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...
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 opacities that were initially mistakenly attributed to COVID-19 pneumonia. A negative reverse transciptase polymerase chain reaction test(performed on a nasopharyngeal swab specimen) was misinterpreted as a false negative. When he subsequently deteriorated a transoesophageal echo cardiogram showed severe mitral regurgitation, flail mitral valve leaflet and papillary muscle rupture. Culture of the mitral valve was positive for Klebsiella pneumoniae.. In retrospect both the breathlessness and the pulmonary opacities had a cardiogenic basis[5].
.
I have no funding and no conflict of interest.
References
[1]Raisi-Estabragh Z., Cooper J., Salih A et al
Cardioascular disease and mortality sequelae of COVID-19 in the UK biobank
Heart 2022 doi:10.1136/heartjnl-2022-321492
Article in Press
[2] Escola-Verge L., Cuervo G., de Alarcon A et al
Impact of the COVID-19 pandemic on the diagnosis management and prognosis of infective endocarditis
Clinical Microbiology and Infection 2021;27:660664
[3]Bajdechi M., Vlad ND., Dumitrascu M et al
Bacterial endocarditis masked by COVID-19: a case report
Experimental and Therapeutic Medicine 2022;23:DOI:10.3892/etm.2021.11109
[4]Davoodi L., Faeli L., Mirzakhani R et al
Catastrophic candida prosthetic valve endocarditis and COVID-19 comorbidity: A rare case
Current Medical Mycology2021;7:43-47
[5] Hayes DE., Rhee D., Hisamoto K et al
Two cases of acute endocarditis misdiagnosed a COVID-19 infection
Echocardiography 2021;38:798-804
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...
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 pressure measuring device must be the one the patient uses in his own home and must be a properly validated device. Technology is available to test its accuracy.
(ii)The protocol for SMBP must be the one prescribed in SPRINT[5[].
(iii) Hospital staff should be allowed to transfer the blood pressure readings from the memory of the device to the patient's health record. (iv)During the period of hospital stay titration of antihypertensive medication should be based on data from self measurement of blood pressure
Self-measurement of blood pressure in the hospital setting helps to mitigate the perception that directly observed treatment might have a punitive dimension. Mitigation of that perception, in turn, restores trust to the doctor-patient relationship, thereby reinforcing compliance with medication.
In the long term SMBP or its variant , automated office blood pressure measurement[6] might even be installed as the standard of care during office visits
I have no conflict of interest.
References
[1] Hardy L
I had a stroke when I was 64. Here's what I wish I had known before www.telegraph.co/health-fitness/mind/had-stroke--when-64-despite-working...
13th November 2022
[2] Soliman EZ., Rahman AKMF., Zhang Z-m et al
Effect of intensive blood pressure lowering on the risk of atrial fibrillation
Hypertension 2020;75:1491-1496
[3[ Upadhya B., Willard JJ., Lovato LC et al
Incidence and outcomes of acute heart failure with preserved versus reduced ejection fraction in SPRINT
Circulation Heart Failure 2021;14:1291-1301
[4]Jolobe OMP
Titrating antihypertensive therapy to mitigate the risk of falls
Clin Med 2022;22:597
[5]Johnson KC., Whelton PK., Cushman WC et al
Blood pressure measurement in SPRINT(Systolic Blood Pressure Intervention Trial)
Hypertension 2018;71:848-857
[6] Myers MG
The great myth of office blood pressure measurement
J Hypertens 2012;30:1894-1898
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...
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 disclosed the presence of a vegetation on the aortic valve[4].
In all three patients splinter haemorrhages were present even though auscultation had not disclosed any cardiac murmurs. Arguably, given the high index of suspicion for IE in the second patient, thrombolytic therapy might have been avoided if splinter haermorrhages had been detected when that patient first presented with stroke[3]. The third patient was fortunate in that thrombolytic treatment of STEMI was avoided altogether, given the risk of iatrogenic intracranial haemorrhage when that treatment modality is implemented in IE-related STEMI[5]. In the latter example intracranial haemorrhage was attributable to thrombolysis-related haemorrhagic transformation of hitherto subclinical IE-related embolic infarcts[5].
All three patients with silent IE had splinter haemorrhages as an early "red flag". In two of the patients[2],[4] iatrogenic harm was avoided as a consequence of that red flag.
