We read with great interest the editorial of Zhu et al (1). The authors have great theoretical knowledge and experience in the treatment of aortic valve regurgitation. We agree with their conclusion concerning personalised external aortic root support (PEARS) that “there are still many questions to be answered”. We would like to try to answer some of them.
Experience based on the first 100 operations in the Czech Republic (2) suggests that the indication for PEARS is limited to the patient with dilatation of the aortic root and/or ascending aorta and only trivial aortic regurgitation regardless of the origin of the disease. Implantation of PEARS should be considered as a preventive operation in group of patients that usually do not meet the criteria for valve sparing aortic valve replacement. In these patients the PEARS procedure can be performed as a measure to prevent further dilatation of the aorta and possible aortic dissection. The possibility of performing the operation without a cardiopulmonary bypass is certainly an advantage for the patient (2).
The authors worried about wall tension after implantation. It is generally known, that decrease of the diameter which is achieved by PEARS implantation, reduces wall tension according to the La Place law. This procedure in fact decreases wall tension and moreover the wall of the aorta is externally supported.
The fears about the viability of the aortic wall due to the continuous circumferential stress...
We read with great interest the editorial of Zhu et al (1). The authors have great theoretical knowledge and experience in the treatment of aortic valve regurgitation. We agree with their conclusion concerning personalised external aortic root support (PEARS) that “there are still many questions to be answered”. We would like to try to answer some of them.
Experience based on the first 100 operations in the Czech Republic (2) suggests that the indication for PEARS is limited to the patient with dilatation of the aortic root and/or ascending aorta and only trivial aortic regurgitation regardless of the origin of the disease. Implantation of PEARS should be considered as a preventive operation in group of patients that usually do not meet the criteria for valve sparing aortic valve replacement. In these patients the PEARS procedure can be performed as a measure to prevent further dilatation of the aorta and possible aortic dissection. The possibility of performing the operation without a cardiopulmonary bypass is certainly an advantage for the patient (2).
The authors worried about wall tension after implantation. It is generally known, that decrease of the diameter which is achieved by PEARS implantation, reduces wall tension according to the La Place law. This procedure in fact decreases wall tension and moreover the wall of the aorta is externally supported.
The fears about the viability of the aortic wall due to the continuous circumferential stress is not well-founded. The porous mesh does not affect the viability of the wall as we proved in our patient that had to be reoperated due to progression of aortic valve disease. The mesh was incorporated into the aortic wall without any signs of scar or necrosis. The same finding was by Pepper at al. (3).
It has been proved that after PEARS implantation there is no progression of aortic dilatation (4,5). This is also our experience with the first 100 patients in the Czech Republic. We found out that PEARS implantation prevented progression in dilatation of ascending aorta during follow-up of 18 months (1). As the longest surviving patient has PEARS implanted for more than 18 years without any progression of dilatation it can be postulated that the durability of this procedure would be excellent (6).
We are not sure if the authors understand well the surgical technique of implantation of the PEARS. The proper technique was published previously (7). In short, the mesh is sutured by several stitches to the aortic anulus that enables the fixation in a proper position. These stitches are not under any tension and therefore there is not any reason for pseudoaneurysm formation. The original seam of the mesh has to be sutured along the entire length by continuous suture
The same suture is performed from the main seam to both coronary ostia. In this way the entire aortic root and ascending aorta are wrapped with the mesh. There is no space between the edges of the seams and therefore no space for any dilatation or aneurysm formation.
We believe that PEARS implantation, if it is done with the proper technique and in a well indicated patient, is a very safe procedure with the potential for a stable long-term result.
Literature:
1. Zhu Y, Woo J. Has personalised surgery made another advancement in aortic root surgery? British Heart Journal. 2023.
2. Němec P, Pirk J, Skalský I, et al. Výsledky léčby externí podpory aortálního kořene a ascendentní aorty u prvních 100 pacientů v České republice. Cor Vasa 2022;64:579–583 https://e-coretvasa.cz/artkey/cor-202206-0002_outcomes-of-personalised-e...
