eLetters

807 e-Letters

  • LTFT trainees: electrophysiology’s loss

    On reading Dobson et al’s enlightening article we were saddened but not surprised to hear that nationally, there were no cardiology LTFT trainees training in electrophysiology (EP). Of course, it remains unclear as the relationship here: do trainees planning LTFT avoid EP, or do EP trainees fear reducing their hours will prove challenging?

    Either way, this represents a great shame for both trainees and subspecialty. For trainees, the fulfilment of electrophysiological problem-solving and skilful intervention should be accessible to all regardless of hours worked. For the subspecialty, a growth in diversity of electrophysiologists as well as flexible working seems very sensible to ensure the continued growth of the subspecialty and its long-term sustainability. Ongoing initiatives by the BCS, BHRS, EHRA and others continue to advocate for a diverse and flexible workforce in EP, and we applaud these efforts.

  • The role of coexisting high-grade carotid artery stenosis in aetiopathogenesis of NVAF-associated stroke

    Given the fact that high-grade carotid artery stenosis(CAS)(50% or more stenosis) is an independent risk factor for stroke in patients with coexisting nonvalvular atrial fibrillation(NVAF)(1), the optimum management of NVAF patients who have symptomatic CAS should be included among the key outstanding research questions enumerated by the authors of the recent review(2). In one study high-grade CAS was prevalent in 12%-14% of NVAF patients aged 71-80(3).. When high-grade CAS gives rise to amaurosis fugax , transient ischaemic attack(TIA), or stroke, the urgent priority is to mitigate the risk of subsequent occurrence of disabling stroke. That priority should prevail irrespective of presence or absence of coexisting NVAF. Strategies to mitigate that risk include initiation of dual antiplatelet therapy(4)(5) followed by interventional treatment of the CAS itself(6).
    For patients in whom symptomatic CAS coexists with NVAF, when the latter is associated with a CHA2DS2-Vasc score that justifies oral anticoagulation to mitigate the risk of cardioembolis stroke , coprescription of oral anticoagulants has to be included in the management strategy. Furthermore after interventional treatment of symptomatic CAS, secondary prevention of neurological events(including stroke) necessitates long term antithrombotic medication with aspirin(5). Concurrently , in the presence of coexisting NVAF, long term primary prevention of cardioembolic stroke necessitates long...

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  • A role for echocardiography when pulmonary embolism presents atypically

    Echocardiography has been shown to generate decisive diagnostic information when pulmonary embolism(PE) presents atypically with paradoxical cerebral embolism in the absence of concurrent PE-related stigmata such as dyspnoea, chest pain, or haemoptysis(1)(2), and also in those cases where the atypical presentation is one which simulates ST segment elevation myocardial infarction(STEMI) in the absence of paradoxical coronary artery embolism(3).
    The following are some anecdotal report which exemplify the diagnostic role of echocardiography:-
    A 32 year old man presented with a stroke , but no concurrent breathlessness or clinical signs of deep vein thrombosis(DVT). Transthoracic echocardiography(TTE) revealed intracardiac thrombus and also a thrombus in the main pulmonary artery. A subsequent Doppler examination revealed a DVT in the right lower limb(1).
    In another report, a 55 year old man presented with a stroke and no concurrent breathlessness. However, he had a blood pressure of 70/40 mm Hg and an elevated serum troponin of 0.07 ng/ml(normal < 0.03 ng/ml). TTE revealed a "positive bubble study" which was followed up with a transoesopahageal echocardiogram(TOE) which showed a patent foramen ovale(PFO). A subsequent Duplex study revealed right lower limb DVT.. His management included intracardiac surgery, which revealed biatrial thrombus straddling a patent foramen ovale. An extensive pulmonary thrombus was also discovered(...

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  • A timely change of focus

    The focus on left atrial dimensions in the risk stratification of patients with atrial fibrillation(AF) and also in those without AF(1), is a timely departure from the prevailing preoccupation with AF-related risk stratification strategies such as the CHA2 DS2-Vasc score which do not include evaluation of left atrial function(2), notwithstanding the hypothesis that the predictive ability of the CHADS2 index to stratify stroke risk may be mechanistically linked to severity of left atrial dysfunction(3). In the latter study left atrial functional index(LAFI) was the parameter utilised to evaluate left atrial function. Regression analysis showed that mean LAFI significantly(p < 0.001) decreased across tertiles of CHADS2(42.8, 37.8, 36.7). After adjustment for age, sex, race, and other parameters , high CHADS2 remained significantly associated with the lowest quartile of LAFI(Odds Ratio 2.34). For every point increase in CHADS2 the LAFI decreased by 4 %. Secondary analyses using CHA2 DS2 Vasc score replicated these results(3). In view of these observations LAFI is a potential modality to risk stratify nonvalvular atrial fibrillation(NVAF) subjects such as those with CHA2DS2 Vasc score of zero , who might otherwise be ineligible for thromboprophylaxis with oral anticoagulants. LAFI could even be utilised to evaluate eligibility for thromboprophylaxis in patients with excessive atrial ectopic activity or short-run atrial tachyarrhythmis, given the fact that each...

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  • 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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