Experts Say Laser Could Make Heart Procedure More Accurate
Sarah Mayberry, M.P.H.
It sounds like a super hero power -- being able to see through blood. But doctors say it's possible, and it's already helping patients suffering from a common heart problem.
Patricia Stroker of Clinton Township, Mich., has suffered from an abnormal heart rhythm for three and a half years.
"It terrified me. I used to come in and tell her, 'I'm afraid to go to sleep at night,'" said Stroker. "It would wake me up from sleep. It would get me when I was eating dinner. Basically any time of the day or night, and it wasn't anything that you could foresee."
The grandmother of two was diagnosed with atrial fibrillation. Experts said it's the most common heart rhythm problem, affecting more than two million Americans.
"Atrial fibrillation is an irregular heart rhythm that starts in the top part of the heart. The top part of the heart goes about 350 to 500 beats a minute. It's a very irregular rhythm," said Dr. Ilana Kutinsky, an electrophysiologist at Beaumont Hospital.
According to the American Heart Association, about 15 percent of strokes occur in people with atrial fibrillation.
"Because the top part of the heart goes so rapidly, it doesn't squeeze effectively, and when it doesn't squeeze effectively, blood can clot and then clots can fleck off and cause a stroke," said Kutinsky.
"I would get lightheaded and dizzy along with it, so I think that scared me more than the rapid heartbeat," said Stroker.
When medicine could no longer control Stroker's symptoms, Kutinsky suggested a procedure to destroy the heart tissue that was causing her problems. Generally, doctors perform this procedure without being able to actually see the heart.
"We use indirect measures of where the heart is. So we'll do a CT scan, or we'll use X-rays, or we use 3-dimensional mapping, but we can't actually see the tissue of the heart," said Kutinsky.
Beaumont offered a different option. The hospital is part of a national clinical trial testing a device called the Cardiofocus Cardiac Laser Ablation system. It's made up of a thin tube with a camera, a balloon, and a rotating laser. It gives doctors a "super power" of sorts.
"It is actually an infrared light that allows us to see through blood," said Kutinsky.
Doctors carefully thread the laser through a vein up to the heart and zap the tissue causing the irregular rhythm.
"It's an incredible advance as far as I'm concerned. I think that is has helped immensely," said Kutinsky. "To actually visualize what I'm doing has made a huge difference. To be able to see through blood is pretty remarkable."
Stroker was the first person in Michigan to be treated with the device. She said she's happy she had access to the latest high-tech advance.
"It makes you feel wonderful that they can see what they're doing, rather than taking a stab in the dark," said Stroker.
A week after the procedure --
"I feel great. I've had a couple little flip flops, which apparently are very normal, but I haven't had any a-fib episodes, and I feel good," said Stroker.
Kutinsky said the traditional procedure has a success rate of about 50 percent on the first attempt, which means many patients need to have a second procedure. She said this laser device could improve that initial success rate. Beaumont plans to enroll more patients in the clinical trial in the months to come.
Wednesday, September 22, 2010
RELEVANCE OF ELEVATED TROPONIN
We are frequently consulted in the hospital about a patient with an elevated troponin. Although a valuable biomarker I thought it would be helpful for our referring physicians to discuss its significance.
Measurement of cardiac troponin (cTn) has revolutionized the evaluation and management of patients with suspected acute coronary syndrome (ACS). Recent consensus statements endorse the use of cTnI or cTnT as the biomarker of choice for such application.1 In order to maximize sensitivity for diagnosis of ACS, as well as for superior prognostication, these same consensus statements endorse the use of the lowest cTn cut-off point, down to the “99th percentile” of a normal population as long as the assay used delivers imprecision < 10% at this cut-off point.1 While the most widely-used conventional cTn methods cannot deliver this combination of sensitivity and precision, novel very high sensitivity cTn (hsTn) assays have now been developed; these assays have a greatly improved detection limit (10- to 100-times lower than that of currently available commercial assays) with improved precision.2 hsTn assays are soon to be more widely used.
Despite the value of cTn for ACS diagnosis, risk stratification and management, it has become quite evident that non-ACS elevation of the marker is not uncommon. In a recent study examining 69,299 patients admitted through the emergency department(ED), 48% had their cTn measured. Of these, 2,344 patients (3.3% overall, or 7.0% of those that had a cTn measured) had an elevated cTn concentration. Of those with a positive cTn, 42.7% of the patients did not have ACS.3
Given this fact, and the emerging use of hsTn assays, clinicians should understand that cTn is not solely a biomarker of ischemic myocardial infarction (MI), and such clinicians must be well-versed in the differential diagnosis of an elevated cTn value outside of ACS, in order to avoid unnecessary and potentially harmful misdiagnosis and treatment for presumed ACS, while also avoiding delay in the correct treatment for the underlying cause of the elevated value. Indeed, independent of mechanism, non-ACS cTn elevations are most often prognostically meaningful (Figure 1).
