By: Hernan Rincon-Choles, MD, MS
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Inhibition of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) is widely used in the treatment of heart failure, hypertension, chronic kidney disease and coronary artery disease with left ventricular dysfunction.
Are ACE Inhibitors better than ARBs?
ACE inhibitors have been the cornerstone of treatment for patients with heart failure with reduced ejection fraction (HFrEF), in whom their use is associated with reduced rates of morbidity and death.2,3The use of ARBs in these patients is also associated with decreased rates of morbidity and death4,5; however, in early comparisons, ACE inhibitors were deemed more effective in decreasing the incidence of myocardial infarction, cardiovascular death, and all-cause mortality in patients with hypertension, diabetes, and increased cardiovascular risk,6and all-cause mortality in patients with HFrEF.7
This presumed superiority of ACE inhibitors over ARBs was thought to be a result of a greater vasodilatory effect caused by inhibiting the degradation of bradykinin and leading to increased levels of nitric oxide and vasoactive prostaglandins.8Another proposed explanation was that because ARBs block angiotensin II AT1 receptors but not AT2 receptors, the increased stimulation of markedly upregulated AT2 receptors in atheromatous plaques in response to elevated serum levels of angiotensin II was deleterious.6Therefore, ACE inhibitors have been recommended as first-line therapy by most guidelines, whereas ARBs are recommended as second-line therapy, when patients are unable to tolerate ACE inhibitors.
Nevertheless, the much debated differences in outcomes between ACE inhibitors and ARBs do not seem to be real and may have originated from a generational gap in the trials.
The ACE inhibitor trials were performed a decade earlier than the ARB trials. Indirect comparisons of their respective placebo-controlled trials assumed that the placebo groups used for comparison in the 2 sets of trials were similar.9,10Actually, the rate of cardiovascular disease decreased nearly 50% between the decades of 1990 to 2000 and 2000 to 2010, the likely result of aggressive primary and secondary prevention strategies in clinical practice, including revascularization and lipid-lowering therapy.10
In fact, a meta-regression analysis showed that the differences between ACE inhibitors and ARBs compared with placebo were due to higher event rates in the placebo groups in the ACE inhibitor trials than in the ARB trials for the outcomes of death, cardiovascular death, and myocardial infarction.11Sensitivity analyses restricted to trials published after 2000 to control for this generational gap showed similar efficacy with ACE inhibitors vs placebo and with ARBs vs placebo for all clinical outcomes.11Moreover, recent studies have shown that ARBs produce a greater decrease in cardiovascular events than ACE inhibitors, especially in patients with established cardiovascular disease.12,13
An advantage of ARBs over ACE inhibitors is fewer adverse effects: in general, ARBs are better tolerated than ACE inhibitors.14There are also ethnic differences in the risks of adverse reactions to these medications. African Americans have a higher risk of developing angioedema with ACE inhibitors compared with the rest of the US population, and Chinese Americans have a higher risk than whites of developing cough with ACE inhibitors.9,15
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How I manage these medications
In my medical practice, I try to make sure patients with HFrEF, hypertension, chronic kidney disease, and coronary artery disease with left ventricular dysfunction receive an inhibitor of the renin-angiotensin-aldosterone system.
I prefer ARBs because patients tolerate them better. I continue ACE inhibitors in patients who are already taking them without adverse effects, and I change to ARBs in patients who later become unable to tolerate ACE inhibitors.
Most antihypertensive agents increase the risk of incident gout, except for calcium channel blockers and losartan.16Losartan is the only ARB with a uricosuric effect, although a mild one,17,18due to inhibition of the urate transporter 1,19and therefore I prefer to use it instead of other ARBs or ACE inhibitors in patients who have a concomitant diagnosis of gout.
The addition of beta-blockers and mineralocorticoid receptor blockers to ACE inhibitors or ARBs is associated with a further decrease in the mortality risk for patients with HFrEF,20–22but some patients cannot tolerate these combinations or optimized doses of these medications because of worsening hypotension or increased risk of developing acute kidney injury or hyperkalemia.
