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Hospitalist Efficiency Impacted by Increased Workloads
Clinical question: Does an increased hospitalist workload lead to increased costs, longer lengths of stay, and worse medical outcomes?
Background: There is evidence that increased resident physician workloads contribute to adverse medical outcomes, but this has not been assessed in the hospital medicine setting. In a recent national survey of hospitalists, almost half reported that they had managed workloads that felt “unsafe.”
Study design: Retrospective cohort study.
Setting: Academic community health system in Delaware.
Synopsis: This study examined the effect of hospital occupancy and hospitalist workloads, using both daily relative value units (RVUs) and hospitalists’ daily patient census, on length of stay (LOS), hospital costs, inpatient mortality, activation of rapid response system (a proxy measure for decompensation), and 30-day readmission rates. Authors reviewed 20,241 hospitalizations and found that when hospitalist daily censuses exceeded 15 patients (or RVU of 25), length of stay increased “exponentially.” Increased workloads were not associated with worsening medical outcomes or diminished patient satisfaction scores.
The authors caution that the significantly increased costs and LOS at higher patient censuses raise concerns that hospital policies that incentivize productivity may “undermine larger system efforts targeting efficiency and costs of care.” They also suggest that hospitalist groups’ staffing approaches need to accommodate fluctuations in hospital occupancy.
Bottom line: When a hospitalist’s workload exceeds a census of 15 patients, the length of stay and cost may increase dramatically.
Article Reference: Elliott DJ, Young RS, Brice J, Aguiar R, Kolm P. Effect of hospitalist workload on the quality and efficiency of care. JAMA Intern Med. 2014;174(5):786-793.
Clinical question: Does an increased hospitalist workload lead to increased costs, longer lengths of stay, and worse medical outcomes?
Background: There is evidence that increased resident physician workloads contribute to adverse medical outcomes, but this has not been assessed in the hospital medicine setting. In a recent national survey of hospitalists, almost half reported that they had managed workloads that felt “unsafe.”
Study design: Retrospective cohort study.
Setting: Academic community health system in Delaware.
Synopsis: This study examined the effect of hospital occupancy and hospitalist workloads, using both daily relative value units (RVUs) and hospitalists’ daily patient census, on length of stay (LOS), hospital costs, inpatient mortality, activation of rapid response system (a proxy measure for decompensation), and 30-day readmission rates. Authors reviewed 20,241 hospitalizations and found that when hospitalist daily censuses exceeded 15 patients (or RVU of 25), length of stay increased “exponentially.” Increased workloads were not associated with worsening medical outcomes or diminished patient satisfaction scores.
The authors caution that the significantly increased costs and LOS at higher patient censuses raise concerns that hospital policies that incentivize productivity may “undermine larger system efforts targeting efficiency and costs of care.” They also suggest that hospitalist groups’ staffing approaches need to accommodate fluctuations in hospital occupancy.
Bottom line: When a hospitalist’s workload exceeds a census of 15 patients, the length of stay and cost may increase dramatically.
Article Reference: Elliott DJ, Young RS, Brice J, Aguiar R, Kolm P. Effect of hospitalist workload on the quality and efficiency of care. JAMA Intern Med. 2014;174(5):786-793.
Clinical question: Does an increased hospitalist workload lead to increased costs, longer lengths of stay, and worse medical outcomes?
Background: There is evidence that increased resident physician workloads contribute to adverse medical outcomes, but this has not been assessed in the hospital medicine setting. In a recent national survey of hospitalists, almost half reported that they had managed workloads that felt “unsafe.”
Study design: Retrospective cohort study.
Setting: Academic community health system in Delaware.
Synopsis: This study examined the effect of hospital occupancy and hospitalist workloads, using both daily relative value units (RVUs) and hospitalists’ daily patient census, on length of stay (LOS), hospital costs, inpatient mortality, activation of rapid response system (a proxy measure for decompensation), and 30-day readmission rates. Authors reviewed 20,241 hospitalizations and found that when hospitalist daily censuses exceeded 15 patients (or RVU of 25), length of stay increased “exponentially.” Increased workloads were not associated with worsening medical outcomes or diminished patient satisfaction scores.
The authors caution that the significantly increased costs and LOS at higher patient censuses raise concerns that hospital policies that incentivize productivity may “undermine larger system efforts targeting efficiency and costs of care.” They also suggest that hospitalist groups’ staffing approaches need to accommodate fluctuations in hospital occupancy.
Bottom line: When a hospitalist’s workload exceeds a census of 15 patients, the length of stay and cost may increase dramatically.
Article Reference: Elliott DJ, Young RS, Brice J, Aguiar R, Kolm P. Effect of hospitalist workload on the quality and efficiency of care. JAMA Intern Med. 2014;174(5):786-793.
Peri-Operative Clonidine Increases Hypotension, Bradycardia, Nonfatal Cardiac Arrest
Clinical question: In patients at risk for vascular complications undergoing noncardiac surgery, do the benefits of aspirin outweigh the risks?
Background: Aspirin has been shown to reduce the rate of myocardial infarction (MI) and major vascular events in patients not undergoing surgery. The benefits of initiating or continuing aspirin in patients undergoing surgery, balanced by the potential increase in bleeding risk, have not been widely studied.
Study design: International randomized placebo-controlled trial with a 2-by-2 factorial design.
Setting: One hundred thirty-five hospitals in 23 countries, from 2010-2013.
Synopsis: The study enrolled 10,010 patients, with a mean age of 68.6 years. Inclusion criteria were age >45 years old and risk for vascular complications, defined as a history of coronary artery disease, peripheral vascular disease, or cerebrovascular accident; major vascular surgery; or at least three of the following: age >70, congestive heart failure, transient ischemic attack, hypertension, diabetes mellitus type 2, creatinine >2 mg/dL, recent smoking, undergoing major surgery, or urgent/emergent surgery.
Groups were stratified by current use of aspirin and then assigned to aspirin or placebo; patients on aspirin held it a median of seven days before surgery. Those in the active group received 200 mg of aspirin pre-operatively. Patients not previously on aspirin then continued aspirin at 100 mg/day for 30 days; those on aspirin previously received 100 mg/day for seven days and then resumed their prior dose.
No difference was found in the primary outcome of death or non-fatal MI at 30 days, but aspirin was noted to increase the risk of major bleeding (4.6% vs. 3.8%, P=0.04), most commonly occurring at the surgical site (78.3%) and the GI tract (9.3%). Because major bleeding can be associated with peri-operative MI, this may have counteracted the cardiovascular benefits of aspirin.
Bottom line: Peri-operative administration of aspirin to patients at risk for vascular complications undergoing noncardiac surgery does not decrease the risk of peri-operative death or MI and may increase the risk of post-operative bleeding.
Citation: Devereaux PJ, Mrkobrada M, Sessler DI, et al. POISE-2 Investigators. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1494-1503.
Clinical question: In patients at risk for vascular complications undergoing noncardiac surgery, do the benefits of aspirin outweigh the risks?
Background: Aspirin has been shown to reduce the rate of myocardial infarction (MI) and major vascular events in patients not undergoing surgery. The benefits of initiating or continuing aspirin in patients undergoing surgery, balanced by the potential increase in bleeding risk, have not been widely studied.
