Apixaban tablets

Photo courtesy of Pfizer

and Bristol-Myers Squibb

ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.

For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.

They found that patients had a similar risk of stroke regardless of which drug they received.

However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.

Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.

“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.

The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.

“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.

During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.

The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.

At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.

“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.

“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”

“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.”

*Information in the abstract differs from that presented at the meeting.

Apixaban tablets

Photo courtesy of Pfizer

and Bristol-Myers Squibb

ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.

For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.

They found that patients had a similar risk of stroke regardless of which drug they received.

However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.

Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.

“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.

The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.

“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.

During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.

The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.

At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.

“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.

“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”

“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.”

*Information in the abstract differs from that presented at the meeting.

Apixaban tablets

Photo courtesy of Pfizer

and Bristol-Myers Squibb

ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.

For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.

They found that patients had a similar risk of stroke regardless of which drug they received.

However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.

Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.

“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.

The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.

“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.

During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.

The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.

At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.

“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.

“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”

“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.”

*Information in the abstract differs from that presented at the meeting.

ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.

Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.

The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.

“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.

However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.

Dr Nakamura presented the results at the congress as abstract 2218.

The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.

All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).

An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.

Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.

There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.

The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.

“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”

Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.

Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.

This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.

ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.

Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.

The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.

“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.

However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.

Dr Nakamura presented the results at the congress as abstract 2218.

The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.

All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).

An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.

Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.

There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.

The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.

“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”

Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.

Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.

This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.

ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.

Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.

The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.

“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.

However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.

Dr Nakamura presented the results at the congress as abstract 2218.

The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.

All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).

An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.

Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.

There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.

The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.

“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”

Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.

Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.

This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.

Cancer patient receiving

chemotherapy

Photo by Rhoda Baer

The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.

The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.

The paper was published in European Heart Journal and on the ESC website.

The document reviews the potential cardiovascular complications of anticancer therapies.

The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.

For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.

Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).

Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.

The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.

The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.

“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”

“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.

“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”

Cancer patient receiving

chemotherapy

Photo by Rhoda Baer

The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.

The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.

The paper was published in European Heart Journal and on the ESC website.

The document reviews the potential cardiovascular complications of anticancer therapies.

The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.

For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.

Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).

Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.

The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.

The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.

“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”

“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.

“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”

Cancer patient receiving

chemotherapy

Photo by Rhoda Baer

The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.

The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.

The paper was published in European Heart Journal and on the ESC website.

The document reviews the potential cardiovascular complications of anticancer therapies.

The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.

For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.

Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).

Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.

The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.

The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.

“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”

“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.

“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”

Blood samples

Photo by Graham Colm

The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.

The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.

The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.

The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.

About the EUA

The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of

in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.

About the test

The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.

Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.

The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.

The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.

Blood samples

Photo by Graham Colm

The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.

The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.

The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.

The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.

About the EUA

The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of

in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.

About the test

The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.

Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.

The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.

The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.

Blood samples

Photo by Graham Colm

The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.

The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.

The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.

The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.

About the EUA

The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of

in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.

About the test

The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.

Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.

The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.

The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.

The factor Xa antidote andexanet achieved effective hemostasis 12 hours after infusion in 79% of patients who had developed serious acute bleeding on factor Xa inhibitor therapy, according to a preliminary analysis of an ongoing study of how reducing anti–factor Xa activity affects clinical hemostatic outcomes.

“The site of bleeding was most often gastrointestinal or intracranial; anti–factor Xa activity was considerably elevated in most patients and, as such, was likely to be a major impediment to clinical hemostasis. The administration of an andexanet bolus and infusion resulted in rapid and substantial reversal of anti–factor Xa activity,” Stuart Connolly, MD, of McMaster University, Hamilton, Ont., and his associates reported at the ESC Congress and in a simultaneously published study (N Engl J Med. 2016 Aug 30. doi: 10.1056/NEJMoa1607887).

Andexanet alfa is a recombinant modified human factor Xa decoy protein that “sharply” reduced plasma levels of unbound factor Xa inhibitors as well as anti-factor Xa activity in healthy older volunteers receiving apixaban or rivaroxaban, the researchers noted. Based on those findings, they designed a prospective, multicenter, single-group, open-label study (Andexanet Alfa, a Novel Antidote to the Anticoagulation Effects of FXA Inhibitors; ANNEXA-4) of andexanet in patients with potentially life-threatening acute major bleeding related to anticoagulation with a factor Xa inhibitor.

This interim report from the ongoing study included 67 patients with data available by June 17, 2016. Participants averaged 77 years of age and were receiving a factor Xa inhibtor because of atrial fibrillation, venous thromboembolism, or both. All patients received a bolus of andexanet for 15 to 30 minutes followed by a 2-hour infusion. Based on previous studies, the researchers used a 400-mg bolus of andexanet followed by a 480-mg infusion when patients had last taken their factor Xa inhibitor more than 7 hours before, and a higher 800-mg bolus followed by a 960-mg infusion when patients had taken their anticoagulant more recently. Bleeding and hemostasis were evaluated based on serial CT or MRI scans of patients with intracranial hemorrhage and corrected hemoglobin and hematocrit levels at 12 hours for patients with gastrointestinal and other nonvisible bleeding.

Among 47 patients in the primary efficacy analysis, 37 (79%) achieved excellent or good hemostasis (95% confidence interval, 64% to 89%), including 81% of patients on rivaroxaban and 75% of patients on enoxaparin, the researchers reported. “The rates of excellent or good efficacy were 84% for gastrointestinal bleeding and 80% for intracranial bleeding, rates that were consistent for other subgroups that were examined,” they said. Among the five patients (10%) with the most residual anti–factor Xa activity, all had received the lower andexanet dose. Four had received rivaroxaban while one had received apixaban.

The safety population included all 67 patients, none of whom developed infusion reactions or antibodies to factors X, Xa, or andexanet. After 30 days of follow-up, 12 patients (18%) had experienced one or more thrombotic events, including deep vein thrombosis (seven patients), stroke (five patients), myocardial infarction (one patient), and pulmonary embolism (one patient). One-third of these events occurred within 3 days of receiving andexanet, while the rest occurred by day 30. A total of 10 patients (15%) died, and six deaths were from cardiovascular causes. “A controlled study would be required to assess whether the frequency of these events exceeded that expected in patients at increased risk for thrombotic events,” the researchers commented.