In most cases, I try not to combine ACE inhibitors with ARBs. This combination may be useful in nondiabetic patients with proteinuria refractory to maximum treatment with 1 class of these agents, but it is associated with an increased risk of hyperkalemia or acute kidney injury in patients with diabetic nephropathy without improving rates of the clinical outcomes of death or cardiovascular events.23I prefer adding a daily low dose of a mineralocorticoid receptor blocker to an ACE inhibitor or an ARB, which is more effective in controlling refractory proteinuria.24This regimen is associated with decreased rates of mortality, cardiovascular mortality, and hospitalization for heart failure in patients with HFrEF,22although it can lead to a higher frequency of hyperkalemia,25and patients on it require frequent dietary education and monitoring of serum potassium.
I avoid combining direct renin inhibitors with ACE inhibitors or ARBs, since this combination has been contraindicated by the US Food and Drug Administration due to lack of reduction in target-organ damage and an associated increased risk of hypotension, hyperkalemia, and kidney failure, and a slight increase in the risk of stroke or death in patients with diabetic nephropathy.26
Valsartan-sacubitril
Neprilysin is a membrane-bound endopeptidase that degrades vasoactive peptides, including B-type natriuretic peptide and atrial natriuretic peptide.27The combination of the ARB valsartan and the neprilysin inhibitor sacubitril is associated with a 20% further decrease in rates of cardiovascular mortality and hospitalization and a 16% decrease in total mortality for patients with HFrEF compared with an ACE inhibitor, although there can also be more hypotension and angioedema with the combination.27,28
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Very importantly, an ACE inhibitor cannot be used together with valsartan-sacubitril due to increased risk of angioedema and cough. I change ACE inhibitors or ARBs to valsartan-sacubitril in patients with HFrEF who still have symptoms of heart failure. Interestingly, a network meta-analysis showed that the combination of valsartan-sacubitril plus a mineralocorticoid receptor blocker and a beta-blocker resulted in the greatest mortality reduction in patients with HFrEF.7A word of caution, though: one can also expect an increased risk of hypotension, hyperkalemia, and kidney failure.
Monitoring
It is crucial to monitor blood pressure, serum potassium, and renal function in patients receiving ACE inhibitors, ARBs, mineralocorticoid receptor blockers, valsartan-sacubitril, or combinations of these medications, particularly in elderly patients, who are more susceptible to complications. I use a multidisciplinary approach in my clinic: a patient educator, dietitian, pharmacist, and advanced practice nurse play key roles in educating and monitoring patients for the development of possible complications from this therapy or interactions with other medications.
A recent population-based cohort study found an association of ACE inhibitor use with a 14% relative increase in lung cancer incidence after 10 years of use, compared with ARBs,29but this may not represent a large absolute risk (calculated number needed to harm of 2,970 after 10 years of ACE inhibitor use) and should be balanced against the improvement in morbidity and mortality gained with use of an ACE inhibitor. Additional studies with long-term follow-up are needed to investigate this possible association.
Takeaway points
- Blockade of the renin-angiotensin-aldosterone system is a cornerstone in the therapy of cardiovascular disease.
- ARBs are as effective as ACE inhibitors and have a better tolerability profile.
- ACE inhibitors cause more angioedema in African Americans and more cough in Chinese Americans than in the rest of the population.
- ACE inhibitors and most ARBs (except for losartan) increase the risk of gout.
- The combination of beta-blockers and mineralocorticoid receptor blockers with ACE inhibitors or ARBs and, lately, the use of the valsartan-sacubitril combination have been increasingly beneficial for patients with HFrEF.
This article was adapted from Cleveland Clinic Journal of Medicine. 2019 September;86(9):608-611
About the Author
Dr. Rincon-Choles practices in the Department of Nephrology and Hypertension within Cleveland Clinic Glickman Urological and Kidney Institute. He is also Assistant Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University and Medical Director of the East Cleveland Dialysis Center, Ohio Renal Care Group.