3. Pepper J, Goddard M, Mohiaddin R, Treasure T. Histology of a Marfan aorta 4.5 years after personalized external aortic root support. Eur J Cardiothorac Surg 2015; 48:502–505
4. Van Hoof L, Rega F, Golesworthy T, et al. Treasure, Personalised external aortic root support for elective treatment of aortic root dilation in 200 patients, Heart 2021;107:1790–1795.
5. Izgi C, Newsome S, Alpendurada F, et al. External Aortic Root Support to Prevent Aortic Dilatation in Patients With Marfan Syndrome. J Am Coll Cardiol 2018;72:1095–1105
6. Treasure T, Austin C, Kenny LA, PepperJ. Personalized external aortic root support in aneurysm disease. Curr Opin Cardiol 2022:37(6):454-458
7. Nemec P, Kolarik M, Fila P. Personalized external aortic root support – how to implant it. Acta Chir Belg 2022;122:70–73
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
Liang et al. conducted a prospective study to predict major adverse cardiovascular events (MACE) in patients with hypertrophic cardiomyopathy (HCM) with special reference to molecular subtypes in HCM (1). Compared with the reference group with molecular subtype A, patients in molecular subtype D presented an increased risk of developing MACE, with the adjusted hazard ratio (HR) (95% CI) of 2.78 (1.18 to 6.55). I have comments about the study.
The authors understand the unstable estimation by multivariate analysis, which would be partly caused by the limited number of events. When conducting Cox regression analysis, they used sex, age, and two conventional cardiac biomarkers. As they classified molecular subtypes into four groups, a total of 7 independent variables were used for the analysis. There is a recommendation that the number of events per independent variable in Cox regression analysis are required ≥10 for prediction model (2,3). If the authors have concerned about the association between molecular subtypes in HCM and MACE events, strict criteria for the number of events can be relaxed (4). Although there is a description that the total number of events was 78 in Table 2, the number of patients with event was 66 in Table 3. I suppose that some patients had more than single event. I recommended to add MACE events by continuing follow-up to fulfill the statistical requirement.
When we see survival curve in Figure 2, remarkable difference in the risk of...
Liang et al. conducted a prospective study to predict major adverse cardiovascular events (MACE) in patients with hypertrophic cardiomyopathy (HCM) with special reference to molecular subtypes in HCM (1). Compared with the reference group with molecular subtype A, patients in molecular subtype D presented an increased risk of developing MACE, with the adjusted hazard ratio (HR) (95% CI) of 2.78 (1.18 to 6.55). I have comments about the study.
The authors understand the unstable estimation by multivariate analysis, which would be partly caused by the limited number of events. When conducting Cox regression analysis, they used sex, age, and two conventional cardiac biomarkers. As they classified molecular subtypes into four groups, a total of 7 independent variables were used for the analysis. There is a recommendation that the number of events per independent variable in Cox regression analysis are required ≥10 for prediction model (2,3). If the authors have concerned about the association between molecular subtypes in HCM and MACE events, strict criteria for the number of events can be relaxed (4). Although there is a description that the total number of events was 78 in Table 2, the number of patients with event was 66 in Table 3. I suppose that some patients had more than single event. I recommended to add MACE events by continuing follow-up to fulfill the statistical requirement.
When we see survival curve in Figure 2, remarkable difference in the risk of MACE event among subtypes was observed after 2 years. Are there any biological explanations for the accelerated risk of MACE events in molecular subtype D ? Anyway, results of genetic testing cannot explain the increased risk of MACE events in molecular subtype D.
Reference
1. Liang LW, Raita Y, Hasegawa K, et al. Proteomics profiling reveals a distinct high-risk molecular subtype of hypertrophic cardiomyopathy. Heart 2022;108(22):1807-14.
