Exam 1: Coronary Artery Disease Flashcards
(211 cards)
1
Q
What is angina?
A
Chest pain/ shortness of breath caused when heart muscles receive insufficient oxygen-rich blood
2
Q
What is ischemia?
A
Condition where blood flow and oxygen are reduced to a part of the body
3
Q
What is the number one cause of death in both men and men?
A
Atherosclerotic CAD
(coronary artery disease)
4
Q
How does age impact the incidence of Atherosclerotic CAD?
A
Increases with age
5
Q
How does gender impact the incidence of Atherosclerotic CAD?
A
More common in men than women until menopause
-After menopause the incidence is equal
6
Q
What fraction of deaths in the US are caused by Atherosclerotic CAD each year?
A
1 in every 3 deaths (1/3)
7
Q
What is the main factor contributing to the increase in Atherosclerotic CAD over time?
A
Diet
-has changed over the last centuries and CAD has increased with it
8
Q
What type of disease is Stable angina pectoris considered?
A
Macrovascular disease
9
Q
What type of disease is Variant or Printzmetal’s angina considered?
A
Vasospastic disease
10
Q
What type of disease is Cardiac Syndrome X considered?
A
Microvascular disease
11
Q
What are the 3 types of angina?
A
-Printzmetal’s Variant Angina
-Chronic Stable Angina
-Unstable Angina
12
Q
What is Printzmetal’s Variant Angina?
A
Vasospasm
*Supply ischemia
-There is a spastic coronary artery, the artery becomes closed by a spasm, and this alters the supply of blood to muscle
13
Q
What is Chronic Stable Angina?
A
Fixed Stenosis (fixed narrowing of artery from a plaque)
*Demand Ischemia (only one)
-Fixed threshold
-Blockage resulting in ischemia upon exertion
14
Q
What is Unstable Angina?
A
*Thrombus
*Supply Ischemia
-Atherosclerotic plaque progresses and forms a thrombus in the artery
-The thrombus added to the plaque eventually causes the vessel to fully close which can lead to tissue death (infarction)
15
Q
What 3 factors contribute to oxygen demand ?
A
*Wall tension
(affected by systolic pressure and left ventricular volume)
*Contractility
*Heart Rate
(all can be targeted by drugs)
16
Q
What 3 things lead to Decreased Coronary Blood Flow?
A
-Fixed Stenosis
-Vasospasm
-Thrombus
(these are all related to the 3 types of angina)
17
Q
What 4 things lead to Increased Oxygen Consumption?
A
-Increased Heart Rate
-Increased Contractility
-Increased Afterload
-Increased Preload
18
Q
How would a patient know they have ischemia?
A
If they experience:
-Angina (chest pain)
-Anginal Equivalents (normally due to other diseases they have like heart failure, ex: SOB)
19
Q
How will a decrease in heart contractility affect O2 consumption?
A
O2 consumption will decrease
20
Q
What affect will a decreased heart rate have on O2 consumption and coronary perfusion?
A
O2 consumption will decrease
Coronary perfusion will increase
21
Q
How is preload decreased?
A
Venodilation
22
Q
What effect does decreasing preload have on O2 Consumption and Myocardial Perfusion?
A
O2 consumption decreases
Myocardial perfusion increases
23
Q
How is afterload decreased?
A
Dilation of arteries
24
Q
A decrease in afterload has what affect on O2 consumption?
A
Decrease in O2 consumption
25
What disease is stable angina pectoris usually associated with?
Single to Multivessel ASCAD (atherosclerotic coronary artery disease)
(plaque buildup in the arteries)
26
What percentage of patients experiencing angina have significant coronary artery disease?
85%
27
What percent of atherosclerotic reduction is defined as "significant coronary artery disease"?
*hint: this is also the percent of blockage typically required to develop a thrombus
>70-75%
28
True or False: 50-70% blockage in a vessel can cause ischemia
FALSE
>70-75% of blockage in a vessel is required to cause ischemia
*this is typically caused by plaque buildup
29
What is myocardial ischemia?