Splinter haemorrhages also occur in atrial myxoma[6], nonbacterial thrombotic endocarditis[7], granulomatosis with polyangiitis[8], and in eosinophilic endocarditis[9]. In granulomatosis with angiitis IE can also be simulated by the presence of vegetations[10]. Vegatations also occur in nonbacterial thrombotic endocarditis[7].
i have no funding and no conflict of interest
References
[1]Schiebert R., Baig W., Wu J., Sandre JA
Diagnostic accuracy of splinter haemorrhages in patients referred with suspected infective endocarditis
Heart 2022;108:1986-1990
[2] Giurgea LT., Lahey T
Haemophilus parainfluenzae mural endocarditis: Case report and review of the literature
Case Reports in Infectious Diseases Volume 2016; Article ID 3639517
DOI.org/10.1155/2016/363517
[3] Bhuva P., Kuo S-H., Hemphill JC., Lopez GA
Intracranial haemorrhage following thrombolytic use for stroke caused by infective endocarditis
Neurocrit care 2010;12:79-82
[4]Rischin AP., Carrillo P., Layland J
Multi-embolic ST-elevation myocardial infarction secondary to aortic valve endocarditis
Heart, Lung and Circulation 2019;24:e1-e3
[5]Di Salvo TG., Tatter SB., O'Gara PT., Nielsen G., DeSanctis RW
Fatal intracerebral haemorrhage following thrimbolytic therapy of embolic myocardial infarction in unsuspected infective endocarditis
Clin Cardiol 1994;17:340-344
[6] May IA., Kimball KG., Goldman PW., Dugan DJ
Left atrial myxoma
Diagnosis, treatment, and pre-and post operative physiological studies
Journal of Thoracic and cardiovascular Surgery 1967;53:805-813
[7] Costenbader KH., Fidias P., Gilman MD., Qureshi A., Tambouret RH
Vase 29-2006:, A 43 year old woman with painful nodules on the fingertips, shortness of breath, and fatigue
N Engl J Med 2006;355:1263-1272
[8] Laurent C., Dion J., Regent A
Splinter haemorrhages .splenic infarcts, and pulmonary embolism in granulomatosis with plyangiitis
Vascular Medicine 2019;24:263-264
Usui S., Dainichi T., Kitoh A., Miyachi Y., Kabashima K
Janeway lesions and spilinte haemorrhages in a patient with eosinophilic endomyocarditis
JAMA Dermatology 2015;151:907-908
[10] Varnier G., Schire N., Christov G., Eleftheriou D., Brogan PA
Granulomatosis with plyangiitis mimicking infective endocarditis in an adolescent male
Clin Rheumatol 2016;35:2369-2372
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...
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 the etiology for her presentation". CTA showed an ascending thoracic aortic aneurysm, moderate pericardial effusion but neither aortic dissection nor PE. Nevertheless , due to concern for a concealed dissection, surgical exploration was undertaken. This disclosed significant haemopericardium and a 1 cm ascending thoracic aortic rupture tamponaded by the pulmonary artery[4].
Diligent evaluation of family history and genetic testing both powerfully augment the index of suspicion , as was the case in a patient whose father experienced DAA at the age of 20 , and had tested positive for a variant of the MYH11 gene. During pregnancy the patient , herself, tested positive for the same variant of the MYH11 gene. She was placed on metoprolol during pregnancy and post partum. Three days post partum she presented with pleuritic pain radiating through to the back, and new diastolic murmur was elicited.. Both transthoracic echocardiography and cardiac computed tomography disclosed the presence of DAA. Aortic repair was successfully undertaken[5].
I have no conflict of interest
References
[1]Bourjeily G., Paidas M., Khalil H., Rosene Montella K., Rodger M
Pulmonary embolism in pregnancy
Lancet 2020;375:500-512
[2]Braverman AC
Acute aortic dissection
Circulation 2010;122:184-188
[3[ Lombaard H., Soma-Pillay P., Farrell E-M
Managing acute collapse in pregnant women
Best Practice & Research Clinical Obstetrics and Gynaecology 2009;23:339-355
[4]Bogaert K., Christensen K., Cagliostro M., Ferrara L
Contained aortic rupture in a term pregnant woman during COVID-19 pandemic
BMJ Case Reports 2020;13:e238370
[5]Sathananthan G., Rychel V., Yam J., Barlow A., Grewal J., Kiess M
A postpartum Type A dissection
JACC Case Reports 2020;2;150-153
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...
