Use Of Renin-angiotensin-aldosterone System Blockers Research Articles

Assessment of Oxidative Stress Markers in Hypertensive Patients under the Use of Renin-Angiotensin-Aldosterone Blockers.

As in other fields, chronotherapy applied to arterial hypertension (AHT) may have implications on oxidative stress. We compared the levels of some redox markers between hypertensive patients with morning and bedtime use of renin-angiotensin-aldosterone system (RAAS) blockers. This was an observational study that included patients older than 18 years with a diagnosis of essential AHT. Blood pressure (BP) figures were measured using twenty-four-hour ambulatory BP monitoring (24-h ABPM). Lipid peroxidation and protein oxidation were assessed using the thiobarbituric acid reactive substances (TBARS) and reduced thiols assays. We recruited 70 patients with a median age of 54 years, of whom 38 (54%) were women. In hypertensive patients with bedtime use of RAAS blockers, reduced thiol levels showed a positive correlation with nocturnal diastolic BP decrease. TBARS levels were associated with bedtime use of RAAS blockers in dipper and non-dipper hypertensive patients. In non-dipper patients, bedtime use of RAAS blockers was also associated with a decrease in nocturnal diastolic BP. Chronotherapy applied to bedtime use of some BP-lowering drugs in hypertensive patients may be linked to a better redox profile.

Chronic use of renin-angiotensin-aldosterone system blockers and mortality in COVID-19: A multicenter prospective cohort and literature review.

AimsThe role of renin‐angiotensin‐aldosterone system (RAAS) blockers on the course of coronavirus disease 2019 (COVID‐19) is debated. We assessed the association between chronic use of RAAS blockers and mortality among inpatients with COVID‐19 and explored reasons for discrepancies in the literature.Methods and resultsWe included adult hypertensive patients from a prospective nationwide cohort of 3512 inpatients with COVID‐19 up to June 30, 2020. Cox proportional hazard models with various adjustment or propensity weighting methods were used to estimate the hazard ratios (HR) of 30‐day mortality for chronic users versus non‐users of RAAS blockers. We analyzed data of 1160 hypertensive patients: 719 (62%) were male and 777 (67%) were older than 65 years. The main comorbidities were diabetes (n = 416, 36%), chronic cardiac disease (n = 401, 35%), and obesity (n = 340, 29%); 705 (61%) received oxygen therapy. We recorded 135 (11.6%) deaths within 30 days of diagnosis. We found no association between chronic use of RAAS blockers and mortality (unadjusted HR = 1.13, 95% CI [0.8–1.6]; propensity inverse probability treatment weighted HR = 1.09 [0.86‐1.39]; propensity standardized mortality ratio weighted HR = 1.08 [0.79–1.47]). Our comprehensive review of previous studies highlighted that significant associations were mostly found in unrestricted populations with inappropriate adjustment, or with biased in‐hospital exposure measurement.ConclusionOur results do not support previous concerns regarding these drugs, nor a potential protective effect as reported in previous poorly designed studies and meta‐analyses. RAAS blockers should not be discontinued during the pandemic, while in‐hospital management of these drugs will be clarified by randomized trials. NCT04262921.

The effect of renin-angiotensin-aldosterone blockers on SARS-CoV-2 infection in adults: a systematic review of studies and meta-analyzes

