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...
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 infection might be mediated by a hypersensitivity reaction to the SARS-2 CoV-2 virus. That would account for the development of eosinophilic myocarditis in the previously healthy 17 year old male in reported by Craver et al[3]. The same aetiopathogenic mechanism might, arguably, even have facilitated the development of eosinophilc myocarditis in the two patients with previous history of asthma[4],[5].
I have no funding and no conflict of interest.
References
[1]Blagova O., Lutokhina Y., Kogan E et al
Chronic biopsy-proven post-COVID myoendocarditis with SARS-CoV-2 persistence and high level of antiheart antibodies
Clin Cardiol 2022;45:952-959
[2]Techasatian W., Gozun M., Vo K et al
Eosinophilic myocarditis: systematic review
Heart 2023 doi:10.1136/heartjnl-2023-323225
[3]Craver R., Huber S., Sandomirsky M et al
Fatal eosinophilic myocarditis in a healthy 17-year old male with acute respiratory syndrome coronavirus 2 (SARS-CoV-2c)
FETAL AND PEDIATRIC PATHOLOGY doi.org/10.1080/15513815.20201761491
[4]Sherafan A., Rachmanian M., Badkoubeh RS et al
Hypereosinophilic syndrome and COVID-19:2 case reports
Journal of Cardiothoracic Surgery 2023:18;158
doi.org/10.1186/s13019-023-02241-1
[5]Rao K., Arustamyan M., Walling A et al
Utility of cardiac magnetic resonance imaging in diagnosing eosinophilic myocarditis in a patient recently recovered from COVID-19: a grand round case report
Eur Heart J Case Reports 2023;7:1-8
[6]Araujo M., Correia S., Lima AL et al
SARS-CoV-2 as a trigger of eosinophilic pneumonia
Pulmonology 2022;28:62-64
In view of the fact that the association of pulmonary embolism (PE) and chronic obstructive pulmonary disease (COPD) is one fraught with the risk of PE recurrence, and fatal outcome, respectively [1], the association of the two disorders is one that should have merited some mention in the review of heightened long term cardiovascular risk after exacerbations of COPD [2], notwithstanding the uncertainty about the true prevalence of PE in patients with COPD [3],[4] . The uncertainty about PE prevalence in COPD is, arguably, in part, attributable to the fact that some COPD patients have coexisting carcinomatosis as a risk factor for PE in its own right [3]. In a systematic review and meta-analysis published in 2009, Rizkallah et al documented a PE prevalence amounting to 19.9%(95% Confidence Interval 6.7% to 33%) among patients with acute exacerbations of COPD[4]. Anecdotal reports also document the association of right heart thrombi (one of the stigmata of pulmonary thromboembolism) and COPD [5-8].
Over and above its association with PE, COPD also appears to be a risk factor for the occurrence of "in situ" thrombosis in the pulmonary arterial vasculature [9],[10], a development which is a long term risk factor for right heart failure.
Arguably, in view of the prothrombotic environment generated by acute exacerbations of COPD, and the fact that atrial fibrillation might be prevalent in approximately 15% of COPD patients [2], there might b...
In view of the fact that the association of pulmonary embolism (PE) and chronic obstructive pulmonary disease (COPD) is one fraught with the risk of PE recurrence, and fatal outcome, respectively [1], the association of the two disorders is one that should have merited some mention in the review of heightened long term cardiovascular risk after exacerbations of COPD [2], notwithstanding the uncertainty about the true prevalence of PE in patients with COPD [3],[4] . The uncertainty about PE prevalence in COPD is, arguably, in part, attributable to the fact that some COPD patients have coexisting carcinomatosis as a risk factor for PE in its own right [3]. In a systematic review and meta-analysis published in 2009, Rizkallah et al documented a PE prevalence amounting to 19.9%(95% Confidence Interval 6.7% to 33%) among patients with acute exacerbations of COPD[4]. Anecdotal reports also document the association of right heart thrombi (one of the stigmata of pulmonary thromboembolism) and COPD [5-8].
