The assertion that natriuretic peptide levels below a defined threshold(for, example, Brain Natriuretic Peptide(BNP) levels < 100 pg/mL) can safely rule out heart failure and may also obviate the need to proceed to early echocardiography[1] should be qualified as follows:-
Early echocardiography does not necessarily confirm or refute the diagnosis of congestive heart failure(CHF) in patients with heart failure characterised by preserved ejection fraction(HFpEF). This is a truism that ought to be valid even in HFpEF patients with BNP levels < 100 pg/mL[2]. In the latter study , among 159 patients who had been hospitalised for CHF, the latter characterised by left ventricular ejection fraction(LVEF) amounting to >50%, in association with pulmonary capillary wedge pressure > 15 mm Hg, 46/159 patients(29%) had BNP equal to or less than 100 pg/mL[2].. Accordingly, if the index of suspicion for CHF is sufficiently high strategies other than echocardiography should be deployed to confirm or refute the diagnosis of CHF. The following are some of those strategies:-
(i) Clinical evaluation of jugular venous pressure(JVP). A raised JVP is indicative of a right atrial pressure beyond the normal upper limit of 8 mm Hg[3]. Furthermore, jugular venous distension is associated with a likelihood ratio amounting to 5.1(95% Confidence Interval, 3.2 to 7.9) in favour of a diagnosis of CHF[4].
(ii)Evaluation of inferior vena cava(IVC) diameter. An...
The assertion that natriuretic peptide levels below a defined threshold(for, example, Brain Natriuretic Peptide(BNP) levels < 100 pg/mL) can safely rule out heart failure and may also obviate the need to proceed to early echocardiography[1] should be qualified as follows:-
Early echocardiography does not necessarily confirm or refute the diagnosis of congestive heart failure(CHF) in patients with heart failure characterised by preserved ejection fraction(HFpEF). This is a truism that ought to be valid even in HFpEF patients with BNP levels < 100 pg/mL[2]. In the latter study , among 159 patients who had been hospitalised for CHF, the latter characterised by left ventricular ejection fraction(LVEF) amounting to >50%, in association with pulmonary capillary wedge pressure > 15 mm Hg, 46/159 patients(29%) had BNP equal to or less than 100 pg/mL[2].. Accordingly, if the index of suspicion for CHF is sufficiently high strategies other than echocardiography should be deployed to confirm or refute the diagnosis of CHF. The following are some of those strategies:-
(i) Clinical evaluation of jugular venous pressure(JVP). A raised JVP is indicative of a right atrial pressure beyond the normal upper limit of 8 mm Hg[3]. Furthermore, jugular venous distension is associated with a likelihood ratio amounting to 5.1(95% Confidence Interval, 3.2 to 7.9) in favour of a diagnosis of CHF[4].
(ii)Evaluation of inferior vena cava(IVC) diameter. An IVC diameter amounting to 20 mm is associated with 73% sensitivity and 85% specificity for predicting a right atrial pressure of > 10 mm Hg[5] In another study, among 110 patients fulfilling the European Society of Cardiology criteria for acute heart failure, comparable values for IVC diameter(mean values of 20-21 mm) were found among 59 patients with LVEF equal to or less than 40% versus 51 counterparts with LVEF > 40% even though the latter subgroup had significantly(p < 0.0001) lower BNP levels(mean levels 1132 pg/mL vs 415 pg/mL)[6]..
Evaluation of patients with normal BNP despite clinical suspicion of CHF should also include a diligent search for stigmata of constrictive pericarditis(CP). The latter is a disorder characterised by marked elevation of JVP which persists despite a response to diuretic treatment that is characterised by pronounced weight loss[7].. Accordingly, the association of persistently high JVP and normal or only modestly elevated lvels of BNP should always raise the index of suspicion for CP. In Melo et al, where 91% of 24 CP subjects had high JVP levels, mean BNP(obtained in 22 subjects) amounted to 170 pg/mL(range 37-468 pg/mL). In the light of those observations the authors commented that "the presence of right heart failure with preserved ejection fraction and BNP levels normal or slightly elevated may suggest the diagnosis[of CP], even with a normal TE(transthoracic echocardiogram)"[8].