The article discusses the role of immune dysregulation of the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of COVID-19 infection, the participation of ACE2 for the penetration of the SARS-CoV-2 coronavirus into cells and the possible role of RAAS blockers, which have a direct effect on the pathological activity of the RAAS, in the development of and the severity of the disease. It is noted that the beneficial organoprotective effects of ACE inhibitors and ARBs may protect against SARS-CoV-2 infection, and their withdrawal may lead to clinical decompensation in patients at high risk of cardiovascular risk. Since then, a number of observational cohort studies have been carried out to address the main questions: does the use of an ACE inhibitor or ARB increase the risk of contracting the novel SARS-CoV-2 coronavirus, and whether the use of RAAS blockers is associated with worse outcomes of COVID-19 disease. The article provides an overview of the scientific evidence on the relationship between the use of RASS blockers and COVID-19 infection. Several cohort studies and two meta-analyzes found no association between prior use of an ACE inhibitor/ARB and the risk of COVID-19 infection (RR 0.96–0.99). In studies on the study of clinical and laboratory features of the action of RAAS blockers in COVID-19, a significantly larger number of subpopulations of T-lymphocytes CD3+ and CD8+, lower concentrations of biomarkers (C-reactive protein, ferritin, IL-6, procalcitonin), as well as a lower viral load. In clinical outcomes, with the use of an ACE inhibitor/ARB, there was a lower incidence of severe/critical forms, and a shorter duration of hospitalization. In large cohort studies with >1000 patients, the use of an ACE inhibitor/ARB was not associated with an increase in the risk of death in patients with COVID-19 (RR < 1.0), and some studies showed a 37–67% decrease in RR. Meta-analyzes also confirmed the absence of the effect of RAAS blockers on the risk of mortality, and in the population of patients with hypertension, a significant reduction in the risk of mortality and severe course of COVID-19 was revealed. Most international associations of specialists, as well as the Russian Cardiological Society, are recommended to continue the use of RAAS blockers in patients with cardiovascular diseases and not to be canceled in case of COVID-19 disease. Further randomized clinical trials are needed to generate new evidence.

Treatment of hypertension during the COVID-19 pandemic: questions about the blockade of the renin-angiotensin-aldosterone system

Arterial hypertension was one of the most common comorbidities associated with a high risk of death in hospitalized patients with COVID-19. Patients with hypertension are routinely and according to standards treated with angiotensinconverting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARB) II. ACE inhibitors or ARB II are included in fixed combinations of antihypertensive drugs recommended for patients with uncomplicated hypertension, as well as when combined with various comorbidities. During the COVID-19 pandemic, there were suggestions about the potential for a negative effect of drugs of these classes on the course and outcomes of a new coronavirus infection. There was a need for a quick response from the most reputable medical organizations to the question of the use of ACE inhibitors and ARB II during the COVID-19 pandemic. The expert position was soon published despite the lack of evidence from randomized clinical trials. Was there any reason for concern about the treatment of ACE inhibitors and ARB II for COVID-19? What are the relationships between the renin-angiotensin-aldosterone system (RAAS) and COVID-19? Is there any new data from clinical trials that can confirm or deny the previously presented position of professional societies regarding the use of RAAS blockers in COVID-19? What is the role of the difference in the mechanism of action of an ACE inhibitor and ARB II in COVID-19? Is it possible that RAAS blockers will be helpful in treating COVID-19? Will the tactics of hypertension pharmacotherapy change in the near future? In this review article, modern concepts on this problem are discussed and answers to the listed questions reflecting the achieved level of knowledge are formulated.

Increasing prescription of renin-angiotensin-aldosterone system blockers associated with improved kidney prognosis in Korean IgA nephropathy patients.

BackgroundWe aimed to describe the characteristics of immunoglobulin A nephropathy (IgAN) in Korea with assessment for time trends.MethodsWe performed a multicenter retrospective observational cohort study including biopsy-confirmed native IgAN cases from four tertiary hospitals in Korea. Time eras of diagnosis were stratified into 1979–2003, 2004–9 and 2010–17. The prognostic variable was progression to end-stage kidney disease (ESKD) analyzed by multivariable Cox regression analysis.ResultsWe included 1366 (from 1979 to 2003), 1636 (from 2004 to 2009) and 1442 (from 2010 to 2017) IgAN patients in this study. In the recent periods, IgAN had relatively better clinical characteristics, as patients had higher estimated glomerular filtration rates and lower baseline blood pressures than before. The use of renin–angiotensin–aldosterone system (RAAS) blockers increased from 57.7% in 1979–2003 to 80.0% in 2010–17. During a median follow-up duration of 11.3 years, 722 patients progressed to ESKD with an incidence rate of 12.5 per 1000 person-years. The 10-year risk of progression to ESKD was lower in 2010–17 compared with that of 1979–2003 [adjusted hazard ratio 0.692 (95% confidence interval 0.523–0.915)], even after adjustment for multiple clinicopathologic characteristics. The use of RAAS blockers was a significant mediator (P < 0.001) for the association between time trends and lower 10-year ESKD risk.ConclusionsClinicopathologic characteristics of IgAN in Korea have changed over time. Although the limitation of a retrospective observational study remains, the result showed that the prognosis of IgAN has improved over the study period, possibly related to increased prescription of RAAS blockers.

