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Noncardiac inpatient has acute hypertension: Treat or not?
ILLUSTRATIVE CASE
A 48-year-old man is admitted to your family medicine service for cellulitis after failed outpatient therapy. He has presumed community-acquired methicillin-resistant Staphylococcus aureus infection of the left lower extremity and is receiving intravenous (IV) vancomycin. His BP this morning is 176/98 mm Hg, and the reading from the previous shift was 168/94 mm Hg. He is asymptomatic from this elevated BP. Based on protocol, his nurse is asking about treatment in response to the multiple elevated readings. How should you address the patient’s elevated BP, knowing that you will see him for a transition management appointment in 2 weeks?
Elevated BP is common in the adult inpatient setting. Prevalence estimates range from 25% to > 50%. Many factors can contribute to elevated BP in the acute illness setting, such as pain, anxiety, medication withdrawal, and volume status.2,3
Treatment of elevated BP in outpatients is well researched, with evidence-based guidelines for physicians. That is not the case for treatment of asymptomatic elevated BP in the inpatient setting. Most published guidance on inpatient management of acutely elevated BP recommends IV medications, such as hydralazine or labetalol, although there is limited evidence to support such recommendations. There is minimal evidence for outcomes-based benefit in treating acute elevations of inpatient BP, such as reduced myocardial injury or stroke; however, there is some evidence of adverse outcomes, such as hypotension and prolonged hospital stays.4-8
Although the possibility of intensifying antihypertensive therapy for those with known hypertension or those with presumed “new-onset” hypertension could theoretically lead to improved outcomes over the long term, there is little evidence to support this presumption. Rather, there is evidence that intensification of antihypertensive therapy at discharge is linked to short-term harms. This was demonstrated in a propensity-matched veteran cohort that included 4056 hospitalized older adults with hypertension (mean age, 77 years; 3961 men), equally split between those who received antihypertensive intensification at hospital discharge and those who did not. Within 30 days, patients receiving intensification had a higher risk of readmission (number needed to harm [NNH] = 27) and serious adverse events (NNH = 63).9
The current study aimed to put all these pieces together by quantifying the prevalence of hypertension in hospitalized patients, characterizing clinician response to patients’ acutely elevated BP, and comparing both short- and long-term outcomes in patients treated for acute BP elevations while hospitalized vs those who were not. The study also assessed the potential effects of antihypertensive intensification at discharge.
STUDY SUMMARY
Treatment of acute hypertension was associated with end-organ injury
This retrospective, propensity score–matched cohort study (N = 22,834) evaluated the electronic health records of all adult patients (age > 18 years) admitted to a medicine service with a noncardiovascular diagnosis over a 1-year period at 10 Cleveland Clinic hospitals, with 1 year of follow-up data.
Exclusion criteria included hospitalization for a cardiovascular diagnosis; admission for a cerebrovascular event or acute coronary syndrome within the previous 30 days; pregnancy; length of stay of less than 2 days or more than 14 days; and lack of outpatient medication data. Patients were propensity-score matched using BP, demographic features, comorbidities, hospital shift, and time since admission. Exposure was defined as administration of IV antihypertensive medication or a new class of oral antihypertensive medication.
Continue to: Outcomes were defined...
Outcomes were defined as a temporal association between acute hypertension treatment and subsequent end-organ damage, such as AKI (serum creatinine increase ≥ 0.3 mg/dL or 1.5 × initial value [Acute Kidney Injury Network definition]), myocardial injury (elevated troponin: > 0.029 ng/mL for troponin T; > 0.045 ng/mL for troponin I), and/or stroke (indicated by discharge diagnosis, with confirmation by chart review). Monitored outcomes included stroke and myocardial infarction (MI) within 30 days of discharge and BP control up to 1 year later.
The 22,834 patients had a mean (SD) age of 65.6 (17.9) years; 12,993 (56.9%) were women, and 15,963 (69.9%) were White. Of the 17,821 (78%) who had at least 1 inpatient hypertensive systolic BP (SBP) episode, defined as an SBP ≥ 140 mm Hg, 5904 (33.1%) received a new treatment. Of those receiving a new treatment, 4378 (74.2%) received only oral treatment, and 1516 (25.7%) received at least 1 dose of IV medication with or without oral dosing.
Using the propensity-matched sample (4520 treated for elevated BP matched to 4520 who were not treated), treated patients had higher rates of AKI (10.3% vs 7.9%; P < .001) and myocardial injury (1.2% vs 0.6%; P = .003). When assessed by SBP, nontreatment of BP was still superior up to an SBP of 199 mm Hg. At an SBP of ≥ 200 mm Hg, there was no difference in rates of AKI or MI between the treatment and nontreatment groups. There was no difference in stroke in either cohort, although the overall numbers were quite low.
Patients with and without antihypertensive intensification at discharge had similar rates of MI (0.1% vs 0.2%; P > .99) and stroke (0.5% vs 0.4%; P > .99) in a matched cohort at 30 days post discharge. At 1 year, BP control in the intensification vs no-intensification groups was nearly the same: maximum SBP was 157.2 mm Hg vs 157.8 mm Hg, respectively (P = .54) and maximum diastolic BP was 86.5 mm Hg vs 86.1 mm Hg, respectively (P = .49).
WHAT’S NEW
Previous research is confirmed in a more diverse population
Whereas previous research showed no benefit to intensification of treatment among hospitalized older male patients, this large, retrospective, propensity score–matched cohort study demonstrated the short- and long-term effects of treating acute, asymptomatic BP elevations in a younger, more generalizable population that included women. Regardless of treatment modality, there appeared to be more harm than good from treating these BP elevations.
In addition, the study appears to corroborate previous research showing that intensification of BP treatment at discharge did not lead to better outcomes.9 At the very least, the study makes a reasonable argument that treating acute BP elevations in noncardiac patients in the hospital setting is not beneficial.
CAVEATS
Impact of existing therapy could be underestimated
This study had several important limitations. First, 23% of treated participants were excluded from the propensity analysis without justification from the authors. Additionally, there was no reporting of missing data and how it was managed. The authors’ definition of treatment excluded dose intensification of existing antihypertensive therapy, which would undercount the number of treated patients. However, this could underestimate the actual harms of the acute antihypertensive therapy. The authors also included patients with atrial fibrillation and heart failure in the study population, even though they already may have been taking antihypertensive agents.
