Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.

A panel of diverse hospital systems shared successes and challenges with SHM's Project BOOST program, which aims to reduce readmissions for older adults. Although each initiative is (purposefully) tailored to the site, each share common themes, including the use of multidisciplinary teams, discharge process redesign, the use of teach back, and the use of follow up phone calls.

Key Takeaways:

• BOOST has been widely successful in improving the discharge process in a variety of hospital settings;
• Mentored implementation is a critical factor to it’s success.

Dr. Scheurer is physician editor of The Hospitalist

A panel of diverse hospital systems shared successes and challenges with SHM's Project BOOST program, which aims to reduce readmissions for older adults. Although each initiative is (purposefully) tailored to the site, each share common themes, including the use of multidisciplinary teams, discharge process redesign, the use of teach back, and the use of follow up phone calls.

Key Takeaways:

• BOOST has been widely successful in improving the discharge process in a variety of hospital settings;
• Mentored implementation is a critical factor to it’s success.

Dr. Scheurer is physician editor of The Hospitalist

A panel of diverse hospital systems shared successes and challenges with SHM's Project BOOST program, which aims to reduce readmissions for older adults. Although each initiative is (purposefully) tailored to the site, each share common themes, including the use of multidisciplinary teams, discharge process redesign, the use of teach back, and the use of follow up phone calls.

Key Takeaways:

• BOOST has been widely successful in improving the discharge process in a variety of hospital settings;
• Mentored implementation is a critical factor to it’s success.

Dr. Scheurer is physician editor of The Hospitalist

Patrick Torcson explained the history behind the ABCs of CMS during a Monday-morning session at HM12.

Medicare Part A currently spends $200 billion annually, and Part B spends $120 billion annually. These costs are unsustainable, said Dr. Torcson, and a 2003 Rand study found the quality of care provided by Medicare to be "untrustworthy." Fee for service is volume-based, not quality-based, said Dr. Torcson. Out of this was born the idea of pay for performance (P4P). The structure of P4P is such that performance is measured, reported, and rewarded. Whether or not P4P actually works is controversial, said Dr. Torcson. Studies are limited, results are conflicting, and nothing suggests better outcomes for patients.

The 3 Stages of P4P

1. Physician Quality Reporting System (PQRS): voluntary reporting system whereby physicians report to CMS on a variety of metrics. There are 10 metrics that hospitalists can report on, such as ACE/ARB for HF, and BB for AMI. PQRS provides a potential percentage increase in medicare payments through 2014. In 2015, failure to participate will result in reductions in payments from Medicare.
2. Physician Feedback Program: A three-phase program that began in 2007, it provides confidential reports to physicians called quality resource use reports (QRUR). These reports will be used to generate physicians' scores for the next:
3. Value-Based Payment Modifier: Each physician will receive a two-digit score assigned to his or her NPI. This will cause reimbursement of E&M scores to be weighted according to quality. Whereas currently a 99233 is reimbursed at $186.19, the range will be from $166.19 to $206.19, depending on a physician's VBP modifier. This will take effect in 2013 in Iowa, Nebraska, Kansas, and Missouri.

Bottom Line

• Value-based purchasing is designed to be budget-neutral; some will earn more, some less.
• Get used to being measured.
• Learn new skills and competencies.
• Embrace it; don't be lulled into complacency.

Patrick Torcson explained the history behind the ABCs of CMS during a Monday-morning session at HM12.

Medicare Part A currently spends $200 billion annually, and Part B spends $120 billion annually. These costs are unsustainable, said Dr. Torcson, and a 2003 Rand study found the quality of care provided by Medicare to be "untrustworthy." Fee for service is volume-based, not quality-based, said Dr. Torcson. Out of this was born the idea of pay for performance (P4P). The structure of P4P is such that performance is measured, reported, and rewarded. Whether or not P4P actually works is controversial, said Dr. Torcson. Studies are limited, results are conflicting, and nothing suggests better outcomes for patients.

