64 e-Letters

published between 2020 and 2023

  • The complexity of the association of eosinophilic myocarditis and COVID-19 infection

    Notwithstanding the fact that Blagova et al did not identify any specific findings related to eosinophilic myocarditis(EM) in their series of 14 patients with post-COVID myoendocarditis[1], anecdotal reports not cited by Techasatian et al[2] have documented an association between COVID 19 infection and eosinophilic myocarditis[3-5].
    Craver et al reported the case of a previously healthy 17 year old male who had a 2 day history of headache, nausea and vomiting , followed by sudden death. At autopsy his heart weighed 500 grams(expected weight fro age was 262-295 grams), with a histological profile characterised by an inflammatory infiltrate which had prominent" eosinophils, in addition to lymphocytes and macrophages. This was associated with multiple foci of myocyte necrosis.. Histological examination of the lungs revealed mild chronic inflammation of the bronchi with only occasional eosinophils. Postmortem nasopharyngeal swabs tested positive for SARS-2 CoV-2[3].
    In two other cases of the association of COVID-19 infection and eosinophilic myocarditis, each of the patients[4],[5] had a previous history of chronic asthma, thereby raising the possibility that eosinophilic myocarditis might have been a manifestation of eosinophilic granulomatosis with polyangiitis.
    However, given the fact that, in its own right, COVID-19 infection can be a trigger for eosinophilic pneumonia[6], the association of eosinophilic myocarditis and COVID-19 infectio...

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  • Covid-19 -related aortitis as a risk factor for aortic dissection

    In their analysis of population-based mortality from dissecting aortic aneurysm(DAA), the authors drew attention to the need for further research to be undertaken to optimise earlier identification of those at risk[1]. Relevant to this task is the increasing awareness of the entity of COVID-19-related aortitis, and the documentation of increasing numbers of anecdotal reports of the association of COVID-19 infection and DAA.
    The report by Shergall et al was one of the first to show a persuasively valid causal relationship between COVID-19 infection and aortitis. In that example a 71 year old man presented with chest pain radiating to the scapula, within a few days of experiencing symptomatic COVID-19 infection. Although, by this time, the nasopharyngeal swab test was negative for COVID-19, he had serological evidence of recent COVID-19 infection. Computed tomography showed evidence of diffuse inflammatory aortitis. Following a course of prednisolone 40 mg/day, subsequent tomography showed partial resolution of the aortitis[2].
    In three subsequent reports, it was the occurrence of DAA(presumably as a complication of aortitis) , rather than aortitis per se, which was the issue of concern, especially because of the pain-free nature of the clinical presentation.
    In one of those patients , a 45 year old previously healthy non-smoker with no comorbidities, the only symptoms comprised a 3 days history of fever, cough, and dyspnoea. He had neither...

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  • Re: Assessment of haemoglobin and serum markers of iron deficiency in people with cardiovascular disease

    Graham et al. reported the prevalence of anaemia and iron deficiency in patients with cardiovascular disease, aged ≥50 years (1). Prevalence of anaemia in patients with and without heart failure were 46%, and 29%, respectively. In addition, low haemoglobin and transferrin saturation, but not low ferritin, were associated with a worse prognosis. I have two comments.

    First, Mahendiran et al. reported that patients with acute coronary syndromes (ACS) and anaemia at admission was significantly associated with 1-year all-cause mortality and cardiovascular events (2). Colombo et al. also conducted a prospective study, with median follow-up of 4.9 years, to investigate the relationship between anaemia and cardiovascular events in patients with ACS (3). The adjusted hazard ratio (95% confidence intervals [CI]) of patients with anaemia at admission against patients without anaemia throughout admission for was 1.51 (1.02-2.25). I suppose that the severity of ACS, including progression of heart failure, may also be closely related to subsequent prognosis.

    Second, Graham et al. made an emphasis that anaemia would contribute to a worse prognosis in patients with cardiovascular disease (1). Salisbury et al. reported the risk of in-hospital mortality in relation to anaemia after hospitalization in patients with acute myocardial infarction (4). When the severity of anaemia was classified into three levels of haemoglobin, mild (>11 g/dL), moderate (9-11 g/dL), and severe...

