eLetters

833 e-Letters

  • ACUTE AUTOIMMUNE REACTION: AN OBSCURE MECHANISM OF COVID-19-RELATED MYOCARDIAL INJURY ?

    ACUTE AUTOIMMUNE REACTION: AN OBSCURE MECHANISM OF COVID-19-RELATED MYOCARDIAL INJURY ?

    Kenan YALTA, MD a
    Ertan YETKIN, MD b
    Gokay TAYLAN, MD a
    Tulin YALTA, MD c

    a Trakya University, Cardiology Department, Edirne, TURKEY
    b Istinye University, Liv Hospital, Cardiology Department, Istanbul, TURKEY
    c Trakya University, Pathology Department, Edirne, TURKEY

    Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
    Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

    Acute myocardial injury has been suggested as an important prognostic factor in Covid-19 patients (1-3). In their recently published article (1), Wei JF, et al. have demonstrated a significant association of acute myocardial injury (defined as elevation of high sensitive troponin-T (hs-TnT) levels) with older age, pre-existing cardiovascular disease, disease severity (and hence; general frailty) and adverse prognosis in Covid-19 patients . The authors have principally attributed this injury to certain factors including systemic inflammation, hypoxemia and direct myocardial invasion by the viral agent (1). However, as described below, an acute autoimmune reaction triggered by the virus might also be considered as an alternative mechanism of myocardial injury par...

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  • Other treatable causes of recurrent pericarditis

    Among the underlying causes of recurrent pericarditis which require specific treatment strategies (1) mention must also be made of recurrent pericarditis attributable to coeliac disease(2)(3), and recurrent pericarditis attributable either to Type 2 autoimmune endocrinopathy(4) or to hypoadrenalism(5).
    Faizallah et al reported 3 patients aged 40, 40, and 56, respectively, with recurrent pericarditis attributable to coeliac disease. The first patient presented with a temperature of 38.5 degrees Celsius, pericardial friction rub, and macrocytic anaemia attributable to folate deficiency. Pericardiocentesis yielded blood stained fluid that tested negative on bacteriological and M tuberculosis culture. Viral studies were negative and there were no malignant cells in the pericardial fluid. He responded well to reducing doses of corticosteroid therapy. However, it was only after a relapse of pericarditis that he had a duodenal biopsy, the latter an evaluation which revealed histological stigmata of coeliac disease. He was subsequently managed with a gluten-free diet(GFD), concurrently with an attempt to taper off the corticosteroid treatment. In spite of two subsequent relapses, corticosteroid treatment was eventually permanently terminated without any further relapse of pericarditis. The second patient was on GFD as well as a small dose of prednisolone at the time of publication of the report. The third patient, characterised by two episodes of pericarditi...

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  • Red flags as an adjunct to clinical decision rules in aortic dissection

    The clinical presentation which simulates ST-segment elevation myocardial infarction(STEMI)(1) is one of the most deceptive manifestations of dissecting aortic aneurysm(DAA), deserving detailed analysis notwithstanding its infrequent(2)(3)(4) occurrence. In Zhu et al DAA was prevalent in only 0.5% of 1576 subjects with suspected STEMI(2). Conversely, Kosuge et al documented a 4%(9 patients) prevalence of ST segment elevation among 233 subjects with confirmed DAA(3). In Hirata et al ST segment elevation was prevalent in 8.2% of 159 subjects with type A aortic dissection(4). When ST segment elevation occurs as a manifestation of DAA, there is a high prevalence of involvement of the inferior leads, exemplified by 6 of the 9 patients in Kosuge et al(3)., and seven of the 13 cases in Hirata et al(4)., arguably because type A aortic dissection is more likely to compromise the ostium of the right coronary artery than the ostium of the left coronary artery(5). In view of the life-threatening nature of DAA clinicians should not rely only on clinical decision rules to raise the index of suspicion. The rationale for a more open-minded approach is that clinical decision rules such as the AAD risk score tend to emphasise typical symptoms, such as the "tearing" character of the back pain(1), almost to the total exclusion of less typical symptoms such as nonspecific back pain, the latter typically radiating from a retrosternal chest pain. For example, a literat...

