Chronic CHD and Chronic Stable Angina Flashcards
What is coronary heart disease (CHD)?
General term that describes various phases a patient may cycle in-between for several decades:
-Asymptomatic disease
-Stable angina
-Unstable angina
-NSTEMI and STEMI
Which phases are considered “ACS”?
Unstable angina, NSTEMI and STEMI
What is chronic stable angina?
A patient w/ predictable angina symptoms during exertion
Is atherosclerosis an inflammatory disease?
Yes
What is atherosclerosis?
Over time, plaque builds up on the endothelial lining of a BV, triggering an inflammatory response leading to enlargement and increased endothelial injury over time
???? Atherosclerosis pics
What are chronic stable angina (CSA) symptoms associated with?
Myocardial ischemia, supply and demand mismatch for oxygen
Are chronic stable angina (CSA) symptoms present at rest?
No, predictable EXERTIONAL angina
What is the O2 mismatch in CSA?
O2 delivery does not meet aerobic O2 demands
Presence of occlusion in CSA may be due to?
Lipid-rich plaques, thrombus, vasospasm
Myocardial ischemia in CSA will lead to…?
Buildup of metabolites (lactate, AMP), metabolic changes, remodeling
What can meds for CSA prevent?
Hypertrophy, remodeling and progression from CSA to ACS by increasing O2 delivery
Oxygen consumption is mainly driven by what factors?
Heart rate, ventricular contractility (force of contraction), afterload (systolic wall tension, vascular resistance)
What does the body release to compensate for O2 demand/delivery mismatch?
Releases NE (increases ventricular contraction, HR, & afterload)
What medication can be used to counteract the increased contraction, HR, and afterload in response to body releasing NE?
Beta Blockers
When does blood fill the coronary arteries?
During diastole
What can be used to increase coronary blood flow?
Nitroglycerin (vasodilation), and BB or CCB (dec. HR)
What causes myocardial ischemia?
Inadequate oxygen supply plus increased oxygen demand that results in predictive anginal pain
Common manifestations of CSA?
Anginal pain or discomfort on presentation, ST-segment changes on ECG, reduced LV function on echo
Medical management of CSA?
Medical therapy and lifestyle modification
Diet/lifestyle changes for CSA?
-DASH Mediterranean diet
-Fasting: can help w/ fluctuating blood sugar in DM
*Physical activity, goal setting
Meds for control of HTN in CSA?
ACEi/ARBs, BBs, BP control
Meds for dyslipidemia in CSA?
Diet, activity, statins
Other medications for CSA?
Antiplatelet therapy, diabetes management, tx to target doses/parameters
What is important to check in CSA follow up?
A1C & LDL in 3 months
The “A” of CSA management?
Aspirin, ACEi’s, anti-anginals
The “B” of CSA management?
Beta blockers, BP control (140/90 mmHg or lower)
The “C” of CSA management?
Cholesterol and cigarettes
*High intensity statins (atorvastatin and rosuvastatin)
The “D” of CSA management?
Diet, diabetes management, depression
The “E” of CSA management?
Exercise: calorie targets, physical activity
(800 kcal/wk vs. 2400 kcal/wk vs. 3000 kcal/wk)
Relative risk reduction of Aspirin in post-MI?
25%
Relative risk reduction of B-Blockers in post-MI?
25%
Relative risk reduction of ACEi’s in post-MI?
25%
Relative risk reduction of lipid lowering agents in post-MI?
30%
5 year CV-event recurrence risk percentage if no medical therapy post-MI?
20%
5 year CV-event recurrence risk percentage if on only aspirin post-MI?
15%
5 year CV-event recurrence risk percentage if on aspirin + BB post-MI?
11.3%
5 year CV-event recurrence risk percentage if on Aspirin + BB + ACEi post-MI?
8.4%
5 year of CV-event recurrence risk percentage if on Aspirin + BB + ACEi + lipid lowering agent post-MI?
5.9%
Cumulative risk reduction if ASA + BB + ACEi + Lipid lowering are used?
~70%
Number needed to treat (NNT) to prevent 1 major CV event in 5 years?
7 (7 people treated will result in reduction of 1 bad outcome, measures effectiveness of therapy post-MI)
What is the role of platelets in atherothrombosis?
- Activation by collagen/thrombin after vascular injury
- Adhesion (to wall)
- Aggregation (platelets stick together, build)
What is the preferred anti-anginal agent (when tolerated)?
Beta blockers (Metoprolol, Bisoprolol, Carvedilol, Atenolol)
*best data for reducing CV events
Which beta-blocker acts on both B1 and a1 receptors?
Carvedilol
What can be used as an alternative for Beta blockers?
Calcium channel blockers (CCBs)
Some CCBs can be used with BBs for what purpose?
Vasodilation
Which CCBs can be used with BBs?
Dihydropyridines: Amlodipine, Felodipine, Nifedipine
Which CCBs are not commonly used with BB due to the risk of bradycardia?