RAAS Blockers and Region-Specific Variations in COVID-19 Outcomes: Findings from a Systematic Review and Meta-Analysis

Background: Coronavirus disease 2019 (COVID-19) has evolved as a global crisis with high mortality seen in elderly and people with cardiometabolic diseases. The use of renin angiotensin aldosterone system (RAAS) blockers in these patients is known to enhance the expression of ACE-2, the chief binding receptor of SARS-CoV-2 and may potentially enhance infectivity.Objective: To provide a pooled estimate of the effect of RAAS blocker usage on COVID-19 outcomes.Data Sources: An electronic literature search was performed for published (using MEDLINE/PubMed and Google Scholar) and preprint (using bioRxiv and medRxiv) studies of interest. The last search was conducted on 9th July 2020.Study Selection: Studies reporting data on RAAS blocker use and COVID-19 mortality and severity were included in the review.Data Extraction and Synthesis: Mortality data and severity data including hospitalization, intensive care unit (ICU) admission, invasive ventilation, steroid use and acute kidney injury (AKI) were recorded. Pooled Odds ratio (OR) estimates were reported with 95% CIs and level of heterogeneity (I2).Main Outcomes and Measures: Odds of mortality in users of RAAS blockers with respect to non-users was the primary outcome. Odds of severity, hospitalization, ICU admission, mechanical ventilation, steroid use, and AKI in users with respect to non-users of RAAS blockers were the secondary outcomes.Results: Of 1348 articles identified, 48 published studies were included in the final analysis, with a total of 26432 patients from 31 studies included in mortality analysis and 20127 patients from 23 studies included in severity analysis. Majority of the studies (41.6%) were from China. No increased risk of mortality (Pooled OR 0.91 (0.65-1.26), I2 =89%) or severity (Pooled OR 1.08 (0.79-1.46), I2 =88%) was seen with RAAS blockers. The drug class was protective in hypertension (pooled OR 0.63 (0.46-0.86), I2 =58%). Severity of COVID-19 outcomes was found to be high for Europeans (Pooled OR 2.08 (1.52-2.85), I2 =77%) and US patients (Pooled OR 1.87 (1.62-2.17) in users of RAAS-blockers. A nearly 4 times higher risk of hospitalization, two times higher risk of ICU admission and mechanical ventilation was observed in US patients on RAAS blockers. No net effect on mortality and severity outcomes was seen in Chinese patients. RAAS blocker usage did not have any effect on corticosteroid use and AKI in Chinese patients.Conclusions and Relevance: Use of RAAS blockers is not associated with increased risk of mortality in COVID-19 patients. Reduced mortality is seen in hypertensive patients with COVID-19 and therefore the drugs should be continued in this subset. US and European patients are at higher risk of severe outcomes. Pharmacogenomic differences may explain the ethnicity related variations.Funding Statement: None.Declaration of Interests: None.

SAT-151 A DILEMMA OF CALCITRIOL IN PRE-DIALYTIC CHRONIC KIDNEY DISEASE: A 1-YEAR STUDY FOR COMBINATION THERAPY OF CALCITRIOL AND RENIN-ANGIOTENSIN ALDOSTERONE BLOCKER IN CHRONIC KIDNEY DISEASE