CHALLENGES TO IMPLEMENTATION
Potential delays in translating findings to patient care
Although several recent studies have shown the potential benefit of not treating asymptomatic acute BP elevations in inpatients, incorporating that information into electronic health record order sets or clinical decision support, and disseminating it to clinical end users, will take time. In the interim, despite these findings, patients may continue to receive IV or oral medications to treat acute, asymptomatic BP elevations while hospitalized for noncardiac diagnoses.
1. Rastogi R, Sheehan MM, Hu B, et al. Treatment and outcomes of inpatient hypertension among adults with noncardiac admissions. JAMA Intern Med. 2021;181:345-352. doi: 10.1001/jamainternmed.2020.7501
2. Jacobs ZG, Najafi N, Fang MC, et al. Reducing unnecessary treatment of asymptomatic elevated blood pressure with intravenous medications on the general internal medicine wards: a quality improvement initiative. J Hosp Med. 2019;14:144-150. doi: 10.12788/jhm.3087
3. Pasik SD, Chiu S, Yang J, et al. Assess before Rx: reducing the overtreatment of asymptomatic blood pressure elevation in the inpatient setting. J Hosp Med. 2019;14:151-156. doi: 10.12788/jhm.3190
4. Campbell P, Baker WL, Bendel SD, et al. Intravenous hydralazine for blood pressure management in the hospitalized patient: its use is often unjustified. J Am Soc Hypertens. 2011;5:473-477. doi: 10.1016/j.jash.2011.07.002
5. Gauer R. Severe asymptomatic hypertension: evaluation and treatment. Am Fam Physician. 2017;95:492-500.
6. Lipari M, Moser LR, Petrovitch EA, et al. As-needed intravenous antihypertensive therapy and blood pressure control. J Hosp Med. 2016;11:193-198. doi: 10.1002/jhm.2510
7. Gaynor MF, Wright GC, Vondracek S. Retrospective review of the use of as-needed hydralazine and labetalol for the treatment of acute hypertension in hospitalized medicine patients. Ther Adv Cardiovasc Dis. 2018;12:7-15. doi: 10.1177/1753944717746613
8. Weder AB, Erickson S. Treatment of hypertension in the inpatient setting: use of intravenous labetalol and hydralazine. J Clin Hypertens (Greenwich). 2010;12:29-33. doi: 10.1111/j.1751-7176.2009.00196.x
9. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536. doi: 10.1001/jamainternmed.2019.3007
ILLUSTRATIVE CASE
A 48-year-old man is admitted to your family medicine service for cellulitis after failed outpatient therapy. He has presumed community-acquired methicillin-resistant Staphylococcus aureus infection of the left lower extremity and is receiving intravenous (IV) vancomycin. His BP this morning is 176/98 mm Hg, and the reading from the previous shift was 168/94 mm Hg. He is asymptomatic from this elevated BP. Based on protocol, his nurse is asking about treatment in response to the multiple elevated readings. How should you address the patient’s elevated BP, knowing that you will see him for a transition management appointment in 2 weeks?
Elevated BP is common in the adult inpatient setting. Prevalence estimates range from 25% to > 50%. Many factors can contribute to elevated BP in the acute illness setting, such as pain, anxiety, medication withdrawal, and volume status.2,3
Treatment of elevated BP in outpatients is well researched, with evidence-based guidelines for physicians. That is not the case for treatment of asymptomatic elevated BP in the inpatient setting. Most published guidance on inpatient management of acutely elevated BP recommends IV medications, such as hydralazine or labetalol, although there is limited evidence to support such recommendations. There is minimal evidence for outcomes-based benefit in treating acute elevations of inpatient BP, such as reduced myocardial injury or stroke; however, there is some evidence of adverse outcomes, such as hypotension and prolonged hospital stays.4-8
Although the possibility of intensifying antihypertensive therapy for those with known hypertension or those with presumed “new-onset” hypertension could theoretically lead to improved outcomes over the long term, there is little evidence to support this presumption. Rather, there is evidence that intensification of antihypertensive therapy at discharge is linked to short-term harms. This was demonstrated in a propensity-matched veteran cohort that included 4056 hospitalized older adults with hypertension (mean age, 77 years; 3961 men), equally split between those who received antihypertensive intensification at hospital discharge and those who did not. Within 30 days, patients receiving intensification had a higher risk of readmission (number needed to harm [NNH] = 27) and serious adverse events (NNH = 63).9
The current study aimed to put all these pieces together by quantifying the prevalence of hypertension in hospitalized patients, characterizing clinician response to patients’ acutely elevated BP, and comparing both short- and long-term outcomes in patients treated for acute BP elevations while hospitalized vs those who were not. The study also assessed the potential effects of antihypertensive intensification at discharge.
STUDY SUMMARY
Treatment of acute hypertension was associated with end-organ injury
This retrospective, propensity score–matched cohort study (N = 22,834) evaluated the electronic health records of all adult patients (age > 18 years) admitted to a medicine service with a noncardiovascular diagnosis over a 1-year period at 10 Cleveland Clinic hospitals, with 1 year of follow-up data.
Exclusion criteria included hospitalization for a cardiovascular diagnosis; admission for a cerebrovascular event or acute coronary syndrome within the previous 30 days; pregnancy; length of stay of less than 2 days or more than 14 days; and lack of outpatient medication data. Patients were propensity-score matched using BP, demographic features, comorbidities, hospital shift, and time since admission. Exposure was defined as administration of IV antihypertensive medication or a new class of oral antihypertensive medication.
Continue to: Outcomes were defined...
Outcomes were defined as a temporal association between acute hypertension treatment and subsequent end-organ damage, such as AKI (serum creatinine increase ≥ 0.3 mg/dL or 1.5 × initial value [Acute Kidney Injury Network definition]), myocardial injury (elevated troponin: > 0.029 ng/mL for troponin T; > 0.045 ng/mL for troponin I), and/or stroke (indicated by discharge diagnosis, with confirmation by chart review). Monitored outcomes included stroke and myocardial infarction (MI) within 30 days of discharge and BP control up to 1 year later.