Over and above its association with PE, COPD also appears to be a risk factor for the occurrence of "in situ" thrombosis in the pulmonary arterial vasculature [9],[10], a development which is a long term risk factor for right heart failure.
Arguably, in view of the prothrombotic environment generated by acute exacerbations of COPD, and the fact that atrial fibrillation might be prevalent in approximately 15% of COPD patients [2], there might be a case for including COPD as one of the parameters in the CHA2DS2Vasc risk assessment formula, so as to generate a rational basis for initiating long-term anticoagulant therapy in patients who have the association of COPD and atrial fibrillation.
For all these reasons all aspects of the relationship between COPD and pulmonary thromboembolism should be the subject of vigilant documentation , verification, and evaluation for long term cardiovascular risk.
I have no conflict of interest.
References
Bertoletti L., Quenet S., Laporte S et al
Pulmonary embolism and 3-month outcomes in 4035 patients with venous thromboembolism and chronic obstructive pulmonary disease: data from RIETE Registry
Respiratory Research 2013;14:75
doi 10.1186/1465-9921-14-75
[2] Hawkins NB., Nordon C., Rhodes K et al
Heightened long term cardiovascular risk after exacerbations of chronic obstructive pulmonary disease
HEART
Epub ahead of print doi:10.1136/heartjnl-2023-323487
[3] Tillie-Leblond I., Marquette C-H., Perez T et al
Pulmonary embolism in patients with unexplained exacerbations of chronic obstructive pulmonary disease: Prevalence and risk factors
Ann Intern Med 2006;144:390-396
[4]Rizkallah J ., Man P., Sin DD
Prevalence of pulmonary embolism in acute exacerbations of COPD
A systematic review and meta-analysis
CHEST 2009;135:786-793
[5] Noji Y., Kojima T., Aoyama T
Free-floating thrombus in right heart and massive pulmonary embolism migrating into pulmonary artery
CIRCULATION 2005;111:e438-e439
[6] Ates BA., Esenboga K., Ozyuncu N
Isolated right ventricular thrombus with severe chronic obstructive pulmonary disease
Journal of Cardiology and Cardiovascular Surgery 2023;1:14-15
[7] Gur H., Keren G., Levo Y
Right ventricular thrombus and pulmonary emboli in a patient with emphysema. An echocardiographic and doppler documentation
Clin Cardiol 1987;10:680-682
[8] Hosna AU., Miller D., Makhoul K., Noff N
SA case of chronic pulmonary embolism resulting in pulmonary hypertension and decompensated right heart failure
CUREUS 2022;14:e32771
doi 10.7759/cureus 32771
[9] Wang C., Du M., Cao D
A pathological study of in situ thrombosis of small pulmonary arteries and arterioles in autopsy cases pf chronic cor pulmonale
Zhaonghua Yi Xue Za Zhi 1997;77:123-125
Article in Chines: Abstract in English
[10] Russo A., De Uca M., Vigna C et al
Central pulmonary artery lesions in chronic obstructive pulmonary disease
CIRCULATION 1999;100: 1808-1815
The data was evaluated by the authors using Fine-Gray competing risk models, with C-19 linked deaths included as competing risks. In the text, they referred to this as "To account for the competing risk of death associated with COVID-19."
When examining the cardiovascular and thromboembolic effects of COVID-19, it is not appropriate to consider COVID-19 associated mortality as a competing risk. Furthermore, these consequences are the primary factors contributing to mortality in cases of C-19 infection.
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...
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 chest pain nor back pain.. The reverse transcriptase test for SARS-2 CoV-2 was positive. Computed tomography showed typical ground glass opacification in the lung fields, and, unexpectedly, also showed DAA[3].
Two other patients, aged 42 and 55, respectively, with proven COVID-19 infection , also experienced a pain-free presentation of DAA[4],[5].
Aortitis has also been reported as a complication of the administration of the BNT162b2 vaccine. In this instance aortitis occurred in association with vaccine-related pericarditis. Aortitis was complicated by the subsequent development of fatal DAA[6].