Portola Pharmaceuticals makes andexanet alfa and funded the study. Dr. Connolly disclosed ties to Bayer, Bristol-Myers Squibb/Pfizer, Daiichi-Sankyo, CSL Behring, Octapharma, and Boehringer Ingelheim outside the submitted work.

The factor Xa antidote andexanet achieved effective hemostasis 12 hours after infusion in 79% of patients who had developed serious acute bleeding on factor Xa inhibitor therapy, according to a preliminary analysis of an ongoing study of how reducing anti–factor Xa activity affects clinical hemostatic outcomes.

“The site of bleeding was most often gastrointestinal or intracranial; anti–factor Xa activity was considerably elevated in most patients and, as such, was likely to be a major impediment to clinical hemostasis. The administration of an andexanet bolus and infusion resulted in rapid and substantial reversal of anti–factor Xa activity,” Stuart Connolly, MD, of McMaster University, Hamilton, Ont., and his associates reported at the ESC Congress and in a simultaneously published study (N Engl J Med. 2016 Aug 30. doi: 10.1056/NEJMoa1607887).

Andexanet alfa is a recombinant modified human factor Xa decoy protein that “sharply” reduced plasma levels of unbound factor Xa inhibitors as well as anti-factor Xa activity in healthy older volunteers receiving apixaban or rivaroxaban, the researchers noted. Based on those findings, they designed a prospective, multicenter, single-group, open-label study (Andexanet Alfa, a Novel Antidote to the Anticoagulation Effects of FXA Inhibitors; ANNEXA-4) of andexanet in patients with potentially life-threatening acute major bleeding related to anticoagulation with a factor Xa inhibitor.

This interim report from the ongoing study included 67 patients with data available by June 17, 2016. Participants averaged 77 years of age and were receiving a factor Xa inhibtor because of atrial fibrillation, venous thromboembolism, or both. All patients received a bolus of andexanet for 15 to 30 minutes followed by a 2-hour infusion. Based on previous studies, the researchers used a 400-mg bolus of andexanet followed by a 480-mg infusion when patients had last taken their factor Xa inhibitor more than 7 hours before, and a higher 800-mg bolus followed by a 960-mg infusion when patients had taken their anticoagulant more recently. Bleeding and hemostasis were evaluated based on serial CT or MRI scans of patients with intracranial hemorrhage and corrected hemoglobin and hematocrit levels at 12 hours for patients with gastrointestinal and other nonvisible bleeding.

Among 47 patients in the primary efficacy analysis, 37 (79%) achieved excellent or good hemostasis (95% confidence interval, 64% to 89%), including 81% of patients on rivaroxaban and 75% of patients on enoxaparin, the researchers reported. “The rates of excellent or good efficacy were 84% for gastrointestinal bleeding and 80% for intracranial bleeding, rates that were consistent for other subgroups that were examined,” they said. Among the five patients (10%) with the most residual anti–factor Xa activity, all had received the lower andexanet dose. Four had received rivaroxaban while one had received apixaban.

The safety population included all 67 patients, none of whom developed infusion reactions or antibodies to factors X, Xa, or andexanet. After 30 days of follow-up, 12 patients (18%) had experienced one or more thrombotic events, including deep vein thrombosis (seven patients), stroke (five patients), myocardial infarction (one patient), and pulmonary embolism (one patient). One-third of these events occurred within 3 days of receiving andexanet, while the rest occurred by day 30. A total of 10 patients (15%) died, and six deaths were from cardiovascular causes. “A controlled study would be required to assess whether the frequency of these events exceeded that expected in patients at increased risk for thrombotic events,” the researchers commented.

Portola Pharmaceuticals makes andexanet alfa and funded the study. Dr. Connolly disclosed ties to Bayer, Bristol-Myers Squibb/Pfizer, Daiichi-Sankyo, CSL Behring, Octapharma, and Boehringer Ingelheim outside the submitted work.

The factor Xa antidote andexanet achieved effective hemostasis 12 hours after infusion in 79% of patients who had developed serious acute bleeding on factor Xa inhibitor therapy, according to a preliminary analysis of an ongoing study of how reducing anti–factor Xa activity affects clinical hemostatic outcomes.

“The site of bleeding was most often gastrointestinal or intracranial; anti–factor Xa activity was considerably elevated in most patients and, as such, was likely to be a major impediment to clinical hemostasis. The administration of an andexanet bolus and infusion resulted in rapid and substantial reversal of anti–factor Xa activity,” Stuart Connolly, MD, of McMaster University, Hamilton, Ont., and his associates reported at the ESC Congress and in a simultaneously published study (N Engl J Med. 2016 Aug 30. doi: 10.1056/NEJMoa1607887).

Andexanet alfa is a recombinant modified human factor Xa decoy protein that “sharply” reduced plasma levels of unbound factor Xa inhibitors as well as anti-factor Xa activity in healthy older volunteers receiving apixaban or rivaroxaban, the researchers noted. Based on those findings, they designed a prospective, multicenter, single-group, open-label study (Andexanet Alfa, a Novel Antidote to the Anticoagulation Effects of FXA Inhibitors; ANNEXA-4) of andexanet in patients with potentially life-threatening acute major bleeding related to anticoagulation with a factor Xa inhibitor.

This interim report from the ongoing study included 67 patients with data available by June 17, 2016. Participants averaged 77 years of age and were receiving a factor Xa inhibtor because of atrial fibrillation, venous thromboembolism, or both. All patients received a bolus of andexanet for 15 to 30 minutes followed by a 2-hour infusion. Based on previous studies, the researchers used a 400-mg bolus of andexanet followed by a 480-mg infusion when patients had last taken their factor Xa inhibitor more than 7 hours before, and a higher 800-mg bolus followed by a 960-mg infusion when patients had taken their anticoagulant more recently. Bleeding and hemostasis were evaluated based on serial CT or MRI scans of patients with intracranial hemorrhage and corrected hemoglobin and hematocrit levels at 12 hours for patients with gastrointestinal and other nonvisible bleeding.