The 22,834 patients had a mean (SD) age of 65.6 (17.9) years; 12,993 (56.9%) were women, and 15,963 (69.9%) were White. Of the 17,821 (78%) who had at least 1 inpatient hypertensive systolic BP (SBP) episode, defined as an SBP ≥ 140 mm Hg, 5904 (33.1%) received a new treatment. Of those receiving a new treatment, 4378 (74.2%) received only oral treatment, and 1516 (25.7%) received at least 1 dose of IV medication with or without oral dosing.
Using the propensity-matched sample (4520 treated for elevated BP matched to 4520 who were not treated), treated patients had higher rates of AKI (10.3% vs 7.9%; P < .001) and myocardial injury (1.2% vs 0.6%; P = .003). When assessed by SBP, nontreatment of BP was still superior up to an SBP of 199 mm Hg. At an SBP of ≥ 200 mm Hg, there was no difference in rates of AKI or MI between the treatment and nontreatment groups. There was no difference in stroke in either cohort, although the overall numbers were quite low.
Patients with and without antihypertensive intensification at discharge had similar rates of MI (0.1% vs 0.2%; P > .99) and stroke (0.5% vs 0.4%; P > .99) in a matched cohort at 30 days post discharge. At 1 year, BP control in the intensification vs no-intensification groups was nearly the same: maximum SBP was 157.2 mm Hg vs 157.8 mm Hg, respectively (P = .54) and maximum diastolic BP was 86.5 mm Hg vs 86.1 mm Hg, respectively (P = .49).
WHAT’S NEW
Previous research is confirmed in a more diverse population
Whereas previous research showed no benefit to intensification of treatment among hospitalized older male patients, this large, retrospective, propensity score–matched cohort study demonstrated the short- and long-term effects of treating acute, asymptomatic BP elevations in a younger, more generalizable population that included women. Regardless of treatment modality, there appeared to be more harm than good from treating these BP elevations.
In addition, the study appears to corroborate previous research showing that intensification of BP treatment at discharge did not lead to better outcomes.9 At the very least, the study makes a reasonable argument that treating acute BP elevations in noncardiac patients in the hospital setting is not beneficial.
CAVEATS
Impact of existing therapy could be underestimated
This study had several important limitations. First, 23% of treated participants were excluded from the propensity analysis without justification from the authors. Additionally, there was no reporting of missing data and how it was managed. The authors’ definition of treatment excluded dose intensification of existing antihypertensive therapy, which would undercount the number of treated patients. However, this could underestimate the actual harms of the acute antihypertensive therapy. The authors also included patients with atrial fibrillation and heart failure in the study population, even though they already may have been taking antihypertensive agents.
CHALLENGES TO IMPLEMENTATION
Potential delays in translating findings to patient care
Although several recent studies have shown the potential benefit of not treating asymptomatic acute BP elevations in inpatients, incorporating that information into electronic health record order sets or clinical decision support, and disseminating it to clinical end users, will take time. In the interim, despite these findings, patients may continue to receive IV or oral medications to treat acute, asymptomatic BP elevations while hospitalized for noncardiac diagnoses.
ILLUSTRATIVE CASE
A 48-year-old man is admitted to your family medicine service for cellulitis after failed outpatient therapy. He has presumed community-acquired methicillin-resistant Staphylococcus aureus infection of the left lower extremity and is receiving intravenous (IV) vancomycin. His BP this morning is 176/98 mm Hg, and the reading from the previous shift was 168/94 mm Hg. He is asymptomatic from this elevated BP. Based on protocol, his nurse is asking about treatment in response to the multiple elevated readings. How should you address the patient’s elevated BP, knowing that you will see him for a transition management appointment in 2 weeks?
Elevated BP is common in the adult inpatient setting. Prevalence estimates range from 25% to > 50%. Many factors can contribute to elevated BP in the acute illness setting, such as pain, anxiety, medication withdrawal, and volume status.2,3
Treatment of elevated BP in outpatients is well researched, with evidence-based guidelines for physicians. That is not the case for treatment of asymptomatic elevated BP in the inpatient setting. Most published guidance on inpatient management of acutely elevated BP recommends IV medications, such as hydralazine or labetalol, although there is limited evidence to support such recommendations. There is minimal evidence for outcomes-based benefit in treating acute elevations of inpatient BP, such as reduced myocardial injury or stroke; however, there is some evidence of adverse outcomes, such as hypotension and prolonged hospital stays.4-8
Although the possibility of intensifying antihypertensive therapy for those with known hypertension or those with presumed “new-onset” hypertension could theoretically lead to improved outcomes over the long term, there is little evidence to support this presumption. Rather, there is evidence that intensification of antihypertensive therapy at discharge is linked to short-term harms. This was demonstrated in a propensity-matched veteran cohort that included 4056 hospitalized older adults with hypertension (mean age, 77 years; 3961 men), equally split between those who received antihypertensive intensification at hospital discharge and those who did not. Within 30 days, patients receiving intensification had a higher risk of readmission (number needed to harm [NNH] = 27) and serious adverse events (NNH = 63).9
The current study aimed to put all these pieces together by quantifying the prevalence of hypertension in hospitalized patients, characterizing clinician response to patients’ acutely elevated BP, and comparing both short- and long-term outcomes in patients treated for acute BP elevations while hospitalized vs those who were not. The study also assessed the potential effects of antihypertensive intensification at discharge.
STUDY SUMMARY
Treatment of acute hypertension was associated with end-organ injury
This retrospective, propensity score–matched cohort study (N = 22,834) evaluated the electronic health records of all adult patients (age > 18 years) admitted to a medicine service with a noncardiovascular diagnosis over a 1-year period at 10 Cleveland Clinic hospitals, with 1 year of follow-up data.
Exclusion criteria included hospitalization for a cardiovascular diagnosis; admission for a cerebrovascular event or acute coronary syndrome within the previous 30 days; pregnancy; length of stay of less than 2 days or more than 14 days; and lack of outpatient medication data. Patients were propensity-score matched using BP, demographic features, comorbidities, hospital shift, and time since admission. Exposure was defined as administration of IV antihypertensive medication or a new class of oral antihypertensive medication.
Continue to: Outcomes were defined...
