eLetters

177 e-Letters

published between 2020 and 2023

  • Valvulopathy in autoimmune disorders as the differential diagnosis of infective endocarditis

    The valvulopathy of autoimmune disorders can simulate infective endocarditis when echocardiography discloses the presence of vegetations on the heart valves[1-4].
    This occurrence was exemplified by valvulitis with vegetations and concurrent congestive heart failure(CHF) as the initial presentation of systemic lupus erythematosus[2]. Blood cultures were sterile.The patient was managed medically with corticosteroid therapy[2].
    In granulomatosis with polyangiitis valvulopathy was exemplified by a patient who presented with pyrexia, dyspnoea, renal failure, and dry gangrene of the toes. Echocardiography revealed a mobile, 7-10 mm vegetation on the chordae of the tricuspid valve. Antineutrophilic cytoplasmic antibodies against proteinase 3 (PR3-ANCA) were strongly positive(194 EU/mL; Reference Range < 1.99). Renal biopsy showed crescentric glomerulonephritis. Blood cultures were sterile. The patient was successfully managed solely with immunosuppressive therapy[3].
    The valvulopathy of eosinophilic granulomatosis with polyangiitis was exemplified by a patient who presented with breathlessness and polyarthralgia superimposed on a long history of eosninophilia, asthma, allergic rhinitis, and sinusitis. Clinical examination disclosed the presence of systolic murmurs and signs of CHF. Echocardiography revealed a 19 mm x 16 mm vegetation on the aortic valve and a 11 mm x 9 mm vegetation on the mitral valve in association with moderate to severe m...

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  • RE: Proteomics profiling reveals a distinct high-risk molecular subtype of hypertrophic cardiomyopathy

    Liang et al. conducted a prospective study to predict major adverse cardiovascular events (MACE) in patients with hypertrophic cardiomyopathy (HCM) with special reference to molecular subtypes in HCM (1). Compared with the reference group with molecular subtype A, patients in molecular subtype D presented an increased risk of developing MACE, with the adjusted hazard ratio (HR) (95% CI) of 2.78 (1.18 to 6.55). I have comments about the study.

    The authors understand the unstable estimation by multivariate analysis, which would be partly caused by the limited number of events. When conducting Cox regression analysis, they used sex, age, and two conventional cardiac biomarkers. As they classified molecular subtypes into four groups, a total of 7 independent variables were used for the analysis. There is a recommendation that the number of events per independent variable in Cox regression analysis are required ≥10 for prediction model (2,3). If the authors have concerned about the association between molecular subtypes in HCM and MACE events, strict criteria for the number of events can be relaxed (4). Although there is a description that the total number of events was 78 in Table 2, the number of patients with event was 66 in Table 3. I suppose that some patients had more than single event. I recommended to add MACE events by continuing follow-up to fulfill the statistical requirement.

    When we see survival curve in Figure 2, remarkable difference in the risk of...

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  • An important rationale for sequential prescription of medication for congestive heart failure

    The occasional, and unforeseen occurrence of drug-related interstitial nephritis is, arguably, an important justification for sequencing the initiation of drug treatment for congestive heart failure or for hypertension.
    Given the fact that interstitial nephritis has been reported after medication with captopril[1], losartan[2], valsartan[3], and empagliflozin[4],[5],, respectively, the challenge of identifying the culprit medication is made much easier if drugs belonging to those subclasses are introduced sequentially. Two examples justify that approach:-
    In one hypertensive patient empagliflozin had been prescribed as an add-on therapy to long-standing medication with losartan, bisoprolol, amlodipine, sitagliptin, and aspirin. Pre empagliflozin serum creatinine was 0.9 mg/dl. Post empgliflozin serum creatinine peaked at 9.22 mg/dl. Renal biopsy showed stigmata of acute interstitial nephritis. Empagliflozin was discontinued, and the patient was managed with haemodialysis and corticosteroid therapy. She improved and was eventually weaned off haemodialysis[4].
    The second example was a hypertensive patient who had been taking enalapril, dilriazem, and atoravastatin for more than 2 years. Pre-empagliflozin serum creatinine was 60 mcmol/l. After empagliflozin was initiated as add-on therapy serum creatnine increased to 381 mcmol/l. Renal biopsy showed stigmata of acute interstitial nephritis. Renal function improved after withdrawal of empagliflozi...