I have no funding and no conflict of interest
References
[1]Eltayeb M., Squire I., Sze S
Biomarkers in heart failure: a focus on natriuretic peptides
Heart
6th September 2023
doi:10.1136/heartjnl-2020-318553
[2]Anjan VY., Loftus TM., Burke MA et al
Prevalence, clinical phenotype, and outcomes associated with normal B type natriuretic peptide levels in heart failure with preserved ejection fraction
Am J Cardiol 2012;110:870-875
[3]Sinisalo J., Rapola J., Rossinen J., Kupari M
Simplifying the estimation of jugular venous pressure
Am J Cardiol 2007;100:1779-1781
[4]Wang CS., Fitzgerald JM., Schulzer M., Mak E., Ayas NT
Does this dyspneic patient in the emergency department have congestive heart failure?
JAMA 2005;294:1944-1956
[5] Brennan J., Blair JE., Goonewardena S et al
Reappraisal of the use of inferior vena cava for estimating right atrial pressure
J Am Soc Echocardiography 2007;20:857-861
[6]Coiro S., Porot G., Rossignol P et al
Prognostic value of pulmonary congestion assessed by lung ultrasound imaging during heart failure hospitalisation: A two centre cohort study
SCIENTIFIC REPORTS
DOI:10.1038/srep39426
[7] Jolobe OMP
Monitoring of the jugular venous pressure response to diuretics in constrictive pericarditis
Int J Cardiol 2015;182:163
[8] Melo DTP., Fernandes F., Salemi VMC et al
Diagnostic challenge in constrictive pericarditis: the role of brain natriuretic peptide and image tools
Eur Heart J 2013;34;Suppl_1:P3893
dio.org/10.1093/eurheartj/eht309.P3893
The establishment of an endocarditis team(ET)[1] is a fundamental requirement for good practice, not only in the narrow context of reactive management of clinically overt infective endocarditis but also in the wider context of frontline mitigation of the risk of missed diagnosis of occult infective endocarditis(IE). It is in the latter context that point of care ultrasound(POCUS) might have a role beacuse of its wider availability and because it can be utilised as an extension of the physical examination to detect manifestations of IE such as splemonegaly and splenic infarction. .
The caveat is that, in the present state of technical expertise and equipment capability, the use of POCUS is associated with a trade-off between availability and diagnostic accuracy. Three cases exemplify this dilemma[2[,[3],[4].. None had cardiac murmurs, notwithstanding the fact that the presence of a murmur is the usual starting point for triggering the index of suspicion for IE. In each instance the use of POCUS appeared to be an extension of the clinical examination, aimed at exploring the differential diagnosis of the presenting clinical scenario.
The first patient, who had a history of intravenous drug use, presented with altered level of consciousness. Auscultation disclosed bilateral crackles but no murmurs. Electrocardiography showed right axis deviation and ST segment elevation in the inferolateral leads. POCUS disclosed the presence of a tricuspid valve vegetati...
The establishment of an endocarditis team(ET)[1] is a fundamental requirement for good practice, not only in the narrow context of reactive management of clinically overt infective endocarditis but also in the wider context of frontline mitigation of the risk of missed diagnosis of occult infective endocarditis(IE). It is in the latter context that point of care ultrasound(POCUS) might have a role beacuse of its wider availability and because it can be utilised as an extension of the physical examination to detect manifestations of IE such as splemonegaly and splenic infarction. .
The caveat is that, in the present state of technical expertise and equipment capability, the use of POCUS is associated with a trade-off between availability and diagnostic accuracy. Three cases exemplify this dilemma[2[,[3],[4].. None had cardiac murmurs, notwithstanding the fact that the presence of a murmur is the usual starting point for triggering the index of suspicion for IE. In each instance the use of POCUS appeared to be an extension of the clinical examination, aimed at exploring the differential diagnosis of the presenting clinical scenario.
The first patient, who had a history of intravenous drug use, presented with altered level of consciousness. Auscultation disclosed bilateral crackles but no murmurs. Electrocardiography showed right axis deviation and ST segment elevation in the inferolateral leads. POCUS disclosed the presence of a tricuspid valve vegetation. Formal transthoracic echocardiography(TTE), however, showed vegetations both on the tricuspid valve and on the mitral valve,. It was the latter which had given rise to coronary embolism and, hence, inferolateral ST segment elevation.. Computed tomography showed multiple areas of hyperdensity consistent with intracranial haemorrhage attributable to septic emboli[2].