Troponin Elevation: Biological and Analytical Considerations
The cTn complex is found both in the sarcomere (accounting for ~95% of cTn in the heart) as well as to a lesser extent in the cytosol of cardiomyocytes. In the setting of irreversible myocardial cell injury, the contents of the cTn complex are released into circulation. With older conventional assays, cTnI or T is typically measurable as early as 3-4 hours following myocardial injury. However, when using hsTn assays, a rising (or falling) pattern may be seen as early as one hour after myocardial injury.4 Importantly, the phenomenon of cTn release is independent of mechanism—thus, cardiomyocyte necrosis of any kind—ischemic, infectious, toxic, or otherwise—is not infrequently detectable.
In general, the prevalence of cTn elevation in the general population is low when currently available assays are used. A community-based sample of 3557 participants showed that the frequency of elevated cTnT using was 0.7%,5 and typically associated with risk factors for heart disease or heart failure (HF). Importantly, even minimally elevated cTn levels in asymptomatic, apparently healthy older adults have been shown to be associated with adverse outcomes; having elevated cTn increased the risk of all-cause and cardiovascular mortality two-fold.6
Chest Pain, non-ACS Cardiac Diagnoses and Elevated cTn
Cardiac Tn is most commonly measured for the evaluation of chest discomfort and in this context, a rising and/or falling pattern of cTn should be interpreted as being reflective of ACS. However, many non-ACS diagnoses should be kept in mind as potential cause for cTn elevation. Both acutely decompensated and chronic HF are associated with elevated cTn values, which may frequently be substantial. Elevation of cTn in the context of HF often occurs in the absence of coronary ischemia, and frequently occurs even in the absence of coronary artery disease. Various mechanisms for HF-related cTn elevation have been proposed, including subendocardial ischemia from wall tension, apoptosis, spontaneous necrosis, as well as inflammation. Linked to ventricular remodeling, elevated cTn in HF should not be discarded as ‘false positive’ as the prognosis associated with elevated cTn in this setting is poor.7
An important non-ACS diagnosis to consider in a patient presenting with chest pain and elevated cTn is acute aortic dissection (AAD). Cardiac Tn is elevated in up to 18% of patients with AAD,8 indicative of the high acuity of illness than specific to aortic dissection itself, although coronary artery occlusion in this setting is well-described.9 Misdiagnosis of AAD may potentially result in incorrect administration of anticoagulation therapy, or lead to a risky delay in the correct diagnosis.10
Another common non-ACS cause of chest pain and cTn elevation is pulmonary embolism (PE).11 The frequency of elevated cTn is 10-50% in such patients,12-13 and may be related to a combination of acute right ventricular strain and injury, hypoxia and tachycardia. Elevated cTn is strongly associated with mortality in acute PE; in a meta-analysis of 20 acute PE studies, patients with an elevated cTn had more than 5-fold increase in mortality (19.7% vs. 3.7%).14
Other relevant cardiac diagnoses that may present with both chest pain and elevated cTn include post-revascularization myocardial injury states, myocarditis (where cTn elevations are common and prognostically meaningful),15-16 acute pericarditis,17 and blunt force trauma to the heart.18
Acute Illness
In the context of life-threatening illness, the prevalence of elevated cTn is considerable (table 1). In 1130 patients presenting to an emergency department (ED) without chest pain, the frequency of elevated cTn was 3.6% and was associated with an increased mortality.19 This prevalence increases further in population presenting with chest pain to 4.5%,20 while in critically ill patients without ACS, the frequency ranges from 27% to 55%.21
An elevation of cTn in such situations may in fact have an ischemic origin: a recent study demonstrated that an elevated hsTnT in patients without ACS was strongly associated with the presence and severity of coronary artery disease and heart muscle disease, implying that non-ACS cTn elevation may result from coronary ischemia in the absence of plaque rupture or coronary thrombosis; this situation of supply-demand mismatch is known as a Type II MI.22
Common causes of non-ACS cTn elevation in the acutely ill patients include severe hypertension or hypotension,23 severe upper gastrointestinal bleeding,24 as well as systemic inflammatory response syndrome (with or without acute respiratory distress syndrome); in each case, elevated cTn is often associated with myocardial dysfunction and worse prognosis.25 Severe central nervous system injury due to an acute stroke or head trauma may cause elevated cTn values.26 Lastly, cardiotoxic chemotherapy is well recognized to increase cTn, and when this occurs, it can help to identify a patient at risk for cardiomyopathy.27-28
Chronic Diseases
A number of chronic diseases are associated with increased frequency of elevated cTn including infiltrative cardiac diseases (e.g. amyloidosis), systemic hypertension, left ventricular hypertrophy, HF, pulmonary hypertension and chronic kidney disease (CKD).28
Troponin elevation in CKD is worth discussion, as the interpretation of elevation of cTn in non-ACS patients may be difficult. Elevated cTn in asymptomatic CKD is common, the frequency which is dependent on the assay (cTnT > cTnI) and cut-off value used. Due to this fact, the specificity of cTn for ACS in this patient population is lower compared with patients without renal disease. This is of course problematic, as the incidence and prevalence of coronary artery disease and ACS is high in this population.