Among 47 patients in the primary efficacy analysis, 37 (79%) achieved excellent or good hemostasis (95% confidence interval, 64% to 89%), including 81% of patients on rivaroxaban and 75% of patients on enoxaparin, the researchers reported. “The rates of excellent or good efficacy were 84% for gastrointestinal bleeding and 80% for intracranial bleeding, rates that were consistent for other subgroups that were examined,” they said. Among the five patients (10%) with the most residual anti–factor Xa activity, all had received the lower andexanet dose. Four had received rivaroxaban while one had received apixaban.

The safety population included all 67 patients, none of whom developed infusion reactions or antibodies to factors X, Xa, or andexanet. After 30 days of follow-up, 12 patients (18%) had experienced one or more thrombotic events, including deep vein thrombosis (seven patients), stroke (five patients), myocardial infarction (one patient), and pulmonary embolism (one patient). One-third of these events occurred within 3 days of receiving andexanet, while the rest occurred by day 30. A total of 10 patients (15%) died, and six deaths were from cardiovascular causes. “A controlled study would be required to assess whether the frequency of these events exceeded that expected in patients at increased risk for thrombotic events,” the researchers commented.

Portola Pharmaceuticals makes andexanet alfa and funded the study. Dr. Connolly disclosed ties to Bayer, Bristol-Myers Squibb/Pfizer, Daiichi-Sankyo, CSL Behring, Octapharma, and Boehringer Ingelheim outside the submitted work.

Invasive coronary therapies deserve credit for the decade-long decline in mortality among patients hospitalized with NSTEMI in the United Kingdom, Marlous Hall, PhD, said at the annual meeting of the European Society of Cardiology.

All-cause mortality improved approximately 3.2% per year in NSTEMI cases during a recent 10-year period, and most of that reduction (88%) was attributed to an increase in guideline-indicated treatment using coronary angiography, PCI, and CABG. Appropriate pharmacologic therapies also accounted for a significant though much smaller portion (10%) of that improvement, said Dr. Hall of the University of Leeds (England) Institute of Cardiovascular and Metabolic Medicine.

Dr. Hall’s findings were presented at the meeting and simultaneously published online Aug. 30 in JAMA (JAMA 2016 Aug 30. doi: 10.1001/jama.2016.1076).

NSTEMI-related deaths have declined globally in recent years, but the underlying reasons have been unclear. Some experts expressed concern that this reduction may not be a real treatment effect but may actually represent the expansion of treatment to a much lower-risk population. This concern worsened after the introduction of a higher-sensitivity troponin assay that identifies milder cases of acute coronary syndrome, Dr. Hall noted.

He and his associates examined this issue by analyzing data in a nationwide ACS registry that tracks patients treated at all 247 hospitals in England and Wales. They focused on time trends in 30-day and 180-day mortality among 389,057 adults treated for NSTEMI in 2003-2013. The median patient age was 72.7 years. Study participants were followed for a median of 2.3 years after diagnosis.

This patient population had a high rate of comorbidities including hypertension, current or former smoking, diabetes, angina, and previous MI. Most patients had an intermediate-to-high cardiac risk score. There were 37,236 deaths.

As expected, all-cause mortality declined over time, at an average of 3.2% per year. In particular, in-hospital mortality decreased from 10.9% in 2003 to 5.0% in 2013.

Only a small portion of this decline could be attributed to lower patient risk at diagnosis. The single most important variable accounting for reduced mortality was the appropriate, guideline-indicated use of invasive therapies. It was estimated that coronary angiography, PCI, and CABG contributed approximately 88% to the improvement in patient survival and that appropriate, guideline-indicated use of pharmacologic therapies contributed approximately 10%.

In a further analysis of the data, “use of an invasive coronary strategy was associated with a relative decrease in mortality of 46.1%. Furthermore, the estimate of the indirect contribution associated with an invasive coronary strategy through the provision of [comprehensive] cardiac rehabilitation was small (3.6%),” Dr. Hall said.

He cautioned that the study results should not be interpreted to mean that medical therapies are unimportant. “In our cohort, aspirin, P2Y12 inhibitors, beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor-blockers, and statins each had a significant association with improved survival,” Dr. Hall said.

Invasive coronary therapies deserve credit for the decade-long decline in mortality among patients hospitalized with NSTEMI in the United Kingdom, Marlous Hall, PhD, said at the annual meeting of the European Society of Cardiology.

All-cause mortality improved approximately 3.2% per year in NSTEMI cases during a recent 10-year period, and most of that reduction (88%) was attributed to an increase in guideline-indicated treatment using coronary angiography, PCI, and CABG. Appropriate pharmacologic therapies also accounted for a significant though much smaller portion (10%) of that improvement, said Dr. Hall of the University of Leeds (England) Institute of Cardiovascular and Metabolic Medicine.

Dr. Hall’s findings were presented at the meeting and simultaneously published online Aug. 30 in JAMA (JAMA 2016 Aug 30. doi: 10.1001/jama.2016.1076).

NSTEMI-related deaths have declined globally in recent years, but the underlying reasons have been unclear. Some experts expressed concern that this reduction may not be a real treatment effect but may actually represent the expansion of treatment to a much lower-risk population. This concern worsened after the introduction of a higher-sensitivity troponin assay that identifies milder cases of acute coronary syndrome, Dr. Hall noted.

He and his associates examined this issue by analyzing data in a nationwide ACS registry that tracks patients treated at all 247 hospitals in England and Wales. They focused on time trends in 30-day and 180-day mortality among 389,057 adults treated for NSTEMI in 2003-2013. The median patient age was 72.7 years. Study participants were followed for a median of 2.3 years after diagnosis.

This patient population had a high rate of comorbidities including hypertension, current or former smoking, diabetes, angina, and previous MI. Most patients had an intermediate-to-high cardiac risk score. There were 37,236 deaths.

As expected, all-cause mortality declined over time, at an average of 3.2% per year. In particular, in-hospital mortality decreased from 10.9% in 2003 to 5.0% in 2013.

Only a small portion of this decline could be attributed to lower patient risk at diagnosis. The single most important variable accounting for reduced mortality was the appropriate, guideline-indicated use of invasive therapies. It was estimated that coronary angiography, PCI, and CABG contributed approximately 88% to the improvement in patient survival and that appropriate, guideline-indicated use of pharmacologic therapies contributed approximately 10%.

