ACE Inhibitors, Angiotensin Receptor Blockers, Mineralocorticoid Receptor Antagonists, and Renin Antagonists

Author(s):  
Norman K. Hollenberg
BMJ Open ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. e044010
Author(s):  
Molly Moore Jeffery ◽  
Nathan W Cummins ◽  
Timothy M Dempsey ◽  
Andrew H. Limper ◽  
Nilay D Shah ◽  
...  

ObjectivesEvaluate associations between ACE inhibitors (ACEis) and angiotensin receptor blockers (ARBs) and clinical outcomes in acute viral respiratory illness (AVRI).DesignRetrospective cohort analysis of claims data.SettingThe USA; 2018–2019 influenza season.ParticipantsMain cohort: people with hypertension (HTN) taking an ACEi, ARB or other HTN medications, and experiencing AVRI. Falsification cohort: parallel cohort receiving elective knee or hip replacement.Main outcome measuresMain cohort: hospital admission, intensive care unit, acute respiratory distress (ARD), ARD syndrome and all-cause mortality. Falsification cohort: complications after surgery and all-cause mortality.ResultsThe main cohort included 236 843 episodes of AVRI contributed by 202 629 unique individuals. Most episodes were in women (58.9%), 81.4% in people with Medicare Advantage and 40.3% in people aged 75+ years. Odds of mortality were lower in the ACEi (0.78 (0.74 to 0.83)) and ARB (0.64 (0.61 to 0.68)) cohorts compared with other HTN medications. On all other outcomes, people taking ARBs (but not ACEis) had a >10% reduction in odds of inpatient stays compared with other HTN medications.In the falsification analysis (N=103 353), both ACEis (0.89 (0.80 to 0.98)) and ARBs (0.82 (0.74 to 0.91)) were associated with decreased odds of complications compared with other HTN medications; ARBs (0.64 (0.47 to 0.87)) but not ACEis (0.79 (0.60 to 1.05)) were associated with lower odds of death compared with other HTN medications.ConclusionsOutpatient use of ARBs was associated with better outcomes with AVRI compared with other medications for HTN. ACEis were associated with reduced risk of death, but with minimal or no reduction in risk of other complications. A falsification analysis conducted to provide context on the possible causal implications of these findings did not provide a clear answer. Further analysis using observational data will benefit from additional approaches to assess causal relationships between these drugs and outcomes in AVRI.