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  • The differential diagnosis of heart failure must include constrictive pericarditis

    The analysis of aetiology, ejection fraction, and mortality in heart failure is one which would benefit from inclusion of constrictive pericarditis(CP) as the differential diagnosis of some of the underlying causes of congestive heart failure(CHF) enumerated by Fritz et al[1].
    The rationale is that some of the underlying causes of CP, such as radiotherapy[2], tuberculosis, sarcoidosis, and Whipple's disease are also causes of myocarditis and, hence, CHF[3]. Conversely, CP might, itself, be a cause of atrophy of myocardial fibres, a state of affairs "which probably occurs in response to ischemia owing to cardiac compression[4]. CP-related myocardial dysfunction is more likely to occur when aetiologies of CP such as radiation therapy, cardiac surgery, and systemic inflammatory diseases are operative[4].
    It is, therefore, likely that the echocardiographic documentation of left ventricular ejection fraction(LVEF) amounting to < 50% in a substantial minority of CP patients[5],[6],[7] might be attributable to coexistence of CP and left ventricular systolic dysfunction, a state of affairs that might make CP clinically and echocardiographically indistinguishable from dilated cardiomyopathy. Conversely, left ventricular diastolic dysfunction might predominate, and the clinical manifestations of CP characterised by LVEF > 50% may be indistinguishable from the clinical manifestations of, for example, restrictive cardiomyopathy[8].
    Among 43...

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  • Limitations of biomarkers in heart failure with preserved ejection fraction and in mimics of that syndrome

    The assertion that natriuretic peptide levels below a defined threshold(for, example, Brain Natriuretic Peptide(BNP) levels < 100 pg/mL) can safely rule out heart failure and may also obviate the need to proceed to early echocardiography[1] should be qualified as follows:-
    Early echocardiography does not necessarily confirm or refute the diagnosis of congestive heart failure(CHF) in patients with heart failure characterised by preserved ejection fraction(HFpEF). This is a truism that ought to be valid even in HFpEF patients with BNP levels < 100 pg/mL[2]. In the latter study , among 159 patients who had been hospitalised for CHF, the latter characterised by left ventricular ejection fraction(LVEF) amounting to >50%, in association with pulmonary capillary wedge pressure > 15 mm Hg, 46/159 patients(29%) had BNP equal to or less than 100 pg/mL[2].. Accordingly, if the index of suspicion for CHF is sufficiently high strategies other than echocardiography should be deployed to confirm or refute the diagnosis of CHF. The following are some of those strategies:-
    (i) Clinical evaluation of jugular venous pressure(JVP). A raised JVP is indicative of a right atrial pressure beyond the normal upper limit of 8 mm Hg[3]. Furthermore, jugular venous distension is associated with a likelihood ratio amounting to 5.1(95% Confidence Interval, 3.2 to 7.9) in favour of a diagnosis of CHF[4].
    (ii)Evaluation of inferior vena cava(IVC) diameter. An...

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  • A more accurate definition of clinical inertia

    It is, indeed, a truism that poor rates blood pressure(BP) control are, in part, attributable to clinical inertia, whereby therapy is not escalated when BP is uncontrolled[1]. However, the criterion for escalation of antihypertensive therapy utilised by the authors, namely, a BP amounting to 140/90 mm Hg or more[1], is inappropriate, given the fact that the goal BP most likely to mitigate the risk of incident hypertension-related atrial fibrillation(AF) and hypertension-related congestive heart failure(CHF), respectively, is a goal BP amounting to < 120/80 mm Hg[2],[3]. In principle, that goal BP can be achieved by ultralow-dose quadruple combination therapy either on its own or in combination with lifestyle antihypertensive strategies such as regular exercise[4] and low-salt diet with or without abstinence from alcohol[5]. The younger the patient the more compelling the requirement to attain a BP amounting to < 120/80 mm Hg because it is theoretically possible that the longer the duration of suboptimal blood pressure the greater the long term risk of AF, CHF, and, arguably, hypertension-related vascular dementia[6].
    Attainment of optimum goal BP crucially depends on accurate measurement of both "office" and home blood pressures[7],[8], and both those goals are predicated on the use of well-validated blood pressure monitors[8]. However, the minimum requirement for ultimate success in the control of BP is an honest conversation between doctor...