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  • Release of troponin after exercise stress test in hypertrophic cardiomyopathy

    Release of troponin after exercise stress test in hypertrophic cardiomyopathy

    Pawel Petkow Dimitrow1, Renata Rajtar-Salwa2, Tomasz Tokarek2
    1 2nd Department of Cardiology, Jagiellonian University Medical College, Kraków, Poland
    2 Department of Cardiology and Cardiovascular Interventions, University Hospital, Krakow, Poland
    Correspondence to: Paweł Petkow Dimitrow, 2nd Department of Cardiology, Jagiellonian University Medical College, Jakubowskiego 2 Str., 30-688 Krakow, Poland, e-mail: dimitrow@mp.pl, tel. 0048 12 400 22 50

    Recently Cramer et al. demonstrated very important observation on troponin level increase after exercise in patients with hypertrophic cardiomyopathy (HCM) [1]. Several concerns regarding to methodology of their study should be explained. Authors decided to perform only one measurement of troponin level at 6 hours after end of exercise. In our opinion, sampling after 6, 12, 18 and 24 hours after exercise provide more adequate profile of troponin level and allow to monitor possible post-exercise ischemia. Furthermore, data on prevalence of silent myocardial ischemia (only troponin increase) should be provided. In our study [2] painless ischemia detected by troponin measurement after normal daily physical activity was present in 25% of HCM patients. In another study [3], among HCM patients monitored by HOLTER ECG during normal daily physical activity, maximum heart rate was higher in th...

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  • ACUTE OR PRE-EXISTING CORONARY SLOW FLOW IN TAKOTSUBO CARDIOMYOPATHY: DOES IT MATTER ?

    ACUTE OR PRE-EXISTING CORONARY SLOW FLOW IN TAKOTSUBO CARDIOMYOPATHY: DOES IT MATTER ?

    Kenan YALTA, MD a
    Tulin YALTA, MD b
    Muhammet GURDOGAN, MD a

    aTrakya University, Cardiology Department, Edirne, TURKEY
    b Trakya University, Pathology Department, Edirne, TURKEY
    Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
    Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 0090505657985

    In the setting of takotsubo cardiomyopathy (TTC), coronary microvascular dysfunction has been mostly considered as a causative factor (1,2). In their recently published article (1), Montone RA et al have demonstrated, for the first time, the prognostic value of coronary slow flow (CSF) phenomenon in TTC patients. Of note, as we previously discussed, on a theoretical basis, the particular prognostic value of CSF phenomenon in these patients (3), we feel now pleased to notice that this theory has been fully confirmed by a well-designed study (1). Nevertheless, we would like to make a few comments on this issue:
    Firstly; temporal emergence of CSF phenomenon might possibly matter in TTC as well. Accordingly; an acutely evolving CSF pattern (due to severe adrenergic discharge (1)) as compared with a sole pre-existing one (emerging long before the index TTC as part of generalized...

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  • Problems with the clinical director role

    I read with interest the super article by Chris Steadman regarding being a clinical director in the NHS. I would add to this article that a particular problem has now become grossly apparent with taking on such a role which is the amount of pension tax that many will find they have to pay in taking such a role on. Previously, leadership and management roles have often attracted a rise in pensionable salary, which was a clear incentive to take them - as per the article, they clearly result in alot of work to the individual and so should be rewarded for this. However with the pension taper which started in 2016 and a low annual allowance, this creates a major problem, with many stories of doctors taking on such roles and receiving a large tax bill as result. How big a bill this may or may not be will depend on the personal circumstances of the individual and the amount of extra pensionable salary the individual trust is offering. For example, under current rules, a £10,000 increase in pensionable pay would result in me doing such a job at a big financial loss in my first year of doing it! Unless the UK government change the pension tax rules, it has created major disincentive for doctors to take on such roles.