References
- Momoniat T, Ilyas D, Bhandari S. ACE inhibitors and ARBs: managing potassium and renal function. Cleve Clin J Med 2019; 86(9):601– 607. doi:10.3949/ccjm.86a.18024
- CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987; 316(23):1429–1435. doi:10.1056/NEJM198706043162301
- SOLVD Investigators; Yusuf S, Pitt B, Davis CE, Hood WB, Cohn JN. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325(5):293–302. doi:10.1056/NEJM199108013250501
- Young JB, Dunlap ME, Pfeffer MA, et al; Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) Investigators and Committees. Mortality and morbidity reduction with candesartan in patients with chronic heart failure and left ventricular systolic dysfunction: results of the CHARM low-left ventricular ejection fraction trials. Circulation 2004; 110(17):2618–2626. doi:10.1161/01.CIR.0000146819.43235.A9
- Cohn JN, Tognoni G; Valsartan Heart Failure Trial Investigators. A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure. N Engl J Med 2001; 345(23):1667–1675. doi:10.1056/NEJMoa010713
- Straus MH, Hall AS. Angiotensin receptor blockers do not reduce risk of myocardial infarction, cardiovascular death, or total mortality: further evidence for the ARB-MI paradox. Circulation 2017; 135(22):2088–2090. doi:10.1161/CIRCULATIONAHA.117.026112
- Burnett H, Earley A, Voors AA, et al. Thirty years of evidence on the efficacy of drug treatments for chronic heart failure with reduced ejection fraction. A network meta-analysis. Circ Heart Fail 2017; 10(1). pii:e003529. doi:10.1161/CIRCHEARTFAILURE.116.003529
- Chobanian AV. Editorial: angiotensin inhibition. N Engl J Med 1974; 291(16):844–845. doi:10.1056/NEJM197410172911611
- Messerli FH, Bangalore S, Bavishi C, Rimoldi SF. Angiotensin-converting enzyme inhibitors in hypertension: to use or not to use? J Am Coll Cardiol 2018; 71(13):1474–1482. doi:10.1016/j.jacc.2018.01.058
- Messerli FH, Bangalore S. Angiotensin receptor blockers reduce cardiovascular events, including the risk of myocardial infarction. Circulation 2017; 135(22):2085–2087. doi:10.1161/CIRCULATIONAHA.116.025950 11. Bangalore S, Fakheri R, Toklu B, Ogedegbe G, Weintraub H, Messerli FH. Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in patients without heart failure? Insights from 254,301 patients from randomized trials. Mayo Clin Proc 2016; 91(1):51–60. doi:10.1016/j.mayocp.2015.10.019
- Potier L, Roussel R, Elbez Y, et al; REACH Registry Investigators. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk. Heart 2017; 103(17):1339–1346. doi:10.1136/heartjnl-2016-310705
- Bangalore S, Kumar S, Wetterslev J, Messerli FH. Angiotensin receptor blockers and risk of myocardial infarction: meta-analyses and trial sequential analyses of 147,020 patients from randomized trials. BMJ 2011; 342:d2234. doi:10.1136/bmj.d2234
- Saglimbene V, Palmer SC, Ruospo M, et al; Long-Term Impact of RAS Inhibition on Cardiorenal Outcomes (LIRICO) Investigators. The long-term impact of renin-angiotensin system (RAS) inhibition on cardiorenal outcomes (LIRICO): a randomized, controlled trial. J Am Soc Nephrol 2018; 29(12):2890–2899. doi:10.1681/ASN.2018040443
- McDowell SE, Coleman JJ, Ferner RE. Systematic review and metaanalysis of ethnic differences in risks of adverse reactions to drugs used in cardiovascular medicine. BMJ 2006; 332(7551):1177–1181. doi:10.1136/bmj.38803.528113.55
- Choi HK, Soriano LC, Zhang Y, Rodríguez LA. Antihypertensive drugs and risk of incident gout among patients with hypertension: population based case-control study. BMJ 2012; 344:d8190. doi:10.1136/bmj.d8190
- Wolff ML, Cruz JL, Vanderman AJ, Brown JN. The effect of angiotensin II receptor blockers on hyperuricemia. Ther Adv Chronic Dis 2015; 6(6):339–346. doi:10.1177/2040622315596119 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 86 • NUMBER 9 SEPTEMBER 2019 611 RINCON-CHOLES