While cTn elevation in CKD necessarily leads to a higher risk for false positive ACS diagnosis, cTn values in this setting are to be taken seriously; a true positive cTn related to ACS in patients with CKD is associated with a heightened risk for mortality29 compared to non CKD patients, while an asymptomatic elevation in cTn in severe CKD is associated with an increased incidence of ACS30 and a 2- to 5-fold increase in mortality.31 Serial measurement, observing for a rise and/or fall of an elevated cTn value in a patient with CKD is recommended to differentiate ACS from non-ACS causes of cTn elevations.
Other Causes
Cardiac Tn elevations have been reported in patients with snake or scorpion bites, and thought to be in part due to myocardial injury by biologic toxins, vasospasm and coagulation abnormalities.28 Elevated cTn levels have been reported to be frequently elevated in asymptomatic athletes who complete endurance exercise. The exact mechanism by which cTn release occurs in this setting remains unknown but may be due to right ventricular injury.32
Conclusion
Elevated cTn values outside of ACS are not uncommon and reflect cardiomyocyte necrosis from a wide array of cardiac, pulmonary and systemic diseases. The growing use of hsTn assays will no doubt lead to more frequent detection of elevated cTn values, thus the topic is timely. The clinician is advised to be familiar with the broad differential diagnosis of an elevated cTn, to avoid false attribution of “acute MI” to a patient without an ACS. Importantly, an elevated cTn in the absence of ACS is most often associated with a worse prognosis and should not be disregarded as a ‘false positive’ result.
acc cardiosource 9-2010
Measurement of cardiac troponin (cTn) has revolutionized the evaluation and management of patients with suspected acute coronary syndrome (ACS). Recent consensus statements endorse the use of cTnI or cTnT as the biomarker of choice for such application.1 In order to maximize sensitivity for diagnosis of ACS, as well as for superior prognostication, these same consensus statements endorse the use of the lowest cTn cut-off point, down to the “99th percentile” of a normal population as long as the assay used delivers imprecision < 10% at this cut-off point.1 While the most widely-used conventional cTn methods cannot deliver this combination of sensitivity and precision, novel very high sensitivity cTn (hsTn) assays have now been developed; these assays have a greatly improved detection limit (10- to 100-times lower than that of currently available commercial assays) with improved precision.2 hsTn assays are soon to be more widely used.
Despite the value of cTn for ACS diagnosis, risk stratification and management, it has become quite evident that non-ACS elevation of the marker is not uncommon. In a recent study examining 69,299 patients admitted through the emergency department(ED), 48% had their cTn measured. Of these, 2,344 patients (3.3% overall, or 7.0% of those that had a cTn measured) had an elevated cTn concentration. Of those with a positive cTn, 42.7% of the patients did not have ACS.3
Given this fact, and the emerging use of hsTn assays, clinicians should understand that cTn is not solely a biomarker of ischemic myocardial infarction (MI), and such clinicians must be well-versed in the differential diagnosis of an elevated cTn value outside of ACS, in order to avoid unnecessary and potentially harmful misdiagnosis and treatment for presumed ACS, while also avoiding delay in the correct treatment for the underlying cause of the elevated value. Indeed, independent of mechanism, non-ACS cTn elevations are most often prognostically meaningful (Figure 1).
Troponin Elevation: Biological and Analytical Considerations
The cTn complex is found both in the sarcomere (accounting for ~95% of cTn in the heart) as well as to a lesser extent in the cytosol of cardiomyocytes. In the setting of irreversible myocardial cell injury, the contents of the cTn complex are released into circulation. With older conventional assays, cTnI or T is typically measurable as early as 3-4 hours following myocardial injury. However, when using hsTn assays, a rising (or falling) pattern may be seen as early as one hour after myocardial injury.4 Importantly, the phenomenon of cTn release is independent of mechanism—thus, cardiomyocyte necrosis of any kind—ischemic, infectious, toxic, or otherwise—is not infrequently detectable.