An imbalance between myocardial oxygen supply and demand
-Usually effort induced!!! when there is a decrease in oxygen supply
-Typically caused by atherosclerotic plaque accumulation
30
What are the effects of myocardial ischemia?
Disturbances in myocardial function without causing myocardial necrosis
31
What is angina?
-The resulting symptoms from ischemia
(chest discomfort)
32
What is the relationship between ischemia and angina?
Ischemia is what happens
Angina is the outward symptom that the patient describes
33
What is the difference between stable and unstable angina?
Stable: occurs predictably with physical activity or emotional stress. Lasts a short time and is typically helped by medication
Unstable: Occurs unpredictably, even at rest or with minimal exertion. It worsens in frequency and severity and is a medical emergency. patient should seek medical attention
34
What is an important thing to remember about stable angina regarding symptom characteristics?
Angina is considered "stable" when characteristics of an anginal episode (quality, frequency, severity, duration, time of day, etc) HAVE NOT CHANGED RECENTLY
(typically over the course of a few months)
35
True or False: Stable angina does not cause myocardial necrosis
TRUE
36
What is the clinical presentation of stable angina?
PQRST
P: precipitating factors: exertion
P: palliative measures: rest and/or sublingual nitroglycerin
Q: quality and quantity of the pain: squeezing, heaviness, tightening
R: region and radiation: substernal
S: severity of the pain: subjective, >5 out of 10 typically
T: timing and temporal pattern: lasts <20min, usually relieved in 5-10min
37
How long does stable angina normally last and how does this differ than MI?
Stable angina: usually relieved in 5-10 minutes
MI: Lasts LONGER than 20 minutes
38
What are some precipitating factors of stable angina?
-Exercise
-Effort involving use of arms above the head
-Weather (cold, warm and humid)
-Walking against wind
-Large meal
-Emotions with exercise
-Fright, anger
-Coitus
*Smoking
39
Where does the pain associated with angina typically radiate to?
-Left arm and shoulder
-Jaw
-Right arm (occasionally but less common)
40
What qualities are typically associated with angina?
-Pressure/heavy weight on chest
-SOB with feelings of constriction in the larynx or upper trachea
-Burning, tightness, crushing or visceral quality
-Gradual increase in intensity followed by gradual fading away
-Anginal equivalents present
41
What is one of the most common causes of hospitalization for patients with CAD?
Snow shoveling
42
Why are women and patients with diabetes often less likely to be properly diagnosed with CAD?
-They tend to have more silent episodes and report pain in different ways
-Providers are often biased toward diagnosing men and not women since men experience it earlier
43
What ECG finding is typically shown with angina?
ST-segment depression during event
-The ST-segment occurs directly before the beginning of the T wave
-Normally the ST-segment is flat, but with angina there is a curve downward
44
How do we diagnose CCD?
-History and physical examination
(determine risk factors)
-Electrocardiogram
(look for ST segment depression [ischemia] or elevation [variant angina])
45
How do we diagnose CHD?
-Treadmill or bicycle exercise testing
-Endpoints (duration, workload achieved, ECG changes, BP and HR responses, Symptoms)
-Double product (HR and Systolic BP used as an index of MVO2)
-Assessment of drug therapy
*Beta-blockers and CCBs may complicate interpretation by decreasing HR*
46
How may beta-blockers and CCBs complicate diagnostic procedures for CHD testing?
They make interpretation of the results of exercise testing and heart rate evaluation difficult since they lower heart rate
47
What are the diagnostic procedures for CHD?
-Cardiac imaging
---Stress testing
---Nuclear imaging
---Electron beam computerized
tomography (EBCT)
-Echocardiography
-Cardiac catheterization and coronary angiography
48
How is stress testing conducted?
-Patient is given dobutamine to increase their heart rate
-This is done when a patient cannot undergo exercise testing
49
How is EBCT (electron beam computerized tomography) conducted?
Non-invasive CT scan that allows you to quantify calcification (via a calcium score) that could be associated with plaque formation
-higher score=higher chance that plaque is more significant
50
How is coronary catheterization and coronary angiography conducted?
