A recent small study suggested that, in the age of endovascular aortic aneurysm repair (EVAR), the mortality rates between symptomatic and asymptomatic abdominal aortic aneurysm (AAA) repair have become similar, according to Peter A. Soden, MD, of Beth Deaconess Medical Center, Boston, and his colleagues. However, in their large database study, Dr. Soden and his colleagues found that outcomes for the repair of abdominal aortic aneurysms were increasingly worse from asymptomatic to symptomatic to ruptured AAA.

The researchers assessed all patients undergoing endovascular and open AAA repair in the 2011-2013 American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) data set, according to a report published in the August issue of the Journal of Vascular Surgery.

D.G.S.V.D. Gajasinghe/Wikimedia Commons/Creative Commons License

Symptomatic AAA was defined as lack of evidence of rupture but with the presence of abdominal or back pain or symptoms from local compression by the aneurysm causing early satiety, hydronephrosis, or deep vein thrombosis. Ruptured aneurysms were divided into two categories: hypotensive (defined as systolic blood pressure less than 90 mmm Hg or drop of greater than 40 mm HG from baseline) and nonhypotensive (J Vasc Surg. 2016;64:297-305).

There were numerous demographic and comorbidity differences between asymptomatic and symptomatic patients and between symptomatic and ruptured patients, with a general trend of increasing of commodities and factors influencing operative risk.

The final study included 5,502 patients undergoing repair of infrarenal (85%; 92% EVAR) or juxtarenal (15%;20% EVAR) aneurysms. These differences in the use of EVAR were statistically significant.

This population comprised 4,495 asymptomatic patients (82% EVAR), 455 symptomatic patients (69% EVAR), and 552 ruptured patients (52% EVAR).

The overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (5.1% vs. 1.9%; P less than .001).Similarly, for EVAR, the overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (3.8% vs. 1.4%; P less than .001). For open repair, there was no significant difference in mortality (7.7% vs. 4.3%) between symptomatic and asymptomatic patients, respectively.

Multivariate analysis showed that symptomatic patients had twice the operative mortality as asymptomatic patients (odds ratio, 2.1). A symptomatic aneurysm was also predictive of a major adverse event (OR, 1.5). Ruptured aneurysms had a significant nearly sevenfold increase in mortality risk vs. symptomatic aneurysms (OR, 6.5) and a fivefold increase of risk of a major adverse event (OR 5.1), with all ORs within their 95% confidence interval levels).

“In this large contemporary study of symptomatic AAA patients, in which the majority were treated with EVAR, we found that symptomatic patients have twice the perioperative mortality compared with asymptomatic patients. Despite this, we also find a reduction in perioperative mortality for symptomatic aneurysms compared with prior reports in which the majority were treated with open repair, and we believe this supports an EVAR-first approach for symptomatic aneurysms with suitable anatomy,” the researchers concluded.

The authors reported that they had no relevant disclosures.

[email protected]

A recent small study suggested that, in the age of endovascular aortic aneurysm repair (EVAR), the mortality rates between symptomatic and asymptomatic abdominal aortic aneurysm (AAA) repair have become similar, according to Peter A. Soden, MD, of Beth Deaconess Medical Center, Boston, and his colleagues. However, in their large database study, Dr. Soden and his colleagues found that outcomes for the repair of abdominal aortic aneurysms were increasingly worse from asymptomatic to symptomatic to ruptured AAA.

The researchers assessed all patients undergoing endovascular and open AAA repair in the 2011-2013 American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) data set, according to a report published in the August issue of the Journal of Vascular Surgery.

D.G.S.V.D. Gajasinghe/Wikimedia Commons/Creative Commons License

Symptomatic AAA was defined as lack of evidence of rupture but with the presence of abdominal or back pain or symptoms from local compression by the aneurysm causing early satiety, hydronephrosis, or deep vein thrombosis. Ruptured aneurysms were divided into two categories: hypotensive (defined as systolic blood pressure less than 90 mmm Hg or drop of greater than 40 mm HG from baseline) and nonhypotensive (J Vasc Surg. 2016;64:297-305).

There were numerous demographic and comorbidity differences between asymptomatic and symptomatic patients and between symptomatic and ruptured patients, with a general trend of increasing of commodities and factors influencing operative risk.

The final study included 5,502 patients undergoing repair of infrarenal (85%; 92% EVAR) or juxtarenal (15%;20% EVAR) aneurysms. These differences in the use of EVAR were statistically significant.

This population comprised 4,495 asymptomatic patients (82% EVAR), 455 symptomatic patients (69% EVAR), and 552 ruptured patients (52% EVAR).

The overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (5.1% vs. 1.9%; P less than .001).Similarly, for EVAR, the overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (3.8% vs. 1.4%; P less than .001). For open repair, there was no significant difference in mortality (7.7% vs. 4.3%) between symptomatic and asymptomatic patients, respectively.

Multivariate analysis showed that symptomatic patients had twice the operative mortality as asymptomatic patients (odds ratio, 2.1). A symptomatic aneurysm was also predictive of a major adverse event (OR, 1.5). Ruptured aneurysms had a significant nearly sevenfold increase in mortality risk vs. symptomatic aneurysms (OR, 6.5) and a fivefold increase of risk of a major adverse event (OR 5.1), with all ORs within their 95% confidence interval levels).