In their systematic review of the association of COVID-19 and DAA, Ramandi et al commented that the level of Van Willebrand Factor appeared to show an increase in COVID-19-infected patients. They postulated that this was indicative of extensive endothelial activation[7].
These observations raise the question"Is COVID-19 the new atherosclerosis?"[8]. This question was posed in the context of yet another report of the association of COVID-19 and DAA[8].
If it were the case that both COVID-19 and vaccination could be risk factors for aortitis and, hence, aortic dissection, there is a potential for a huge upsurge in DAA prevalence and incidence following the COVID-19 pandemic. This upsurge could be monitored by evaluating the prevalence of aortitis in patience with long COVID, the latter presumably a disorder in which there is a continuous background of COVID-19-related activity arguably involving varying degrees of proinflammatory cytokine activity. Imaging studies for identification of aortitis could go hand in hand with evaluation of Von Willebrand Factor. Those strategies for quantifying background prevalence of COVID-19-related aortitis might give some indication of whether or not previous COVID-19 infection is a substantial risk factor for DAA.
I have no conflict of interest
References
[1] Hamilton BCS and Eagle KA
Winning the battle but losing the war: increased population-based mortality from aortic dissection
Heart 2023;doi:10.1136/heartjnl-2023-323302
[2]Shergill S., Davies J., Bloomfield J
Florid aortitis following SARS-CoV-2 infection
Eur Heart J 2020;41:4286
[3]Jariwala P., Kambie R., Sridhar S., Mishra KC., Jadhav KP
A fatal association of COVID-19 and acute complicated Type B aortic dissection
Interventional management in a difficult situation
IHJ Cardiovascular Case Reports 2021;5:94-97
[4] Alrjoob M., Alkhatib A., Khan AM et al
COVID-19 It's not over yet:A case of COVID-19-induced aortitis complicated by aortic dissection
CHEST 2023
DOI.org/10.1016/j.chest.2023.07.232
[5]Gebril A., Nawaz A., Ashour S., Nasr MK., Eebelihy OE
Silent Type B aortic dissection accidentally discovered in a COVID-19-positive patient
CUREUS 2023;15:e41373 DOI:10.7759/cureus.41373
[6]Takahashi M., Kondo T., Yamasaki G et al
An autopsy case report of aortic dissection complicated with histiolymphocytic pericarditis and aortic inflammation after m RNA Covid-19 vaccination
Legal Medicine 2022;59:102154
[7] Ramandi A., Akbarzadeh M., Khaheshi I., Khalilian MR
Aortic dissection and COVID-19: A comprehensive systematic review
Curr Probl Cardiol 2023;48:101129
[8] Vergopoulos S., Evalgeliou A., Boulmpou A et al
Acute aortic dissection Type A in the early period after COVID-19 infection
HSOA Journal of Angiology & Vascular Surgery 2022;7:085
DOI:10.24966/AVS-7397/100085
[9] Ahamed J., Laurence J
Long covid endotheliopathy: hypthesized mechanisms and potential therapeutic approaches
J Clin Invest 2022;132;e161167
doi;10.1172/JCI161167
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...
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 CP patients evaluated by Oreto et al, nine(20.9%) had LVEF < 40%. . Brain Natriuretic Peptide levels(inter quatrile range) ranged from 114 pg/ml-782 pg/ml[5]. Among 140 CP patients evaluated by Porta-Sanchez et al, twenty eight(20%) had LVEF less than or equal to 50%. There was no documentation of concomitant BNP values[6]. Among 97% CP patients evaluated by Busch et al , three(3.1%) had LVEF < 30%, twenty-three (23.7%) had LVEF 31%-55%, and seventy-one(72.2%) had LVEF > 56%. There was no documentation of concomitant BNP data[7]. When 6 CP patients , each with LVEF amounting to 60%, were compared with 5 patients with restrictive cardiomyopathy(RCMP), in whom LVEF amounted to 30%, 40%, 55%, 60% and 60%, respectively, BNP ranged from 50 pg/ml to 186 pg/ml in the CP subgroup versus 639 pg/ml to 1,060 pg/ml in the RCMP subgroup[8]. All patients, both in the CP subgroup and in the RCMP subgroup, were in New York Heart Association functional class III or IV[8]. Accordingly, the differential diagnosis of the association of symptomatic CHF and normal or only marginally elevated BNP levels should include, not only heart failure with preserved ejection fraction, even in the absence of a specific diagnosis of RCMP, as was the case in 46 subjects with clinically overt CHF who were characterised by pulmonary capillary wedge pressure > 15 mm Hg,[9], but, also, CP[8].