Catheterization: A catheter is introduced into the heart through the groin or wrist. Used to clear clogged arteries
Coronary angiography: A picture/visualization of the vessel. Is the only way to definitively assess a patient's coronary anatomy
**very invasive and expensive, most commonly performed medical procedure in US
51
What is the first desired outcome for treatment of chronic coronary disease?
PREVENT DEATH
-Risk factor modification
-Prevent future events/death
52
What is the second desired outcome for treatment of chronic coronary disease?
ALLEVIATE OR PREVENT SYMPTOMS
-Manage anginal episodes
-Alleviate acute symptoms
-Prevent recurrent symptoms of ischemia
53
What is the MOA of aspirin?
Acetylates and irreversibly inactivates platelet COX-1
Has antiplatelet activity (blocks TXA2 synthesis)
--interferes with platelet aggregation
-prolongs bleeding time
-blocks arterial thrombi formation
***Aspirin DOES NOT affect thrombi that are already formed, only blocks creation of new ones
54
True or False: Aspirin will break up thrombi that are already formed
FALSE
-only blocks the formation of thrombi
-does not affect already made thrombi
-must be used chronically
55
What is the function of TXA2?
Formed by COX-1 to recruit and activate platelets
(COX-1 is blocked by aspirin which indirectly blocks TXA2)
56
Why do we only use low dose (81mg) aspirin and not high dose aspirin for CAD?
Low dose aspirin only inhibits COX-1 whereas high doe aspirin will inhibit both COX-1 and COX-2
COX-1 increases platelet aggregation and vasoconstriction which we want inhibited by aspirin
COX-2 inhibits platelet aggregation and induces vasodilation which we do not want inhibited!! Inhibiting this increases the risk of a thrombosis
57
What molecule does COX-1 synthesize?
Thromboxan A2 (TXA2)
-this promotes platelet aggregation and vasoconstriction)
-pro-thrombotic
58
What molecule does COX-2 synthesize?
Prostacyclin PGI2
-this inhibits platelet aggregation and increases vasodilation
-anti-thrombotic
59
What drugs are selective COX-2 inhibitors?
"coxibs"
60
What is the loading dose of aspirin? (soluble or EC)
162-325mg
61
What are the P2Y12 Inhibitor Platelet Drugs?
Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)
Cangrelor (Kengreal)
62
What is the MOA of the P2Y12 inhibitors?
Selectively inhibit adenosine diphosphate (ADP) induced platelet aggregation
*no direct effect on TXA2
63
What is the loading and regular dose of Clopidogrel (Plavix)?
L: 300-600mg *
R: 75 mg daily
64
What is the loading and regular dose of Prasugrel (Effient)?
L: 60mg *
R: 10 mg daily
65
What is the loading and regular dose of Ticagrelor (Brilinta)?
L: 180mg*
R: 90 mg BID
66
What is the dosing of Cangrelor (Kengreal)?
IV only
67
What are the adverse effects of aspirin?
-GI bleeding
-Hematologic: bleeding (intracranial and extracranial)
-Hypersensitivity
-Major bleeding (2-3% in first year)
68
What is the purpose of enteric coated aspirins?
They do not dissolve in the stomach and only dissolve in the small intestine (alkaline environment)
-Reduces GI side effects and GI bleeding
69
If a patient thinks they are having a heart attack, how should we instruct them to take an aspirin?
-Tell the patient to take a low dose aspirin and CHEW it
-Otherwise the aspirin will take 4 hours to pass through the stomach and dissolve which is too much time
70
What is the recommended dose of aspirin for cardiovascular prevention?
81 mg
71
True or False: Antiplatelet medications can be used together
TRUE
-because they have different mechanisms of action in the aggregation cascade
72
Which two P2Y12 inhibitors are members of the Thienopyridine class?
Clopidogrel (Plavix)
Prasugrel (Effient)
73
Which two P2Y12 Inhibitors need to be activated by CYP (prodrugs)?
Clopidogrel (Plavix)
Prasugrel (Effient)
74
What P2Y12 Inhibitor does NOT need to be activated by CYP/ is direct acting?
