803 e-Letters

  • raising the index of suspicion for pulmonary embolism in LBBB-associated troponinosis

    Given the fact that acute myocardial infarction(AMI)(1), left bundle branch block(LBBB)(2), and pulmonary embolism(PE), are all age-related disorders, the authors of the recent study correctly highlighted the importance of including PE in the differential diagnosis of the association of suspected AMI and LBBB(2). For the purpose of identifying those patients who are most likely to have AMI the authors proposed the use of serum troponin as a rule-in criterion during the first 3 hours of hospital admission . By implication the inclusion of PE in the differential diagnosis should be deferred for at least 3 hours, and only activated in patients who do not have a raised serum troponin level.
    However, in view of the fact that elevation in serum troponin may be a feature in the presentation of PE(4), and also in view of the fact that transient LBBB has been reported in a 59 year old patient with PE(5), the latter disorder should be included in the differential diagnosis of the association of acute coronary syndrome and LBBB. In the 59 year old patient who was reported with PE and LBBB, serial troponin levels were 0.38, 0.41, and 1.12 ng/ml(reference range 0-0.04)(5), arguably justifying early coronary angiography(2). That patient had neither pleuritic pain nor breathlessness to raise the index of suspicion for PE. Coronary angiography ruled out coronary artery occlusion, and helical computed tomography revealed extensive PE involving the main branches of both pul...

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  • A novel strategy to distinguish between an infective and a non infective vegetation

    In the context of suspected cardiac implantable electronic device infection a fundamental flaw in transoesophageal echocardiography(TOE) is that this modality does not distinguish between infective and non infective masses situated on the electronic device lead. For example, in one study 25 patients who underwent TOE were shown to have either a lead vegetation(11 cases) or lead strands(13 cases) or both(1 case). Nevertheless, 18 of of those 25 patients proved, after exhaustive evaluation, to have no evidence of infection(1). According to a recent report, however, guided biopsy of a lead-associated mass, by means of a biotome, can facilitate the distinction between an infective versus non infective device-related mass. In Case 1 of that report an 80 year old woman with a pacemaker presented with mild leucocytosis in the setting of a recent dental procedure, but was afebrile. Transoesophageal echocardiography(TOE) disclosed a 1.6 X 1.0 cm mass on her right atrial lead. Using femoral access and fluoroscopic guidance the mass was biopsied under TOE guidance. The mass proved to be a thrombus with irregular fragments of soft tissue. The gram stain showed no polymorphonuclear cells and the tissue culture confirmed no growth. Case 2 in that report was a 29 year old man with an implantable cardioverter-defibrillator in the setting of intermittent fever and night sweats. TOE revealed a 2.9 cm X 1.2 mass encasing the device lead. A single blood culture grew a Propionib...

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  • compelling evidence of the utility of PET/CT in optimising the diagnosis of cardiac implantable electronic device infection

    Notwithstanding the high costs and lack of reimbursement associated with the use of positron emission tomography/computed tomography(PET/CT) in suspected cardiac implantable electronic device (CIED) infection(1), the ability of this modality to distinguish between infective and non infective vegetations is a powerful argument for its inclusion in the workup of suspected CIED. Evidence of the ability to make this distinction comes from two sources(2)(3). Firstly, in a retrospective study of 177 transoesophageal echocardiographic studies performed on 153 consecutive patients, a visible mass was observed on a device lead in 25 instances. In 11 studies this was a lead vegetation, in 13 instances only lead strands were seen, and in one instance a lead vegetation coexisted with a lead strand. Nevertheless, 18 of the 25 patients with lead-associated masses had no other evidence of infection. In that study the presence or absence of infection was adjudicated by three clinical investigators who independently reviewed all available clinical data without knowledge of the echocardiographic results(2). In another study, 63 consecutive patients(mean age 68.6) with suspected CIED were evaluated both by echocardiography(tranasthoracic and transoesophageal) and by PET/CT. Echocardiography was associated with a positive predictive value(PPV) of 83.3%, and a negative predictive value(NPV) of 69.2%. For PET/CT, PPV and NPV amounted to 100% and 93.9%, respectively(3). The additional ut...