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 which occurs in patients with spontaneous or revealed symptoms. By comparison, in asymptomatic patients the stroke volume rises in early exercise. Hence, a normal HR response to exercise test is clinically useful and reassuring when the presenting symptoms are doubtful. A positive exercise test (revealed symptoms, abnormal blood pressure response, arrhythmias or significant decline in functional capacity) or left ventricular (LV) dysfunction by echocardiography at baseline are guideline indications for valve intervention,4 and in these patients valve intervention rather than exercise prescription is necessary. However, exercise-based rehabilitation or training differs from formal exercise testing, and is useful both before and after valve intervention. Pre-intervention exercise training or exercise-based rehabilitation is associated with better post-intervention outcome, shorter hospital stay,5 and an early return to work or other activities. Pre-intervention obesity is often a concern for surgeons with regard to the potential for post-intervention rehabilitation. However, in daily clinical practice we encounter patients who are turned down for valve intervention (transcatheter valve implantation [TAVI] or conventional surgery) by the Heart team due to complex comorbidity, frailty and higher age, and are therefore assigned for conservative treatment. The question arises whether these patients may benefit from a low-intensity training or regular physical activity or not, and what will be the prescribed exercise intensity and frequency. Exercise-based rehabilitation or training is probably necessary for these patients to maintain and improve their physical function. However, there is a paucity of evidence in the literature to assess the benefit of exercise-based rehabilitation in patients with significant AS who are not found eligible for valve intervention, and hence no dedicated exercise recommendations exist. This should be investigated in prospective research studies in future.
Furthermore, we agree with the authors that most cardiologists dealing with patients with VHD may have limited knowledge of exercise prescription. However, this should ideally be incorporated into the remit of cardiac rehabilitation teams, which is often comprised of physicians and other health and fitness professionals in most European Hospitals, particularly in Scandinavia. Next, a comparison between aortic regurgitation related pressure and volume overload and the athletic heart was presented. However, a resting echo in athletic heart will exclude aortic regurgitation. Furthermore, in addition to borderline (low-normal) LV ejection fraction in the context of bradycardia, and significant improvement during exercise (contractile reserve), an athletic heart may typically show normal/higher systolic tissue Doppler velocities (S’), global longitudinal strain by speckle tracking echocardiography and other more sensitive marker of systolic LV function, such as the novel first-phase ejection fraction,6 compared with patients with VHD. Finally, a reduced LV ejection fraction in severe AS may be reversible reflecting “contractility-afterload mismatch”; i.e. reduced transaortic flow or LV ejection fraction but preserved contractile function. A relief of valve resistance (AS) in these patients either by TAVI or surgical valve replacement often leads to immediate increase in LV ejection fraction and/or normalization of transaortic flow.
Contributors SS wrote the first draft, RR revised it. Both authors approved the final version.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this work.
Patient consent for publication Not applicable.
Ethics approval This work does not involve human participants.
References
1. Chatrath N, Papadakis M. Physical activity and exercise recommendations for patients with valvular heart disease. Heart 2022 Mar 2:heartjnl-2021-319824.
2. Saeed S, Rajani R, Seifert R, et al. Exercise testing in patients with asymptomatic moderate or severe aortic stenosis. Heart 2018 Nov;104(22):1836-1842.
3. Chambers JB, Rajani R, Parkin D, et al. Rapid early rise in heart rate on treadmill exercise in patients with asymptomatic moderate or severe aortic stenosis: a new prognostic marker? Open Heart 2019;6(1):e000950. doi: 10.1136/openhrt-2018-000950. eCollection 2019.
4. Baumgartner H, Falk V, Bax JJ, et al. ESC Scientific Document Group. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2017; 38: 2739-2791.
5. Marmelo F, Rocha V, Moreira-Gonçalves D. The impact of prehabilitation on post-surgical complications in patients undergoing non-urgent cardiovascular surgical intervention: systematic review and meta-analysis. Eur J Prev Cardiol 2018;25:404–17.
