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Does Low Muscle Strength Predict Parkinson’s Disease?
Low muscle strength in late adolescence may indicate the presence of subclinical motor deficits and predict a subsequent diagnosis of Parkinson’s disease, according to data published May 5 in Neurology. “The pattern of reduced muscle strength only in the upper extremities is of interest, as motor symptoms of Parkinson’s disease debut most commonly at these sites,” said Helena Gustafsson, MD, a postgraduate student in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden.
A prodromal phase of unknown length precedes the clinical onset of Parkinson’s disease. Research has suggested associations between nonspecific symptoms such as constipation, depression, sleep disorders, and olfactory impairment and a diagnosis of Parkinson’s disease as long as 20 years later. Koller and Kase found reduced muscle strength in patients with early Parkinson’s disease in 1986.
The Swedish National Patient Register
To investigate the potential association between muscle strength and Parkinson’s disease later in life, Dr. Gustafsson and colleagues examined data for cohort of 1,317,713 Swedish men who had been conscripted at age 18 for compulsory military service between 1969 and 1996. All conscripts underwent two-day physical examinations during which isometric maximal muscle force was measured by knee extension, elbow flexion, and handgrip tests. Each muscle group was measured three times. If the third value was highest, the conscript was tested until the test value became stable.
The investigators identified diagnoses of Parkinson’s disease through December 31, 2012, in the study cohort using the participants’ personal identification numbers from the National Patient Register. Participants were followed up for a mean of 29 years. The researchers used linear regression models to test whether men diagnosed with Parkinson’s disease during follow-up had lower muscle strength at baseline than the rest of the cohort, after adjustment for confounders. They also used Cox proportional hazard models to investigate associations between variables assessed at baseline and the later risk of Parkinson’s disease.
Parents’ Diagnosis Influenced Strength
Dr. Gustafsson and colleagues found that participants with greater handgrip strength generally were heavier, taller, and more physically fit at conscription, and less educated 15 years later, than participants with less handgrip strength. A total of 977 men in the cohort were diagnosed with Parkinson’s disease during follow-up at a mean age of 50. Participants with a diagnosis of Parkinson’s disease were more likely to have a parent with the disease, compared with participants without this diagnosis.
Linear regression models adjusted for age, year of conscription, weight, and height indicated that participants diagnosed with Parkinson’s disease during follow-up had less handgrip strength (mean difference [MD] –10.1 N) and elbow flexion strength (MD –5.8 N) than participants without this diagnosis. The difference in knee extension strength (–3.9 N) was not significant. Further adjustments for other variables such as physical fitness, income, and education did not change the significance of the results.
When Dr. Gustafsson and colleagues adjusted Cox regression models for several variables, the lowest fifths of handgrip strength (hazard ratio [HR] 1.38) and elbow flexion strength (HR 1.34), but not knee extension strength (HR 1.24), were associated with an increased risk of Parkinson’s disease diagnosis during follow-up, compared with the highest fifth.
After the researchers adjusted for age, year of conscription, weight, and height, they found that men whose mothers had been diagnosed with Parkinson’s disease had less handgrip strength (MD –3.9 N) and elbow flexion strength (MD –2.7 N), but not knee extension strength (MD 0.9 N), than those whose mothers had not received this diagnosis. Handgrip strength (MD –4.6 N) and elbow flexion strength (MD –3.3 N) values, but not knee extension strength values (MD 0.8 N), were lower in men whose fathers had been diagnosed with Parkinson’s disease than in men whose fathers did not receive this diagnosis.
Exercise May Not Play a Role
The data suggest a genetic link between low muscle strength in young men and later risk of Parkinson’s disease. “As the differences in muscle strength were detected in late adolescence, it would be of interest, although difficult, to study whether these deficits are present already in childhood or perhaps even at birth,” said Dr. Gustafsson.
The investigators observed substantial relationships between physical fitness and muscle strength, but the associations between muscle strength and Parkinson’s disease were independent of physical fitness, and physical fitness was not associated with the risk of Parkinson’s disease. “Thus, exercise habits are unlikely to underlie the associations between Parkinson’s disease and muscle strength observed in this study,” said Dr. Gustafsson.
Findings May Be Sex-Specific
The strengths of Dr. Gustafsson’s study are its large population and long follow-up, said Cuiling Wang, PhD, Associate Professor in the Department of Epidemiology and Population Health at Albert Einstein College of Medicine in Bronx, New York, in an accompanying editorial. The large number of 977 incident cases of Parkinson’s disease is uncommon for this type of study. “Possibly as both a strength and as a cautionary note, the modest magnitude of association found here would be difficult to detect in smaller studies,” Dr. Wang added.
“The finding from this study needs to be interpreted with caution, as it might not be applicable to women or other races and ethnicities. However, it presents an intriguing hypothetical biomarker that prompts further study,” she concluded.
—Erik Greb
Suggested Reading
Gustafsson H, Aasly J, Stråhle S, et al. Low muscle strength in late adolescence and Parkinson disease later in life. Neurology. 2015;84(18):1862-1869.
Wang C. Comment: Muscle strength at age 18 and Parkinson disease among Swedish men from a nationwide cohort. Neurology. 2015;84(18):1868.
Low muscle strength in late adolescence may indicate the presence of subclinical motor deficits and predict a subsequent diagnosis of Parkinson’s disease, according to data published May 5 in Neurology. “The pattern of reduced muscle strength only in the upper extremities is of interest, as motor symptoms of Parkinson’s disease debut most commonly at these sites,” said Helena Gustafsson, MD, a postgraduate student in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden.
A prodromal phase of unknown length precedes the clinical onset of Parkinson’s disease. Research has suggested associations between nonspecific symptoms such as constipation, depression, sleep disorders, and olfactory impairment and a diagnosis of Parkinson’s disease as long as 20 years later. Koller and Kase found reduced muscle strength in patients with early Parkinson’s disease in 1986.
The Swedish National Patient Register
To investigate the potential association between muscle strength and Parkinson’s disease later in life, Dr. Gustafsson and colleagues examined data for cohort of 1,317,713 Swedish men who had been conscripted at age 18 for compulsory military service between 1969 and 1996. All conscripts underwent two-day physical examinations during which isometric maximal muscle force was measured by knee extension, elbow flexion, and handgrip tests. Each muscle group was measured three times. If the third value was highest, the conscript was tested until the test value became stable.
