The Wall Street Journal (2/8, McCartney, Subscription Publication) reports that the American College of Chest Physicians has released new guidelines recommending that travelers at an increased risk for developing deep vein thrombosis (DVT) use compression stockings when on long flights.
The AP (2/8, Tanner) reports that "the guidelines were released online Tuesday in the group's journal, Chest. They're based on a review of recent research and other medical evidence on deep vein thrombosis, blood clots that form deep in leg veins." The AP adds, "There's no proof that flying economy-class increases your chances of dangerous blood clots, according to" the "new guidelines."
MedPage Today (2/8, Fiore) reports, meanwhile, that "clinicians should not recommend that all travelers use aspirin for prevention of deep vein thrombosis during long plane trips, according to" the "new recommendation."
POSTED BY BRIAN D. WILLIAMSON, MD
Friday, March 30, 2012
Tuesday, March 27, 2012
SMOKING ASSOCIATED WITH FASTER COGNITIVE DECLINE IN MIDDLE-AGED MEN
The Los Angeles Times (2/7, Brown) "Booster Shots" blog reports, "Middle-aged men who smoke suffered more rapid cognitive decline than peers who have never smoked or who have been ex-smokers for at least 10 years," according to a study published online Feb. 6 in the Archives of General Psychiatry.
On its website, ABC News (2/7, Gann) explains, "Researchers from University College in London studied more than 5,000 men and 2,000 women from Britain's long-running Whitehall II study, which has surveyed the health of thousands of British civil service employees." After examining "each participant's performance on tests of memory, verbal skills and reasoning over a period of 10 years, beginning when the participants were about 56 years old," researchers "found that men who smoked showed a greater decline in these mental functions than those who had never smoked."
"But there was good news for people who had laid off cigarettes for at least a decade: Men who were long-term ex smokers did not have greater mental decline than men who never took up tobacco," WebMD (2/7, Nierenberg) reports.
Still, HealthDay (2/7, Preidt) pointed out that "quitting didn't necessarily help right away: Men who kicked the habit in the 10 years before their first assessment were still at risk of more mental decline, particularly in their so-called 'executive' functioning, which includes various complex mental processes involved in planning and achieving a particular goal." Nevertheless, "men who were long-term ex-smokers did not have faster decline." Notably, the study authors "found no link between smoking and declines in mental abilities in women. The reasons for this gender difference aren't clear, but the fact that men tend to smoke more cigarettes than women may be one explanation, they suggested." Also covering the story are Reuters (2/7, Kelland), and MedPage Today (2/7, Phend).
POSTED BY BRIAN D. WILLIAMSON, MD
On its website, ABC News (2/7, Gann) explains, "Researchers from University College in London studied more than 5,000 men and 2,000 women from Britain's long-running Whitehall II study, which has surveyed the health of thousands of British civil service employees." After examining "each participant's performance on tests of memory, verbal skills and reasoning over a period of 10 years, beginning when the participants were about 56 years old," researchers "found that men who smoked showed a greater decline in these mental functions than those who had never smoked."
"But there was good news for people who had laid off cigarettes for at least a decade: Men who were long-term ex smokers did not have greater mental decline than men who never took up tobacco," WebMD (2/7, Nierenberg) reports.
Still, HealthDay (2/7, Preidt) pointed out that "quitting didn't necessarily help right away: Men who kicked the habit in the 10 years before their first assessment were still at risk of more mental decline, particularly in their so-called 'executive' functioning, which includes various complex mental processes involved in planning and achieving a particular goal." Nevertheless, "men who were long-term ex-smokers did not have faster decline." Notably, the study authors "found no link between smoking and declines in mental abilities in women. The reasons for this gender difference aren't clear, but the fact that men tend to smoke more cigarettes than women may be one explanation, they suggested." Also covering the story are Reuters (2/7, Kelland), and MedPage Today (2/7, Phend).