Ticagrelor (Brilinta)
75
What is the typical half-lives of the P2Y12 Inhibitors?
5 days or 7 days
**keep this in mind before surgery
76
True or False: P2Y12 Inhibitors increase the risk of bleeding more significantly than aspirin
True
77
What are the adverse effects of the P2Y12 inhibitors?
Clopidogrel: Bleeding, Diarrhea, rash
Prasugrel: Bleeding, Diarrhea, Rash
Ticagrelor: Bleeding, Bradycardia, Heart Block, Dyspnea (SOB)
78
When added to aspirin, by how much do the P2Y12 inhibitors increase the risk of major bleeding?
Clopidogrel: 1% increase
Prasugrel: 0.6% increase
Ticagrelor: 1% increase
79
All patients with a history of CCD should receive which medication?
Aspirin 75-100 mg/day indefinitely
(prefer 81mg)
80
If a patient has an absolute contraindication to aspirin or a significant intolerance, what medication should they be started on instead?
Clopidogrel 75 mg/day indefinitely
81
What medication is considered SAPT (Single-Antiplatelet Therapy)?
Aspirin 75-100mg/day
OR
Clopidogrel 75 mg/day
(when aspirin is contraindicated)
82
What two medications are considered DAPT (Dual-Antiplatelet Therapy)?
Aspirin 81mg/day
+
P2Y12 Inhibitor (ex: Clopidogrel 75 mg/day)
*certain high risk patients receive both
83
What treatment should patients with No History of Stent Implantation receive?
(secondary prevention)
SAPT (Single-Antiplatelet Therapy)
High-risk patients: DAPT (Dual-Antiplatelet Therapy)
84
How is a stent placed?
-The stent (metal tubing) is put over an uninflated balloon and inserted into an artery
-The balloon is expanded at the site
-Cells surround the stent (endothelialize) and leave the vessel open
-Need to use antiplatelet therapy after the fact
85
What are the 2 types of stents?
Bare Metal Stents (rarely used)
Drug Eluting Stents
--3 generations
--2nd and 3rd mostly used
--Contain antiproliferative drugs to
prevent cell proliferation at site
--"limus" drugs
86
Before an elective PCI (Percutaneous Coronary intervention) + Drug Eluting Stent, what medications are a patient given?
Aspirin loading dose (325mg)
and
P2Y12 Inhibitor loading dose
87
After an elective PCI (percutaneous coronary intervention) + Drug Eluting Stent, if a patient has a LOW BLEEDING RISK, what medications are they given and for how long?
DAPT: Minimum 6 months
SAPT: Indefinitely
88
After an elective PCA (percutaneous coronary intervention) + Drug Eluting Stent, if a patient has a HIGH BLEEDING RISK/OVERT BLEEDING, what medications are they given and for how long?
DAPT: 1-3 months
SAPT: P2Y12 inhibitor until 12 months
SAPT: Aspirin indefinitely
89
Which P2Y12 Inhibitor is preferred for use with Elective PCI + Drug Eluting Stent placement?
NO DISTINGUISHMENT BETWEEN CHOICES, ANY ARE CORRECT
*Prefer to avoid Ticagrelor 90 mg BID because of dosing
Prefer: Clopidogrel 75mg daily or Prasugrel 10 mg daily
90
When a patient undergoes CABG (coronary artery bypass graft), what medication regimen should they be put on?
DAPT for 12 MONTHS!
(aspirin 81 mg/day + clopidogrel 70 mg/day)
SAPT indefinitely
(aspirin 81 mg/day for life)
91
If a patient is on both ticagrelor (Brilinta) and aspirin, how does this affect the dosing of aspirin used?
***KNOW THIS***
The dose of aspirin must be BELOW 100mg
92
When a patient is taking both ticagrelor (Brilinta) and aspirin, the risk of which disease states increase?
-Cerebral Hemorrhage
-Stroke
**this is why the aspirin dose must be below 100mg!!!
93
What are the benefits provided by ACE inhibitors and ARBs for CCD?
-Stabilize plaque formation
-Improve endothelial function
-Inhibit VSM (vascular smooth muscle) cell growth
-Decrease macrophage migration
-Anti-oxidant properties??