The second patient presented with congestive heart failure but no murmurs. Although formal TTE was thought to be desirable it was not available on that day. In its place POCUS was implemented, and it showed mitral regurgitation as well as aortic regurgitation but vegetations were detected only on the mitral valve. On the strength of the POCUS findings the patient was transferred to a tertiary hospital where formal TTE showed vegetations on both the mitral valve and the aortic valves.[3[.
The third patient presented with fever. cough, and weight loss but no murmurs. POCUS showed a vegetation on the aortic valve and some irregularity on the mitral valve. Subsequent formal TTE showed vegetations on both the aortic and mitral valves[4].
Comment
These examples show POCUS to be a readily available frontline resource for initial work up of occult IE, albeit with the limitation of suboptimal diagnostic accuracy. To some extent, however, POCUS compensates for that deficiency, not only by being more readily available(thereby reinforcing the principle of "same day echocardiography", but also because POCUS has a multiorgan dimension whereby it can be utilised to detect extracardiac manifestations of IE such as splenomegaly, and embolic manifestations of IE such as splenic infarction and hepatic infarction[5]. In the latter study, where POCUS was utilised as an extension of the physical examination(to detect splenomegaly and hepatomegaly) in patients with bacteremia or candidemia, POCUS had a positive predictive value of 78% for detection of splenomegaly, positive predictive value of 100% for detection of splenic infarction, and a positive predictive value of 75% for detection of hepatic infarction[5]. POCUS (with back up from TTE) could also be utilised to screen for IE in prospective candidates for thrombolytic therapy of stroke so as to mitigate the risk of inappropriate thrombolysis attributable to missed diagnosis of IE as the underlying cause of stroke. The second case , where IE was the underlying cause of intracranial embolism[2],reinforces that principle.
I have no funding and no conflict of interest
References
[1]Sandoe JAT., Ahmed F., Arumugam P et al
Expert consensus recommendations for the use of provision of infective endocarditis services: updated guidance from the JJoint British Societies
Heart doi:10.1136/heartjnl-2022-321791
. [2] Cohen S., Ford L., Situ-LaCasse E., Tolby N
Infective endocarditis causing acute myocardial infarction
CUREUS 2020 DOI:10.7759/cureus.11245
[3] Kobenson L., Ma IWY., Olszynski P
A sinister point of care ultrasound(POCUS) finding in a patient with new heart failure
Canadian Journal of General Internal Medicine 2022;17:6-12
[4]Bugg CW., Berona K
Point-of -care ultrasound diagnosis of left-sided endocarditis
Western Journal of Emergency Medicine 2016;17:383--383
[5]Palmero SL., Zuniga MAL., Martinez VR et al
Point-of care ultrasound(POCUS) as an extension of the physical examination in patients with bacteremia or candidemia
Journal of Clinical; Medicine 2022;11:3636
DOI.org/10.3390/jcm 11133636
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
This study, in which subjects with systolic blood pressure(SBP) in the range 130 mm Hg-139 mm Hg were defined as being in the category of "high normal" blood pressure[1] is a reaffirmation of the dictum that "Essential hypertension can be defined as a rise in blood pressure....that increases risk of cerebral, cardiac, and renal events"[2]. According to that definition of hypertension subjects such as the ones shown to be at risk of a cardiac event such as atrial fibrillation(with its attendant risk of cerebral embolism) , as a consequence of a SBP of 130 mm Hg-139 mm Hg , should be allocated to the category of hypertension instead of being categorised as having "high normal" blood pressure. A similar categorisation should have been applied to otherwise healthy middle-aged men(mean aged 50) with SBP in the range 129 mm Hg-138 mm Hg who were shown to have a 1.5-fold increase in risk of atrial fibrillation(95% Confidence Interval 1.10 to 2.03) compared with middle aged men with SBP < 128 mm Hg[3].
Given the observation that "Throughout middle and old age, usual blood pressure is strongly and directly related to vascular(and overall) mortality , without any evidence of a threshold, down to at least 115/75 mm Hg"[4], the time might, perhaps, be overdue to invoke the concept proposed by Messerli et al that we should abandon the hypertension/normotension dichotomy and focus on global risk reduction, instead [2]. In that s...