POSTED BY BRIAN D. WILLIAMSON, MD
Friday, March 23, 2012
EXPERIMENTAL DRUG CUT HEART ATTACK RISK, BUT INCREASED BLEEDING
The Wall Street Journal (2/8, Loftus, Subscription Publication) reports that Merck's experimental anticlotting medication vorapaxar cut heart attack risk, but increased the risk of bleeding in a clinical trial. The findings are scheduled to be presented at an American College of Cardiology conference next month.
The AP (2/8) reports, "A year ago, the same bleeding problem led safety monitors to halt a late-stage study of vorapaxar called TRACER. That international study included nearly 13,000 patients who had had a heart attack or severe chest pain from clogged arteries." Also covering the story were Reuters (2/8) and MedPage Today (2/8, Kaiser
POSTED BY BRIAN D. WILLIAMSON, MD
The AP (2/8) reports, "A year ago, the same bleeding problem led safety monitors to halt a late-stage study of vorapaxar called TRACER. That international study included nearly 13,000 patients who had had a heart attack or severe chest pain from clogged arteries." Also covering the story were Reuters (2/8) and MedPage Today (2/8, Kaiser
POSTED BY BRIAN D. WILLIAMSON, MD
Tuesday, March 20, 2012
CDC SURVEY FINDS BREAD IS TOP SOURCE OF SODIUM IN US DIET
ABC World News (2/7, story 7, 0:35, Sawyer) reported that "the Center for Diseases Control said nine out of ten adults eat too much salt. And the number one source of their salt is a surprise -- bread and rolls."
The CBS Evening News (2/7, story 9, 0:20, Pelley) reported, "The Centers for Disease Control said today that salty snacks like potato chips are not our biggest source of sodium."
NBC Nightly News (2/7, story 8, 2:25, Williams) reported that CDC Director Thomas Frieden, MD, said, "We're eating more food made by others, in restaurants or prepared food from grocery stores. And when other people make food for us, they put a lot more salt in it." NBC's Costello added, "More fruits, veggies and home cooking are the solution, says the CDC."
The AP (2/8, Stobbe) reports, "Bread and rolls are the No. 1 source of salt in the American diet, accounting for more than twice as much sodium as salty junk food like potato chips. That surprising finding comes in a government report released Tuesday that includes a list of the top 10 sources of sodium." CDC officials "are encouraging consumers to read labels and, for example, buy brands of bread that have lower sodium." CDC Director Frieden noted, "Potato chips, pretzels, and popcorn -- which we think of as the saltiest foods in our diet -- are only No. 10."
"Most sodium in the US diet comes from bread, lunch meat, pizza, chicken, soup, and burgers, the CDC found," according to the National Journal (2/8, Fox, Subscription Publication). In a statement, CDC Director Frieden said, "We're encouraged that some food manufacturers are already taking steps to reduce sodium," noting that manufacturers such as Kraft and Leprino Foods are "actively working on providing customers and consumers with healthier options."
The NPR (2/8, Barclay) "The Salt" blog reports, "According to the CDC, the average American consumes about 3,300 milligrams of sodium per day, not including any salt that may be added during a meal. ... The US Dietary Guidelines recommend no more than 2,300 mg a day, except if you're over 51 years or African American or have high blood pressure, diabetes or chronic kidney disease."
The Atlanta Journal-Constitution (2/8, Jeffries) lists the "10 types of foods are responsible for more than 40 percent of people's sodium intake," according to the CDC list. The foods are "breads and rolls; luncheon meat, such as deli ham or turkey; pizza; poultry; soups; cheeseburgers and other sandwiches; cheese; pasta dishes; meat dishes such as meat loaf; and snack foods such as potato chips, pretzels and popcorn." The Journal-Constitution points out that "breads and rolls aren't saltier than many of the other foods on the CDC list, but people tend to eat a lot of them," which makes them the cop source of salt in the diet.
MedPage Today (2/8, Fiore) notes, "The data come from the 'What We Eat in America' portion of the National Health and Nutrition Examination Survey (NHANES) 2007-2008. NHANES is a survey that relies on self-reported data, a fact that may introduce bias and also raises questions about the generalizability of its findings." The study is published in the CDC's Morbidity and Mortality Weekly Report. CQ (2/8, Subscription Publication) and the Los Angeles Times (2/8, Muskal) "Nation Now" blog also cover the story.