The 3 Stages of P4P

1. Physician Quality Reporting System (PQRS): voluntary reporting system whereby physicians report to CMS on a variety of metrics. There are 10 metrics that hospitalists can report on, such as ACE/ARB for HF, and BB for AMI. PQRS provides a potential percentage increase in medicare payments through 2014. In 2015, failure to participate will result in reductions in payments from Medicare.
2. Physician Feedback Program: A three-phase program that began in 2007, it provides confidential reports to physicians called quality resource use reports (QRUR). These reports will be used to generate physicians' scores for the next:
3. Value-Based Payment Modifier: Each physician will receive a two-digit score assigned to his or her NPI. This will cause reimbursement of E&M scores to be weighted according to quality. Whereas currently a 99233 is reimbursed at $186.19, the range will be from $166.19 to $206.19, depending on a physician's VBP modifier. This will take effect in 2013 in Iowa, Nebraska, Kansas, and Missouri.

Bottom Line

• Value-based purchasing is designed to be budget-neutral; some will earn more, some less.
• Get used to being measured.
• Learn new skills and competencies.
• Embrace it; don't be lulled into complacency.

Patrick Torcson explained the history behind the ABCs of CMS during a Monday-morning session at HM12.

Medicare Part A currently spends $200 billion annually, and Part B spends $120 billion annually. These costs are unsustainable, said Dr. Torcson, and a 2003 Rand study found the quality of care provided by Medicare to be "untrustworthy." Fee for service is volume-based, not quality-based, said Dr. Torcson. Out of this was born the idea of pay for performance (P4P). The structure of P4P is such that performance is measured, reported, and rewarded. Whether or not P4P actually works is controversial, said Dr. Torcson. Studies are limited, results are conflicting, and nothing suggests better outcomes for patients.

The 3 Stages of P4P

1. Physician Quality Reporting System (PQRS): voluntary reporting system whereby physicians report to CMS on a variety of metrics. There are 10 metrics that hospitalists can report on, such as ACE/ARB for HF, and BB for AMI. PQRS provides a potential percentage increase in medicare payments through 2014. In 2015, failure to participate will result in reductions in payments from Medicare.
2. Physician Feedback Program: A three-phase program that began in 2007, it provides confidential reports to physicians called quality resource use reports (QRUR). These reports will be used to generate physicians' scores for the next:
3. Value-Based Payment Modifier: Each physician will receive a two-digit score assigned to his or her NPI. This will cause reimbursement of E&M scores to be weighted according to quality. Whereas currently a 99233 is reimbursed at $186.19, the range will be from $166.19 to $206.19, depending on a physician's VBP modifier. This will take effect in 2013 in Iowa, Nebraska, Kansas, and Missouri.

Bottom Line

• Value-based purchasing is designed to be budget-neutral; some will earn more, some less.
• Get used to being measured.
• Learn new skills and competencies.
• Embrace it; don't be lulled into complacency.

As part of the Affordable Care Act, the value-based purchasing program (VBP) is being rolled out this year. Beginning in October, VBP will put hospitals at financial risk for a defined set of clinical and patient satisfaction metrics. Because of the significant impact that this will have on hospitals and HM, SHM had a pre-course focused on this topic at HM12.

Pat Torscon and Joe Miller led the pre-course, which focused on VBP's key components. Through a series of vignettes and studies, the faculty provided nearly 100 attendess a better understanding of the impact.

Key Takeaways

1. VBP is budget neutral. Some Hospitals will receive bonuses, some will not. This will depend on where hospitals fall in the performance score. To receive a bonus, a hospital will have to exceed the 50% threshold. If below, then no opportunity for performance bonus. The model is based on a floor, a threshold (50%), and benchmark, which is presently a bell-shaped curve.

2. The performance score will be 70% clinical process domain and 30% patient experience domain. Hospitalists will have a major role in the perfromance measures around AMI, CHF, pneumonia, SCIP, and patient experience.

3. Hospitalists will need to understand the data and where it comes from. When you combine VBP, Inpatient Quality Reporting, readmissions, hospital-acquired conditions, and meaningful use, the actual amount of payment at risk is 7%. With most hospital profit margins around 1-3% this amount will be significant. Of those hospitals that have been studied, 10% in high performance, and 74% were inconsistent performance across four clinical measures.