In conclusion, given the considerable overlap in clinical features and in BNP levels between the subgroups of CHF patients evaluated by Fritz et al[1] and the subgoups of patients I have enumerated[5-9], a mediation analysis can only be complete if the evaluation also includes CP patients with LVEF ranging from <40% to > 50%, and the corresponding range of BNP values. A comprehensive and detailed evaluation along those lines has not yet been done although it is long overdue, given the fact that CP , when diagnosed early, is an eminently reversible underlying cause of CHF[4].
I have no conflict of interest
References
[1] Fritz J., Belovari K., Ulmer H et al
Aetiology, ejection fraction, and mortality in chronic heart failure: a mediation analysis
Heart E pub ahead of print
DOI:10.1136/heartjnl-2023-322803
[2]Saiki H., Petersen IA., Scott CG et al
Risk of heart failure with preserved ejection fraction in older women after contemporary radiotherapy for breast caner
Circulation 2017;135:1388-1396
[3] Jolobe, OMP
High-risk and low prevalence disease: Cardiac sarcoidosis and some of its mimics
IJC Heart & Vasculature 2023;47:101221
doi.org/10.1016/j.ijcha.2023.101221
[4]Syed FF., Schaff HV., Oh JK
Constrictive pericarditis: a curable diastolic heart failure
Nat Rev Cardiol 20114;11:530-544
[5] Oreto L., Mayer A., Todaro MC et al
Contemporary clinical spectrum of constrictive pericarditis: a 10 year experience
International Journal of Cardiology 2013;163:339-341
[6] Porta-Sanchez A., Sagrista-Sauleda J., Ferreira-Gonzalez I et al
Constrictive pericarditis. Etiologic spectrum, patterns of clinical presentation, prognostic factors, and long-term follow up
Rev Esp Cardiol 2015;68:1092-1100
[7] Busch C., Penov K., Amorim PA et al
Risk factors for mortality after pericardiectomy for chronic constrictive pericarditis in a large single-centre cohort
European Journal of Cardio-Thoracic Surgery 2015;48:e110-e116
[8]Leya FS., Arab D., Joyal D et al
The efficacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy
JACC 2005;45:1900-1902.
[9]Anjan VY., Loftus TH., Burke MA et al
Prevalence, clinical phenotype, and outcomes associated with normal B type natriuretic peptide levels in heart failure with preserved ejection fraction
Am J Cardiol 2012;110:870-875
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...
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 attributable to intracardiac devices such as permanent pacemekers and implantable cardioverter defibrillators. The diagnosis of device-related IE comes to mind most readily when the patient has concurrent inflammatory signs of of infection of the device pocket[5]. Regardless of presence or absence of signs of device pocket infection , however, the presence of endogenous endophthalmitis should, also, raise the index of suspicion for device -related IE, especially when stigmata of septic pulmonary embolism are also present[6]. In the latter example, where no mention was made of the appearance of the device pocket, TOE showed a 20 mm mobile vegetation attached to the right atrial lead[6]. The association of endophthalmitis, pulmonary consolidation(with or without cavitation) , and hypotension(the latter attributable to systemic sepsis), is a "triad" that should raise the index of suspicion for device-related IE[7].
Echocardiography expedites the workup of suspected intracardiac device-related IE. TOE has greater sensitivity than TTE for identifying vegetations on the leads and for identifying vegetations on the heart valves. Accordingly, TOE can be offered as the first echocardiographic test if clinical suspicion is sufficiently high[8]. Nuclear imaging, using 18 Fluoro Deoxy Glucose positron emission tomography computed tomography is highly specific for lead endocarditis given the fact that, unlike TOE, it can also distinguish between infected thrombi and uninfected thrombi attached to the leads[8]. Sensitivity is however, suboptimal, given the the negative results believed to be attributable to previous antibiotic therapy or attributable to vegetation size being lower than the spatial resolution of nuclear imaging[9].
