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Chronic Stable
Angina
NUR 506
Valparaiso University
"I have neither given or received, nor have I tolerated others’ use of unauthorized
aid."
OBJECTIVES
Ultimately the student will be able to :
 Summarize the epidemiology of Chronic stable
angina (CSA)
 Analyze the pathophysiology of CSA
 Understand the difference between CSA &
Acute coronary syndrome (ACS)
 Learn the different pharmacological approach
for CSA
 Determine the various nursing educational
plans for patients with CSA and are on
medications.
Definition
The term “angina,” however, derives from a neologism of two
Latin words “ angor animi ,” which literally translates as “fear of life
being extinguished,” according to Heberden’s original description
in 1768. Angina is a chronic condition in which short episodes of
chest pain can occur periodically when the heart has a temporary
deficiency in its blood supply.
Angina is a syndrome, a constellation of symptoms that results
from myocardial oxygen demand being greater than the oxygen
supply.
(Arcangelo & Peterson, 2013, Healey, 2012, Flather, Bhatt, & Geisler, 2012)
Epidemiology
Despite the declining incidence of myocardial infarction, the
prevalence of angina remains high with direct costs in the United
States in 2000 estimated at over $75 billion.
In the United States, approximately 10.2 million Americans were
reported to have angina in 2006 with 4.7% of Caucasian men and
4.5% of Caucasian women over the age of 20 years affected.
Ethnic differences in angina occurrence are well illustrated in the
United States where the prevalence in men over the age of 20
years is 3.8% in Caucasians, 3.3% in African Americans, and
3.6% in the Hispanic population. The equivalent prevalence
amongst females is 3.7%, 5.6% and 3.7%.
(Beltrame, Dreyer & Tavella, 2012)
Pathophysiology
Atherosclerosis
The pathophysiology of angina involves atherosclerosis , which is a disorder of lipid
metabolism causing cholesterol deposition in the blood vessels
Picture – A.D.A.M Inc, 2013
This causes a reactive endothelial injury that eventually results in narrowing of the
vessels by episodes of acute thrombosis
The narrow arteries impair the ability of
oxygen and nutrients to reach the
myocardium.
Impaired myocardial metabolism
(Arcangelo & Peterson, 2013)
Contd..
Coronary Artery Vasospasm
Coronary vasospasm by the narrowing of the coronary artery lumen
Narrowing is caused arterial muscle spasm which limits blood supply to the myocardium
The smooth muscles of the coronary arteries contract in response to neurogenic
stimulation
Ciggarette smoking and hyperlipidemia appear to play a role in this type of angina
(Arcangelo & Peterson, 2013)
(Pic – A.D.A.M Inc, 2013)
Differences b/w CSA & Acute coronary syndrome
1. CSA or Stable angina is chest pain
that occurs with stress or activity. It is
due to poor blood blood flow to the
heart. It is called as Non ACS anginal
chest pain.
2. A chronic limited ability to increase
oxygen supply to the myocardium in
the setting of increased oxygen
demand results in CSA
3. vWF is not significant in CSA
4. Management for CSA includes
aggressive life-style and risk factor
modification to control cardiac risk
factors; pharmacologic interventions
such as beta-blockers, nitrates, CCBs,
anti-platelet agents, and statins remain
the standard of care.
1. The term acute coronary syndrome
(ACS) refers to any group of clinical
symptoms compatible with acute
myocardial ischemia and includes
unstable angina (UA), non–ST-segment
elevation myocardial infarction
(NSTEMI), and ST-segment elevation
myocardial infarction (STEMI)
2. The reduction in coronary blood flow
(CBF) leads to a decline in oxygen
supply, resulting in development of an
ACS.
3. High levels of vWF can be seen in ACS
4. ACS) should receive aggressive care,
including aspirin, clopidogrel,
unfractionated heparin or low–
molecular-weight heparin (LMWH), IV
platelet glycoprotein IIb/IIIa complex
blockers (eg, tirofiban, eptifibatide), and
a beta blocker. The goal is early
Drugs used for Rx of CSA
• Beta Blockers
o Atenolol: 25 – 100 mg qd.
o Metoprolol: 25 – 200 mg tid.
o Metoprolol succinate – 50 -100mg qd,
o Propranolol – IR – 40 – 160mg bid & ER – 80 – 240 mg qd
These drugs must all be given in an individually titrated dose to control
symptoms and attenuate postural and exercise-induced tachycardia.
• Beta-blockers are usually started at a low dose, then titrated upward as
tolerated.
• In general, the dose is titrated to control of symptoms or resting heart rate in
the 60s (beats/min).
(Flather, Bhatt & Geisler, 2012; Reid, Walters & Gerard, 2010, Arcangelo & Peterson, 2013)
Calcium channel blockers(CCBs)
• If the patient cant tolerate BB, CCBs may be given.
• Nifedipine ( ER)
30-60 mg qd
May cause marked tachycardia
May cause less myocardial depression than the other drugs in this group
• Amlodipine
2.5-10 mg qd, Ultralong-acting
• Verapamil
IR - 80-320 mg bid, ER – 120 – 480 mg qd
Commonly causes constipation; useful anti-arrhythmic properties
• Diltiazem (ER)
180-420 mg qd
Similar anti-arrhythmic properties to verapamil
(Fauci, et al, 2008, Arcangelo & Peterson, 2013)
Nitrates
 Short acting nitrates – NTG (nitrostat, nitroquick) – 0.4mg SL prn
-- Isosorbide dinitrate: 5 mg SL prn
 Long acting nitrates – NTG – Topical ointment – ½ to 1 in bid/tid Transdermal GTN:
0.2- 0.8mg /hr. Nitrate patches should be removed at night to ensure efficacy during
the day.
 Isosorbide mononitrate – 5 – 20mg bid, ER (Imdur) – 30 – 120 mg bid
• To prevent nitrate tolerance, a 12-hour nitrate-free interval is often required.
Combining nitrates with hydralazine, folic acid, and antioxidants like vitamin
E may reduce the development of nitrate tolerance
(Ogle, 2010; Flather, Bhatt & Geisler, 2012, Arcangelo & Peterson, 2013)
Antiplatelet agents
• Aspirin should be started at 81to 325 mg qd and continued
indefinitely in all patients unless contraindicated.
