential to:
-restore blood
-decrease the risk for damaged myocardium
-decrease the risk of death
89
What are the components of pre-PCI therapy?
antiplatelets are started prior to PCI procedures:
-protect against platelet activation that occurs during
placement of stents (stent placement can cause endothelial
damage)
-ASA 81-325mg (325mg if not taking ASA currently)
-loading dose of P2Y12 inhibitor: clopidogrel, prasugrel,
ticagrelor
anticoagulants before PCI:
-options: LMWH, UFH, bivalirudin
90
Which patients should not receive prasugrel for pre-PCL therapy?
prior history of stroke or TIA
91
How do ADP receptor antagonists work?
inhibits the ADP/P2Y12 receptor on platelets
-prevents platelet activation
92
Describe clopidogrel.
prodrug-->requires activation in liver by CYP2C19
inhibits ADP receptor
irreversible inhibitor
requirement for activation may be a disadvantage in some patients
93
Describe prasugrel.
prodrug, but less intra-subject variability
ADP receptor antagonist
concern regarding risk of serious bleeding in:
-patients > 75yrs
-patients < 60kg
94
Describe ticagrelor.
not a prodrug
reversible inhibitor of ADP receptor
becoming much more common in post-MI setting
95
How long is DAPT for someone who received PCI after a STEMI?
1 year
-ASA 81mg OD + ticagrelor 90mg BID or prasugrel 10mg OD
preferred over clopidogrel 75mg OD
*then determine bleeding risk at 1 year and follow elective PCI as described in previous card*
96
What are the factors increasing bleeding risk on DAPT?
need for OAC, NSAIDs, or prednisone
age > 75
frailty
anemia with Hb <110
CrCl < 40ml/min
body weight < 60kg
prior stroke/intracranial bleed
bleeding hospitalization within previous year
97
What are the issues pertaining to DAPT?
DAPT increases bleeding risk over monotherapy
optimal duration of DAPT still unclear (current 1 yr target)
if bleeding risk is high, DAPT d/c can be considered
-after 1 month with DES
-after 3 months DES
98
What is a unique ADR with ticagrelor+ASA?
significant dyspnea
99
What are the current conditions that are recommended for beta-blockers post MI?
LVSD/heart failure=absolute indication (not in acute phase)
arrythmia=absolute indication
STEMI=absolute indication
STEMI without residual dysfunction-3 years and re-evaluate
NSTEMI without residual dysfunction-"consider" BB
*the less severe the MI, the less benefit to be realized*
100
True or false: ACEI shown to decrease mortality in patients with recent MI
true
used in virtually ALL people with MI
*ARBs are reasonable option if ACEI not tolerated*
101
What are some strong indications for ACEI?
EF<40%
hypertension
chronic kidney disease
102
What is the time frame for caution of ACEI after MI?
caution in first 24 hrs of MI because of risk of hypotension or renal dysfunction
short acting ACEI (captopril or enalapril) may be used initially in patients with increased risk of ADRs
if significant renal dysfunction, may wish to wait until kidneys are stabilized
103
Describe ACEI based on the following: efficacy, safety, DI, convenience, CI (big table)
efficacy:
-mechanism decreases RAAS
-first line in HTN when: CKD, ACVD, HF
-considered in all high risk patients even without HTN
-protects against CV events and renal diseases
safety:
-general bp related side effects
-renal specific effects: drop in GFR expected after starting ACEI
(up to 25% is safe)
-cough (can be quite common)
-increased K (through RAAS effect)
-angioedema (rare swelling reaction...often around
mouth/lips)
DI:
-anything that increases K
-anything that decreases renal perfusion (NSAIDs, diuretics)
convenience:
-most are once (or twice daily)
-many single pill combinations available
CI:
-teratogenic
-bilateral renal artery stenosis
-history of angioedema
-first line in renal disease but need caution in renal disease
104
What is the role of MRAs post-MI?
may be added to ACEI and BB with EF <40%
associated with decreased mortality
105
When are MRAs not prescribed post-MI even if EF<40%?
significant renal dysfunction (Cr>170)
high K
106
What is normal ejection fraction?
50-75%
*ejection fraction is the % of blood in the left ventricle that is pumped out during contraction*
107
What is the role of CABG in STEMI?
urgent CABG indicated when coronary anatomy not amendable to PCI and ischemia persists
*CABG poses a much higher risk for bleeding during the procedure*
108
How does antiplatelet/anticoagulant guidelines differ in CABG compared to PCI?
ASA should be used before surgery
in non-urgent situations, ADP inhibitors should be dc for at least 5 days before surgery
if urgent, ADP inhibitors should be stopped at least 24hrs before surgery
109
What is the antiplatelet therapy post CABG?
depends on situation
STEMI or NSTEMI-->eligible for DAPT
elective CABG-->ASA only
110
Differ between NSTEMI and unstable angina.
NSTEMI: cell death proven in the context of ACS and ST depression
unstable angina: no cell death proven in context of ACS and ST depression
111
True or false: ST depression always indicates the need for primary PCI
false
112
What are the features favouring primary PCI?
STEMI
refractory angina
hemodynamic/electrical instability
high risk features (diabetes, previous MI, HF, etc)
113
What may a reasonable duration of DAPT for low-risk patients? This is not in the Canadian guidelines yet.
1-3 months
114
What can complicate the use of DAPT due to risk of bleeding?
atrial fibrillation
115
Describe atrial fibrillation.
an arrhythmia of the atrium removing the atrial contraction altogether
clots can form in the left atrium due to pooling of blood
these clots can embolize into the carotid artery and cause ischemia to the brain
anticoagulants are effective for this condition
116
What are guidelines for afib patients and elective PCI without high risk features for thrombotic CV events?
dual therapy (OAC + clopidogrel) 1-12 months post PCI
stable CAD/PAD-->OAC
117
What are the guidelines for afib patients and ACS with PCI or elective PCI with high risk features for thrombotic CV events?
triple therapy (OAC + ASA + clopidogrel) 1 day-1month
dual therapy (OAC + clopidogrel) up to 12 months post PCI
stable CAD/PAD-->OAC
118
What are the guidelines for afib patients and ACS without PCI?
dual therapy (OAC + clopidogrel) 1-12 months post ACS
stable CAD/PAD-->OAC
119
What is the management of unstable angina?
less clear for those who quickly resolve and have few high-risk markers
for ongoing medication management, often can be treated similar to fixed-obstruction angina
-DAPT could be avoided
-BB could be delayed if no ongoing angina
many people will be scheduled for elective PCI at a later date