4. Concurrent patient management will be important. Hospitalists will become the drivers and champions of this. To move either your HCAHPS score or Press Ganey performance scores will take time. It is important to convey that to the C-suite. An example of the impact of VBP for a 146-bed hospital over five years could be more than $5 million at stake; a 541-bed hospital would be $40 million.

As part of the Affordable Care Act, the value-based purchasing program (VBP) is being rolled out this year. Beginning in October, VBP will put hospitals at financial risk for a defined set of clinical and patient satisfaction metrics. Because of the significant impact that this will have on hospitals and HM, SHM had a pre-course focused on this topic at HM12.

Pat Torscon and Joe Miller led the pre-course, which focused on VBP's key components. Through a series of vignettes and studies, the faculty provided nearly 100 attendess a better understanding of the impact.

Key Takeaways

1. VBP is budget neutral. Some Hospitals will receive bonuses, some will not. This will depend on where hospitals fall in the performance score. To receive a bonus, a hospital will have to exceed the 50% threshold. If below, then no opportunity for performance bonus. The model is based on a floor, a threshold (50%), and benchmark, which is presently a bell-shaped curve.

2. The performance score will be 70% clinical process domain and 30% patient experience domain. Hospitalists will have a major role in the perfromance measures around AMI, CHF, pneumonia, SCIP, and patient experience.

3. Hospitalists will need to understand the data and where it comes from. When you combine VBP, Inpatient Quality Reporting, readmissions, hospital-acquired conditions, and meaningful use, the actual amount of payment at risk is 7%. With most hospital profit margins around 1-3% this amount will be significant. Of those hospitals that have been studied, 10% in high performance, and 74% were inconsistent performance across four clinical measures.

4. Concurrent patient management will be important. Hospitalists will become the drivers and champions of this. To move either your HCAHPS score or Press Ganey performance scores will take time. It is important to convey that to the C-suite. An example of the impact of VBP for a 146-bed hospital over five years could be more than $5 million at stake; a 541-bed hospital would be $40 million.

As part of the Affordable Care Act, the value-based purchasing program (VBP) is being rolled out this year. Beginning in October, VBP will put hospitals at financial risk for a defined set of clinical and patient satisfaction metrics. Because of the significant impact that this will have on hospitals and HM, SHM had a pre-course focused on this topic at HM12.

Pat Torscon and Joe Miller led the pre-course, which focused on VBP's key components. Through a series of vignettes and studies, the faculty provided nearly 100 attendess a better understanding of the impact.

Key Takeaways

1. VBP is budget neutral. Some Hospitals will receive bonuses, some will not. This will depend on where hospitals fall in the performance score. To receive a bonus, a hospital will have to exceed the 50% threshold. If below, then no opportunity for performance bonus. The model is based on a floor, a threshold (50%), and benchmark, which is presently a bell-shaped curve.

2. The performance score will be 70% clinical process domain and 30% patient experience domain. Hospitalists will have a major role in the perfromance measures around AMI, CHF, pneumonia, SCIP, and patient experience.

3. Hospitalists will need to understand the data and where it comes from. When you combine VBP, Inpatient Quality Reporting, readmissions, hospital-acquired conditions, and meaningful use, the actual amount of payment at risk is 7%. With most hospital profit margins around 1-3% this amount will be significant. Of those hospitals that have been studied, 10% in high performance, and 74% were inconsistent performance across four clinical measures.

4. Concurrent patient management will be important. Hospitalists will become the drivers and champions of this. To move either your HCAHPS score or Press Ganey performance scores will take time. It is important to convey that to the C-suite. An example of the impact of VBP for a 146-bed hospital over five years could be more than $5 million at stake; a 541-bed hospital would be $40 million.

HM12 formally kicked off for thousands of hospitalists on Monday morning with two plenary addresses that couldn't have been more different.