2. Concato J, Peduzzi P, Holford TR, et al. Importance of events per independent variable in proportional hazards analysis. I. Background, goals, and general strategy. J Clin Epidemiol 1995;48(12):1495-501.
3. Peduzzi P, Concato J, Feinstein AR et al. Importance of events per independent variable in proportional hazards regression analysis. II. Accuracy and precision of regression estimates. J Clin Epidemiol 1995;48(12):1503-10.
4. Vittinghoff E, McCulloch CE. Relaxing the rule of ten events per variable in logistic and Cox regression. Am J Epidemiol 2007;165(6):710-8.
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
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
Unfortunately, the review of cardiovascular disease and mortality sequelae of COVID-19[1] did not encompass the infective endocarditis(IE) dimension. By contrast, a multicentre retrospective observational study conducted at 26 Spanish referral centres for infective endocarditis and cardiac surgery made the following observations:-
When data from 2020 were compared with data from 2019, the year 2020 was characterised by a 34% reduction in the absolute number of definite IE episodes. The authors attributed this decline to the possibility that people with occult IE were either obeying strict instructions to stay at home or were reluctant to seek medical attention for fear of contracting COVID-19 in a medical facility[2]. Anecdotal reports, however, reflect the reality that people with severe symptoms of COVID 19 have no choice but to go to hospital whether or not they unknowingly have coexisting IE.. Included in that category was a patient with coexistence of native valve bacterial endocarditis and COVID-19 pneumonia[3], and the patient with catastrophic Candida prosthetic valve endocarditis and COVID-19 pneumonia[4].. By contrast some patients who attend hospital with symptoms and radiographic stigmata suggestive of COVID-19 infection ultimately prove to have complications of infective endocarditis in the total absence of coexistence ofr COVID-19 infection.[5]. In the latter report the chest radiograph of a patient with breathlessness showed bilateral opaciti...
Unfortunately, the review of cardiovascular disease and mortality sequelae of COVID-19[1] did not encompass the infective endocarditis(IE) dimension. By contrast, a multicentre retrospective observational study conducted at 26 Spanish referral centres for infective endocarditis and cardiac surgery made the following observations:-
When data from 2020 were compared with data from 2019, the year 2020 was characterised by a 34% reduction in the absolute number of definite IE episodes. The authors attributed this decline to the possibility that people with occult IE were either obeying strict instructions to stay at home or were reluctant to seek medical attention for fear of contracting COVID-19 in a medical facility[2]. Anecdotal reports, however, reflect the reality that people with severe symptoms of COVID 19 have no choice but to go to hospital whether or not they unknowingly have coexisting IE.. Included in that category was a patient with coexistence of native valve bacterial endocarditis and COVID-19 pneumonia[3], and the patient with catastrophic Candida prosthetic valve endocarditis and COVID-19 pneumonia[4].. By contrast some patients who attend hospital with symptoms and radiographic stigmata suggestive of COVID-19 infection ultimately prove to have complications of infective endocarditis in the total absence of coexistence ofr COVID-19 infection.[5]. In the latter report the chest radiograph of a patient with breathlessness showed bilateral opacities that were initially mistakenly attributed to COVID-19 pneumonia. A negative reverse transciptase polymerase chain reaction test(performed on a nasopharyngeal swab specimen) was misinterpreted as a false negative. When he subsequently deteriorated a transoesophageal echo cardiogram showed severe mitral regurgitation, flail mitral valve leaflet and papillary muscle rupture. Culture of the mitral valve was positive for Klebsiella pneumoniae.. In retrospect both the breathlessness and the pulmonary opacities had a cardiogenic basis[5].
.
I have no funding and no conflict of interest.