Outcomes were defined as a temporal association between acute hypertension treatment and subsequent end-organ damage, such as AKI (serum creatinine increase ≥ 0.3 mg/dL or 1.5 × initial value [Acute Kidney Injury Network definition]), myocardial injury (elevated troponin: > 0.029 ng/mL for troponin T; > 0.045 ng/mL for troponin I), and/or stroke (indicated by discharge diagnosis, with confirmation by chart review). Monitored outcomes included stroke and myocardial infarction (MI) within 30 days of discharge and BP control up to 1 year later.
The 22,834 patients had a mean (SD) age of 65.6 (17.9) years; 12,993 (56.9%) were women, and 15,963 (69.9%) were White. Of the 17,821 (78%) who had at least 1 inpatient hypertensive systolic BP (SBP) episode, defined as an SBP ≥ 140 mm Hg, 5904 (33.1%) received a new treatment. Of those receiving a new treatment, 4378 (74.2%) received only oral treatment, and 1516 (25.7%) received at least 1 dose of IV medication with or without oral dosing.
Using the propensity-matched sample (4520 treated for elevated BP matched to 4520 who were not treated), treated patients had higher rates of AKI (10.3% vs 7.9%; P < .001) and myocardial injury (1.2% vs 0.6%; P = .003). When assessed by SBP, nontreatment of BP was still superior up to an SBP of 199 mm Hg. At an SBP of ≥ 200 mm Hg, there was no difference in rates of AKI or MI between the treatment and nontreatment groups. There was no difference in stroke in either cohort, although the overall numbers were quite low.
Patients with and without antihypertensive intensification at discharge had similar rates of MI (0.1% vs 0.2%; P > .99) and stroke (0.5% vs 0.4%; P > .99) in a matched cohort at 30 days post discharge. At 1 year, BP control in the intensification vs no-intensification groups was nearly the same: maximum SBP was 157.2 mm Hg vs 157.8 mm Hg, respectively (P = .54) and maximum diastolic BP was 86.5 mm Hg vs 86.1 mm Hg, respectively (P = .49).
WHAT’S NEW
Previous research is confirmed in a more diverse population
Whereas previous research showed no benefit to intensification of treatment among hospitalized older male patients, this large, retrospective, propensity score–matched cohort study demonstrated the short- and long-term effects of treating acute, asymptomatic BP elevations in a younger, more generalizable population that included women. Regardless of treatment modality, there appeared to be more harm than good from treating these BP elevations.
In addition, the study appears to corroborate previous research showing that intensification of BP treatment at discharge did not lead to better outcomes.9 At the very least, the study makes a reasonable argument that treating acute BP elevations in noncardiac patients in the hospital setting is not beneficial.
CAVEATS
Impact of existing therapy could be underestimated
This study had several important limitations. First, 23% of treated participants were excluded from the propensity analysis without justification from the authors. Additionally, there was no reporting of missing data and how it was managed. The authors’ definition of treatment excluded dose intensification of existing antihypertensive therapy, which would undercount the number of treated patients. However, this could underestimate the actual harms of the acute antihypertensive therapy. The authors also included patients with atrial fibrillation and heart failure in the study population, even though they already may have been taking antihypertensive agents.
CHALLENGES TO IMPLEMENTATION
Potential delays in translating findings to patient care
Although several recent studies have shown the potential benefit of not treating asymptomatic acute BP elevations in inpatients, incorporating that information into electronic health record order sets or clinical decision support, and disseminating it to clinical end users, will take time. In the interim, despite these findings, patients may continue to receive IV or oral medications to treat acute, asymptomatic BP elevations while hospitalized for noncardiac diagnoses.
1. Rastogi R, Sheehan MM, Hu B, et al. Treatment and outcomes of inpatient hypertension among adults with noncardiac admissions. JAMA Intern Med. 2021;181:345-352. doi: 10.1001/jamainternmed.2020.7501
2. Jacobs ZG, Najafi N, Fang MC, et al. Reducing unnecessary treatment of asymptomatic elevated blood pressure with intravenous medications on the general internal medicine wards: a quality improvement initiative. J Hosp Med. 2019;14:144-150. doi: 10.12788/jhm.3087
3. Pasik SD, Chiu S, Yang J, et al. Assess before Rx: reducing the overtreatment of asymptomatic blood pressure elevation in the inpatient setting. J Hosp Med. 2019;14:151-156. doi: 10.12788/jhm.3190
4. Campbell P, Baker WL, Bendel SD, et al. Intravenous hydralazine for blood pressure management in the hospitalized patient: its use is often unjustified. J Am Soc Hypertens. 2011;5:473-477. doi: 10.1016/j.jash.2011.07.002
5. Gauer R. Severe asymptomatic hypertension: evaluation and treatment. Am Fam Physician. 2017;95:492-500.
6. Lipari M, Moser LR, Petrovitch EA, et al. As-needed intravenous antihypertensive therapy and blood pressure control. J Hosp Med. 2016;11:193-198. doi: 10.1002/jhm.2510
7. Gaynor MF, Wright GC, Vondracek S. Retrospective review of the use of as-needed hydralazine and labetalol for the treatment of acute hypertension in hospitalized medicine patients. Ther Adv Cardiovasc Dis. 2018;12:7-15. doi: 10.1177/1753944717746613
8. Weder AB, Erickson S. Treatment of hypertension in the inpatient setting: use of intravenous labetalol and hydralazine. J Clin Hypertens (Greenwich). 2010;12:29-33. doi: 10.1111/j.1751-7176.2009.00196.x
9. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536. doi: 10.1001/jamainternmed.2019.3007
1. Rastogi R, Sheehan MM, Hu B, et al. Treatment and outcomes of inpatient hypertension among adults with noncardiac admissions. JAMA Intern Med. 2021;181:345-352. doi: 10.1001/jamainternmed.2020.7501
2. Jacobs ZG, Najafi N, Fang MC, et al. Reducing unnecessary treatment of asymptomatic elevated blood pressure with intravenous medications on the general internal medicine wards: a quality improvement initiative. J Hosp Med. 2019;14:144-150. doi: 10.12788/jhm.3087
3. Pasik SD, Chiu S, Yang J, et al. Assess before Rx: reducing the overtreatment of asymptomatic blood pressure elevation in the inpatient setting. J Hosp Med. 2019;14:151-156. doi: 10.12788/jhm.3190
4. Campbell P, Baker WL, Bendel SD, et al. Intravenous hydralazine for blood pressure management in the hospitalized patient: its use is often unjustified. J Am Soc Hypertens. 2011;5:473-477. doi: 10.1016/j.jash.2011.07.002