- Schmidt A, Gruber U, Böhmig G, Köller E, Mayer G. The effect of ACE inhibitor and angiotensin II receptor antagonist therapy on serum uric acid levels and potassium homeostasis in hypertensive renal transplant recipients treated with CsA. Nephrol Dial Transplant 2001; 16(5):1034–1037. pmid:11328912
- Hamada T, Ichida K, Hosoyamada M, et al. Uricosuric action of losartan via the inhibition of urate transporter 1 (URAT1) in hypertensive patients. Am J Hypertens 2008; 21(10):1157–1162. doi:10.1038/ajh.2008.245 20. Packer M, Coats AJ, Fowler MB, et al; Carvedilol Prospective Randomized Cumulative Survival Study Group. Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med 2001; 344(22):1651–1658. doi:10.1056/NEJM200105313442201
- Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341(10):709–717. doi:10.1056/NEJM199909023411001
- Zannad F, McMurray JJ, Krum H, et al; EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011;364(1):11-21. doi: 10.1056/NEJMoa1009492
- Fried LF, Emanuele N, Zhang JH, et al. Combined angiotensin inhibition for the treatment of diabetic nephropathy. N Engl J Med 2011; 364(1):11–21. doi:10.1056/NEJMoa1009492
- Chrysostomou A, Pedagogos E, MacGregor L, Becker GJ. Doubleblind, placebo-controlled study on the effect of the aldosterone receptor antagonist spironolactone in patients who have persistent proteinuria and are on long-term angiotensin-converting enzyme inhibitor therapy, with or without an angiotensin II receptor blocker. Clin J Am Soc Nephrol 2006; 1(2):256–262. doi:10.2215/CJN.01040905
- Abbas S, Ihle P, Harder S, Schubert I. Risk of hyperkalemia and combined use of spironolactone and long-term ACE inhibitor/angiotensin receptor blocker therapy in heart failure using real-life data: a population- and insurance-based cohort. Pharmacoepidemiol Drug Saf 2015; 24(4):406–413. doi:10.1002/pds.3748
- US Food and Drug Administration. FDA drug safety communication: new warning and contraindication for blood pressure medicines containing aliskiren (Tekturna). www.fda.gov/Drugs/DrugSafety/ ucm300889.htm. Accessed March 8, 2019.
- Jhund PS, McMurray JJ. The neprilysin pathway in heart failure: a review and guide on the use of sacubitril/valsartan. Heart 2016; 102(17):1342–1347. doi:10.1136/heartjnl-2014-306775
- McMurray JJ, Packer M, Desai AS, et al; PARADIGM-HF Investigators and Committees. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 2014; 371(11):993–1004. doi:10.1056/NEJMoa1409077
- Hicks BM, Filion KB, Yin H, Sakr L, Udell JA, Azoulay L. Angiotensin converting enzyme inhibitors and risk of lung cancer: population based cohort study. BMJ 2018; 363:k4209. doi:10.1136/bmj.k4209
- McMurray JJ, Packer M, Desai AS, et al; PARADIGM-HF Investigators and Committees. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 2014; 371(11):993–1004. doi:10.1056/NEJMoa1409077
- Hicks BM, Filion KB, Yin H, Sakr L, Udell JA, Azoulay L. Angiotensin converting enzyme inhibitors and risk of lung cancer: population based cohort study. BMJ 2018; 363:k4209. doi:10.1136/bmj.k4209
FAQs
Can you prescribe ACE inhibitor and ARB together? ›
Avoid prescribing an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) for patients at high risk of vascular events or renal dysfunction. The combination does not reduce poor outcomes, and leads to more adverse drug-related events than an ACE inhibitor or ARB alone.
When are ACE inhibitors and ARBs used together? ›Accordingly, blockade of the angiotensin receptor can further decrease angiotensin II–induced vasoconstriction. Two indications for combination therapy with ACE inhibitors and ARBs are prominently cited in the literature: heart failure and CKD with proteinuria.