References
[1]Raisi-Estabragh Z., Cooper J., Salih A et al
Cardioascular disease and mortality sequelae of COVID-19 in the UK biobank
Heart 2022 doi:10.1136/heartjnl-2022-321492
Article in Press
[2] Escola-Verge L., Cuervo G., de Alarcon A et al
Impact of the COVID-19 pandemic on the diagnosis management and prognosis of infective endocarditis
Clinical Microbiology and Infection 2021;27:660664
[3]Bajdechi M., Vlad ND., Dumitrascu M et al
Bacterial endocarditis masked by COVID-19: a case report
Experimental and Therapeutic Medicine 2022;23:DOI:10.3892/etm.2021.11109
[4]Davoodi L., Faeli L., Mirzakhani R et al
Catastrophic candida prosthetic valve endocarditis and COVID-19 comorbidity: A rare case
Current Medical Mycology2021;7:43-47
[5] Hayes DE., Rhee D., Hisamoto K et al
Two cases of acute endocarditis misdiagnosed a COVID-19 infection
Echocardiography 2021;38:798-804
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Self-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood p...
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Self-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood pressure measuring device must be the one the patient uses in his own home and must be a properly validated device. Technology is available to test its accuracy.
(ii)The protocol for SMBP must be the one prescribed in SPRINT[5[].
(iii) Hospital staff should be allowed to transfer the blood pressure readings from the memory of the device to the patient's health record. (iv)During the period of hospital stay titration of antihypertensive medication should be based on data from self measurement of blood pressure
Self-measurement of blood pressure in the hospital setting helps to mitigate the perception that directly observed treatment might have a punitive dimension. Mitigation of that perception, in turn, restores trust to the doctor-patient relationship, thereby reinforcing compliance with medication.
In the long term SMBP or its variant , automated office blood pressure measurement[6] might even be installed as the standard of care during office visits
I have no conflict of interest.
References
[1] Hardy L
I had a stroke when I was 64. Here's what I wish I had known before www.telegraph.co/health-fitness/mind/had-stroke--when-64-despite-working...
13th November 2022
[2] Soliman EZ., Rahman AKMF., Zhang Z-m et al
Effect of intensive blood pressure lowering on the risk of atrial fibrillation
Hypertension 2020;75:1491-1496
[3[ Upadhya B., Willard JJ., Lovato LC et al
Incidence and outcomes of acute heart failure with preserved versus reduced ejection fraction in SPRINT
Circulation Heart Failure 2021;14:1291-1301
[4]Jolobe OMP
Titrating antihypertensive therapy to mitigate the risk of falls
Clin Med 2022;22:597
[5]Johnson KC., Whelton PK., Cushman WC et al
Blood pressure measurement in SPRINT(Systolic Blood Pressure Intervention Trial)
Hypertension 2018;71:848-857
[6] Myers MG
The great myth of office blood pressure measurement
J Hypertens 2012;30:1894-1898
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
In the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation...
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
In the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation disclosed the presence of a vegetation on the aortic valve[4].
In all three patients splinter haemorrhages were present even though auscultation had not disclosed any cardiac murmurs. Arguably, given the high index of suspicion for IE in the second patient, thrombolytic therapy might have been avoided if splinter haermorrhages had been detected when that patient first presented with stroke[3]. The third patient was fortunate in that thrombolytic treatment of STEMI was avoided altogether, given the risk of iatrogenic intracranial haemorrhage when that treatment modality is implemented in IE-related STEMI[5]. In the latter example intracranial haemorrhage was attributable to thrombolysis-related haemorrhagic transformation of hitherto subclinical IE-related embolic infarcts[5].
All three patients with silent IE had splinter haemorrhages as an early "red flag". In two of the patients[2],[4] iatrogenic harm was avoided as a consequence of that red flag.