POSTED BY BRIAN D. WILLIAMSON, MD
The CBS Evening News (2/7, story 9, 0:20, Pelley) reported, "The Centers for Disease Control said today that salty snacks like potato chips are not our biggest source of sodium."
NBC Nightly News (2/7, story 8, 2:25, Williams) reported that CDC Director Thomas Frieden, MD, said, "We're eating more food made by others, in restaurants or prepared food from grocery stores. And when other people make food for us, they put a lot more salt in it." NBC's Costello added, "More fruits, veggies and home cooking are the solution, says the CDC."
The AP (2/8, Stobbe) reports, "Bread and rolls are the No. 1 source of salt in the American diet, accounting for more than twice as much sodium as salty junk food like potato chips. That surprising finding comes in a government report released Tuesday that includes a list of the top 10 sources of sodium." CDC officials "are encouraging consumers to read labels and, for example, buy brands of bread that have lower sodium." CDC Director Frieden noted, "Potato chips, pretzels, and popcorn -- which we think of as the saltiest foods in our diet -- are only No. 10."
"Most sodium in the US diet comes from bread, lunch meat, pizza, chicken, soup, and burgers, the CDC found," according to the National Journal (2/8, Fox, Subscription Publication). In a statement, CDC Director Frieden said, "We're encouraged that some food manufacturers are already taking steps to reduce sodium," noting that manufacturers such as Kraft and Leprino Foods are "actively working on providing customers and consumers with healthier options."
The NPR (2/8, Barclay) "The Salt" blog reports, "According to the CDC, the average American consumes about 3,300 milligrams of sodium per day, not including any salt that may be added during a meal. ... The US Dietary Guidelines recommend no more than 2,300 mg a day, except if you're over 51 years or African American or have high blood pressure, diabetes or chronic kidney disease."
The Atlanta Journal-Constitution (2/8, Jeffries) lists the "10 types of foods are responsible for more than 40 percent of people's sodium intake," according to the CDC list. The foods are "breads and rolls; luncheon meat, such as deli ham or turkey; pizza; poultry; soups; cheeseburgers and other sandwiches; cheese; pasta dishes; meat dishes such as meat loaf; and snack foods such as potato chips, pretzels and popcorn." The Journal-Constitution points out that "breads and rolls aren't saltier than many of the other foods on the CDC list, but people tend to eat a lot of them," which makes them the cop source of salt in the diet.
MedPage Today (2/8, Fiore) notes, "The data come from the 'What We Eat in America' portion of the National Health and Nutrition Examination Survey (NHANES) 2007-2008. NHANES is a survey that relies on self-reported data, a fact that may introduce bias and also raises questions about the generalizability of its findings." The study is published in the CDC's Morbidity and Mortality Weekly Report. CQ (2/8, Subscription Publication) and the Los Angeles Times (2/8, Muskal) "Nation Now" blog also cover the story.
POSTED BY BRIAN D. WILLIAMSON, MD
Friday, March 16, 2012
GENETIC DATA NIX FOLATE ROLE IN HEART DISEASE
By: Michael Smith, North American Correspondent, MedPage Today
Published: February 22, 2012
Reviewed by: Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
The final nail may have been placed in the coffin of homocysteine-lowering therapy as a preventive measure for coronary heart disease.
The overall result from large, unpublished data sets shows lifelong moderate homocysteine elevation has little or no effect on coronary heart disease.
A comprehensive analysis -- including published and unpublished research that involved more than 236,000 participants -- suggests that even lifelong exposure to elevated homocysteine "has little or no effect," according to Robert Clarke, MD, of the Clinical Trial Service Unit at the University of Oxford, in Oxford, England, and colleagues.
The key finding is that, in several large unpublished data sets, genetic variation that increases or decreases natural homocysteine levels did not significantly affect the risk of coronary heart disease, Clarke and colleagues reported online in PLoS Medicine.