Non-dihydropyridines: Verapamil, Diltiazem
Which nitrate is used as an anti-anginal?
Nitroglycerin (in short and longer acting forms)
Does nitroglycerin have any outcome effect, or just symptom relief?
Only for symptoms, no outcome data
What form of nitroglycerin is short-acting?
Sublingual
What form of nitroglycerin is long-acting?
Oral (can be controlled or immediate release)
Outcome benefits of beta blocker treatment are derived from what?
Lowering myocardial oxygen demand
Effects of BBs in CSA?
Reduced ischemic time, decreased HR, decreased BP/workload, decreased contractility
How does slower HR (from BBs) improve outcome of CSA?
Improves venous perfusion and ventricular filling
What reflects BBs use (before vs. after differences)?
EKGs
Caution using BBs in patients with what condition?
Pulmonary disease
What can sudden d/c of BBs lead to?
Rebound tachycardia (must taper BBs if d/c)
What can BBs mask in patients with DM?
Can mask signs of hypoglycemia (ex. tachycardia)
What effect can BBs have on EKG?
Slowed PR-interval, ventricular rate
What effect do BBs have on the renal system?
Reduction in renin output, reduces RAAS activity
What other condition can BBs be useful for?
Open-angle glaucoma (enhanced outflow and drainage)
What kind of selectivity is important to consider when choosing BBs for therapy?
Beta-1 vs. Beta-2 selectivity
*All BB’s have dose-related B-1/B-2 activity
What can selective Beta-1 drugs do at higher doses?
They can also block B-2 receptors at higher doses
Bronchioles and peripheral vascular tissue uses what activity for some vasodilation?
Beta-2 activity
Blocking Beta-2 receptors may result in what?
Unopposed alpha constriction
Ideally, what treatment w/ BBs will avoid excessive alpha constriction/increased afterload?
Minimize use of nonselective BBs with some Beta-2 blockade
Non-selective BBs?
Labetalol, Carvedilol, Nadolol, Sotalol, Timolol
Selective BBs?
Metoprolol, Atenolol, Bisoprolol
Many patients with pulmonary disease can tolerate BBs at what doses?
Lower doses
Typically, CCBs are given in what setting for CSA & at what dose?
The ER, and typically dosed once daily
Blocking of calcium channels inhibits what?
Inhibits Ca2+ mediated depolarization, facilitates muscle relaxation
What kind of CCBs are Verapamil and Diltiazem?
Non-dihydropyridines
Verapamil and Diltiazem can be used in place of what medications?
Beta-blockers
What benefits do Verapamil and Diltiazem provide?
Rate control, Anti-anginal effects, BP lowering
How do Verapamil and Diltiazem lower BP?
Depression of AV node conduction, coronary & arterial vessel dilation
What kind of vasodilation activity do dihydropyridine CCB’s have?
Selective vasodilation with minimal AV node activity
Calcium channel blockers have what similar effect between classes?
Similar BP reduction
Calcium channel blockers may have differences in what effects?
Hemodynamics and tolerability may be different among classes
Which dosage forms of CCB’s are once daily?
XR, ER, XL are once daily (be mindful of dosage form!)
In HFrEF, which medications should be avoided?
Non-dihydropyridine Calcium channel blockers
Which meds can be used in HFrEF?
Can use BB, ACEi, diuretics
What do Diltiazem and Verapamil reduce?
Myocardial O2 demand, HR, contractility, peripheral vascular resistance, ischemic time, BP, workload
Do EKGs reflect CCB use (before vs. after)?
Yes
Which has better effect on cardiac conduction/output: Verapamil or Diltiazem?
Verapamil
Which dosage forms of Verapamil & Diltiazem give the best 24 hour HR and BP control?
Long acting dosage forms
Which CCBs are dihydropyridines?
Nifedipine, Amlodipine, Felodipine
Which dihydropyridine gives the best 24 hour HR and BP control?
Long acting drugs (i.e. Amplodipine)
Which dihydropyridine is short acting and can be associated with rebound sympathetic activity, rebound HTN, & tachycardia?
Nifedipine
When can Nifedipine use be dangerous?
In BP labile (easily changing/altering) patients w/ severe CAD & HTN
What do nitrates dilate: arteries or veins?
Mixed venous AND arterial dilating
Which vasodilates more from nitrates: arteries or veins?
Venous vasodilation > arterial vasodilation
Nitrate effects?
Increase venous capacity, decrease ventricular preload, improves venous/later arterial filling
Benefits of nitrates come from what?
Symptom relief, reduced hospitalization (HOWEVER, NO CV OUTCOME BENEFITS)
What are nitrates useful for?
Controlling symptoms and delaying ED/urgent care visits
Which meds for CSA have extensive first pass metabolism?
Oral Nitrates (must be broken down by liver before they get to the heart)
Which nitrate route of administration can avoid the first pass metabolism?