Splinter haemorrhages also occur in atrial myxoma[6], nonbacterial thrombotic endocarditis[7], granulomatosis with polyangiitis[8], and in eosinophilic endocarditis[9]. In granulomatosis with angiitis IE can also be simulated by the presence of vegetations[10]. Vegatations also occur in nonbacterial thrombotic endocarditis[7].
i have no funding and no conflict of interest
References
[1]Schiebert R., Baig W., Wu J., Sandre JA
Diagnostic accuracy of splinter haemorrhages in patients referred with suspected infective endocarditis
Heart 2022;108:1986-1990
[2] Giurgea LT., Lahey T
Haemophilus parainfluenzae mural endocarditis: Case report and review of the literature
Case Reports in Infectious Diseases Volume 2016; Article ID 3639517
DOI.org/10.1155/2016/363517
[3] Bhuva P., Kuo S-H., Hemphill JC., Lopez GA
Intracranial haemorrhage following thrombolytic use for stroke caused by infective endocarditis
Neurocrit care 2010;12:79-82
[4]Rischin AP., Carrillo P., Layland J
Multi-embolic ST-elevation myocardial infarction secondary to aortic valve endocarditis
Heart, Lung and Circulation 2019;24:e1-e3
[5]Di Salvo TG., Tatter SB., O'Gara PT., Nielsen G., DeSanctis RW
Fatal intracerebral haemorrhage following thrimbolytic therapy of embolic myocardial infarction in unsuspected infective endocarditis
Clin Cardiol 1994;17:340-344
[6] May IA., Kimball KG., Goldman PW., Dugan DJ
Left atrial myxoma
Diagnosis, treatment, and pre-and post operative physiological studies
Journal of Thoracic and cardiovascular Surgery 1967;53:805-813
[7] Costenbader KH., Fidias P., Gilman MD., Qureshi A., Tambouret RH
Vase 29-2006:, A 43 year old woman with painful nodules on the fingertips, shortness of breath, and fatigue
N Engl J Med 2006;355:1263-1272
[8] Laurent C., Dion J., Regent A
Splinter haemorrhages .splenic infarcts, and pulmonary embolism in granulomatosis with plyangiitis
Vascular Medicine 2019;24:263-264
Usui S., Dainichi T., Kitoh A., Miyachi Y., Kabashima K
Janeway lesions and spilinte haemorrhages in a patient with eosinophilic endomyocarditis
JAMA Dermatology 2015;151:907-908
[10] Varnier G., Schire N., Christov G., Eleftheriou D., Brogan PA
Granulomatosis with plyangiitis mimicking infective endocarditis in an adolescent male
Clin Rheumatol 2016;35:2369-2372
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
For example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as t...
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
For example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as the etiology for her presentation". CTA showed an ascending thoracic aortic aneurysm, moderate pericardial effusion but neither aortic dissection nor PE. Nevertheless , due to concern for a concealed dissection, surgical exploration was undertaken. This disclosed significant haemopericardium and a 1 cm ascending thoracic aortic rupture tamponaded by the pulmonary artery[4].
Diligent evaluation of family history and genetic testing both powerfully augment the index of suspicion , as was the case in a patient whose father experienced DAA at the age of 20 , and had tested positive for a variant of the MYH11 gene. During pregnancy the patient , herself, tested positive for the same variant of the MYH11 gene. She was placed on metoprolol during pregnancy and post partum. Three days post partum she presented with pleuritic pain radiating through to the back, and new diastolic murmur was elicited.. Both transthoracic echocardiography and cardiac computed tomography disclosed the presence of DAA. Aortic repair was successfully undertaken[5].