This study, in which subjects with systolic blood pressure(SBP) in the range 130 mm Hg-139 mm Hg were defined as being in the category of "high normal" blood pressure[1] is a reaffirmation of the dictum that "Essential hypertension can be defined as a rise in blood pressure....that increases risk of cerebral, cardiac, and renal events"[2]. According to that definition of hypertension subjects such as the ones shown to be at risk of a cardiac event such as atrial fibrillation(with its attendant risk of cerebral embolism) , as a consequence of a SBP of 130 mm Hg-139 mm Hg , should be allocated to the category of hypertension instead of being categorised as having "high normal" blood pressure. A similar categorisation should have been applied to otherwise healthy middle-aged men(mean aged 50) with SBP in the range 129 mm Hg-138 mm Hg who were shown to have a 1.5-fold increase in risk of atrial fibrillation(95% Confidence Interval 1.10 to 2.03) compared with middle aged men with SBP < 128 mm Hg[3].
Given the observation that "Throughout middle and old age, usual blood pressure is strongly and directly related to vascular(and overall) mortality , without any evidence of a threshold, down to at least 115/75 mm Hg"[4], the time might, perhaps, be overdue to invoke the concept proposed by Messerli et al that we should abandon the hypertension/normotension dichotomy and focus on global risk reduction, instead [2]. In that spirit of reduction of the risk of incident adverse cardiac events it has been shown that reduction of the risk of incident atrial fibrillation is achievable through intensive lowering of systolic blood pressure to a target level of <120 mm Hg[5]. Accordingly, the conversation that should take place between doctor and patient should be about goal blood pressure for mitigating the risk of complications such as incident atrial fibrillation, and atrial fibrillation-related stroke. That is the kind of dialogue that is most likely to generate compliance with medication and compliance with home blood pressure monitoring.
I have no conflict of interest.
References
[1]Kim J., Kim D., Jange E et al
Association of high normal blood pressure and impaired fasting glucose with atrial fibrillation
Heart doi.org/10.1136/heartjnl.2022-322094
[2] Messerli FH., Williams B., Eitz E
Essential hypertension
Lancet 2007;370:591-601
[3] Prospective Studies Collaboration
Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies
Lancet 2002;360:1903-1913
[4[ Grundvold I., Skretteberg PT., Liestol K et al
Upper normal blood pressures predict incident atrial fibrillation in healthy middle aged men
A 35 year follow up study
Hypertension 2012;59:198-204
[5]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
The association of chronic obstructive pulmonary disease(COPD) and heart failure with preserved ejection fraction(HFpEF) justifies the special mention accorded to it by the authors[1]. In part, the rationale is that COPD is a risk factor for for atrial fibrillation(AF), and, hence, worsening of heart failure. Furthermore, both AF and COPD are risk factors for pulmonary embolism [4],[5]], the latter a complication that might, in turn, lead to worsening of heart failure. Additionally, in its own right, hypoxic COPD generates a mortality risk which is favourably modified by prescription of long term oxygen therapy(LTOT)[6]. Accordingly, all HFpEF patients with coexisting COPD should be evaluated for eligibility for LTOT, and should receive the benefit of LTOT if found to be eligible.
SGLT2 inhibitor therapy sits well with the management of HFpEF in the COPD context, given the fact that SGLT2 inhibition mitigates the risk of worsening of congestive heart failure(CHF) to a comparable degree in HFpEF patients with and without coexisting COPD[7]. In the latter study the prevalence of AF was significantly(p < 0.001) higher in HFpEF patients with COPD than in counterparts who did not have coexisting COPD[7].
Hypertension is another important comorbidity of HFpEF[1]. In its most recent report, the American College of Cardiology Expert Consensus Decision Pathway recommends a goal systolic blood pressure(SBP) of < 130 mm Hg in the presence of HFpEF[8]...
The association of chronic obstructive pulmonary disease(COPD) and heart failure with preserved ejection fraction(HFpEF) justifies the special mention accorded to it by the authors[1]. In part, the rationale is that COPD is a risk factor for for atrial fibrillation(AF), and, hence, worsening of heart failure. Furthermore, both AF and COPD are risk factors for pulmonary embolism [4],[5]], the latter a complication that might, in turn, lead to worsening of heart failure. Additionally, in its own right, hypoxic COPD generates a mortality risk which is favourably modified by prescription of long term oxygen therapy(LTOT)[6]. Accordingly, all HFpEF patients with coexisting COPD should be evaluated for eligibility for LTOT, and should receive the benefit of LTOT if found to be eligible.