The investigators identified diagnoses of Parkinson’s disease through December 31, 2012, in the study cohort using the participants’ personal identification numbers from the National Patient Register. Participants were followed up for a mean of 29 years. The researchers used linear regression models to test whether men diagnosed with Parkinson’s disease during follow-up had lower muscle strength at baseline than the rest of the cohort, after adjustment for confounders. They also used Cox proportional hazard models to investigate associations between variables assessed at baseline and the later risk of Parkinson’s disease.
Parents’ Diagnosis Influenced Strength
Dr. Gustafsson and colleagues found that participants with greater handgrip strength generally were heavier, taller, and more physically fit at conscription, and less educated 15 years later, than participants with less handgrip strength. A total of 977 men in the cohort were diagnosed with Parkinson’s disease during follow-up at a mean age of 50. Participants with a diagnosis of Parkinson’s disease were more likely to have a parent with the disease, compared with participants without this diagnosis.
Linear regression models adjusted for age, year of conscription, weight, and height indicated that participants diagnosed with Parkinson’s disease during follow-up had less handgrip strength (mean difference [MD] –10.1 N) and elbow flexion strength (MD –5.8 N) than participants without this diagnosis. The difference in knee extension strength (–3.9 N) was not significant. Further adjustments for other variables such as physical fitness, income, and education did not change the significance of the results.
When Dr. Gustafsson and colleagues adjusted Cox regression models for several variables, the lowest fifths of handgrip strength (hazard ratio [HR] 1.38) and elbow flexion strength (HR 1.34), but not knee extension strength (HR 1.24), were associated with an increased risk of Parkinson’s disease diagnosis during follow-up, compared with the highest fifth.
After the researchers adjusted for age, year of conscription, weight, and height, they found that men whose mothers had been diagnosed with Parkinson’s disease had less handgrip strength (MD –3.9 N) and elbow flexion strength (MD –2.7 N), but not knee extension strength (MD 0.9 N), than those whose mothers had not received this diagnosis. Handgrip strength (MD –4.6 N) and elbow flexion strength (MD –3.3 N) values, but not knee extension strength values (MD 0.8 N), were lower in men whose fathers had been diagnosed with Parkinson’s disease than in men whose fathers did not receive this diagnosis.
Exercise May Not Play a Role
The data suggest a genetic link between low muscle strength in young men and later risk of Parkinson’s disease. “As the differences in muscle strength were detected in late adolescence, it would be of interest, although difficult, to study whether these deficits are present already in childhood or perhaps even at birth,” said Dr. Gustafsson.
The investigators observed substantial relationships between physical fitness and muscle strength, but the associations between muscle strength and Parkinson’s disease were independent of physical fitness, and physical fitness was not associated with the risk of Parkinson’s disease. “Thus, exercise habits are unlikely to underlie the associations between Parkinson’s disease and muscle strength observed in this study,” said Dr. Gustafsson.
Findings May Be Sex-Specific
The strengths of Dr. Gustafsson’s study are its large population and long follow-up, said Cuiling Wang, PhD, Associate Professor in the Department of Epidemiology and Population Health at Albert Einstein College of Medicine in Bronx, New York, in an accompanying editorial. The large number of 977 incident cases of Parkinson’s disease is uncommon for this type of study. “Possibly as both a strength and as a cautionary note, the modest magnitude of association found here would be difficult to detect in smaller studies,” Dr. Wang added.
“The finding from this study needs to be interpreted with caution, as it might not be applicable to women or other races and ethnicities. However, it presents an intriguing hypothetical biomarker that prompts further study,” she concluded.
—Erik Greb
Low muscle strength in late adolescence may indicate the presence of subclinical motor deficits and predict a subsequent diagnosis of Parkinson’s disease, according to data published May 5 in Neurology. “The pattern of reduced muscle strength only in the upper extremities is of interest, as motor symptoms of Parkinson’s disease debut most commonly at these sites,” said Helena Gustafsson, MD, a postgraduate student in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden.
A prodromal phase of unknown length precedes the clinical onset of Parkinson’s disease. Research has suggested associations between nonspecific symptoms such as constipation, depression, sleep disorders, and olfactory impairment and a diagnosis of Parkinson’s disease as long as 20 years later. Koller and Kase found reduced muscle strength in patients with early Parkinson’s disease in 1986.
The Swedish National Patient Register
To investigate the potential association between muscle strength and Parkinson’s disease later in life, Dr. Gustafsson and colleagues examined data for cohort of 1,317,713 Swedish men who had been conscripted at age 18 for compulsory military service between 1969 and 1996. All conscripts underwent two-day physical examinations during which isometric maximal muscle force was measured by knee extension, elbow flexion, and handgrip tests. Each muscle group was measured three times. If the third value was highest, the conscript was tested until the test value became stable.
The investigators identified diagnoses of Parkinson’s disease through December 31, 2012, in the study cohort using the participants’ personal identification numbers from the National Patient Register. Participants were followed up for a mean of 29 years. The researchers used linear regression models to test whether men diagnosed with Parkinson’s disease during follow-up had lower muscle strength at baseline than the rest of the cohort, after adjustment for confounders. They also used Cox proportional hazard models to investigate associations between variables assessed at baseline and the later risk of Parkinson’s disease.
Parents’ Diagnosis Influenced Strength
Dr. Gustafsson and colleagues found that participants with greater handgrip strength generally were heavier, taller, and more physically fit at conscription, and less educated 15 years later, than participants with less handgrip strength. A total of 977 men in the cohort were diagnosed with Parkinson’s disease during follow-up at a mean age of 50. Participants with a diagnosis of Parkinson’s disease were more likely to have a parent with the disease, compared with participants without this diagnosis.
Linear regression models adjusted for age, year of conscription, weight, and height indicated that participants diagnosed with Parkinson’s disease during follow-up had less handgrip strength (mean difference [MD] –10.1 N) and elbow flexion strength (MD –5.8 N) than participants without this diagnosis. The difference in knee extension strength (–3.9 N) was not significant. Further adjustments for other variables such as physical fitness, income, and education did not change the significance of the results.
When Dr. Gustafsson and colleagues adjusted Cox regression models for several variables, the lowest fifths of handgrip strength (hazard ratio [HR] 1.38) and elbow flexion strength (HR 1.34), but not knee extension strength (HR 1.24), were associated with an increased risk of Parkinson’s disease diagnosis during follow-up, compared with the highest fifth.
After the researchers adjusted for age, year of conscription, weight, and height, they found that men whose mothers had been diagnosed with Parkinson’s disease had less handgrip strength (MD –3.9 N) and elbow flexion strength (MD –2.7 N), but not knee extension strength (MD 0.9 N), than those whose mothers had not received this diagnosis. Handgrip strength (MD –4.6 N) and elbow flexion strength (MD –3.3 N) values, but not knee extension strength values (MD 0.8 N), were lower in men whose fathers had been diagnosed with Parkinson’s disease than in men whose fathers did not receive this diagnosis.