6. Saeed S, Gu H, Rajani R, et al. First phase ejection fraction in aortic stenosis: A useful new measure of early left ventricular systolic dysfunction. J Clin Ultrasound 2021 Nov;49(9):932-935.
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...
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 aortic diameters in the general population aged 55 years or older. Heart 2022 doi: 10.1136/heartjnl-2021-320574
2. Ferrara A, Totaro P, Morganti S, et al. Effects of clinico-pathological risk factors on in-vitro mechanical properties of human dilated ascending aorta. J Mech Behav Biomed Mater 2018;77:1-11.
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
When the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however,...
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
When the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however, as emphasized, the dilatory activity can selectively be damped by low dosage beta – blockade. [5] This potential has been shown in a baby born with right ventricular hypertrophy, when the beta-blockers given at low doses produced complete remission of the hypertrophy [6].
Biopsies have confirmed that myocardial hypertrophy is part and parcel of the of Takotsubo cardiomyopathy [7]. It is likely that, in this setting, selective hypertrophy of the transmural aggregates is induced by the slightly elevated levels of adrenalin known to prevail in these patients [8]. Selective damping of the transmural aggregates by low dose beta-blockade, therefore, can be anticipated to be a more appropriate treatment than use of the higher doses, as currently recommended. [1,2]
References:
1: Silverio A, Parodi G, Scudiero F, Bossone E , Di Maio M Vriz O et al [2022] Beta-blockers are associated with better long-term survival in patients with Takotsubo syndrome . Heart 108(17):1369-1376. doi: 10.1136/heartjnl-2021-320543.
2: Kummer M, El-Battrawy I, Gietzen T, Ansari U, Behnes M, Lang S, Zhou X Borggrefe M , Akin I [ 2020] The Use of Beta Blockers in Takotsubo Syndrome as Compared to Acute Coronary Syndrome. Front Pharmacol. 211: 681-689 doi: 10.3389/fphar.2020.00681
3: Lunkenheimer PP, Redmann K, Cryer CW, Batista RIV, Stanton JJ, Niederer P, Anderson RH (2007) Beta-blockade at low doses restoring the physiological balance in myocytic antagonism. Eur J Cardio Thorac Surg 32: 225-230, DOI: 10.1016/j.ejcts.2007.03.048
4: Lunkenheimer PP, Redmann K, Hoffmeier A, Niederer P, Stephenson R, Schmitt B, L Theilmann L, Becker F, Anderson RH (2017) The Ventricular Structure Functioning as an Antagonistic Continuum. J Biomed Tech Res 3 (1): 104-114
5: Schmitt B, Li T, Kutty SH, Klasheei AL, Schmitt KRL, Anderson RH, Lunkenheimer PP, Berger F, Kühne T, Peters B (2015) Effects of incremental beta-blocker dosing on myocardial mechanics of the human left ventricle: MRI 3D-tagging insight into pharmacodynamics supports theory of inner antagonism. Am J Physiol Heart Circ Physiol 309:H45-52, DOI: 10.1152/ajpheart.00746.2014
6: Emeis M, Lunze FI, Miera O, Berger F, Rossi R, Schmitt B. (2020) Congenital hypertrophy of the right ventricle successfully treated with very low dose beta blockers. Cardiology and Cardiovascular Medicine 4,760-765
7: Nef HM, Möllmann H, Kostin S, Troidl C, Voss S, Weber M, Dill T, Brandt R, Hamm CW [2007] Takotsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. European Heart Journal 28, 20: 2456–2464, https://doi.org/10.1093/eurheartj/ehl570
8: Templin C, Hänggi J, Klein , et al. [2019] Altered limbic and autonomic processing supports brain-heart axis in takotsubo syndrome. European Heart Journal. 40(15):1183–1187. doi: 10.1093/eurheartj/ehz068.
I take great concern in regards to the conclusions that this and multiple other previous cardiology articles have laid claim to in regards to calcium supplementation. Many providers read these articles and tell patients to stop taking calcium, this then results in osteoporosis and fractures which also has a high mortality rate. There must be significant caution in making the conclusions that this article makes. The amount of calcium the patients were taking was quite varied between 500-2,000 mg a day, patients with bone disease need 1200 mg a day in order to maintain normal bone turnover and rebuilding by the osteoblast. There needs to be data from this study showing the poor outcome patient’s calcium supplement amounts. To insinuate that all calcium supplements are bad is not only a disservice but a detriment to our patients. Patients now have access to articles more than ever and will read this and now won’t take their calcium supplements, this means that anyone treating osteoporosis will now have to explain this and other articles. Patients are more likely to believe bad data than good data. The truth is that calcium is needed for good bone health and there is a safe amount that is not a risk to cardiac health. This article amongst others does not bring in that side of the story.