5. Gauer R. Severe asymptomatic hypertension: evaluation and treatment. Am Fam Physician. 2017;95:492-500.
6. Lipari M, Moser LR, Petrovitch EA, et al. As-needed intravenous antihypertensive therapy and blood pressure control. J Hosp Med. 2016;11:193-198. doi: 10.1002/jhm.2510
7. Gaynor MF, Wright GC, Vondracek S. Retrospective review of the use of as-needed hydralazine and labetalol for the treatment of acute hypertension in hospitalized medicine patients. Ther Adv Cardiovasc Dis. 2018;12:7-15. doi: 10.1177/1753944717746613
8. Weder AB, Erickson S. Treatment of hypertension in the inpatient setting: use of intravenous labetalol and hydralazine. J Clin Hypertens (Greenwich). 2010;12:29-33. doi: 10.1111/j.1751-7176.2009.00196.x
9. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536. doi: 10.1001/jamainternmed.2019.3007
PRACTICE CHANGER
Manage blood pressure (BP) elevations conservatively in patients admitted for noncardiac diagnoses, as acute hypertension treatment may increase the risk for acute kidney injury (AKI) and myocardial injury.
STRENGTH OF RECOMMENDATION
C: Based on a single, large, retrospective cohort study.1
Rastogi R, Sheehan MM, Hu B, et al. Treatment and outcomes of inpatient hypertension among adults with noncardiac admissions. JAMA Intern Med. 2021;181:345-352.
Alcohol abstinence reduces A-fib burden in drinkers
ILLUSTRATIVE CASE
A 61-year-old man with hypertension and paroxysmal AF presents to your office shortly after experiencing his third episode of AF in the past 6 months. He describes these episodes, which last for several days, as “just awful,” noting that when he experiences AF, he has fatigue, palpitations, and shortness of breath and “can’t stop paying attention to my heart.” The patient, who has a body mass index of 32, consumes more than 15 alcoholic drinks per week. What can you recommend to him that will decrease his likelihood of experiencing more episodes of AF?
AF is the most common sustained cardiac arrhythmia. It is associated with significant morbidity and mortality. Known risk factors include obesity, physical inactivity, sleep apnea, diabetes, and hypertension.2
According to the Centers for Disease Control and Prevention, an estimated 12.1 million people in the United States will have AF by 2030. In 2018, AF was mentioned on more than 183,000 death certificates and was the underlying cause of more than 26,000 of those deaths.3 AF is the primary diagnosis in 450,000 hospitalizations annually,4 and the death rate from AF as the primary or contributing cause of death has been rising for more than 2 decades.3
More than 50% of Americans report alcohol consumption within the past month.5 Although alcohol use is associated with new and recurrent AF, only limited prospective data show a clear and causal association between abstaining from alcohol and decreasing AF recurrence.
STUDY SUMMARY
Reduction in AF recurrence and total AF burden following alcohol abstinence
This multicenter, prospective, open-label, randomized controlled trial (N = 140) from 6 sites in Australia evaluated the impact of alcohol abstinence on both the recurrence of AF and the amount of time in AF. Study participants were ages 18 to 85 years, consumed 10 or more standard alcohol-containing drinks per week, had paroxysmal or persistent AF, and were in sinus rhythm at the time of enrollment, regardless of antiarrhythmic therapy. Exclusion criteria included alcohol dependence or abuse, severe left ventricular systolic dysfunction (ejection fraction < 35%), clinically significant noncardiac illness, and/or coexisting psychiatric disorder.1
After a 4-week run-in period, patients were randomized to either an abstinence or a control group in a 1:1 fashion. Patients enrolled in the abstinence group were encouraged to abstain from alcohol consumption for 6 months and were provided with written and oral instructions to assist with abstaining. Control group patients continued their same level of alcohol consumption. Comprehensive rhythm monitoring occurred for all patients after randomization.
Alcohol consumption was reported by both groups using a weekly alcohol diary, supplemented with a visual guide showing pictures of standard alcohol drinks. For the abstinence group, random urine testing for ethyl glucuronide (an alcohol metabolite) was possible if no alcohol intake was reported. Primary outcomes during the 6-month study included recurrence of AF and total AF burden (percentage of time in AF).
Continue to: Secondary outcomes included hospitalizations...
Secondary outcomes included hospitalizations for AF, AF symptom severity, and change in weight. Blood pressure, quality-of-life, and depression scores were missing for > 35% of patients.1
Patients were randomized evenly to the control and abstinence groups. The typical patient was an overweight male in his early 60s with paroxysmal AF, who was taking an antiarrhythmic agent. Patients in the abstinence group decreased their alcohol consumption from 16.8 to 2.1 drinks per week (87.5% reduction; mean difference = –14.7; 95% CI, –12.7 to –16.7). Patients in the control group reduced their intake from 16.4 to 13.2 drinks per week (19.5% reduction; mean difference = –3.2; 95% CI, –1.9 to –4.4).1
AF recurred in 53% vs 73% of the abstinence and control groups, respectively, with a longer period before recurrence in the abstinence group than in the control group (hazard ratio = 0.55; 95% CI, 0.36-0.84; P = .005; number needed to treat = 5). The AF burden was also lower in the abstinence group (0.5%; interquartile range [IQR] = 0.0-3.0) than in the control group (1.2%; IQR = 0.0-10.3; P = .01). The abstinence group had a lower percentage of AF hospitalizations compared with the control group (9% vs 20%), and fewer patients reporting moderate or severe AF symptoms (10% vs 32%). In addition, the abstinence group lost 3.7 kg more weight than did the control group at 6 months.1
WHAT’S NEW
Objective new evidence for effective patient counseling
Alcohol consumption and its association with the onset and recurrence of AF has been documented previously.6 This study was the first to prospectively examine if abstaining from alcohol reduces paroxysmal AF episodes in moderate drinkers.