In general, the prevalence of cTn elevation in the general population is low when currently available assays are used. A community-based sample of 3557 participants showed that the frequency of elevated cTnT using was 0.7%,5 and typically associated with risk factors for heart disease or heart failure (HF). Importantly, even minimally elevated cTn levels in asymptomatic, apparently healthy older adults have been shown to be associated with adverse outcomes; having elevated cTn increased the risk of all-cause and cardiovascular mortality two-fold.6
Chest Pain, non-ACS Cardiac Diagnoses and Elevated cTn
Cardiac Tn is most commonly measured for the evaluation of chest discomfort and in this context, a rising and/or falling pattern of cTn should be interpreted as being reflective of ACS. However, many non-ACS diagnoses should be kept in mind as potential cause for cTn elevation. Both acutely decompensated and chronic HF are associated with elevated cTn values, which may frequently be substantial. Elevation of cTn in the context of HF often occurs in the absence of coronary ischemia, and frequently occurs even in the absence of coronary artery disease. Various mechanisms for HF-related cTn elevation have been proposed, including subendocardial ischemia from wall tension, apoptosis, spontaneous necrosis, as well as inflammation. Linked to ventricular remodeling, elevated cTn in HF should not be discarded as ‘false positive’ as the prognosis associated with elevated cTn in this setting is poor.7
An important non-ACS diagnosis to consider in a patient presenting with chest pain and elevated cTn is acute aortic dissection (AAD). Cardiac Tn is elevated in up to 18% of patients with AAD,8 indicative of the high acuity of illness than specific to aortic dissection itself, although coronary artery occlusion in this setting is well-described.9 Misdiagnosis of AAD may potentially result in incorrect administration of anticoagulation therapy, or lead to a risky delay in the correct diagnosis.10
Another common non-ACS cause of chest pain and cTn elevation is pulmonary embolism (PE).11 The frequency of elevated cTn is 10-50% in such patients,12-13 and may be related to a combination of acute right ventricular strain and injury, hypoxia and tachycardia. Elevated cTn is strongly associated with mortality in acute PE; in a meta-analysis of 20 acute PE studies, patients with an elevated cTn had more than 5-fold increase in mortality (19.7% vs. 3.7%).14
Other relevant cardiac diagnoses that may present with both chest pain and elevated cTn include post-revascularization myocardial injury states, myocarditis (where cTn elevations are common and prognostically meaningful),15-16 acute pericarditis,17 and blunt force trauma to the heart.18
Acute Illness
In the context of life-threatening illness, the prevalence of elevated cTn is considerable (table 1). In 1130 patients presenting to an emergency department (ED) without chest pain, the frequency of elevated cTn was 3.6% and was associated with an increased mortality.19 This prevalence increases further in population presenting with chest pain to 4.5%,20 while in critically ill patients without ACS, the frequency ranges from 27% to 55%.21
An elevation of cTn in such situations may in fact have an ischemic origin: a recent study demonstrated that an elevated hsTnT in patients without ACS was strongly associated with the presence and severity of coronary artery disease and heart muscle disease, implying that non-ACS cTn elevation may result from coronary ischemia in the absence of plaque rupture or coronary thrombosis; this situation of supply-demand mismatch is known as a Type II MI.22
Common causes of non-ACS cTn elevation in the acutely ill patients include severe hypertension or hypotension,23 severe upper gastrointestinal bleeding,24 as well as systemic inflammatory response syndrome (with or without acute respiratory distress syndrome); in each case, elevated cTn is often associated with myocardial dysfunction and worse prognosis.25 Severe central nervous system injury due to an acute stroke or head trauma may cause elevated cTn values.26 Lastly, cardiotoxic chemotherapy is well recognized to increase cTn, and when this occurs, it can help to identify a patient at risk for cardiomyopathy.27-28
Chronic Diseases
A number of chronic diseases are associated with increased frequency of elevated cTn including infiltrative cardiac diseases (e.g. amyloidosis), systemic hypertension, left ventricular hypertrophy, HF, pulmonary hypertension and chronic kidney disease (CKD).28
Troponin elevation in CKD is worth discussion, as the interpretation of elevation of cTn in non-ACS patients may be difficult. Elevated cTn in asymptomatic CKD is common, the frequency which is dependent on the assay (cTnT > cTnI) and cut-off value used. Due to this fact, the specificity of cTn for ACS in this patient population is lower compared with patients without renal disease. This is of course problematic, as the incidence and prevalence of coronary artery disease and ACS is high in this population.