I have no conflict of interest
References
[1]Bourjeily G., Paidas M., Khalil H., Rosene Montella K., Rodger M
Pulmonary embolism in pregnancy
Lancet 2020;375:500-512
[2]Braverman AC
Acute aortic dissection
Circulation 2010;122:184-188
[3[ Lombaard H., Soma-Pillay P., Farrell E-M
Managing acute collapse in pregnant women
Best Practice & Research Clinical Obstetrics and Gynaecology 2009;23:339-355
[4]Bogaert K., Christensen K., Cagliostro M., Ferrara L
Contained aortic rupture in a term pregnant woman during COVID-19 pandemic
BMJ Case Reports 2020;13:e238370
[5]Sathananthan G., Rychel V., Yam J., Barlow A., Grewal J., Kiess M
A postpartum Type A dissection
JACC Case Reports 2020;2;150-153
To the Editor We read with interest the review article “Physical activity and exercise recommendations for patients with valvular heart disease” by Doctors Nikhil Chatrath and Michael Papadakis, which was published in a recent edition of Heart.1 The focused clinical review is particularly useful for physicians and other health care workers dealing with patients with valvular heart disease (VHD). However, we would like to share some additional thoughts based upon our own experiences from Heart Valve Clinics and our previous publications derived from the EXTAS (exercise testing in aortic stenosis) cohort study.2 Indeed, some notions in their work, were previously explored by us in the EXTAS study and deserve mention. We showed that exercise testing (modified Bruce protocol) was safe, tolerable and revealed symptoms not confirmed on the history in approximately 40% of patients with asymptomatic severe and 24% moderate AS.2 Serial exercise testing added incremental prognostic information to baseline testing. Furthermore, in another follow-up study we showed that an early rapid rise in heart rate (defined as achieving at least 85% of target heart rate or ≥50% increase from baseline within the first 6 min) was associated with revealed symptoms later in the test and an increased risk of death in moderate AS in the following 2 years.3 We speculated that rapid risk in heart rate was probably a compensation for a fall in stroke volume to maintain cardiac output in early exercise whi...
To the Editor We read with interest the review article “Physical activity and exercise recommendations for patients with valvular heart disease” by Doctors Nikhil Chatrath and Michael Papadakis, which was published in a recent edition of Heart.1 The focused clinical review is particularly useful for physicians and other health care workers dealing with patients with valvular heart disease (VHD). However, we would like to share some additional thoughts based upon our own experiences from Heart Valve Clinics and our previous publications derived from the EXTAS (exercise testing in aortic stenosis) cohort study.2 Indeed, some notions in their work, were previously explored by us in the EXTAS study and deserve mention. We showed that exercise testing (modified Bruce protocol) was safe, tolerable and revealed symptoms not confirmed on the history in approximately 40% of patients with asymptomatic severe and 24% moderate AS.2 Serial exercise testing added incremental prognostic information to baseline testing. Furthermore, in another follow-up study we showed that an early rapid rise in heart rate (defined as achieving at least 85% of target heart rate or ≥50% increase from baseline within the first 6 min) was associated with revealed symptoms later in the test and an increased risk of death in moderate AS in the following 2 years.3 We speculated that rapid risk in heart rate was probably a compensation for a fall in stroke volume to maintain cardiac output in early exercise which occurs in patients with spontaneous or revealed symptoms. By comparison, in asymptomatic patients the stroke volume rises in early exercise. Hence, a normal HR response to exercise test is clinically useful and reassuring when the presenting symptoms are doubtful. A positive exercise test (revealed symptoms, abnormal blood pressure response, arrhythmias or significant decline in functional capacity) or left ventricular (LV) dysfunction by echocardiography at baseline are guideline indications for valve intervention,4 and in these patients valve intervention rather than exercise prescription is necessary. However, exercise-based rehabilitation or training differs from formal exercise testing, and is useful both before and after valve intervention. Pre-intervention exercise training or exercise-based rehabilitation is associated with better post-intervention outcome, shorter hospital stay,5 and an early return to work or other activities. Pre-intervention obesity is often a concern for surgeons with regard to the potential for post-intervention rehabilitation. However, in daily clinical practice we encounter patients who are turned down for valve intervention (transcatheter valve implantation [TAVI] or conventional surgery) by the Heart team due to complex comorbidity, frailty and higher age, and are therefore assigned for conservative treatment. The question arises whether these patients may benefit from a low-intensity training or regular physical activity or not, and what will be the prescribed exercise intensity and frequency. Exercise-based rehabilitation or training is probably necessary for these patients to maintain and improve their physical function. However, there is a paucity of evidence in the literature to assess the benefit of exercise-based rehabilitation in patients with significant AS who are not found eligible for valve intervention, and hence no dedicated exercise recommendations exist. This should be investigated in prospective research studies in future.