Study design: International randomized placebo-controlled trial with a 2-by-2 factorial design.
Setting: One hundred thirty-five hospitals in 23 countries, from 2010-2013.
Synopsis: The study enrolled 10,010 patients, with a mean age of 68.6 years. Inclusion criteria were age >45 years old and risk for vascular complications, defined as a history of coronary artery disease, peripheral vascular disease, or cerebrovascular accident; major vascular surgery; or at least three of the following: age >70, congestive heart failure, transient ischemic attack, hypertension, diabetes mellitus type 2, creatinine >2 mg/dL, recent smoking, undergoing major surgery, or urgent/emergent surgery.
Groups were stratified by current use of aspirin and then assigned to aspirin or placebo; patients on aspirin held it a median of seven days before surgery. Those in the active group received 200 mg of aspirin pre-operatively. Patients not previously on aspirin then continued aspirin at 100 mg/day for 30 days; those on aspirin previously received 100 mg/day for seven days and then resumed their prior dose.
No difference was found in the primary outcome of death or non-fatal MI at 30 days, but aspirin was noted to increase the risk of major bleeding (4.6% vs. 3.8%, P=0.04), most commonly occurring at the surgical site (78.3%) and the GI tract (9.3%). Because major bleeding can be associated with peri-operative MI, this may have counteracted the cardiovascular benefits of aspirin.
Bottom line: Peri-operative administration of aspirin to patients at risk for vascular complications undergoing noncardiac surgery does not decrease the risk of peri-operative death or MI and may increase the risk of post-operative bleeding.
Citation: Devereaux PJ, Mrkobrada M, Sessler DI, et al. POISE-2 Investigators. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1494-1503.
Clinical question: In patients at risk for vascular complications undergoing noncardiac surgery, do the benefits of aspirin outweigh the risks?
Background: Aspirin has been shown to reduce the rate of myocardial infarction (MI) and major vascular events in patients not undergoing surgery. The benefits of initiating or continuing aspirin in patients undergoing surgery, balanced by the potential increase in bleeding risk, have not been widely studied.
Study design: International randomized placebo-controlled trial with a 2-by-2 factorial design.
Setting: One hundred thirty-five hospitals in 23 countries, from 2010-2013.
Synopsis: The study enrolled 10,010 patients, with a mean age of 68.6 years. Inclusion criteria were age >45 years old and risk for vascular complications, defined as a history of coronary artery disease, peripheral vascular disease, or cerebrovascular accident; major vascular surgery; or at least three of the following: age >70, congestive heart failure, transient ischemic attack, hypertension, diabetes mellitus type 2, creatinine >2 mg/dL, recent smoking, undergoing major surgery, or urgent/emergent surgery.
Groups were stratified by current use of aspirin and then assigned to aspirin or placebo; patients on aspirin held it a median of seven days before surgery. Those in the active group received 200 mg of aspirin pre-operatively. Patients not previously on aspirin then continued aspirin at 100 mg/day for 30 days; those on aspirin previously received 100 mg/day for seven days and then resumed their prior dose.
No difference was found in the primary outcome of death or non-fatal MI at 30 days, but aspirin was noted to increase the risk of major bleeding (4.6% vs. 3.8%, P=0.04), most commonly occurring at the surgical site (78.3%) and the GI tract (9.3%). Because major bleeding can be associated with peri-operative MI, this may have counteracted the cardiovascular benefits of aspirin.
Bottom line: Peri-operative administration of aspirin to patients at risk for vascular complications undergoing noncardiac surgery does not decrease the risk of peri-operative death or MI and may increase the risk of post-operative bleeding.
Citation: Devereaux PJ, Mrkobrada M, Sessler DI, et al. POISE-2 Investigators. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1494-1503.
Fibrinolytics Increase Stroke Risk, Hemorrhage in Intermediate-Risk Pulmonary Emboli
Clinical question: Do fibrinolytics decrease mortality rates in intermediate-risk pulmonary emboli?
Background: Over the past 40 years, fibrinolytics have been studied in fewer than 1,000 patients with pulmonary emboli. Previous studies have shown improvement in hemodynamic response, though the evidence for clinical outcomes such as death and hemodynamic collapse have not been studied adequately in intermediate-risk pulmonary emboli.
Study design: Randomized, double-blinded, placebo-controlled trial.
Setting: Seventy-six sites in 13 countries.
Synopsis: The PEITHO [Pulmonary EmbolIsm THrOmbolysis] trial randomized 1,006 patients in a double-blind fashion. All patients had acute pulmonary emboli with evidence of right ventricular dysfunction on computed tomography scan or echocardiogram, as well as an elevated troponin, in the absence of hemodynamic compromise. Patients received tenecteplase and heparin or placebo and heparin. The primary outcome was death and hemodynamic decompensation.
The primary outcome was found in 2.6% of the treatment group and 5.6% in the placebo group (P=0.02), favoring the treatment group; however, there was no difference in death at seven days (1.2% vs. 1.8%; P=0.42) and 30 days (2.4% vs. 3.2%; P=0.42). Additionally, there were higher rates of extracranial bleeding (6.3% vs. 1.2%; P=<0.001) and stroke (2.4% vs. 0.2%; P=0.003) in the tenecteplase group than in the placebo group. Of the 12 strokes in the treatment group, 11 were hemorrhagic.
Bottom line: Treatment of intermediate-risk pulmonary emboli with fibrinolytics may improve hemodynamics; however, there is no mortality benefit, and fibrinolytic therapy carries an increased risk of bleeding and stroke.
Citation: Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411.
Clinical question: Do fibrinolytics decrease mortality rates in intermediate-risk pulmonary emboli?
Background: Over the past 40 years, fibrinolytics have been studied in fewer than 1,000 patients with pulmonary emboli. Previous studies have shown improvement in hemodynamic response, though the evidence for clinical outcomes such as death and hemodynamic collapse have not been studied adequately in intermediate-risk pulmonary emboli.
Study design: Randomized, double-blinded, placebo-controlled trial.
Setting: Seventy-six sites in 13 countries.
Synopsis: The PEITHO [Pulmonary EmbolIsm THrOmbolysis] trial randomized 1,006 patients in a double-blind fashion. All patients had acute pulmonary emboli with evidence of right ventricular dysfunction on computed tomography scan or echocardiogram, as well as an elevated troponin, in the absence of hemodynamic compromise. Patients received tenecteplase and heparin or placebo and heparin. The primary outcome was death and hemodynamic decompensation.
The primary outcome was found in 2.6% of the treatment group and 5.6% in the placebo group (P=0.02), favoring the treatment group; however, there was no difference in death at seven days (1.2% vs. 1.8%; P=0.42) and 30 days (2.4% vs. 3.2%; P=0.42). Additionally, there were higher rates of extracranial bleeding (6.3% vs. 1.2%; P=<0.001) and stroke (2.4% vs. 0.2%; P=0.003) in the tenecteplase group than in the placebo group. Of the 12 strokes in the treatment group, 11 were hemorrhagic.
Bottom line: Treatment of intermediate-risk pulmonary emboli with fibrinolytics may improve hemodynamics; however, there is no mortality benefit, and fibrinolytic therapy carries an increased risk of bleeding and stroke.
Citation: Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411.
Clinical question: Do fibrinolytics decrease mortality rates in intermediate-risk pulmonary emboli?