“In this large contemporary study of symptomatic AAA patients, in which the majority were treated with EVAR, we found that symptomatic patients have twice the perioperative mortality compared with asymptomatic patients. Despite this, we also find a reduction in perioperative mortality for symptomatic aneurysms compared with prior reports in which the majority were treated with open repair, and we believe this supports an EVAR-first approach for symptomatic aneurysms with suitable anatomy,” the researchers concluded.

The authors reported that they had no relevant disclosures.

[email protected]

A recent small study suggested that, in the age of endovascular aortic aneurysm repair (EVAR), the mortality rates between symptomatic and asymptomatic abdominal aortic aneurysm (AAA) repair have become similar, according to Peter A. Soden, MD, of Beth Deaconess Medical Center, Boston, and his colleagues. However, in their large database study, Dr. Soden and his colleagues found that outcomes for the repair of abdominal aortic aneurysms were increasingly worse from asymptomatic to symptomatic to ruptured AAA.

The researchers assessed all patients undergoing endovascular and open AAA repair in the 2011-2013 American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) data set, according to a report published in the August issue of the Journal of Vascular Surgery.

D.G.S.V.D. Gajasinghe/Wikimedia Commons/Creative Commons License

Symptomatic AAA was defined as lack of evidence of rupture but with the presence of abdominal or back pain or symptoms from local compression by the aneurysm causing early satiety, hydronephrosis, or deep vein thrombosis. Ruptured aneurysms were divided into two categories: hypotensive (defined as systolic blood pressure less than 90 mmm Hg or drop of greater than 40 mm HG from baseline) and nonhypotensive (J Vasc Surg. 2016;64:297-305).

There were numerous demographic and comorbidity differences between asymptomatic and symptomatic patients and between symptomatic and ruptured patients, with a general trend of increasing of commodities and factors influencing operative risk.

The final study included 5,502 patients undergoing repair of infrarenal (85%; 92% EVAR) or juxtarenal (15%;20% EVAR) aneurysms. These differences in the use of EVAR were statistically significant.

This population comprised 4,495 asymptomatic patients (82% EVAR), 455 symptomatic patients (69% EVAR), and 552 ruptured patients (52% EVAR).

The overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (5.1% vs. 1.9%; P less than .001).Similarly, for EVAR, the overall 30-day mortality rate was significantly higher in symptomatic over asymptomatic patients (3.8% vs. 1.4%; P less than .001). For open repair, there was no significant difference in mortality (7.7% vs. 4.3%) between symptomatic and asymptomatic patients, respectively.

Multivariate analysis showed that symptomatic patients had twice the operative mortality as asymptomatic patients (odds ratio, 2.1). A symptomatic aneurysm was also predictive of a major adverse event (OR, 1.5). Ruptured aneurysms had a significant nearly sevenfold increase in mortality risk vs. symptomatic aneurysms (OR, 6.5) and a fivefold increase of risk of a major adverse event (OR 5.1), with all ORs within their 95% confidence interval levels).

“In this large contemporary study of symptomatic AAA patients, in which the majority were treated with EVAR, we found that symptomatic patients have twice the perioperative mortality compared with asymptomatic patients. Despite this, we also find a reduction in perioperative mortality for symptomatic aneurysms compared with prior reports in which the majority were treated with open repair, and we believe this supports an EVAR-first approach for symptomatic aneurysms with suitable anatomy,” the researchers concluded.

The authors reported that they had no relevant disclosures.

[email protected]

One of PHM16’s most highly-attended sessions was an update on the anticipated AAP guidelines for febrile infants between ages 7-90 days given by Dr. Kenneth Roberts. The goal is to give evidence-based guidelines, not rules, from the most recent literature available. It also stresses the need to separate individual components of serious bacterial infections (UTI, bacteremia, and meningitis) as the incidence and clinical course can vary greatly in this population.

The inclusion criteria for infants for this upcoming algorithm require an infant to be full-term (37-43 weeks gestation), aged 7-90 days, well-appearing, and presenting with a temperature of 38 degrees Celsius.

Exclusion criteria include perinatal/prenatal/neonatal: maternal fever, infection, or antimicrobial treatment, the presence of any evident infection, being technology-dependent, and the presence of congenital anomalies.

The updated guideline will aim to stratify management by age 7-28 days, 29-60 days, and 61 to 90 days to provide the most appropriate and directed treatment.

It will also include a role for inflammatory markers, and allow for a “kinder, gentler” approach to the management of febrile infants aged 7-90 days including withholding certain treatments and procedures if infants are at low risk of infection. An active, not passive, need for observation may be appropriate for certain infants as well. These guidelines should be tailored for individual patients to provide the best care possible while minimizing risk in this population.

Key Takeaway:

An updated AAP Practice guideline algorithm for the management of well-appearing febrile infants 7-28 days, 29-60 days, and 60-90 days will be coming in the near future that will help standardize care in this population, but should not be used as a substitute for clinical judgment.

One of PHM16’s most highly-attended sessions was an update on the anticipated AAP guidelines for febrile infants between ages 7-90 days given by Dr. Kenneth Roberts. The goal is to give evidence-based guidelines, not rules, from the most recent literature available. It also stresses the need to separate individual components of serious bacterial infections (UTI, bacteremia, and meningitis) as the incidence and clinical course can vary greatly in this population.

The inclusion criteria for infants for this upcoming algorithm require an infant to be full-term (37-43 weeks gestation), aged 7-90 days, well-appearing, and presenting with a temperature of 38 degrees Celsius.

