Chronic stable angina

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

AtherosclerosisThe 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 VasospasmCoronary 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


(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

revascularization.

Drugs used for Rx of CSA

• Beta Blockerso 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


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


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


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.


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


Pic- A.D.A.M Inc

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.

http://doi.org/10.1016/j.mcna.2010.01.008

http://doi.org/10.1093/eurheartj/ehn321

• 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

http://site.ebrary.com/id/10483324


• 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

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http://doi.org/10.1161/CIR.0b013e318277d6a0

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diagnostics and treatment, Dr. David Gaze (Ed.), ISBN: 978-

953-51-0262-5

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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

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(pp. 168-175). Oxford: Willey-Blackwell.

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pharmacology to evidence-based therapeutics. Hoboken, New

Jersey: John Wiley & Sons, Inc.

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Management of coronary artery disease and its complications.

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Wiley-Blackwell. Retrieved from books.google

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Easy!, 8(6), 9–12.

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• Timby, B. K & Smith, E, N., (2010). Introductory medical-

surgical nursing (10th ed). Philadelphia: Wolters Kluwer

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Health & Medicine

Chronic stable angina