Background: Over the past 40 years, fibrinolytics have been studied in fewer than 1,000 patients with pulmonary emboli. Previous studies have shown improvement in hemodynamic response, though the evidence for clinical outcomes such as death and hemodynamic collapse have not been studied adequately in intermediate-risk pulmonary emboli.
Study design: Randomized, double-blinded, placebo-controlled trial.
Setting: Seventy-six sites in 13 countries.
Synopsis: The PEITHO [Pulmonary EmbolIsm THrOmbolysis] trial randomized 1,006 patients in a double-blind fashion. All patients had acute pulmonary emboli with evidence of right ventricular dysfunction on computed tomography scan or echocardiogram, as well as an elevated troponin, in the absence of hemodynamic compromise. Patients received tenecteplase and heparin or placebo and heparin. The primary outcome was death and hemodynamic decompensation.
The primary outcome was found in 2.6% of the treatment group and 5.6% in the placebo group (P=0.02), favoring the treatment group; however, there was no difference in death at seven days (1.2% vs. 1.8%; P=0.42) and 30 days (2.4% vs. 3.2%; P=0.42). Additionally, there were higher rates of extracranial bleeding (6.3% vs. 1.2%; P=<0.001) and stroke (2.4% vs. 0.2%; P=0.003) in the tenecteplase group than in the placebo group. Of the 12 strokes in the treatment group, 11 were hemorrhagic.
Bottom line: Treatment of intermediate-risk pulmonary emboli with fibrinolytics may improve hemodynamics; however, there is no mortality benefit, and fibrinolytic therapy carries an increased risk of bleeding and stroke.
Citation: Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411.
AHA/ACC Atrial Fibrillation Guidelines Updated
Clinical question: What new recommendations are made in the AHA/ACC/HRS atrial fibrillation guidelines?
Background: This is the AHA’s first comprehensive update on atrial fibrillation since 2006; there were two intervening focused updates in 2011.
Synopsis: The majority of the new recommendations center on patient selection for anticoagulation and the role of the new oral anticoagulants.
CHA2DS2-VASc is now recommended over CHADS2 for evaluation of stroke risk, with anticoagulation recommended for a score of two or greater, or for a patient with any prior history of stroke or transient ischemic attack.
Warfarin, direct thrombin inhibitors, or factor Xa inhibitors may be considered in patients with normal renal function. Reduced doses of these medications may be considered in patients with moderate to severe renal dysfunction but have not been studied in clinical trials.
Warfarin remains the drug of choice for patients on hemodialysis and those with hemodynamically significant mitral stenosis or aortic valve replacement.
The clinical utility of bleeding risk scores remains insufficient for formal recommendations. There is sparse evidence on which to base recommendations for bridging, but additional studies, such as the BRIDGE trial, are ongoing. A liberal rate control strategy targeting heart rates <110 in asymptomatic patients with preserved systolic function is reasonable; ideal rate control targets remain controversial.
Citation: January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society [published online ahead of print April 10, 2014]. Circulation.
Clinical question: What new recommendations are made in the AHA/ACC/HRS atrial fibrillation guidelines?
Background: This is the AHA’s first comprehensive update on atrial fibrillation since 2006; there were two intervening focused updates in 2011.
Synopsis: The majority of the new recommendations center on patient selection for anticoagulation and the role of the new oral anticoagulants.
CHA2DS2-VASc is now recommended over CHADS2 for evaluation of stroke risk, with anticoagulation recommended for a score of two or greater, or for a patient with any prior history of stroke or transient ischemic attack.
Warfarin, direct thrombin inhibitors, or factor Xa inhibitors may be considered in patients with normal renal function. Reduced doses of these medications may be considered in patients with moderate to severe renal dysfunction but have not been studied in clinical trials.
Warfarin remains the drug of choice for patients on hemodialysis and those with hemodynamically significant mitral stenosis or aortic valve replacement.
The clinical utility of bleeding risk scores remains insufficient for formal recommendations. There is sparse evidence on which to base recommendations for bridging, but additional studies, such as the BRIDGE trial, are ongoing. A liberal rate control strategy targeting heart rates <110 in asymptomatic patients with preserved systolic function is reasonable; ideal rate control targets remain controversial.
Citation: January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society [published online ahead of print April 10, 2014]. Circulation.
Clinical question: What new recommendations are made in the AHA/ACC/HRS atrial fibrillation guidelines?
Background: This is the AHA’s first comprehensive update on atrial fibrillation since 2006; there were two intervening focused updates in 2011.
Synopsis: The majority of the new recommendations center on patient selection for anticoagulation and the role of the new oral anticoagulants.
CHA2DS2-VASc is now recommended over CHADS2 for evaluation of stroke risk, with anticoagulation recommended for a score of two or greater, or for a patient with any prior history of stroke or transient ischemic attack.
Warfarin, direct thrombin inhibitors, or factor Xa inhibitors may be considered in patients with normal renal function. Reduced doses of these medications may be considered in patients with moderate to severe renal dysfunction but have not been studied in clinical trials.
Warfarin remains the drug of choice for patients on hemodialysis and those with hemodynamically significant mitral stenosis or aortic valve replacement.
The clinical utility of bleeding risk scores remains insufficient for formal recommendations. There is sparse evidence on which to base recommendations for bridging, but additional studies, such as the BRIDGE trial, are ongoing. A liberal rate control strategy targeting heart rates <110 in asymptomatic patients with preserved systolic function is reasonable; ideal rate control targets remain controversial.
Citation: January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society [published online ahead of print April 10, 2014]. Circulation.
Peri-Operative Aspirin Impact on Risk of Bleeding, Death, Myocardial Infarction Examined
Clinical question: Does peri-operative clonidine prevent myocardial infarction (MI)?
Background: A meta-analysis showed that peri-operative clonidine decreased death and MI compared to placebo in patients undergoing vascular surgery. It also showed that rates of death and MI were the same for patients taking clonidine vs. placebo undergoing nonvascular surgery without significant effects on hemodynamics.
Study design: Randomized controlled trial.
Setting: One hundred thirty-five centers across 23 countries.
Synopsis: The POISE-II [PeriOperative Ischemic Evaluation-II] study randomized 10,010 patients in a 1:1:1:1 fashion to analyze peri-operative clonidine and aspirin against placebo. This paper specifically examined the effects of peri-operative clonidine vs. placebo. The average age of the population was 69 years old. The most common comorbidities were diabetes (38%) and coronary artery disease (23%).
The outcomes showed that clonidine vs. placebo yielded insignificant results with respect to the primary endpoints (death, MI, or stroke: 7.6% vs. 7.0%; P=0.30); however, there were significantly higher rates of clinically significant hypotension (47.6% vs. 37.1%; P<0.001), bradycardia (12.0% vs. 8.1%; P<0.001), and nonfatal cardiac arrest (0.3% vs. 0.1%; P=0.02) in the clonidine group.
These results differ from previous, smaller studies, which suggested that there were no significant hemodynamic changes when patients received peri-operative clonidine.
Bottom line: Peri-operative clonidine does not affect the rate of MI but increases clinically significant hypotension, bradycardia, and nonfatal cardiac arrest.
Citation: Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1504-1513.
Clinical question: Does peri-operative clonidine prevent myocardial infarction (MI)?