2021 ◽  
Vol 54 (3) ◽  
pp. 275-276
Author(s):  
Kanwal Ashiq ◽  
Sana Ashiq

Dear Editor, In December 2019, a new virus which is known as SARS-COV-2 (COVID-19) was identified. In a short period, this virus spread rapidly and caused significant morbidities and mortalities across the earth. On March 11, 2020, the World Health Organization (WHO) declared a pandemic due to the logarithmic expansion of COVID-19 cases globally.1 Various guidelines were issued, and a complete lockdown has been observed on a large scale to stop the spread of the virus. Currently, there is no specific treatment for COVID-19 is available. Throughout the year 2020, scientists struggled a lot to find the COVID-19 cure, and many vaccines are successfully developed which would be helpful in the prevention of disease. Nevertheless, the emergence of virus variants remains an issue. The epidemiological trends and clinical features of this disease have been reported in several publications.2 Due to comorbidities, COVID-19 disease can exacerbate and may result in increased severity and deadly consequences. In a study, the most common comorbidities in COVID-19 patients were reported as following; diabetes (19%), hypertension (30%), and coronary heart disease (8%). In hypertension, blood pressure elevates from the threshold level. The occurrence of hypertension is not necessarily to be associated with COVID-19 as hypertension is quite frequent in geriatric patients, and these patients are at higher risk of being infected with COVID-19.3,4 Angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors are widely prescribed for the cure of hypertension and other cardiovascular-related diseases. On the other hand, the COVID-19 virus binds with ACE2 to gain entry into the lung cells. ACE inhibitors and ARBs escalate ACE2 that could hypothetically increase the chance of COVID-19 binding to lung cells and could headway to more damage. Conversely, in experimental studies, ACE2 showed a protective effect against lung injury. Due to the anti-inflammatory potential of ACE inhibitors and ARBs, these agents can reduce the incidence of developing myocarditis and acute respiratory distress syndrome in COVID-19 patients. There is no evidence that hypertension is linked with the COVID-19 and anti-hypertensive medicines (ACE inhibitors and ARBs) are either harmful or beneficial during the COVID-19 pandemic.5 During this unprecedented situation, the Council on Hypertension of the European Society of Cardiology released a statement that “The Council on Hypertension strongly recommends that physicians and patients should continue treatment with their usual anti-hypertensive therapy because there is no clinical or scientific evidence to suggest that treatment with ACEIs or ARBs should be discontinued because of the COVID-19 infection.” After this announcement, many other societies also recommend that patients should continue using their current hypertensive therapy and if necessary, after careful assessment, changes can be made in the hypertensive regimen.6 According to estimation, globally, 1.5 billion people can suffer from hypertension by 2025 which may contribute approximately 75% of stroke risk and 50% of heart disease risk. CVDs accounts almost 38% of deaths related to the non-communicated disease (NCDs). In Pakistan, hypertension is a chief health concern that leads to significant morbidity and mortality. Blood pressure can be control with medications and lifestyle modifications. One of the best approaches to control and improve blood pressure is team-based care consisting of doctors, pharmacists, and nurses. During COVID-19, collaborative efforts are required to improve patient’s quality of life and to reduce the healthcare burden.7,8 Keywords: COVID-19, Hypertension, Pandemic, ACE inhibitors References Ashiq K, Bajwa MA, Ashiq S. COVID-19 Pandemic and its Impact on Pharmacy Education. Turkish J Pharma Sci. 2021;18(2):122. Ashiq K, Ashiq S, Bajwa MA, Tanveer S, Qayyum M. Knowledge, attitude and practices among the inhabitants of Lahore, Pakistan towards the COVID-19 pandemic: an immediate online based cross-sectional survey while people are under the lockdown. Bangladesh J Med Sci. 2020:69-S 76. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-62. Ashiq S, Ashiq K. The Role of Paraoxonase 1 (PON1) Gene Polymorphisms in Coronary Artery Disease: A Systematic Review and Meta-Analysis. Biochem Genet. 2021:1-21. Schiffrin EL, Flack JM, Ito S, Muntner P, Webb RC. Hypertension and COVID-19. Am J Hypertens. 2020;33(5):373–374. Patel AB, Verma A. COVID-19 and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what is the evidence? JAMA. 2020;323(18):1769-70. Riaz M, Shah G, Asif M, Shah A, Adhikari K, Abu-Shaheen A. Factors associated with hypertension in Pakistan: A systematic review and meta-analysis. PLoS One. 2021;16(1):e0246085. Zarei L, Karimzadeh I, Moradi N, Peymani P, Asadi S, Babar Z-U-D. Affordability assessment from a static to dynamic concept: a scenario-based assessment of cardiovascular medicines. Int J Environ Res Public Health. 2020;17(5):1710.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Prabhjot Grewal ◽  
Jeanwoo Yoo ◽  
Aikaterini Papamanoli ◽  
Azad Mojahedi ◽  
Simrat Dhaliwal ◽  
...  

Introduction: Angiotensin converting enzyme (ACE) 2, is a co-receptor for the entry of SARS-CoV-2 into target cells. The impact of ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) on outcomes in patients with coronavirus disease 19 (COVID-19) is under investigation. Hypothesis: ACEIs/ARBs are associated with worse outcomes in patients hospitalized with COVID-19. Methods: We evaluated the in-hospital course of 469 adults admitted to Stony Brook University Hospital, NY, from March 1 to April 15, 2020 with severe COVID-19 pneumonia (need for high-flow O2). We excluded patients who required mechanical ventilation (MV) or died within 24h of admission. We used Cox regression models to examine the association of previous (home) use of ACEIs or ARBs with mortality and the composite of death or MV. Results: Table 1 summarizes the patient characteristics according to ACEI/ARB use (ACEI: 73; ARB: 73; 146/469 patients, 31.1%). After a median of 13 days (8-22), 123 patients (26.2%) died and 105 patients (22.4%) required MV and survived. In models adjusting for age, sex, race, body mass index, hypertension, diabetes, coronary artery disease, heart failure, atrial fibrillation, chronic lung disease, chronic kidney disease, and baseline 0 2 saturation, ACEIs/ARBs were not associated with mortality (HR 1.00; 95%CI 0.62-1.61; P=0.99). There was no difference between classes in mortality (ACEI vs. ARB: HR 1.14; 95%CI 0.61-2.15; P=0.68). However, there was a trend towards lower rates of death or MV with ACEI/ARB (HR 0.75; 95%CI 0.54-1.05; P=0.095), mainly because of lower MV rates. The protective effect of ARBs on the composite was significant (HR 0.66; 95%CI 0.44-0.99; P=0.046) whereas that of ACEIs was not (HR 0.87; 95%CI 0.57-1.31; P=0.50), albeit difference was not significant (P=0.28). Conclusions: In patients with severe COVID-19 pneumonia, ACEI/ARB use was not associated with mortality. Especially ARBs may reduce need for MV in this high-risk COVID-19 population.