Exercise May Not Play a Role
The data suggest a genetic link between low muscle strength in young men and later risk of Parkinson’s disease. “As the differences in muscle strength were detected in late adolescence, it would be of interest, although difficult, to study whether these deficits are present already in childhood or perhaps even at birth,” said Dr. Gustafsson.
The investigators observed substantial relationships between physical fitness and muscle strength, but the associations between muscle strength and Parkinson’s disease were independent of physical fitness, and physical fitness was not associated with the risk of Parkinson’s disease. “Thus, exercise habits are unlikely to underlie the associations between Parkinson’s disease and muscle strength observed in this study,” said Dr. Gustafsson.
Findings May Be Sex-Specific
The strengths of Dr. Gustafsson’s study are its large population and long follow-up, said Cuiling Wang, PhD, Associate Professor in the Department of Epidemiology and Population Health at Albert Einstein College of Medicine in Bronx, New York, in an accompanying editorial. The large number of 977 incident cases of Parkinson’s disease is uncommon for this type of study. “Possibly as both a strength and as a cautionary note, the modest magnitude of association found here would be difficult to detect in smaller studies,” Dr. Wang added.
“The finding from this study needs to be interpreted with caution, as it might not be applicable to women or other races and ethnicities. However, it presents an intriguing hypothetical biomarker that prompts further study,” she concluded.
—Erik Greb
Suggested Reading
Gustafsson H, Aasly J, Stråhle S, et al. Low muscle strength in late adolescence and Parkinson disease later in life. Neurology. 2015;84(18):1862-1869.
Wang C. Comment: Muscle strength at age 18 and Parkinson disease among Swedish men from a nationwide cohort. Neurology. 2015;84(18):1868.
Suggested Reading
Gustafsson H, Aasly J, Stråhle S, et al. Low muscle strength in late adolescence and Parkinson disease later in life. Neurology. 2015;84(18):1862-1869.
Wang C. Comment: Muscle strength at age 18 and Parkinson disease among Swedish men from a nationwide cohort. Neurology. 2015;84(18):1868.
AAN Revises Epilepsy Update Quality Measurement Set
The American Academy of Neurology’s Epilepsy Update Quality Measurement Set workgroup retired 3 of the 2009 recommendations; revised 5 recommendations; and added 2 more. The new quality measurement set includes:
At each encounter:
o Specify etiology, seizure type, and epilepsy syndrome
o Ask about side effects of antiepileptic therapy and offer intervention
Once a year:
o Counsel women of childbearing potential with epilepsy
Every 2 years:
Fountain NB, Van Ness PC, Bennett A, et al. Quality improvement in neurology: epilepsy update quality measurement set. Neurology. 2015;84(14):1483-1487.
The American Academy of Neurology’s Epilepsy Update Quality Measurement Set workgroup retired 3 of the 2009 recommendations; revised 5 recommendations; and added 2 more. The new quality measurement set includes:
At each encounter:
o Specify etiology, seizure type, and epilepsy syndrome
o Ask about side effects of antiepileptic therapy and offer intervention
Once a year:
o Counsel women of childbearing potential with epilepsy
Every 2 years:
Fountain NB, Van Ness PC, Bennett A, et al. Quality improvement in neurology: epilepsy update quality measurement set. Neurology. 2015;84(14):1483-1487.
The American Academy of Neurology’s Epilepsy Update Quality Measurement Set workgroup retired 3 of the 2009 recommendations; revised 5 recommendations; and added 2 more. The new quality measurement set includes:
At each encounter:
o Specify etiology, seizure type, and epilepsy syndrome
o Ask about side effects of antiepileptic therapy and offer intervention
Once a year:
o Counsel women of childbearing potential with epilepsy
Every 2 years:
Fountain NB, Van Ness PC, Bennett A, et al. Quality improvement in neurology: epilepsy update quality measurement set. Neurology. 2015;84(14):1483-1487.
Are Status Epilepticus Hospitalizations Increasing?
Over 400,000 status epilepticus-related hospital visits between January 1, 1999 and December 31, 2010 were examined in 2 retrospective serial cross-sectional studies. Status epilepticus-related mortality was relatively stable over the 12-year range but there was a marked increase in status epilepticus hospitalizations (increase of 56.4% from 1999 to 2010). The authors suggest this change could be due to an increase in status epilepticus diagnoses through advanced diagnostic sensitivity or adjustments in medical billing and coding. The authors advocate that the standard approach to status epilepticus should evolve with these new epidemiologic trends.
Betjemann JP, Josephson SA, Lowenstein DH, Burke JF. Trends in status epilepticus-related hospitalizations and mortality: redefined in US practice over time [published online ahead of print April 27, 2015]. JAMA Neurol. 2015:doi:10.1001/jamaneurol.2015.0188.
Over 400,000 status epilepticus-related hospital visits between January 1, 1999 and December 31, 2010 were examined in 2 retrospective serial cross-sectional studies. Status epilepticus-related mortality was relatively stable over the 12-year range but there was a marked increase in status epilepticus hospitalizations (increase of 56.4% from 1999 to 2010). The authors suggest this change could be due to an increase in status epilepticus diagnoses through advanced diagnostic sensitivity or adjustments in medical billing and coding. The authors advocate that the standard approach to status epilepticus should evolve with these new epidemiologic trends.
Betjemann JP, Josephson SA, Lowenstein DH, Burke JF. Trends in status epilepticus-related hospitalizations and mortality: redefined in US practice over time [published online ahead of print April 27, 2015]. JAMA Neurol. 2015:doi:10.1001/jamaneurol.2015.0188.
Over 400,000 status epilepticus-related hospital visits between January 1, 1999 and December 31, 2010 were examined in 2 retrospective serial cross-sectional studies. Status epilepticus-related mortality was relatively stable over the 12-year range but there was a marked increase in status epilepticus hospitalizations (increase of 56.4% from 1999 to 2010). The authors suggest this change could be due to an increase in status epilepticus diagnoses through advanced diagnostic sensitivity or adjustments in medical billing and coding. The authors advocate that the standard approach to status epilepticus should evolve with these new epidemiologic trends.
Betjemann JP, Josephson SA, Lowenstein DH, Burke JF. Trends in status epilepticus-related hospitalizations and mortality: redefined in US practice over time [published online ahead of print April 27, 2015]. JAMA Neurol. 2015:doi:10.1001/jamaneurol.2015.0188.
