Wake Up CALL

Wake-up call for sleep related CVD risk

 

Geneva, Switzerland - Those who sleep badly, and not for long, have a 65% increased risk of cardiovascular disease—and an even greater risk of coronary heart disease—compared with normal sleepers, according to new research presented at the EuroPRevent 2011 meeting this past weekend.

 

Researcher Marieke Hoevenaar-Blom (National Institute for Public Health and the Environment, Bilthoven, the Netherlands) explained that several investigations have found an increased risk of CVD in short sleepers compared with normal sleepers, but this is the first study to take into account whether people rise feeling rested. The results should help confirm that suboptimal sleep is a risk factor for cardiovascular disease, something she says is not widely appreciated in the cardiology community.

 

Hoevenaar-Blom, who is studying for a PhD in primary prevention of cardiovascular disease by lifestyle, reported her findings from 12 years of follow-up in a Dutch cohort during an oral session; she was nominated for a young investigator award for her research, which has also been accepted by the journal Sleep for publication [1].

 

"The message is that you have to assess sleep, and especially sleep quality, when you see a patient, because it might be a risk factor for cardiovascular diseases," Said Hoevenaar-Blom "When a patient is sleeping poorly, you can very easily fix that," she noted, although she acknowledged that this involves figuring out what is causing the sleep disturbance. However, simple advice—such as restricting intake of caffeinated drinks after a certain time and not watching TV late—can often be useful, she suggested.

 

Is sleep quality a modifying factor in association with CVD?

 

In the Monitoring Project on Risks Factors and Chronic Diseases in the Netherlands (MORGEN) study, Hoevenaar-Blom and her colleagues explored the combined associations of sleep duration and quality with CVD and CHD incidence.

The message is that you have to assess sleep, and especially sleep quality, when you see a patient, because it might be a risk factor for cardiovascular diseases.

Information on sleep duration and quality was obtained by a self-administered questionnaire filled in by 20 432 participants (9217 men and 11 215 women aged 20 to 65 years) between 1993 and 1997. Over 10 to 15 years of follow-up, data on morbidity and causes of death were obtained through linkage with several national registries.

 

Average sleep duration was assessed by asking participants how many hours of sleep they usually got in a 24-hour period. Short sleep duration was defined as six hours or less, while long sleep duration was sleeping for nine hours or more per 24-hour period. Sleeping for seven to eight hours was designated "normal." Sleep quality was assessed in the first two years of baseline measurements with the question, "Do you usually rise feeling rested?"

"Our research questions were: 'What is the association between sleep duration and cardiovascular disease and coronary heart disease? And is sleep quality a modifying factor in this association?' " Hoevenaar-Blom explained.

 

After 10 to 15 years of follow-up (mean 11.9 years), 1486 participants developed CVD, of whom 177 had a fatal event. After adjustment for multivariate confounders, short sleepers had a 15% higher risk of incident CVD compared with participants with normal sleep duration, a finding that was significant, and short sleepers had an even stronger, 23% higher risk of CHD compared with normal sleepers.

 

It's not just quantity, but quality, that is important

 

On its own, no association was found between sleep quality and CVD incidence, but when assessing quality in combination with sleep duration, short sleepers with poor-quality sleep had a 65% higher risk of CVD and an 85% higher risk of CHD than participants with a normal sleep duration and good sleep quality.

 

The investigators found no association between long sleep duration and CVD, a finding that contradicts previous studies, said Hoevenaar-Blom. She noted that there has never been any biological mechanism to explain why people who sleep longer have increased risk, but she hypothesized it could be due to reverse causality—that these people were perhaps ill in the first place and therefore slept longer.

 

Asked whether psychosocial stress could be contributing to poor sleep quality and short duration of sleep, she acknowledged that, of course, this was likely. "We do need more research," she observed.

 

"In conclusion, short sleepers have an increased risk of total CVD and CHD; the risk in short sleepers is the largest when they are not rising rested; it's really the combination" that is important, she said.