What labs should be monitored with ACE inhibitors? ›When you start on an ACE inhibitor, you will need blood tests to monitor your kidney function and potassium levels. Be aware: If you take an ACE inhibitor, keep a written log of your heart rate (pulse) and blood pressure.
Why are ACE inhibitors and ARBs sometimes given together? ›Data synthesis: ACE inhibitors provide incomplete blockade of the renin-angiotensin system, sometimes leading to loss of blood pressure control. Addition of ARBs may in theory further reduce blood pressure.
Can losartan and lisinopril be taken together? ›Should I take lisinopril and losartan together? No. Although some blood pressure medications are used in combination (such as losartan or lisinopril in combination with a diuretic), lisinopril and losartan should not be taken together.
How do I switch from lisinopril to losartan? ›switching from lisinopril to losartan - YouTube
Why do ACE and ARBs cause hyperkalemia? ›Main mechanisms contributing to hyperkalemia with ACEi/ARB include decreased aldosterone concentrations, decreased delivery of sodium to the distal nephron, abnormal collecting tubule function, and excessive potassium intake (Table 1).
Can I switch from ACE to ARB? ›Therefore switching from ACE inhibitors to ARB might be beneficial in patients at risk or with COVID-19 in prevention of such sequelae when they are already on therapy affecting the Renin-Angiotensin System.
Which is safer ARB or ACE inhibitor? ›“Our study largely confirmed that both antihypertensive drug classes are similarly effective, though ARBs may be a little safer than ACE inhibitors,” Hripcsak says.
Do ARBs increase creatinine? ›Many such patients experience a transient rise in serum creatinine levels after treatment with an ACEI or angiotensin receptor blocker (ARB) is started or after blood pressure is adequately reduced. A rise in the serum creatinine level consequently leads to physician reticence to stay the course with a given therapy.
When should I check potassium after ACE inhibitors? ›
Clinical practice guidelines recommend routine kidney function and serum potassium testing within 30 days of initiating ACE (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker therapy.
Do ARBs increase potassium? ›ACEIs, ARBs, and DRIs increase serum potassium levels by interfering with angiotensin II-mediated stimulation of aldosterone secretion from the adrenal gland and by decreasing renal blood flow and GFR in special patient populations.
What are some side effects of ACE inhibitors and ARBs? ›- Cough.
- Elevated blood potassium levels.
- Low blood pressure,
- dizziness.
- Headache.
- Drowsiness.
- Weakness.
- Abnormal taste (metallic or salty taste)
In patients with higher uric acid levels, the ARB of choice should be losartan. Irbesartan may also have a protective effect at therapeutic doses. Telmisartan is a neutral agent regarding uric acid excretion, while candesartan, olmesartan and valsartan may increase the risk of hyperuricemia.
What happens when ACE inhibitors and ARBs are stopped because of hyperkalemia? ›Stopping ACE Inhibitors, ARBs After Hyperkalemia Episode Ups Death Risk in CKD. Patients with CKD who discontinued ACE inhibitors or angiotensin receptor blockers after a hyperkalemia episode had a 2.6-fold increased risk of all-cause mortality compared with patients who continued taking the drugs.
What is the first choice drug for hypertension? ›First-line (first choice) options include these blood pressure medication names: Thiazide diuretics, calcium channel blockers and ― for people who have kidney disease and heart failure ― angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs).
Does losartan lower systolic or diastolic pressure? ›Results: All doses of losartan potassium significantly decreased mean systolic 24-h ambulatory blood pressure (range -9.4 to -14.2 mmHg; P < or = 0.01) and mean diastolic 24-h ambulatory blood pressure (range -5.6 to -9.0 mmHg; P < or = 0.01) compared with placebo.
Is it better to take losartan in the morning or in the evening? ›Take losartan tablets once a day. Your doctor may suggest that you take your first dose before bedtime, because it can make you feel dizzy. After your first dose, you can take losartan at any time of day. But try to take it at the same time every day.