SGLT2 inhibitor therapy sits well with the management of HFpEF in the COPD context, given the fact that SGLT2 inhibition mitigates the risk of worsening of congestive heart failure(CHF) to a comparable degree in HFpEF patients with and without coexisting COPD[7]. In the latter study the prevalence of AF was significantly(p < 0.001) higher in HFpEF patients with COPD than in counterparts who did not have coexisting COPD[7].
Hypertension is another important comorbidity of HFpEF[1]. In its most recent report, the American College of Cardiology Expert Consensus Decision Pathway recommends a goal systolic blood pressure(SBP) of < 130 mm Hg in the presence of HFpEF[8]. Arguably, this goal blood pressure can be justified on the basis of the study which showed that, on 4.6 year follow up, that on-treatment goal SBP was associated with a 40% reduction in risk of incident AF(95% Confidence Interval 18% to 55%)[9]
Last but not least, in the event of the coexistence of iron deficiency and CHF, intravenous iron should be prescribed because, in that context, intravenous iron improves exercise capacity as well as quality of life, and does so both in anaemic and in non anaemic iron deficiency[10].
I have no funding, and no conflict of interest.
References
[1] Jasinska-Piadlo A., Campbell P
Management of patients with heart failure and preserved ejection fraction
Heart
DOI:10.1136/heqrtjnl-2022-321097
[2]Francesco G., Corica B., Pipitone E et al
Prevalence , amagement an impact of chronic obstructive pulmonary disease in atrial fibrillation: a systematic review and meta-analysis of 4,200,000 patients
Eur Heart J 2021;42:3541-3554
[3] Grymonprez M., Vankaet V., Kavousi M et al
Chronic obstructive pulmonary disease and the development of atrial fibrillation
Int J Cardiol 2019;276:118-124
[4] Bikdeli B,m Ziki MDH., LipGYH
Pulmonary embolism and atrial fibrillation, two sides of the same coin: A systematic review
Semin Thromb Hemost 2017;43:849-863
[5] Aleva FE., Voets LWM., Simons SO et al
Prevalence aqnd localisation of pulmonary embolism in unexplained acute exacerbations of COPD
CHEST 2017;151:544-554
[6[ Lim V., Beneditt JO., Wise RA., Sharafkhaneh A
Oxygen therapy in chronic obstructive pulmonary disease
Proc Am Thorac Assoc 2008;5:513-518
[7] Dewan P., Docherty KF., Bengtsson O et al
Effects of dapliflozin in heart failure with reduced ejection fraction and chronic obstructive pulmonary disease: an analysis of DAPA-HF
Eur Heart J 2021;23:632-643
[8] Kittleson M., Panraj GS., Amancheria K et al
2023 ACC Expert Consnsus Decision Pathway on management of heart failure with preserved ejection fraction
JACC
Article in Press
DOI.org/10.1016/j.jacc.2023.03.393
[9]Okin PM., Hille DA., Larstorp AC et al
Effect of lower on-treatment systolic blood pressure on risk of atrial fibrillation in hypertensive subjects
HYPERTENSION 2015;66:368-373
[10] Anker SD., Colet JC., Filippatos G et al
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
The assertion that natriuretic peptide levels below a defined threshold(for, example, Brain Natriuretic Peptide(BNP) levels < 100 pg/mL) can safely rule out heart failure and may also obviate the need to proceed to early echocardiography[1] should be qualified as follows:-
Show MoreEarly echocardiography does not necessarily confirm or refute the diagnosis of congestive heart failure(CHF) in patients with heart failure characterised by preserved ejection fraction(HFpEF). This is a truism that ought to be valid even in HFpEF patients with BNP levels < 100 pg/mL[2]. In the latter study , among 159 patients who had been hospitalised for CHF, the latter characterised by left ventricular ejection fraction(LVEF) amounting to >50%, in association with pulmonary capillary wedge pressure > 15 mm Hg, 46/159 patients(29%) had BNP equal to or less than 100 pg/mL[2].. Accordingly, if the index of suspicion for CHF is sufficiently high strategies other than echocardiography should be deployed to confirm or refute the diagnosis of CHF. The following are some of those strategies:-
(i) Clinical evaluation of jugular venous pressure(JVP). A raised JVP is indicative of a right atrial pressure beyond the normal upper limit of 8 mm Hg[3]. Furthermore, jugular venous distension is associated with a likelihood ratio amounting to 5.1(95% Confidence Interval, 3.2 to 7.9) in favour of a diagnosis of CHF[4].
