Adverse Effects
Most Common
Dry Cough: Commonly, patients on ACE inhibitors have reported dry cough between the one week of initiation and up to six months. Some sources cite up to one year after initiation. Discontinuing therapy usually resolves the cough 1 to 4 days after, but it can be prolonged for up to a month.[15] The concern for dry cough with therapy initiation is a decrease in the patient’s medication adherence. Additionally, there is an increased propensity to develop bronchospasm in these patients.[16]
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ACE metabolizes bradykinin and other local molecules. Inhibiting ACE in the lung increases the concentration of kinins, causing bronchial irritation.[17] After discontinuation of ACE inhibitor therapy, an angiotensin receptor blocker (ARB) can be initiated as an alternate therapy. ARBs have a lower incidence of cough recurrence than reinitiating ACE inhibitor therapy.[18] If cough recurs on ARB therapy, switch to a different drug class entirely.
Angioedema: Angioedema is a rare but potentially life-threatening side effect of ACE inhibitor use. Angioedema is an adverse drug reaction characterized by swelling of the face, lips, and upper airway in an episodic nature. The inflammation creates difficulty in the patient’s ability to maintain an airway; therefore, endotracheal intubation is necessary to secure the airway. The mechanism of angioedema is thought to be through an extensive accumulation of bradykinins in select individuals. Bradykinin induces prominent vasodilation and plasma extravasation into the local tissue. Therefore, the primary treatment of ACE inhibitor-induced angioedema is the discontinuation of ACE inhibitor therapy. It is also suggested to avoid ACE inhibitor therapy in individuals with hereditary angioedema or a history of angioedema episodes. Ghouse J. et al. conducted a genome-wide association study on patients who developed ACE inhibitor-related angioedema.[19] The investigators found variants located near the bradykinin receptor B2 gene.
Hyperkalemia: Hyperkalemia from ACE inhibitors directly results from its mechanism of action. The blockade of angiotensin II prevents the downstream secretion of aldosterone. Aldosterone causes reabsorption of sodium and, subsequently, water. Consequently, protons and potassium get secreted into the urine. Without potassium secretion through aldosterone, potassium can easily increase in patients on ACE inhibitors.[20] Co-morbidities that decrease kidney function or medications that cause potassium retention can increase the risk of hyperkalemia.
Increased BUN and creatinine: A slight reduction of glomerular filtration rate (GFR) is common when initiating therapy. Patients with heart failure, chronic kidney disease, and bilateral renal artery stenosis with poor renal perfusion can further reduce GFR, which mandates discontinuation of ACE-Inhibitor therapy.[21]
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Hypotension: Hypotension can cause intolerance to therapy leading to discontinuation in a small population of patients, which is more common in patients with increased renin baseline concentrations. Allowing the repletion of fluids and discontinuing diuretic medication before therapy can minimize hypotensive episodes.[22]
Dizziness: Dizziness is a common adverse drug reaction of ACE inhibitor therapy that can be mitigated by adequate volume status and avoiding concomitant diuretic therapy.[4][23]
Post-marketing surveillance: Significant adverse events are reported in less than one percent population in post-marketing surveillance. These adverse drug reactions include anaphylactoid reactions, cardiac arrest, cutaneous pseudolymphoma, eosinophilic pneumonitis, hepatic necrosis, hyponatremia, intestinal angioedema, malignant neoplasm of the lung, pulmonary embolism, systemic lupus erythematosus, Steven-Johnson Syndrome, toxic epidermal necrolysis, and transient ischemic attack.
Khera R. et al. found no association between ACE inhibitors and angiotensin II receptor blockers in COVID-19 hospitalization and mortality.[24]
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This post was last modified on November 16, 2024 5:15 am