That was coupled with a null effect in an updated meta-analysis of 10 clinical trials testing the effect of folic acid, a homocysteine-lowering compound.
Taken together, that evidence suggests that a significant but modest benefit of lower homocysteine in an updated meta-analysis of 86 published case-control studies was an "artifact of publication bias," the researchers argued.
Clarke and colleagues noted that a common genetic variant -- named C677T -- in the methylene tetrahydrofolate reductase gene (MTHFR) markedly affects homocysteine levels.
Specifically, people with the TT genotype (individuals in whom both copies of the MTHFR gene have the nucleotide thymine at position 677) of the C677T polymorphism have natural levels that are about 20% higher than those with the CC variant. The CT variant has an effect that is intermediate but closer to CC than TT.
That suggests the possibility of a natural "Mendelian" experiment, and luckily the increasing use of large scale-genomics analysis has led to the creation of 19 large datasets -- with a total of more than 100,000 participants -- in which variation in the MTHFR gene was analyzed, although not as a primary focus.
Clarke and colleagues designated those studies as "unpublished" because odds ratios for coronary heart disease were not the primary aim and have not been reported. The studies had a total of 48,175 coronary heart disease cases and 67,961 controls.
If the associations seen in the earlier case-control studies were causal, the researchers argued, the 20% higher homocysteine in those with the TT variant should imply about an 8% increase in coronary heart disease risk, compared with CC carriers.
But a meta-analysis of the effect of the TT variant in the 19 studies showed a nonsignificant odds ratio of 1.02, with a 95% confidence interval from 0.98 to 1.07, they reported.
Even in the sub-population of participants who had not been given folate supplements in food, where the effect of the TT variant might be expected to be stronger, it remained nonsignificant, with an odds ratio of 1.01.
On the other hand, Clarke and colleagues reported, the updated analysis of the 86 biochemical studies -- with 28,617 cases and 41,857 controls -- suggested that having the TT variant increased the risk of coronary heart disease by 15% (odds ratio 1.15, 95% CI from 1.09 to 1.21).
The results of the two analyses are "discrepant," the researchers noted, and the discrepancy "is too extreme to be plausibly dismissed as a chance finding."
Instead, they argued for a "substantial" effect of publication bias.
To bolster the argument, they noted that their analysis of the 10 intervention studies, with a total of more than 50,000 participants, found that lowering homocysteine for at least five years had no significant effect on the risk of coronary heart disease. The odds ratio was 1.02 (95% CI from 0.96 to 1.08).
"Both the genetic studies and the trials argue against the use of (homocysteine-lowering agents) as a means of reducing coronary heart disease risk," they concluded.
The journal editors agreed, noting that "these findings reveal a serious example of publication bias and argue against the use of folate supplements as a means of reducing [coronary heart disease] risk."
POSTED BY DAVID R. CRAGG, MD
Primary source: PLoS Medicine
Source reference:
Clarke R, et al "Homocysteine and coronary heart disease: meta-analysis of MTHFR case-control studies, avoiding publication bias" PLoS Med 2012; 9(2): e1001177.
Published: February 22, 2012
Reviewed by: Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
The final nail may have been placed in the coffin of homocysteine-lowering therapy as a preventive measure for coronary heart disease.
The overall result from large, unpublished data sets shows lifelong moderate homocysteine elevation has little or no effect on coronary heart disease.
A comprehensive analysis -- including published and unpublished research that involved more than 236,000 participants -- suggests that even lifelong exposure to elevated homocysteine "has little or no effect," according to Robert Clarke, MD, of the Clinical Trial Service Unit at the University of Oxford, in Oxford, England, and colleagues.
The key finding is that, in several large unpublished data sets, genetic variation that increases or decreases natural homocysteine levels did not significantly affect the risk of coronary heart disease, Clarke and colleagues reported online in PLoS Medicine.
That was coupled with a null effect in an updated meta-analysis of 10 clinical trials testing the effect of folic acid, a homocysteine-lowering compound.
Taken together, that evidence suggests that a significant but modest benefit of lower homocysteine in an updated meta-analysis of 86 published case-control studies was an "artifact of publication bias," the researchers argued.
