eLetters

16 e-Letters

  • The effect of linoleic acid on coronary heart disease may be increased coagulation rather than oxidation

    We agree with DiNicolantonio´s and O´Keefe´s hypothesis that a high intake of omega-6 vegetable oils may promote coronary heart disease (CHD).1 However, we think that the mechanism is not oxidation of LDL-cholesterol (LDL-C). It is a solidly documented but little-known fact that LDL partake in the immune system by adhering to and inactivating almost all types of microorganisms.2 As the LDL-covered microorganisms are oxidized after having been taken up by macrophages, we think that the oxidation of LDL is a secondary phenomenon. The crucial event is most likely, as explained in our papers,2,3 that complexes of LDL-covered microorganisms may aggregate, in particular in the presence of
    hyperhomocysteinemia, because homocysteine thiolactone causes aggregation and precipitation of thiolated LDL. Because of the high extra-capillary tissue pressure, aggregates of such complexes may be trapped in vasa vasorum of the major arteries and result in ischemia of the arterial wall. The reason why omega-6 oils promote CHD may be that these oils may result in increased coagulation,4 which is a well-known risk factor for CHD, even among individuals with familial hypercholesterolemia.5

    References
    1. DiNicolantonio JJ, O’Keefe JH. Omega-6 vegetable oils as a driver of coronary heart
    disease: the oxidized linoleic acid hypothesis. Open Heart 2018;5:e000898. doi:10.1136/openhrt-2018-000898
    2. Ravnskov U, McCully KS. Vulnerable plaque formation from obstruction of...

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  • Response to CardioBrief blog post

    Clinical practice has been historically driven by evidence-based medicine. Properly sized randomized controlled trials have been the basis of accepting or rejecting research hypotheses, and clinical guidelines are developed based on data reported in such trials. Clinical research is not perfect. However, most clinical trials are conducted in a highly regulated environment and accepted for publication following a strict peer review process led by independent experts. While limitations exist in conducting and reporting clinical trials, investigators are judged at very high ethical and academic standards.

    A blog posted on September 11, 2017[1] questioned the integrity of the data and ethical conduct of the investigators of this study published in Open Heart. Due to the respect I have for the editor and this journal, I am obliged to respond on behalf of the authors.

    First, I did not receive ANY type of financial compensation as the principal investigator for this study. Second, no financial obligations or equity arrangements exist between the sponsor of the study, myself or my current Institution. Third, although all financial disclosures of all authors were properly disclosed to the journal at the time of submission, they were unfortunately not included in the final published article and therefore published subsequently as a correction[2]. Fourth, the objective of the study was to assess the 3-week healing properties of a surface-modified stent. The patient wi...

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  • The long and the short of it

    Lee et al in trying to define the accuracy of one method illustrate the huge weakness in echo vs MRI comparative data. First and foremost neither FAC or TAPSE correlated that well with RVEF ( FAC only slightly better) although statistically significant this difference is clinically of negligible importance. Secondly in assuming that MRI provides a gold standard for RVEF. As with echo there are strengths and weaknesses of MRI. On is the rather lower sensitivity to long axis abnormalities because ventricular volumes are usually defined using the short axis plane. So a reduced correlation between a purely long axis technique, a moderate correlation with a technique that has both long and short axis components and one which is defined using predominantly radial function is entirely to be expected. Long axis dysfunction is usually the first sign of ventricular deterioration with short axis hyperactivity to compensate - exactly the example cited post cardiac surgery. Finally in their conclusions they state that FAC provides a better guide to RV systolic function. This is not justified - what it does do is provide a slightly better estimate of RVEF -these two are not synonymous. So as there are no clinical correlates - prognosis, symptoms, exercise performance, hospitalisations , the comparison between the techniques tells us nothing we did not already know - all methods of defining systolic function are different - we have not answered which one is best.

  • This was so helpful

    This was so helpful and easy! Do you have any aricelts on rehab?

  • Increased mortality associated with low cholesterol does not reflect reverse causality, but causes it.