While cTn elevation in CKD necessarily leads to a higher risk for false positive ACS diagnosis, cTn values in this setting are to be taken seriously; a true positive cTn related to ACS in patients with CKD is associated with a heightened risk for mortality29 compared to non CKD patients, while an asymptomatic elevation in cTn in severe CKD is associated with an increased incidence of ACS30 and a 2- to 5-fold increase in mortality.31 Serial measurement, observing for a rise and/or fall of an elevated cTn value in a patient with CKD is recommended to differentiate ACS from non-ACS causes of cTn elevations.
Other Causes
Cardiac Tn elevations have been reported in patients with snake or scorpion bites, and thought to be in part due to myocardial injury by biologic toxins, vasospasm and coagulation abnormalities.28 Elevated cTn levels have been reported to be frequently elevated in asymptomatic athletes who complete endurance exercise. The exact mechanism by which cTn release occurs in this setting remains unknown but may be due to right ventricular injury.32
Conclusion
Elevated cTn values outside of ACS are not uncommon and reflect cardiomyocyte necrosis from a wide array of cardiac, pulmonary and systemic diseases. The growing use of hsTn assays will no doubt lead to more frequent detection of elevated cTn values, thus the topic is timely. The clinician is advised to be familiar with the broad differential diagnosis of an elevated cTn, to avoid false attribution of “acute MI” to a patient without an ACS. Importantly, an elevated cTn in the absence of ACS is most often associated with a worse prognosis and should not be disregarded as a ‘false positive’ result.
acc cardiosource 9-2010
HEART DISEASE AND TYPE D PERSONALITIES
In the Washington Post (09/14/10) "The Checkup" blog, Rob Stein wrote that research reported in the journal Circulation: Cardiovascular Quality and Outcomes suggests people with type D personalities may be "prone to heart problems." These people tend "to experience a lot of negative emotions, such as pessimism, anxiety, irritation, depressed mood," don't often share their emotions, and fear disapproval.
According to US News & World Report (09/14/10, Haupt), type D personalities "are at three times the risk for future heart problems, including peripheral artery disease, heart failure, and death, compared to more optimistic sorts." Researchers "analyzed 49 previous studies involving more than 6,000 people" to arrive at their conclusions. Barry Jacobs, a clinical psychologist and American Heart Association spokesman, said, "It really adds weight to the argument that this core, hostile personality is a concern -- or ought to be a concern -- for people who have it."
According to MedPage Today (09/14/10, Walsh), the researchers wrote that "there are plausible biological and behavioral pathways linking type D to cardiac risk," as "this personality type is associated with elevations in blood pressure, heart rate, and cardiac output, as well as with increases in the activity of proinflammatory cytokines," increased cortisol, and increased oxidative stress. "In addition, patients with the distressed personality type D, also are less likely to seek timely medical care or to adhere to medication, according to the researchers."
Steven Almany, MD
According to US News & World Report (09/14/10, Haupt), type D personalities "are at three times the risk for future heart problems, including peripheral artery disease, heart failure, and death, compared to more optimistic sorts." Researchers "analyzed 49 previous studies involving more than 6,000 people" to arrive at their conclusions. Barry Jacobs, a clinical psychologist and American Heart Association spokesman, said, "It really adds weight to the argument that this core, hostile personality is a concern -- or ought to be a concern -- for people who have it."
According to MedPage Today (09/14/10, Walsh), the researchers wrote that "there are plausible biological and behavioral pathways linking type D to cardiac risk," as "this personality type is associated with elevations in blood pressure, heart rate, and cardiac output, as well as with increases in the activity of proinflammatory cytokines," increased cortisol, and increased oxidative stress. "In addition, patients with the distressed personality type D, also are less likely to seek timely medical care or to adhere to medication, according to the researchers."
Steven Almany, MD
Tuesday, September 21, 2010
INTRESTING ARTICLE- posted by Joel Kahn, MD
A study, published in the October/November, 2009 issue of the Journal of Clinical Endocrinology and Metabolism, has found that reducing the amounts of processed and fried foods in the diet can promote weight loss, reduce inflammation and restore the body's natural defenses against disease for both young and old, regardless of the status of their health. Cutting back on the processed and fried foods can reduce your family's risk of kidney disease, heart disease, hypertension, diabetes and obesity, and may even increase longevity.
Processed and fried foods are high in glycotoxins called Advanced Glycation End products (AGEs). AGEs proliferate when food is heated, pasteurized, fried, smoked or grilled. Once they are inside the body, they bind themselves to tissues and oxidize them. This oxidation process causes inflammation, which in turn can cause disease. These toxins, or oxidants, may be more responsible than genetics for causing certain diseases and conditions.