Exclusion criteria include perinatal/prenatal/neonatal: maternal fever, infection, or antimicrobial treatment, the presence of any evident infection, being technology-dependent, and the presence of congenital anomalies.

The updated guideline will aim to stratify management by age 7-28 days, 29-60 days, and 61 to 90 days to provide the most appropriate and directed treatment.

It will also include a role for inflammatory markers, and allow for a “kinder, gentler” approach to the management of febrile infants aged 7-90 days including withholding certain treatments and procedures if infants are at low risk of infection. An active, not passive, need for observation may be appropriate for certain infants as well. These guidelines should be tailored for individual patients to provide the best care possible while minimizing risk in this population.

Key Takeaway:

An updated AAP Practice guideline algorithm for the management of well-appearing febrile infants 7-28 days, 29-60 days, and 60-90 days will be coming in the near future that will help standardize care in this population, but should not be used as a substitute for clinical judgment.

One of PHM16’s most highly-attended sessions was an update on the anticipated AAP guidelines for febrile infants between ages 7-90 days given by Dr. Kenneth Roberts. The goal is to give evidence-based guidelines, not rules, from the most recent literature available. It also stresses the need to separate individual components of serious bacterial infections (UTI, bacteremia, and meningitis) as the incidence and clinical course can vary greatly in this population.

The inclusion criteria for infants for this upcoming algorithm require an infant to be full-term (37-43 weeks gestation), aged 7-90 days, well-appearing, and presenting with a temperature of 38 degrees Celsius.

Exclusion criteria include perinatal/prenatal/neonatal: maternal fever, infection, or antimicrobial treatment, the presence of any evident infection, being technology-dependent, and the presence of congenital anomalies.

The updated guideline will aim to stratify management by age 7-28 days, 29-60 days, and 61 to 90 days to provide the most appropriate and directed treatment.

It will also include a role for inflammatory markers, and allow for a “kinder, gentler” approach to the management of febrile infants aged 7-90 days including withholding certain treatments and procedures if infants are at low risk of infection. An active, not passive, need for observation may be appropriate for certain infants as well. These guidelines should be tailored for individual patients to provide the best care possible while minimizing risk in this population.

Key Takeaway:

An updated AAP Practice guideline algorithm for the management of well-appearing febrile infants 7-28 days, 29-60 days, and 60-90 days will be coming in the near future that will help standardize care in this population, but should not be used as a substitute for clinical judgment.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

An updated risk model based on data from patients presenting after acute myocardial infarction to a broad spectrum of U.S. hospitals appears to predict with a high degree of accuracy which patients are at the greatest risk for in-hospital mortality, investigators say.

Created from data on more than 240,000 patients presenting to one of 655 U.S. hospitals in 2012 and 2013 following ST-segment elevation myocardial infarction (STEMI) or non–ST-segment elevation MI (NSTEMI), the model identified the following independent risk factors for in-hospital mortality: age, heart rate, systolic blood pressure, presentation to the hospital after cardiac arrest, presentation in cardiogenic shock, presentation in heart failure, presentation with STEMI, creatinine clearance, and troponin ratio, reported Robert L. McNamara, MD, of Yale University, New Haven, Conn.

megaflopp/ThinkStock

The investigators are participants in the ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry–GWTG (Get With the Guidelines).

“The new ACTION Registry–GWTG in-hospital mortality risk model and risk score represent robust, parsimonious, and contemporary risk adjustment methodology for use in routine clinical care and hospital quality assessment. The addition of risk adjustment for patients presenting after cardiac arrest is critically important and enables a fairer assessment across hospitals with varied case mix,” they wrote (J Am Coll Cardiol. 2016 Aug 1;68[6]:626-35).

The revised risk model has the potential to facilitate hospital quality assessments and help investigators to identify specific factors that could help clinicians even further lower death rates, the investigators write.

Further mortality reductions?

Although improvements in care of patients with acute MI over the last several decades have driven the in-hospital death rate from 29% in 1969 down to less than 7% today, there are still more than 100,000 AMI-related in-hospital deaths in the United States annually, with wide variations across hospitals, Dr. McNamara and colleagues noted.

A previous risk model published by ACTION Registry–GWTG members included data on patients treated at 306 U.S. hospitals and provided a simple, validated in-hospital mortality and risk score.

Since that model was published, however, the dataset was expanded to include patients presenting after cardiac arrest at the time of AMI presentation.

“Being able to adjust for cardiac arrest is critical because it is a well-documented predictor of mortality. Moreover, continued improvement in AMI care mandates periodic updates to the risk models so that hospitals can assess their quality as contemporary care continues to evolve,” the authors wrote.

To see whether they could develop a new and improved model and risk score, they analyzed data on 243,440 patients treated at one of 655 hospitals in the voluntary network. Data on 145,952 patients (60% of the total), 57,039 of whom presented with STEMI, and 88,913 of whom presented with NSTEMI, were used to for the derivation sample.

Data on the remaining 97,488 (38,060 with STEMI and 59,428 with NSTEMI) were used to create the validation sample.

The authors found that for the total cohort, the in-hospital mortality rate was 4.6%. In multivariate models controlled for demographic and clinical factors, independent risk factors significantly associated with in-hospital mortality (validation cohort) were:

• Presentation after cardiac arrest (odds ratio, 5.15).

• Presentation in cardiogenic shock (OR, 4.22).

