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 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
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the association of type 1 diabetes and fulminant viral , the latter characterised by ST segment elevation, serum troponin elevation and severe left ventricular systolic dysfunction giving rise to cardiogenic pulmonary oedema[3]. In the latter example parainfluenza-3 was believed to be the underlying cause of both the diabetic decompensation and the severe left ventricular systolic dysfunction[3]. A viral aetiology was also suspected but not serologically proven in a 47 year old patient who experienced a prodrome of fever, vomiting, and diahrroea before she was admitted with severe DKA and pain-free ST segment elevation associted with serum troponin elevation but no angiographically demonstrable coronary occlusion. Endomyocardial biopsy showed a mild accumulation of mononuclear cells in the myocardial interstitium[4].
Diabetic ketoacidosis can also be complicated by the occurrence of pain-free Takotsubo myocarditis with STEMI-like presentation[5][6]]. In both cases coronary angiography did not reveal any coronary occlusion.
The differential diagnosis of pain-free DKA-related STEMI extends to the association of DKA-related hyperkalaemia and ST segment elevation[7],[8]. Only one of the two patients had a raised serum troponin[8]. Both patients had total absence of coronary artery occlusion on coronary angiography. In another severely hyperkalaemic patient(serum potassium 9.0 mmol/l) the ST segment elevation had a Brugada syndrome configuration. Serum troponin peaked at 20.452 mcg/L but no occlusive lesion was documented on coronary angiography[9].
DKA-related ST segment elevation can also occur in patients who are normokalaemic, and have normal serum troponin and no abnormality on coronary angiography[10]. Euglycaemic DKA was the associated feature in the latter patient[10].
Comment
Patients with unrecognised Type 1 STEMI complicated by decompensated CHF incur the double jeopardy of “missing out on coronary reperfusion therapy and also run the risk of inappropriate administration of large volumes of intravenous fluids for the management of DKA-related metabolic decompensation.
DKA patients with hyperkalaemia related ST elevation and serum troponin elevation run the risk of mistaken diagnosis of type 2 acute myocardial infarction
Clinicians must be vigilant for both types of eventualities in DKA patients presenting with pain-free ST segment elevation
I have no funding and no conflict of interest
References
[1]Kumar A., Sanghera A., Sanghera B et al
Chest pain symptoms during myocardial infarction in patients with and without diabetes: a systematic review and meta-analysis
Heart doi. 10.1136/heartjnl-2022-322289
[2]Baral N., Montalbano A., KhanA., Qureshi M., Luitel P
Silent myocardial infarction and acute multiorgan failure in a COVID-19 patient: A case report
J Nepal Med Assoc 2021;59:1048-1051
[3]Ohara N., Kaneko M., Kuwano H et al
Fulminant Type 1 diabetes mellitus and fulminant viral myocarditis: A case report and literature review
Int Heart J 2015;56:239-244
[4]Hiramatsu S., Komori K., Mori E et al
A case of fulminant type 1 diabetes mellitus accompoanied by myocarditis
Endocrine Journal 2011;58:553-557
[5]Patel KKHP., Soe HM
Association of diabetic ketoacidosis with Takotsubo cardiomyopathy
CHEST doi:https://doi.org/10.1016/chest.2020.08.283
[6] Gordon A., LaCapra G., Roberti R
DKA-induced Takotsubo cardiomyopathy in patient with known HOCM
Case Reports in Critical Care 2017 doi.org/10.1155/2017/4287125
[7]Ziakas A., Basangiannis C., Stiliadis I
Pseudoinfarction pattern in a patient with hyperkalaemia, diabetic ketoacidosis and normal coronary vessels: a case report
Journal of Medical Case Reports 2020;4:115
[8]Sharma E., Dagal S., Sharma P., Ghimire DKC., Dahal S
A case of pseudo infarction pattern in diabetic ketoacidosis
A diagnostic and therapeutic dilemma
Cardiol Res 2018;9:250-252
[9] Pfirman KS., Donley CJ., Fryman EB., Champaneria SU., Gatewood WT
Brugada pattern manifesting during hyperkalaemia, diabetic ketoacidosis, and acute alcohol intoxication
American Journal of Case Reports 2021;22;e932048
[10]Jay DR., Henry TD., Sharkey SW
Acute inferior myocardial infarction or Not?