Findings show that people can benefit from a diet low in AGEs without reducing calories or nutrient intake. That means it is possible to lose weight and improve your health without reducing calories. Of course, if you are overeating, reducing the amount you put in your mouth is a good idea, but this study could give your weight loss efforts an added boost.
Eliminating processed foods from your family's diet may seem impossible. They have become the mainstay of the Western diet. Manufacturers make it even easier to consume these foods at a "savings" with coupons and special offers. The truth is that the processed foods you eat are not saving you any money in the long run. They may actually be costing you money in the form of future medical bills, time lost at work due to illness, and even unemployment or disability due to serious illness. Eating an AGEless diet may mean a little more work in the kitchen, but the long term health benefits far outweigh any inconvenience.
Read more: How to Restore Your Body's Defenses: The AGEless Diet | eHow.com http://www.ehow.com/how_5609065_restore-bodys-defenses-ageless-diet.html#ixzz0ywGbgwpL
Processed and fried foods are high in glycotoxins called Advanced Glycation End products (AGEs). AGEs proliferate when food is heated, pasteurized, fried, smoked or grilled. Once they are inside the body, they bind themselves to tissues and oxidize them. This oxidation process causes inflammation, which in turn can cause disease. These toxins, or oxidants, may be more responsible than genetics for causing certain diseases and conditions.
Findings show that people can benefit from a diet low in AGEs without reducing calories or nutrient intake. That means it is possible to lose weight and improve your health without reducing calories. Of course, if you are overeating, reducing the amount you put in your mouth is a good idea, but this study could give your weight loss efforts an added boost.
Eliminating processed foods from your family's diet may seem impossible. They have become the mainstay of the Western diet. Manufacturers make it even easier to consume these foods at a "savings" with coupons and special offers. The truth is that the processed foods you eat are not saving you any money in the long run. They may actually be costing you money in the form of future medical bills, time lost at work due to illness, and even unemployment or disability due to serious illness. Eating an AGEless diet may mean a little more work in the kitchen, but the long term health benefits far outweigh any inconvenience.
Read more: How to Restore Your Body's Defenses: The AGEless Diet | eHow.com http://www.ehow.com/how_5609065_restore-bodys-defenses-ageless-diet.html#ixzz0ywGbgwpL
Wednesday, September 8, 2010
CURBSIDE- September 2010
STUDY ONE:
Title: Waist Circumference and All-Cause Mortality in a Large US Cohort
Date Posted: August 9, 2010
Authors: Jacobs EJ, Newton CC, Wang Y, et al.
Citation: Arch Intern Med 2010;170:1293-1301.
Study Question:
Is waist circumference associated with risk of death within body mass index (BMI) categories?
Methods:
Data from the Cancer Prevention Study II (CPS-II) Nutrition Cohort (established in 1992) were used for the current study. The CPS-II Nutrition Cohort is a subset of the CPS-II cohort established by the American Cancer Society in 1982. Subjects enrolled between 1992 and 1993 and were mailed questionnaires in 1997, in which they were asked to measure their waist circumference. Validity of self-report was not completed. Body mass index (BMI) was calculated from reported weight on the 1997 survey, and height was reported in the 1982 survey. Subjects who had lost ≥10 lbs or gained more than 25 lbs between 1992 and 1997 were excluded. Subjects with missing data on waist circumference or BMI were also excluded. Mortality was assessed through the National Death Index through December 31, 2006.
Results:
A total of 48,500 men and 56,343 women, 50 years or older, were included in this analysis. Median age at baseline was 69 years for men and 67 years for women. The cohort was predominately white. Subjects in the highest category of waist circumference were more likely to be less educated, have a high BMI, be sedentary, and were former smokers compared to subjects with lower waist circumference. This group was also more likely to have a history of cardiovascular disease, cancer, or respiratory disease. Between 1997 and 2006, 9,315 men and 5,332 women had died. After adjustment for BMI and other risk factors, increased waist circumference (≥120 cm compared to <90 cm) was associated with a twofold higher risk of mortality among men (relative risk [RR], 2.20; 95% confidence interval [CI], 1.71-2.39). For women, a waist circumference ≥110 cm compared to <75 cm was also associated with increased risk of death (RR, 2.36; 95% CI, 1.98-2.82). Waist circumference was positively associated with mortality in all categories of BMI. In men, a 10 cm increase in waist circumference was associated with RRs of 1.16 (95% CI, 1.09-1.23) for normal (18.5 to <25) BMI, 1.18 (95% CI, 1.12-1.24) for overweight (25 to <30) BMI, and 1.21 (95% CI, 1.13-1.30) for obese (≥30) BMI. In women, corresponding RRs were 1.25 (95% CI, 1.18-1.32), 1.15 (95% CI, 1.08-1.22), and 1.13 (95% CI, 1.06-1.20).