2010 ◽  
pp. 2728-2728
Author(s):  
John G.F Cleland ◽  
Andrew L Clark

Heart failure is a common clinical syndrome, often presenting with breathlessness, fatigue and peripheral oedema. It is predominantly a disease of older people. The prevalence is increasing, exceeding 2% of the adult population in developed countries. The pathophysiology of heart failure is complex. A common feature is salt and water retention, possibly triggered by a relative fall in renal perfusion pressure. Common aetiologies include ischaemic heart disease, hypertension, and valvular heart disease. The early diagnosis of heart failure relies on a low threshold of suspicion and screening of people at risk before the onset of obvious symptoms or signs. In patients with suspected heart failure, routine investigation with electrocardiography and blood tests for urea and electrolytes, haemoglobin and BNP/NT-proBNP are recommended. Low plasma concentrations of BNP/NT-proBNP exclude most forms of heart failure. Intermediate or high concentrations should prompt referral for echocardiography to identify possible causes of heart failure and the left ventricular ejection fraction (LVEF). Patients can be classified as reduced (<40%) LVEF (HFrEF), normal (>50%) LVEF (HFnEF), or borderline (40–50%) LVEF (HFbEF). Currently HFbEF and HFnEF are managed similarly by current guidelines. Treatable causes for heart failure (e.g. valvular disease, tachyarrhythmias, thyrotoxicosis, anaemia or hypertension) should be identified and corrected. Patients with heart failure will generally benefit from lifestyle advice (diet, exercise, vaccination). Pharmacological therapy is given to improve symptoms and prognosis. Diuretic therapy is the mainstay for control of congestion and symptoms; it may be life-saving for patients with acute heart failure but its effect on long-term prognosis is unknown. For patients with HFrEF, either angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, or, more recently, angiotensin receptor neprilysin inhibitors, combined with β‎-blockers and mineralocorticoid receptor antagonists (triple therapy) provide both symptomatic and prognostic benefit. Ivabridine may be added for those in sinus rhythm where the heart rate remains above 70 bpm. Whether digoxin still has a role in contemporary management is uncertain. Cardiac resynchronization therapy is appropriate for symptomatic patients with HFrEF if they are in sinus rhythm and have a broad QRS (>140 ms). Implantable defibrillators provide additional prognostic benefit in selected patients with an ejection fraction below 35%. For patients with HFnEF, treatments directed at comorbid conditions (e.g. hypertension, atrial fibrillation) and congestion (e.g. diuretics and mineralocorticoid receptor antagonists) are appropriate but there is no robust evidence that any treatment can improve prognosis. Heart transplantation or assist devices may be options for highly selected patients with endstage heart failure; many others may benefit from palliative care services. Effective management of chronic heart failure requires a coordinated multidisciplinary team, including heart failure nurse specialists, primary care physicians, and cardiologists. New treatments have improved the prognosis of heart failure substantially over the past two decades. The annual mortality is now probably less than 5% for patients with HFrEF receiving good contemporary care whose symptoms are stable and controlled. For patients with recurrent or recalcitrant congestion requiring admission to hospital, the prognosis is much worse. In-patient mortality is about 5% for those aged less than 75 years but threefold higher for older patients; mortality in the year after discharge ranges from 20% to 40% depending on age.


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