Furthermore, we agree with the authors that most cardiologists dealing with patients with VHD may have limited knowledge of exercise prescription. However, this should ideally be incorporated into the remit of cardiac rehabilitation teams, which is often comprised of physicians and other health and fitness professionals in most European Hospitals, particularly in Scandinavia. Next, a comparison between aortic regurgitation related pressure and volume overload and the athletic heart was presented. However, a resting echo in athletic heart will exclude aortic regurgitation. Furthermore, in addition to borderline (low-normal) LV ejection fraction in the context of bradycardia, and significant improvement during exercise (contractile reserve), an athletic heart may typically show normal/higher systolic tissue Doppler velocities (S’), global longitudinal strain by speckle tracking echocardiography and other more sensitive marker of systolic LV function, such as the novel first-phase ejection fraction,6 compared with patients with VHD. Finally, a reduced LV ejection fraction in severe AS may be reversible reflecting “contractility-afterload mismatch”; i.e. reduced transaortic flow or LV ejection fraction but preserved contractile function. A relief of valve resistance (AS) in these patients either by TAVI or surgical valve replacement often leads to immediate increase in LV ejection fraction and/or normalization of transaortic flow.
Contributors SS wrote the first draft, RR revised it. Both authors approved the final version.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this work.
Patient consent for publication Not applicable.
Ethics approval This work does not involve human participants.
References
1. Chatrath N, Papadakis M. Physical activity and exercise recommendations for patients with valvular heart disease. Heart 2022 Mar 2:heartjnl-2021-319824.
2. Saeed S, Rajani R, Seifert R, et al. Exercise testing in patients with asymptomatic moderate or severe aortic stenosis. Heart 2018 Nov;104(22):1836-1842.
3. Chambers JB, Rajani R, Parkin D, et al. Rapid early rise in heart rate on treadmill exercise in patients with asymptomatic moderate or severe aortic stenosis: a new prognostic marker? Open Heart 2019;6(1):e000950. doi: 10.1136/openhrt-2018-000950. eCollection 2019.
4. Baumgartner H, Falk V, Bax JJ, et al. ESC Scientific Document Group. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2017; 38: 2739-2791.
5. Marmelo F, Rocha V, Moreira-Gonçalves D. The impact of prehabilitation on post-surgical complications in patients undergoing non-urgent cardiovascular surgical intervention: systematic review and meta-analysis. Eur J Prev Cardiol 2018;25:404–17.
6. Saeed S, Gu H, Rajani R, et al. First phase ejection fraction in aortic stenosis: A useful new measure of early left ventricular systolic dysfunction. J Clin Ultrasound 2021 Nov;49(9):932-935.
We read with great interest the editorial of Zhu et al (1). The authors have great theoretical knowledge and experience in the treatment of aortic valve regurgitation. We agree with their conclusion concerning personalised external aortic root support (PEARS) that “there are still many questions to be answered”. We would like to try to answer some of them.
Show MoreExperience based on the first 100 operations in the Czech Republic (2) suggests that the indication for PEARS is limited to the patient with dilatation of the aortic root and/or ascending aorta and only trivial aortic regurgitation regardless of the origin of the disease. Implantation of PEARS should be considered as a preventive operation in group of patients that usually do not meet the criteria for valve sparing aortic valve replacement. In these patients the PEARS procedure can be performed as a measure to prevent further dilatation of the aorta and possible aortic dissection. The possibility of performing the operation without a cardiopulmonary bypass is certainly an advantage for the patient (2).
The authors worried about wall tension after implantation. It is generally known, that decrease of the diameter which is achieved by PEARS implantation, reduces wall tension according to the La Place law. This procedure in fact decreases wall tension and moreover the wall of the aorta is externally supported.