Is MEG a Valuable Tool for Interictal Spike Mapping before Epilepsy Surgery?
A retrospective cohort study of 132 patients with focal epilepsy who received MEG and underwent resective surgery found that magnetoencephalography (MEG) was a valuable tool for noninvasive interictal spike mapping. Prior to the results of this study, the clinical utility of MEG in presurgical evaluation of patients with epilepsy was not fully understood because of the lack of long-term outcomes or small sample sizes. The reliability of MEG was comparable in patients with or without localized scalp EEG and the use of MEG to localize the epileptogenic zone was associated with improved seizure outcomes.
Englot DJ, Nagarajan SS, Imber BS, et al. Epileptogenic zone localization using magnetoencephalography predicts seizure freedom in epilepsy surgery [published online ahead of print April 29, 2015]. Epilepsia. 2015:doi:10.1111/epi.13002.
A retrospective cohort study of 132 patients with focal epilepsy who received MEG and underwent resective surgery found that magnetoencephalography (MEG) was a valuable tool for noninvasive interictal spike mapping. Prior to the results of this study, the clinical utility of MEG in presurgical evaluation of patients with epilepsy was not fully understood because of the lack of long-term outcomes or small sample sizes. The reliability of MEG was comparable in patients with or without localized scalp EEG and the use of MEG to localize the epileptogenic zone was associated with improved seizure outcomes.
Englot DJ, Nagarajan SS, Imber BS, et al. Epileptogenic zone localization using magnetoencephalography predicts seizure freedom in epilepsy surgery [published online ahead of print April 29, 2015]. Epilepsia. 2015:doi:10.1111/epi.13002.
A retrospective cohort study of 132 patients with focal epilepsy who received MEG and underwent resective surgery found that magnetoencephalography (MEG) was a valuable tool for noninvasive interictal spike mapping. Prior to the results of this study, the clinical utility of MEG in presurgical evaluation of patients with epilepsy was not fully understood because of the lack of long-term outcomes or small sample sizes. The reliability of MEG was comparable in patients with or without localized scalp EEG and the use of MEG to localize the epileptogenic zone was associated with improved seizure outcomes.
Englot DJ, Nagarajan SS, Imber BS, et al. Epileptogenic zone localization using magnetoencephalography predicts seizure freedom in epilepsy surgery [published online ahead of print April 29, 2015]. Epilepsia. 2015:doi:10.1111/epi.13002.
SIRS Criteria Could Identify More Patients with Severe Sepsis
Clinical question: Does inclusion of two or more SIRS criteria in the definition of severe sepsis accurately identify patients with higher mortality risk, as compared with patients with infection and organ failure but with fewer than two SIRS criteria?
Background: SIRS describes dysregulation of the inflammatory response to illness. The current definition of severe sepsis includes evidence of infection, organ failure, and two or more SIRS criteria. This study sought to test the validity of inclusion of two or more SIRS criteria in the definition of severe sepsis to differentiate patients at higher mortality risk.
Study design: 14-year, retrospective study.
Setting: One hundred seventy-two ICUs in Australia and New Zealand.
Synopsis: Investigators evaluated 109,663 patients; 87.9% had SIRS-positive severe sepsis, and 12.1% had SIRS-negative severe sepsis. Patients with SIRS-positive sepsis were younger, more ill with higher mortality, and more likely to have community-acquired infections. Both groups had decreased mortality over the 14-year study period; SIRS-positive patients decreased to 18.3% from 36.1%; SIRS-negative patients decreased to 8.5% from 27.7%.
Being SIRS-positive independently increased the risk of death by 26%; however, modeling showed a linear relationship between mortality and presence of SIRS criteria with each additional criteria, from zero to four, increasing mortality by 13%. There was no transitional increase in risk of mortality using two criteria as a cut-off.
Limiting the severe sepsis definition to two or more SIRS criteria missed one of eight patients admitted to ICU with organ failure and infection alone. SIRS-negative severe sepsis patients had significant mortality but showed similarities to SIRS-positive severe sepsis patients, suggesting they are separate phenotypes of the same condition.
Bottom line: This study challenges the sensitivity, face validity, and construct validity of the two-criteria SIRS cutoff. Redefining severe sepsis to include a lower number of SIRS criteria may diagnose more patients with organ failure and infection.
Citation: Kaukonen KM, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response syndrome criteria in defining severe sepsis. N Engl J Med. 2015;372:1629-1638.
Clinical question: Does inclusion of two or more SIRS criteria in the definition of severe sepsis accurately identify patients with higher mortality risk, as compared with patients with infection and organ failure but with fewer than two SIRS criteria?
Background: SIRS describes dysregulation of the inflammatory response to illness. The current definition of severe sepsis includes evidence of infection, organ failure, and two or more SIRS criteria. This study sought to test the validity of inclusion of two or more SIRS criteria in the definition of severe sepsis to differentiate patients at higher mortality risk.
Study design: 14-year, retrospective study.
Setting: One hundred seventy-two ICUs in Australia and New Zealand.
Synopsis: Investigators evaluated 109,663 patients; 87.9% had SIRS-positive severe sepsis, and 12.1% had SIRS-negative severe sepsis. Patients with SIRS-positive sepsis were younger, more ill with higher mortality, and more likely to have community-acquired infections. Both groups had decreased mortality over the 14-year study period; SIRS-positive patients decreased to 18.3% from 36.1%; SIRS-negative patients decreased to 8.5% from 27.7%.
Being SIRS-positive independently increased the risk of death by 26%; however, modeling showed a linear relationship between mortality and presence of SIRS criteria with each additional criteria, from zero to four, increasing mortality by 13%. There was no transitional increase in risk of mortality using two criteria as a cut-off.
Limiting the severe sepsis definition to two or more SIRS criteria missed one of eight patients admitted to ICU with organ failure and infection alone. SIRS-negative severe sepsis patients had significant mortality but showed similarities to SIRS-positive severe sepsis patients, suggesting they are separate phenotypes of the same condition.
Bottom line: This study challenges the sensitivity, face validity, and construct validity of the two-criteria SIRS cutoff. Redefining severe sepsis to include a lower number of SIRS criteria may diagnose more patients with organ failure and infection.
Citation: Kaukonen KM, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response syndrome criteria in defining severe sepsis. N Engl J Med. 2015;372:1629-1638.
Clinical question: Does inclusion of two or more SIRS criteria in the definition of severe sepsis accurately identify patients with higher mortality risk, as compared with patients with infection and organ failure but with fewer than two SIRS criteria?