• Presentation in heart failure (OR, 1.83).

• STEMI on electrocardiography (OR, 1.81).

• Age, per 5 years (OR, 1.24).

• Systolic BP, per 10 mm Hg decrease (OR, 1.19).

• Creatinine clearance per 5/mL/min/1.73 m² decrease (OR, 1.11).

• Heart rate per 10 beats/min (OR, 1.09).

• Troponin ratio, per 5 units (OR, 1.05).

The 95% confidence intervals for all of the above factors were significant.

The C-statistic, a standard measure of the predictive accuracy of a logistic regression model, was 0.88, indicating that the final ACTION Registry–GWTG in-hospital mortality model had a high level of discrimination in both the derivation and validation populations, the authors state.

The ACTION Registry–GWTG is a Program of the American College of Cardiology and the American Heart Association, with funding from Schering-Plough and the Bristol-Myers Squibb/Sanofi Pharmaceutical Partnership. Dr. McNamara serves on a clinical trials endpoint adjudication committee for Pfizer. Other coauthors reported multiple financial relationships with pharmaceutical and medical device companies.

When our second daughter was born, she came home from the hospital in a box. All the babies born at Duke University Medical Center in 1973 were sent home in a cardboard box that had served as their bassinets during their stay in the newborn nursery. As I recall, the boxes were decorated with storks and musical notes; had spaces for the babies’ names, measurements, and birth dates; and had open slots that functioned as carrying handles.

Of course, 1973 predated crash-tested car seats, and so we put little Emily and her box in what we referred to as the “wayback” of our Ford Pinto wagon, a car that subsequently earned a reputation for turning into a fireball when involved in a rear-end collision. However, I believe I did take the extra precaution of “securing” the box in place with a bungee cord.

But Emily survived, and I filed away the memory of her cardboard bassinet until a few weeks ago when I read a story in the New York Times, “Why Finland’s Newborns Sleep in Cardboard Cribs” (Eli Rosenberg, July 6, 2016). It turns out the Finnish government gives out 40,000 cardboard boxes to pregnant women who agree to have a medical exam during the first trimester of their pregnancy. The gift boxes come along with 50 items of baby ware appropriate for Finland’s frigid climate, including a warm coat and a balaclava.

The baby box program began in the late 1930s as a way to encourage mothers to visit physicians. The current Finnish infant mortality is one of the lowest in the world and less than half of ours in the United States. There are some who have been tempted to attribute this dramatic decline to the baby box program. But it is hard to tease out one factor in a country that offers a 10-month paid parental leave and guarantees that a stay-at-home parent may return to his or her job at any time before the child’s third birthday.

Even without a broad social service support system, the cardboard box crib can save lives. For families who can’t afford a crib, the box offers a safer alternative to a couch with soft cushions and face-trapping gaps between its cushions, or to a bed shared with a sleep-deprived or inebriated parent, or to an antique crib with neck-pinching slats and layers of lead-laced paint.

Given this high costs of raising a child, the option of a no-cost cardboard box crib should appeal to most young families. But you know as well as I do that parents to be (and grandparents to be) are primed to buy and are focused on creating nurseries that match the images they see in the glossy magazines targeted at their vulnerable demographic.

It will require a major public relations campaign to counteract the image that bedding one’s precious newborn in a cardboard box conjures up. But maybe there is a role for us. If pediatricians began promoting the advantages of cardboard cribs, they might just catch on. On second thought, maybe we should focus our energies on promoting more child-friendly parental leave policies.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

When our second daughter was born, she came home from the hospital in a box. All the babies born at Duke University Medical Center in 1973 were sent home in a cardboard box that had served as their bassinets during their stay in the newborn nursery. As I recall, the boxes were decorated with storks and musical notes; had spaces for the babies’ names, measurements, and birth dates; and had open slots that functioned as carrying handles.

Of course, 1973 predated crash-tested car seats, and so we put little Emily and her box in what we referred to as the “wayback” of our Ford Pinto wagon, a car that subsequently earned a reputation for turning into a fireball when involved in a rear-end collision. However, I believe I did take the extra precaution of “securing” the box in place with a bungee cord.

But Emily survived, and I filed away the memory of her cardboard bassinet until a few weeks ago when I read a story in the New York Times, “Why Finland’s Newborns Sleep in Cardboard Cribs” (Eli Rosenberg, July 6, 2016). It turns out the Finnish government gives out 40,000 cardboard boxes to pregnant women who agree to have a medical exam during the first trimester of their pregnancy. The gift boxes come along with 50 items of baby ware appropriate for Finland’s frigid climate, including a warm coat and a balaclava.

The baby box program began in the late 1930s as a way to encourage mothers to visit physicians. The current Finnish infant mortality is one of the lowest in the world and less than half of ours in the United States. There are some who have been tempted to attribute this dramatic decline to the baby box program. But it is hard to tease out one factor in a country that offers a 10-month paid parental leave and guarantees that a stay-at-home parent may return to his or her job at any time before the child’s third birthday.

Even without a broad social service support system, the cardboard box crib can save lives. For families who can’t afford a crib, the box offers a safer alternative to a couch with soft cushions and face-trapping gaps between its cushions, or to a bed shared with a sleep-deprived or inebriated parent, or to an antique crib with neck-pinching slats and layers of lead-laced paint.