• Clopidogrel – 75mg qd
• If the patient cannot tolerate aspirin, thienopyridines like
clopidogrel or ticopidine hydrochloride may be given.
(Fraker & Fihn, 2007, Flather, Bhatt & Geisler, 2012, Arcangelo & Peterson, 2013 )
Renin-Angiotensin-Aldosterone system blockers
• Captopril – Start – 6.25mg or 12.5 mg tid, therapeutic range –
25 – 100 mg tid
• Enalpril – start 2.5mg qd or bid, range – 5 – 20 mg qd or bid
daily
• Fosinopril – start – 10mg qd, range – 10-40mg qd
• Lisinopril –start -5mg qd, range -5-20mg qd
• Quinapril- start- 5mg bid, range 20-40mg bid
• Ramipril – start 1.25mg twice daily, range – 1.25- 5mg twice
daily.
(Fraker & Fihn, 2007; Kaplow & Hardin, 2007, Arcangelo & Peterson, 2013)
Ranolazine
• It is used in combination with beta blockers,nitrates, CCBs,
antiplatelet therapy, lipid lowering therapy, angiotensing
converting enyme inhibitors and angiotensin receptor blockers.
• For treating CSA, initial dose of 500mg – 1000mg qd
(Li, 2015, Arcangelo & Peterson, 2013)
Recommendations for pharmacological therapy to improve prognosis in patients with stable
angina
Class I
•Aspirin 75 mg daily in all patients without specific contraindications (ie active GI bleeding, aspirin
allergy or previous aspirin intolerance) (level of evidence A)
•Statin therapy for all patients with coronary disease (level of evidence A)
•ACE-inhibitor therapy in patients with coincident indications for ACE-inhibition, such as
hypertension, heart failure, LV dysfunction, prior MI with LV dysfunction, or diabetes (level of
evidence A)
•Oral beta blocker therapy in patients post-MI or with heart failure (level of evidence A)
Class IIa
•ACE-inhibitor therapy in all patients with angina and proven coronary disease (level of evidence B)
•Clopidogrel as an alternative antiplatelet agent in patients with stable angina who cannot take
aspirin eg Aspirin allergic (level of evidence B)
•High-dose statin therapy in high risk (>2% annual CV mortality) patients with proven coronary
disease (level of evidence B)
Class IIb
•Fibrate therapy in patients with low HDL and high triglycerides who have diabetes or the metabolic
syndrome (level of evidence B)
(Fox et al., 2006)
Step care for CSA
• First line therapy –Beta blockers with CCB
• Second line therapy - Long acting nitrate with beta blocker plus
a CCB like nifedipine
• Third line therapy – Adding long acting nitrates , CCB and
betablockers
(Arcangelo & Peterson, 2013)
Drugs differ for Acute Rx v/s Chronic prevention
of angina episodes.
• Acute Rx
Short acting nitrate
• Chronic Prevention
Aspirin. Beta blockers, CCB and Long acting nitrates
(Arcangelo & Peterson, 2013)
Patient Education – Effects of the drug.
•Beta blockers -These slow the heart rate, decreasing blood pressure, and
thereby reducing the oxygen demand of the heart. Beta-blockers’ principal
effects are negative chronotropic (slow heart rate) and, to a variable extent,
negative inotropic (decrease cardiac contractility)
•CCBs - These agents block the action of calcium. They effect different areas
like coronary artery (CA) and systemic vasodilation, decreased contractility of
the heart(negative ionotropy) and decreased heartrate and conduction through
the atrioventricular(AV) node.
•Aspirin – It is given for a thrombogenic effect through platelet inhibition and it
also reduces anti-inflammatory response in atherosclerosis
(Li, 2015, Arcangelo & Peterson, 2013)
Contd..Patient Education – Effects of the drug.
• Ranolazine - It blocks the late cardiac sodium current (Ina) thereby reducing the
accumulation of intracellular Ca+ during diastole and thereby decreases wall tension.
• ACE inhibitors - These drugs block the conversion of angiotensin I to angiotensin II
which in turn causes arterial vasodilation and it lowers the blood pressure. In the end
it it decreases myocardial oxygen demand by decreasing the workload of the heart.
• Nitrates – It reduces the myocardial oxygen demand through increased venous
capacitance which leads to decreased LV volume/preload; they also dilate coronary
arteries and enhances subendocardial perfusion.
(Li, 2015, Arcangelo & Peterson, 2013)
Potential adverse effects of medications.
• Betablockers - Primary side effects include excessive bradycardia, prolongation of
the PR interval and heart block, exacerbation of congestive heart failure, and
exacerbation of severe reactive airway disease. Peripheral edema, nausea and
vomiting, and diarrhoea. Sexual dysfunction in men is also a common adverse
reaction.
• CCBs - One of the possible adverse reactions is hypotension. Other possible
adverse reactions include dizziness, bradycardia, headache, and edema.
• Nitrates - The most common adverse reaction to nitrates
is hypotension accompanied by dizziness, so patients should be sitting or lying down
when taking the medication. Nitrates may also cause headache.
(Li, 2015, Kones, 2010, Arcangelo & Peterson, 2013)
Contd…
• Aspirin - Contrary to the antiplatelet effects, the gastrointestinal side-effects of aspirin
increase at higher doses. The relative risk of suffering an intracranial haemorrhage
increases by 30%, but the absolute risk of such complications attributable to
antiplatelet drug therapy is less than 1 per 1000 patient years of treatment with
aspirin at doses ≥75 mg/day.
• Ranolazine - The most common side effects are dizziness, headache, constipation
and nausea.
• ACE inhibitors - Postural hypotension, dry cough, rash. Rare: hyperkalaemia,
worsening of renal function (in those with underlying renal ischemia or severe heart
failure), angioneurotic oedema, haematological toxicity (e.g. neutropenia,
agranulocytosis).
(Li, 2015; Kones, 2010; Chatu, 2012, Arcangelo & Peterson, 2013)
Drug interactions
• Beta blockers - Diltiazem: concomitant use of diltiazem and atenolol increases the risk
of bradycardia and AV block. Verapamil: the risk of heart failure, severe hypotension
and asystole is increased if atenolol is given with verapamil.
