In the context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Criteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identi...
In the context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Criteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identified a low number of acid and alcohol fast bacilli[4].
A fatal outcome was documented in a patient in whom diagnostic ambiguity could only be resolved by recourse to the nested polymerase chain reaction(PCR) method. This was a patient previously in good health, who died suddenly. Autopsy disclosed nodules in the myocardium, lymph nodes, and spleen. Histological examination of the myocardium showed granulomas, epithelial cells, and lymphocytes immersed in fibrous tissue. No acid fast bacilli were seen. However, nested PCR was positive for Mycobacterium avium in samples of the myocardium, liver, spleen, right lung, and kidney[5].
A fatal outcome was also documented in a patient who had presented with severe biventricular heart failure characterised by an echocardiogram which showed biventricular dysfunction. Furthermore the right ventricle was almost akinetic. Computed tomography showed asymmetrical hilar lymphadenoipathy. Endobronchial aspiration demonstrated non-caseating granulomatous inflammation that was negative for acid-fast bacilli. Given a differential diagnosis that included both cardiac sarcoidosis and tuberculous myocarditis, and also in view of rapid clinical deterioration in spite of optimised treatment for congestive heart failure, the clinicians opted for empirical concurrent high dose corticosteroid therapy and antituberculous chemotherapy. In spite of these measures the patient subsequently died. Autopsy showed almost complete replacement of the right ventricular myocardium by scar tissue and patchy fibrosis of the left ventricle. Histology showed giant cell invasion of the cardiac myocytes. Ziehl-nielsen stain for mycobacterium of the hilar lymph nodes was positive[6].
I have no conflict of interest
References
[1]Sohn D-W., Park J-B
Cardiac sarcoidosis
Heart doi.10.1136/heartjnl-2022-321379
[2]Sundaraila S., Sulaiman A., Rajendran A
Cardiac tuberculosis on 18F-FDG PET imaging-A great masquerader of cardiac sarcoidosis
Indian J Radiol Imaging 2021;31:1002-1007
[3]Srikala J., Subramanyam PB., Rao BH
Granulomatous myocarditis: cardiac MRI and PET CT findings
Indian Journal of Ckinical Cardiology 2022;3:213-214
[4[] Khurana R., Shalhoub J., Verma A et al
Tubercular myocarditis presenting with ventricular tachycardia
Nature Clinical Practice Cardiovascular Medicine ;5:169-174
[5]Silingardi E., Rivasci F., Santanione AL., Garagnani L
Sudden death from tubercular myocarditis
J Foresnsic Sci 2006;51:667-669
[6]Cowley A., Dobson L., Kurian J., Saunderson C
Acute myocarditis secondary to tuberculosis : a case report
Echo Research and Practice
ID:17-0024;September 2017
DOI:10.1530/ERP-17-0024
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
The occasional, and unforeseen occurrence of drug-related interstitial nephritis is, arguably, an important justification for sequencing the initiation of drug treatment for congestive heart failure or for hypertension.
Given the fact that interstitial nephritis has been reported after medication with captopril[1], losartan[2], valsartan[3], and empagliflozin[4],[5],, respectively, the challenge of identifying the culprit medication is made much easier if drugs belonging to those subclasses are introduced sequentially. Two examples justify that approach:-
In one hypertensive patient empagliflozin had been prescribed as an add-on therapy to long-standing medication with losartan, bisoprolol, amlodipine, sitagliptin, and aspirin. Pre empagliflozin serum creatinine was 0.9 mg/dl. Post empgliflozin serum creatinine peaked at 9.22 mg/dl. Renal biopsy showed stigmata of acute interstitial nephritis. Empagliflozin was discontinued, and the patient was managed with haemodialysis and corticosteroid therapy. She improved and was eventually weaned off haemodialysis[4].
The second example was a hypertensive patient who had been taking enalapril, dilriazem, and atoravastatin for more than 2 years. Pre-empagliflozin serum creatinine was 60 mcmol/l. After empagliflozin was initiated as add-on therapy serum creatnine increased to 381 mcmol/l. Renal biopsy showed stigmata of acute interstitial nephritis. Renal function improved after withdrawal of empagliflozi...
The occasional, and unforeseen occurrence of drug-related interstitial nephritis is, arguably, an important justification for sequencing the initiation of drug treatment for congestive heart failure or for hypertension.
Given the fact that interstitial nephritis has been reported after medication with captopril[1], losartan[2], valsartan[3], and empagliflozin[4],[5],, respectively, the challenge of identifying the culprit medication is made much easier if drugs belonging to those subclasses are introduced sequentially. Two examples justify that approach:-
In one hypertensive patient empagliflozin had been prescribed as an add-on therapy to long-standing medication with losartan, bisoprolol, amlodipine, sitagliptin, and aspirin. Pre empagliflozin serum creatinine was 0.9 mg/dl. Post empgliflozin serum creatinine peaked at 9.22 mg/dl. Renal biopsy showed stigmata of acute interstitial nephritis. Empagliflozin was discontinued, and the patient was managed with haemodialysis and corticosteroid therapy. She improved and was eventually weaned off haemodialysis[4].