Given this high costs of raising a child, the option of a no-cost cardboard box crib should appeal to most young families. But you know as well as I do that parents to be (and grandparents to be) are primed to buy and are focused on creating nurseries that match the images they see in the glossy magazines targeted at their vulnerable demographic.

It will require a major public relations campaign to counteract the image that bedding one’s precious newborn in a cardboard box conjures up. But maybe there is a role for us. If pediatricians began promoting the advantages of cardboard cribs, they might just catch on. On second thought, maybe we should focus our energies on promoting more child-friendly parental leave policies.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

When our second daughter was born, she came home from the hospital in a box. All the babies born at Duke University Medical Center in 1973 were sent home in a cardboard box that had served as their bassinets during their stay in the newborn nursery. As I recall, the boxes were decorated with storks and musical notes; had spaces for the babies’ names, measurements, and birth dates; and had open slots that functioned as carrying handles.

Of course, 1973 predated crash-tested car seats, and so we put little Emily and her box in what we referred to as the “wayback” of our Ford Pinto wagon, a car that subsequently earned a reputation for turning into a fireball when involved in a rear-end collision. However, I believe I did take the extra precaution of “securing” the box in place with a bungee cord.

But Emily survived, and I filed away the memory of her cardboard bassinet until a few weeks ago when I read a story in the New York Times, “Why Finland’s Newborns Sleep in Cardboard Cribs” (Eli Rosenberg, July 6, 2016). It turns out the Finnish government gives out 40,000 cardboard boxes to pregnant women who agree to have a medical exam during the first trimester of their pregnancy. The gift boxes come along with 50 items of baby ware appropriate for Finland’s frigid climate, including a warm coat and a balaclava.

The baby box program began in the late 1930s as a way to encourage mothers to visit physicians. The current Finnish infant mortality is one of the lowest in the world and less than half of ours in the United States. There are some who have been tempted to attribute this dramatic decline to the baby box program. But it is hard to tease out one factor in a country that offers a 10-month paid parental leave and guarantees that a stay-at-home parent may return to his or her job at any time before the child’s third birthday.

Even without a broad social service support system, the cardboard box crib can save lives. For families who can’t afford a crib, the box offers a safer alternative to a couch with soft cushions and face-trapping gaps between its cushions, or to a bed shared with a sleep-deprived or inebriated parent, or to an antique crib with neck-pinching slats and layers of lead-laced paint.

Given this high costs of raising a child, the option of a no-cost cardboard box crib should appeal to most young families. But you know as well as I do that parents to be (and grandparents to be) are primed to buy and are focused on creating nurseries that match the images they see in the glossy magazines targeted at their vulnerable demographic.

It will require a major public relations campaign to counteract the image that bedding one’s precious newborn in a cardboard box conjures up. But maybe there is a role for us. If pediatricians began promoting the advantages of cardboard cribs, they might just catch on. On second thought, maybe we should focus our energies on promoting more child-friendly parental leave policies.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

Of the almost 9 million children and adolescents aged 17 years and younger estimated to be measles susceptible in the United States, those 3 years and younger show the highest levels of risk for infection, according to the results of a study published in the American Journal of Epidemiology.

Robert A. Bednarczyk, MD, and his colleagues at Emory University, Atlanta, developed a model based on age-specific measles vaccination data from the National Immunization Survey–Teen collected between 2008 and 2013 (18 cumulative birth cohorts) to estimate the number of U.S. children (birth–age 12 years ) and adolescents (aged 13-17 years) susceptible to measles infection (Am J Epidemiol. 2016 Jul 15;184[2]:148-56).

CDC/Dr. Heinz F. Eichenwald

The model was developed using the survey data in conjunction with assumptions designed to account for several potentially confounding variables. These included the effectiveness of the vaccine used, whether infants were protected by maternally derived, vaccine-induced antibodies, and any loss of immunity attributable to treatment for cancer during childhood. The model also allowed for an examination of susceptibility by different age groupings, as well as by state. Additionally, the study authors were able to estimate the impact of decreased measles-containing vaccine effectiveness on susceptibility to infection in adolescents.

Results from the model indicated that 12.5% of the over 69 million of U.S. children and adolescents in the 18 birth cohorts are susceptible to measles infection. Those with the highest percentage of susceptibility were children 3 years of age and younger (24.7%), compared with 9.0% of children and adolescents aged 4-17 years. Geographic differences in susceptibility also were apparent. In addition to the District of Columbia, 10 states had adolescent susceptibility levels of at least 6%, and 14 states each had over 20,000 susceptible adolescents.

Using the model to simulate a 1% decrease in vaccine effectiveness for both the first (93%-92%) and second (97%-96%) measles-containing vaccine doses, the study authors reported the addition of almost 1 million children and adolescents (13.4%) to the measles-susceptible category. This finding indicates that very small changes in vaccine effectiveness can have a substantial impact on susceptibility through a slow accumulation of additional susceptible children and adolescents each year, culminating in a steady decline in the proportion of children and adolescents immune to measles.

Regarding their overall findings, Dr. Bednarczyk and his colleagues stated, “the overall level of immunity to measles is generally at or higher than the operational threshold of 92%. This is compatible with the experience to date that, despite substantial numbers of importations, endemic measles transmission has not been reestablished.”

As for broader implications, the investigators said that “These estimates underscore the need to help public health professionals plan for future immunization programs and potential measles outbreaks, and to maintain appropriate levels of immunity in the population to prevent widespread transmission of this highly infectious disease.”