First up, Patrick Conway, MD, MSc, FAAP, SFHM, a pediatric hospitalist and chief medical officer of the Centers for Medicare & Medicaid Services (CMS), provided a rapid-fire insight into the breadth of CMS and asked hospitalists to consider the government behemoth as a partner in systems change. Political analyst Norman Ornstein, PhD, MA, then presented a global view of the dysfunction racking the political system (once he finished an opening monologue of political jibes that would have made late-night writers proud).

But while the plenary perspectives differed in theme, they converged on implication: The next few years will be a period of change for healthcare and HM.

"The fact is if we had a political system operating on all cylinders at this point, if we had a law put into place and then assurances that it would continue, and that everybody would be making a good faith effort to make it work, it would still hold years of tumult ahead as we try to figure out how we can change cultures, change behaviors, and still along the way provide quality care at a price that is going to be acceptable enough in the system to make it work,” Ornstein said.

Dr. Conway summed it up this way: “better health, better care, and lower cost.”

Dr. Conway, who maintains a presence in the clinical world by working unpaid weekend shifts at Children's National Medical Center in Washington, D.C., says that while individual hospitalists might feel their contribution is too small to translate to systems change, they are wrong. Change, he says, begins at the local level.

"My challenge to you is: Please don't sit on the sidelines," Dr. Conway said. "Please be actively engaged in your local system in creating this change."

HM12 formally kicked off for thousands of hospitalists on Monday morning with two plenary addresses that couldn't have been more different.

First up, Patrick Conway, MD, MSc, FAAP, SFHM, a pediatric hospitalist and chief medical officer of the Centers for Medicare & Medicaid Services (CMS), provided a rapid-fire insight into the breadth of CMS and asked hospitalists to consider the government behemoth as a partner in systems change. Political analyst Norman Ornstein, PhD, MA, then presented a global view of the dysfunction racking the political system (once he finished an opening monologue of political jibes that would have made late-night writers proud).

But while the plenary perspectives differed in theme, they converged on implication: The next few years will be a period of change for healthcare and HM.

"The fact is if we had a political system operating on all cylinders at this point, if we had a law put into place and then assurances that it would continue, and that everybody would be making a good faith effort to make it work, it would still hold years of tumult ahead as we try to figure out how we can change cultures, change behaviors, and still along the way provide quality care at a price that is going to be acceptable enough in the system to make it work,” Ornstein said.

Dr. Conway summed it up this way: “better health, better care, and lower cost.”

Dr. Conway, who maintains a presence in the clinical world by working unpaid weekend shifts at Children's National Medical Center in Washington, D.C., says that while individual hospitalists might feel their contribution is too small to translate to systems change, they are wrong. Change, he says, begins at the local level.

"My challenge to you is: Please don't sit on the sidelines," Dr. Conway said. "Please be actively engaged in your local system in creating this change."

HM12 formally kicked off for thousands of hospitalists on Monday morning with two plenary addresses that couldn't have been more different.

First up, Patrick Conway, MD, MSc, FAAP, SFHM, a pediatric hospitalist and chief medical officer of the Centers for Medicare & Medicaid Services (CMS), provided a rapid-fire insight into the breadth of CMS and asked hospitalists to consider the government behemoth as a partner in systems change. Political analyst Norman Ornstein, PhD, MA, then presented a global view of the dysfunction racking the political system (once he finished an opening monologue of political jibes that would have made late-night writers proud).

But while the plenary perspectives differed in theme, they converged on implication: The next few years will be a period of change for healthcare and HM.

"The fact is if we had a political system operating on all cylinders at this point, if we had a law put into place and then assurances that it would continue, and that everybody would be making a good faith effort to make it work, it would still hold years of tumult ahead as we try to figure out how we can change cultures, change behaviors, and still along the way provide quality care at a price that is going to be acceptable enough in the system to make it work,” Ornstein said.

Dr. Conway summed it up this way: “better health, better care, and lower cost.”

Dr. Conway, who maintains a presence in the clinical world by working unpaid weekend shifts at Children's National Medical Center in Washington, D.C., says that while individual hospitalists might feel their contribution is too small to translate to systems change, they are wrong. Change, he says, begins at the local level.

"My challenge to you is: Please don't sit on the sidelines," Dr. Conway said. "Please be actively engaged in your local system in creating this change."