Background: A meta-analysis showed that peri-operative clonidine decreased death and MI compared to placebo in patients undergoing vascular surgery. It also showed that rates of death and MI were the same for patients taking clonidine vs. placebo undergoing nonvascular surgery without significant effects on hemodynamics.
Study design: Randomized controlled trial.
Setting: One hundred thirty-five centers across 23 countries.
Synopsis: The POISE-II [PeriOperative Ischemic Evaluation-II] study randomized 10,010 patients in a 1:1:1:1 fashion to analyze peri-operative clonidine and aspirin against placebo. This paper specifically examined the effects of peri-operative clonidine vs. placebo. The average age of the population was 69 years old. The most common comorbidities were diabetes (38%) and coronary artery disease (23%).
The outcomes showed that clonidine vs. placebo yielded insignificant results with respect to the primary endpoints (death, MI, or stroke: 7.6% vs. 7.0%; P=0.30); however, there were significantly higher rates of clinically significant hypotension (47.6% vs. 37.1%; P<0.001), bradycardia (12.0% vs. 8.1%; P<0.001), and nonfatal cardiac arrest (0.3% vs. 0.1%; P=0.02) in the clonidine group.
These results differ from previous, smaller studies, which suggested that there were no significant hemodynamic changes when patients received peri-operative clonidine.
Bottom line: Peri-operative clonidine does not affect the rate of MI but increases clinically significant hypotension, bradycardia, and nonfatal cardiac arrest.
Citation: Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1504-1513.
Clinical question: Does peri-operative clonidine prevent myocardial infarction (MI)?
Background: A meta-analysis showed that peri-operative clonidine decreased death and MI compared to placebo in patients undergoing vascular surgery. It also showed that rates of death and MI were the same for patients taking clonidine vs. placebo undergoing nonvascular surgery without significant effects on hemodynamics.
Study design: Randomized controlled trial.
Setting: One hundred thirty-five centers across 23 countries.
Synopsis: The POISE-II [PeriOperative Ischemic Evaluation-II] study randomized 10,010 patients in a 1:1:1:1 fashion to analyze peri-operative clonidine and aspirin against placebo. This paper specifically examined the effects of peri-operative clonidine vs. placebo. The average age of the population was 69 years old. The most common comorbidities were diabetes (38%) and coronary artery disease (23%).
The outcomes showed that clonidine vs. placebo yielded insignificant results with respect to the primary endpoints (death, MI, or stroke: 7.6% vs. 7.0%; P=0.30); however, there were significantly higher rates of clinically significant hypotension (47.6% vs. 37.1%; P<0.001), bradycardia (12.0% vs. 8.1%; P<0.001), and nonfatal cardiac arrest (0.3% vs. 0.1%; P=0.02) in the clonidine group.
These results differ from previous, smaller studies, which suggested that there were no significant hemodynamic changes when patients received peri-operative clonidine.
Bottom line: Peri-operative clonidine does not affect the rate of MI but increases clinically significant hypotension, bradycardia, and nonfatal cardiac arrest.
Citation: Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1504-1513.
Confusion Assessment Method (CAM-S) Evaluates Delirium Severity, Gauges Clinical Outcome
Clinical question: Can a delirium severity score that coincides with clinical outcomes be developed?
Background: Quantification of the severity of delirium is important. Building on the Confusion Assessment Method (CAM) scoring system, the CAM-S was developed to help evaluate the severity of delirium.
Study design: Validation analysis in two independent cohorts.
Setting: Three academic medical centers.
Synopsis: Two cohorts of patients were included. The sample from the SAGES [Successful Aging after Elective Surgery] study included 300 patients aged 70 years or older undergoing major surgery. The sample from the Project Recovery study included 919 medical patients aged 70 years or older. There was a predominance of women in both studies. Patients were excluded if they had delirium or dementia present at baseline, recent hospitalization, a terminal diagnosis, vision and auditory impairment, or inability to speak English. A short, four-item form and 10-item longer form were developed, and scores on forms were correlated with outcomes both in the hospital and after discharge.
A higher severity score in both short and long forms was associated with a higher length of stay, as well as relative risk of death and nursing home residence at 90 days.
Limitations to the study were that all patients in the study were 70 years and older and that the Project Recovery sample used an older data set from 1995-1998.
Bottom line: The CAM-S represents a new delirium severity measurement system; it is associated with several clinical outcomes.
Citation: Inouye SK, Kosar CM, Tommet D, et al. The CAM-S: development and validation of a new scoring system for delirium severity in 2 cohorts. Ann Intern Med. 2014;160(8):526-533.
Clinical question: Can a delirium severity score that coincides with clinical outcomes be developed?
Background: Quantification of the severity of delirium is important. Building on the Confusion Assessment Method (CAM) scoring system, the CAM-S was developed to help evaluate the severity of delirium.
Study design: Validation analysis in two independent cohorts.
Setting: Three academic medical centers.
Synopsis: Two cohorts of patients were included. The sample from the SAGES [Successful Aging after Elective Surgery] study included 300 patients aged 70 years or older undergoing major surgery. The sample from the Project Recovery study included 919 medical patients aged 70 years or older. There was a predominance of women in both studies. Patients were excluded if they had delirium or dementia present at baseline, recent hospitalization, a terminal diagnosis, vision and auditory impairment, or inability to speak English. A short, four-item form and 10-item longer form were developed, and scores on forms were correlated with outcomes both in the hospital and after discharge.
A higher severity score in both short and long forms was associated with a higher length of stay, as well as relative risk of death and nursing home residence at 90 days.
Limitations to the study were that all patients in the study were 70 years and older and that the Project Recovery sample used an older data set from 1995-1998.
Bottom line: The CAM-S represents a new delirium severity measurement system; it is associated with several clinical outcomes.
Citation: Inouye SK, Kosar CM, Tommet D, et al. The CAM-S: development and validation of a new scoring system for delirium severity in 2 cohorts. Ann Intern Med. 2014;160(8):526-533.
Clinical question: Can a delirium severity score that coincides with clinical outcomes be developed?
Background: Quantification of the severity of delirium is important. Building on the Confusion Assessment Method (CAM) scoring system, the CAM-S was developed to help evaluate the severity of delirium.
Study design: Validation analysis in two independent cohorts.
Setting: Three academic medical centers.
Synopsis: Two cohorts of patients were included. The sample from the SAGES [Successful Aging after Elective Surgery] study included 300 patients aged 70 years or older undergoing major surgery. The sample from the Project Recovery study included 919 medical patients aged 70 years or older. There was a predominance of women in both studies. Patients were excluded if they had delirium or dementia present at baseline, recent hospitalization, a terminal diagnosis, vision and auditory impairment, or inability to speak English. A short, four-item form and 10-item longer form were developed, and scores on forms were correlated with outcomes both in the hospital and after discharge.
A higher severity score in both short and long forms was associated with a higher length of stay, as well as relative risk of death and nursing home residence at 90 days.
Limitations to the study were that all patients in the study were 70 years and older and that the Project Recovery sample used an older data set from 1995-1998.
Bottom line: The CAM-S represents a new delirium severity measurement system; it is associated with several clinical outcomes.