In a further analysis of the data, “use of an invasive coronary strategy was associated with a relative decrease in mortality of 46.1%. Furthermore, the estimate of the indirect contribution associated with an invasive coronary strategy through the provision of [comprehensive] cardiac rehabilitation was small (3.6%),” Dr. Hall said.

He cautioned that the study results should not be interpreted to mean that medical therapies are unimportant. “In our cohort, aspirin, P2Y12 inhibitors, beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor-blockers, and statins each had a significant association with improved survival,” Dr. Hall said.

Invasive coronary therapies deserve credit for the decade-long decline in mortality among patients hospitalized with NSTEMI in the United Kingdom, Marlous Hall, PhD, said at the annual meeting of the European Society of Cardiology.

All-cause mortality improved approximately 3.2% per year in NSTEMI cases during a recent 10-year period, and most of that reduction (88%) was attributed to an increase in guideline-indicated treatment using coronary angiography, PCI, and CABG. Appropriate pharmacologic therapies also accounted for a significant though much smaller portion (10%) of that improvement, said Dr. Hall of the University of Leeds (England) Institute of Cardiovascular and Metabolic Medicine.

Dr. Hall’s findings were presented at the meeting and simultaneously published online Aug. 30 in JAMA (JAMA 2016 Aug 30. doi: 10.1001/jama.2016.1076).

NSTEMI-related deaths have declined globally in recent years, but the underlying reasons have been unclear. Some experts expressed concern that this reduction may not be a real treatment effect but may actually represent the expansion of treatment to a much lower-risk population. This concern worsened after the introduction of a higher-sensitivity troponin assay that identifies milder cases of acute coronary syndrome, Dr. Hall noted.

He and his associates examined this issue by analyzing data in a nationwide ACS registry that tracks patients treated at all 247 hospitals in England and Wales. They focused on time trends in 30-day and 180-day mortality among 389,057 adults treated for NSTEMI in 2003-2013. The median patient age was 72.7 years. Study participants were followed for a median of 2.3 years after diagnosis.

This patient population had a high rate of comorbidities including hypertension, current or former smoking, diabetes, angina, and previous MI. Most patients had an intermediate-to-high cardiac risk score. There were 37,236 deaths.

As expected, all-cause mortality declined over time, at an average of 3.2% per year. In particular, in-hospital mortality decreased from 10.9% in 2003 to 5.0% in 2013.

Only a small portion of this decline could be attributed to lower patient risk at diagnosis. The single most important variable accounting for reduced mortality was the appropriate, guideline-indicated use of invasive therapies. It was estimated that coronary angiography, PCI, and CABG contributed approximately 88% to the improvement in patient survival and that appropriate, guideline-indicated use of pharmacologic therapies contributed approximately 10%.

In a further analysis of the data, “use of an invasive coronary strategy was associated with a relative decrease in mortality of 46.1%. Furthermore, the estimate of the indirect contribution associated with an invasive coronary strategy through the provision of [comprehensive] cardiac rehabilitation was small (3.6%),” Dr. Hall said.

He cautioned that the study results should not be interpreted to mean that medical therapies are unimportant. “In our cohort, aspirin, P2Y12 inhibitors, beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor-blockers, and statins each had a significant association with improved survival,” Dr. Hall said.

Off-hours presentation to the hospital with STEMI did not affect PCI outcomes in the international prospective randomized CHAMPION PHOENIX trial.

The newer findings are reassuring and, in contrast with findings from several previous retrospective registry–based studies, suggest that presenting to the hospital at night or on weekends or holidays is no more hazardous than presenting during regular working hours, Senthil Selvaraj, MD, said in a presentation at the annual congress of the European Society of Cardiology. The results may reflect global quality improvement measures in STEMI care.

In the study, which was simultaneously published in Journal of the American College of Cardiology, researchers assessed the outcomes of 1,992 patients with STEMI participating in a large, industry-sponsored clinical trial. The primary efficacy outcome – a combination of all-cause mortality, MI, stent thrombosis, or ischemia-driven revascularization at 48 hours – was no different between patients who presented at 7 a.m. through 7 p.m. Monday through Friday than in those who presented during off hours (RR, 1.00), said Dr. Selvaraj of Brigham and Women’s Hospital Heart & Vascular Center, Boston.

There also was no difference between the two study groups in the primary safety outcome, which was moderate to severe bleeding events.

PCI yielded consistent benefits regardless of the timing of patient presentation, Dr. Selvaraj said.

CHAMPION PHOENIX was sponsored by the Medicines Company.

Off-hours presentation to the hospital with STEMI did not affect PCI outcomes in the international prospective randomized CHAMPION PHOENIX trial.

The newer findings are reassuring and, in contrast with findings from several previous retrospective registry–based studies, suggest that presenting to the hospital at night or on weekends or holidays is no more hazardous than presenting during regular working hours, Senthil Selvaraj, MD, said in a presentation at the annual congress of the European Society of Cardiology. The results may reflect global quality improvement measures in STEMI care.

In the study, which was simultaneously published in Journal of the American College of Cardiology, researchers assessed the outcomes of 1,992 patients with STEMI participating in a large, industry-sponsored clinical trial. The primary efficacy outcome – a combination of all-cause mortality, MI, stent thrombosis, or ischemia-driven revascularization at 48 hours – was no different between patients who presented at 7 a.m. through 7 p.m. Monday through Friday than in those who presented during off hours (RR, 1.00), said Dr. Selvaraj of Brigham and Women’s Hospital Heart & Vascular Center, Boston.

There also was no difference between the two study groups in the primary safety outcome, which was moderate to severe bleeding events.

PCI yielded consistent benefits regardless of the timing of patient presentation, Dr. Selvaraj said.

CHAMPION PHOENIX was sponsored by the Medicines Company.

Off-hours presentation to the hospital with STEMI did not affect PCI outcomes in the international prospective randomized CHAMPION PHOENIX trial.

The newer findings are reassuring and, in contrast with findings from several previous retrospective registry–based studies, suggest that presenting to the hospital at night or on weekends or holidays is no more hazardous than presenting during regular working hours, Senthil Selvaraj, MD, said in a presentation at the annual congress of the European Society of Cardiology. The results may reflect global quality improvement measures in STEMI care.