Which is safer losartan or lisinopril? ›In general, losartan causes fewer side effects than does lisinopril (losartan doesn't cause a nagging cough and has a lower risk for facial swelling).
Is losartan better for kidneys than lisinopril? ›Cozaar (Losartan) is a good blood pressure-lowering medicine that protects kidney function like an ACE inhibitor, but with fewer side effects. Lowers blood pressure. Zestril (lisinopril) is a good blood pressure-lowering medicine that protects kidney function.
What is the safest high blood pressure medication? ›
Safe medications to use include methyldopa and potentially some diuretics and beta-blockers, including labetalol.
Can ARBs cause kidney damage? ›We reviewed the literature along these lines and submit that ACEIs and ARBs often cause unrecognized significant worsening renal failure in CKD patients, sometimes irreversible, and that more caution is required regarding their use, especially in the older hypertensive patients, with likely ischemic hypertensive ...
When should I check renal function after starting ACE inhibitors? ›Adverse effects
Renal impairment — check renal function and electrolytes before starting and 1–2 weeks after starting an ACE inhibitor, after each increase in dose, and regularly throughout treatment.
The BP lowering effect of ARBs is modest and similar to ACE inhibitors as a class; the magnitude of average trough BP lowering for ARBs at maximum recommended doses and above is ‐8/‐5 mmHg. Furthermore, 60 to 70% of this trough BP lowering effect occurs with recommended starting doses.
Who should not take ARBs? ›Although doctors often prescribe ARBs to help protect the kidneys, people with certain kidney conditions — like narrowing of the arteries feeding the kidneys (renal artery stenosis) or very poor kidney function — shouldn't take ARBs.
When Should ACE inhibitors not be used? ›The following are people who shouldn't take ACE inhibitors: Pregnant women. An ACE inhibitor might hurt the baby during the last six months of pregnancy. If you were already taking an ACE inhibitor and stop taking it during the first three months of pregnancy, the risk to your baby is very low.
Why is ACE first line for hypertension? ›ACE (angiotensin-converting enzyme) inhibitors and angiotensin receptor blockers (ARBs) effectively lower blood pressure (BP) through inhibition of the renin-angiotensin system and are equally recommended as first-line medications in the treatment of hypertension.
What is the most common side effect of ARBs? ›- Dizziness, lightheadedness, or faintness upon rising, This side effect may be strongest after the first dose, especially if you have been taking a diuretic (water pill). ...
- Physical problems. ...
- Confusion. ...
- Severe vomiting or diarrhea.
Patients taking angiotensin receptor blockers (ARBs) for the treatment of high blood pressure experienced fewer side effects than those taking angiotensin-converting enzyme (ACE) inhibitors, according to a new study published in Hypertension.
Can ARBs cause liver damage? ›As a class, the ARBs have been associated with rare instances of acute liver injury that is usually self limited in duration, but varies in clinical expression, being usually hepatocellular but occasional cholestatic in nature.
Are ARBs safe for kidneys? ›
Background: Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-II receptor blockers (ARBs) are considered to be equally effective for patients with diabetic kidney disease, but renal and not mortality outcomes have usually been considered.
Do ARBs lower GFR? ›Most clinical studies have also shown that the GFR remains stable when an ARB is administered. However, a significant reduction in GFR by treatment with an ARB has often been seen in patients with severe renal disease [18, 19].
Why does creatinine increase after starting ACE inhibitors? ›The rise in serum creatinine values usually begins a few days after beginning therapy with an ACE inhibitor or an ARB, as angiotensin II levels are rapidly reduced or blocked from binding. This results in efferent arteriolar dilatation and decreased effective GFR.
Do ARBs cause less hyperkalemia than ACE inhibitors? ›Hyperkalemia is more common with ARBs than ACEIs. ARB use, when compared to ACEI use, may significantly and independently be associated with increased odds of hyperkalemia.
How much do ACE inhibitors increase potassium? ›Previous studies demonstrate that ACE inhibitors generally raise serum potassium levels an average of 15% above baseline after a one-month period2, 3, 4, 5, 6, 7, 8, 9. Conversely, ARBs raise serum potassium levels an average of 5% above baseline over the same period10, 11, 12.