Renin-angiotensin aldosterone system blockers (RASB) is main stream of management of chronic kidney disease (CKD). Vitamin D (vitD) is known as a potent negative regulator of renin-angiotensin aldosterone system via vitamin D receptor. VitD deficiency often presents, even in early CKD. However, there is no a definite guideline of use of vitD in CKD. In addition, the use of vitD should be given a careful attention due to development of hypercalcemia or vascular calcification in CKD. Now, we report results of a 1-year study for combination therapy of calcitriol and RASB in patients with pre-dialytic CKD and vitD deficiency. Forty five patients with pre-dialytic CKD and proteinuria >500 mg/day despites of RASB during at least 6 months were enrolled. We prescribed calcitriol of 0.5 μg, thrice weekly only in patients with serum calclium <10 mg/dL and 25(OH)vitD of <15 ng/mL. Only a total 27 patients received combination therapy of calcitriol and RASB, and laboratory data were retrospectively analyzed. Urine albumin-creatinine ratio (UACR) at baseline was measured. UACR and serum creatinine were followed with 6-month interval. We also divided the enrolled patients into two groups, early CKD and advanced CKD group, based on eGFR of 60 mL/min/1.73m2. We performed a comparative analysis for impacts of combination therapy on albuminuria and renal function in the groups based on eGFR. Total 27 patients used calcitriol and RASB. Eleven patients among the 27 patients were classified into early CKD group and sixteen patients were classified into advanced CKD group. Total 18 patients used only RASB. Twelve patients among the 18 patients were classified into early CKD group and six patients were classified into advanced CKD group. (Table 1,2: not shown in the abstract) In combination group, UACR were 3.15 g/g ± 3.82 at baseline and fell to 2.28 g/g ± 2.90 and 1.91 g/g ± 2.75 after 6 and 12 months. (p=0.031 and p=0.096, respectively) (Table 3) Moreover, in RASB only group, UACR were 1.05 g/d ± 1.71 at baseline and fell to 0.34 g/g ± 0.37 and 0.74 g/g ± 1.13 after 6 and 12 months. (p=0.039 and p=0.133, respectively) (Table 4) Change of UACR after 6 months from baseline did not show statistical significance in both groups. However, in combination group, when subgroup analyses were performed in early CKD and advanced CKD, UACR were 3.61 g/g ± 4.13 at baseline and significantly fell to 2.44 g/g ± 3.04 and 1.17 g/g ± 1.68 after 6 and 12 months (p=0.005 and p=0.022, respectively) in only early CKD. In addition, change of GFR in early CKD patients received combination therapy did not decrease significantly during 12 months. (p=0.099) (Table 3) Moreover, we performed a comparative analysis between combination and RASB only to identify effect of calcitriol on UACR according to time. The difference of decreasing UACR between combination and RASB only group was not statistically significant in both groups, however, in early CKD patients, the difference based on time between both groups seemed to be significant. (p=0.05) (Table 4 and Figure 1) View Large Image Figure ViewerDownload Hi-res image Download (PPT) Our study didnot show a significant impact on albuminuria of vitD combination therapy compared with only RASB therapy. However, if sample size and study-duration are expanded, combination therapy might show negative impact on albuminuria, particularly in early CKD patients with persistent proteinuria despites of use of RASB.

The influence of renin angiotensin aldosterone system blockers on asymmetric dimethylarginine levels in patients with chronic glomerulonephritis

AbstractEndothelial dysfunction could be related to the limited availability of nitric oxide (NO). NO is synthesized with the participation of an NO synthase whose activity is inhibited by asymmetric dimethylarginine (ADMA). The synthesis of ADMA is exacerbated by oxidative stress, and several studies have shown the efficacy of drugs acting on the renin-angiotensin-aldosterone system (RAAS) (converting enzyme inhibitors and angiotensin II receptor antagonists) in reducing the level of ADMA. The probable mechanism of drug action is a reduction of oxidative stress through a decrease of angiotensin II formation. The aim of this study was to assess the influence of RAAS blockers on the plasma concentration of ADMA in patients with chronic glomerulonephritis (ChGN). The study included 37 patients, placed into group A and group B, depending on the treatment. Both groups were treated with RAAS blockers. In group B, immunosuppressive drugs were additionally administered. The control visits were at the 0, 6 and 12 months of observation. In both the studied groups (A+B), a significant reduction of ADMA (0.77 vs 0.4 μmol/l; p&lt;0.05) was noticed. In patients suffering from ChGN, the use of RAAS blockers resulted in a significant decrease of plasma ADMA concentration, independently of immunosupressive treatment.

PS 10-06 ALDOSTERONE MODULATES EXPRESSION OF AN ACID-SECRETING AMMONIA TRANSPORTER Rhcg IN INTERCALATED CELLS OF THE COLLECTING DUCTS