Of the almost 9 million children and adolescents aged 17 years and younger estimated to be measles susceptible in the United States, those 3 years and younger show the highest levels of risk for infection, according to the results of a study published in the American Journal of Epidemiology.

Robert A. Bednarczyk, MD, and his colleagues at Emory University, Atlanta, developed a model based on age-specific measles vaccination data from the National Immunization Survey–Teen collected between 2008 and 2013 (18 cumulative birth cohorts) to estimate the number of U.S. children (birth–age 12 years ) and adolescents (aged 13-17 years) susceptible to measles infection (Am J Epidemiol. 2016 Jul 15;184[2]:148-56).

CDC/Dr. Heinz F. Eichenwald

The model was developed using the survey data in conjunction with assumptions designed to account for several potentially confounding variables. These included the effectiveness of the vaccine used, whether infants were protected by maternally derived, vaccine-induced antibodies, and any loss of immunity attributable to treatment for cancer during childhood. The model also allowed for an examination of susceptibility by different age groupings, as well as by state. Additionally, the study authors were able to estimate the impact of decreased measles-containing vaccine effectiveness on susceptibility to infection in adolescents.

Results from the model indicated that 12.5% of the over 69 million of U.S. children and adolescents in the 18 birth cohorts are susceptible to measles infection. Those with the highest percentage of susceptibility were children 3 years of age and younger (24.7%), compared with 9.0% of children and adolescents aged 4-17 years. Geographic differences in susceptibility also were apparent. In addition to the District of Columbia, 10 states had adolescent susceptibility levels of at least 6%, and 14 states each had over 20,000 susceptible adolescents.

Using the model to simulate a 1% decrease in vaccine effectiveness for both the first (93%-92%) and second (97%-96%) measles-containing vaccine doses, the study authors reported the addition of almost 1 million children and adolescents (13.4%) to the measles-susceptible category. This finding indicates that very small changes in vaccine effectiveness can have a substantial impact on susceptibility through a slow accumulation of additional susceptible children and adolescents each year, culminating in a steady decline in the proportion of children and adolescents immune to measles.

Regarding their overall findings, Dr. Bednarczyk and his colleagues stated, “the overall level of immunity to measles is generally at or higher than the operational threshold of 92%. This is compatible with the experience to date that, despite substantial numbers of importations, endemic measles transmission has not been reestablished.”

As for broader implications, the investigators said that “These estimates underscore the need to help public health professionals plan for future immunization programs and potential measles outbreaks, and to maintain appropriate levels of immunity in the population to prevent widespread transmission of this highly infectious disease.”

Of the almost 9 million children and adolescents aged 17 years and younger estimated to be measles susceptible in the United States, those 3 years and younger show the highest levels of risk for infection, according to the results of a study published in the American Journal of Epidemiology.

Robert A. Bednarczyk, MD, and his colleagues at Emory University, Atlanta, developed a model based on age-specific measles vaccination data from the National Immunization Survey–Teen collected between 2008 and 2013 (18 cumulative birth cohorts) to estimate the number of U.S. children (birth–age 12 years ) and adolescents (aged 13-17 years) susceptible to measles infection (Am J Epidemiol. 2016 Jul 15;184[2]:148-56).

CDC/Dr. Heinz F. Eichenwald

The model was developed using the survey data in conjunction with assumptions designed to account for several potentially confounding variables. These included the effectiveness of the vaccine used, whether infants were protected by maternally derived, vaccine-induced antibodies, and any loss of immunity attributable to treatment for cancer during childhood. The model also allowed for an examination of susceptibility by different age groupings, as well as by state. Additionally, the study authors were able to estimate the impact of decreased measles-containing vaccine effectiveness on susceptibility to infection in adolescents.

Results from the model indicated that 12.5% of the over 69 million of U.S. children and adolescents in the 18 birth cohorts are susceptible to measles infection. Those with the highest percentage of susceptibility were children 3 years of age and younger (24.7%), compared with 9.0% of children and adolescents aged 4-17 years. Geographic differences in susceptibility also were apparent. In addition to the District of Columbia, 10 states had adolescent susceptibility levels of at least 6%, and 14 states each had over 20,000 susceptible adolescents.

Using the model to simulate a 1% decrease in vaccine effectiveness for both the first (93%-92%) and second (97%-96%) measles-containing vaccine doses, the study authors reported the addition of almost 1 million children and adolescents (13.4%) to the measles-susceptible category. This finding indicates that very small changes in vaccine effectiveness can have a substantial impact on susceptibility through a slow accumulation of additional susceptible children and adolescents each year, culminating in a steady decline in the proportion of children and adolescents immune to measles.

Regarding their overall findings, Dr. Bednarczyk and his colleagues stated, “the overall level of immunity to measles is generally at or higher than the operational threshold of 92%. This is compatible with the experience to date that, despite substantial numbers of importations, endemic measles transmission has not been reestablished.”

As for broader implications, the investigators said that “These estimates underscore the need to help public health professionals plan for future immunization programs and potential measles outbreaks, and to maintain appropriate levels of immunity in the population to prevent widespread transmission of this highly infectious disease.”

Look ahead to next summer, and be sure to save the dates of May 31 to June 3 for the 2017 Vascular Annual Meeting. Plenaries and exhibits will be from June 1 to 3.

Next year’s meeting will take place at the San Diego Convention Center in sunny San Diego, Calif.