To the Editor
We read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could...
To the Editor
We read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could occur due to complete obstruction of valvular orifice, and this convinced the authors of the necessity of a prompt operation once the diagnosis is made, regardless of the size and location of the tumour.
Sugimoto et al [5] believed that a cardiac myxoma should be excised as soon as possible because it may produce serious complications. While optimal timing of surgery after the onset of embolic complications (especially cerebral or myocardial infarction) remained controversial, the authors believed that early surgery may have to be performed when there is a threat of new embolic events.
Lijoi et al [6] advocated that surgical excision is undertaken as soon as possible after diagnosis in order to avoid such complications as systemic embolization and valvular incompetence with rapid deterioration.
Meyns et al [7] noted that embolization was not related to the size of the myxoma, but was dictated by the friability of the tissues. The authors recommended immediate excision of atrial myxoma once the diagnosis is established.
Keeling et al [8] highlighted that embolization risk was increased in patients presenting with a cardiac rhythm other than sinus rhythm, and in large, left-sided, polypoid and mitral valve myxomas. Their study concluded that immediate resection of cardiac myxomas should be performed to prevent sudden death and embolic events and that, by immediate resection, these risks may be very low.
Selkane et al [9] advocated that surgery for cardiac myxoma should comply with the usual recommendations for preoperative coronary angiography, and that emergency surgery should be available to acute symptomatic patients and those at a high risk of embolization.
Khan et al [10] performed immediate surgical treatment in all their patients, and this was associated with low rates of morbidity and mortality. The authors recommended that surgical excision should be carried out without delay, while coronary angiography was advised if coronary artery disease is suspected or if patient’s age was over 40 years.
Kuroczyński et al [11] recommended urgent resection of cardiac myxomas after establishing the diagnosis to prevent complications such as embolization or obstruction of the mitral orifice. They also recommended performing pre-operative coronary angiography in patients aged over 40 with risk factors for coronary heart disease.
Garatti et al [12] recommended that surgical excision of cardiac myxomas must be done as soon as possible after the diagnosis is established because of the high risk of valvular obstruction or systemic embolization.
Lastly, Rushel et al [13] believed that immediate surgical excision was indicated in all patients to prevent sudden death and embolic complications.
In summary, our “best evidence topic” review indicates that, even though comparative data is lacking, there is sufficient data to indicate that excision of an atrial myxoma qualifies as an emergency procedure in acute symptomatic patients, where acute valvular obstruction was conceivable (such as in large mobile left atrial myxomas) and where tumour embolization was more likely to occur (e.g. lobulated and gelatinous myxomas). Excision of other atrial myxomas can be performed on an urgent basis, which allows for a thorough preoperative optimization and assessment (including coronary angiography).