Citation: Inouye SK, Kosar CM, Tommet D, et al. The CAM-S: development and validation of a new scoring system for delirium severity in 2 cohorts. Ann Intern Med. 2014;160(8):526-533.
Risk-Prediction Model for Recurrent Clostridium difficile Infection
Clinical question: What are the risk factors identified at the onset of illness that are associated with recurrent C. diff infection?
Background: After initial infection, 10%-25% of patients experience recurrent C. diff infection (CDI). The identification of patients at high risk of recurrence would be beneficial for therapeutic decision making.
Study design: Retrospective cohort study.
Setting: Large, urban, academic medical center.
Synopsis: Authors included 4,196 patients with an initial infection, defined by a positive C. diff toxin assay and unformed stools. A repeat positive toxin within 42 days of completing treatment for the initial infection represented recurrent CDI. Multiple characteristics were examined to identify risks of recurrent infection, including demographics and those related to acute and chronic disease. A logistic regression model was used to identify risk factors for recurrence.
Four hundred twenty-five patients (10.1%) had recurrent infection. Age, fluoroquinolone and high-risk antibiotic use, community-acquired healthcare-associated infection, multiple hospitalizations, and gastric acid suppression were found to predict recurrent infection through multivariate analysis.
Limitations of the study included potential confounding, use of observational data, and generalizability, given the urban academic medical center setting. This prediction model differs from previously developed models in that it identifies factors present at the onset of infection.
Bottom line: Multiple factors identified at the onset of illness can predict CDI recurrence.
Citation: Zilberberg MD, Reske K, Olsen M, Yan Y, Dubberke ER. Development and validation of a recurrent Clostridium difficile risk-prediction model. J Hosp Med. 2014;9(7):418-423.
Clinical question: What are the risk factors identified at the onset of illness that are associated with recurrent C. diff infection?
Background: After initial infection, 10%-25% of patients experience recurrent C. diff infection (CDI). The identification of patients at high risk of recurrence would be beneficial for therapeutic decision making.
Study design: Retrospective cohort study.
Setting: Large, urban, academic medical center.
Synopsis: Authors included 4,196 patients with an initial infection, defined by a positive C. diff toxin assay and unformed stools. A repeat positive toxin within 42 days of completing treatment for the initial infection represented recurrent CDI. Multiple characteristics were examined to identify risks of recurrent infection, including demographics and those related to acute and chronic disease. A logistic regression model was used to identify risk factors for recurrence.
Four hundred twenty-five patients (10.1%) had recurrent infection. Age, fluoroquinolone and high-risk antibiotic use, community-acquired healthcare-associated infection, multiple hospitalizations, and gastric acid suppression were found to predict recurrent infection through multivariate analysis.
Limitations of the study included potential confounding, use of observational data, and generalizability, given the urban academic medical center setting. This prediction model differs from previously developed models in that it identifies factors present at the onset of infection.
Bottom line: Multiple factors identified at the onset of illness can predict CDI recurrence.
Citation: Zilberberg MD, Reske K, Olsen M, Yan Y, Dubberke ER. Development and validation of a recurrent Clostridium difficile risk-prediction model. J Hosp Med. 2014;9(7):418-423.
Clinical question: What are the risk factors identified at the onset of illness that are associated with recurrent C. diff infection?
Background: After initial infection, 10%-25% of patients experience recurrent C. diff infection (CDI). The identification of patients at high risk of recurrence would be beneficial for therapeutic decision making.
Study design: Retrospective cohort study.
Setting: Large, urban, academic medical center.
Synopsis: Authors included 4,196 patients with an initial infection, defined by a positive C. diff toxin assay and unformed stools. A repeat positive toxin within 42 days of completing treatment for the initial infection represented recurrent CDI. Multiple characteristics were examined to identify risks of recurrent infection, including demographics and those related to acute and chronic disease. A logistic regression model was used to identify risk factors for recurrence.
Four hundred twenty-five patients (10.1%) had recurrent infection. Age, fluoroquinolone and high-risk antibiotic use, community-acquired healthcare-associated infection, multiple hospitalizations, and gastric acid suppression were found to predict recurrent infection through multivariate analysis.
Limitations of the study included potential confounding, use of observational data, and generalizability, given the urban academic medical center setting. This prediction model differs from previously developed models in that it identifies factors present at the onset of infection.
Bottom line: Multiple factors identified at the onset of illness can predict CDI recurrence.
Citation: Zilberberg MD, Reske K, Olsen M, Yan Y, Dubberke ER. Development and validation of a recurrent Clostridium difficile risk-prediction model. J Hosp Med. 2014;9(7):418-423.
Does Vitamin D Deficiency Increase the Risk of Dementia?
Baseline vitamin D concentrations are strongly associated with the risk of incident all-cause dementia and Alzheimer’s disease, according to research published September 2 in Neurology.
People who are deficient in serum 25-hydroxyvitamin D (25[OH]D) may have a 51% increased risk of all-cause dementia, and people who are severely deficient in 25(OH)D may have an approximately 122% increased risk of all-cause dementia. The association between vitamin D deficiency and incident Alzheimer’s disease may be similarly strong, said the researchers.
“We have conducted what is to our knowledge the first large, prospective, population-based study to examine vitamin D concentrations in relation to a comprehensive adjudicated assessment of dementia and Alzheimer’s disease,” said Thomas J. Littlejohns, a doctoral student at the University of Exeter Medical School in the United Kingdom, and colleagues. “Our results clarify that the threshold above which older adults are unlikely to benefit from supplementation with regard to dementia risk is likely to lie in the region of 50 nmol/L when 25(OH)D concentrations are measured using [liquid chromatography–mass spectrometry].”
The researchers analyzed data for 1,658 participants in the Cardiovascular Health Study, a prospective, population-based study in the United States. Participants were ambulatory and did not have dementia, cardiovascular disease, or stroke. Their mean age was approximately 74. Blood samples were collected in 1992 and 1993, and serum 25(OH)D concentrations were measured by liquid chromatography–mass spectrometry.
In 1998 and 1999, a committee of neurologists and psychiatrists assessed participants’ dementia and Alzheimer’s disease status using annual cognitive assessments, MRI scans, medical records, questionnaires, and proxy interviews. Diagnoses were based on criteria from the National Institute of Neurological and Communicative Disorders and Stroke and from the Alzheimer’s Disease and Related Disorders Association. Mean follow-up was 5.6 years.
During follow-up, 171 patients developed all-cause dementia and 102 developed Alzheimer’s disease. The risk of developing all-cause dementia and Alzheimer’s disease was significantly higher among participants who were deficient or severely deficient in 25(OH)D. Adjustment for potential confounders (eg, age, season of blood collection, education, sex, BMI, smoking status, and alcohol use) did not alter the pattern of results.
A linear trend across groups in all analyses suggested a monotonic association between 25(OH)D deficiency and dementia risk. Multivariate adjusted smoothing spline plots indicated that the risk of all-cause dementia and Alzheimer’s disease increased sharply at 25(OH)D concentrations lower than 50 nmol/L.
Multivariate adjusted risks for incident all-cause dementia and incident Alzheimer’s disease decreased by 18% and 20%, respectively, for each 1-SD increase in 25(OH)D.