Make a note of it!

And for a list of the next five years of future VAMs click here.

Look ahead to next summer, and be sure to save the dates of May 31 to June 3 for the 2017 Vascular Annual Meeting. Plenaries and exhibits will be from June 1 to 3.

Next year’s meeting will take place at the San Diego Convention Center in sunny San Diego, Calif.

Make a note of it!

And for a list of the next five years of future VAMs click here.

Look ahead to next summer, and be sure to save the dates of May 31 to June 3 for the 2017 Vascular Annual Meeting. Plenaries and exhibits will be from June 1 to 3.

Next year’s meeting will take place at the San Diego Convention Center in sunny San Diego, Calif.

Make a note of it!

And for a list of the next five years of future VAMs click here.

Still haven’t claimed CME or MOC credits from the Vascular Annual Meeting?

Access the CME site via the 2016 VAM app or by visiting www.vsweb.org/ClaimCME. Provide either the registration ID number OR first and last names and the ZIP code used to register (either five- or nine-digit code). Follow the extensive directions to list sessions, provide evaluations, take exams and generate credit certificates.

Credits must be claimed by Dec. 31. For information or help, email [email protected].

Still haven’t claimed CME or MOC credits from the Vascular Annual Meeting?

Access the CME site via the 2016 VAM app or by visiting www.vsweb.org/ClaimCME. Provide either the registration ID number OR first and last names and the ZIP code used to register (either five- or nine-digit code). Follow the extensive directions to list sessions, provide evaluations, take exams and generate credit certificates.

Credits must be claimed by Dec. 31. For information or help, email [email protected].

Still haven’t claimed CME or MOC credits from the Vascular Annual Meeting?

Access the CME site via the 2016 VAM app or by visiting www.vsweb.org/ClaimCME. Provide either the registration ID number OR first and last names and the ZIP code used to register (either five- or nine-digit code). Follow the extensive directions to list sessions, provide evaluations, take exams and generate credit certificates.

Credits must be claimed by Dec. 31. For information or help, email [email protected].

Abdominal compartment syndrome (ACS) was common after ruptured abdominal aortic aneurysm (AAA) repair, with a similar incidence for both open surgical and endovascular repair (EVAR), according to a report published in the European Journal of Vascular and Endovascular Surgery.

Samuel Ersryd, a doctoral student, and his colleagues at Uppsala (Sweden) University performed their study to determine the contemporary incidence, treatment, and outcomes of ACS after AAA repair.

BruceBlaus/Wikimedia Commons/Creative Commons License

The analysis included 6,634 patients in the Swedish vascular registry who were treated for abdominal aortic aneurysm repair at 31 institutions from May 2008 to December 2013. The mean patient age was 72.8 years, and 16.6% were women. There were 5,271 intact AAA (iAAA) repairs and 1,341 ruptured AAA (rAAA repairs). A total of 41.9% of iAAA repairs were open, as were 72.0% of the rAAA repairs (Eur J Vasc Endovasc Surg. 2016;52:158-65).The study found an incidence of ACS in the rAAA group of 6.8% after open surgery and 6.9% after EVAR.

The morbidity and mortality rates for iAAA and rAAA with ACS were “devastating” in both groups, according to the authors.

Mortality at 90 days for patients with ACS after rAAA was 58.7%, twice that of patients without ACS. In patients with iAAA repair with ACS, the 90-day mortality was 19.2%, six times higher than for those without ACS.

Prophylactic open abdomen treatment was performed in 10.7% of open-surgery patients.

The researchers found no differences in mortality among patients in either group that developed ACS, whether they were treated with decompression laparotomy or not.

Age, sex, and perioperative comorbidities were not associated with ACS, Mr. Ersryd and his associates said. Within the rAAA group, however, ACS was associated with the lowest measured preoperative blood pressure and with preoperative unconsciousness. In addition, ACS was more common in both the iAAA and rAAA groups after perioperative bleeding greater than 5 L, in the iAAA group after reimplantation of a renal artery, and in the rAAA group after the use of balloon occlusion after EVAR. In those patients operated on for iAAA, the risk of developing ACS was 8.1% in patients who had perioperative bleeding greater than 5 L, compared with only 0.8% if bleeding was less than 5 L (P less than .001).

“With such poor results among patients who developed ACS, prevention is the obvious key to success. Massive transfusion protocols and permissive hypotension in patients with ongoing bleeding are important, as well as being restrictive with crystalloids,” the authors said. In addition, they recommended a proactive strategy treating intra-abdominal hypertension with medical therapy, effective pain relief, and neuromuscular blockade as important preventive measures.

“ACS is associated with a devastating effect on outcome after surgery for both ruptured and intact AAA. There was no difference in outcome among those who developed ACS, depending on whether the primary treatment had been performed with an open or endovascular technique,” the researchers concluded.

The authors reported they had no conflicts of interest and the study was funded by the Swedish Research Council and Uppsala University.

[email protected]

On Twitter @VascularTweets

Abdominal compartment syndrome (ACS) was common after ruptured abdominal aortic aneurysm (AAA) repair, with a similar incidence for both open surgical and endovascular repair (EVAR), according to a report published in the European Journal of Vascular and Endovascular Surgery.

Samuel Ersryd, a doctoral student, and his colleagues at Uppsala (Sweden) University performed their study to determine the contemporary incidence, treatment, and outcomes of ACS after AAA repair.