• CCBs - These drugs should be used with caution when combined with cyclosporine,
carbamazepine, lithium carbonate, amiodarone, or digoxin (ie, 50% to 70% increase
in digoxin concentrations in first week of therapy). Combining verapamil or diltiazem
with beta blockers generally should be avoided because of potentially profound
adverse effects on AV nodal conduction, heart rate, or cardiac contractility.
• Nitrates - Coadministration of the phosphodiesterase inhibitors sildenafil, tadalafil, or
vardenafil with long-acting nitrates should be strictly avoided within 24 hours of nitrate
administration because of the risk of profound hypotension (eg, 25–mm Hg drop in
systolic BP).
(Fihn et al., 2012)
Contd..
• Ranolazine - Ranolazine is contraindicated in combination with potent inhibitors of
the CYP3A4 pathway, including ketoconazole (3.2-fold increase in ranolazine plasma
levels) and other azole antifungals, macrolide antibiotics, HIV (human
immunodeficiency virus) protease inhibitors, grapefruit products or juice, diltiazem
(1.8- to 2.3-fold increase in ranolazine plasma levels), itraconazole, clarithromycin,
and certain HIV protease inhibitors.
• ACE inhibitors : NSAIDs: these increase the risk of renal impairment. Potassium-
sparing diuretics: concomitant use with an ACE inhibitor increases the risk of
hyperkalaemia.
• Aspirin - Selective serotonin reuptake inhibitors (SSRIs): concomitant use of aspirin
and SSRIs increases the risk of GI bleeding. Warfarin: concomitant use of aspirin
and warfarin increases the risk of bleeding.
(Fihn et al., 2012)
Lab monitoring
• Betablockers – Monitor blood glucose levels, measure serum
Potassium.
• ACE inhibitors – Monitor BUN, creatinine and K levels
(Arcangelo & Peterson, 2013)
Dietary, Exercise and Social life.
• Nitrates
If you miss a dose of this medicine, take it as soon as possible. However, if it is almost time for
your next dose, skip the missed dose and go back to your regular dosing schedule. Do not double
doses.
Other advices to be given :
• • If you smoke, stop.
• If you’re overweight, talk to your healthcare provider about
losing weight.
• Increase your physical activity. Ask your healthcare provider
about the kinds of activities that are safe for you.
• Eat a healthy, low-fat diet. Include lots of whole grains, fruits,
and vegetables.
• If you have diabetes, keep your blood sugar under control.
•Avoid eating large meals that make you feel stuffed.
• Find ways to relax and manage stress.
(Timby & Smith, 2010)
References
• Agarwal, M., Mehta, P. K., & Bairey Merz, C. N. (2010).
Nonacute coronary syndrome anginal chest pain. Medical
Clinics of North America, 94(2), 201–216.
http://doi.org/10.1016/j.mcna.2010.01.008
• Agewall, S. (2008). Acute and stable coronary heart disease:
different risk factors. European Heart Journal, 29(16), 1927–
1929. http://doi.org/10.1093/eurheartj/ehn321
• Arcangelo, V. P., & Peterson, A. M. (2013).
Pharmacotherapeutics for advanced practice: A practical
approach (3rd ed., pp. 265-266). Ambler, PA: Lippincott
Williams & Wilkins.
• Chatu, S., & Tofield, C. (2010). The hands-on guide to clinical
pharmacology. Chichester, West Sussex, UK: Wiley-Blackwell.
Retrieved from http://site.ebrary.com/id/10483324
• Fauci, A. S. (Ed.). (2008). Harrison’s principles of internal
medicine (17th ed). New York: McGraw-Hill Medicine
• Flather, M., Bhatt, D., & Geisler, T. (Eds.). (2012).
Cardiovascular clinical trials : Putting the evidence into practice.
Somerset, NJ, USA: John Wiley & Sons. Retrieved from
http://www.ebrary.com
• Fox, K., Garcia, M. A. A., Ardissino, D., Buszman, P., Camici,
P. G., Crea, F., … Weis, M. (2006). Guidelines on the
management of stable angina pectoris: executive summary.
European Heart Journal, 27(11), 1341–1381.
http://doi.org/10.1093/eurheartj/ehl001
• Fihn, S. D., Gardin, J. M., Abrams, J., Berra, K., Blankenship, J.
C., Dallas, A. P., … Anderson, J. L. (2012). 2012
ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the
diagnosis and management of patients With stable ischemic
heart disease: A report of the American college of cardiology
foundation/American heart association task force on practice
guidelines, and the American college of physicians, American
association for thoracic surgery, preventive cardiovascular
nurses association, society for cardiovascular angiography and
interventions, and society of thoracic surgeons. Circulation,
126(25), e354–e471.
http://doi.org/10.1161/CIR.0b013e318277d6a0
• Healey, J. (Ed.). (2012). Issues in society, Volume 340 :
Cardiovascular Health. Thirroul, NSW, AUS: The Spinney
Press. Retrieved from http://www.ebrary.com
• John F. Beltrame, Rachel Dreyer and Rosanna Tavella (2012).
Epidemiology of coronary artery disease, Coronary artery
disease – Current concepts in epidemiology, pathophysiology,
diagnostics and treatment, Dr. David Gaze (Ed.), ISBN: 978-
953-51-0262-5
• Kones, R. (2010). Recent advances in the management of
chronic stable angina II. Anti-ischemic therapy, options for
refractory angina, risk factor reduction, and revascularization.
Vascular Health and Risk Management, 749.
http://doi.org/10.2147/VHRM.S11100
• Kucia, A., & Quinn, T. (2010). Presentations of Acute Coronary
Syndromes Acute cardiac care: A practical guide for nurses
(pp. 168-175). Oxford: Willey-Blackwell.
• Li, Y. (2015). Cardiovascular diseases: from molecular
pharmacology to evidence-based therapeutics. Hoboken, New
Jersey: John Wiley & Sons, Inc.
• McKay, G. A., Reid, J. L., & Walters, M. R. (2010).
Management of coronary artery disease and its complications.