The study identified clinically meaningful findings among those who abstained from alcohol, including decreased AF recurrence rates, increased time to recurrence, and lower overall AF burden. This provides objective evidence that can be used for motivational interviewing in patients with paroxysmal AF who may be receptive to reducing or abstaining from alcohol consumption.
Continue to: CAVEATS
CAVEATS
The narrow study population may not be widely applicable
The study population was predominantly male, in their seventh decade of life (mean age, 61), and living in Australia. Rates of AF and symptomatology differ by gender and age, making this information challenging to apply to women or older populations. The study excluded patients with alcohol dependence or abuse, left ventricular systolic dysfunction (ejection fraction < 35%), coexisting psychiatric disorders, and clinically significant noncardiac illnesses, limiting the study’s generalizability to these patient populations. Overall, AF recurrence was low in both groups despite the intervention, and the study did not evaluate the efficacy of the counseling method for abstinence.
Since publication of this article, a prospective cohort study of approximately 3800 Swiss patients with AF evaluated the effect of alcohol consumption on the rate of stroke and embolic events. That study did not find statistically significant correlations between patients who drank no alcohol per day, > 0 to < 1, 1 to < 2, or ≥ 2 drinks per day and their rate of stroke.7 However, this study did not specifically evaluate the rate of AF recurrence or time spent in AF among the cohort, which is clinically meaningful for patient morbidity.1
CHALLENGES TO IMPLEMENTATION
Patient willingness to cut alcohol consumption may be limited
The largest challenge to implementation of this intervention is most likely the willingness of patients to cut their alcohol consumption. In this study population, 697 patients were screened for enrollment and met inclusion criteria; however, 491 patients (70.4%) were not willing to consider abstinence from alcohol, and after the run-in phase, another 17 declined randomization. Many primary care physicians would likely agree that while it is easy to encourage patients to drink less, patient adherence to these recommendations, particularly abstaining, is likely to be limited.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med. 2020;382:20-28. doi: 10.1056/NEJMoa1817591
2. Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and risk factor modification for reduction of atrial fibrillation: a scientific statement from the American Heart Association. Circulation. 2020;141:e750-e772. doi: 10.1161/CIR.0000000000000748
3. Atrial fibrillation. Centers for Disease Control and Prevention. Last reviewed September 27, 2021. Accessed February 9, 2022. www.cdc.gov/heartdisease/atrial_fibrillation.htm
4. Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics—2019 update: a report from the American Heart Association. Circulation. 2019;139:e56-e528. doi: 10.1161/CIR.0000000000000659
5. Alcohol facts and statistics. National Institute on Alcohol Abuse and Alcoholism. Updated June 2021. Accessed February 9, 2022. www.niaaa.nih.gov/publications/brochures-and-fact-sheets/alcohol-facts-and-statistics
6. Kodama S, Saito K, Tanaka S, et al. Alcohol consumption and risk of atrial fibrillation: a meta-analysis. J Am Coll Cardiol. 2011;57:427-436. doi: 10.1016/j.jacc.2010.08.641
7. Reddiess P, Aeschbacher S, Meyre P, et al. Alcohol consumption and risk of cardiovascular outcomes and bleeding in patients with established atrial fibrillation. CMAJ. 2021;193:E117-E123. doi: 10.1503/cmaj.200778
ILLUSTRATIVE CASE
A 61-year-old man with hypertension and paroxysmal AF presents to your office shortly after experiencing his third episode of AF in the past 6 months. He describes these episodes, which last for several days, as “just awful,” noting that when he experiences AF, he has fatigue, palpitations, and shortness of breath and “can’t stop paying attention to my heart.” The patient, who has a body mass index of 32, consumes more than 15 alcoholic drinks per week. What can you recommend to him that will decrease his likelihood of experiencing more episodes of AF?
AF is the most common sustained cardiac arrhythmia. It is associated with significant morbidity and mortality. Known risk factors include obesity, physical inactivity, sleep apnea, diabetes, and hypertension.2
According to the Centers for Disease Control and Prevention, an estimated 12.1 million people in the United States will have AF by 2030. In 2018, AF was mentioned on more than 183,000 death certificates and was the underlying cause of more than 26,000 of those deaths.3 AF is the primary diagnosis in 450,000 hospitalizations annually,4 and the death rate from AF as the primary or contributing cause of death has been rising for more than 2 decades.3
More than 50% of Americans report alcohol consumption within the past month.5 Although alcohol use is associated with new and recurrent AF, only limited prospective data show a clear and causal association between abstaining from alcohol and decreasing AF recurrence.
STUDY SUMMARY
Reduction in AF recurrence and total AF burden following alcohol abstinence
This multicenter, prospective, open-label, randomized controlled trial (N = 140) from 6 sites in Australia evaluated the impact of alcohol abstinence on both the recurrence of AF and the amount of time in AF. Study participants were ages 18 to 85 years, consumed 10 or more standard alcohol-containing drinks per week, had paroxysmal or persistent AF, and were in sinus rhythm at the time of enrollment, regardless of antiarrhythmic therapy. Exclusion criteria included alcohol dependence or abuse, severe left ventricular systolic dysfunction (ejection fraction < 35%), clinically significant noncardiac illness, and/or coexisting psychiatric disorder.1
After a 4-week run-in period, patients were randomized to either an abstinence or a control group in a 1:1 fashion. Patients enrolled in the abstinence group were encouraged to abstain from alcohol consumption for 6 months and were provided with written and oral instructions to assist with abstaining. Control group patients continued their same level of alcohol consumption. Comprehensive rhythm monitoring occurred for all patients after randomization.
Alcohol consumption was reported by both groups using a weekly alcohol diary, supplemented with a visual guide showing pictures of standard alcohol drinks. For the abstinence group, random urine testing for ethyl glucuronide (an alcohol metabolite) was possible if no alcohol intake was reported. Primary outcomes during the 6-month study included recurrence of AF and total AF burden (percentage of time in AF).
Continue to: Secondary outcomes included hospitalizations...