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  • Antibiotic prophylaxis for vulnerable prospective candidates for intraarticular corticosteroid injections

    Intra-articular corticosteroid injections were notably absent from the list of invasive procedures which were evaluated for temporal association with infective endocarditis. Although the randomised trial that involved use of intra-articular corticosteroids painted a favourable benefit/risk profile in the comparison between intra-articular steroids plus best current advice(BCT)(66 subjects with hip osteoarthritis) versus intraarticuar lidocaine plus BCT(66 subjects also with hip osteoarthritis) , "one event was considered possibly related to trial treatment"[1]. This event was a fatal episode of infective endocarditis in a patient who had a bioprosthetic aortic valve antedating the intra-articular corticosteroid injection[1].
    Previous post traumatic splenectomy was the risk factor in a 60 year old woman who developed infective endocarditis 2 weeks after she received intra-articular corticosteroids for shoulder pain[2].
    In a study which involved 6066 patients of mean age 66.8 who received intraarticular facet joint corticosteroid injections one patient developed infective endocarditis with fatal, outcome. This was a patient with previous mitral valve replacement surgery and a previous episode of infective endocarditis[3].
    A congenital heart defect was the risk factor in a 38 year old woman who developed tricuspid valve infective endocarditis after lumbar spine corticosteroid injection[4].
    Concurrent immunosuppressive treatment for...

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  • Infective endocarditis as a casualty of COVID-19

    Unfortunately, the review of cardiovascular disease and mortality sequelae of COVID-19[1] did not encompass the infective endocarditis(IE) dimension. By contrast, a multicentre retrospective observational study conducted at 26 Spanish referral centres for infective endocarditis and cardiac surgery made the following observations:-
    When data from 2020 were compared with data from 2019, the year 2020 was characterised by a 34% reduction in the absolute number of definite IE episodes. The authors attributed this decline to the possibility that people with occult IE were either obeying strict instructions to stay at home or were reluctant to seek medical attention for fear of contracting COVID-19 in a medical facility[2]. Anecdotal reports, however, reflect the reality that people with severe symptoms of COVID 19 have no choice but to go to hospital whether or not they unknowingly have coexisting IE.. Included in that category was a patient with coexistence of native valve bacterial endocarditis and COVID-19 pneumonia[3], and the patient with catastrophic Candida prosthetic valve endocarditis and COVID-19 pneumonia[4].. By contrast some patients who attend hospital with symptoms and radiographic stigmata suggestive of COVID-19 infection ultimately prove to have complications of infective endocarditis in the total absence of coexistence ofr COVID-19 infection.[5]. In the latter report the chest radiograph of a patient with breathlessness showed bilateral opaciti...

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  • Self-measurement of blood pressure during directly observed treatment

    Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
    Self-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
    The following are the minimum requirements for in-hospital SMBP:-
    (i)The blood p...

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  • A caveat for splinter haemorrhages

    A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
    In the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
    In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
    The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation...

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  • Poor index of suspicion as a major hinderance to optimum management

    In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
    For example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
    Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as t...

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  • Correspondence on “Physical activity and exercise recommendations for patients with valvular heart disease” by Chatrath et al

    To the Editor We read with interest the review article “Physical activity and exercise recommendations for patients with valvular heart disease” by Doctors Nikhil Chatrath and Michael Papadakis, which was published in a recent edition of Heart.1 The focused clinical review is particularly useful for physicians and other health care workers dealing with patients with valvular heart disease (VHD). However, we would like to share some additional thoughts based upon our own experiences from Heart Valve Clinics and our previous publications derived from the EXTAS (exercise testing in aortic stenosis) cohort study.2 Indeed, some notions in their work, were previously explored by us in the EXTAS study and deserve mention. We showed that exercise testing (modified Bruce protocol) was safe, tolerable and revealed symptoms not confirmed on the history in approximately 40% of patients with asymptomatic severe and 24% moderate AS.2 Serial exercise testing added incremental prognostic information to baseline testing. Furthermore, in another follow-up study we showed that an early rapid rise in heart rate (defined as achieving at least 85% of target heart rate or ≥50% increase from baseline within the first 6 min) was associated with revealed symptoms later in the test and an increased risk of death in moderate AS in the following 2 years.3 We speculated that rapid risk in heart rate was probably a compensation for a fall in stroke volume to maintain cardiac output in early exercise whi...

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  • Re: Longitudinal changes of thoracic aortic diameters in the general population aged 55 years or older

    Thijssen et al. reported factors affecting the diameters of the thoracic aorta in participants (1). By using non-enhanced cardiac CT, the diameters of the ascending (AA) and descending aorta (DA) were measured. The median absolute change in diameters during follow-up with mean scan interval of 14.1 years, was 1 mm for both the AA and DA. Absolute changes per decade in AA and AD diameters were significantly larger in males than in females. Significant determinants of changes in AA diameter were age, body mass index (BMI) and diastolic blood pressure (DBP) in female, and BMI in males. In addition, significant determinants of changes in DA diameter were age, BMI, DBP, and current smoking in female, and age and BMI in males. I have a comment about the study.

    There are some sex differences in significant determinants for the change of AA and AD diameters, and BMI is a common risk factor. Ferrara et al. reported that there were no effects of gender, BMI, AA diameter, aortic stiffness index, smoking habits, diabetes mellitus, and Marfan syndrome on AA tissue in patients with AA aneurysms. In contrast, aging and hypertension made the AA tissue weaker (2). The significant determinants for dilation of AA and DA diameters may not directly relate to the risk of thoracic aneurysm, and BMI management is important to prevent thoracic aorta dilations in general population.

    Reference
    1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic...

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