****DO NOT PROVIDE SYMPTOM RELIEF****
94
Why are ACEi and ARBs used for CCD?
They reduce the progression of the disease and decrease the likelihood of having cardiovascular events
**They do not reduce symptoms**
95
True or False: ACEi and ARBs improve symptomatic ischemia
FALSE
-they do not reduce angina or other disease symptoms
96
True or False: All patients with CCD should receive an ACEi or an ARB
TRUE
-these drugs should be considered in all patients with CCD
-may have a lower benefit in lower risk patients though
97
What patient populations have the greatest benefit from receiving an ACEi or an ARB?
LVEF <40% (left ventricular ejection fraction)
HTN
DM
CKD
98
Who should receive ARBs instead of ACEi's?
-Patients intolerant to ACEi
(cough or adverse effects)
99
True or False: ACEi and ARBs can be used together to treat CCD
FALSE
-never use these drugs together
100
What is colchicine normally used to treat?
Gout
101
What is the mechanism of action of colchicine/ how does it work?
Reduces inflammation
by: reducing IL-1B and IL-18
102
What is the role of colchicine in treating CCD, and which patients should this medication be considered in?
This medication is reserved for high risk patients with elevated levels of hsCRP (>2)
(hsCRP is an inflammatory marker)
*Note: atherosclerosis and CV disease are inflammatory diseases
103
What level of the inflammatory marker hsCRP is considered "elevated"?
>2
**consider initiating colchicine when patients are at this level and have high risk CCD
104
When is colchicine contraindicated?
Severe renal disease
Severe hepatic disease
105
What is the role of statins in CCD?
All patients should be on a high intensity statin!!!
(if high intensity is not tolerated, moderate intensity statins can be used)
106
Which patients have beta blockers been shown to reduce mortality in?
Post-ACS
Heart failure (with reduced ejection fraction) (HFrEF)
***data has not shown reduced mortality in any other patient populations regarding CCD
107
True or False: If a patient experiences angina from CCD while exercising, we want them to stop exercising
FALSE, we want to treat the symptom so that the patient can continue exercising
(still may be difficult with heart rate lowering effects of beta blockers)
108
What 3 conditions lead to decreased coronary blood flow?
-Fixed stenosis
-Vasospasm
-Thrombus
109
What 4 states contribute to increased oxygen consumption?
Increased Heart Rate
Increased Contractility
Increased Afterload
Increased Preload
110
What two things contribute to ischemia?
-Decreased coronary blood flow
-Increased oxygen consumption
111
What drugs decrease heart rate?
Beta Blockers
Verapamil + Diltiazem
112
What drugs increase heart rate?
Nitrates
*Nifedipine (DHP CCB)
113
What drugs decrease myocardial contractility?
Beta blockers
Nifedipine (DHP CCB) (or no effect)
Verapamil
Diltiazem (or no effect)
114
What is another term for afterload?
Systolic blood pressure
115
What is another term for preload?
Left-ventricular end-diastolic volume
(LV volume)
116
What drugs decrease preload the most?
Nitrates
117
What drugs INCREASE preload?
Beta-blockers
118
What drug classes are used to prevent ACUTE ischemia and angina symptoms?
Nitrates
(nitroglycerin)
119
What is the mechanism of action of nitrates?
Nitric oxide donors/releasers
-Activate guanylate cyclase
120
What action of nitrates decreases preload?
Venodilation
121
What are the 3 activities of nitrates?
-Marked venodilation (decreases preload)
-Less arteriole dilation (coronary and peripheral)
-Inhibition of platelet aggregation (minor)
122
What molecule leads to the relaxation caused by nitrates?
Increase in cGMP
-impacts the myosin chain contraction
*NOTE: PDE5i do this as well
123
Do nitrates affect the natural history of CAD?
NO
*do not keep people alive, only treat symptoms!!!!!
124
What is the dosing for SL Nitroglycerine Tablets?
0.3-0.6 mg
125
What is the dosing interval/frequency of SL Nitroglycerin Tablets and Spray?