The second example was a hypertensive patient who had been taking enalapril, dilriazem, and atoravastatin for more than 2 years. Pre-empagliflozin serum creatinine was 60 mcmol/l. After empagliflozin was initiated as add-on therapy serum creatnine increased to 381 mcmol/l. Renal biopsy showed stigmata of acute interstitial nephritis. Renal function improved after withdrawal of empagliflozin and initiation of corticosteroid therapy[5].
Comment
In both cases[4],[5] the culprit medication was more easily identifiable because medications belonging to subclasses that were potential candidates for the role of causative agents for interstitial nephritis, namely, losartan[4] and enalapril[5] , respectively, were already in place by the time empagliflozin was introduced.
I have no conflict of interest
References
[1]Smith WR., Neill J., Cushman WC., Butkus DE
Captopril-associated acute interstitial nephritis
Am J Nephrol 1989;9:230-235
[2]Weinert LS., Triches CB., Laitao B et al
Losartan-induced acute interstitial nephritis
REV HCPA 2007;27:61-64
[3]Chen T., Xu P-c., Hu S-y et al
Severe acute interstitial nephritis induced by valsartan A case report
Medicine 2019;98;6
[4] Bnaya A., Itzkowitz E., Atrash J., Abu-Alfeilat M., Shavit L
Acute interstitial nephritis related to SGLT-2 inhibitor
Postgrad Med J 2022;98:740-741
[5] Ryan R., Choo S., Willows J et al
Acute interstitial nephritis due to sodium-glucose-co-transporter 2 inhibitor empagliflozin
Clinical Kidney Journal 2021;14:1020-1022
The valvulopathy of autoimmune disorders can simulate infective endocarditis when echocardiography discloses the presence of vegetations on the heart valves[1-4].
This occurrence was exemplified by valvulitis with vegetations and concurrent congestive heart failure(CHF) as the initial presentation of systemic lupus erythematosus[2]. Blood cultures were sterile.The patient was managed medically with corticosteroid therapy[2].
In granulomatosis with polyangiitis valvulopathy was exemplified by a patient who presented with pyrexia, dyspnoea, renal failure, and dry gangrene of the toes. Echocardiography revealed a mobile, 7-10 mm vegetation on the chordae of the tricuspid valve. Antineutrophilic cytoplasmic antibodies against proteinase 3 (PR3-ANCA) were strongly positive(194 EU/mL; Reference Range < 1.99). Renal biopsy showed crescentric glomerulonephritis. Blood cultures were sterile. The patient was successfully managed solely with immunosuppressive therapy[3].
The valvulopathy of eosinophilic granulomatosis with polyangiitis was exemplified by a patient who presented with breathlessness and polyarthralgia superimposed on a long history of eosninophilia, asthma, allergic rhinitis, and sinusitis. Clinical examination disclosed the presence of systolic murmurs and signs of CHF. Echocardiography revealed a 19 mm x 16 mm vegetation on the aortic valve and a 11 mm x 9 mm vegetation on the mitral valve in association with moderate to severe m...
The valvulopathy of autoimmune disorders can simulate infective endocarditis when echocardiography discloses the presence of vegetations on the heart valves[1-4].
This occurrence was exemplified by valvulitis with vegetations and concurrent congestive heart failure(CHF) as the initial presentation of systemic lupus erythematosus[2]. Blood cultures were sterile.The patient was managed medically with corticosteroid therapy[2].
In granulomatosis with polyangiitis valvulopathy was exemplified by a patient who presented with pyrexia, dyspnoea, renal failure, and dry gangrene of the toes. Echocardiography revealed a mobile, 7-10 mm vegetation on the chordae of the tricuspid valve. Antineutrophilic cytoplasmic antibodies against proteinase 3 (PR3-ANCA) were strongly positive(194 EU/mL; Reference Range < 1.99). Renal biopsy showed crescentric glomerulonephritis. Blood cultures were sterile. The patient was successfully managed solely with immunosuppressive therapy[3].
The valvulopathy of eosinophilic granulomatosis with polyangiitis was exemplified by a patient who presented with breathlessness and polyarthralgia superimposed on a long history of eosninophilia, asthma, allergic rhinitis, and sinusitis. Clinical examination disclosed the presence of systolic murmurs and signs of CHF. Echocardiography revealed a 19 mm x 16 mm vegetation on the aortic valve and a 11 mm x 9 mm vegetation on the mitral valve in association with moderate to severe mitral regurgitation. Blood cultures were sterile. The patient was managed by mitral and aortic valve replacement. Ten months after discharge the patient was readmitted with severe CHF from which the patient died.