Adjusting the data for diabetes, hypertension, ethnicity, income, and occupation did not change the pattern of results. After excluding participants who developed all-cause dementia and Alzheimer’s disease within one year of baseline, the researchers found that the hazard ratio for incident all-cause dementia was 2.42 in participants who were severely 25(OH)D deficient and 1.54 in those who were 25(OH)D deficient, compared with participants with sufficient 25(OH)D. The hazard ratio for Alzheimer’s disease was 2.36 in participants who were severely 25(OH)D deficient and 1.69 for those who were 25(OH)D deficient. These results suggest that the association is not caused by early converters.
“Our findings support the hypothesis that vitamin D may be neuroprotective and that ‘sufficiency’ in the context of dementia risk may be in the region of 50 nmol/L,” they concluded.
—Erik Greb
Suggested Reading
Littlejohns TJ, Henley WE, Lang IA, et al. Vitamin D and the risk of dementia and Alzheimer disease. Neurology. 2014 Aug 6 [Epub ahead of print].
Baseline vitamin D concentrations are strongly associated with the risk of incident all-cause dementia and Alzheimer’s disease, according to research published September 2 in Neurology.
People who are deficient in serum 25-hydroxyvitamin D (25[OH]D) may have a 51% increased risk of all-cause dementia, and people who are severely deficient in 25(OH)D may have an approximately 122% increased risk of all-cause dementia. The association between vitamin D deficiency and incident Alzheimer’s disease may be similarly strong, said the researchers.
“We have conducted what is to our knowledge the first large, prospective, population-based study to examine vitamin D concentrations in relation to a comprehensive adjudicated assessment of dementia and Alzheimer’s disease,” said Thomas J. Littlejohns, a doctoral student at the University of Exeter Medical School in the United Kingdom, and colleagues. “Our results clarify that the threshold above which older adults are unlikely to benefit from supplementation with regard to dementia risk is likely to lie in the region of 50 nmol/L when 25(OH)D concentrations are measured using [liquid chromatography–mass spectrometry].”
The researchers analyzed data for 1,658 participants in the Cardiovascular Health Study, a prospective, population-based study in the United States. Participants were ambulatory and did not have dementia, cardiovascular disease, or stroke. Their mean age was approximately 74. Blood samples were collected in 1992 and 1993, and serum 25(OH)D concentrations were measured by liquid chromatography–mass spectrometry.
In 1998 and 1999, a committee of neurologists and psychiatrists assessed participants’ dementia and Alzheimer’s disease status using annual cognitive assessments, MRI scans, medical records, questionnaires, and proxy interviews. Diagnoses were based on criteria from the National Institute of Neurological and Communicative Disorders and Stroke and from the Alzheimer’s Disease and Related Disorders Association. Mean follow-up was 5.6 years.
During follow-up, 171 patients developed all-cause dementia and 102 developed Alzheimer’s disease. The risk of developing all-cause dementia and Alzheimer’s disease was significantly higher among participants who were deficient or severely deficient in 25(OH)D. Adjustment for potential confounders (eg, age, season of blood collection, education, sex, BMI, smoking status, and alcohol use) did not alter the pattern of results.
A linear trend across groups in all analyses suggested a monotonic association between 25(OH)D deficiency and dementia risk. Multivariate adjusted smoothing spline plots indicated that the risk of all-cause dementia and Alzheimer’s disease increased sharply at 25(OH)D concentrations lower than 50 nmol/L.
Multivariate adjusted risks for incident all-cause dementia and incident Alzheimer’s disease decreased by 18% and 20%, respectively, for each 1-SD increase in 25(OH)D.
Adjusting the data for diabetes, hypertension, ethnicity, income, and occupation did not change the pattern of results. After excluding participants who developed all-cause dementia and Alzheimer’s disease within one year of baseline, the researchers found that the hazard ratio for incident all-cause dementia was 2.42 in participants who were severely 25(OH)D deficient and 1.54 in those who were 25(OH)D deficient, compared with participants with sufficient 25(OH)D. The hazard ratio for Alzheimer’s disease was 2.36 in participants who were severely 25(OH)D deficient and 1.69 for those who were 25(OH)D deficient. These results suggest that the association is not caused by early converters.
“Our findings support the hypothesis that vitamin D may be neuroprotective and that ‘sufficiency’ in the context of dementia risk may be in the region of 50 nmol/L,” they concluded.
—Erik Greb
Baseline vitamin D concentrations are strongly associated with the risk of incident all-cause dementia and Alzheimer’s disease, according to research published September 2 in Neurology.
People who are deficient in serum 25-hydroxyvitamin D (25[OH]D) may have a 51% increased risk of all-cause dementia, and people who are severely deficient in 25(OH)D may have an approximately 122% increased risk of all-cause dementia. The association between vitamin D deficiency and incident Alzheimer’s disease may be similarly strong, said the researchers.
“We have conducted what is to our knowledge the first large, prospective, population-based study to examine vitamin D concentrations in relation to a comprehensive adjudicated assessment of dementia and Alzheimer’s disease,” said Thomas J. Littlejohns, a doctoral student at the University of Exeter Medical School in the United Kingdom, and colleagues. “Our results clarify that the threshold above which older adults are unlikely to benefit from supplementation with regard to dementia risk is likely to lie in the region of 50 nmol/L when 25(OH)D concentrations are measured using [liquid chromatography–mass spectrometry].”
The researchers analyzed data for 1,658 participants in the Cardiovascular Health Study, a prospective, population-based study in the United States. Participants were ambulatory and did not have dementia, cardiovascular disease, or stroke. Their mean age was approximately 74. Blood samples were collected in 1992 and 1993, and serum 25(OH)D concentrations were measured by liquid chromatography–mass spectrometry.
In 1998 and 1999, a committee of neurologists and psychiatrists assessed participants’ dementia and Alzheimer’s disease status using annual cognitive assessments, MRI scans, medical records, questionnaires, and proxy interviews. Diagnoses were based on criteria from the National Institute of Neurological and Communicative Disorders and Stroke and from the Alzheimer’s Disease and Related Disorders Association. Mean follow-up was 5.6 years.
During follow-up, 171 patients developed all-cause dementia and 102 developed Alzheimer’s disease. The risk of developing all-cause dementia and Alzheimer’s disease was significantly higher among participants who were deficient or severely deficient in 25(OH)D. Adjustment for potential confounders (eg, age, season of blood collection, education, sex, BMI, smoking status, and alcohol use) did not alter the pattern of results.
A linear trend across groups in all analyses suggested a monotonic association between 25(OH)D deficiency and dementia risk. Multivariate adjusted smoothing spline plots indicated that the risk of all-cause dementia and Alzheimer’s disease increased sharply at 25(OH)D concentrations lower than 50 nmol/L.
Multivariate adjusted risks for incident all-cause dementia and incident Alzheimer’s disease decreased by 18% and 20%, respectively, for each 1-SD increase in 25(OH)D.
Adjusting the data for diabetes, hypertension, ethnicity, income, and occupation did not change the pattern of results. After excluding participants who developed all-cause dementia and Alzheimer’s disease within one year of baseline, the researchers found that the hazard ratio for incident all-cause dementia was 2.42 in participants who were severely 25(OH)D deficient and 1.54 in those who were 25(OH)D deficient, compared with participants with sufficient 25(OH)D. The hazard ratio for Alzheimer’s disease was 2.36 in participants who were severely 25(OH)D deficient and 1.69 for those who were 25(OH)D deficient. These results suggest that the association is not caused by early converters.