Sublingual (SL)
How fast do SL nitrates take effect? How long do the effects last?
Rapid vasodilation (fast acting), but only 30 minutes of effect
If needed for chronic use, which form of nitrates should be avoided?
Short acting nitrates
Which dose intervals of nitrates should be used for chronic management?
12 and 24 hour dose intervals
When should short-acting nitrates be used?
To treat occasional angina symptoms
If using nitrates chronically, what should be done in order to avoid building a tolerance to the meds?
Windows of drug vacation
Venodilation is more prominent in what doses of nitrates: higher or lower?
Lower doses
Arterial dilitation is more prominent in what doses of nitrates: higher or lower?
Higher doses
What can occur due to venous dilation by nitrates?
Orthostasis due to venous pooling: dangerous if dehydrated, upright/not moving, or using alcohol
What can happen with temporal and meningeal arteries when using nitrates?
Vasodilate triggering intense, throbbing, disorienting migraine-like headaches
What percentage of patients experience migraines from temporal and meningeal vasodilation when taking nitrates?
> 60% of patients
What can happen in patients are using nitrates inappropriately (not using PRN) and then stop using them abruptly?
Rebound tachycardia (preferably prescribe BB or non-dhp CCB along w nitrates)
What is nitrate tachyphylaxis?
Long term exposure to short acting nitrates will desensitize response to nitrates
What medications should absolutely be avoided if using nitrate therapy?
Phosphodiesterase inhibitors: Viagra (Sildenafil), Cialis (Tadalafil), etc.
How long should phosphodiesterase inhibitors be held after any nitrate?
24 hours
What interaction can nitrates have with posphodiesterase inhibitors?
CAN BE DEADLY, causes a massive shift of blood away from the heart
What causes nitrate toxicity?
Excess nitrate combines w hemoglobin (Hb) causing methemoglobinemia –> oxygen delivery impaired
What is nitrate toxicity/methemoglobinema treated with?
Methylene blue
Quick acting nitrates to treat angina symptoms?
Nitroglycerin (Nitrostat, NitroBID)
What is nitroglycerin intended for?
Rapid relief of angina (insufficient for background dilation)
How does nitroglycerin act on vascular smooth muscle?
Relaxes vascular smooth muscle via increased cGMP
What are the effects of nitroglycerin?
Reduces O2 demand, preload, afterload
Improves collateral/backup circulation
Reduces sx, hospitalization
**NO IMPROVEMENT ON CV OUCTOMES
Duration of sublingual (SL) nitroglycerin?
20-30 minutes
Duration of transdermal (TD) nitroglycerin?
6-8 hours
When should TD nitroglycerin patches be removed?
Before MRI and defibrillation
Half life of nitroglycerin?
1-4 minutes
What nitrate-free interval is necessary for avoiding tolerance of oral nitroglycerin?
Interval of 10-12 hours
What should you instruct patients to avoid when using nitrates?
Alcohol
First dose of nitrates should be given where?
Under supervision to monitor for headache or reflux
Which nitrates are long-acting for angina prevention?
Isosorbide mononitrate (Imdur, Ismo, Monoket) and Dinitrate (Isordil)
How do long-acting nitrates work?
Systemic vasodilation by increasing cGMP
What do long-acting nitrates reduce?
Reduce preload, LV end diastolic volume & pressure
Is there any data of improved CV outcome for long-acting nitrates?
NO, only symptom relief data
Dosage for chronic use of long-acting nitrates?
5-10mg at:
7AM and 3PM
OR
9AM and 5PM
*allows nitrate-free interval to reduce tachyphylaxis
Mononitrate formulations allow what duration?
XR tablet allows 24 hours (once daily)
Dinitrate formulations allow what duration?
XR tablet allows 12 hours (twice daily)
What is important to educate patients on when using XR tablets (long-acting nitrates)?
DO NOT confuse with SL nitroglycerin or chew like aspirin
How to manage nocturnal angina with long-acting nitrates?
Adjust scheduled doses/dose spacing
Medication combo for angina/chest pain?
BB + long-acting nitrates + PRN SL/spray nitroglycerin
Medication combo for angina/chest pain in unable to take BB?
Non-DHP CCB + long-acting nitrates + PRN SL/spray nitroglycerin
Management for lipid-lowering in CSA?
Counsel on lifestyle habits, baseline lipid and liver panel, if LDL > 190 investigate cause (may be genetically predisposed), high intensity statins
When to use PCSK9i’s for lipid-lowering?
Not routinely used, but if LDL remains >190 even after high intensity statins, initiate PCSK9i therapy
ACEi (or ARB if intolerant) therapy for CSA?
Evidence supports dec. in CV events w/ CHD
Also consider for: CKD, DM, EF < 40%
*plaque stabilization
Which medication should only be used if necessary?
Non-DHP CCBs in place of BB’s - lack data for benefits in preventing MI
Meds for plaque stabilization?
DAPT, ACEi, statins