Secondary outcomes included hospitalizations for AF, AF symptom severity, and change in weight. Blood pressure, quality-of-life, and depression scores were missing for > 35% of patients.1
Patients were randomized evenly to the control and abstinence groups. The typical patient was an overweight male in his early 60s with paroxysmal AF, who was taking an antiarrhythmic agent. Patients in the abstinence group decreased their alcohol consumption from 16.8 to 2.1 drinks per week (87.5% reduction; mean difference = –14.7; 95% CI, –12.7 to –16.7). Patients in the control group reduced their intake from 16.4 to 13.2 drinks per week (19.5% reduction; mean difference = –3.2; 95% CI, –1.9 to –4.4).1
AF recurred in 53% vs 73% of the abstinence and control groups, respectively, with a longer period before recurrence in the abstinence group than in the control group (hazard ratio = 0.55; 95% CI, 0.36-0.84; P = .005; number needed to treat = 5). The AF burden was also lower in the abstinence group (0.5%; interquartile range [IQR] = 0.0-3.0) than in the control group (1.2%; IQR = 0.0-10.3; P = .01). The abstinence group had a lower percentage of AF hospitalizations compared with the control group (9% vs 20%), and fewer patients reporting moderate or severe AF symptoms (10% vs 32%). In addition, the abstinence group lost 3.7 kg more weight than did the control group at 6 months.1
WHAT’S NEW
Objective new evidence for effective patient counseling
Alcohol consumption and its association with the onset and recurrence of AF has been documented previously.6 This study was the first to prospectively examine if abstaining from alcohol reduces paroxysmal AF episodes in moderate drinkers.
The study identified clinically meaningful findings among those who abstained from alcohol, including decreased AF recurrence rates, increased time to recurrence, and lower overall AF burden. This provides objective evidence that can be used for motivational interviewing in patients with paroxysmal AF who may be receptive to reducing or abstaining from alcohol consumption.
Continue to: CAVEATS
CAVEATS
The narrow study population may not be widely applicable
The study population was predominantly male, in their seventh decade of life (mean age, 61), and living in Australia. Rates of AF and symptomatology differ by gender and age, making this information challenging to apply to women or older populations. The study excluded patients with alcohol dependence or abuse, left ventricular systolic dysfunction (ejection fraction < 35%), coexisting psychiatric disorders, and clinically significant noncardiac illnesses, limiting the study’s generalizability to these patient populations. Overall, AF recurrence was low in both groups despite the intervention, and the study did not evaluate the efficacy of the counseling method for abstinence.
Since publication of this article, a prospective cohort study of approximately 3800 Swiss patients with AF evaluated the effect of alcohol consumption on the rate of stroke and embolic events. That study did not find statistically significant correlations between patients who drank no alcohol per day, > 0 to < 1, 1 to < 2, or ≥ 2 drinks per day and their rate of stroke.7 However, this study did not specifically evaluate the rate of AF recurrence or time spent in AF among the cohort, which is clinically meaningful for patient morbidity.1
CHALLENGES TO IMPLEMENTATION
Patient willingness to cut alcohol consumption may be limited
The largest challenge to implementation of this intervention is most likely the willingness of patients to cut their alcohol consumption. In this study population, 697 patients were screened for enrollment and met inclusion criteria; however, 491 patients (70.4%) were not willing to consider abstinence from alcohol, and after the run-in phase, another 17 declined randomization. Many primary care physicians would likely agree that while it is easy to encourage patients to drink less, patient adherence to these recommendations, particularly abstaining, is likely to be limited.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
ILLUSTRATIVE CASE
A 61-year-old man with hypertension and paroxysmal AF presents to your office shortly after experiencing his third episode of AF in the past 6 months. He describes these episodes, which last for several days, as “just awful,” noting that when he experiences AF, he has fatigue, palpitations, and shortness of breath and “can’t stop paying attention to my heart.” The patient, who has a body mass index of 32, consumes more than 15 alcoholic drinks per week. What can you recommend to him that will decrease his likelihood of experiencing more episodes of AF?
AF is the most common sustained cardiac arrhythmia. It is associated with significant morbidity and mortality. Known risk factors include obesity, physical inactivity, sleep apnea, diabetes, and hypertension.2
According to the Centers for Disease Control and Prevention, an estimated 12.1 million people in the United States will have AF by 2030. In 2018, AF was mentioned on more than 183,000 death certificates and was the underlying cause of more than 26,000 of those deaths.3 AF is the primary diagnosis in 450,000 hospitalizations annually,4 and the death rate from AF as the primary or contributing cause of death has been rising for more than 2 decades.3
More than 50% of Americans report alcohol consumption within the past month.5 Although alcohol use is associated with new and recurrent AF, only limited prospective data show a clear and causal association between abstaining from alcohol and decreasing AF recurrence.
STUDY SUMMARY
Reduction in AF recurrence and total AF burden following alcohol abstinence
This multicenter, prospective, open-label, randomized controlled trial (N = 140) from 6 sites in Australia evaluated the impact of alcohol abstinence on both the recurrence of AF and the amount of time in AF. Study participants were ages 18 to 85 years, consumed 10 or more standard alcohol-containing drinks per week, had paroxysmal or persistent AF, and were in sinus rhythm at the time of enrollment, regardless of antiarrhythmic therapy. Exclusion criteria included alcohol dependence or abuse, severe left ventricular systolic dysfunction (ejection fraction < 35%), clinically significant noncardiac illness, and/or coexisting psychiatric disorder.1
After a 4-week run-in period, patients were randomized to either an abstinence or a control group in a 1:1 fashion. Patients enrolled in the abstinence group were encouraged to abstain from alcohol consumption for 6 months and were provided with written and oral instructions to assist with abstaining. Control group patients continued their same level of alcohol consumption. Comprehensive rhythm monitoring occurred for all patients after randomization.
Alcohol consumption was reported by both groups using a weekly alcohol diary, supplemented with a visual guide showing pictures of standard alcohol drinks. For the abstinence group, random urine testing for ethyl glucuronide (an alcohol metabolite) was possible if no alcohol intake was reported. Primary outcomes during the 6-month study included recurrence of AF and total AF burden (percentage of time in AF).
Continue to: Secondary outcomes included hospitalizations...