In the study, which was simultaneously published in Journal of the American College of Cardiology, researchers assessed the outcomes of 1,992 patients with STEMI participating in a large, industry-sponsored clinical trial. The primary efficacy outcome – a combination of all-cause mortality, MI, stent thrombosis, or ischemia-driven revascularization at 48 hours – was no different between patients who presented at 7 a.m. through 7 p.m. Monday through Friday than in those who presented during off hours (RR, 1.00), said Dr. Selvaraj of Brigham and Women’s Hospital Heart & Vascular Center, Boston.

There also was no difference between the two study groups in the primary safety outcome, which was moderate to severe bleeding events.

PCI yielded consistent benefits regardless of the timing of patient presentation, Dr. Selvaraj said.

CHAMPION PHOENIX was sponsored by the Medicines Company.

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 55-year-old woman with a past medical history of hypertension was brought to a local emergency department by ambulance after a co-worker noticed her repeating the phrase “I have to close the store, I have to close the store” to herself after the store was already closed. The patient did not recall this time period.

In the emergency room a drug screen was negative and a computed tomography (CT) scan of the head was negative. A routine EEG was normal. A diagnosis of a seizure was made and the patient was started on levetiracetam (Keppra) 1000 mg PO q12hrs.

The patient had a consultation with an epileptologist the following week. The consultation revealed that the patient family noticed that she had periods where she would stare, her speech would not make sense, and it would appear as though she was “chewing something.” The patient denied such symptoms. The patient’s family believed these symptoms had been present for at least 5 years, but thought they were due to tiredness. When questioned, the patient recalled at least 2 instances where she has fallen asleep in bed and woken up on the floor.

When asked about potential head trauma, the patient stated she was involved in a car accident 7 months ago, but the cause was not determined. The patient was driving, there was no inclement weather, and her car veered off the road and into the ditch. The patient was not intoxicated. She was not injured as a result of the accident.

Diagnosis: partial epilepsy with and without secondary generalization.

Questions and Discussion:

• Although the patient only recently received an official diagnosis of seizure, it is likely that she was having seizures for many years (at least 5 years per history).
  • Because of the long patient history with seizures, the more accurate diagnosis for this patient is complex partial epilepsy with secondary generalization.
• Does a normal routine EEG change the diagnosis?
  • No. An EEG can be normal in a patient with epilepsy.
• What further testing should be ordered?
  • The standard of care is to use dedicated magnetic resonance imaging (MRI) testing MRI-protocol for epilepsy.
• What was the likely cause of the car accident?
  • A seizure was the likely cause of the car accident.

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 55-year-old woman with a past medical history of hypertension was brought to a local emergency department by ambulance after a co-worker noticed her repeating the phrase “I have to close the store, I have to close the store” to herself after the store was already closed. The patient did not recall this time period.

In the emergency room a drug screen was negative and a computed tomography (CT) scan of the head was negative. A routine EEG was normal. A diagnosis of a seizure was made and the patient was started on levetiracetam (Keppra) 1000 mg PO q12hrs.

The patient had a consultation with an epileptologist the following week. The consultation revealed that the patient family noticed that she had periods where she would stare, her speech would not make sense, and it would appear as though she was “chewing something.” The patient denied such symptoms. The patient’s family believed these symptoms had been present for at least 5 years, but thought they were due to tiredness. When questioned, the patient recalled at least 2 instances where she has fallen asleep in bed and woken up on the floor.

When asked about potential head trauma, the patient stated she was involved in a car accident 7 months ago, but the cause was not determined. The patient was driving, there was no inclement weather, and her car veered off the road and into the ditch. The patient was not intoxicated. She was not injured as a result of the accident.

Diagnosis: partial epilepsy with and without secondary generalization.

Questions and Discussion:

• Although the patient only recently received an official diagnosis of seizure, it is likely that she was having seizures for many years (at least 5 years per history).
  • Because of the long patient history with seizures, the more accurate diagnosis for this patient is complex partial epilepsy with secondary generalization.
• Does a normal routine EEG change the diagnosis?
  • No. An EEG can be normal in a patient with epilepsy.
• What further testing should be ordered?
  • The standard of care is to use dedicated magnetic resonance imaging (MRI) testing MRI-protocol for epilepsy.
• What was the likely cause of the car accident?
  • A seizure was the likely cause of the car accident.

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 55-year-old woman with a past medical history of hypertension was brought to a local emergency department by ambulance after a co-worker noticed her repeating the phrase “I have to close the store, I have to close the store” to herself after the store was already closed. The patient did not recall this time period.

In the emergency room a drug screen was negative and a computed tomography (CT) scan of the head was negative. A routine EEG was normal. A diagnosis of a seizure was made and the patient was started on levetiracetam (Keppra) 1000 mg PO q12hrs.

The patient had a consultation with an epileptologist the following week. The consultation revealed that the patient family noticed that she had periods where she would stare, her speech would not make sense, and it would appear as though she was “chewing something.” The patient denied such symptoms. The patient’s family believed these symptoms had been present for at least 5 years, but thought they were due to tiredness. When questioned, the patient recalled at least 2 instances where she has fallen asleep in bed and woken up on the floor.

When asked about potential head trauma, the patient stated she was involved in a car accident 7 months ago, but the cause was not determined. The patient was driving, there was no inclement weather, and her car veered off the road and into the ditch. The patient was not intoxicated. She was not injured as a result of the accident.

Diagnosis: partial epilepsy with and without secondary generalization.

Questions and Discussion:

• Although the patient only recently received an official diagnosis of seizure, it is likely that she was having seizures for many years (at least 5 years per history).
  • Because of the long patient history with seizures, the more accurate diagnosis for this patient is complex partial epilepsy with secondary generalization.
• Does a normal routine EEG change the diagnosis?
  • No. An EEG can be normal in a patient with epilepsy.
• What further testing should be ordered?
  • The standard of care is to use dedicated magnetic resonance imaging (MRI) testing MRI-protocol for epilepsy.
• What was the likely cause of the car accident?
  • A seizure was the likely cause of the car accident.

The European Society of Clinical Microbiology and Infectious Diseases has updated its clinical guideline for diagnosing Clostridium difficile infection, according to a report in Clinical Microbiology and Infection.