Clinical pharmacology and therapeutics.(Eds.) Chichester:
Wiley-Blackwell. Retrieved from books.google
• Ogle, K. T. (2010). Analyzing angina. Nursing Made Incredibly
Easy!, 8(6), 9–12.
http://doi.org/10.1097/01.NME.0000388531.96402.68
• Timby, B. K & Smith, E, N., (2010). Introductory medical-
surgical nursing (10th ed). Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.

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Chronic stable angina

  • 1. Chronic Stable Angina NUR 506 Valparaiso University "I have neither given or received, nor have I tolerated others’ use of unauthorized aid."
  • 2. OBJECTIVES Ultimately the student will be able to :  Summarize the epidemiology of Chronic stable angina (CSA)  Analyze the pathophysiology of CSA  Understand the difference between CSA & Acute coronary syndrome (ACS)  Learn the different pharmacological approach for CSA  Determine the various nursing educational plans for patients with CSA and are on medications.
  • 3. Definition The term “angina,” however, derives from a neologism of two Latin words “ angor animi ,” which literally translates as “fear of life being extinguished,” according to Heberden’s original description in 1768. Angina is a chronic condition in which short episodes of chest pain can occur periodically when the heart has a temporary deficiency in its blood supply. Angina is a syndrome, a constellation of symptoms that results from myocardial oxygen demand being greater than the oxygen supply. (Arcangelo & Peterson, 2013, Healey, 2012, Flather, Bhatt, & Geisler, 2012)
  • 4. Epidemiology Despite the declining incidence of myocardial infarction, the prevalence of angina remains high with direct costs in the United States in 2000 estimated at over $75 billion. In the United States, approximately 10.2 million Americans were reported to have angina in 2006 with 4.7% of Caucasian men and 4.5% of Caucasian women over the age of 20 years affected. Ethnic differences in angina occurrence are well illustrated in the United States where the prevalence in men over the age of 20 years is 3.8% in Caucasians, 3.3% in African Americans, and 3.6% in the Hispanic population. The equivalent prevalence amongst females is 3.7%, 5.6% and 3.7%. (Beltrame, Dreyer & Tavella, 2012)
  • 5. Pathophysiology Atherosclerosis The pathophysiology of angina involves atherosclerosis , which is a disorder of lipid metabolism causing cholesterol deposition in the blood vessels Picture – A.D.A.M Inc, 2013 This causes a reactive endothelial injury that eventually results in narrowing of the vessels by episodes of acute thrombosis The narrow arteries impair the ability of oxygen and nutrients to reach the myocardium. Impaired myocardial metabolism (Arcangelo & Peterson, 2013)
  • 6. Contd.. Coronary Artery Vasospasm Coronary vasospasm by the narrowing of the coronary artery lumen Narrowing is caused arterial muscle spasm which limits blood supply to the myocardium The smooth muscles of the coronary arteries contract in response to neurogenic stimulation Ciggarette smoking and hyperlipidemia appear to play a role in this type of angina (Arcangelo & Peterson, 2013) (Pic – A.D.A.M Inc, 2013)
  • 7. Differences b/w CSA & Acute coronary syndrome 1. CSA or Stable angina is chest pain that occurs with stress or activity. It is due to poor blood blood flow to the heart. It is called as Non ACS anginal chest pain. 2. A chronic limited ability to increase oxygen supply to the myocardium in the setting of increased oxygen demand results in CSA 3. vWF is not significant in CSA 4. Management for CSA includes aggressive life-style and risk factor modification to control cardiac risk factors; pharmacologic interventions such as beta-blockers, nitrates, CCBs, anti-platelet agents, and statins remain the standard of care. 1. The term acute coronary syndrome (ACS) refers to any group of clinical symptoms compatible with acute myocardial ischemia and includes unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) 2. The reduction in coronary blood flow (CBF) leads to a decline in oxygen supply, resulting in development of an ACS. 3. High levels of vWF can be seen in ACS 4. ACS) should receive aggressive care, including aspirin, clopidogrel, unfractionated heparin or low– molecular-weight heparin (LMWH), IV platelet glycoprotein IIb/IIIa complex blockers (eg, tirofiban, eptifibatide), and a beta blocker. The goal is early
  • 8. Drugs used for Rx of CSA • Beta Blockers o Atenolol: 25 – 100 mg qd. o Metoprolol: 25 – 200 mg tid. o Metoprolol succinate – 50 -100mg qd, o Propranolol – IR – 40 – 160mg bid & ER – 80 – 240 mg qd These drugs must all be given in an individually titrated dose to control symptoms and attenuate postural and exercise-induced tachycardia. • Beta-blockers are usually started at a low dose, then titrated upward as tolerated. • In general, the dose is titrated to control of symptoms or resting heart rate in the 60s (beats/min). (Flather, Bhatt & Geisler, 2012; Reid, Walters & Gerard, 2010, Arcangelo & Peterson, 2013)
  • 9. Calcium channel blockers(CCBs) • If the patient cant tolerate BB, CCBs may be given. • Nifedipine ( ER) 30-60 mg qd May cause marked tachycardia May cause less myocardial depression than the other drugs in this group • Amlodipine 2.5-10 mg qd, Ultralong-acting • Verapamil IR - 80-320 mg bid, ER – 120 – 480 mg qd Commonly causes constipation; useful anti-arrhythmic properties • Diltiazem (ER) 180-420 mg qd Similar anti-arrhythmic properties to verapamil (Fauci, et al, 2008, Arcangelo & Peterson, 2013)
  • 10. Nitrates  Short acting nitrates – NTG (nitrostat, nitroquick) – 0.4mg SL prn -- Isosorbide dinitrate: 5 mg SL prn  Long acting nitrates – NTG – Topical ointment – ½ to 1 in bid/tid Transdermal GTN: 0.2- 0.8mg /hr. Nitrate patches should be removed at night to ensure efficacy during the day.  Isosorbide mononitrate – 5 – 20mg bid, ER (Imdur) – 30 – 120 mg bid • To prevent nitrate tolerance, a 12-hour nitrate-free interval is often required. Combining nitrates with hydralazine, folic acid, and antioxidants like vitamin E may reduce the development of nitrate tolerance (Ogle, 2010; Flather, Bhatt & Geisler, 2012, Arcangelo & Peterson, 2013)