Clarke and colleagues noted that a common genetic variant -- named C677T -- in the methylene tetrahydrofolate reductase gene (MTHFR) markedly affects homocysteine levels.
Specifically, people with the TT genotype (individuals in whom both copies of the MTHFR gene have the nucleotide thymine at position 677) of the C677T polymorphism have natural levels that are about 20% higher than those with the CC variant. The CT variant has an effect that is intermediate but closer to CC than TT.
That suggests the possibility of a natural "Mendelian" experiment, and luckily the increasing use of large scale-genomics analysis has led to the creation of 19 large datasets -- with a total of more than 100,000 participants -- in which variation in the MTHFR gene was analyzed, although not as a primary focus.
Clarke and colleagues designated those studies as "unpublished" because odds ratios for coronary heart disease were not the primary aim and have not been reported. The studies had a total of 48,175 coronary heart disease cases and 67,961 controls.
If the associations seen in the earlier case-control studies were causal, the researchers argued, the 20% higher homocysteine in those with the TT variant should imply about an 8% increase in coronary heart disease risk, compared with CC carriers.
But a meta-analysis of the effect of the TT variant in the 19 studies showed a nonsignificant odds ratio of 1.02, with a 95% confidence interval from 0.98 to 1.07, they reported.
Even in the sub-population of participants who had not been given folate supplements in food, where the effect of the TT variant might be expected to be stronger, it remained nonsignificant, with an odds ratio of 1.01.
On the other hand, Clarke and colleagues reported, the updated analysis of the 86 biochemical studies -- with 28,617 cases and 41,857 controls -- suggested that having the TT variant increased the risk of coronary heart disease by 15% (odds ratio 1.15, 95% CI from 1.09 to 1.21).
The results of the two analyses are "discrepant," the researchers noted, and the discrepancy "is too extreme to be plausibly dismissed as a chance finding."
Instead, they argued for a "substantial" effect of publication bias.
To bolster the argument, they noted that their analysis of the 10 intervention studies, with a total of more than 50,000 participants, found that lowering homocysteine for at least five years had no significant effect on the risk of coronary heart disease. The odds ratio was 1.02 (95% CI from 0.96 to 1.08).
"Both the genetic studies and the trials argue against the use of (homocysteine-lowering agents) as a means of reducing coronary heart disease risk," they concluded.
The journal editors agreed, noting that "these findings reveal a serious example of publication bias and argue against the use of folate supplements as a means of reducing [coronary heart disease] risk."
POSTED BY DAVID R. CRAGG, MD
Primary source: PLoS Medicine
Source reference:
Clarke R, et al "Homocysteine and coronary heart disease: meta-analysis of MTHFR case-control studies, avoiding publication bias" PLoS Med 2012; 9(2): e1001177.
Tuesday, March 13, 2012
UNDERSTANDING BLEEDING RISKS WITH DABIGATRAN
In 2011, the use of Dabigatran (Pradaxa) became commonplace in the anti-coagulation regimen for atrial fibrillation. In the US, FDA approval was based on the RELY Trial showing improved efficacy and safety compared with Warfarin in the setting of non-valvular atrial fibrillation (defined as valvular disease that was either insignificant or not meeting criteria for surgical correction). Dabigatran is an oral direct thrombin inhibitor and a twice daily regimen of 150 mg in patients with adequate renal clearance showing significant benefit in reducing stroke rates and reducing bleeding risk in patients compared with Warfarin.
Importantly, this study involved a higher percentage of patients with lower risk for CVA (CHADS 1), suggesting benefits even in lower risk patients. The ease of its use (no blood tests or dietary limitations) is a significant draw for patients, and it's no wonder that it's use is on a rapid upwards trajectory. In RELY, the primary subgroup that did not show benefit with Dabigatran were those with a history of GI bleeding. Their bleeding risks were substantially higher on Dabigatran. It should also be stated that there is no direct antidote for Dabigatran. Emergency management might require emergency dialysis which does clear the drug and eliminates most of the anticoagulant effect within an hour. For those with significant renal impairment (creatinine clearance less than 39ml), a reduced dose of Dabigatran 75 mg bid is available.