I have no conflict of interest
References
[1]Gartshteyn Y., Bhave N., Joseph MS., Askenase A
Inflammatory and thrombotic valvulopathies in autoimmune disease
Heart doi 10.1136/heartjnl 2021-319603
[2]Louthernoo W., Kanjanavanit R., Sukitawut W
Acute aortic valvulitis as an initial presentation of systemic lupus erythematosus
Asian Pacific Journal of Allergy and Immunology 1999;17:121-124
[3[ Varnier G., Schire N., Christov G., Eleftheriou D., Brogan PA
Granulomatosis with polyangiitis mimicking infective endocarditis
Clin Rheumatol 2016;35:2369-2372
[4] Karthikeyan K., Balla S., SAlpert MA
Non infectious aortic and mitral vegetations in a patient with eosinophilic granulomatosis with polyangiitis
BMJ case Reporst 2019;12:e225947
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
Intra-articular corticosteroid injections were notably absent from the list of invasive procedures which were evaluated for temporal association with infective endocarditis. Although the randomised trial that involved use of intra-articular corticosteroids painted a favourable benefit/risk profile in the comparison between intra-articular steroids plus best current advice(BCT)(66 subjects with hip osteoarthritis) versus intraarticuar lidocaine plus BCT(66 subjects also with hip osteoarthritis) , "one event was considered possibly related to trial treatment"[1]. This event was a fatal episode of infective endocarditis in a patient who had a bioprosthetic aortic valve antedating the intra-articular corticosteroid injection[1].
Previous post traumatic splenectomy was the risk factor in a 60 year old woman who developed infective endocarditis 2 weeks after she received intra-articular corticosteroids for shoulder pain[2].
In a study which involved 6066 patients of mean age 66.8 who received intraarticular facet joint corticosteroid injections one patient developed infective endocarditis with fatal, outcome. This was a patient with previous mitral valve replacement surgery and a previous episode of infective endocarditis[3].
A congenital heart defect was the risk factor in a 38 year old woman who developed tricuspid valve infective endocarditis after lumbar spine corticosteroid injection[4].
Concurrent immunosuppressive treatment for...
Intra-articular corticosteroid injections were notably absent from the list of invasive procedures which were evaluated for temporal association with infective endocarditis. Although the randomised trial that involved use of intra-articular corticosteroids painted a favourable benefit/risk profile in the comparison between intra-articular steroids plus best current advice(BCT)(66 subjects with hip osteoarthritis) versus intraarticuar lidocaine plus BCT(66 subjects also with hip osteoarthritis) , "one event was considered possibly related to trial treatment"[1]. This event was a fatal episode of infective endocarditis in a patient who had a bioprosthetic aortic valve antedating the intra-articular corticosteroid injection[1].
Previous post traumatic splenectomy was the risk factor in a 60 year old woman who developed infective endocarditis 2 weeks after she received intra-articular corticosteroids for shoulder pain[2].
In a study which involved 6066 patients of mean age 66.8 who received intraarticular facet joint corticosteroid injections one patient developed infective endocarditis with fatal, outcome. This was a patient with previous mitral valve replacement surgery and a previous episode of infective endocarditis[3].
A congenital heart defect was the risk factor in a 38 year old woman who developed tricuspid valve infective endocarditis after lumbar spine corticosteroid injection[4].
Concurrent immunosuppressive treatment for Hepatitis C virus was the risk factor in a 59 year old woman who developed infective endocarditis after corticosteroid sacroiliac joint injection for low back pain[5].
There was no obvious risk factor in a 68 year old man who developed infective endocarditis(with florid mucocutaneous stigmata) after facet joint corticosteroid injection[6].
None of these patients were reported to have received prophylactic antibiotics.
]I have no conflict of interest
References
[1] Paskins Z., Bromley K., Lewis M et al
Clinical effetiveness of one ultrasound guided intraarticular corticosteroid and local anaesthetic injection in addition to advice and education for hip osteoarthritis(HIT trial): single blind, parallel group, three arm, randomised controlled trial
BMJ 2022;377:e068446 doi.org/10.1136/bmj;2021-068446
(2) Medani S., O'Callaghan P
Rare manifestations of infective endocarditis ;the long known, never to be forgotten diagnosis
BMJ Case Reports doi;10.1136/bcr-2015-211276[3]Kim
[3]]Kim BR., Lee JW., Lee E., et al
Intra-articular facet joint steroid injection-related adverse events encounbtered during 11,980 procedures
European Rafiology 2020;30:1507-1516
[4] Al-Khalaila ON., Tbishat LF., Abdelghani MS et al
Native tricuspid valve infective endocarditis with Staphylococcus ligdenesis An unusual complication post spinal epidural injection Case report and literature reiew
IDCases 2021;24:eo1o97
[5]Nagpal G., Flaherty JP., Benzon HT
Diskitis, osteomyelitis, spinal epidural absecess, meningitis and endocarditis following sacroliliac joint injection for the treatment of low-back pain in a patient on therapy for hepatitis C virus
Regional anesthesia and Pain Medicine 2017;42:517-520
[6] Hoelzer BC., Weingarten TN., Hooten WM et al
Parasinal abscess complicated by endocarditis following a facet joint injection
European Journal of Pain 2008;12:261-265l
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.
