Tag Archives: cardiovascular disease

Who needs aspirin?

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Despite a lot of good press for aspirin with regards to prevention of cardiovascular events and cancer prevention, determining who should take aspirin is quite tricky.  This blog entry will discuss the vascular rationale and a subsequent post will tackle the potential of aspirin for colorectal cancer prevention.

At this time, the cardiovascular disease (CVD) rationale includes preventing myocardial infarction [MI] and stroke.  These are the main determinants of risk/benefit for taking aspirin.  In 2009, guidelines from US Preventive Services Task Force (USPSTF) for taking aspirin were published (Ann Intern Med 2009; 150: 396-404).  The following link can be used to access this article:

http://www.uspreventiveservicestaskforce.org/uspstf09/aspirincvd/aspcvdrs.pdf

The recommendations include the following:

Men <45:  Not encourage aspirin for MI prevention

Women <55: Not encourage aspirin for stroke prevention

Men 45-79:  Encourage aspirin when CVD benefit.  Benefit likely if:

  • 45-59 years, 10 -year CVD risk ≥4%
  • 60-69 years, 10-year CVD risk ≥9%
  • 70-79 years, 10-year CVD risk ≥12%
To calculate 10-year CVD risk: http://www.mcw.edu/calculators.htm
Risk factors: age, high blood pressure, diabetes, smoking, history of CVD, total cholesterol level, and HDL cholesterol level

Women 55-79:  Encourage aspirin when stroke benefit.  Benefit likely if:

  • 55-59 years, 10 -year stroke risk ≥3%
  • 60-69 years, 10 -year stroke risk ≥8%
  • 70-59 years, 10 -year stroke risk ≥11%

To calculate 10 -year stroke risk: http://my.clevelandclinic.org/p2/stroke-risk-calculator.aspx

Risk factors: age, high blood pressure, diabetes, smoking, history of CVD, atrial fibrillation, and left ventricular hypertrophy

In addition, it is noted that aspirin is NOT recommended when other NSAIDs are being administered or if history of GI ulcers/risk of serious GI bleeding.

While these recommendations are a useful starting point and the risk calculators are fascinating, the absolute benefit of aspirin remains unclear.  A recent article on this subject indicates that aspirin may not improve mortality (Arch Intern Med. 2012;172(3):209-216. doi:10.1001/archinternmed.2011.628).  This article reviewed nine large randomized placebo-controlled studies, each with at least 1000 participants.  In total, more than 100,000 patients were described in these studies.  While CVD events were reduced by 10%, there was no reduction in mortality for cardiovascular disease (OR 0.99) or for cancer (OR 0.93) among aspirin takers over a mean of 6 years.  Most of the reduction in CVD events were due to a lower rate of non-fatal MI (OR 0.80).  In addition, there was an increase in significant GI bleeding among patients taking aspirin (OR 1.31)

Due to these results, the authors conclude that routine use as primary prevention is not warranted; “treatment decisions need to be considered on a case-by-case basis.”

Additional reference:

  • –Arch Intern Med 2012;172:217-218.  Aspirin Therapy in Primary Prevention: Comment on “Effect of Aspirin on Vascular and Nonvascular Outcomes”

Lower leptin with physical activity

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Leptin is a cytokine expressed primarily by adipose tissue and helps regulate energy homeostasis in the body.  Higher leptin levels are found in obesity and associated with an increase risk of cardiovascular disease, insulin resistance, and type 2 diabetes.  In a recent study, physical activity, especially vigorous physical activity, has been shown to be negatively associated with leptin levels (J Pediatr 2012; 160: 598-603).

This study was conducted in school settings in 10 European cities from 9 countries (n=902) with ages 12-18 years.  Several fitness tests including handgrip, long jump, and shuttle runs were measured along with serum fasting leptin, insulin, and glucose.

Vigorous activity and fitness test results were associated with lower leptin levels; these findings were maintained when controlling for confounders.  It is not known the exact mechanisms whereby physical activity can lower leptin levels as this finding is independent of total body fat.  The authors note that previous studies have shown some contradictory results; the authors note that this could be related to drawbacks in how some studies measured physical activity.