Secondary outcomes included hospitalizations for AF, AF symptom severity, and change in weight. Blood pressure, quality-of-life, and depression scores were missing for > 35% of patients.1
Patients were randomized evenly to the control and abstinence groups. The typical patient was an overweight male in his early 60s with paroxysmal AF, who was taking an antiarrhythmic agent. Patients in the abstinence group decreased their alcohol consumption from 16.8 to 2.1 drinks per week (87.5% reduction; mean difference = –14.7; 95% CI, –12.7 to –16.7). Patients in the control group reduced their intake from 16.4 to 13.2 drinks per week (19.5% reduction; mean difference = –3.2; 95% CI, –1.9 to –4.4).1
AF recurred in 53% vs 73% of the abstinence and control groups, respectively, with a longer period before recurrence in the abstinence group than in the control group (hazard ratio = 0.55; 95% CI, 0.36-0.84; P = .005; number needed to treat = 5). The AF burden was also lower in the abstinence group (0.5%; interquartile range [IQR] = 0.0-3.0) than in the control group (1.2%; IQR = 0.0-10.3; P = .01). The abstinence group had a lower percentage of AF hospitalizations compared with the control group (9% vs 20%), and fewer patients reporting moderate or severe AF symptoms (10% vs 32%). In addition, the abstinence group lost 3.7 kg more weight than did the control group at 6 months.1
WHAT’S NEW
Objective new evidence for effective patient counseling
Alcohol consumption and its association with the onset and recurrence of AF has been documented previously.6 This study was the first to prospectively examine if abstaining from alcohol reduces paroxysmal AF episodes in moderate drinkers.
The study identified clinically meaningful findings among those who abstained from alcohol, including decreased AF recurrence rates, increased time to recurrence, and lower overall AF burden. This provides objective evidence that can be used for motivational interviewing in patients with paroxysmal AF who may be receptive to reducing or abstaining from alcohol consumption.
Continue to: CAVEATS
CAVEATS
The narrow study population may not be widely applicable
The study population was predominantly male, in their seventh decade of life (mean age, 61), and living in Australia. Rates of AF and symptomatology differ by gender and age, making this information challenging to apply to women or older populations. The study excluded patients with alcohol dependence or abuse, left ventricular systolic dysfunction (ejection fraction < 35%), coexisting psychiatric disorders, and clinically significant noncardiac illnesses, limiting the study’s generalizability to these patient populations. Overall, AF recurrence was low in both groups despite the intervention, and the study did not evaluate the efficacy of the counseling method for abstinence.
Since publication of this article, a prospective cohort study of approximately 3800 Swiss patients with AF evaluated the effect of alcohol consumption on the rate of stroke and embolic events. That study did not find statistically significant correlations between patients who drank no alcohol per day, > 0 to < 1, 1 to < 2, or ≥ 2 drinks per day and their rate of stroke.7 However, this study did not specifically evaluate the rate of AF recurrence or time spent in AF among the cohort, which is clinically meaningful for patient morbidity.1
CHALLENGES TO IMPLEMENTATION
Patient willingness to cut alcohol consumption may be limited
The largest challenge to implementation of this intervention is most likely the willingness of patients to cut their alcohol consumption. In this study population, 697 patients were screened for enrollment and met inclusion criteria; however, 491 patients (70.4%) were not willing to consider abstinence from alcohol, and after the run-in phase, another 17 declined randomization. Many primary care physicians would likely agree that while it is easy to encourage patients to drink less, patient adherence to these recommendations, particularly abstaining, is likely to be limited.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med. 2020;382:20-28. doi: 10.1056/NEJMoa1817591
2. Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and risk factor modification for reduction of atrial fibrillation: a scientific statement from the American Heart Association. Circulation. 2020;141:e750-e772. doi: 10.1161/CIR.0000000000000748
3. Atrial fibrillation. Centers for Disease Control and Prevention. Last reviewed September 27, 2021. Accessed February 9, 2022. www.cdc.gov/heartdisease/atrial_fibrillation.htm
4. Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics—2019 update: a report from the American Heart Association. Circulation. 2019;139:e56-e528. doi: 10.1161/CIR.0000000000000659
5. Alcohol facts and statistics. National Institute on Alcohol Abuse and Alcoholism. Updated June 2021. Accessed February 9, 2022. www.niaaa.nih.gov/publications/brochures-and-fact-sheets/alcohol-facts-and-statistics
6. Kodama S, Saito K, Tanaka S, et al. Alcohol consumption and risk of atrial fibrillation: a meta-analysis. J Am Coll Cardiol. 2011;57:427-436. doi: 10.1016/j.jacc.2010.08.641
7. Reddiess P, Aeschbacher S, Meyre P, et al. Alcohol consumption and risk of cardiovascular outcomes and bleeding in patients with established atrial fibrillation. CMAJ. 2021;193:E117-E123. doi: 10.1503/cmaj.200778
1. Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med. 2020;382:20-28. doi: 10.1056/NEJMoa1817591
2. Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and risk factor modification for reduction of atrial fibrillation: a scientific statement from the American Heart Association. Circulation. 2020;141:e750-e772. doi: 10.1161/CIR.0000000000000748
3. Atrial fibrillation. Centers for Disease Control and Prevention. Last reviewed September 27, 2021. Accessed February 9, 2022. www.cdc.gov/heartdisease/atrial_fibrillation.htm
4. Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics—2019 update: a report from the American Heart Association. Circulation. 2019;139:e56-e528. doi: 10.1161/CIR.0000000000000659
5. Alcohol facts and statistics. National Institute on Alcohol Abuse and Alcoholism. Updated June 2021. Accessed February 9, 2022. www.niaaa.nih.gov/publications/brochures-and-fact-sheets/alcohol-facts-and-statistics
6. Kodama S, Saito K, Tanaka S, et al. Alcohol consumption and risk of atrial fibrillation: a meta-analysis. J Am Coll Cardiol. 2011;57:427-436. doi: 10.1016/j.jacc.2010.08.641
7. Reddiess P, Aeschbacher S, Meyre P, et al. Alcohol consumption and risk of cardiovascular outcomes and bleeding in patients with established atrial fibrillation. CMAJ. 2021;193:E117-E123. doi: 10.1503/cmaj.200778
PRACTICE CHANGER
Counsel patients with paroxysmal or persistent atrial fibrillation (AF) who drink moderately (≥ 10 drinks per week) that they can reduce their time in AF, as well as their overall recurrence of AF, by decreasing their alcohol consumption by half or more.
STRENGTH OF RECOMMENDATION
B: Based on a well-performed randomized controlled trial1
Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med. 2020;382:20-28.