Background: SIRS describes dysregulation of the inflammatory response to illness. The current definition of severe sepsis includes evidence of infection, organ failure, and two or more SIRS criteria. This study sought to test the validity of inclusion of two or more SIRS criteria in the definition of severe sepsis to differentiate patients at higher mortality risk.
Study design: 14-year, retrospective study.
Setting: One hundred seventy-two ICUs in Australia and New Zealand.
Synopsis: Investigators evaluated 109,663 patients; 87.9% had SIRS-positive severe sepsis, and 12.1% had SIRS-negative severe sepsis. Patients with SIRS-positive sepsis were younger, more ill with higher mortality, and more likely to have community-acquired infections. Both groups had decreased mortality over the 14-year study period; SIRS-positive patients decreased to 18.3% from 36.1%; SIRS-negative patients decreased to 8.5% from 27.7%.
Being SIRS-positive independently increased the risk of death by 26%; however, modeling showed a linear relationship between mortality and presence of SIRS criteria with each additional criteria, from zero to four, increasing mortality by 13%. There was no transitional increase in risk of mortality using two criteria as a cut-off.
Limiting the severe sepsis definition to two or more SIRS criteria missed one of eight patients admitted to ICU with organ failure and infection alone. SIRS-negative severe sepsis patients had significant mortality but showed similarities to SIRS-positive severe sepsis patients, suggesting they are separate phenotypes of the same condition.
Bottom line: This study challenges the sensitivity, face validity, and construct validity of the two-criteria SIRS cutoff. Redefining severe sepsis to include a lower number of SIRS criteria may diagnose more patients with organ failure and infection.
Citation: Kaukonen KM, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response syndrome criteria in defining severe sepsis. N Engl J Med. 2015;372:1629-1638.
Trimethoprim-Sulfamethoxazole Use in Older Patients Taking Spironolactone
Clinical question: Does trimethoprim-sulfamethoxazole (TMP-SMX) increase the risk of sudden death in older patients taking spironolactone?
Background: TMP-SMX increases the risk of hyperkalemia when used with spironolactone; however, previous studies have not examined whether the drug interaction is associated with an increased risk of sudden cardiac death, a predictable consequence of hyperkalemia.
Study design: Population-based, nested, case-control study.
Setting: Ontario, Canada.
Synopsis: Investigators identified 11,968 patients aged 66 years or older who suffered sudden death between 1994 and 2011 while receiving spironolactone; for 328 of these patients, death occurred within 14 days of antibiotic exposure. The rate of sudden death in patients receiving TMP-SMX was compared to the rate of sudden death in patients who instead received other study antibiotics.
Compared with amoxicillin, TMP-SMX was associated with a more than twofold increase in the risk of sudden death (OR 2.46, 95%; CI 1.55-3.90). The absolute rate of death of patients taking spironolactone who were prescribed TMP-SMX was 0.74%, compared to 0.35% in patients prescribed amoxicillin.
Because TMP-SMX and spironolactone are common medications, the likelihood of co-prescription leading to drug interaction is high. Although the study does not establish causality, it suggests that alternate antibiotics should be used in elderly patients on spironolactone when possible.
Bottom line: TMP-SMX increases the risk of sudden death in older patients taking spironolactone.
Citation: Antoniou T, Hollands S, Macdonald EM, Gomes T, Mamdani MM, Juurlink DN. Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. CMAJ. 2015;187(4):E138-E143
Clinical question: Does trimethoprim-sulfamethoxazole (TMP-SMX) increase the risk of sudden death in older patients taking spironolactone?
Background: TMP-SMX increases the risk of hyperkalemia when used with spironolactone; however, previous studies have not examined whether the drug interaction is associated with an increased risk of sudden cardiac death, a predictable consequence of hyperkalemia.
Study design: Population-based, nested, case-control study.
Setting: Ontario, Canada.
Synopsis: Investigators identified 11,968 patients aged 66 years or older who suffered sudden death between 1994 and 2011 while receiving spironolactone; for 328 of these patients, death occurred within 14 days of antibiotic exposure. The rate of sudden death in patients receiving TMP-SMX was compared to the rate of sudden death in patients who instead received other study antibiotics.
Compared with amoxicillin, TMP-SMX was associated with a more than twofold increase in the risk of sudden death (OR 2.46, 95%; CI 1.55-3.90). The absolute rate of death of patients taking spironolactone who were prescribed TMP-SMX was 0.74%, compared to 0.35% in patients prescribed amoxicillin.
Because TMP-SMX and spironolactone are common medications, the likelihood of co-prescription leading to drug interaction is high. Although the study does not establish causality, it suggests that alternate antibiotics should be used in elderly patients on spironolactone when possible.
Bottom line: TMP-SMX increases the risk of sudden death in older patients taking spironolactone.
Citation: Antoniou T, Hollands S, Macdonald EM, Gomes T, Mamdani MM, Juurlink DN. Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. CMAJ. 2015;187(4):E138-E143
Clinical question: Does trimethoprim-sulfamethoxazole (TMP-SMX) increase the risk of sudden death in older patients taking spironolactone?
Background: TMP-SMX increases the risk of hyperkalemia when used with spironolactone; however, previous studies have not examined whether the drug interaction is associated with an increased risk of sudden cardiac death, a predictable consequence of hyperkalemia.
Study design: Population-based, nested, case-control study.
Setting: Ontario, Canada.
Synopsis: Investigators identified 11,968 patients aged 66 years or older who suffered sudden death between 1994 and 2011 while receiving spironolactone; for 328 of these patients, death occurred within 14 days of antibiotic exposure. The rate of sudden death in patients receiving TMP-SMX was compared to the rate of sudden death in patients who instead received other study antibiotics.
Compared with amoxicillin, TMP-SMX was associated with a more than twofold increase in the risk of sudden death (OR 2.46, 95%; CI 1.55-3.90). The absolute rate of death of patients taking spironolactone who were prescribed TMP-SMX was 0.74%, compared to 0.35% in patients prescribed amoxicillin.
Because TMP-SMX and spironolactone are common medications, the likelihood of co-prescription leading to drug interaction is high. Although the study does not establish causality, it suggests that alternate antibiotics should be used in elderly patients on spironolactone when possible.
Bottom line: TMP-SMX increases the risk of sudden death in older patients taking spironolactone.
Citation: Antoniou T, Hollands S, Macdonald EM, Gomes T, Mamdani MM, Juurlink DN. Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. CMAJ. 2015;187(4):E138-E143
Medicare Nonpayment for Hospital-Acquired Conditions May Have Reduced Infection Rates
Clinical question: What was the effect of the Centers for Medicare and Medicaid Services’ (CMS) nonpayment for hospital-acquired conditions?