This study’s information, when combined with previous studies (see below) on hormonal adaptations with weight loss, suggest a reason why exercise is important to maintain weight loss.  Losing weight without exercise could result in increased appetite and make it more difficult to achieve long-term results.  In contrast, physical activity may help maintain weight loss by improving hormonal adaptation.

Additional references:

  • -NEJM 2011; 365: 1597.  Persistence of hormonal adaptations with weight loss.  Due to persistent changes in hormones like leptin & peptide YY, hard to keep wt off -result is increased appetite.
  • -NEJM 2009; 360: 859.  Obesity-wt loss: composition of diet does not seem to be important.  Total calories important.
  • -NEJM 2007; 356: 237.  Leptin receptor deficiency present in 3% of 300 patients with early-onset obesity and hyperphagia.
  • -Pediatrics 2007; 120: suppl 4: S164-S287.
  • -NEJM 2007; 357: 370.  Obestiy spread in social network.
  • -Gastroenterology 2007; 132: 2085-2276.  Special issue on obesity issues.
  • -NEJM 2006; 355: 1593.  Case review on obesity c DDx and mgt.

Cardiovascular disease for the entire family

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This month’s Journal of Pediatrics features an article for the entire family (J Pediatr 2012; 160: 590-7 [editorial pg 539]).  The authors demonstrate that children screened for cholesterol can serve as an index case for the entire family.  During a 26-year prospective followup of 852 pediatric patients (5-19 years old at enrollment) from Cincinnati, the authors assessed relationships of childhood risk factors with parental cardiovascular disease (CVD), type 2 diabetes (T2DM), and high blood pressure (HBP).

  • Pediatric HBP and low HDL cholesterol were predictive of parental CVD ≤age 50
  • Pediatric HBP and high triglycerides were predictive of parental CVD ≤age 60
  • Pediatric high triglycerides and high LDL cholesterol were predictive of parental CVD ≤age 66

The related editorial reviews large studies regarding lipid assessments, including the Bogalusa study with more than 3000 children and the Muscatine study with more than 14,000 children.  In addition, the editorial reviews the recommendations from an expert pediatric panel which suggested screening all children for dyslipidemia between 9 and 11 years. Interestingly, the editorial reviews the fact that screening for cholesterol has not been shown to harm children.  “The evidence is not sufficient to demonstrate any adverse affects.”

Although no harm has been proven, the expert recommendations do not have prospective data demonstrating benefit either.  While it is known that atherosclerotic lesions, including fatty streaks and calcifications, can develop in childhood, it is not known that current treatment strategies will improve long-term outcomes.  This study, however, provides an additional rationale for screening; namely, by identifying children with dyslipidemia, primary care providers can identify parents with cardiovascular disease who are more likely to benefit from urgent intervention.

Additional references:

  • http://hin.nhlbi.nih.gov/atpiii/calculator.asp?usertype=prof (cholesterol risk calculator)
  • Pediatrics 2011; 128 (suppl 5): S213-56.  Expert panel guidelines for cardiovascular health and risk reduction in children and adolescents.
  • -NEJM 2011; 365: 2078.  Use of statins to lower LDL to 60-70 range halted progression of coronary artery disease.
  • -Pediatrics 2007; 120: e189, e215.  US Preventive Services Task Force:  “the evidence is insufficient to recommend for or against routine screening for lipid disorders” up to age 20.  Consider pediatric drug Rx:
    1. After dietary failure
    2. LDL >190
    3. LDL >160 & FHx of CVD before age 55
    4. triglycerides >250-500 persistently
  • Pediatric Nutrition Handbook AAP Lipid types:type I -increased trig  (rare)
    type IIa -increased chol & LDL
    (most common)
       Homozygous: chol >500
         xanthomas before 10 yrs, vascular dz before age 20
       Heterozygotes with lower chol
    type IIb -elevated trig & chol/LDL
    (3rd most common)
    type III -abnormal LDL density (rare)
    type IV -elevated trig (2nd most common)
         may be increased with diabetes, obesity, inadequate fasting; may need to study parents to establish dx
    type V -increased trig/VLDL (rare)
         exclude nephrotic synd, hypothyroid, diabetes