  • 11. Antiplatelet agents • Aspirin should be started at 81to 325 mg qd and continued indefinitely in all patients unless contraindicated. • Clopidogrel – 75mg qd • If the patient cannot tolerate aspirin, thienopyridines like clopidogrel or ticopidine hydrochloride may be given. (Fraker & Fihn, 2007, Flather, Bhatt & Geisler, 2012, Arcangelo & Peterson, 2013 )
  • 12. Renin-Angiotensin-Aldosterone system blockers • Captopril – Start – 6.25mg or 12.5 mg tid, therapeutic range – 25 – 100 mg tid • Enalpril – start 2.5mg qd or bid, range – 5 – 20 mg qd or bid daily • Fosinopril – start – 10mg qd, range – 10-40mg qd • Lisinopril –start -5mg qd, range -5-20mg qd • Quinapril- start- 5mg bid, range 20-40mg bid • Ramipril – start 1.25mg twice daily, range – 1.25- 5mg twice daily. (Fraker & Fihn, 2007; Kaplow & Hardin, 2007, Arcangelo & Peterson, 2013)
  • 13. Ranolazine • It is used in combination with beta blockers,nitrates, CCBs, antiplatelet therapy, lipid lowering therapy, angiotensing converting enyme inhibitors and angiotensin receptor blockers. • For treating CSA, initial dose of 500mg – 1000mg qd (Li, 2015, Arcangelo & Peterson, 2013)
  • 14. Recommendations for pharmacological therapy to improve prognosis in patients with stable angina Class I •Aspirin 75 mg daily in all patients without specific contraindications (ie active GI bleeding, aspirin allergy or previous aspirin intolerance) (level of evidence A) •Statin therapy for all patients with coronary disease (level of evidence A) •ACE-inhibitor therapy in patients with coincident indications for ACE-inhibition, such as hypertension, heart failure, LV dysfunction, prior MI with LV dysfunction, or diabetes (level of evidence A) •Oral beta blocker therapy in patients post-MI or with heart failure (level of evidence A) Class IIa •ACE-inhibitor therapy in all patients with angina and proven coronary disease (level of evidence B) •Clopidogrel as an alternative antiplatelet agent in patients with stable angina who cannot take aspirin eg Aspirin allergic (level of evidence B) •High-dose statin therapy in high risk (>2% annual CV mortality) patients with proven coronary disease (level of evidence B) Class IIb •Fibrate therapy in patients with low HDL and high triglycerides who have diabetes or the metabolic syndrome (level of evidence B) (Fox et al., 2006)
  • 15. Step care for CSA • First line therapy –Beta blockers with CCB • Second line therapy - Long acting nitrate with beta blocker plus a CCB like nifedipine • Third line therapy – Adding long acting nitrates , CCB and betablockers (Arcangelo & Peterson, 2013)
  • 16. Drugs differ for Acute Rx v/s Chronic prevention of angina episodes. • Acute Rx Short acting nitrate • Chronic Prevention Aspirin. Beta blockers, CCB and Long acting nitrates (Arcangelo & Peterson, 2013)
  • 17. Patient Education – Effects of the drug. •Beta blockers -These slow the heart rate, decreasing blood pressure, and thereby reducing the oxygen demand of the heart. Beta-blockers’ principal effects are negative chronotropic (slow heart rate) and, to a variable extent, negative inotropic (decrease cardiac contractility) •CCBs - These agents block the action of calcium. They effect different areas like coronary artery (CA) and systemic vasodilation, decreased contractility of the heart(negative ionotropy) and decreased heartrate and conduction through the atrioventricular(AV) node. •Aspirin – It is given for a thrombogenic effect through platelet inhibition and it also reduces anti-inflammatory response in atherosclerosis (Li, 2015, Arcangelo & Peterson, 2013)
  • 18. Contd..Patient Education – Effects of the drug. • Ranolazine - It blocks the late cardiac sodium current (Ina) thereby reducing the accumulation of intracellular Ca+ during diastole and thereby decreases wall tension. • ACE inhibitors - These drugs block the conversion of angiotensin I to angiotensin II which in turn causes arterial vasodilation and it lowers the blood pressure. In the end it it decreases myocardial oxygen demand by decreasing the workload of the heart. • Nitrates – It reduces the myocardial oxygen demand through increased venous capacitance which leads to decreased LV volume/preload; they also dilate coronary arteries and enhances subendocardial perfusion. (Li, 2015, Arcangelo & Peterson, 2013)
  • 19. Potential adverse effects of medications. • Betablockers - Primary side effects include excessive bradycardia, prolongation of the PR interval and heart block, exacerbation of congestive heart failure, and exacerbation of severe reactive airway disease. Peripheral edema, nausea and vomiting, and diarrhoea. Sexual dysfunction in men is also a common adverse reaction. • CCBs - One of the possible adverse reactions is hypotension. Other possible adverse reactions include dizziness, bradycardia, headache, and edema. • Nitrates - The most common adverse reaction to nitrates is hypotension accompanied by dizziness, so patients should be sitting or lying down when taking the medication. Nitrates may also cause headache. (Li, 2015, Kones, 2010, Arcangelo & Peterson, 2013)
  • 20. Contd… • Aspirin - Contrary to the antiplatelet effects, the gastrointestinal side-effects of aspirin increase at higher doses. The relative risk of suffering an intracranial haemorrhage increases by 30%, but the absolute risk of such complications attributable to antiplatelet drug therapy is less than 1 per 1000 patient years of treatment with aspirin at doses ≥75 mg/day. • Ranolazine - The most common side effects are dizziness, headache, constipation and nausea. • ACE inhibitors - Postural hypotension, dry cough, rash. Rare: hyperkalaemia, worsening of renal function (in those with underlying renal ischemia or severe heart failure), angioneurotic oedema, haematological toxicity (e.g. neutropenia, agranulocytosis). (Li, 2015; Kones, 2010; Chatu, 2012, Arcangelo & Peterson, 2013)
  • 21. Drug interactions • Beta blockers - Diltiazem: concomitant use of diltiazem and atenolol increases the risk of bradycardia and AV block. Verapamil: the risk of heart failure, severe hypotension and asystole is increased if atenolol is given with verapamil. • CCBs - These drugs should be used with caution when combined with cyclosporine, carbamazepine, lithium carbonate, amiodarone, or digoxin (ie, 50% to 70% increase in digoxin concentrations in first week of therapy). Combining verapamil or diltiazem with beta blockers generally should be avoided because of potentially profound adverse effects on AV nodal conduction, heart rate, or cardiac contractility. • Nitrates - Coadministration of the phosphodiesterase inhibitors sildenafil, tadalafil, or vardenafil with long-acting nitrates should be strictly avoided within 24 hours of nitrate administration because of the risk of profound hypotension (eg, 25–mm Hg drop in systolic BP). (Fihn et al., 2012)