Background: In 2008, CMS implemented the Hospital-Acquired Conditions (HAC) initiative, denying incremental payment to hospitals for complications of hospital care, including central-line associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), hospital-acquired pressure ulcers, and injurious patient falls.
Study design: Quasi-experimental data review, pre-post comparison of outcomes.
Setting: Nearly 1,400 U.S. hospitals contributing data to the National Database of Nursing Quality Indicators (NDNQI).
Synopsis: Using time points before and after implementation of the CMS initiative, the authors found that the rates of CLABSIs and CAUTIs dropped significantly after implementation (11% reduction of CLABSIs, 10% reduction of CAUTIs). The rates of pressure ulcers and falls did not change significantly.
Findings differ from an earlier study, which found the HAC initiative did not lead to a reduction in the rates of CLABSIs or CAUTIs. The authors point out that the databases used were different, as was the time frame of data collection.
The authors hypothesize that the reason CLABSI and CAUTI rates decreased while fall and pressure ulcer rates were unchanged was better evidence supporting infection prevention practices for the former. An accompanying editorial argues that the differential outcomes may have been due to increased challenges in implementing practices for the latter measures rather than differential evidence.
Limitations of the study include characteristics of hospitals reporting to the NDNQI and accuracy of data capture by individual reporting hospitals. Changes over time may also be attributed to factors other than the HAC initiative.
Bottom line: Nonpayment for HACs may have led to decreases in rates of CLABSIs and CAUTIs, but rates of pressure ulcers and falls remained unchanged.
Citation: Waters TM, Daniels MJ, Bazzoli GJ, et al. Effect of Medicare’s nonpayment for hospital-acquired conditions. JAMA Intern Med. 2015;175(3):347-354.
Clinical question: What was the effect of the Centers for Medicare and Medicaid Services’ (CMS) nonpayment for hospital-acquired conditions?
Background: In 2008, CMS implemented the Hospital-Acquired Conditions (HAC) initiative, denying incremental payment to hospitals for complications of hospital care, including central-line associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), hospital-acquired pressure ulcers, and injurious patient falls.
Study design: Quasi-experimental data review, pre-post comparison of outcomes.
Setting: Nearly 1,400 U.S. hospitals contributing data to the National Database of Nursing Quality Indicators (NDNQI).
Synopsis: Using time points before and after implementation of the CMS initiative, the authors found that the rates of CLABSIs and CAUTIs dropped significantly after implementation (11% reduction of CLABSIs, 10% reduction of CAUTIs). The rates of pressure ulcers and falls did not change significantly.
Findings differ from an earlier study, which found the HAC initiative did not lead to a reduction in the rates of CLABSIs or CAUTIs. The authors point out that the databases used were different, as was the time frame of data collection.
The authors hypothesize that the reason CLABSI and CAUTI rates decreased while fall and pressure ulcer rates were unchanged was better evidence supporting infection prevention practices for the former. An accompanying editorial argues that the differential outcomes may have been due to increased challenges in implementing practices for the latter measures rather than differential evidence.
Limitations of the study include characteristics of hospitals reporting to the NDNQI and accuracy of data capture by individual reporting hospitals. Changes over time may also be attributed to factors other than the HAC initiative.
Bottom line: Nonpayment for HACs may have led to decreases in rates of CLABSIs and CAUTIs, but rates of pressure ulcers and falls remained unchanged.
Citation: Waters TM, Daniels MJ, Bazzoli GJ, et al. Effect of Medicare’s nonpayment for hospital-acquired conditions. JAMA Intern Med. 2015;175(3):347-354.
Clinical question: What was the effect of the Centers for Medicare and Medicaid Services’ (CMS) nonpayment for hospital-acquired conditions?
Background: In 2008, CMS implemented the Hospital-Acquired Conditions (HAC) initiative, denying incremental payment to hospitals for complications of hospital care, including central-line associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), hospital-acquired pressure ulcers, and injurious patient falls.
Study design: Quasi-experimental data review, pre-post comparison of outcomes.
Setting: Nearly 1,400 U.S. hospitals contributing data to the National Database of Nursing Quality Indicators (NDNQI).
Synopsis: Using time points before and after implementation of the CMS initiative, the authors found that the rates of CLABSIs and CAUTIs dropped significantly after implementation (11% reduction of CLABSIs, 10% reduction of CAUTIs). The rates of pressure ulcers and falls did not change significantly.
Findings differ from an earlier study, which found the HAC initiative did not lead to a reduction in the rates of CLABSIs or CAUTIs. The authors point out that the databases used were different, as was the time frame of data collection.
The authors hypothesize that the reason CLABSI and CAUTI rates decreased while fall and pressure ulcer rates were unchanged was better evidence supporting infection prevention practices for the former. An accompanying editorial argues that the differential outcomes may have been due to increased challenges in implementing practices for the latter measures rather than differential evidence.
Limitations of the study include characteristics of hospitals reporting to the NDNQI and accuracy of data capture by individual reporting hospitals. Changes over time may also be attributed to factors other than the HAC initiative.
Bottom line: Nonpayment for HACs may have led to decreases in rates of CLABSIs and CAUTIs, but rates of pressure ulcers and falls remained unchanged.
Citation: Waters TM, Daniels MJ, Bazzoli GJ, et al. Effect of Medicare’s nonpayment for hospital-acquired conditions. JAMA Intern Med. 2015;175(3):347-354.
Peri-Operative Phlebotomy Might Cause Significant Blood Loss in Cardiac Surgery Patients
Clinical question: What are the frequency of laboratory testing, the average total blood volume drawn per patient, and the resulting transfusion utilization in patients undergoing cardiac surgery?
Background: Healthcare providers seldom recognize the amount of phlebotomy, and, therefore, its consequences and possible solutions have not been fully evaluated.
Study design: Retrospective, cohort study.
Setting: Major U.S. academic medical center.
Synopsis: The authors examined 1,894 patients undergoing cardiac surgery over a six-month period. They determined the number and type of lab tests drawn on each patient during hospitalization, as well as the estimated total blood volume drawn on each patient.
Patients averaged 115 lab tests during their hospitalization and had cumulative median phlebotomy volume of 454 ml (equivalent to one to two units of red blood cells). They also found that increasing total phlebotomy volume correlated with increased blood product use and that increasing length of stay correlated with higher levels of both.
During an average patient day in the ICU, of the average 116 ml of blood drawn, 80 ml was discarded at the bedside.