JAMA Internal Medicine 2022;182:224-225
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
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.
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
In the context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Criteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identi...
In the context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Criteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identified a low number of acid and alcohol fast bacilli[4].
A fatal outcome was documented in a patient in whom diagnostic ambiguity could only be resolved by recourse to the nested polymerase chain reaction(PCR) method. This was a patient previously in good health, who died suddenly. Autopsy disclosed nodules in the myocardium, lymph nodes, and spleen. Histological examination of the myocardium showed granulomas, epithelial cells, and lymphocytes immersed in fibrous tissue. No acid fast bacilli were seen. However, nested PCR was positive for Mycobacterium avium in samples of the myocardium, liver, spleen, right lung, and kidney[5].
A fatal outcome was also documented in a patient who had presented with severe biventricular heart failure characterised by an echocardiogram which showed biventricular dysfunction. Furthermore the right ventricle was almost akinetic. Computed tomography showed asymmetrical hilar lymphadenoipathy. Endobronchial aspiration demonstrated non-caseating granulomatous inflammation that was negative for acid-fast bacilli. Given a differential diagnosis that included both cardiac sarcoidosis and tuberculous myocarditis, and also in view of rapid clinical deterioration in spite of optimised treatment for congestive heart failure, the clinicians opted for empirical concurrent high dose corticosteroid therapy and antituberculous chemotherapy. In spite of these measures the patient subsequently died. Autopsy showed almost complete replacement of the right ventricular myocardium by scar tissue and patchy fibrosis of the left ventricle. Histology showed giant cell invasion of the cardiac myocytes. Ziehl-nielsen stain for mycobacterium of the hilar lymph nodes was positive[6].
I have no conflict of interest
References
[1]Sohn D-W., Park J-B
Cardiac sarcoidosis
Heart doi.10.1136/heartjnl-2022-321379
[2]Sundaraila S., Sulaiman A., Rajendran A
Cardiac tuberculosis on 18F-FDG PET imaging-A great masquerader of cardiac sarcoidosis
Indian J Radiol Imaging 2021;31:1002-1007
[3]Srikala J., Subramanyam PB., Rao BH
Granulomatous myocarditis: cardiac MRI and PET CT findings
Indian Journal of Ckinical Cardiology 2022;3:213-214
[4[] Khurana R., Shalhoub J., Verma A et al
Tubercular myocarditis presenting with ventricular tachycardia
Nature Clinical Practice Cardiovascular Medicine ;5:169-174
[5]Silingardi E., Rivasci F., Santanione AL., Garagnani L
Sudden death from tubercular myocarditis
J Foresnsic Sci 2006;51:667-669
[6]Cowley A., Dobson L., Kurian J., Saunderson C
Acute myocarditis secondary to tuberculosis : a case report
Echo Research and Practice
ID:17-0024;September 2017
DOI:10.1530/ERP-17-0024
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Self-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood p...
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Self-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood pressure measuring device must be the one the patient uses in his own home and must be a properly validated device. Technology is available to test its accuracy.
(ii)The protocol for SMBP must be the one prescribed in SPRINT[5[].
(iii) Hospital staff should be allowed to transfer the blood pressure readings from the memory of the device to the patient's health record. (iv)During the period of hospital stay titration of antihypertensive medication should be based on data from self measurement of blood pressure
Self-measurement of blood pressure in the hospital setting helps to mitigate the perception that directly observed treatment might have a punitive dimension. Mitigation of that perception, in turn, restores trust to the doctor-patient relationship, thereby reinforcing compliance with medication.