BruceBlaus/Wikimedia Commons/Creative Commons License

The analysis included 6,634 patients in the Swedish vascular registry who were treated for abdominal aortic aneurysm repair at 31 institutions from May 2008 to December 2013. The mean patient age was 72.8 years, and 16.6% were women. There were 5,271 intact AAA (iAAA) repairs and 1,341 ruptured AAA (rAAA repairs). A total of 41.9% of iAAA repairs were open, as were 72.0% of the rAAA repairs (Eur J Vasc Endovasc Surg. 2016;52:158-65).The study found an incidence of ACS in the rAAA group of 6.8% after open surgery and 6.9% after EVAR.

The morbidity and mortality rates for iAAA and rAAA with ACS were “devastating” in both groups, according to the authors.

Mortality at 90 days for patients with ACS after rAAA was 58.7%, twice that of patients without ACS. In patients with iAAA repair with ACS, the 90-day mortality was 19.2%, six times higher than for those without ACS.

Prophylactic open abdomen treatment was performed in 10.7% of open-surgery patients.

The researchers found no differences in mortality among patients in either group that developed ACS, whether they were treated with decompression laparotomy or not.

Age, sex, and perioperative comorbidities were not associated with ACS, Mr. Ersryd and his associates said. Within the rAAA group, however, ACS was associated with the lowest measured preoperative blood pressure and with preoperative unconsciousness. In addition, ACS was more common in both the iAAA and rAAA groups after perioperative bleeding greater than 5 L, in the iAAA group after reimplantation of a renal artery, and in the rAAA group after the use of balloon occlusion after EVAR. In those patients operated on for iAAA, the risk of developing ACS was 8.1% in patients who had perioperative bleeding greater than 5 L, compared with only 0.8% if bleeding was less than 5 L (P less than .001).

“With such poor results among patients who developed ACS, prevention is the obvious key to success. Massive transfusion protocols and permissive hypotension in patients with ongoing bleeding are important, as well as being restrictive with crystalloids,” the authors said. In addition, they recommended a proactive strategy treating intra-abdominal hypertension with medical therapy, effective pain relief, and neuromuscular blockade as important preventive measures.

“ACS is associated with a devastating effect on outcome after surgery for both ruptured and intact AAA. There was no difference in outcome among those who developed ACS, depending on whether the primary treatment had been performed with an open or endovascular technique,” the researchers concluded.

The authors reported they had no conflicts of interest and the study was funded by the Swedish Research Council and Uppsala University.

[email protected]

On Twitter @VascularTweets

Abdominal compartment syndrome (ACS) was common after ruptured abdominal aortic aneurysm (AAA) repair, with a similar incidence for both open surgical and endovascular repair (EVAR), according to a report published in the European Journal of Vascular and Endovascular Surgery.

Samuel Ersryd, a doctoral student, and his colleagues at Uppsala (Sweden) University performed their study to determine the contemporary incidence, treatment, and outcomes of ACS after AAA repair.

BruceBlaus/Wikimedia Commons/Creative Commons License

The analysis included 6,634 patients in the Swedish vascular registry who were treated for abdominal aortic aneurysm repair at 31 institutions from May 2008 to December 2013. The mean patient age was 72.8 years, and 16.6% were women. There were 5,271 intact AAA (iAAA) repairs and 1,341 ruptured AAA (rAAA repairs). A total of 41.9% of iAAA repairs were open, as were 72.0% of the rAAA repairs (Eur J Vasc Endovasc Surg. 2016;52:158-65).The study found an incidence of ACS in the rAAA group of 6.8% after open surgery and 6.9% after EVAR.

The morbidity and mortality rates for iAAA and rAAA with ACS were “devastating” in both groups, according to the authors.

Mortality at 90 days for patients with ACS after rAAA was 58.7%, twice that of patients without ACS. In patients with iAAA repair with ACS, the 90-day mortality was 19.2%, six times higher than for those without ACS.

Prophylactic open abdomen treatment was performed in 10.7% of open-surgery patients.

The researchers found no differences in mortality among patients in either group that developed ACS, whether they were treated with decompression laparotomy or not.

Age, sex, and perioperative comorbidities were not associated with ACS, Mr. Ersryd and his associates said. Within the rAAA group, however, ACS was associated with the lowest measured preoperative blood pressure and with preoperative unconsciousness. In addition, ACS was more common in both the iAAA and rAAA groups after perioperative bleeding greater than 5 L, in the iAAA group after reimplantation of a renal artery, and in the rAAA group after the use of balloon occlusion after EVAR. In those patients operated on for iAAA, the risk of developing ACS was 8.1% in patients who had perioperative bleeding greater than 5 L, compared with only 0.8% if bleeding was less than 5 L (P less than .001).

“With such poor results among patients who developed ACS, prevention is the obvious key to success. Massive transfusion protocols and permissive hypotension in patients with ongoing bleeding are important, as well as being restrictive with crystalloids,” the authors said. In addition, they recommended a proactive strategy treating intra-abdominal hypertension with medical therapy, effective pain relief, and neuromuscular blockade as important preventive measures.

“ACS is associated with a devastating effect on outcome after surgery for both ruptured and intact AAA. There was no difference in outcome among those who developed ACS, depending on whether the primary treatment had been performed with an open or endovascular technique,” the researchers concluded.

The authors reported they had no conflicts of interest and the study was funded by the Swedish Research Council and Uppsala University.

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