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Antianginal drugs – how do they work?

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Antianginal drugs – how do they work?

Angina is severe chest pain attributable to reduced blood flow to the center. Antianginal drugs include a gaggle of medicine that either reduce the consumption of oxygen in the center muscle or increase the availability of oxygen to the center muscle to forestall the symptoms of angina. These classes of medicine include antianginal drugs (ranolazine), beta-blockers, calcium channel blockers, and nitrates.
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How do they work?

Angina occurs when the coronary arteries (the center’s primary source of oxygen) supply the center muscle with insufficient oxygen. This increases the load on the center by increasing heart rate, preload (the amount of blood within the ventricle at the top of diastole), afterload (the pressure within the arteries leaving the ventricle), and the contractile force of the center muscle.
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Antianginal medications relieve angina by reducing a number of of those 4 aspects. This diagram summarizes the results of antianginal drugs on the cardiovascular system. AND

Approved antianginal medications

(Lippincott Williams and Wilkins, 2022)
: chronic angina Ranolazine (Ranexa) The mechanism of motion and antianginal effect haven’t been determined.
moderate to severe angina pectoris Atenolol
Bisoprolol fumarate
Metoprolol
Nadolol
Propranolol hydrochloride
Prevent catecholamines from stimulating B1 adrenergic receptors, which causes a discount in heart rate, blood pressure and heart muscle contraction.
exercise-induced angina and Printzmetal’s angina Amlodipine besilate
Diltiazem hydrochloride
Nicardipine hydrochloride
Nifedipine
Verapamil hydrochloride
They inhibit the flow of calcium through muscle cells, dilating coronary arteries, slowing the center rate and increasing the availability of oxygen to the center muscle. They also dilate peripheral arteries, which reduces systemic vascular resistance (afterload).
recurrent angina, acute angina, unstable angina Isosorbide (dinitrate, mononitrate)
Nitroglycerin
It dilates veins, arteries and coronary arteries by relaxing vascular smooth muscles, leading to reduced afterload and left ventricular end-diastolic pressure (preload) and increased blood flow through the lateral coronary vessels.

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Contraindications

Ranolazine use is contraindicated in case of strong CYP3A inhibitors and inducers and in patients with clinically significant hepatic impairment (Facts and Comparisons, 2022).
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Beta-blockers are contraindicated in patients with heart block greater than first degree; cardiogenic shock; decompensated, overt or uncontrolled heart failure; bronchial asthma; and sick sinus syndrome (apart from patients with a functioning everlasting pacemaker) (Facts and comparisons, 2020).
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Calcium channel antagonists are contraindicated in patients taking beta-blockers or in patients with heart failure with reduced ejection fraction, sick sinus syndrome, or second- or third-degree atrioventricular block.
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Nitrates are contraindicated in the next cases (Kannam and Gersh, 2021):

  • Patients who’ve taken sildenafil or vardenafil inside 24 hours or tadalafil inside 48 hours as this may occasionally cause severe hypotension.
  • Patients with hypertrophic cardiomyopathy in whom nitrates may increase outflow tract obstruction.
  • Patients with suspected right ventricular infarction as this may occasionally cause hypotension.

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Full information and dosing will be present in the leaflet that comes with each medicine or within the Nursing2022 Medicines Manual + medicines updates.
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Facts and Comparisons (2022, May 4). Ranolazine orally. . https://fco.factsandcomparisons.com/lco/action/doc/retrieve/docid/fc_dfc/5548914?cesid=4LdUlCXOPQN

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Facts and comparisons. (2020, September 17). Beta-adrenergic blocking agents (beta-blockers) https://online.factsandcomparisons.com/lco/action/doc/retrieve/docid/fc_dfc/5545850

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Kannam, J. P., & Gersh, B. J. (2021, March 31). Nitrates within the treatment of chronic coronary syndrome. . https://www.uptodate.com/contents/nitrates-in-the-management-of-chronic-coronary-syndrome

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Lippincott Williams and Wilkins (2022). . Wolters Kluwer.

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