Conclusions:
The investigators concluded that waist circumference is important as a risk factor for mortality among older adults, regardless of BMI.
Perspective:
These data highlight the clinical significance of waist circumference. Clinicians may want to consider making waist circumference part of the vital signs for each patient, and to make clear to patients the potential benefits of preventing abdominal obesity.
STUDY TWO:
Title: Effect of Low Doses of N-3 Fatty Acids on Cardiovascular Diseases in Post-MI Patients
Trial Sponsor: Netherlands Heart Foundation, The Hague, The Netherlands, National Institutes of Health, Unilever
Year Presented: 2010
Summary Posted: 09/08/2010
Reviewer Disclosure: RESEARCH/RESEARCH GRANTS: Astra Zeneca, Heartscape, Eisai, Sanofi Aventis, The Medicines Company, Ethicon, Bristol Myers Squibb Cogentus, PLx Pharma, Takeda
Description:
The goal of the trial was to evaluate treatment with supplemental omega-3 fatty acids (N-3) among patients with prior myocardial infarction (MI). Fatty acids in fish are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), whereas fatty acids in plants are alpha-linolenic acid (ALA).
Hypothesis:
Omega-3 fatty acids will be more effective at reducing major adverse cardiovascular events.
Drugs/Procedures Used:
Patients who had suffered an MI within the last 4 years were randomized to one of four margarines for dietary consumption: 1) EPA-DHA 400 mg daily + ALA placebo (n = 1,192), 2) EPA-DHA placebo + ALA 2 g daily (n = 1,197), 3) EPA-DHA 400 mg daily + ALA 2 g daily (n = 1,212), or 4) EPA-DHA placebo + ALA placebo (n = 1,236).
Concomitant Medications:
At baseline in the EPA-DHA + ALA group, the use of lipid-lowering drugs was 87%.
Principal Findings:
Overall 4,837 patients were randomized. In the EPA-DHA + ALA group, the mean age was 69 years, 22% were women, 20% were diabetic, systolic blood pressure was 141 mm Hg, and body mass index was 28 kg/m2. Compliance with study medication was verified by measurement of serum fatty acids.
The primary outcome, major adverse cardiovascular events (MACE), was similar between the EPA-DHA group and placebo group (hazard ratio [HR] 1.01, p = 0.93) and between the ALA group and placebo group (HR 0.91, p = 0.20). Among women in the ALA group, there was a nonsignificant reduction in the primary outcome (HR 0.73, p = 0.07) and among diabetics in the ALA group, there was a significant reduction in ventricular arrhythmia-related adverse events (HR 0.39, p = 0.002).
Interpretation:
Among patients with prior MI, dietary supplementation of omega-3 fatty acids was not beneficial since this therapy did not reduce MACE. Subgroup analysis revealed a nonsignificant reduction in MACE among women treated with ALA, and a significant reduction in ventricular arrhythmia-related adverse events among diabetics treated with ALA. Both of these subgroups should be interpreted with caution until further analysis can be performed. We continue to use FISH Oil capsules in patients that have very high triglycerides >500). The patients need follow up lipid evaluations as the LDL CAN UP AS MUCH AS 20% in patients taking fish oil. Most side effects are tolerable. Patients who get GERD with fish oil capsules might benefit from freezing the capsules.
Steven Almany, MD
Title: Waist Circumference and All-Cause Mortality in a Large US Cohort
Date Posted: August 9, 2010
Authors: Jacobs EJ, Newton CC, Wang Y, et al.
Citation: Arch Intern Med 2010;170:1293-1301.
Study Question:
Is waist circumference associated with risk of death within body mass index (BMI) categories?
Methods:
Data from the Cancer Prevention Study II (CPS-II) Nutrition Cohort (established in 1992) were used for the current study. The CPS-II Nutrition Cohort is a subset of the CPS-II cohort established by the American Cancer Society in 1982. Subjects enrolled between 1992 and 1993 and were mailed questionnaires in 1997, in which they were asked to measure their waist circumference. Validity of self-report was not completed. Body mass index (BMI) was calculated from reported weight on the 1997 survey, and height was reported in the 1982 survey. Subjects who had lost ≥10 lbs or gained more than 25 lbs between 1992 and 1997 were excluded. Subjects with missing data on waist circumference or BMI were also excluded. Mortality was assessed through the National Death Index through December 31, 2006.