A comprehensive account of best practice in the work up of suspected device-related IE was made by Dilsizian et al[8].
I have no conflict of interest.
References
[1]Ng JY., Zarook E., Nicholson L et al
Eyes and the heart: what a clinician should know
Heart 2023
Epub ahead of print
DOI 10.1136/heartjnl-2022-322081
[2]Carmelli G., Surles T., Brown A
Endophthalmitis and myocotic aneurysm: The only clues to underlying endocarditis
Clin Pract Cases Emerg Med 2018 https://doi.org/10.5811/cpcem.2017.8.34723
[3]Sim YR., Lee YJ., Park SW et al
Infective endocarditis presenting as endogenous endophthalmitis secondary to streptococcus agalactiae in a healthy adult
CSE Rep Literat Rev Infect Chemother 2017;49:286-292
[4]Nakata M., Mashidori T., Higa N et al
Infective endocarditis with no underlying disease for which bacterial endophthalmitis have been first symptom
Intern Med 2020;59:2061-2065
[5]Looser PM., Saleh L., Thomas G., Cheung JW
Systemic infection due to subcutaneous implantable cardioverter defibrillator implantation: Importance of early recognition and treatment of device pocket related complications
Heart Rhythm Case Reports 2017;3:40-42
[6] Patel N., McDonald ML., Bradford NS et al
AngioVac debulking in endocarditis patients with large, device-related vegetations
The Journal of Innovations in Cardiac Rhythm Management 2018;9:3291-3296
[7]Sarvat B., Sarria JC
Implantable cardioverter-defibrillator infection due to Scetosporium apiospermum
Journal of Infection 2007;55:e109-e113
[8]Dilsizian V., Budde RPJ., Chen W et al
Best practice for imaging cardiac device-related infections and endocarditis
A JACC Cardiovascular imaging expert panel statement
JACC Cardiovascular Imaging 2022;15:891-911
[9]Cautela J., Alessandrini S., Carmmiller S et al
Diagnostic yield of FDG positron emission tomography/computed tomography in patients with CEID infection: a pilot study
Europace 2013;15:252-257
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...
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 and patient about the goals of treatment. The patient should be told that achievable treatment goals include mitigation of risk of hypertension-related AF and, hence, AF-related stroke, and mitigation of risk of hypertension-related CHF. The doctor can then proceed to spell out their role, which consists of checking the "office" BP and instigating regular ambulatory blood pressure measurements, as well as titrating antihypertensive medication on the basis of all the available blood pressure readings, including home blood pressure readings. The role of the patient is to do home blood pressure checks, to comply with medication and to adhere to a lifestyle which is compliant with good BP control.
That might well be the most cost-effective strategy for hypertension control.
I have no funding and no conflict of interest
References
[1] Bellows BK., Kazi DS
Ultralow-dose quadruple combination therapy. A cost effective solution for hypertension control
HEART doi.org/10.1136/heartjnl-2023-323007
[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., Rocco M., Lewis CE et al
Effect of intensive blood pressure treatment on heart failure events in the systolic blood pressure reduction intervention trial
Circ Heart Faul 2017 doi.:10.1161/CIRCHEARTFAILURE.116.003613
[4] Jolobe OMP
Regular exercise as an adjunct to antihypertensive therapy
American Journal of Emergency Medicine 2019;37:530-531
[5] Tse Y-H., Tuet C-Y., Lau K-K., Tse H-F
Dietary modification for prevention and control of high blood pressure
Postgrad Med J 2023 doi.org/10.1093postmjqgad021
[6] Li C., Zhu Y., Ma Y et al
Association of cumulative blood pressure with cognitive decline, dementia, and mortality
JACC 2022;79:1321-1335
[7] Johnson KC., Whelton PK., Cushman WC et al
Blood pressure measurement in SPRINT(systolic blood pressure intervention trial)
HYPERTENSION 2018;71:848-857
[8] Cheung AK., Whelton PK., Muntner P et al
International consensus on standardized cliic blood pressure measurement-a call to action
Am J Med drg/10/1016/j.amje,d.2022.12.015
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...
