ACE Inhibitors: Congestive Heart Failure: Difference between revisions

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Angiotensin Converting Enzyme (ACE) Inhibitors have become popular by increasing vasodilation and decreasing workload of the heart in patients with CHF.  ACE inhibitors prevent vasoconstriction by suppressing the angiotensin converting enzyme, preventing angiotensin I from converting into angiotensin II. Angiotensin converting enzyme is responsible for converting angiotensin I to angiotensin II which is responsible for vasoconstriction<ref>Montezano AC, Nguyen Dinh Cat A, Rios FJ, Touyz RM. Angiotensin II and vascular injury. ''Current Hypertension Reports''. 2014;16(6):431</ref>. In addition to being a powerful vasoconstrictor, Angiotensin II is also responsible for hypertrophy of vascular tissues and aldosterone secretion.  Hypertrophy of vascular tissues causes vessels to become narrow resulting in increased workload on the heart.  Aldosterone secretion is primarily responsible for water retention which can increase vascular fluid volume also increasing the workload on the heart. Therefore, the inhibition of angiotensin II decreases the amount of pressure in the heart which decreases workload on the heart<ref>Katragadda S, Arora RR. Role of angiotensin-converting enzyme inhibitors in vascular modulation: beyond the hypertensive effects. ''American Journal of Therapeutics.'' 2010;17(1):e11-23</ref>.  Another beneficial effect of ACE inhibitors is that they increase bradykinin levels in the blood by decreasing their breakdown.  Bradykinin is responsible for vasodilation<ref>Regoli D, Plante GE, Gobeil F Jr. Impact of kinins in the treatment of cardiovascular diseases. ''Pharmacology & Therapeutics''. 2012;135(1):94-111.</ref>. Common ACE inhibitors for patients with CHF are benazepril, fosinopril, and captropil<ref name=":0">Ciccone CD. Renin Angiotensin System Inhibitors. ''Pharmacology in rehabilitation.'' 5th ed. Philadelphia: F.A. Davis Company; 2016</ref>. Benazepril and fosinopril is given 10 mg once daily and gradually increased to 20-40 mg per day with a half-life of 10-11 hours and 12 hours respectively.  If given with a diuretic the initial dose should be 5mg<ref>U.S. Food and Drug Administration (FDA). Lotensin (benazepril hydrochloride). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019851s042lbl.pdf</nowiki>. Last accessed 11/29/18.</ref><ref>U.S. Food and Drug Administration (FDA). MONOPRIL (fosinopril sodium tablets). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/19915se5-037_monopril_lbl.pdf</nowiki>. Last accessed 11/29/18.</ref>.Captropil is given 25 mg 3 times daily and has a shorter half-life of 3.3 hours requiring the patient to take it more frequently<ref>U.S. Food and Drug Administration (FDA). CAPOTEN® (Captopril Tablets, USP). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/018343s084lbl.pdf</nowiki>.  Last accessed 11/29/18.</ref>. In general, these medications help decrease cardiac output by limiting vasoconstriction and inhibiting aldosterone secretion promoting vasodilation.   
Angiotensin Converting Enzyme (ACE) Inhibitors have become popular by increasing [[Vasodilators in the Treatment of Hypertension|vasodilation]] and decreasing workload of the heart in patients with [[Heart Failure|Congestive Heart Failure]] (CHF).  ACE inhibitors prevent vasoconstriction by suppressing the angiotensin converting enzyme, preventing angiotensin I from converting into angiotensin II. Angiotensin converting enzyme is responsible for converting angiotensin I to angiotensin II which is responsible for vasoconstriction<ref>Montezano AC, Nguyen Dinh Cat A, Rios FJ, Touyz RM. Angiotensin II and vascular injury. ''Current Hypertension Reports''. 2014;16(6):431</ref>. In addition to being a powerful vasoconstrictor, Angiotensin II is also responsible for hypertrophy of vascular tissues and aldosterone secretion.  Hypertrophy of vascular tissues causes vessels to become narrow resulting in increased workload on the heart.  Aldosterone secretion is primarily responsible for water retention which can increase vascular fluid volume also increasing the workload on the heart. Therefore, the inhibition of angiotensin II decreases the amount of pressure in the heart which decreases workload on the heart<ref>Katragadda S, Arora RR. Role of angiotensin-converting enzyme inhibitors in vascular modulation: beyond the hypertensive effects. ''American Journal of Therapeutics.'' 2010;17(1):e11-23</ref>.  Another beneficial effect of ACE inhibitors is that they increase bradykinin levels in the blood by decreasing their breakdown.  Bradykinin is responsible for vasodilation<ref>Regoli D, Plante GE, Gobeil F Jr. Impact of kinins in the treatment of cardiovascular diseases. ''Pharmacology & Therapeutics''. 2012;135(1):94-111.</ref>. Common ACE inhibitors for patients with CHF are benazepril, fosinopril, and captropil<ref name=":0">Ciccone CD. Renin Angiotensin System Inhibitors. ''Pharmacology in rehabilitation.'' 5th ed. Philadelphia: F.A. Davis Company; 2016</ref>. Benazepril and fosinopril is given 10 mg once daily and gradually increased to 20-40 mg per day with a half-life of 10-11 hours and 12 hours respectively.  If given with a diuretic the initial dose should be 5mg<ref>U.S. Food and Drug Administration (FDA). Lotensin (benazepril hydrochloride). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019851s042lbl.pdf</nowiki>. Last accessed 11/29/18.</ref><ref>U.S. Food and Drug Administration (FDA). MONOPRIL (fosinopril sodium tablets). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/19915se5-037_monopril_lbl.pdf</nowiki>. Last accessed 11/29/18.</ref>.Captropil is given 25 mg 3 times daily and has a shorter half-life of 3.3 hours requiring the patient to take it more frequently<ref>U.S. Food and Drug Administration (FDA). CAPOTEN® (Captopril Tablets, USP). Available online at: <nowiki>https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/018343s084lbl.pdf</nowiki>.  Last accessed 11/29/18.</ref>. In general, these medications help decrease cardiac output by limiting vasoconstriction and inhibiting aldosterone secretion promoting vasodilation.   