PRN, repeat dose 1-3 times every 5 minutes
126
What is the dosing for SL Nitroglycerin Spray?
0.4 mg/spray
127
If patient experiences lasting chest pain and is instructed to chew an aspirin, what dose should they chew?
162-325 mg
128
If patient is experiencing chest pain, when should they call 911?
If the pain is unimproved or worsening after 5 minutes
*this goes for both patients prescribed NTG and not
129
What are 6 important counseling points for nitroglycerin tablets?
-Keep tablets in original container
-Do not swallow, place under tongue
-Do not store in bathroom or humid area
-Sit down before taking
-Keep the tablets on you at all times
-Take up to 3 doses 5 mins apart
130
What are 2 important unique counseling points for nitroglycerin spray?
-Spray under tongue, do not inhale
-DO NOT SHAKE
131
What are the adverse effects of nitrates?
-Headache (throbbing or pulsing)
-Hypotension
-Dizziness/ lightheadedness
-Facial flushing!
**Reflex tachycardia**
132
What drug class causes reflex tachycardia?
Nitrates
-BP reduced and baroreceptors sense it. catecholamines get released and BP goes up
**want to use lowest dose possible
133
What drug class should be used with extreme caution with PDE5 inhibitors?
Nitrates
*risk of hypotension and death
*vasodilatory effects of nitrates are substantially enhanced when used in combo
134
If a patient takes Avanafil (PDE5i), how long do they have to wait before taking a nitrate?
12 hours
135
If a patient takes Sildenafil or Vardenafil, how long do they have to wait before taking a nitrate?
24 hours
136
If a patient takes Tadalafil, how long do they have to wait before taking a nitrate?
48 hours
137
What patients should receive sublingual nitroglycerin?
ALL patients with CCD
(either spray or tablet)
138
True or False: nitroglycerin can be useful for the prevention of angina by taking it right before a patient exerts themself
True
139
Which beta receptor is more present in heart cells (B1 or B2)?
B1
(80% B1 and 20% B2)
140
What drug classes are used to prevent RECURRENT/CHRONIC ischemia and angina symptoms?
-Beta blockers
-Calcium channel blockers
-Nitrates
141
How does the distribution of beta cells change in heart failure?
B1: 60%
B2: 40%
*B2 becomes more important
142
What affect do beta blockers have in cardiac myocytes?
Block B1 (and possibly B2) receptors which prevents release of cAMP
This decreases heart rate, contractility, and conduction velocity
143
What is chronotropy?
Changes made to heart rate
144
What is inotropy?
A change in contractility
145
What is dromotropy?
A change in conduction velocity/speed
146
What affect do beta blockers have in vascular smooth muscle cells?
B2 receptors in smooth muscles (vascular, GI, uterine) cause relaxation
-beta blockers block this
147
What is the mechanism of action of beta blockers?
Competitive, reversible inhibitors of beta-adrenergic stimulation by catecholamines
148
In what 3 ways do beta blockers decrease myocardial oxygen demand?
Reduce HR
Reduce myocardial contractility
Reduce arterial BP (afterload)
149
What negative effect do beta blockers have on myocardial oxygen demand?
They reduce heart rate which increases diastolic filling time
*ultimately this INCREASES preload
150
What affects do beta blockers have on preload and afterload?
Preload: increase it (bad)
After load: decrease it
151
Beta blockers are associated with a reduction of what two (bad) events in the heart?
Ventricular arrhythmias
Remodeling
152
What two prototype beta blockers are cardio selective for B1?
Atenolol
Metoprolol
153
What two prototype beta blockers are nonselective?
Propranolol
Carvedilol
154
What two prototype beta blockers have intrinsic sympathomimetic activity?
Pindolol
Acebutolol
155
What contraindications are associated with intrinsic sympathomimetic activity beta blockers?
Contraindicated in post-MI patients
*May increase heart rate at rest
*May cause angina
DO NOT USE THESE FOR ANGINA EITHER
(pindolol, acebutolol)
156
Which non-selective beta blocker has both alpha and beta blocking effects?