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 (< 9 g/dL), the adjusted odds ratios (95% CIs) of moderate and severe anaemia against no anaemia for in-hospital mortality were 1.38 (1.10-1.73) and 3.39 (2.59-4.44), respectively. Severity of anaemia may be a key factor to assess the in-hospital mortality. Severity of anaemia in patients with ACS would contribute to the increased risk of mortality, and controlling anaemia might relate to subsequent prognosis, which should be examined by interventional studies (5).
References
1. Graham FJ, Friday JM, Pellicori P, et al. Assessment of haemoglobin and serum markers of iron deficiency in people with cardiovascular disease. Heart 2023;109(17):1294-1301.
2. Mahendiran T, Nanchen D, Gencer B, et al. Prognosis of patients with chronic and hospital-acquired anaemia after acute coronary syndromes. J Cardiovasc Transl Res 2020;13(4):618-628.
3. Colombo C, Rebora P, Montalto C, et al. Hospital-acquired anemia in patients with acute coronary syndromes: epidemiology and potential impact on long-term outcome. Am J Med. 2023 Sep 11. doi: 10.1016/j.amjmed.2023.08.012. [Epub ahead of print]
4. Salisbury AC, Amin AP, Reid KJ, et al. Hospital-acquired anemia and in-hospital mortality in patients with acute myocardial infarction. Am Heart J 2011;162(2):300-309.e3.
5. Kang SH, Moon JY, Kim SH, et al. Association of hemoglobin levels with clinical outcomes in acute coronary syndromes in Koreans. Medicine (Baltimore). 2022;101(52):e32579.
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the association of type 1 diabetes and fulminant viral , the latter characterised by ST segment elevation, serum troponin elevation and severe left ventricular systolic dysfunction giving rise to cardiogenic pulmonary oedema[3]. In the latter example parainfluenza-3 was believed to be the underlying cause of both the diabetic decompensation and the severe left ventricular systolic dysfunction[3]. A viral aetiology was also suspected but not serologically proven in a 47 year old patient who experienced a prodrome of fever, vomiting, and diahrroea before she was admitted with severe DKA and pain-free ST segment elevation associted with serum troponin elevation but no angiographically demonstrable coronary occlusion. Endomyocardial biopsy showed a mild accumulation of mononuclear cells in the myocardial interstitium[4].
Diabetic ketoacidosis can also be complicated by the occurrence of pain-free Takotsubo myocarditis with STEMI-like presentation[5][6]]. In both cases coronary angiography did not reveal any coronary occlusion.
The differential diagnosis of pain-free DKA-related STEMI extends to the association of DKA-related hyperkalaemia and ST segment elevation[7],[8]. Only one of the two patients had a raised serum troponin[8]. Both patients had total absence of coronary artery occlusion on coronary angiography. In another severely hyperkalaemic patient(serum potassium 9.0 mmol/l) the ST segment elevation had a Brugada syndrome configuration. Serum troponin peaked at 20.452 mcg/L but no occlusive lesion was documented on coronary angiography[9].
DKA-related ST segment elevation can also occur in patients who are normokalaemic, and have normal serum troponin and no abnormality on coronary angiography[10]. Euglycaemic DKA was the associated feature in the latter patient[10].
Comment
Patients with unrecognised Type 1 STEMI complicated by decompensated CHF incur the double jeopardy of “missing out on coronary reperfusion therapy and also run the risk of inappropriate administration of large volumes of intravenous fluids for the management of DKA-related metabolic decompensation.