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 context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Show MoreCriteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identi...
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...
The occasional, and unforeseen occurrence of drug-related interstitial nephritis is, arguably, an important justification for sequencing the initiation of drug treatment for congestive heart failure or for hypertension.
Show MoreGiven the fact that interstitial nephritis has been reported after medication with captopril[1], losartan[2], valsartan[3], and empagliflozin[4],[5],, respectively, the challenge of identifying the culprit medication is made much easier if drugs belonging to those subclasses are introduced sequentially. Two examples justify that approach:-
In one hypertensive patient empagliflozin had been prescribed as an add-on therapy to long-standing medication with losartan, bisoprolol, amlodipine, sitagliptin, and aspirin. Pre empagliflozin serum creatinine was 0.9 mg/dl. Post empgliflozin serum creatinine peaked at 9.22 mg/dl. Renal biopsy showed stigmata of acute interstitial nephritis. Empagliflozin was discontinued, and the patient was managed with haemodialysis and corticosteroid therapy. She improved and was eventually weaned off haemodialysis[4].
The second example was a hypertensive patient who had been taking enalapril, dilriazem, and atoravastatin for more than 2 years. Pre-empagliflozin serum creatinine was 60 mcmol/l. After empagliflozin was initiated as add-on therapy serum creatnine increased to 381 mcmol/l. Renal biopsy showed stigmata of acute interstitial nephritis. Renal function improved after withdrawal of empagliflozi...
The valvulopathy of autoimmune disorders can simulate infective endocarditis when echocardiography discloses the presence of vegetations on the heart valves[1-4].
Show MoreThis occurrence was exemplified by valvulitis with vegetations and concurrent congestive heart failure(CHF) as the initial presentation of systemic lupus erythematosus[2]. Blood cultures were sterile.The patient was managed medically with corticosteroid therapy[2].
In granulomatosis with polyangiitis valvulopathy was exemplified by a patient who presented with pyrexia, dyspnoea, renal failure, and dry gangrene of the toes. Echocardiography revealed a mobile, 7-10 mm vegetation on the chordae of the tricuspid valve. Antineutrophilic cytoplasmic antibodies against proteinase 3 (PR3-ANCA) were strongly positive(194 EU/mL; Reference Range < 1.99). Renal biopsy showed crescentric glomerulonephritis. Blood cultures were sterile. The patient was successfully managed solely with immunosuppressive therapy[3].
The valvulopathy of eosinophilic granulomatosis with polyangiitis was exemplified by a patient who presented with breathlessness and polyarthralgia superimposed on a long history of eosninophilia, asthma, allergic rhinitis, and sinusitis. Clinical examination disclosed the presence of systolic murmurs and signs of CHF. Echocardiography revealed a 19 mm x 16 mm vegetation on the aortic valve and a 11 mm x 9 mm vegetation on the mitral valve in association with moderate to severe m...
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...
Intra-articular corticosteroid injections were notably absent from the list of invasive procedures which were evaluated for temporal association with infective endocarditis. Although the randomised trial that involved use of intra-articular corticosteroids painted a favourable benefit/risk profile in the comparison between intra-articular steroids plus best current advice(BCT)(66 subjects with hip osteoarthritis) versus intraarticuar lidocaine plus BCT(66 subjects also with hip osteoarthritis) , "one event was considered possibly related to trial treatment"[1]. This event was a fatal episode of infective endocarditis in a patient who had a bioprosthetic aortic valve antedating the intra-articular corticosteroid injection[1].
Show MorePrevious post traumatic splenectomy was the risk factor in a 60 year old woman who developed infective endocarditis 2 weeks after she received intra-articular corticosteroids for shoulder pain[2].
In a study which involved 6066 patients of mean age 66.8 who received intraarticular facet joint corticosteroid injections one patient developed infective endocarditis with fatal, outcome. This was a patient with previous mitral valve replacement surgery and a previous episode of infective endocarditis[3].
A congenital heart defect was the risk factor in a 38 year old woman who developed tricuspid valve infective endocarditis after lumbar spine corticosteroid injection[4].
Concurrent immunosuppressive treatment for...
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,...
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
Show More1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic...
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