In the long term SMBP or its variant , automated office blood pressure measurement[6] might even be installed as the standard of care during office visits
I have no conflict of interest.
References
[1] Hardy L
I had a stroke when I was 64. Here's what I wish I had known before www.telegraph.co/health-fitness/mind/had-stroke--when-64-despite-working...
13th November 2022
[2] Soliman EZ., Rahman AKMF., Zhang Z-m et al
Effect of intensive blood pressure lowering on the risk of atrial fibrillation
Hypertension 2020;75:1491-1496
[3[ Upadhya B., Willard JJ., Lovato LC et al
Incidence and outcomes of acute heart failure with preserved versus reduced ejection fraction in SPRINT
Circulation Heart Failure 2021;14:1291-1301
[4]Jolobe OMP
Titrating antihypertensive therapy to mitigate the risk of falls
Clin Med 2022;22:597
[5]Johnson KC., Whelton PK., Cushman WC et al
Blood pressure measurement in SPRINT(Systolic Blood Pressure Intervention Trial)
Hypertension 2018;71:848-857
[6] Myers MG
The great myth of office blood pressure measurement
J Hypertens 2012;30:1894-1898
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
In the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation...
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
In the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation disclosed the presence of a vegetation on the aortic valve[4].
In all three patients splinter haemorrhages were present even though auscultation had not disclosed any cardiac murmurs. Arguably, given the high index of suspicion for IE in the second patient, thrombolytic therapy might have been avoided if splinter haermorrhages had been detected when that patient first presented with stroke[3]. The third patient was fortunate in that thrombolytic treatment of STEMI was avoided altogether, given the risk of iatrogenic intracranial haemorrhage when that treatment modality is implemented in IE-related STEMI[5]. In the latter example intracranial haemorrhage was attributable to thrombolysis-related haemorrhagic transformation of hitherto subclinical IE-related embolic infarcts[5].
All three patients with silent IE had splinter haemorrhages as an early "red flag". In two of the patients[2],[4] iatrogenic harm was avoided as a consequence of that red flag.
Splinter haemorrhages also occur in atrial myxoma[6], nonbacterial thrombotic endocarditis[7], granulomatosis with polyangiitis[8], and in eosinophilic endocarditis[9]. In granulomatosis with angiitis IE can also be simulated by the presence of vegetations[10]. Vegatations also occur in nonbacterial thrombotic endocarditis[7].
i have no funding and no conflict of interest
References
[1]Schiebert R., Baig W., Wu J., Sandre JA
Diagnostic accuracy of splinter haemorrhages in patients referred with suspected infective endocarditis
Heart 2022;108:1986-1990
[2] Giurgea LT., Lahey T
Haemophilus parainfluenzae mural endocarditis: Case report and review of the literature
Case Reports in Infectious Diseases Volume 2016; Article ID 3639517
DOI.org/10.1155/2016/363517
[3] Bhuva P., Kuo S-H., Hemphill JC., Lopez GA
Intracranial haemorrhage following thrombolytic use for stroke caused by infective endocarditis
Neurocrit care 2010;12:79-82
[4]Rischin AP., Carrillo P., Layland J
Multi-embolic ST-elevation myocardial infarction secondary to aortic valve endocarditis
Heart, Lung and Circulation 2019;24:e1-e3
[5]Di Salvo TG., Tatter SB., O'Gara PT., Nielsen G., DeSanctis RW
Fatal intracerebral haemorrhage following thrimbolytic therapy of embolic myocardial infarction in unsuspected infective endocarditis
Clin Cardiol 1994;17:340-344
[6] May IA., Kimball KG., Goldman PW., Dugan DJ
Left atrial myxoma
Diagnosis, treatment, and pre-and post operative physiological studies
Journal of Thoracic and cardiovascular Surgery 1967;53:805-813
[7] Costenbader KH., Fidias P., Gilman MD., Qureshi A., Tambouret RH
Vase 29-2006:, A 43 year old woman with painful nodules on the fingertips, shortness of breath, and fatigue
N Engl J Med 2006;355:1263-1272
[8] Laurent C., Dion J., Regent A
Splinter haemorrhages .splenic infarcts, and pulmonary embolism in granulomatosis with plyangiitis
Vascular Medicine 2019;24:263-264
Usui S., Dainichi T., Kitoh A., Miyachi Y., Kabashima K
Janeway lesions and spilinte haemorrhages in a patient with eosinophilic endomyocarditis
JAMA Dermatology 2015;151:907-908
[10] Varnier G., Schire N., Christov G., Eleftheriou D., Brogan PA
Granulomatosis with plyangiitis mimicking infective endocarditis in an adolescent male
Clin Rheumatol 2016;35:2369-2372
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
For example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as t...