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So is niacin a dead drug? Dayspring

Commentary on Niacin’s Effect on Lp(a) in AIM HIGH

Here are my thoughts as a clinical lipidologist (By: Thomas Dayspring, MD, FACP, FNLA, NCMP)

We must get apoB (LDL-P) to goal in all at-risk patients. Lifestyle therapies and statins are the mainstay of therapy. However residual risk is high if apoB (LDL) remains elevated despite at-goal LDL-C, non-HDL-C), any level of HDL-C or if Lp(a) mass is elevated.

So I would have no hesitancy in adding niacin to high and very high risk patients who have not achieved apoB (LDL-P) goals with whatever therapies they are using or using niacin as a monotherapy in those intolerant of other apoB lowering meds.

Data from HPS THRIVE 2 (discussed in a recent commentary) suggested statin plus ezetimibe was better at event reduction than statin plus niacin [9]. In view of that and the very significant side effects reported in HPS THRIVE 2 [bleeding (GI, intracranial, other) in the niacin group: 326 (2.5%) to 238 (1.9%) and infection 1031(8%) to 853 (6.6%)] [3] makes niacin a tertiary or quaternary add-on drug (some may prefer the bile acid sequestrant colesevelam as an apoB lowering medication).
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The angioplasty and stent of President George W. Bush - Dayspring

Commentary regarding the angioplasty and stent of President George W. Bush           

By: Thomas Dayspring, MD, FACP, FNLA, NCMP

  

Commentary from Thomas Dayspring MD, FACP, FNLA regarding the angioplasty and stent of President George W. Bush 

George W. Bush underwent stent placement because during a routine physical a stress test (which is rarely indicated in an asymptomatic person) revealed an abnormality that led to a CT-angiogram test (which is rarely indicated in an asymptomatic person) that led to a coronary angiogram test (which is rarely indicated in an asymptomatic person) that as usual led to a stent (which is rarely indicated in an asymptomatic person). Why was an angiogram done on an asymptomatic person? Did the test show early marked ST depression that suggested a main stem lesion? There is a bit of a history here – all public knowledge. During his second year in office during a yearly physical at Bethesda his physician did a routine coronary calcium level which was 4 (trivial). Even though his LDL-C was fine (~100 mg/dL superb by 2001 standards) they started him on a statin and as one would suspect, a low fat diet. It is well known what a super exercise routine Mr. Bush pursues (then and now): secret service men cannot keep up with him on jogs or bike rides. Now we find out that he suddenly needed a stent. Well do not clogged pipes; I mean arteries – need plumbers to fix them? And is it not dietary fat and cholesterol that clogs the arteries? For more opinions on the inappropriateness of the workup please see  http://www.theheart.org/article/1567069.do

 

Earlier in the year I posted a commentary on LecturePad.org regarding “Clogged Arteries.” (click here to review) That posting was provoked by a perspective authored by Michael Rothberg of the Cleveland Clinic which was published in Circulation Cardiovascular Quality Outcomes. (Circ Cardiovasc Qual Outcomes. 2013;6:129-132) entitled Coronary Artery Disease as Clogged Pipes A Misconceptual Model. It is a brilliant piece and needs to be read by all providers including Mr. Bush’s physicians. Here are some of the many highlights verbatim from that perspective ....

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Read the complete article here.

I also recommend The Doc's Opinion on President Bush here.

Listen to podcast by Dr. William Blanchet here.