Carvedilol
157
Which two prototype beta blockers are lipid soluble and how are they removed from the body?
Propranolol
Carvedilol
(*removed by the kidneys*)
158
Which two prototype beta blockers are water soluble?
Atenolol
Bisoprolol
(*removed unchanged*)
159
What cardiac adverse effects do beta blockers have?
-Sinus bradycardia
(<60)
-Sinus arrest
(no sinus pulse, all comes from below sinus node)
-AV block
(no beats conducted from atrium to ventricle)
-Reduced LVEF
160
What general side effects do beta blockers have (not cardiac related)?
-*Bronchoconstriction*
-Fatigue
-Depression
-Nightmares
-Sexual dysfunction
-Exercise intolerance
161
Why should patients be tapered off of beta blockers?
Beta blocker withdrawal syndrome
-androgen hypersensitivity due to increased receptors being made while on beta blockers to try and overcome the beta blocker
-When the beta blocker is removed, all of these receptors are activated
-causes a rise in BP and HR
162
How should beta blocker dosing be handled?
Start at lowest dose
-titrate to symptom reduction
163
What are the goal heart rates for beta blockers?
Rest: 50-60 bpm
Exercise: <100 bpm
164
What is the MOA of Calcium Chanel Blockers?
Block L-type calcium channels
*this blocks the contraction effects of calcium
165
What effects do calcium channel blockers have in cardiac cells?
-Decrease influx of Ca
-Decrease chronotropy and inotropy
166
What effects do calcium channel blockers have in vascular cells?
Vasodilation (relaxation)
167
Which group of CCB is a more potent vasodilator?
DHPs
*non-DHPs act more like beta blockers, still vasodilate but less
168
What two CCBs do we never use in CCD?
And why?
Nifedipine (Procardia, Adalat)
Nicardipine (Cardene)
*cause substantial reflex tachycardia
169
What are the side effects of DHPs?
-Hypotension
-Flushing
-Headache
-Dizziness
*Peripheral edema (due to vasodilation)
*Reduced myocardial contractility
*Reflex adrenergic activation
170
If a patient develops peripheral edema while on a DHP CCB what should be done?
Decrease the dose
-this is a dose-related side effect
-some patients may not tolerate any dose
171
What are the side effects of Non-DHPs?
*Reduce myocardial contractility (V>D)
*Bradycardia and AV block (V>D)
-Hypotension
-Flushing
-Headache
-Dizziness
**Constipation** (V>D)
172
Which two drug classes have constipation as a side effect?
Non-DHP CCB
Ranolazine
*note: may not be great in elderly patients
173
How should CCB dosing be initiated?
-Initiate at lowest dose
-Titrate to symptom relief
174
In what patients can calcium channel blockers have an added benefit?
-Patients with increased BP
175
What causes the biggest challenge in a patient taking a nitrate?
Nitrate tolerance
*this can happen within a single day, patients need to be given increasingly higher doses
*why nitrate-free periods are important
176
To prevent nitrate tolerance, how long should a nitrate free period last each day?
10-12 hours
177
For a NTG patch, how long should it be on and how long should it be off?
-What times should it be put on and taken off?
On for 12-14 hrs, off for 10-12 hrs
On: 7 am
Off: 7-9 pm
178
For ISDN tablets dosed TID, what times should they be taken?
8am, 12pm, 4pm
179
For ISMN tablets dosed BID, what times should they be taken?
8am, 3pm
180
For ISMN SR tablets taken once daily, what time should they be taken?
8am
*so that drug is out of system by 8pm
181
Why are nitrates typically only used as combination therapy?
Because patients do not get any protection at night with nitrates alone due to the nitrate free period
182
What are the important counseling points for nitroglycerin patches?
-Apply between elbows and knees
-Apply to clean, dry, hairless, unmarked area
-Choose different area each day
-You CAN shower with the patch
-Do not cut
-Wash hands before and after
183
What are 2 additional important counseling points for application of nitroglycerin ointment?
-Do not rub or massage in ointment
-Do not cover the area with any kind of wrap
184
How can vasodilators cause tachycardia?