References
1. Griborio-Guzman AG, Aseyev OI, Shah H, Sadreddini M. Cardiac myxomas: clinical presentation, diagnosis and management. Heart. 2021 Sep 7:heartjnl-2021-319479. doi: 10.1136/heartjnl-2021-319479
2. Dunning J, Prendergast B, Mackway-Jones K. Towards evidence-based medicine in cardiothoracic surgery: best BETS. Interact CardioVasc Thorac Surg 2003, 2:405-9
3. Semb BKH. Surgical considerations in the treatment of cardiac myxoma. J Thorac Cardiovasc Surg 10984; 87:251-259
4. Livi U, Bortolotti U, Milano A, Valente M, Prandi A, Frugoni C, de Mozzi P, Valfre C, Mazzucco A, Gallucci V. Cardiac myxomas: results of 14 years' experience. Thorac Cardiovasc Surg. 1984; 32:143-7
5. Sugimoto T, Ogawa K, Asada T, Mukohara N, Nishiwaki M, Higami T, Kawamura T. Surgical treatment of cardiac myxoma and its complications. Cardiovasc Surg. 1993; 1:395-8
6. Lijoi A, Scoti P, Faveto C, Canale C, Parodi E, Passerone GC, Dottori V, Venere G. Surgical management of intracardiac myxomas. A 16-year experience. Tex Heart Inst J. 1993; 20:231-4
7. Meyns B, Vancleemput J, Flameng W, Daenen W. Surgery for cardiac myxoma. A 20-year experience with long-term follow-up. Eur J Cardiothorac Surg. 1993; 7:437-40
8. Keeling IM, Oberwalder P, Anelli-Monti M, Schuchlenz H, Demel U, Tilz GP, Rehak P, Rigler B. Cardiac myxomas: 24 years of experience in 49 patients. Eur J Cardiothorac Surg. 2002; 22:971-7
9. Selkane C, Amahzoune B, Chavanis N, Raisky O, Robin J, Ninet J, Obadia JF. Changing management of cardiac myxoma based on a series of 40 cases with long-term follow-up. Ann Thorac Surg. 2003; 76:1935-8
10. Khan MA, Khan AA, Waseem M. Surgical experience with cardiac myxomas. J Ayub Med Coll Abbottabad. 2008; 20:76-9
11. Kuroczyński W, Peivandi AA, Ewald P, Pruefer D, Heinemann M, Vahl CF. Cardiac myxomas: short- and long-term follow-up. Cardiol J. 2009; 16:447-54
12. Garatti A, Nano G, Canziani A, Gagliardotto P, Mossuto E, Frigiola A, Menicanti L. Surgical excision of cardiac myxomas: twenty years’ experience at a single institution. Ann Thorac Surg. 2012; 93:825-31
13. Rushel SS, Mandal SC, Moinuddin S, Alamgir MK. Surgical Treatment of Cardiac Tumours: a 17-year Experience at Department of Cardiac Surgery, NICVD, Dhaka. Mymensingh Med J. 2019; 28:562-566
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5...
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5
Noticeably, the authors,3 commenting on the Ikezaki et al. study, claimed exactly the following: “A prospective observational study in Japan including 4014 participants showed that the dietary intake of omega-3 fatty acids was negatively associated with successful eradicarion.9” That is an incomplete - inaccurate and rather unacceptable “biased” comment, made by the authors. Actually, Ikezaki et al.6 concluded exactly as follows: “Our results indicate that higher egg and fish intake may be negatively correlated with successful H. pylori eradication therapy in H. pylori-positive subjects with gastritis and/or duodenal ulcers”,6 thereby meaning that both high cholesterol and omega-3 fatty acid intake, but not omega-3 fatty acid intake alone, may be negatively correlated with successful H. pylori eradication therapy.
In this respect, relative data suggest that mainly high cholesterol intake rather than omega-3 fatty acid intake, is negatively linked with successful H. pylori eradication regimen. For instance, a recent large-scale study reported that H. pylori infection could play a pathophysiologic role in the development of dyslipidemia, whereas H. pylori eradication may decrease the risk of dyslipidemia; significant reduction in total cholesterol was observed in the successful eradication of H. pylori arm compared to the persistent H. pylori-positive arm (P<0.001).7 A meta-analysis investigating the association between H. pylori infection and the serum lipid profile, revealed that H. pylori infection is positively associated with LDL-C, TC, and TG and negatively associated with HDL-C.8 Another recent meta-analysis also revealed that the post-H. pylori eradication HDL-C concentrations were increased while LDL-C concentrations were marginally or not influenced, and thus further investigation is necessary to clarify the effects of lipid alterations following H. pylori eradication on CVD.9 Likewise, a multicenter national study reported that H. pylori infection appears to play an independent role in the pathophysiology of the mentioned MetS; H. pylori-positive participants exhibit significantly higher body mass index, waist circumference, TC, LDL-C, and lower HDL-C, when compared with seronegative participants (P < 0.05).10 As a final example, simvastatin significantly improves H. pylori eradication rate.11
All in all, the potential effect of omega-3 supplementation on MetS and/or H. pylori-related risk of cardio-cerebrovascular events needs further evaluation before considering the introduction of low and/or high dosage of omega-3 as a possible regular regimen against cardio-cerebrovascular disorders.
References
1. Rizos EC, Markozannes G, Tsapas A, et al. Omega-3 supplementation and cardiovascular disease: formulation-based systematic review and meta-analysis with trial sequential analysis. Heart 2020;107:150-58.