(ii)Evaluation of inferior vena cava(IVC) diameter. An...
The establishment of an endocarditis team(ET)[1] is a fundamental requirement for good practice, not only in the narrow context of reactive management of clinically overt infective endocarditis but also in the wider context of frontline mitigation of the risk of missed diagnosis of occult infective endocarditis(IE). It is in the latter context that point of care ultrasound(POCUS) might have a role beacuse of its wider availability and because it can be utilised as an extension of the physical examination to detect manifestations of IE such as splemonegaly and splenic infarction. .
Show MoreThe caveat is that, in the present state of technical expertise and equipment capability, the use of POCUS is associated with a trade-off between availability and diagnostic accuracy. Three cases exemplify this dilemma[2[,[3],[4].. None had cardiac murmurs, notwithstanding the fact that the presence of a murmur is the usual starting point for triggering the index of suspicion for IE. In each instance the use of POCUS appeared to be an extension of the clinical examination, aimed at exploring the differential diagnosis of the presenting clinical scenario.
The first patient, who had a history of intravenous drug use, presented with altered level of consciousness. Auscultation disclosed bilateral crackles but no murmurs. Electrocardiography showed right axis deviation and ST segment elevation in the inferolateral leads. POCUS disclosed the presence of a tricuspid valve vegetati...
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...
This study, in which subjects with systolic blood pressure(SBP) in the range 130 mm Hg-139 mm Hg were defined as being in the category of "high normal" blood pressure[1] is a reaffirmation of the dictum that "Essential hypertension can be defined as a rise in blood pressure....that increases risk of cerebral, cardiac, and renal events"[2]. According to that definition of hypertension subjects such as the ones shown to be at risk of a cardiac event such as atrial fibrillation(with its attendant risk of cerebral embolism) , as a consequence of a SBP of 130 mm Hg-139 mm Hg , should be allocated to the category of hypertension instead of being categorised as having "high normal" blood pressure. A similar categorisation should have been applied to otherwise healthy middle-aged men(mean aged 50) with SBP in the range 129 mm Hg-138 mm Hg who were shown to have a 1.5-fold increase in risk of atrial fibrillation(95% Confidence Interval 1.10 to 2.03) compared with middle aged men with SBP < 128 mm Hg[3].
Show MoreGiven the observation that "Throughout middle and old age, usual blood pressure is strongly and directly related to vascular(and overall) mortality , without any evidence of a threshold, down to at least 115/75 mm Hg"[4], the time might, perhaps, be overdue to invoke the concept proposed by Messerli et al that we should abandon the hypertension/normotension dichotomy and focus on global risk reduction, instead [2]. In that s...
The association of chronic obstructive pulmonary disease(COPD) and heart failure with preserved ejection fraction(HFpEF) justifies the special mention accorded to it by the authors[1]. In part, the rationale is that COPD is a risk factor for for atrial fibrillation(AF), and, hence, worsening of heart failure. Furthermore, both AF and COPD are risk factors for pulmonary embolism [4],[5]], the latter a complication that might, in turn, lead to worsening of heart failure. Additionally, in its own right, hypoxic COPD generates a mortality risk which is favourably modified by prescription of long term oxygen therapy(LTOT)[6]. Accordingly, all HFpEF patients with coexisting COPD should be evaluated for eligibility for LTOT, and should receive the benefit of LTOT if found to be eligible.
Show MoreSGLT2 inhibitor therapy sits well with the management of HFpEF in the COPD context, given the fact that SGLT2 inhibition mitigates the risk of worsening of congestive heart failure(CHF) to a comparable degree in HFpEF patients with and without coexisting COPD[7]. In the latter study the prevalence of AF was significantly(p < 0.001) higher in HFpEF patients with COPD than in counterparts who did not have coexisting COPD[7].
Hypertension is another important comorbidity of HFpEF[1]. In its most recent report, the American College of Cardiology Expert Consensus Decision Pathway recommends a goal systolic blood pressure(SBP) of < 130 mm Hg in the presence of HFpEF[8]...
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...
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