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  • Kidney injury attributable to treatment of acute gout in heart failure

    Under the heading "Changes in kidney function during intercurrent illness"(1) mention must be made of the risk of acute kidney injury when nonsteroidal anti inflammatory drugs(NSAIDs) are prescribed for acute gout, the latter complication(the equivalent of "intercurrent illness") sometimes documented as a consequence of diuretic use in congestive heart failure(CHF)(2). Coprescription of NSAIDs, diuretics, and angiotensin converting enzyme inhibitors(or angiotensin receptor blockers), so-called triple therapy, is associated with increased risk of acute kidney injury(rate ratio 1.31, 95% Confidence Interval 1.12 to 1.53)(3). This was shown in a nested case-control study which enrolled patients in whom hypertension was the indication for prescription of diuretics and/or angiotensin converting enzyme inhibitors(or angiotensin receptor blockers)(3), but might be equally applicable in the context of CHF. Additionally, among CHF patients who have a drug regime which includes spironolactone, the use of NSAIDs might increase the risk of hyperkalaemia. The rationale is that NSAIDs "interfere with the stimulatory effect of prostaglandins on the release of renin"(4). The risk of hyperkalaemia may be compounded by concurrent use of beta adrenergic blocking agents(4).
    For all the above reasons, NSAIDs should be contraindicated in CHF patients with gout. The recommended alternatives include colcichine(5) and intraarticuoar corticosteroids(6), resp...

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  • Re: Sub-optimal cholesterol response to initiation of statins and future risk of cardiovascular disease

    We are grateful for the comments by David P Foley, Zoe Harcombe and Uffe Ravnsker on our paper.

    Both American and UK guidelines for the treatment of cholesterol,[1,2] recommend monitoring percent reduction in low-density lipoprotein cholesterol (LDL-C) among patients initiating statins as an indication of response and adherence. Our recently published paper [3] examined LDL-C reduction among patients initiating statins in the real-world setting.

    With regard to the points raised:

    Why didn’t you analyse the possible reasons for the observed ‘findings’?

    Our study was not designed to establish causality so we are unable to analyse possible reasons for the observed findings. We are, however, undertaking further research to establish these latter.
    David P Foley notes in his response, ‘it is already well proven that only moderate to high dose statin therapy has a proven biological anti-atherogenic effect’. However, it is important to avoid any erroneous impression that patients are started on low dose statins in primary care. As shown in Table 1, most patients in this study were actually prescribed moderate and high potency statins (70.9% in the sub-optimal responders compared to 81.8% in the optimal responders).
    A study by Vupputuri et al,[4] examined LDL-C reduction and adherence among high-risk patients initiating statins in a real-world setting using electronic health records of 1,066 patients in the US. Of patients with high adherence...

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  • Why didnt you analyse the possible resons for the observed 'findings' ?

    This study has already been inappropriately quoted in the media which is what the public read and misinformation is propagating. The authors need to take some responsibility for failing to point out that the dosing of the statins prescribed (most likely archaic low dose simvastatin) isn't analysed and long term compliance isn't addressed in this ' primary prevention population based longitudinal non interventional study'
    Cardiologists are going to inundated with questions from patients with coronary disease on statins who have misinterpreted information which is incomplete and misrepresented - the title of the study needs to be highlighted 'Initiation of statins' is well put and needs to be remembered. The study cannot address the 'ongoing management' of cardiovascular risk with appropriate cardiovascular investigation of patients and optimization of preventative strategies as this study does not address this crucial aspect.
    It is already well proven that only moderate to high dose statin therapy has a proven biological anti-atherogenic effect so that low doses initiated in general practice are actually ineffective and this is what the study shows NOT that statins are ineffective but that medical practice of blanket prescribing of low doses of statins is ineffective without monitoring of response and ongoing titration to achieve evidence based targets. This omission from the conclusions needs to be corrected and it ne...

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  • This paper needs to be corrected to adjust for lifestyle differences

    The conclusion of this article was twofold: 1) approximately half of primary care patients put on statins did not achieve at least a 40% reduction in LDL-Cholesterol (the sub-optimal group) and 2) those who did (the optimal group) had fewer cardiovascular incidents over the next (approximately six) years.

    Table 1 in the paper shows that the sub-optimal group have 1.43 times the “alcohol misuse” of the optimal group. There is no more information on alcohol consumption beyond this. Were the alcohol misusers also far less likely to be non or moderate drinkers and far more likely to be heavy and frequent drinkers?

    The smoking information shows that, from the limited information available, the sub-optimal group were 25% more likely to be smokers. However, there is no smoking information for 96% of patients. There is no activity information – were the drinking/smokers more likely to be sedentary? Were they more likely to be obese?