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  • The association of endogenous endophthalmitis and infective endocarditis also deserves mention

    Over and above the scenario cited by the authors, where the presence of Roth spots became a "red flag" for infective endocarditis(IE)[1], clinicians also need to take note of endogenous endophthalmitis as a "red flag" for IE, both in the context of native valve IE, and in the context of intracardiac device-related IE.
    Endophthalmitis and native valve infective endocarditis:-
    Awareness of endophthalmitis as a manifestation of IE is of heightened value when IE presents in the absence of a cardiac murmur, so-called "silent" infective endocarditis. In one patient with silent IE , Roth spots were identified in the same eye that was affected by endogenous endophthalmitis[2]. In another patient with silent IE initial transthoracic echocardiography(TTE) did not disclose any vegetations. Ten days later, however, transoesophageal echocardiography(TOE) disclosed the presence of vegetations[3]. The clinical course of another patient with silent IE was characterised by non diagnostic initial TTE, and nondiagnostic TOE on day 12. On day 31, however, TOE showed severe aortic regurgitation and what appeared to be a vegetation on the aortic valve. Intraoperatively, however, what had previously appeared to be a vegetation proved to be a destroyed non coronary valve tip[4].
    Endophthalmitis and infective endocarditis attributable to intracardiac devices:-

    Endogenous endophthalmitis is also a red flag for infective endocarditis attr...

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  • The absolute risk of having chest pain during a heart attack in a patient with diabetes remains higher

    I have known this for years. A silent heart attack is relatively more common in a patient with diabetes than in a patient without diabetes. However this then leads to the medical myth that patients with diabetes mostly get silent ischaemia, leading to possible over-investigation of patients with diabetes and non-cardiac pain. It should thus be part of teaching that most patients with diabetes still get typical chest pain during a heart attack - I have long used a 80/20 vs 90/10 rule, the % of patients who have chest pain during a heart attack/do not have chest pain, diabetics vs non-diabetics.

  • Response to “Has personalised surgery made another advancement in aortic root surgery?” by Zhu and Woo

    We read with great interest the editorial of Zhu et al (1). The authors have great theoretical knowledge and experience in the treatment of aortic valve regurgitation. We agree with their conclusion concerning personalised external aortic root support (PEARS) that “there are still many questions to be answered”. We would like to try to answer some of them.
    Experience based on the first 100 operations in the Czech Republic (2) suggests that the indication for PEARS is limited to the patient with dilatation of the aortic root and/or ascending aorta and only trivial aortic regurgitation regardless of the origin of the disease. Implantation of PEARS should be considered as a preventive operation in group of patients that usually do not meet the criteria for valve sparing aortic valve replacement. In these patients the PEARS procedure can be performed as a measure to prevent further dilatation of the aorta and possible aortic dissection. The possibility of performing the operation without a cardiopulmonary bypass is certainly an advantage for the patient (2).
    The authors worried about wall tension after implantation. It is generally known, that decrease of the diameter which is achieved by PEARS implantation, reduces wall tension according to the La Place law. This procedure in fact decreases wall tension and moreover the wall of the aorta is externally supported.
    The fears about the viability of the aortic wall due to the continuous circumferential stress...

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  • Management of HFpEF and its comorbidities

    The association of chronic obstructive pulmonary disease(COPD) and heart failure with preserved ejection fraction(HFpEF) justifies the special mention accorded to it by the authors[1]. In part, the rationale is that COPD is a risk factor for for atrial fibrillation(AF), and, hence, worsening of heart failure. Furthermore, both AF and COPD are risk factors for pulmonary embolism [4],[5]], the latter a complication that might, in turn, lead to worsening of heart failure. Additionally, in its own right, hypoxic COPD generates a mortality risk which is favourably modified by prescription of long term oxygen therapy(LTOT)[6]. Accordingly, all HFpEF patients with coexisting COPD should be evaluated for eligibility for LTOT, and should receive the benefit of LTOT if found to be eligible.
    SGLT2 inhibitor therapy sits well with the management of HFpEF in the COPD context, given the fact that SGLT2 inhibition mitigates the risk of worsening of congestive heart failure(CHF) to a comparable degree in HFpEF patients with and without coexisting COPD[7]. In the latter study the prevalence of AF was significantly(p < 0.001) higher in HFpEF patients with COPD than in counterparts who did not have coexisting COPD[7].
    Hypertension is another important comorbidity of HFpEF[1]. In its most recent report, the American College of Cardiology Expert Consensus Decision Pathway recommends a goal systolic blood pressure(SBP) of < 130 mm Hg in the presence of HFpEF[8]...

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