DKA patients with hyperkalaemia related ST elevation and serum troponin elevation run the risk of mistaken diagnosis of type 2 acute myocardial infarction
Clinicians must be vigilant for both types of eventualities in DKA patients presenting with pain-free ST segment elevation
I have no funding and no conflict of interest
References
[1]Kumar A., Sanghera A., Sanghera B et al
Chest pain symptoms during myocardial infarction in patients with and without diabetes: a systematic review and meta-analysis
Heart doi. 10.1136/heartjnl-2022-322289
[2]Baral N., Montalbano A., KhanA., Qureshi M., Luitel P
Silent myocardial infarction and acute multiorgan failure in a COVID-19 patient: A case report
J Nepal Med Assoc 2021;59:1048-1051
[3]Ohara N., Kaneko M., Kuwano H et al
Fulminant Type 1 diabetes mellitus and fulminant viral myocarditis: A case report and literature review
Int Heart J 2015;56:239-244
[4]Hiramatsu S., Komori K., Mori E et al
A case of fulminant type 1 diabetes mellitus accompoanied by myocarditis
Endocrine Journal 2011;58:553-557
[5]Patel KKHP., Soe HM
Association of diabetic ketoacidosis with Takotsubo cardiomyopathy
CHEST doi:https://doi.org/10.1016/chest.2020.08.283
[6] Gordon A., LaCapra G., Roberti R
DKA-induced Takotsubo cardiomyopathy in patient with known HOCM
Case Reports in Critical Care 2017 doi.org/10.1155/2017/4287125
[7]Ziakas A., Basangiannis C., Stiliadis I
Pseudoinfarction pattern in a patient with hyperkalaemia, diabetic ketoacidosis and normal coronary vessels: a case report
Journal of Medical Case Reports 2020;4:115
[8]Sharma E., Dagal S., Sharma P., Ghimire DKC., Dahal S
A case of pseudo infarction pattern in diabetic ketoacidosis
A diagnostic and therapeutic dilemma
Cardiol Res 2018;9:250-252
[9] Pfirman KS., Donley CJ., Fryman EB., Champaneria SU., Gatewood WT
Brugada pattern manifesting during hyperkalaemia, diabetic ketoacidosis, and acute alcohol intoxication
American Journal of Case Reports 2021;22;e932048
[10]Jay DR., Henry TD., Sharkey SW
Acute inferior myocardial infarction or Not?
JAMA Internal Medicine 2022;182:224-225
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.
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].
Show MoreCraver 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...
In view of the fact that the association of pulmonary embolism (PE) and chronic obstructive pulmonary disease (COPD) is one fraught with the risk of PE recurrence, and fatal outcome, respectively [1], the association of the two disorders is one that should have merited some mention in the review of heightened long term cardiovascular risk after exacerbations of COPD [2], notwithstanding the uncertainty about the true prevalence of PE in patients with COPD [3],[4] . The uncertainty about PE prevalence in COPD is, arguably, in part, attributable to the fact that some COPD patients have coexisting carcinomatosis as a risk factor for PE in its own right [3]. In a systematic review and meta-analysis published in 2009, Rizkallah et al documented a PE prevalence amounting to 19.9%(95% Confidence Interval 6.7% to 33%) among patients with acute exacerbations of COPD[4]. Anecdotal reports also document the association of right heart thrombi (one of the stigmata of pulmonary thromboembolism) and COPD [5-8].
Show MoreOver and above its association with PE, COPD also appears to be a risk factor for the occurrence of "in situ" thrombosis in the pulmonary arterial vasculature [9],[10], a development which is a long term risk factor for right heart failure.
Arguably, in view of the prothrombotic environment generated by acute exacerbations of COPD, and the fact that atrial fibrillation might be prevalent in approximately 15% of COPD patients [2], there might b...
The data was evaluated by the authors using Fine-Gray competing risk models, with C-19 linked deaths included as competing risks. In the text, they referred to this as "To account for the competing risk of death associated with COVID-19."
When examining the cardiovascular and thromboembolic effects of COVID-19, it is not appropriate to consider COVID-19 associated mortality as a competing risk. Furthermore, these consequences are the primary factors contributing to mortality in cases of C-19 infection.
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.
Show MoreThe 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...
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].
Show MoreThe 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...
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...
Show MoreIt 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].
Show MoreAttainment 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...
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...
Show MoreOver and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
Show MoreIn the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
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.
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