  • APICAL ANEURYSM ? OR TRANSIENT APICAL BALLOONING ? : A POTENTIAL DILEMMA IN RISK-STRATIFICATION OF HYPERTROPHIC CARDIOMYOPATHY

    APICAL ANEURYSM ? OR TRANSIENT APICAL BALLOONING ? : A POTENTIAL DILEMMA IN RISK-STRATIFICATION OF HYPERTROPHIC CARDIOMYOPATHY

    Kenan YALTA, MD a
    Muhammet GURDOGAN, MD a
    Orkide PALABIYIK, MD b

    a,Trakya University, Cardiology Department, Edirne, TURKEY
    b Trakya University, Department of Biophysics, Edirne, TURKEY
    Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
    Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

    Left ventricular apical aneurysm (LVAA) formation in the setting of hypertrophic cardiomyopathy (HCM) usually appears to be associated with a significant mid-ventricular obstruction, and is potentially associated with adverse cardiovascular events (1). In their recently published article (1), Ramchand J et al have suggested LVAA as a major risk marker in this setting. Though we fully agree with the authors on this point, we would like to draw attention to certain other conditions including transient LV apical ballooning that might strongly mimick LVAA leading to a potential misdiagnosis in patients with HCM:
    Takotsubo cardiomyopathy (TTC) presenting with a transient apical ballooning pattern has been recently suggested to have a pure mechanical basis in certain patients with pre-existing structural heart diseas...

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  • A minor correction to the variant nomenclature

    As a physician dealing with patients with confirmed or suspected Fabry disease, I've read with great interest this editorial. This is a very thought-provoking article, which introduces the process of reclassification of a prevalent variant in the GLA gene associated with the cardiac variant of Fabry disease. I would like to make only a minor correction regarding the nomenclature of the variant mentioned. As written in the article of Valtola et al, the referred variant is c.427G> A and not c.472G> A¹ (transcript NM_000169.2).

    1. Valtola K, Nino-Quintero J, Hedman M, et al. Cardiomyopathy associated with the Ala143Thr variant of the α-galactosidase A gene. Heart 2020;:heartjnl-2019-315933. doi:10.1136/heartjnl-2019-315933

  • LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS

    LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS

    Kenan YALTA, MD
    Muhammet GURDOGAN, MD
    Gokay TAYLAN, MD

    a,Trakya University, Cardiology Department, Edirne, TURKEY

    Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
    Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

    In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
    Firstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wal...

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  • Response to letter to the editor

    We thank Dr Althouse for his letter and the interests in our article and for taking time to send us his comments. We appreciate it very much.

    In Figure 1, in scenario C, we incorporated the findings of “equivalence” in cases of equivalence trials. We stated in the article under the section of “Equivalence trials versus non-inferiority trials” that, in equivalence trials, the significance level is set as a two-sided p value of 0.05. We agree that, in non-inferiority trials, a one-sided p value of 0.025 is usually set as the significant level, although in some non-inferiority trials in cardiology, a significance level of one-sided p value of 0.05 was used. This is also mentioned under the same section. We have considered using a separate figure in the submission. However, we decided to submit a single figure as the separate figure incorporating only equivalence trials may be too simple and not the focus of the discussion.

    In scenario E, the lower limit of the confidence intervals is below 1 and the upper limit of the confidence interval is above the non-inferior margin. Therefore, the null hypothesis that the new treatment is inferior to standard treatment cannot be rejected and the alternative hypothesis that the new treatment is non-inferior to standard treatment cannot be accepted. We agree that the interpretation is more correctly stated as “New treatment not non-inferior to standard treatment”. Alternatively, as Dr Althouse suggested “New treatment...

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