Does losartan cause hyperkalemia or hypokalemia? ›Losartan should be used with caution patients with hyperkalemia. Although hyperkalemia is infrequent with losartan, angiotensin II blockade can elevate serum potassium concentrations by blocking aldosterone secretion and could worsen pre-existing hyperkalemia.
Do ARBs cause water retention? ›ARBs reduce the action of the hormone angiotensin II. This hormone has a powerful constricting effect on blood vessels, increasing blood pressure. Angiotensin II also stimulates salt and water retention in the body, which further increases blood pressure.
Do ARBs affect heart rate? ›ARB increased both the day/night HR ratio (1.17 ± 0.09 to 1.21 ± 0.13; P = 0.04) and HRV (10.6 ± 2.9 to 11.7 ± 4.2; P = 0.04), which were lower when baseline renal function deteriorated. Conclusion: The present study indicates that there exists a close correlation in circadian rhythms between HR and MAP in CKD.
Which ARB is best for CKD? ›Angiotensin receptor blockers (ARBs) are better tolerated than angiotensin-converting enzyme inhibitors and, thus, may be a more practical therapeutic option. Clinical studies have demonstrated the efficacy of irbesartan, losartan, telmisartan and valsartan in the management of CKD.
Why ACE inhibitors and ARBs should not be combined? ›Avoid prescribing an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) for patients at high risk of vascular events or renal dysfunction. The combination does not reduce poor outcomes, and leads to more adverse drug-related events than an ACE inhibitor or ARB alone.
What important teaching points should be addressed for patients receiving antihypertensive drugs? ›
Educate patient on importance of healthy lifestyle choices which include regular exercise, weight loss, smoking cessation, and low-sodium diet to maximize the effect of antihypertensive therapy. Administer drug on empty stomach one hour before or two hours after meal to ensure optimum drug absorption.
Is ACE or ARB better for hypertension? ›Choose ARBs Over ACE Inhibitors for First-line Hypertension Treatment, Large New Analysis Suggests. For first-line treatment of hypertension, angiotensin receptor blockers (ARBs) work as well as angiotensin-converting enzyme (ACE) inhibitors but are safer, according to a head-to-head analysis of the 2 drug classes.
Can you take ACE inhibitor and ARB together? ›However, we maintain that based on the data from ValHeFT and CHARM-Added, ARBs can be safely combined with ACE-inhibitors in patients with heart failure without serious risk of renal failure or hyperkalemia and regardless of background beta blocker therapy.
Why are ACE inhibitors and ARBs sometimes given together? ›Data synthesis: ACE inhibitors provide incomplete blockade of the renin-angiotensin system, sometimes leading to loss of blood pressure control. Addition of ARBs may in theory further reduce blood pressure.
Which ARB has the longest half-life? ›Telmisartan is the longest acting angiotensin II receptor blocker in the market with a mean half-life of 24 hours.
Do ARBs increase creatinine? ›Many such patients experience a transient rise in serum creatinine levels after treatment with an ACEI or angiotensin receptor blocker (ARB) is started or after blood pressure is adequately reduced. A rise in the serum creatinine level consequently leads to physician reticence to stay the course with a given therapy.
Why do ACE and ARBs cause hyperkalemia? ›Main mechanisms contributing to hyperkalemia with ACEi/ARB include decreased aldosterone concentrations, decreased delivery of sodium to the distal nephron, abnormal collecting tubule function, and excessive potassium intake (Table 1).
How do ACE and ARBs protect kidneys? ›ACE and ARB medicines lower the pressure inside of the kidneys to a better level. They are especially helpful for kidneys that are letting protein leak into the urine. Kidneys are not supposed to release protein into the urine.
Can ramipril and losartan be taken together? ›A fixed dose combination of losartan and ramipril showed good to excellent efficacy response in 98% of patients. The combination of losartan and ramipril is effective in reducing blood pressure levels in patients with both hypertension and diabetes.