The fears about the viability of the aortic wall due to the continuous circumferential stress...
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...
Liang et al. conducted a prospective study to predict major adverse cardiovascular events (MACE) in patients with hypertrophic cardiomyopathy (HCM) with special reference to molecular subtypes in HCM (1). Compared with the reference group with molecular subtype A, patients in molecular subtype D presented an increased risk of developing MACE, with the adjusted hazard ratio (HR) (95% CI) of 2.78 (1.18 to 6.55). I have comments about the study.
The authors understand the unstable estimation by multivariate analysis, which would be partly caused by the limited number of events. When conducting Cox regression analysis, they used sex, age, and two conventional cardiac biomarkers. As they classified molecular subtypes into four groups, a total of 7 independent variables were used for the analysis. There is a recommendation that the number of events per independent variable in Cox regression analysis are required ≥10 for prediction model (2,3). If the authors have concerned about the association between molecular subtypes in HCM and MACE events, strict criteria for the number of events can be relaxed (4). Although there is a description that the total number of events was 78 in Table 2, the number of patients with event was 66 in Table 3. I suppose that some patients had more than single event. I recommended to add MACE events by continuing follow-up to fulfill the statistical requirement.
When we see survival curve in Figure 2, remarkable difference in the risk of...
Show MoreThe 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...
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...
Unfortunately, the review of cardiovascular disease and mortality sequelae of COVID-19[1] did not encompass the infective endocarditis(IE) dimension. By contrast, a multicentre retrospective observational study conducted at 26 Spanish referral centres for infective endocarditis and cardiac surgery made the following observations:-
Show MoreWhen data from 2020 were compared with data from 2019, the year 2020 was characterised by a 34% reduction in the absolute number of definite IE episodes. The authors attributed this decline to the possibility that people with occult IE were either obeying strict instructions to stay at home or were reluctant to seek medical attention for fear of contracting COVID-19 in a medical facility[2]. Anecdotal reports, however, reflect the reality that people with severe symptoms of COVID 19 have no choice but to go to hospital whether or not they unknowingly have coexisting IE.. Included in that category was a patient with coexistence of native valve bacterial endocarditis and COVID-19 pneumonia[3], and the patient with catastrophic Candida prosthetic valve endocarditis and COVID-19 pneumonia[4].. By contrast some patients who attend hospital with symptoms and radiographic stigmata suggestive of COVID-19 infection ultimately prove to have complications of infective endocarditis in the total absence of coexistence ofr COVID-19 infection.[5]. In the latter report the chest radiograph of a patient with breathlessness showed bilateral opaciti...
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Show MoreSelf-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood p...
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
Show MoreIn the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation...
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
Show MoreFor example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as t...
To the Editor We read with interest the review article “Physical activity and exercise recommendations for patients with valvular heart disease” by Doctors Nikhil Chatrath and Michael Papadakis, which was published in a recent edition of Heart.1 The focused clinical review is particularly useful for physicians and other health care workers dealing with patients with valvular heart disease (VHD). However, we would like to share some additional thoughts based upon our own experiences from Heart Valve Clinics and our previous publications derived from the EXTAS (exercise testing in aortic stenosis) cohort study.2 Indeed, some notions in their work, were previously explored by us in the EXTAS study and deserve mention. We showed that exercise testing (modified Bruce protocol) was safe, tolerable and revealed symptoms not confirmed on the history in approximately 40% of patients with asymptomatic severe and 24% moderate AS.2 Serial exercise testing added incremental prognostic information to baseline testing. Furthermore, in another follow-up study we showed that an early rapid rise in heart rate (defined as achieving at least 85% of target heart rate or ≥50% increase from baseline within the first 6 min) was associated with revealed symptoms later in the test and an increased risk of death in moderate AS in the following 2 years.3 We speculated that rapid risk in heart rate was probably a compensation for a fall in stroke volume to maintain cardiac output in early exercise whi...
Show MorePages