“Our aim is to not only improve diagnosis of C. difficile infection, but also to standardize the diagnostic process across Europe to allow for improved surveillance of the disease,” Ed J. Kuijper, MD, of the Centre for Infectious Diseases, Leiden (the Netherlands) University Medical Centre and lead investigator for the new guideline, said in a press statement.

CDC/Jennifer Hulsey

The Society released its first guideline regarding C. difficile diagnosis in 2009, but it required revision because many new diagnostic tests have become commercially available since then. The updated guideline focuses on diagnosing patients of all ages with diarrhea who are suspected of having C. difficile infection and is intended for use by medical microbiologists, gastroenterologists, infectious disease specialists, and infection control practitioners, said Monique J.T. Crobach, MD, who is also of Leiden University and is first author of the guideline, and her associates (Clin Microbiol Infect. 2016;22:S63-81).

They performed a comprehensive meta-analysis of 56 studies that compared 24 commercially available diagnostic assays against either of the current “gold standard” tests, the cell cytotoxicity neutralization assay or the toxigenic culture. Forty-one of these studies were published after 2009. Based on their findings, Dr. Crobach and her associates formulated 16 recommendations and suggestions, noting the quality of evidence supporting each one.

The updated guideline strongly recommends against using any single diagnostic assay to diagnose C. difficile infection, regardless of the technology on which it is based. Instead, diagnosis should rest on clinical signs and symptoms together with a two-step algorithm starting with either a nucleic acid amplification test or a glutamate dehydrogenase enzyme immunoassay. Samples with positive results on this initial test should be tested further with a toxin A/B enzyme immunoassay.

An alternative algorithm is to initially test samples with both a glutamate dehydrogenase and a toxin A/B enzyme immunoassay. The guideline spells out what actions to take in the event of concordant positive results, concordant negative results, or discordant results.

Testing for C. difficile should not be limited to samples with a specific request from a physician. All unformed stool samples from patients aged 3 years and older should be tested for the organism. In contrast, formed stool samples shouldn’t be tested for C. difficile unless the patient has paralytic ileus.

The guideline also addresses repeat testing. Performing a repeat test after an initial negative result during the same diarrheal episode may be useful in selected cases with ongoing clinical suspicion during an epidemic situation, or even in cases with high clinical suspicion during endemic situations. But repeat testing after an initial positive result generally is not recommended. Repeat testing to assess whether the patient is cured is definitely not recommended.

However, the decision to treat patients for C. difficile infection is a clinical one and may be justified even if all laboratory results are negative, Dr. Crobach and her associates noted.

The European Society of Clinical Microbiology and Infectious Diseases has updated its clinical guideline for diagnosing Clostridium difficile infection, according to a report in Clinical Microbiology and Infection.

“Our aim is to not only improve diagnosis of C. difficile infection, but also to standardize the diagnostic process across Europe to allow for improved surveillance of the disease,” Ed J. Kuijper, MD, of the Centre for Infectious Diseases, Leiden (the Netherlands) University Medical Centre and lead investigator for the new guideline, said in a press statement.

CDC/Jennifer Hulsey

The Society released its first guideline regarding C. difficile diagnosis in 2009, but it required revision because many new diagnostic tests have become commercially available since then. The updated guideline focuses on diagnosing patients of all ages with diarrhea who are suspected of having C. difficile infection and is intended for use by medical microbiologists, gastroenterologists, infectious disease specialists, and infection control practitioners, said Monique J.T. Crobach, MD, who is also of Leiden University and is first author of the guideline, and her associates (Clin Microbiol Infect. 2016;22:S63-81).

They performed a comprehensive meta-analysis of 56 studies that compared 24 commercially available diagnostic assays against either of the current “gold standard” tests, the cell cytotoxicity neutralization assay or the toxigenic culture. Forty-one of these studies were published after 2009. Based on their findings, Dr. Crobach and her associates formulated 16 recommendations and suggestions, noting the quality of evidence supporting each one.

The updated guideline strongly recommends against using any single diagnostic assay to diagnose C. difficile infection, regardless of the technology on which it is based. Instead, diagnosis should rest on clinical signs and symptoms together with a two-step algorithm starting with either a nucleic acid amplification test or a glutamate dehydrogenase enzyme immunoassay. Samples with positive results on this initial test should be tested further with a toxin A/B enzyme immunoassay.

An alternative algorithm is to initially test samples with both a glutamate dehydrogenase and a toxin A/B enzyme immunoassay. The guideline spells out what actions to take in the event of concordant positive results, concordant negative results, or discordant results.

Testing for C. difficile should not be limited to samples with a specific request from a physician. All unformed stool samples from patients aged 3 years and older should be tested for the organism. In contrast, formed stool samples shouldn’t be tested for C. difficile unless the patient has paralytic ileus.

The guideline also addresses repeat testing. Performing a repeat test after an initial negative result during the same diarrheal episode may be useful in selected cases with ongoing clinical suspicion during an epidemic situation, or even in cases with high clinical suspicion during endemic situations. But repeat testing after an initial positive result generally is not recommended. Repeat testing to assess whether the patient is cured is definitely not recommended.

However, the decision to treat patients for C. difficile infection is a clinical one and may be justified even if all laboratory results are negative, Dr. Crobach and her associates noted.

The European Society of Clinical Microbiology and Infectious Diseases has updated its clinical guideline for diagnosing Clostridium difficile infection, according to a report in Clinical Microbiology and Infection.

“Our aim is to not only improve diagnosis of C. difficile infection, but also to standardize the diagnostic process across Europe to allow for improved surveillance of the disease,” Ed J. Kuijper, MD, of the Centre for Infectious Diseases, Leiden (the Netherlands) University Medical Centre and lead investigator for the new guideline, said in a press statement.

CDC/Jennifer Hulsey

The Society released its first guideline regarding C. difficile diagnosis in 2009, but it required revision because many new diagnostic tests have become commercially available since then. The updated guideline focuses on diagnosing patients of all ages with diarrhea who are suspected of having C. difficile infection and is intended for use by medical microbiologists, gastroenterologists, infectious disease specialists, and infection control practitioners, said Monique J.T. Crobach, MD, who is also of Leiden University and is first author of the guideline, and her associates (Clin Microbiol Infect. 2016;22:S63-81).