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
For example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as the etiology for her presentation". CTA showed an ascending thoracic aortic aneurysm, moderate pericardial effusion but neither aortic dissection nor PE. Nevertheless , due to concern for a concealed dissection, surgical exploration was undertaken. This disclosed significant haemopericardium and a 1 cm ascending thoracic aortic rupture tamponaded by the pulmonary artery[4].
Diligent evaluation of family history and genetic testing both powerfully augment the index of suspicion , as was the case in a patient whose father experienced DAA at the age of 20 , and had tested positive for a variant of the MYH11 gene. During pregnancy the patient , herself, tested positive for the same variant of the MYH11 gene. She was placed on metoprolol during pregnancy and post partum. Three days post partum she presented with pleuritic pain radiating through to the back, and new diastolic murmur was elicited.. Both transthoracic echocardiography and cardiac computed tomography disclosed the presence of DAA. Aortic repair was successfully undertaken[5].
I have no conflict of interest
References
[1]Bourjeily G., Paidas M., Khalil H., Rosene Montella K., Rodger M
Pulmonary embolism in pregnancy
Lancet 2020;375:500-512
[2]Braverman AC
Acute aortic dissection
Circulation 2010;122:184-188
[3[ Lombaard H., Soma-Pillay P., Farrell E-M
Managing acute collapse in pregnant women
Best Practice & Research Clinical Obstetrics and Gynaecology 2009;23:339-355
[4]Bogaert K., Christensen K., Cagliostro M., Ferrara L
Contained aortic rupture in a term pregnant woman during COVID-19 pandemic
BMJ Case Reports 2020;13:e238370
[5]Sathananthan G., Rychel V., Yam J., Barlow A., Grewal J., Kiess M
A postpartum Type A dissection
JACC Case Reports 2020;2;150-153
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 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]...
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
Show MoreIn the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
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...
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 MoreThis 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...
In the context of cardiac sarcoidosis, diagnostic ambiguities which deserve mention include, not only the entity of arrhythmogenic right ventricular dysplasia(highlighted by the authors[1], but, also, tuberculous myocarditis[2][3],[4], which can have a fatal outcome[5][6].
Show MoreCriteria for cardiac sarcoidosis such as ventricular tachycardia(VT), left ventricular dysfunction characterised by left ventricular ejection fraction as low as 32%, and patchy regions of increased 19-Fluoro Deoxy Glucose(18-FDG) uptake were documented in a patient in whom the diagnosis of a tuberculous aetiology was established after needle biopsy of a paraaortic lymph node revealed necrotising granulomatous inflammation consistent with a diagnosis of tuberculosis[2].
In another example, a patient with documented VT and global hypokinesia of the left ventricle had an imaging study which showed increased 18-FDG uptake in the anteroseptal myocardial segment. Delayed gadolinium enhancement images showed intense subepicardial enhancement in the inferior and inferoseptal segments of the heart. Excision biopsy of an axillary lymph node showed necrotising granulomatous inflammation consistent with tuberculosis[3].