  • 22. Contd.. • Ranolazine - Ranolazine is contraindicated in combination with potent inhibitors of the CYP3A4 pathway, including ketoconazole (3.2-fold increase in ranolazine plasma levels) and other azole antifungals, macrolide antibiotics, HIV (human immunodeficiency virus) protease inhibitors, grapefruit products or juice, diltiazem (1.8- to 2.3-fold increase in ranolazine plasma levels), itraconazole, clarithromycin, and certain HIV protease inhibitors. • ACE inhibitors : NSAIDs: these increase the risk of renal impairment. Potassium- sparing diuretics: concomitant use with an ACE inhibitor increases the risk of hyperkalaemia. • Aspirin - Selective serotonin reuptake inhibitors (SSRIs): concomitant use of aspirin and SSRIs increases the risk of GI bleeding. Warfarin: concomitant use of aspirin and warfarin increases the risk of bleeding. (Fihn et al., 2012)
  • 23. Lab monitoring • Betablockers – Monitor blood glucose levels, measure serum Potassium. • ACE inhibitors – Monitor BUN, creatinine and K levels (Arcangelo & Peterson, 2013)
  • 24. Dietary, Exercise and Social life. • Nitrates If you miss a dose of this medicine, take it as soon as possible. However, if it is almost time for your next dose, skip the missed dose and go back to your regular dosing schedule. Do not double doses.
  • 25. Other advices to be given : • • If you smoke, stop. • If you’re overweight, talk to your healthcare provider about losing weight. • Increase your physical activity. Ask your healthcare provider about the kinds of activities that are safe for you. • Eat a healthy, low-fat diet. Include lots of whole grains, fruits, and vegetables. • If you have diabetes, keep your blood sugar under control. •Avoid eating large meals that make you feel stuffed. • Find ways to relax and manage stress. (Timby & Smith, 2010)
  • 26. References • Agarwal, M., Mehta, P. K., & Bairey Merz, C. N. (2010). Nonacute coronary syndrome anginal chest pain. Medical Clinics of North America, 94(2), 201–216. http://doi.org/10.1016/j.mcna.2010.01.008 • Agewall, S. (2008). Acute and stable coronary heart disease: different risk factors. European Heart Journal, 29(16), 1927– 1929. http://doi.org/10.1093/eurheartj/ehn321 • Arcangelo, V. P., & Peterson, A. M. (2013). Pharmacotherapeutics for advanced practice: A practical approach (3rd ed., pp. 265-266). Ambler, PA: Lippincott Williams & Wilkins.
  • 27. • Chatu, S., & Tofield, C. (2010). The hands-on guide to clinical pharmacology. Chichester, West Sussex, UK: Wiley-Blackwell. Retrieved from http://site.ebrary.com/id/10483324 • Fauci, A. S. (Ed.). (2008). Harrison’s principles of internal medicine (17th ed). New York: McGraw-Hill Medicine • Flather, M., Bhatt, D., & Geisler, T. (Eds.). (2012). Cardiovascular clinical trials : Putting the evidence into practice. Somerset, NJ, USA: John Wiley & Sons. Retrieved from http://www.ebrary.com
  • 28. • Fox, K., Garcia, M. A. A., Ardissino, D., Buszman, P., Camici, P. G., Crea, F., … Weis, M. (2006). Guidelines on the management of stable angina pectoris: executive summary. European Heart Journal, 27(11), 1341–1381. http://doi.org/10.1093/eurheartj/ehl001 • Fihn, S. D., Gardin, J. M., Abrams, J., Berra, K., Blankenship, J. C., Dallas, A. P., … Anderson, J. L. (2012). 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients With stable ischemic heart disease: A report of the American college of cardiology foundation/American heart association task force on practice guidelines, and the American college of physicians, American association for thoracic surgery, preventive cardiovascular nurses association, society for cardiovascular angiography and interventions, and society of thoracic surgeons. Circulation, 126(25), e354–e471. http://doi.org/10.1161/CIR.0b013e318277d6a0
  • 29. • Healey, J. (Ed.). (2012). Issues in society, Volume 340 : Cardiovascular Health. Thirroul, NSW, AUS: The Spinney Press. Retrieved from http://www.ebrary.com • John F. Beltrame, Rachel Dreyer and Rosanna Tavella (2012). Epidemiology of coronary artery disease, Coronary artery disease – Current concepts in epidemiology, pathophysiology, diagnostics and treatment, Dr. David Gaze (Ed.), ISBN: 978- 953-51-0262-5 • Kones, R. (2010). Recent advances in the management of chronic stable angina II. Anti-ischemic therapy, options for refractory angina, risk factor reduction, and revascularization. Vascular Health and Risk Management, 749. http://doi.org/10.2147/VHRM.S11100
  • 30. • Kucia, A., & Quinn, T. (2010). Presentations of Acute Coronary Syndromes Acute cardiac care: A practical guide for nurses (pp. 168-175). Oxford: Willey-Blackwell. • Li, Y. (2015). Cardiovascular diseases: from molecular pharmacology to evidence-based therapeutics. Hoboken, New Jersey: John Wiley & Sons, Inc. • McKay, G. A., Reid, J. L., & Walters, M. R. (2010). Management of coronary artery disease and its complications. Clinical pharmacology and therapeutics.(Eds.) Chichester: Wiley-Blackwell. Retrieved from books.google • Ogle, K. T. (2010). Analyzing angina. Nursing Made Incredibly Easy!, 8(6), 9–12. http://doi.org/10.1097/01.NME.0000388531.96402.68
  • 31. • Timby, B. K & Smith, E, N., (2010). Introductory medical- surgical nursing (10th ed). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Editor's Notes

  1. Angina is the sensation of discomfort experienced during periods of myocardial ischemia or myocardial infarction. It may occur when myocardial oxygen demand exceeds myocardial oxygen supply. Myocardial ischemia and angina are most commonly the result of significant stenosis of one or more coronary arteries. Typically, coronary artery stenosis that is 70% or more of the coronary artery diameter is flow restricting and may cause angina. In patients with chronic stable angina, myocardial ischemia results when myocardial oxygen demand increases, such as during physical exertion. Coronary vasoconstriction, particularly at the site of a preexisting stenosis, can also contribute to myocardial ischemia and produce angina.