Objective: Main adverse effects of renin-angiotensin-aldosterone system (RAAS) blockers are metabolic acidosis and hyperkalemia, which limit the use of RAAS blockers for treatment of patients with chronic kidney disease. The mechanism of urinary acid secretion by the RAAS has not been fully understood. Rhesus blood group C glycoprotein (Rhcg) is an ammonia transporter which cooperates with H+-ATPase to secrete H+ from the intercalated cells of the collecting duct in the kidney. We hypothesize that aldosterone increases acid secretion by regulating Rhcg. Design and Method: In the present study, effects of aldosterone on the regulation of Rhcg were examined in vivo and in vitro. Mice were continuously administered aldosterone (40 μg/body/day) or vehicle for a week. Urinary pH, ammonia excretion, and titratable acids were measured. Membrane fraction of the whole kidney was extracted. IN-IC cells (a rat intercalated cell line) were treated with aldosterone (10–6 M) for 24 h, and then mRNA, whole cell protein, and membrane fraction were extracted. The Rhcg mRNA and protein expressions were measured by real-time PCR and Western blotting, respectively. The expression of serum and glucocorticoid-regulated kinase 1 (Sgk1) mRNA was also measured in IN-IC cells. Results: Administration of aldosterone increased ammonia in urine and Rhcg protein expression in membrane fraction of the whole kidney by 90%, respectively. In IN-IC cells, treatment with aldosterone increased expressions of Rhcg protein in membrane fraction by 220% and Sgk1 mRNA by 200%, respectively. Similarly to the endogenous Rhcg expression, aldosterone increased the expression of Flag-tagged mice Rhcg in membrane fraction. Conclusions: These results suggest that RAAS blockers cause metabolic acidosis, in part, by inhibiting the effect of aldosterone on membrane distribution of Rhcg in the intercalated cells of the collecting ducts.

Has RAAS Blockade Reached Its Limits in the Treatment of Diabetic Nephropathy?

Medications that block the renin-angiotensin-aldosterone system (RAAS) are a cornerstone of diabetic nephropathy treatment. These agents play an important role in slowing the nephropathy progression in patients with diabetes. Clinical outcome trials that investigated use of these drug classes in patients with diabetic nephropathy have demonstrated clinical significant benefit in slowing nephropathy progression only in people with >300 mg/day of proteinuria. Thus, guidelines mandate their use in such patients. Conversely, combinations of RAAS blocking agents in these patients can worsen renal outcomes. Moreover, use of RAAS blockers in patients with a glomerular filtration rate below 45 mL/min/1.73 m(2) is limited by hyperkalemia. New agents that predictably bind excess potassium in the colon offer the possibility of extending RAAS inhibitor use in advanced chronic kidney disease (CKD) to allow evaluation of RAAS blockade for nephropathy and cardiovascular outcomes. These new potassium-binding agents may provide an opportunity to continue full-dose RAAS inhibition and assess if the benefits of RAAS blockade seen in stage 3 CKD can be extrapolated to persons with stages 4 and 5 CKD, not previously tested due to hyperkalemia.

Renin-Angiotensin-Aldosterone System Blockade in Critically Ill Patients Is Associated with Increased Risk for Acute Kidney Injury.

Acute kidney injury (AKI) is a major clinical problem and a predictor of outcomes in critically ill patients who frequently required treatments in the intensive care unit (ICU). Renin-angiotensin-aldosterone system (RAAS) blockers are commonly used for treating hypertension but demands caution because of accompanying illnesses including AKI. The aim of this study was to evaluate whether the use of RAAS blockers affected the incidence of AKI in ICU patients. From a total of 26,287 patients who were admitted to the ICU from January 2003 to December 2013 were included in the final analyses. The primary outcome was the incidence of AKI based on the prescription of RAAS blockers. The secondary outcomes were all-cause mortality. RAAS blocker users were more likely to develop AKI (P < 0.001) and remained an independent risk factor for AKI (odds ratio [OR], 1.56; 95% confidence interval [CI], 1.37-1.79; P < 0.001) after adjusting confounding factors. There was no significant difference in the cumulative 90-day survival rate between the RAAS blocker users and non-users (P = 0.381). However, the adjusted mortality risk associated with AKI was 1.38 (95% CI, 1.22 to 1.56; P < 0.001) and increased as the severity of AKI stage increased from 1 to 3: 1.17 (1.02 to 1.36), 1.77 (1.45 to 2.16), and 1.93 (1.55 to 2.41; P < 0.01 for the trend). RAAS blockers may have a harmful influence to increase the incidence of AKI and temporary withholding of these medications may deserve careful consideration in ICU patients.

Renin-Angiotensin-Aldosterone System Blockers in Elderly Adults with Chronic Kidney Disease without Diabetes Mellitus or Proteinuria.