Can an ARB be given to patients who have had angioedema on an ACE inhibitor? ›Angioedema related to ARBs is reported to be less severe and occurs earlier compared to angioedema that develops during ACEI therapy. Conclusions: ARBs may be an alternative for patients who develop angioedema while using an ACEI but should be reserved for patients with high therapeutic need for angiotensin inhibition.
Can you take ARB and beta blocker together? ›
An ACE inhibitor or ARB is likely to be less effective in patients treated with a beta blocker since beta blockers reduce renin secretion and therefore angiotensin II formation [110], and a beta blocker should be used with caution in combination with verapamil and to a lesser degree diltiazem.
Why would you not give an ACE ARB and potassium sparing diuretic like spironolactone all together? ›Potassium sparing diuretics
Amiloride acts on the distal nephron, while spironolactone is a competitive aldosterone inhibitor. Potassium sparing diuretics have generally been avoided in patients receiving ACE inhibitors, owing to the potential risk of hyperkalaemia.
Some medicines can affect the way losartan works. Tell your doctor if you're taking: other medicines to help lower your blood pressure, including aliskiren, enalapril, captopril, lisinopril or ramipril. painkillers such as ibuprofen, naproxen, diclofenac, celecoxib or etoricoxib.
Is it better to take losartan at night or morning? ›Take losartan tablets once a day. Your doctor may suggest that you take your first dose before bedtime, because it can make you feel dizzy. After your first dose, you can take losartan at any time of day.
Should you take potassium with losartan? ›Potential Negative Interaction
Potassium supplements, potassium-containing salt substitutes (No Salt, Morton Salt Substitute, and others), and even high-potassium foods (including Noni juice) should be avoided by those taking losartan, unless directed otherwise by their doctor.
Therefore switching from ACE inhibitors to ARB might be beneficial in patients at risk or with COVID-19 in prevention of such sequelae when they are already on therapy affecting the Renin-Angiotensin System.
Why does ARB cause angioedema? ›Angioedema associated with angiotensin converting enzyme inhibitors (ACEIs) is due to the accumulation of bradykinin and its metabolites. Angiotensin receptor blockers (ARBs) produce anti-hypertensive effects by blocking the angiotensin II AT1 receptor action; hence bradykinin-related side effects are not expected.
Are ARBs safer than ACE inhibitors? ›Moreover, recent studies have shown that ARBs produce a greater decrease in cardiovascular events than ACE inhibitors, especially in patients with established cardiovascular disease. An advantage of ARBs over ACE inhibitors is fewer adverse effects: in general, ARBs are better tolerated than ACE inhibitors.
What is the first choice drug for hypertension? ›First-line (first choice) options include these blood pressure medication names: Thiazide diuretics, calcium channel blockers and ― for people who have kidney disease and heart failure ― angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs).
What is the best combination of blood pressure meds? ›The greatest antihypertensive effect occurred with the combination of 50 mg of losartan and 12.5 mg of hydrochlorothiazide. This treatment reduced diastolic blood pressure to less than 90 mm Hg (or a reduction of 10 mm Hg or greater) in 78 percent of patients.
Which ARB is best for hypertension? ›
In patients with higher uric acid levels, the ARB of choice should be losartan. Irbesartan may also have a protective effect at therapeutic doses. Telmisartan is a neutral agent regarding uric acid excretion, while candesartan, olmesartan and valsartan may increase the risk of hyperuricemia.
Why do ACE and ARBs cause hyperkalemia? ›Main mechanisms contributing to hyperkalemia with ACEi/ARB include decreased aldosterone concentrations, decreased delivery of sodium to the distal nephron, abnormal collecting tubule function, and excessive potassium intake (Table 1).
Do ARBs increase creatinine? ›Many such patients experience a transient rise in serum creatinine levels after treatment with an ACEI or angiotensin receptor blocker (ARB) is started or after blood pressure is adequately reduced. A rise in the serum creatinine level consequently leads to physician reticence to stay the course with a given therapy.
Are ACE and ARBs nephrotoxic? ›This triple therapy can increase the risk of acute renal failure. This triple therapy can increase the risk of acute renal failure.