  2. These data are primarily based upon patient self- report of a history of angina and thus subject to limited validity. Although the prevalence of angina in the UK and USA are similar, it is affected by age, gender, ethnicity, and geographic region, within the UK, the prevalence is almost 17% amongst males and 12% in females over the age of 75 years but is less than 1% of all those under 45 years of age. Furthermore for all ages, the prevalence of angina in men from Northern Ireland is approximately 6% whereas amongst Welshman it is 4%.
  3. The alternative names for CSA are Angina: stable, Angina: Chronic or Angina pectoris. Angina is the sensation of discomfort experienced during periods of myocardial ischemia or myocardial infarction. It may occur when myocardial oxygen demand exceeds myocardial oxygen supply. Myocardial ischemia and angina are most commonly the result of significant stenosis of one or more coronary arteries. Typically, coronary artery stenosis that is 70% or more of the coronary artery diameter is flow restricting and may cause angina. In patients with chronic stable angina, myocardial ischemia results when myocardial oxygen demand increases, such as during physical exertion. Coronary vasoconstriction, particularly at the site of a preexisting stenosis, can also contribute to myocardial ischemia and produce angina. 2. When atherosclerotic plaques are present, blood flow is impeded, but the process of autoregulation can compensate to a degree. Autoregulation is the dilation of the myocardial vessels in response to decreased oxygen delivery. Through autoregulation, blood flow to the heart changes rapidly as a result of higher demand. The most important mediators involved in myocardial perfusion are adenosine (a potent vasodilator), other nucleotides, nitric oxide, prostaglandins, carbon dioxide, and hydrogen ions. Obstructions to the coronary blood flow can be fixed, as with atherosclerosis, or dynamic, as with coronary spasm. Some patients may have both characteristics, and this is termed mixed angina.
  4. A less common cause of restricted coronary blood supply is by coronary artery vasospasm. There is narrowing of the coronary artery lumen. This narrowing is produced by arterial muscle spasm and limits the blood supply to the myocardium. The exact cause is not known. But contraction of arteries are seen in relation with the neurogenic stimulation. Cigarette smoking and hyperlipidemia are the major leads to this type of angina as they interfere with the normal neurogenic control of the arterial intima.
  5. vWF ( von Willebrand factor) - vWF has been detected in coronary thrombi rich in platelets and fibrin in acute myocardial infarction (AMI). It is elevated and peaks 2-3 days after the event. So in a healthy population, vWF is a weak predictor of future cardiovascular disease. But in a patient with AMI, it is highly significant.
  6. Negative chronotropic and negative ionotropic actions serve to decrease cardiac oxygen demand. Thus, generally they are not initiated in patients with baseline bradycardia, significantly prolonged PR interval (more than 220–240 m sec), acute decompensated heart failure as a result of systolic dysfunction, and severe reactive airway disease The combination of beta-blockers and nitrates is more effective than either agent alone
  7. They act mainly as vasodilators, lowering blood pressure and likely having some coronary vasodilating effects. Thus, they may be used instead of beta-blockers in patients with severe reactive airway disease. Generally they are not used in patients already on beta-blockers and are contraindicated in patients with depressed ejection fractions (less than 40%) because of their negative inotropic effects and because studies in the 1980s suggested a worse outcome with their use in such patients.
  8. Sublingual nitroglycerin is used to treat the acute onset of anginal symptoms as well as to act as a prophylaxis for angina symptoms prior to activities known to cause angina. Isosorbide dinitrate and its active metabolite isosorbide mononitrate are used as an oral preparation for the longer-term control of angina. Extended-release preparations like transdermal nitrate patches and isosorbide mononitrate offer the convenience of once-daily regimens. Due to the development of tachyphylaxis, none of the nitrate preparations provides truly 24-hour prophylaxis.. Nitrates are generally well tolerated.
  9. In all patients with stable angina who do not have evidence of aspirin resistance or allergy . In the case of true aspirin allergy, clopidogrel is recommended. In the CAPRIE (Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events) study, the use of clopidogrel alone was associated with an 8.7% relative reduction in vascular death, ischemic stroke, and MI . Clopidogrel should be considered and continued indefinitely when aspirin is absolutely contraindicated. Clopidogrel should be given following percutaneous coronary intervention for at least 12 months following implantation of a drug-eluting stent. Clopidogrel should be given following percutaneous coronary intervention for at least 1 month and, ideally, up to 12 months following implantation of a bare metal stent.Low-intensity anticoagulation [target international normalized ratio (INR): 1.5] with warfarin in addition to aspirin. Use of warfarin in combination with aspirin and/or clopidogrel is associated with an increased risk of bleeding and should be monitored closely • Use of dipyridamole should be avoided in patients with chronic stable angina.