To compare the effect of renin-angiotensin-aldosterone system (RAAS) blockers with that of other antihypertensive agents on outcomes in a cohort of elderly veterans with incident chronic kidney disease (CKD) without diabetes mellitus or proteinuria. Retrospective cohort study. Veterans Affairs (VA) Upstate New York Healthcare System. All participants were seen in primary care clinic in Veterans Integrated Service Network 2, which comprises five VA medical centers and 29 community-based outpatient clinics, from April 2001 to April 2008. Veterans with incident CKD who were taking antihypertensive medications and did not have proteinuria or diabetes mellitus on the date of onset of CKD were selected from this population. The outcome variables studied were progression of kidney disease (doubling of serum creatinine level or Stage 5 CKD (estimated glomerular filtration rate <15mL/min per 1.73m2 )), all-cause mortality, and combined outcome. Analysis included 2,474 participants, 47.9% of whom were taking RAAS blockers at baseline and the rest other antihypertensives. Time-varying Cox proportional hazards analyses did not reveal a statistically significant difference in primary combined outcome in participants taking RAAS blockers and those taking other antihypertensives (hazard ratio=1.09, 95% confidence interval=0.93-1.27). There was also no significant effect on individual outcomes (death or progression of kidney disease). Use of RAAS blockers was not associated with less hazard of combined and individual outcomes (doubling of serum creatinine, Stage 5 CKD, death) in elderly veterans with incident CKD without diabetes mellitus or proteinuria.

Major Barriers against Renin–Angiotensin–Aldosterone System Blocker Use in Chronic Kidney Disease Stages 3–5 in Clinical Practice: A Safety Concern?

Renin–angiotensin–aldosterone system (RAAS) blockers are underutilized in patients with chronic kidney disease (CKD). We aimed to determine barriers against the use of RAAS blockers in these patients. Patients with stage 3–5 CKD referred to Hacettepe University Hospital Nephrology Unit during a 1 year period were evaluated for RAAS blocker use. Two hundred and seventy-nine patients (166 male, 113 female) were analyzed. The mean age of the patients was 56.7 ± 15.2 years, mean serum creatinine was 2.45 ± 1.44 mg/dL, and mean glomerular filtration rate was 33.3 ± 15.1 mL/min. The mean follow-up time was 22.0 ± 21.9 months and the clinical visit number was 4.0 ± 3.5. Angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers were used by 68.8% of all patients and 67.7% of diabetic patients at the time of analysis. In 82.1% of patients, RAAS blockers had either been used earlier or were being used. Hyperkalemia was the principal reason for both not starting and also discontinuing these drugs in patients with CKD. In 37.4% of patients, reasons for not starting RAAS blockers were unclear. This study showed that hyperkalemia is the major barrier against the use of RAAS blockers in patients with CKD. There was, however, a subset of patients who did not receive RAAS blockers even without clear contraindications.

The effect of pretreatment with renin-angiotensin-aldosterone system blockers on cardioversion success and acute recurrence of atrial fibrillation

Renin-angiotensin-aldosterone system (RAS) may be activated during atrial fibrillation (AF). It is unclear whether RAS inhibition may facilitate cardioversion from AF and may prevent acute recurrence of AF (ARAF). We thus investigated the effect of pretreatment with RAS blockers on cardioversion success and ARAF in patients with AF scheduled for elective cardioversion. This observational study included 356 patients with AF undergoing elective pharmacological or electrical cardioversion. Of these patients, 135 were not included based on exclusion criteria and the remaining 221 patients were divided into RAS group (n = 116, 69 male) or non-RAS group (n = 105, 58 male) based on precardioversion use of any RAS blocker. Hypertension, coronary heart disease and heart failure were more frequent in the RAS group. Cardioversion from AF was more successful in the RAS group than in the non-RAS group (%92 vs. %82, p = 0.026). The rate of ARAF was lower in RAS group compared with that in non-RAS group (17% vs. 31%, p = 0.026). In multivariate analysis, pretreatment with RAS blockers in addition to shock number and enlarged left atrium, independently predicted ARAF (OR: 0.33, 95% CI: 0.15-0.75, p = 0.008). Independent predictors of cardioversion success were shock number and left atrial dilatation, but not use of RAS blocker. Precardioversion use of RAS blockers may reduce ARAF following successful cardioversion of AF, but did not improve electrical cardioversion.