The association of VT and mediastinal lymphadenopathy simulating sarcoidosis was documented in a patient in whom mediastinal lymph node biopsy(via mediastinoscopy) showed large numbers of confluent granulomas with multinucleated giant cells. Ziehl-Nielsen staining identi...
Self-measurement of blood pressure(SMBP), spanning the entire duration of hospital stay, might have been a better way to generate motivation and engage compliance with medication in members of this cohort of hypertensive subjects with suspected non-compliance with medication. Both motivation and compliance can, arguably, be reinforced when the rationale for regular self-measurement of blood pressure is explained to patients in terms that they can understand and identify with,. The risk of stroke [1],[2]] and congestive heart failure(CHF)[3]], is, for example, one that most patients can identify with. Patients also need to be aware that the benefits of antihypertensive medication also carry the risk of symptomatic hypotension, exemplified by dizziness and falls, if hypertension is overtreated, hence the need for twice daily self-monitoring of blood pressure so as to generate an opportunity to titrate antihypertensive medication[4].
Show MoreSelf-measurement of blood pressure in the hospital environment, using the SPRINT protocol[5], also mitigates the risk of of overdiagnosis of suboptimal blood pressure control in those cases where overdiagnosis of suboptimal blood pressure control is attributable to the "white coat" effect of the threatening hospital environment.. Mitigation of the risk of white coat hypertension, in turn, mitigates the risk of overtreatment.
The following are the minimum requirements for in-hospital SMBP:-
(i)The blood p...
A caveat is required to qualify the assertion that splinter hemorrhages are an insensitive marker for infective endocarditis(IE)[1]. The caveat is that silent infective endocarditis, where murmurs are absent, may have splinter haemorrhages as the sole mucocutaneous feature of IE[2],[3],[4]].
Show MoreIn the first patient, splinter who had been admitted with intracranial embolism, haemorrhages were documented on "day 2" of hospital admission, and it was their presence which prompted the performance of echocardiography. That investigation disclosed the presence of a mobile mass in the left ventricle, even though no murmurs were elicited[. It was only on day 11 that a murmur was elicited. Repeat echocardiography disclosed a vegetation on the mitral valve [2].
In the second patient, admitted with stroke, for which he was prescribed thrombolytic therapy, echocardiography antedated the discovery of splinter haemorrhages. That investigation was nondiagnostic, but the diagnosis of IE was subsequently made at autopsy following his death from thrombolysis-related intracranial haemorrhage[3].
The third patient had an afebrile presentation characterised by ST segment elevation myocardial infarction(STEMI), the latter attributable to coronary embolism). Finger clubbing and splinter haemorrhages were present even though no murmurs were elicited. The presence of splinter haemorrhages prompted the initiation of echocardigraphy. That investigation...
In the event of the occurrence of aortic dissection as a complication of aortopathy in pregnancy a low index of suspicion for aortic dissection can be a major hinderance to correct diagnosis. Suboptimal diagnostic awareness is attributable to the fact that, clinicians confronted with the crisis of "collapse in a pregnant woman" , are likely to prioritise recognition of PE over recognition of dissecting aortic aneurysm(DAA) , given the fact that PE is the leading cause of maternal mortality in the developed world[1]. This cognitive bias is most likely to operate when symptoms of DAA overlap with symptoms of PE.
Show MoreFor example, when a woman at 37 weeks gestation presented with the association of chest pain, breathlessness and raised D-dimer levels, the referral for computed tomography angiography(CTA) was prompted by the intention "to evaluate for pulmonary embolism". In the event CTA disclosed the presence of DAA[2].
Women with undifferentiated the "collapse" in pregnancy" syndrome are best served by a multidimensional evaluation which includes a differential diagnosis with a minimum of 3 parameters, namely, PE, acute myocardial infarction, and DAA[3]. The workings of that diagnostic approach were exemplified in a woman who presented at 28 weeks gestation with breathlessness, throat pain, and syncope . In view of elevated D-dimer and T wave inversion in lead III "there was concern for a pulmonary embolism....as t...
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