  10. ACE inhibitors should be started and continued indefinitely in all patients with left ventricular ejection fraction less than or equal to 40% and in those with hypertension, diabetes, or chronic kidney disease unless contraindicated. ACE inhibitors should be started and continued indefinitely in patients who are not lower risk (lower risk defined as those with normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated. It is reasonable to use ACE inhibitors among lower-risk patients with mildly reduced or normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed. Angiotensin receptor blockers are recommended for patients who have hypertension, have indications for but are intolerant of ACE inhibitors, have heart failure, or have had a myocardial infarction with left ventricular ejection fraction less than or equal to 40%. Angiotensin receptor blockers may be considered in combination with ACE inhibitors for heart failure due to left ventricular systolic dysfunction. Aldosterone blockade is recommended for use in post-MI patients without significant renal dysfunction¶ or hyperkalemia􏰆 who are already receiving therapeutic doses of an ACE inhibitor and a beta blocker, have a left ventricular ejection fraction less than or equal to 40%, and have either diabetes or heart failure.
  11. Ranolazine is approved by FDA only for the treatment of CSA. The maximum recommended dose can be brought up to 1000mg twice a day. The most common side effects are dizziness, headache, constipation and nausea. This drug should not be used with strong CYP3A inhibitors like ketoconazole and with CYP3A inducers like rifampin,phenytoin etc. Concomitant use of ranolazine and P-glycoprotein inhibitors like cyclosporine can increase the ranolazine concentration. The dose of this drug should be titrated according to clinical response of the patient with P-glycoprotein inhibitors. It can also inhibit the pathways involving the metabolism of digoxin and simvastatin which may require dose reduction.
  12. Reference (Fox et al., 2006)
  13. First line therapy - When there are no contraindications BB are the first choice of medication for angina for the prevention of acute anginal attacks with out without the history of MI. BB reduce the frequency and likelihood of anginal episodes and reduces CHD related morbidity and mortality. In addition to this it also acts as antihypertensive and antiarrhythmic agent. Anginal pain related to physical exertion is well controlled by BB. But for patients who have their anginal pain due to coronary vasospasm, CCB should be administered. Second line – For patients who don’t respond to single anti anginal agents, combination therapy must be started, When BB alone don’t work, CCB or long acting nitrate can be added. Long acting nitrates are safe and cost effective, they are complementary with the BB. Third line – For patients who don’t tolerate 2 drugs, a 3 drug regimen is used. BB+CCB+ Long acting nitrates are used. Patients who don’t respond to 2 antianginal gents must be referred to specialist doctor.
  14. Acute Rx – Short acting nitrates should be given for treating acute anginal episodes. They are good for patients who hav infrequent attacks or predictable pain on exertion. Chronic prevention – Patients having repeated episodes of angina should receive long acting therapy for chronic prophylaxis. All patients should be administered aspirin. In addition to these they should be given Betablockers, CCB and long acting nitrates. The initial choice of antianginal depends on the patients symptoms.
  15. Betablockers - Beta-blockers are given a class IA recommendation for the initial therapy of patients with prior MI. However, the fewer data for patients without a prior MI have led the American College of Cardiology (ACC)/American Heart Association (AHA) to give beta-blockers a class IB recommendation for these patients. Beta-blockers reduce heart rate and contractility, and myocardial oxygen demand. Reduction in heart rate increases diastolic filling time during which the coronaries receive blood flow. This enhances myocardial tissue perfusion. Beta-blockers can be non-selective (e.g., propranolol), selective (e.g., atenolol and metoprolol), have intrinsic sympathomimetic activity (pindolol, acebutolol) or have alpha-blocking properties (labetolol or carvedilol). All beta-blockers have been studied for the treatment of stable angina. Beta-blockers have been shown to improve survival in patients with previous MI, primary angioplasty for acute ST elevation MI, and heart failure from LV systolic dysfunction. CCBs – Calcium plays a vital role in the electrical excitation and contraction of cardiac and vascular smooth muscle cells. CCB inhibits muscular contraction and therby causes vasodilatation. They reduce heart rate by slowing the conduction through sinoatrial and atrioventricular nodes and they depress caridac contractility. Aspirin – It inhibits the platelet activation through irreversible enzyme antagonism. Antiplatelet (AP) therapy limits the formation of thrombus. When patients are treated with AP agents the risk of MI is reduced. Aspirin blocks prostaglandin synthesis which prevents the formation of thromboxane A2
  16. Ranolazine – It blocks the late phase sodium channels which often remain open during hypoxic or ischemic events. It decreases calcium overload and breaks the cycle of ischemia. ACE Inhibitor – This affect the enzyme that converts AG1 to AG2. ARBs block the vasoconstriction and aldosterone secreting effects of angiotensin. It reduces preload, afterload, and ejection fraction. Nitrates – These cause dilation of the peripheral arteries and veins. When dilated the veins return less blood to the heart thereby reducing the LV filling volume and pressure. This reduces the workload of the heart. Another effect is coronary artery dilation which increases the blood flow and oxygen to the myocardium.
  17. CCB-Leg edema is a common side effect. Nitrates - Nitrates should be avoided within 24 hours of taking phosphodiesterase inhibitors (such as sildenafil) as hypotension may ensue.
  18. As explained above.
  19. Reference - (Fihn et al., 2012) Antiarrhythmics: diltiazem may potentiate the myocardial depression caused by other antiarrhythmic drugs. Beta blockers: these increase the risk of AV block and bradycardia if given with diltiazem. Digoxin: diltiazem increases the plasma concentration of digoxin. Theophylline: diltiazem enhances the effects of theophylline.
  20. Reference - (Fihn et al., 2012)
  21. Beta blockers – As betablockers reduce the flight or fight response , the clinical symptoms may be masked . Therefore patients with diabetes should be closely monitored for serum glucose to avoid severe hypoglycemia. Tyical symptoms of hypoglycemia like tachycardia, tremor, or sweating may be decreased or absent in patients on betablockers. ACE Inhibitors – Renal impairment is seen related to ACE inhibitors. Serum creatinine can be increased and azotemia can be seen in the beginning of the therapy.
  22. As explained in (Arcangelo & Peterson, 2013, Timby & Smith, 2010) Nitrates are contraindicated if patients are taking Viagra and Levitra or tadafil as it can cause severe hypotension. Beta blockers can cause adverse central nervous system effectswhich include drowsiness and depression, the patient must be told to be cautious while driving or doing heavy physical activiites like worlking with a machinery etc,
  23. The patient must be taught when to seek medical attention . The patient can be taught how to use websites that are user friendly and are informative in relation to angina.