A recent report out of New Zealand, Harper et al, NEJM 3/1/12 meticulously reviewed dozens of serious bleeds on Dabigatran (Pradaxa). In nearly half of the cases, patients were noted to have significant renal impairment, and many of the bleeds occurred in octogenarians. It was felt that many of the bleeds might have been caused by poor patient selection, including very elderly patients with impaired creatinine clearance, and/or a history of GI bleeds.
With any new advance in medicine, excitement for adoption of its use must be tempered by knowledge and experience with its use. Understanding when to use a drug is only trumped by the knowledge of when not to use it. Dabigatran continues to offer significant advantages in most patient subsets. Understanding which subsets those are should help substantially in avoid untoward outcomes
POSTED BY STEVEN C. AJLUNI, MD
Importantly, this study involved a higher percentage of patients with lower risk for CVA (CHADS 1), suggesting benefits even in lower risk patients. The ease of its use (no blood tests or dietary limitations) is a significant draw for patients, and it's no wonder that it's use is on a rapid upwards trajectory. In RELY, the primary subgroup that did not show benefit with Dabigatran were those with a history of GI bleeding. Their bleeding risks were substantially higher on Dabigatran. It should also be stated that there is no direct antidote for Dabigatran. Emergency management might require emergency dialysis which does clear the drug and eliminates most of the anticoagulant effect within an hour. For those with significant renal impairment (creatinine clearance less than 39ml), a reduced dose of Dabigatran 75 mg bid is available.
A recent report out of New Zealand, Harper et al, NEJM 3/1/12 meticulously reviewed dozens of serious bleeds on Dabigatran (Pradaxa). In nearly half of the cases, patients were noted to have significant renal impairment, and many of the bleeds occurred in octogenarians. It was felt that many of the bleeds might have been caused by poor patient selection, including very elderly patients with impaired creatinine clearance, and/or a history of GI bleeds.
With any new advance in medicine, excitement for adoption of its use must be tempered by knowledge and experience with its use. Understanding when to use a drug is only trumped by the knowledge of when not to use it. Dabigatran continues to offer significant advantages in most patient subsets. Understanding which subsets those are should help substantially in avoid untoward outcomes
POSTED BY STEVEN C. AJLUNI, MD
Friday, March 9, 2012
PAD IN WOMEN IS UNRECOGNIZED LEADING TO POOR OUTCOMES
A recent AHA Scientific Statement (Hirsch et al, Circulation, 2012) underscores the importance of diagnosing PAD in patients in general, and women in particular. It is thought that 8-12 million people in the US have significant PAD, but only a tiny fraction know it. This is particularly apparent in elderly patients where the prevalence of significant arterial disease may be as high as 15-25%. Despite this, less than 2% of patients in that age group have undergone non-invasive testing. In terms of the population as a whole this discrepancy is even more apparent in women.
Similar to myocardial ischemic syndromes, symptoms of PAD in women are often atypical. Rather than classic claudication type pain, where muscular groups will ache or cramp after exertion, women might have a localizing discomfort in the heel or toes that might not be confined to muscle groups and might not be exertional. Women often only get recognized as having PAD late in the disease course and then they are at risk for worsened outcomes and a greater risk of failure after revascularization. Women with a rest ABI < 0.9 demonstrated trends towards higher event rates. Such patients tend to have more diffuse disease involvement, and that, coupled with smaller caliber vessels might lead to such poor outcomes. The risk of limb loss and amputation consequently are increased.
Much of this is analogous to the situation in coronary disease where atypical presentation and inadequate noninvasive testing result in a poor rate of diagnosis (particularly in high risk groups like diabetics). The problem seems to be compounded in minority populations where diabetes is more prevalent and access to care might be more fragmented.
Would recommended being more proactive in soliciting a history of cold extremities and atypical pain, particularly in high risk groups (smokers, diabetics, those with a history of CAD or cerebrovascular disease) and doing the appropriate testing (screening ABI) when such historical features may be present.