Reduce arterial pressure which leads to increased heart rate
-ultimately increases cardiac output and increases demand
185
Which drugs can cause vasodilator induced tachycardia?
-Nitrates
-Dihydropyridines
186
What is the mechanism of action of Ranolazine (Ranexa)
Inhibits late inward sodium channels in ischemic myocytes (this leads to a decreased Ca influx)
-interrupts the cycle leading to ischemia
187
What is the titration for ranolazine dosing?
Start at 500mg BID and increase to 1000mg BID over 1-2weeks
188
What is Ranolazine (Ranexa) indicated for in the US?
Treatment of chronic angina
189
When do we use Ranolazine (Ranexa)?
-As an add-on to CCBs, BBs, or Nitrates
*Monotherapy only when patients have a BP/HR too low with first-line options
*Typically only add on when BP or HR is low but patient is uncontrolled
190
What drugs should Ranolazine not be used with?
3A inhibitors:
-Ketoconazole + Itraconazole
-Clarithromycin
3A Inducers:
-Carbamazepine
-Rifampin
-St John's Wort
191
With what drugs should the dosing of Rifampin be limited to 500 mg BID?
*Diltiazem + Verapamil
-Erythromycin
-Fluconazole
192
What are the adverse effects of Ranolazine (Ranexa)?
*Constipation
-Nausea
-Dizziness
-Headache
**Increases QT-Interval**
193
What is the first drug class we choose for treatment of stable angina?
Beta Blockers
194
What drug classes do not have any effect on the natural progression of CCD?
-BBs
-CCBs
-Nitrates
-Ranolazine
195
When should beta blockers be avoided?
-Prinzmetal's Angina (vasospastic)
-Conduction Disturbances (SA node block, AV node block)
196
What are the contraindications for beta blockers?
-Bradycardia (HR<50)
-High degree AV block/sick sinus syndrome (with no pacemaker)
197
When are non-DHPs preferred?
*If a beta blocker cannot be used due to contraindications or side effects
198
When are Non-DHPs and DHPs contraindicated?
Non-DHP:
-HFrEF
-Bradycardia (HR < 50)
-AV node block or sick sinus syndrome (with no pacemaker)
DHP:
-HFrEF (except amlodipine and felodipine)
199
Which two drug classes should never be combined?
Beta blockers
+
Non-DHP CCB
200
When using NSAIDs in CV disease, what considerations should be made?
-Only use temporarily!
-Lowest dose for shortest time period
*Check for Benefit or AEs within one week of initiation
201
What two NSAIDs should be chosen first to be used with CV disease?
Ibuprofen
Naproxen
*with gastroprotection
202
What other NSAID can be used and at what dose to have similar cardiovascular risk as Ibuprofen and Naproxen?
Celecoxib doses up to 200mg per day
*Note: this medication seems to have poorer analgesic effects
*Note: Increasing dose above 200mg increases CV risk
203
What NSAID should be absolutely avoided in CV disease?
Diclofenac
*highest risk of aspirin interaction
204
If a patient is taking both Aspirin and an NSAID, how much time should they space the doses out by?
Take aspirin AT LEAST 2 HOURS BEFORE the NSAID
*this gives aspirin the chance to acetylate the COX so the NSAID has less of a chance to compete with it
205
What CV drug do NSAIDs interact with?
Aspirin
(minimize its effects)
206
What are the 3 names for ischemia associated with vasospasm?
-Prinzmetal's angina
-Vasospastic angina
-Variant angina
207
What are the symptoms of vasospastic angina?
-Ischemia/angina occurs at rest
(not brought on by exercise or emotional stress)
-ECG ST-segment elevation
-Ischemic episodes occur mostly in the early morning hours
-Does not have to be associated with atherosclerosis (plaque buildup)
208
What affect does vasospastic angina have on an ECG?
ECG ST-segment elevation
209
What time of day does vasospastic angina typically occur?
Early morning hours
210
What is the first-line treatment for vasospastic angina?
BP > or =130/80: CCB
*most patients
BP <130/80: LA Nitrate
211
What drug class should be avoided in vasospastic angina?
Beta Blockers