“Our findings support the hypothesis that vitamin D may be neuroprotective and that ‘sufficiency’ in the context of dementia risk may be in the region of 50 nmol/L,” they concluded.
—Erik Greb
Suggested Reading
Littlejohns TJ, Henley WE, Lang IA, et al. Vitamin D and the risk of dementia and Alzheimer disease. Neurology. 2014 Aug 6 [Epub ahead of print].
Suggested Reading
Littlejohns TJ, Henley WE, Lang IA, et al. Vitamin D and the risk of dementia and Alzheimer disease. Neurology. 2014 Aug 6 [Epub ahead of print].
Can Lesion Volume and Brain Atrophy Predict Outcomes in Early MS?
Baseline MRI measures of lesion volume and brain atrophy predict distinct long-term clinical changes in patients with early multiple sclerosis (MS), according to a small study published online ahead of print July 23 in Multiple Sclerosis and Related Disorders.
The study identified several interesting potential biomarkers that are strongly associated with clinical worsening in early MS, said Amir-Hadi Maghzi, MD, postdoctoral research fellow at the University of California, San Francisco, and his associates.
The study included 43 patients with early MS, of whom 22 completed the three-year assessment. The patients had participated in a randomized, double-blind, placebo-controlled trial at two centers that assessed the possible neuroprotective effects of riluzole in combination with intramuscular interferon beta-1a. T2 lesion volume, as measured on MRI, significantly predicted longitudinal changes in the Paced Auditory Serial Addition Test, the authors reported.
In addition, three baseline measures of atrophy—brain parenchymal volume and normal-appearing white and gray matter volumes—predicted longitudinal changes in the MS Functional Composite score and the Timed 25-Foot Walk. The different findings for lesion and brain volume could reflect distinct disease processes, said the investigators.
Dr. Maghzi and his colleagues calculated longitudinal changes in brain volume by using the Structural Image Evaluation Using Normalization of Atrophy analysis. The researchers counted T2 and contrast-enhancing lesions by visualizing T2 and T1 images simultaneously before and after enhancement. Most MRI measures did not correlate with clinical outcomes at baseline, the researchers noted.
In longitudinal analyses, every 1% decrease in brain volume was associated with a 1.14-point decrease on the Symbol Digit Modalities Test (SDMT). For patients with MS, a four- to five-point decrease in SDMT score is associated with job loss, according to the authors. For every 1% decrease in brain volume, low-contrast letter acuity also declined by an average of nearly 1.5 letters, the investigators said.
—Amy Karon
Suggested Reading
Giannetti P, Politis M, Su P, et al. Microglia activation in multiple sclerosis black holes predicts outcome in progressive patients: an in vivo [(11)C](R)-PK11195-PET pilot study. Neurobiol Dis. 2014;65:203-210.
Temel S, Keklikoglu HD, Vural G, et al. Diffusion tensor magnetic resonance imaging in patients with multiple sclerosis and its relationship with disability. Neuroradiol J. 2013;26(1):3-17.
Baseline MRI measures of lesion volume and brain atrophy predict distinct long-term clinical changes in patients with early multiple sclerosis (MS), according to a small study published online ahead of print July 23 in Multiple Sclerosis and Related Disorders.
The study identified several interesting potential biomarkers that are strongly associated with clinical worsening in early MS, said Amir-Hadi Maghzi, MD, postdoctoral research fellow at the University of California, San Francisco, and his associates.
The study included 43 patients with early MS, of whom 22 completed the three-year assessment. The patients had participated in a randomized, double-blind, placebo-controlled trial at two centers that assessed the possible neuroprotective effects of riluzole in combination with intramuscular interferon beta-1a. T2 lesion volume, as measured on MRI, significantly predicted longitudinal changes in the Paced Auditory Serial Addition Test, the authors reported.
In addition, three baseline measures of atrophy—brain parenchymal volume and normal-appearing white and gray matter volumes—predicted longitudinal changes in the MS Functional Composite score and the Timed 25-Foot Walk. The different findings for lesion and brain volume could reflect distinct disease processes, said the investigators.
Dr. Maghzi and his colleagues calculated longitudinal changes in brain volume by using the Structural Image Evaluation Using Normalization of Atrophy analysis. The researchers counted T2 and contrast-enhancing lesions by visualizing T2 and T1 images simultaneously before and after enhancement. Most MRI measures did not correlate with clinical outcomes at baseline, the researchers noted.
In longitudinal analyses, every 1% decrease in brain volume was associated with a 1.14-point decrease on the Symbol Digit Modalities Test (SDMT). For patients with MS, a four- to five-point decrease in SDMT score is associated with job loss, according to the authors. For every 1% decrease in brain volume, low-contrast letter acuity also declined by an average of nearly 1.5 letters, the investigators said.
—Amy Karon
Baseline MRI measures of lesion volume and brain atrophy predict distinct long-term clinical changes in patients with early multiple sclerosis (MS), according to a small study published online ahead of print July 23 in Multiple Sclerosis and Related Disorders.
The study identified several interesting potential biomarkers that are strongly associated with clinical worsening in early MS, said Amir-Hadi Maghzi, MD, postdoctoral research fellow at the University of California, San Francisco, and his associates.
The study included 43 patients with early MS, of whom 22 completed the three-year assessment. The patients had participated in a randomized, double-blind, placebo-controlled trial at two centers that assessed the possible neuroprotective effects of riluzole in combination with intramuscular interferon beta-1a. T2 lesion volume, as measured on MRI, significantly predicted longitudinal changes in the Paced Auditory Serial Addition Test, the authors reported.
In addition, three baseline measures of atrophy—brain parenchymal volume and normal-appearing white and gray matter volumes—predicted longitudinal changes in the MS Functional Composite score and the Timed 25-Foot Walk. The different findings for lesion and brain volume could reflect distinct disease processes, said the investigators.
Dr. Maghzi and his colleagues calculated longitudinal changes in brain volume by using the Structural Image Evaluation Using Normalization of Atrophy analysis. The researchers counted T2 and contrast-enhancing lesions by visualizing T2 and T1 images simultaneously before and after enhancement. Most MRI measures did not correlate with clinical outcomes at baseline, the researchers noted.
In longitudinal analyses, every 1% decrease in brain volume was associated with a 1.14-point decrease on the Symbol Digit Modalities Test (SDMT). For patients with MS, a four- to five-point decrease in SDMT score is associated with job loss, according to the authors. For every 1% decrease in brain volume, low-contrast letter acuity also declined by an average of nearly 1.5 letters, the investigators said.
—Amy Karon
Suggested Reading
Giannetti P, Politis M, Su P, et al. Microglia activation in multiple sclerosis black holes predicts outcome in progressive patients: an in vivo [(11)C](R)-PK11195-PET pilot study. Neurobiol Dis. 2014;65:203-210.
Temel S, Keklikoglu HD, Vural G, et al. Diffusion tensor magnetic resonance imaging in patients with multiple sclerosis and its relationship with disability. Neuroradiol J. 2013;26(1):3-17.