POSTED BY STEVEN C. AJLUNI, MD
Similar to myocardial ischemic syndromes, symptoms of PAD in women are often atypical. Rather than classic claudication type pain, where muscular groups will ache or cramp after exertion, women might have a localizing discomfort in the heel or toes that might not be confined to muscle groups and might not be exertional. Women often only get recognized as having PAD late in the disease course and then they are at risk for worsened outcomes and a greater risk of failure after revascularization. Women with a rest ABI < 0.9 demonstrated trends towards higher event rates. Such patients tend to have more diffuse disease involvement, and that, coupled with smaller caliber vessels might lead to such poor outcomes. The risk of limb loss and amputation consequently are increased.
Much of this is analogous to the situation in coronary disease where atypical presentation and inadequate noninvasive testing result in a poor rate of diagnosis (particularly in high risk groups like diabetics). The problem seems to be compounded in minority populations where diabetes is more prevalent and access to care might be more fragmented.
Would recommended being more proactive in soliciting a history of cold extremities and atypical pain, particularly in high risk groups (smokers, diabetics, those with a history of CAD or cerebrovascular disease) and doing the appropriate testing (screening ABI) when such historical features may be present.
POSTED BY STEVEN C. AJLUNI, MD
Tuesday, March 6, 2012
DOES THE BENEFICIAL ANTITHROMBIC EFFECT OF ASPIRIN WARRANT IT'S USE IN PRIMARY PREVENTION?
The latest guidelines from the "ACCP Thrombosis Guidelines" states "yes" but perhaps just barely. Aspirin has long been known for its valuable role in secondary protection whether it be in post-MI management, as well as in post-CVA or PVOD care. It also has clear benefit and a critical role in patients undergoing vascular interventions. Whether these benefits translate into the broader general population for primary prevention is muted by the increased risk for bleeding and gastrointestinal irritation. Beneficial effects on mortality in some cancers has also been described for aspirin. The answer from this leading panel suggests a small mortality benefit for the general population, thus warranting it in patients over the age of 50 who do not suffer from gastrointestinal distress. The recommendations state that individual choices should be made based on the patient's risk status for either thrombotic events or bleeding risk.
Data is further complicated by a lack of clear consensus on aspirin dose-whether a baby aspirin or an adult aspirin will suffice, and in whom. A recent example of this came out in the Plato trial on Ticargrelor for dual anti platelet effect in the setting of ACS patients undergoing PCI. In that trial, "usual use" aspirin dosing differed between European and American sites, leading to conflicting results and prompting the FDA to approve Ticargrelor but only for use with baby aspirin at 81mg, but not with adult dose aspirin at 325mg.
POSTED BY STEVEN C. AJLUNI, MD
Data is further complicated by a lack of clear consensus on aspirin dose-whether a baby aspirin or an adult aspirin will suffice, and in whom. A recent example of this came out in the Plato trial on Ticargrelor for dual anti platelet effect in the setting of ACS patients undergoing PCI. In that trial, "usual use" aspirin dosing differed between European and American sites, leading to conflicting results and prompting the FDA to approve Ticargrelor but only for use with baby aspirin at 81mg, but not with adult dose aspirin at 325mg.
POSTED BY STEVEN C. AJLUNI, MD
Saturday, March 3, 2012
MICHIGAN HEART GROUP'S PHYSICIAN LIAISON IS HERE TO HELP YOU
Michigan Heart Group has a Physician Liaison on staff to assist with questions, concerns or problems you, your staff or your patients may have with our office.
Stacie Batur is available Monday through Thursday at (248) 267-5050 (x6509). She is often between two buildings or visiting referring physician offices. If you get her voice mail, please leave a message and she will call you back shortly. If you need to speak to her immediately you can reach her on her cell phone at (248) 765-4466.
Stacie Batur is available Monday through Thursday at (248) 267-5050 (x6509). She is often between two buildings or visiting referring physician offices. If you get her voice mail, please leave a message and she will call you back shortly. If you need to speak to her immediately you can reach her on her cell phone at (248) 765-4466.
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