Limitations include the broad applicability of this study, which focused on cardiac surgery patients, all of whom stayed in an ICU and had central lines as the source of the majority of their blood draws. Appropriateness of lab testing and transfusions were not examined in this study.
Bottom line: Blood volumes equivalent to one to two units of red blood cells are drawn for lab tests on patients undergoing cardiac surgery, with a large portion of that blood being wasted at the bedside. Initiatives to reduce blood draw volume may help to reduce resource utilization related to such high rates of blood loss from phlebotomy.
Citation: Koch CG, Reinecks EZ, Tang AS, et al. Contemporary bloodletting in cardiac surgical care. Ann Thorac Surg. 2015;99(3):779-784.
Clinical question: What are the frequency of laboratory testing, the average total blood volume drawn per patient, and the resulting transfusion utilization in patients undergoing cardiac surgery?
Background: Healthcare providers seldom recognize the amount of phlebotomy, and, therefore, its consequences and possible solutions have not been fully evaluated.
Study design: Retrospective, cohort study.
Setting: Major U.S. academic medical center.
Synopsis: The authors examined 1,894 patients undergoing cardiac surgery over a six-month period. They determined the number and type of lab tests drawn on each patient during hospitalization, as well as the estimated total blood volume drawn on each patient.
Patients averaged 115 lab tests during their hospitalization and had cumulative median phlebotomy volume of 454 ml (equivalent to one to two units of red blood cells). They also found that increasing total phlebotomy volume correlated with increased blood product use and that increasing length of stay correlated with higher levels of both.
During an average patient day in the ICU, of the average 116 ml of blood drawn, 80 ml was discarded at the bedside.
Limitations include the broad applicability of this study, which focused on cardiac surgery patients, all of whom stayed in an ICU and had central lines as the source of the majority of their blood draws. Appropriateness of lab testing and transfusions were not examined in this study.
Bottom line: Blood volumes equivalent to one to two units of red blood cells are drawn for lab tests on patients undergoing cardiac surgery, with a large portion of that blood being wasted at the bedside. Initiatives to reduce blood draw volume may help to reduce resource utilization related to such high rates of blood loss from phlebotomy.
Citation: Koch CG, Reinecks EZ, Tang AS, et al. Contemporary bloodletting in cardiac surgical care. Ann Thorac Surg. 2015;99(3):779-784.
Clinical question: What are the frequency of laboratory testing, the average total blood volume drawn per patient, and the resulting transfusion utilization in patients undergoing cardiac surgery?
Background: Healthcare providers seldom recognize the amount of phlebotomy, and, therefore, its consequences and possible solutions have not been fully evaluated.
Study design: Retrospective, cohort study.
Setting: Major U.S. academic medical center.
Synopsis: The authors examined 1,894 patients undergoing cardiac surgery over a six-month period. They determined the number and type of lab tests drawn on each patient during hospitalization, as well as the estimated total blood volume drawn on each patient.
Patients averaged 115 lab tests during their hospitalization and had cumulative median phlebotomy volume of 454 ml (equivalent to one to two units of red blood cells). They also found that increasing total phlebotomy volume correlated with increased blood product use and that increasing length of stay correlated with higher levels of both.
During an average patient day in the ICU, of the average 116 ml of blood drawn, 80 ml was discarded at the bedside.
Limitations include the broad applicability of this study, which focused on cardiac surgery patients, all of whom stayed in an ICU and had central lines as the source of the majority of their blood draws. Appropriateness of lab testing and transfusions were not examined in this study.
Bottom line: Blood volumes equivalent to one to two units of red blood cells are drawn for lab tests on patients undergoing cardiac surgery, with a large portion of that blood being wasted at the bedside. Initiatives to reduce blood draw volume may help to reduce resource utilization related to such high rates of blood loss from phlebotomy.
Citation: Koch CG, Reinecks EZ, Tang AS, et al. Contemporary bloodletting in cardiac surgical care. Ann Thorac Surg. 2015;99(3):779-784.
Clostridium Difficile Infection Rates in the U.S. in 2011
Clinical question: What are the incidence, recurrence rate, and mortality rate of Clostridium difficile infection (CDI) in the U.S. in 2011?
Background: CDI has continued to change, and its impact on healthcare has continued to increase.
Study design: Cross-sectional analysis.
Setting: U.S.
Synopsis: The incidence, rate of recurrence, and rate of mortality of C. diff were estimated using 10 sites from the CDC Emerging Infections Program. C. diff incidence was estimated at 453,000 cases, with higher rates among females, whites, and those over age 65. One-third of the cases were community associated. There were an estimated 83,000 first-time recurrent infections and 29,300 estimated deaths within 30 days of diagnosis, with half of those deaths attributable to CDI itself.
This study was limited by the reliance of the case definition solely on positive test results and the trend of labs transitioning to nucleic acid amplification testing (NAAT), both of which can lead to inclusion of colonization (not just actual disease). Also, the recurrence and mortality rates were underestimated, because the study only included first-time recurrences and deaths that were documented in the medical record.
Bottom line: C. diff caused nearly half a million infections and was associated with roughly 29,000 deaths in the U.S. in 2011.
Citation: Less FC, Mu Y, Bamberg WM, et al. Burden of Clostridium difficile infection in the United States. N Engl J Med. 2015;372:825-834.
Clinical question: What are the incidence, recurrence rate, and mortality rate of Clostridium difficile infection (CDI) in the U.S. in 2011?
Background: CDI has continued to change, and its impact on healthcare has continued to increase.
Study design: Cross-sectional analysis.
Setting: U.S.
Synopsis: The incidence, rate of recurrence, and rate of mortality of C. diff were estimated using 10 sites from the CDC Emerging Infections Program. C. diff incidence was estimated at 453,000 cases, with higher rates among females, whites, and those over age 65. One-third of the cases were community associated. There were an estimated 83,000 first-time recurrent infections and 29,300 estimated deaths within 30 days of diagnosis, with half of those deaths attributable to CDI itself.
This study was limited by the reliance of the case definition solely on positive test results and the trend of labs transitioning to nucleic acid amplification testing (NAAT), both of which can lead to inclusion of colonization (not just actual disease). Also, the recurrence and mortality rates were underestimated, because the study only included first-time recurrences and deaths that were documented in the medical record.
Bottom line: C. diff caused nearly half a million infections and was associated with roughly 29,000 deaths in the U.S. in 2011.
Citation: Less FC, Mu Y, Bamberg WM, et al. Burden of Clostridium difficile infection in the United States. N Engl J Med. 2015;372:825-834.
Clinical question: What are the incidence, recurrence rate, and mortality rate of Clostridium difficile infection (CDI) in the U.S. in 2011?