Suggested Reading
Giannetti P, Politis M, Su P, et al. Microglia activation in multiple sclerosis black holes predicts outcome in progressive patients: an in vivo [(11)C](R)-PK11195-PET pilot study. Neurobiol Dis. 2014;65:203-210.
Temel S, Keklikoglu HD, Vural G, et al. Diffusion tensor magnetic resonance imaging in patients with multiple sclerosis and its relationship with disability. Neuroradiol J. 2013;26(1):3-17.
Midlife Hypertension May Increase Risk of Cognitive Decline
Hypertension at midlife and elevated midlife systolic blood pressure are associated with increased cognitive decline during a 20-year period, according to research published online ahead of print August 4 in JAMA Neurology. The decline is greater among Caucasians with high blood pressure than among African Americans with high blood pressure, said the authors.
Rebecca F. Gottesman, MD, PhD, Associate Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues analyzed data for 13,476 African Americans and Caucasians in the Atherosclerosis Risk in Communities cohort. Baseline cognitive assessment was conducted from 1990 to 1992, and follow-up assessments occurred from 1996 to 1998 and from 2011 to 2013. A majority (58.0%) of living participants completed the 20-year cognitive follow-up.
During the follow-up, baseline hypertension was associated with an additional decline of 0.056 global z score points, and prehypertension was associated nonsignificantly with 0.040 additional global z score points of decline, compared with normal blood pressure. People with hypertension who took antihypertensives had less decline during the study period than untreated individuals with hypertension. Having an indication for initiating antihypertensive treatment at baseline (based on Eighth Joint National Committee hypertension guidelines) was associated with a greater 20-year decline than not having an indication.
The authors’ observations are important, but “they are not those of a randomized clinical trial representing a higher-level evidence-based medical decision-making source,” said Philip B. Gorelick, MD, Medical Director of Saint Mary’s Hauenstein Neuroscience Center in Grand Rapids, Michigan, in an accompanying editorial.
Lowering blood pressure is effective for reducing the risk of poststroke dementia in patients with a history of stroke, he added. Blood pressure lowering also can help prevent late-life dementia for people who are middle aged or for the younger elderly.
Given the current evidence, “on a case-by-case basis, the practitioner will need to balance the benefit of blood pressure lowering on cardiovascular disease risk reduction with the possible benefit or risk to cognition,” Dr. Gorelick concluded.
—Erik Greb
Suggested Reading
Gorelick PB. Blood pressure and the prevention of cognitive impairment. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Gottesman RF, Schneider AL, Albert M, et al. Midlife hypertension and 20-year cognitive change: The Atherosclerosis Risk in Communities Neurocognitive Study. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Yaffe K, Vittinghoff E, Pletcher MJ, et al. Early adult to midlife cardiovascular risk factors and cognitive function. Circulation. 2014;129(15):1560-1567.
Hypertension at midlife and elevated midlife systolic blood pressure are associated with increased cognitive decline during a 20-year period, according to research published online ahead of print August 4 in JAMA Neurology. The decline is greater among Caucasians with high blood pressure than among African Americans with high blood pressure, said the authors.
Rebecca F. Gottesman, MD, PhD, Associate Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues analyzed data for 13,476 African Americans and Caucasians in the Atherosclerosis Risk in Communities cohort. Baseline cognitive assessment was conducted from 1990 to 1992, and follow-up assessments occurred from 1996 to 1998 and from 2011 to 2013. A majority (58.0%) of living participants completed the 20-year cognitive follow-up.
During the follow-up, baseline hypertension was associated with an additional decline of 0.056 global z score points, and prehypertension was associated nonsignificantly with 0.040 additional global z score points of decline, compared with normal blood pressure. People with hypertension who took antihypertensives had less decline during the study period than untreated individuals with hypertension. Having an indication for initiating antihypertensive treatment at baseline (based on Eighth Joint National Committee hypertension guidelines) was associated with a greater 20-year decline than not having an indication.
The authors’ observations are important, but “they are not those of a randomized clinical trial representing a higher-level evidence-based medical decision-making source,” said Philip B. Gorelick, MD, Medical Director of Saint Mary’s Hauenstein Neuroscience Center in Grand Rapids, Michigan, in an accompanying editorial.
Lowering blood pressure is effective for reducing the risk of poststroke dementia in patients with a history of stroke, he added. Blood pressure lowering also can help prevent late-life dementia for people who are middle aged or for the younger elderly.
Given the current evidence, “on a case-by-case basis, the practitioner will need to balance the benefit of blood pressure lowering on cardiovascular disease risk reduction with the possible benefit or risk to cognition,” Dr. Gorelick concluded.
—Erik Greb
Hypertension at midlife and elevated midlife systolic blood pressure are associated with increased cognitive decline during a 20-year period, according to research published online ahead of print August 4 in JAMA Neurology. The decline is greater among Caucasians with high blood pressure than among African Americans with high blood pressure, said the authors.
Rebecca F. Gottesman, MD, PhD, Associate Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues analyzed data for 13,476 African Americans and Caucasians in the Atherosclerosis Risk in Communities cohort. Baseline cognitive assessment was conducted from 1990 to 1992, and follow-up assessments occurred from 1996 to 1998 and from 2011 to 2013. A majority (58.0%) of living participants completed the 20-year cognitive follow-up.
During the follow-up, baseline hypertension was associated with an additional decline of 0.056 global z score points, and prehypertension was associated nonsignificantly with 0.040 additional global z score points of decline, compared with normal blood pressure. People with hypertension who took antihypertensives had less decline during the study period than untreated individuals with hypertension. Having an indication for initiating antihypertensive treatment at baseline (based on Eighth Joint National Committee hypertension guidelines) was associated with a greater 20-year decline than not having an indication.
The authors’ observations are important, but “they are not those of a randomized clinical trial representing a higher-level evidence-based medical decision-making source,” said Philip B. Gorelick, MD, Medical Director of Saint Mary’s Hauenstein Neuroscience Center in Grand Rapids, Michigan, in an accompanying editorial.
Lowering blood pressure is effective for reducing the risk of poststroke dementia in patients with a history of stroke, he added. Blood pressure lowering also can help prevent late-life dementia for people who are middle aged or for the younger elderly.
Given the current evidence, “on a case-by-case basis, the practitioner will need to balance the benefit of blood pressure lowering on cardiovascular disease risk reduction with the possible benefit or risk to cognition,” Dr. Gorelick concluded.
—Erik Greb
Suggested Reading
Gorelick PB. Blood pressure and the prevention of cognitive impairment. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Gottesman RF, Schneider AL, Albert M, et al. Midlife hypertension and 20-year cognitive change: The Atherosclerosis Risk in Communities Neurocognitive Study. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Yaffe K, Vittinghoff E, Pletcher MJ, et al. Early adult to midlife cardiovascular risk factors and cognitive function. Circulation. 2014;129(15):1560-1567.
Suggested Reading
Gorelick PB. Blood pressure and the prevention of cognitive impairment. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Gottesman RF, Schneider AL, Albert M, et al. Midlife hypertension and 20-year cognitive change: The Atherosclerosis Risk in Communities Neurocognitive Study. JAMA Neurol. 2014 Aug 4 [Epub ahead of print].
Yaffe K, Vittinghoff E, Pletcher MJ, et al. Early adult to midlife cardiovascular risk factors and cognitive function. Circulation. 2014;129(15):1560-1567.