A few adverse effects which are rare include hypotension and renal failure because ACE inhibitors are primarily excreted through the kidneys. Some minor side effects may include “angioedema, skin rashes, GI discomfort, and dizziness.” These are normally resolved with adjusting the dosage<ref name=":0" />.
A few adverse effects which are rare include hypotension and renal failure because ACE inhibitors are primarily excreted through the kidneys. Some minor side effects may include “angioedema, skin rashes, GI discomfort, and dizziness.” These are normally resolved with adjusting the dosage<ref name=":0" />.


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Revision as of 18:17, 13 December 2018

Angiotensin Converting Enzyme (ACE) Inhibitors have become popular by increasing vasodilation and decreasing workload of the heart in patients with Congestive Heart Failure (CHF).  ACE inhibitors prevent vasoconstriction by suppressing the angiotensin converting enzyme, preventing angiotensin I from converting into angiotensin II. Angiotensin converting enzyme is responsible for converting angiotensin I to angiotensin II which is responsible for vasoconstriction[1]. In addition to being a powerful vasoconstrictor, Angiotensin II is also responsible for hypertrophy of vascular tissues and aldosterone secretion.  Hypertrophy of vascular tissues causes vessels to become narrow resulting in increased workload on the heart.  Aldosterone secretion is primarily responsible for water retention which can increase vascular fluid volume also increasing the workload on the heart. Therefore, the inhibition of angiotensin II decreases the amount of pressure in the heart which decreases workload on the heart[2].  Another beneficial effect of ACE inhibitors is that they increase bradykinin levels in the blood by decreasing their breakdown.  Bradykinin is responsible for vasodilation[3]. Common ACE inhibitors for patients with CHF are benazepril, fosinopril, and captropil[4]. Benazepril and fosinopril is given 10 mg once daily and gradually increased to 20-40 mg per day with a half-life of 10-11 hours and 12 hours respectively.  If given with a diuretic the initial dose should be 5mg[5][6].Captropil is given 25 mg 3 times daily and has a shorter half-life of 3.3 hours requiring the patient to take it more frequently[7]. In general, these medications help decrease cardiac output by limiting vasoconstriction and inhibiting aldosterone secretion promoting vasodilation. 

A few adverse effects which are rare include hypotension and renal failure because ACE inhibitors are primarily excreted through the kidneys. Some minor side effects may include “angioedema, skin rashes, GI discomfort, and dizziness.” These are normally resolved with adjusting the dosage[4].

  1. ↑ Montezano AC, Nguyen Dinh Cat A, Rios FJ, Touyz RM. Angiotensin II and vascular injury. Current Hypertension Reports. 2014;16(6):431
  2. ↑ Katragadda S, Arora RR. Role of angiotensin-converting enzyme inhibitors in vascular modulation: beyond the hypertensive effects. American Journal of Therapeutics. 2010;17(1):e11-23
  3. ↑ Regoli D, Plante GE, Gobeil F Jr. Impact of kinins in the treatment of cardiovascular diseases. Pharmacology & Therapeutics. 2012;135(1):94-111.
  4. ↑ 4.0 4.1 Ciccone CD. Renin Angiotensin System Inhibitors. Pharmacology in rehabilitation. 5th ed. Philadelphia: F.A. Davis Company; 2016
  5. ↑ U.S. Food and Drug Administration (FDA). Lotensin (benazepril hydrochloride). Available online at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019851s042lbl.pdf. Last accessed 11/29/18.
  6. ↑ U.S. Food and Drug Administration (FDA). MONOPRIL (fosinopril sodium tablets). Available online at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/19915se5-037_monopril_lbl.pdf. Last accessed 11/29/18.
  7. ↑ U.S. Food and Drug Administration (FDA). CAPOTEN® (Captopril Tablets, USP). Available online at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/018343s084lbl.pdf.  Last accessed 11/29/18.
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