    DiNicolantonio and McCarty suggest that the inverse association between low cholesterol and mortality in elderly people reflects reverse causality; meaning that the low cholesterol is caused by the disorder being treated.1 One of their arguments is that those whose cholesterol decreases with increasing age die more frequently from cancer and other diseases, compared to those with low cholesterol prior to treatment. However, many studies have shown that low cholesterol may predispose to cancer2 as well as infectious diseases.3 In a previous paper2 we identified nine cohort studies including more than 140,000 individuals, in which cancer was inversely associated with cholesterol measured 10–30 years earlier, and where the association persisted after exclusion of cancer cases appearing during the first 4 years.
    The authors claim that statin treatment does not increase the risk of cancer based on a meta-analysis of 27 randomised trials published by the Cholesterol Treatment Trialists’ (CTT) Collaborators. But very few statin trials have continued for more than five years, and most carcinogenic chemicals need more time to create cancer. In spite of that cancer appeared significantly more often in three statin trials (2). In two other trials, non-melanoma skin cancer appeared more often and with statistical significance if the figures from the two trials were calculated together (2). Since then the number of non-melanoma skin cancers has not been reported in any trial. Fu...

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  • Multidisciplinary infective endocarditis care teams should address substance use disorders and harm reduction services

    We read with great interest Kaura and colleagues’ evaluation of a multidisciplinary care team for hospital inpatients with infective endocarditis (IE) (1). The study provides further evidence for the effectiveness of a team-based approach to IE care – a model endorsed by both European (2) and American (3) guidelines. Despite limitations inherent in a before-and-after study design, it is clear that the IE team provides patients rapid access to cardiology, microbiology, and surgical care with coordination between services.

    Notably absent from this multidisciplinary approach, however, is care for substance use disorders. We wish to draw readers’ attention to the 10% of study participants for whom injection drug use (IDU) was identified as a predisposing factor in their IE. We believe a coordinated IE team offers enormous potential to provide addictions care and harm reduction services for patients with IE who inject drugs.

    Compared with people who do not inject drugs, people who inject drugs are far more likely to have recurrences and repeat hospitalizations for IE, and face increased mortality risk after a first episode of IE (4,5). Rates of hospitalization for IDU-associated IE also appear to be increasing (4,6–8).

    Evidence-based interventions can be provided in-hospital to reduce both rates of injecting and harms associated with ongoing injection. These interventions include initiating opioid agonist therapies (e.g. methadone or buprenorphine) for opi...

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  • India is struggling under a staggering burden of chronic disease
    David E. Brown

    The citizenry of India are especially sensitive to excessive linoleic acid intake as noted by S. L. Malhotra in a research paper published back in 1967. Excerpt: "Much evidence indicates that consumption of even small quantities of unsaturated fatty acids decreases the liability to ischaemic heart disease (Bronte-Stewart et al., 1956; Kinsell et al., 1952). This hypothesis, too, does not find support in our data. The South...

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  • Re: Evidence from RCTs did not support introduction of dietary fat guidelines in 1977 & 1983
    Vivien S. Lund

    Dietary advice that reducing fat and saturated fat consumption will reduce the risk of coronary heart disease was introduced in the UK in 1983. The authors of this systematic review and meta-analysis conclude that evidence from randomised controlled trials, available at the time, did not support that advice.

    It is important to highlight that the review looks at the results of just six relatively short-term ra...

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  • Randomised controlled trials and diet-heart recommendations
    Christine M Williams

    Re: Harcombe et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983:

    The claim made by the authors of this paper that guidelines on dietary fat introduced in the 1970s and 1980s were not based on good scientific evidence is misguided and potentially dangerous. Whilst it is important to ensure an ongoing interrogation of the evidence linking d...

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  • Re:Letter to the Editor: Evidence from randomised controlled trials not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis
    Zoe Harcombe

    We would like to thank you for your interesting and helpful comments.

    We are currently finalising the follow-up paper, which is to consider all RCT evidence for current dietary guidelines before and since their introduction, to see if they have been supported in hindsight. We will review the risk of bias assessment tool, as suggested.

    We do accept the role that cohort studies can play but wanted to focu...

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