2. Kountouras J, Doulberis M, Kazakos E, et al. Impact of omega-3 supplement on metabolic syndrome and/or Helicobacter pylori-related risk of cardiovascular disease. Heart 2022 Feb 9:heartjnl-2020-318776.
3. Markozannes G, Ntzani EE, Rizos EC. Correspondence on 'Impact of omega-3 supplement on metabolic syndrome and/or Helicobacter pylori-related risk of cardiovascular disease' by Kountouras et al. Heart 2022 Feb 9:heartjnl-2022-320822.
4. Elagizi A, Lavie CJ, O'Keefe E, et al. An Update on Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Health. Nutrients 2021;13:204.
5. Jo SH, Han SH, Kim SH, et al. Cardiovascular effects of omega-3 fatty acids: Hope or hype? Atherosclerosis 2021;322:15-23.
6. Ikezaki H, Furusyo N, Jacques PF, et al. Higher dietary cholesterol and omega-3 fatty acid intakes are associated with a lower success rate of Helicobacter pylori eradication therapy in Japan. Am J Clin Nutr 2017;106:581-88.
7. Park Y, Kim TJ, Lee H, et al. Eradication of Helicobacter pylori infection decreases risk for dyslipidemia: A cohort study. Helicobacter 2021;26:e12783.
8. Shimamoto T, Yamamichi N, Gondo K, et al. The association of Helicobacter pylori infection with serum lipid profiles: An evaluation based on a combination of meta-analysis and a propensity score-based observational approach. PLoS One 2020;15:e0234433.
9. Watanabe J, Hamasaki M, Kotani K. The Effect of Helicobacter pylori Eradication on Lipid Levels: A Meta-Analysis. J Clin Med 2021;10:904.
10. Lim SH, Kim N, Kwon JW, et al. Positive Association Between Helicobacter pylori Infection and Metabolic Syndrome in a Korean Population: A Multicenter Nationwide Study. Dig Dis Sci 2019;64:2219-30.
11. Hassan AM, Shawky MAE, Mohammed AQ, et al. Simvastatin improves the eradication rate of Helicobacter pylori: upper Egypt experience. Infect Drug Resist 2019;12:1529-34.
Corresponding to: Jannis Kountouras, MD, PhD
Professor of Medicine
Gastroenterologist
8 Fanariou St, Byzantio 551 33,
Thessaloniki, Macedonia, Greece
Tel: +30-2310-892238, Fax: +30-2310-992794
E-mail: jannis@auth.gr, ancoratus2010@gmail.com
Contributors: JK wrote the draft of the document. AP, EV, DC, MT-C and MD critically revised it.
Funding: Dr Doulberis has received a travel grant by Gilead Sciences Switzerland Sàrl. Rest of the authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Patient and public involvement: Patients and/or public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication: This study does not involve human participants.
Prevalence and peer review: Not commissioned; internally peer reviewed
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:-
Show MoreWhen 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...
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].
Show MoreSelf-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...
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]].
Show MoreIn 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...
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.
Show MoreFor 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...
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...
Show MoreThijssen 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
Show More1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic...
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
Show MoreWhen the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however,...
I take great concern in regards to the conclusions that this and multiple other previous cardiology articles have laid claim to in regards to calcium supplementation. Many providers read these articles and tell patients to stop taking calcium, this then results in osteoporosis and fractures which also has a high mortality rate. There must be significant caution in making the conclusions that this article makes. The amount of calcium the patients were taking was quite varied between 500-2,000 mg a day, patients with bone disease need 1200 mg a day in order to maintain normal bone turnover and rebuilding by the osteoblast. There needs to be data from this study showing the poor outcome patient’s calcium supplement amounts. To insinuate that all calcium supplements are bad is not only a disservice but a detriment to our patients. Patients now have access to articles more than ever and will read this and now won’t take their calcium supplements, this means that anyone treating osteoporosis will now have to explain this and other articles. Patients are more likely to believe bad data than good data. The truth is that calcium is needed for good bone health and there is a safe amount that is not a risk to cardiac health. This article amongst others does not bring in that side of the story.
To the Editor
Show MoreWe read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could...
To the Editor,
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5...
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