Association Between Omega-3 Fatty Acid Supplementation & Risk of Major Cardiovasular Disease - Harris

Comment On JAMA publication by Rizo et.al: Association Between Omega-3 Fatty Acid Supplementation & Risk of Major Cardiovasular Disease

               

Written by William Harris PhD

 

 

Response on the JAMA publication: Association Between Omega-3 Fatty Acid Supplementation and Risk of Cardiovascular Disease Events: On September 12, 2012 Rizos et al. published a meta-analysis titled: “Association Between Omega-3 Fatty Acid Supplementation and Risk of Major Cardiovascular Disease Events” on fish oil and concluded no benefit. Spokespeople from the AHA have been on TV saying that omega-3 supplements clearly don’t ‘work’. here are some of my thoughts…

Positve view of the study

They included all relevant studies; they did not exclude (like the previous meta-analysis (Kwak) did) the non-placebo controlled trials (GISSI-Prevenzione and JELIS)

First negative view about the study

They showed in Figure 3 that there was a significant benefit of omega-3 on cardiac death, and trends towards benefit in total mortality, sudden death and MI (plus trends towards increased stroke). But in the text, they said that there was NO significant effect on cardiac death – this is because they set the p-value for significance at 0.006, a much higher hurdle (than the usual 0.05) for concluding benefit. In my view, this is completely inappropriate and excessively conservative, especially for a very safe intervention. In other words, if you are testing a new drug that has potential benefits AND side/adverse effects, then you want to be very conservative in concluding “benefit” (i.e., you want to require a very small p-value) since – if you’re wrong and the drug really isn’t helpful (false positive) - your ‘endorsement’ of the drug will lead to increased use and thus the potential for increased adverse effects. However, for very low risk interventions (n-3 fatty acids), you don’t worry about adverse effects… you want people to use the treatment even if there is only a trend towards benefit. A favorable benefit-risk ratio. (I’d even suggest that in this setting, a p-value for ‘significant effect’ should be 0.1 instead of the traditional 0.05). In addition, nobody I know of ever adjusts for multiple testing (sets a lower p-value than 0.05 as the target for significance) in a meta-analysis. Therefore, I believe that the authors were far too conservative in this analysis, which led to their “no benefit” conclusion.

Second negative view about the sudy

They should have been much more nuanced in their conclusions. They said, “Our findings do not justify the use of omega-3 in structured [?] intervention in everyday clinical practice or guidelines supporting dietary omega-3 PUFA administration.” They should have said, “In patients of average age 63, with existing cardiovascular disease and under optimal medical care (which, by the way, is very UNcommon), the administration of about 1 g of EPA+DHA for 4 years will not affect major clinical outcomes.” Their study does NOT show that treating with a higher dose for a longer period of time, or treating patients earlier in the disease process or those who are not receiving “optimal medical therapy” will NOT be beneficial.

There may (or may not!) be a slight silver lining to all of this: Here is what Tom Barringer and I ended a chapter on n3 and CVD with in an upcoming book on “Omega-3 Deficiency”:
It should be stressed that future research will be significantly hampered if clinicians and patients are dogmatic in their belief that the value of n-3 fatty acids in CVD is already well-established. If such unfounded certainty is widespread, it will become very difficult to find patients (and investigators and IRBs) willing to participate in or approve the placebo-controlled clinical trials that are so desperately needed to properly evaluate the value of these nutrients in the treatment and prevention of CVD.”
Clearly with Rizos’ paper, we now won’t have any problem convincing the world that the question of omega-3s and CHD risk is still open.

In summary, they were too conservative in their analysis and they were not thoughtful in drawing their conclusions. It’s quite likely true that 1 g of EPA+DHA won’t affect outcomes over a few years in older people started later in life who are well-treated pharmacologically – but that’s a far cry from USA Today’s Headline “Fish oil pills with omega-3 don’t help against disease”
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William Harris PhD
Senior Scientist
William Harris holds a PhD in Nutritional Biochemistry from the University of Minnesota, and did 4 years of post-doctoral research at the Oregon Health Sciences University. He was Director of the Lipid Research Laboratories at the University of Kansas Medical Center (KUMC) and at the Mid America Heart Institute, both in Kansas City, MO, for 22 years, and was on the faculty at KUMC and at the University of Missouri-Kansas City School of Medicine. Between 2006 and 2011 was the Director of the Cardiovascular Health Research Center at Sanford Research/USD (Sioux Falls, SD).
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