They performed a comprehensive meta-analysis of 56 studies that compared 24 commercially available diagnostic assays against either of the current “gold standard” tests, the cell cytotoxicity neutralization assay or the toxigenic culture. Forty-one of these studies were published after 2009. Based on their findings, Dr. Crobach and her associates formulated 16 recommendations and suggestions, noting the quality of evidence supporting each one.

The updated guideline strongly recommends against using any single diagnostic assay to diagnose C. difficile infection, regardless of the technology on which it is based. Instead, diagnosis should rest on clinical signs and symptoms together with a two-step algorithm starting with either a nucleic acid amplification test or a glutamate dehydrogenase enzyme immunoassay. Samples with positive results on this initial test should be tested further with a toxin A/B enzyme immunoassay.

An alternative algorithm is to initially test samples with both a glutamate dehydrogenase and a toxin A/B enzyme immunoassay. The guideline spells out what actions to take in the event of concordant positive results, concordant negative results, or discordant results.

Testing for C. difficile should not be limited to samples with a specific request from a physician. All unformed stool samples from patients aged 3 years and older should be tested for the organism. In contrast, formed stool samples shouldn’t be tested for C. difficile unless the patient has paralytic ileus.

The guideline also addresses repeat testing. Performing a repeat test after an initial negative result during the same diarrheal episode may be useful in selected cases with ongoing clinical suspicion during an epidemic situation, or even in cases with high clinical suspicion during endemic situations. But repeat testing after an initial positive result generally is not recommended. Repeat testing to assess whether the patient is cured is definitely not recommended.

However, the decision to treat patients for C. difficile infection is a clinical one and may be justified even if all laboratory results are negative, Dr. Crobach and her associates noted.

The platysma muscle has been widely studied in its course through the cervical region in an attempt to develop more effective surgical approaches for rejuvenation. As a person ages, the platysma muscle becomes thinner, less defined, and ptotic, which results in the clinical appearance of a sagging neck that prompts patients to undergo neck-lift procedures. However, little is known about the course of the platysma in the mid and lower face and the implications on facial aging.

Bae et al (Plast Reconstr Surg. 2016;138:365-371) performed a cadaveric dissection of the facial portion of the platysma muscle to delineate the morphology and extension of the muscle in the mid and lower face. Thirty-four adult hemifaces were dissected. The demographics were broken down by age (mean, 71.4 years; range, 41–93 years), gender (29 men; 5 women), and ethnicity (14 Korean; 20 Thai). The extension of the platysma was documented according to a grid the authors created. The grid was divided along 3 horizontal lines (H1–H3) and 3 vertical lines (V1–V3). The intersection of these lines created a grid that was comprised of 3×3 squares and was labeled superior (S1–S3), middle (M1–M3), and inferior (I1–I3). H1 was a line drawn horizontally from the tragus to the lateral orbit, H2 was a line from the earlobe to the nasal ala, and H3 was a line from the angle of the mandible to the corner of the mouth.

The extension pattern of the facial portion of the platysma muscle was classified into patterns: A (n=3; S1–S2, M1–M3, and I1-I3 were covered by the muscle), B-1 (n=20; M1–M3, I1–I3), B-2 (n=9; M1–M2, I1–I3), and C (n=2; I1-I3).

The platysma muscle is divided into anterior and posterior portions. The anterior platysma ascends superiorly and medially in the face to interdigitate with the depressor anguli oris and the depressor labii inferioris muscles. The morphology pattern of the posterior platysma varied and was classified into 1 of 3 patterns: straight (n=13), straight-curved (n=18), and curved (n=3). The straight pattern showed platysma fibers that travel parallel to the mandibular malar line and head toward the zygomaticus major or the orbicularis oculi muscles. The straight-curved type has fibers that travel straight from the neck to the face but then curve, heading toward the risorius, zygomaticus major, or orbicularis oculi muscle depending on the extent of the platysma muscle in the area. The curved type has fibers that run parallel to the zygomaticus arch and interdigitate with the orbicularis oculi muscle and either the risorius or zygomaticus major muscle.

What’s the issue?

For many years, the cervical platysma muscle was studied and surgical approaches were modified to enhance results. The authors of this study have taken the study of the platysma muscle further to delineate its course through the face. Knowledge of the various pathways of the muscle can help us determine the most natural direction to resuspend ptotic facial tissue during surgery and minimally invasive procedures such as thread-lifting. The most salient points include: (1) the lower one-third of the masseter muscle is covered by the platysma, and (2) straight-curved was the most common morphology type, suggesting that the vector for repositioning the platysma muscle is vertical.

Although Bae et al do not discuss the use of botulinum toxin (BTX) in the treatment of the platysma, the results of this study further support the importance of BTX to the lower face. We can look back at more than 14 years of cosmetic use of BTX for the glabella and see the reduced number of brow-lift surgeries nationwide. Although the preventative effects of BTX on brow depression still need to be scientifically proven, it may behoove us to think preventatively on the use of BTX in the platysma to minimize ptosis of the lower face and neck. The results of this anatomic study support the importance of tailoring the approach to the dynamic lines caused by the platysma muscle in each patient to address jowls and neck bands. Have you been offering lower face BTX treatments to patients in an effort to reduce lower face aging?

We want to know your views! Tell us what you think.

The platysma muscle has been widely studied in its course through the cervical region in an attempt to develop more effective surgical approaches for rejuvenation. As a person ages, the platysma muscle becomes thinner, less defined, and ptotic, which results in the clinical appearance of a sagging neck that prompts patients to undergo neck-lift procedures. However, little is known about the course of the platysma in the mid and lower face and the implications on facial aging.

Bae et al (Plast Reconstr Surg. 2016;138:365-371) performed a cadaveric dissection of the facial portion of the platysma muscle to delineate the morphology and extension of the muscle in the mid and lower face. Thirty-four adult hemifaces were dissected. The demographics were broken down by age (mean, 71.4 years; range, 41–93 years), gender (29 men; 5 women), and ethnicity (14 Korean; 20 Thai). The extension of the platysma was documented according to a grid the authors created. The grid was divided along 3 horizontal lines (H1–H3) and 3 vertical lines (V1–V3). The intersection of these lines created a grid that was comprised of 3×3 squares and was labeled superior (S1–S3), middle (M1–M3), and inferior (I1–I3). H1 was a line drawn horizontally from the tragus to the lateral orbit, H2 was a line from the earlobe to the nasal ala, and H3 was a line from the angle of the mandible to the corner of the mouth.