Background: CDI has continued to change, and its impact on healthcare has continued to increase.
Study design: Cross-sectional analysis.
Setting: U.S.
Synopsis: The incidence, rate of recurrence, and rate of mortality of C. diff were estimated using 10 sites from the CDC Emerging Infections Program. C. diff incidence was estimated at 453,000 cases, with higher rates among females, whites, and those over age 65. One-third of the cases were community associated. There were an estimated 83,000 first-time recurrent infections and 29,300 estimated deaths within 30 days of diagnosis, with half of those deaths attributable to CDI itself.
This study was limited by the reliance of the case definition solely on positive test results and the trend of labs transitioning to nucleic acid amplification testing (NAAT), both of which can lead to inclusion of colonization (not just actual disease). Also, the recurrence and mortality rates were underestimated, because the study only included first-time recurrences and deaths that were documented in the medical record.
Bottom line: C. diff caused nearly half a million infections and was associated with roughly 29,000 deaths in the U.S. in 2011.
Citation: Less FC, Mu Y, Bamberg WM, et al. Burden of Clostridium difficile infection in the United States. N Engl J Med. 2015;372:825-834.
CT Angiography Effect on Outcome for Patients with Symptomatic Chest Pain
Clinical question: Does CT angiography (CTA) improve clinical outcomes in patients with new-onset stable chest pain more than functional testing?
Background: Chest pain is a common clinical problem, and multiple noninvasive tests are available to detect coronary artery disease (CAD). CT angiography is more accurate than noninvasive testing and may decrease unnecessary invasive testing and improve outcomes in patients with new-onset stable chest pain.
Study design: Pragmatic, comparative-effectiveness design.
Setting: One hundred ninety-three North American sites.
Synopsis: Ten thousand three symptomatic outpatients, mean age 60 years, with at least one cardiovascular risk factor, were randomized to CTA or functional testing to detect CAD. Primary endpoints including death, myocardial infarction, hospitalization for unstable angina, or major procedural complication occurred in 3.3% of CTA patients and 3.0% of functional testing patients (adjusted hazard ratio, 1.04; 95% confidence interval, 0.83 to 1.29; P=0.75). CTA patients received fewer catheterizations showing nonobstructive CAD (3.4% of versus 4.3%, P=0.02).
More CTA patients underwent catheterization within 90 days after randomization (12.2% vs 8.1%), however. Patients in the CTA group had higher exposures to radiation overall, but, per patient, their mean cumulative radiation dose was lower than that of the functional testing group (10.0 mSv vs. 11.3 mSv).
Interestingly, 6.2% of CTA patients versus 3.2% of functional testing patients underwent revascularization, but the study was not powered to assess invasive catheterization or revascularization rates on outcomes.
This study is interesting because results are generalizable to real-world settings; CTA did not improve outcomes compared to functional testing in patients undergoing testing for CAD.
Bottom line: No improvement was seen in clinical outcomes for symptomatic patients undergoing evaluation for CAD with CTA compared with those receiving functional testing.
Citation: Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300.
Clinical question: Does CT angiography (CTA) improve clinical outcomes in patients with new-onset stable chest pain more than functional testing?
Background: Chest pain is a common clinical problem, and multiple noninvasive tests are available to detect coronary artery disease (CAD). CT angiography is more accurate than noninvasive testing and may decrease unnecessary invasive testing and improve outcomes in patients with new-onset stable chest pain.
Study design: Pragmatic, comparative-effectiveness design.
Setting: One hundred ninety-three North American sites.
Synopsis: Ten thousand three symptomatic outpatients, mean age 60 years, with at least one cardiovascular risk factor, were randomized to CTA or functional testing to detect CAD. Primary endpoints including death, myocardial infarction, hospitalization for unstable angina, or major procedural complication occurred in 3.3% of CTA patients and 3.0% of functional testing patients (adjusted hazard ratio, 1.04; 95% confidence interval, 0.83 to 1.29; P=0.75). CTA patients received fewer catheterizations showing nonobstructive CAD (3.4% of versus 4.3%, P=0.02).
More CTA patients underwent catheterization within 90 days after randomization (12.2% vs 8.1%), however. Patients in the CTA group had higher exposures to radiation overall, but, per patient, their mean cumulative radiation dose was lower than that of the functional testing group (10.0 mSv vs. 11.3 mSv).
Interestingly, 6.2% of CTA patients versus 3.2% of functional testing patients underwent revascularization, but the study was not powered to assess invasive catheterization or revascularization rates on outcomes.
This study is interesting because results are generalizable to real-world settings; CTA did not improve outcomes compared to functional testing in patients undergoing testing for CAD.
Bottom line: No improvement was seen in clinical outcomes for symptomatic patients undergoing evaluation for CAD with CTA compared with those receiving functional testing.
Citation: Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300.
Clinical question: Does CT angiography (CTA) improve clinical outcomes in patients with new-onset stable chest pain more than functional testing?
Background: Chest pain is a common clinical problem, and multiple noninvasive tests are available to detect coronary artery disease (CAD). CT angiography is more accurate than noninvasive testing and may decrease unnecessary invasive testing and improve outcomes in patients with new-onset stable chest pain.
Study design: Pragmatic, comparative-effectiveness design.
Setting: One hundred ninety-three North American sites.
Synopsis: Ten thousand three symptomatic outpatients, mean age 60 years, with at least one cardiovascular risk factor, were randomized to CTA or functional testing to detect CAD. Primary endpoints including death, myocardial infarction, hospitalization for unstable angina, or major procedural complication occurred in 3.3% of CTA patients and 3.0% of functional testing patients (adjusted hazard ratio, 1.04; 95% confidence interval, 0.83 to 1.29; P=0.75). CTA patients received fewer catheterizations showing nonobstructive CAD (3.4% of versus 4.3%, P=0.02).
More CTA patients underwent catheterization within 90 days after randomization (12.2% vs 8.1%), however. Patients in the CTA group had higher exposures to radiation overall, but, per patient, their mean cumulative radiation dose was lower than that of the functional testing group (10.0 mSv vs. 11.3 mSv).
Interestingly, 6.2% of CTA patients versus 3.2% of functional testing patients underwent revascularization, but the study was not powered to assess invasive catheterization or revascularization rates on outcomes.
This study is interesting because results are generalizable to real-world settings; CTA did not improve outcomes compared to functional testing in patients undergoing testing for CAD.
Bottom line: No improvement was seen in clinical outcomes for symptomatic patients undergoing evaluation for CAD with CTA compared with those receiving functional testing.
Citation: Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300.