Results:
A total of 48,500 men and 56,343 women, 50 years or older, were included in this analysis. Median age at baseline was 69 years for men and 67 years for women. The cohort was predominately white. Subjects in the highest category of waist circumference were more likely to be less educated, have a high BMI, be sedentary, and were former smokers compared to subjects with lower waist circumference. This group was also more likely to have a history of cardiovascular disease, cancer, or respiratory disease. Between 1997 and 2006, 9,315 men and 5,332 women had died. After adjustment for BMI and other risk factors, increased waist circumference (≥120 cm compared to <90 cm) was associated with a twofold higher risk of mortality among men (relative risk [RR], 2.20; 95% confidence interval [CI], 1.71-2.39). For women, a waist circumference ≥110 cm compared to <75 cm was also associated with increased risk of death (RR, 2.36; 95% CI, 1.98-2.82). Waist circumference was positively associated with mortality in all categories of BMI. In men, a 10 cm increase in waist circumference was associated with RRs of 1.16 (95% CI, 1.09-1.23) for normal (18.5 to <25) BMI, 1.18 (95% CI, 1.12-1.24) for overweight (25 to <30) BMI, and 1.21 (95% CI, 1.13-1.30) for obese (≥30) BMI. In women, corresponding RRs were 1.25 (95% CI, 1.18-1.32), 1.15 (95% CI, 1.08-1.22), and 1.13 (95% CI, 1.06-1.20).
Conclusions:
The investigators concluded that waist circumference is important as a risk factor for mortality among older adults, regardless of BMI.
Perspective:
These data highlight the clinical significance of waist circumference. Clinicians may want to consider making waist circumference part of the vital signs for each patient, and to make clear to patients the potential benefits of preventing abdominal obesity.
STUDY TWO:
Title: Effect of Low Doses of N-3 Fatty Acids on Cardiovascular Diseases in Post-MI Patients
Trial Sponsor: Netherlands Heart Foundation, The Hague, The Netherlands, National Institutes of Health, Unilever
Year Presented: 2010
Summary Posted: 09/08/2010
Reviewer Disclosure: RESEARCH/RESEARCH GRANTS: Astra Zeneca, Heartscape, Eisai, Sanofi Aventis, The Medicines Company, Ethicon, Bristol Myers Squibb Cogentus, PLx Pharma, Takeda
Description:
The goal of the trial was to evaluate treatment with supplemental omega-3 fatty acids (N-3) among patients with prior myocardial infarction (MI). Fatty acids in fish are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), whereas fatty acids in plants are alpha-linolenic acid (ALA).
Hypothesis:
Omega-3 fatty acids will be more effective at reducing major adverse cardiovascular events.
Drugs/Procedures Used:
Patients who had suffered an MI within the last 4 years were randomized to one of four margarines for dietary consumption: 1) EPA-DHA 400 mg daily + ALA placebo (n = 1,192), 2) EPA-DHA placebo + ALA 2 g daily (n = 1,197), 3) EPA-DHA 400 mg daily + ALA 2 g daily (n = 1,212), or 4) EPA-DHA placebo + ALA placebo (n = 1,236).
Concomitant Medications:
At baseline in the EPA-DHA + ALA group, the use of lipid-lowering drugs was 87%.
Principal Findings:
Overall 4,837 patients were randomized. In the EPA-DHA + ALA group, the mean age was 69 years, 22% were women, 20% were diabetic, systolic blood pressure was 141 mm Hg, and body mass index was 28 kg/m2. Compliance with study medication was verified by measurement of serum fatty acids.
The primary outcome, major adverse cardiovascular events (MACE), was similar between the EPA-DHA group and placebo group (hazard ratio [HR] 1.01, p = 0.93) and between the ALA group and placebo group (HR 0.91, p = 0.20). Among women in the ALA group, there was a nonsignificant reduction in the primary outcome (HR 0.73, p = 0.07) and among diabetics in the ALA group, there was a significant reduction in ventricular arrhythmia-related adverse events (HR 0.39, p = 0.002).
Interpretation:
Among patients with prior MI, dietary supplementation of omega-3 fatty acids was not beneficial since this therapy did not reduce MACE. Subgroup analysis revealed a nonsignificant reduction in MACE among women treated with ALA, and a significant reduction in ventricular arrhythmia-related adverse events among diabetics treated with ALA. Both of these subgroups should be interpreted with caution until further analysis can be performed. We continue to use FISH Oil capsules in patients that have very high triglycerides >500). The patients need follow up lipid evaluations as the LDL CAN UP AS MUCH AS 20% in patients taking fish oil. Most side effects are tolerable. Patients who get GERD with fish oil capsules might benefit from freezing the capsules.
Steven Almany, MD
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