The extension pattern of the facial portion of the platysma muscle was classified into patterns: A (n=3; S1–S2, M1–M3, and I1-I3 were covered by the muscle), B-1 (n=20; M1–M3, I1–I3), B-2 (n=9; M1–M2, I1–I3), and C (n=2; I1-I3).

The platysma muscle is divided into anterior and posterior portions. The anterior platysma ascends superiorly and medially in the face to interdigitate with the depressor anguli oris and the depressor labii inferioris muscles. The morphology pattern of the posterior platysma varied and was classified into 1 of 3 patterns: straight (n=13), straight-curved (n=18), and curved (n=3). The straight pattern showed platysma fibers that travel parallel to the mandibular malar line and head toward the zygomaticus major or the orbicularis oculi muscles. The straight-curved type has fibers that travel straight from the neck to the face but then curve, heading toward the risorius, zygomaticus major, or orbicularis oculi muscle depending on the extent of the platysma muscle in the area. The curved type has fibers that run parallel to the zygomaticus arch and interdigitate with the orbicularis oculi muscle and either the risorius or zygomaticus major muscle.

What’s the issue?

For many years, the cervical platysma muscle was studied and surgical approaches were modified to enhance results. The authors of this study have taken the study of the platysma muscle further to delineate its course through the face. Knowledge of the various pathways of the muscle can help us determine the most natural direction to resuspend ptotic facial tissue during surgery and minimally invasive procedures such as thread-lifting. The most salient points include: (1) the lower one-third of the masseter muscle is covered by the platysma, and (2) straight-curved was the most common morphology type, suggesting that the vector for repositioning the platysma muscle is vertical.

Although Bae et al do not discuss the use of botulinum toxin (BTX) in the treatment of the platysma, the results of this study further support the importance of BTX to the lower face. We can look back at more than 14 years of cosmetic use of BTX for the glabella and see the reduced number of brow-lift surgeries nationwide. Although the preventative effects of BTX on brow depression still need to be scientifically proven, it may behoove us to think preventatively on the use of BTX in the platysma to minimize ptosis of the lower face and neck. The results of this anatomic study support the importance of tailoring the approach to the dynamic lines caused by the platysma muscle in each patient to address jowls and neck bands. Have you been offering lower face BTX treatments to patients in an effort to reduce lower face aging?

We want to know your views! Tell us what you think.

The platysma muscle has been widely studied in its course through the cervical region in an attempt to develop more effective surgical approaches for rejuvenation. As a person ages, the platysma muscle becomes thinner, less defined, and ptotic, which results in the clinical appearance of a sagging neck that prompts patients to undergo neck-lift procedures. However, little is known about the course of the platysma in the mid and lower face and the implications on facial aging.

Bae et al (Plast Reconstr Surg. 2016;138:365-371) performed a cadaveric dissection of the facial portion of the platysma muscle to delineate the morphology and extension of the muscle in the mid and lower face. Thirty-four adult hemifaces were dissected. The demographics were broken down by age (mean, 71.4 years; range, 41–93 years), gender (29 men; 5 women), and ethnicity (14 Korean; 20 Thai). The extension of the platysma was documented according to a grid the authors created. The grid was divided along 3 horizontal lines (H1–H3) and 3 vertical lines (V1–V3). The intersection of these lines created a grid that was comprised of 3×3 squares and was labeled superior (S1–S3), middle (M1–M3), and inferior (I1–I3). H1 was a line drawn horizontally from the tragus to the lateral orbit, H2 was a line from the earlobe to the nasal ala, and H3 was a line from the angle of the mandible to the corner of the mouth.

The extension pattern of the facial portion of the platysma muscle was classified into patterns: A (n=3; S1–S2, M1–M3, and I1-I3 were covered by the muscle), B-1 (n=20; M1–M3, I1–I3), B-2 (n=9; M1–M2, I1–I3), and C (n=2; I1-I3).

The platysma muscle is divided into anterior and posterior portions. The anterior platysma ascends superiorly and medially in the face to interdigitate with the depressor anguli oris and the depressor labii inferioris muscles. The morphology pattern of the posterior platysma varied and was classified into 1 of 3 patterns: straight (n=13), straight-curved (n=18), and curved (n=3). The straight pattern showed platysma fibers that travel parallel to the mandibular malar line and head toward the zygomaticus major or the orbicularis oculi muscles. The straight-curved type has fibers that travel straight from the neck to the face but then curve, heading toward the risorius, zygomaticus major, or orbicularis oculi muscle depending on the extent of the platysma muscle in the area. The curved type has fibers that run parallel to the zygomaticus arch and interdigitate with the orbicularis oculi muscle and either the risorius or zygomaticus major muscle.

What’s the issue?

For many years, the cervical platysma muscle was studied and surgical approaches were modified to enhance results. The authors of this study have taken the study of the platysma muscle further to delineate its course through the face. Knowledge of the various pathways of the muscle can help us determine the most natural direction to resuspend ptotic facial tissue during surgery and minimally invasive procedures such as thread-lifting. The most salient points include: (1) the lower one-third of the masseter muscle is covered by the platysma, and (2) straight-curved was the most common morphology type, suggesting that the vector for repositioning the platysma muscle is vertical.

Although Bae et al do not discuss the use of botulinum toxin (BTX) in the treatment of the platysma, the results of this study further support the importance of BTX to the lower face. We can look back at more than 14 years of cosmetic use of BTX for the glabella and see the reduced number of brow-lift surgeries nationwide. Although the preventative effects of BTX on brow depression still need to be scientifically proven, it may behoove us to think preventatively on the use of BTX in the platysma to minimize ptosis of the lower face and neck. The results of this anatomic study support the importance of tailoring the approach to the dynamic lines caused by the platysma muscle in each patient to address jowls and neck bands. Have you been offering lower face BTX treatments to patients in an effort to reduce lower face aging?

We want to know your views! Tell us what you think.