    There were more men in the sub-optimal group. The sub-optimal patients were more likely to be poorly-controlled diabetics and less likely to have hypertension treated.

    Correspondence with the researchers confirmed that the HRs in Table 2 were not adjusted for anything other than age and baseline LDL-Cholesterol. They were not adjusted for alcohol misuse, or smoking, or gender, or any other lifestyle factors that were known to be different between the two groups – even with vast amounts of missing information.

    The enti...

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  • Questionable Benefit of Increasing the Degree of Cholesterol Lowering

    In their prospective cohort study of 165,411 primary care patients, Akyea et al. claim that suboptimal responders on statin treatment will experience significantly increased risk of future cardiovascular disease (CVD)(1). As many cardiovascular events may heal without serious health problems, we consider mortality as the most important outcome. Among the 80,802 patients with optimal cholesterol lowering, 821 (1.01 %) died from CVD. Among the 84,609 patients with suboptimal cholesterol-lowering 873 (1.03 %) died. This means that to prevent one cardiovascular death by optimal cholesterol lowering you have to increase the degree of lowering in 5,000 patients for six years. This is hardly a benefit because several independent researchers have reported that serious side effects from statin treatment are much more common than reported in the statin trials (2). The small numbers reported in the trial reports are achieved by excluding participants who suffer from side effects of the drug during a few weeks long run-in period before the start of the trial. That this is an effective method to lower the number of side effects appeared in the IDEAL trial where this method wasn´t used and where a high statin dose was compared with a low dose, because in that trial almost half of the participants in both groups suffered from serious side effects (2).

    Furthermore, Akyea et al. have not reported total mortality in the two groups. This failure may introduce another bias because tota...

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  • Adrenal function also needs to be evaluated in hypothyroidism-related pericardial effusion(revised version of my recent rapid response)

    Under the "diagnosis" heading the authors asserted that "hypothyroidism can be deemed the aetiology of pericardial effusion or cardiac tamponade if a high TSH level has been found, after excluding other secondary causes like a neoplastic, bacterial or an inflammatory process"(1).. I would add that, if the patient's hypothyroidism is of autoimmune aetiology, Addison's disease is a secondary cause that also requires urgent exclusion(2).
    In one report, a 21 year old man presented with cardiac tamponade, in association with a TSH level of 17.9 microUnits/L(normal range 0.35-5.0 microUnits/L), and serum thyroxine and serum tri-iodothyronine levels which were both at the lower limit of the normal range. Serum cortisol, however, was 0.5 micrograms/dl(normal range 3.0-23.0 mcd/dl). Tests for thyroid and adrenal autoantibodies were positive, thereby fulfilling the criteria for Type 2 autoimmune polyglandular syndrome(Type-2 APS).
    On the basis of the above observations the work-up of patients with pericardial effusion of presumed hypothyroid aetiology should include evaluation of adrenal function, because Addison's disease can, in its own right, be the underlying cause of cardiac tamponade(3). Furthermore, irrespective of hormonal status, pericardial effusion in a patient with Type 2 APS may ultimately be attributable to the "serositis" component of that syndrome, rendering the effusion capable of relapsing...

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  • The effect of chronic total occlusion revascularisation to the long-term outcome: what is the reason?

    To the Editor

    We read the article by Godino et al describing the risk of non-revascularisation of a coronary chronic total occlusion (CTO) for the cardiac death, sudden cardiac death and sustained ventricular arrhythmias (SCD/SVA) with great interest 1. After reading in detail, we have the following comments.
    At first, although the authors mentioned a little in the DISCUSSION, the effect of medications for the prevention of cardiac death and SCD/SVA may better be clarified in the subjects. As they stated, because those who received CTO lesion revascularisation tend to have longer dual antiplatelet therapy and receive more hospital visit for follow-up coronary angiography to recheck, there might be such confounding factors. For example, the third generation P2Y12 class of adenosine diphosphate (ADP) receptors inhibitor was approved in 2009 in Europe 2. How was its distribution compared to conventional clopidogrel treatment? And appropriate statin treatment would be also associated with plaque stability and reduced cardiac adverse events as well as the beta-blocker administration for the prevention of SCD/SVA 3. Because the follow-up period was long as up to 12-years, the difference of these medication strategies between two groups should be clarified. The same also applies to the used stent types. The importance of current manuscript would be much better after these concerns were clarified.
    Second, the multivariate analysis of Table 3 contains 2 factors,...

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