Over and above the scenario cited by the authors, where the presence of Roth spots became a "red flag" for infective endocarditis(IE)[1], clinicians also need to take note of endogenous endophthalmitis as a "red flag" for IE, both in the context of native valve IE, and in the context of intracardiac device-related IE.
Endophthalmitis and native valve infective endocarditis:-
Awareness of endophthalmitis as a manifestation of IE is of heightened value when IE presents in the absence of a cardiac murmur, so-called "silent" infective endocarditis. In one patient with silent IE , Roth spots were identified in the same eye that was affected by endogenous endophthalmitis[2]. In another patient with silent IE initial transthoracic echocardiography(TTE) did not disclose any vegetations. Ten days later, however, transoesophageal echocardiography(TOE) disclosed the presence of vegetations[3]. The clinical course of another patient with silent IE was characterised by non diagnostic initial TTE, and nondiagnostic TOE on day 12. On day 31, however, TOE showed severe aortic regurgitation and what appeared to be a vegetation on the aortic valve. Intraoperatively, however, what had previously appeared to be a vegetation proved to be a destroyed non coronary valve tip[4].
Endophthalmitis and infective endocarditis attributable to intracardiac devices:-
Endogenous endophthalmitis is also a red flag for infective endocarditis attr...
Over and above the scenario cited by the authors, where the presence of Roth spots became a "red flag" for infective endocarditis(IE)[1], clinicians also need to take note of endogenous endophthalmitis as a "red flag" for IE, both in the context of native valve IE, and in the context of intracardiac device-related IE.
Endophthalmitis and native valve infective endocarditis:-
Awareness of endophthalmitis as a manifestation of IE is of heightened value when IE presents in the absence of a cardiac murmur, so-called "silent" infective endocarditis. In one patient with silent IE , Roth spots were identified in the same eye that was affected by endogenous endophthalmitis[2]. In another patient with silent IE initial transthoracic echocardiography(TTE) did not disclose any vegetations. Ten days later, however, transoesophageal echocardiography(TOE) disclosed the presence of vegetations[3]. The clinical course of another patient with silent IE was characterised by non diagnostic initial TTE, and nondiagnostic TOE on day 12. On day 31, however, TOE showed severe aortic regurgitation and what appeared to be a vegetation on the aortic valve. Intraoperatively, however, what had previously appeared to be a vegetation proved to be a destroyed non coronary valve tip[4].
Endophthalmitis and infective endocarditis attributable to intracardiac devices:-
Endogenous endophthalmitis is also a red flag for infective endocarditis attributable to intracardiac devices such as permanent pacemekers and implantable cardioverter defibrillators. The diagnosis of device-related IE comes to mind most readily when the patient has concurrent inflammatory signs of of infection of the device pocket[5]. Regardless of presence or absence of signs of device pocket infection , however, the presence of endogenous endophthalmitis should, also, raise the index of suspicion for device -related IE, especially when stigmata of septic pulmonary embolism are also present[6]. In the latter example, where no mention was made of the appearance of the device pocket, TOE showed a 20 mm mobile vegetation attached to the right atrial lead[6]. The association of endophthalmitis, pulmonary consolidation(with or without cavitation) , and hypotension(the latter attributable to systemic sepsis), is a "triad" that should raise the index of suspicion for device-related IE[7].
Echocardiography expedites the workup of suspected intracardiac device-related IE. TOE has greater sensitivity than TTE for identifying vegetations on the leads and for identifying vegetations on the heart valves. Accordingly, TOE can be offered as the first echocardiographic test if clinical suspicion is sufficiently high[8]. Nuclear imaging, using 18 Fluoro Deoxy Glucose positron emission tomography computed tomography is highly specific for lead endocarditis given the fact that, unlike TOE, it can also distinguish between infected thrombi and uninfected thrombi attached to the leads[8]. Sensitivity is however, suboptimal, given the the negative results believed to be attributable to previous antibiotic therapy or attributable to vegetation size being lower than the spatial resolution of nuclear imaging[9].
A comprehensive account of best practice in the work up of suspected device-related IE was made by Dilsizian et al[8].
I have no conflict of interest.
References
[1]Ng JY., Zarook E., Nicholson L et al
Eyes and the heart: what a clinician should know
Heart 2023
Epub ahead of print
DOI 10.1136/heartjnl-2022-322081
[2]Carmelli G., Surles T., Brown A
Endophthalmitis and myocotic aneurysm: The only clues to underlying endocarditis
Clin Pract Cases Emerg Med 2018 https://doi.org/10.5811/cpcem.2017.8.34723
[3]Sim YR., Lee YJ., Park SW et al
Infective endocarditis presenting as endogenous endophthalmitis secondary to streptococcus agalactiae in a healthy adult
CSE Rep Literat Rev Infect Chemother 2017;49:286-292
[4]Nakata M., Mashidori T., Higa N et al
Infective endocarditis with no underlying disease for which bacterial endophthalmitis have been first symptom
Intern Med 2020;59:2061-2065
[5]Looser PM., Saleh L., Thomas G., Cheung JW
Systemic infection due to subcutaneous implantable cardioverter defibrillator implantation: Importance of early recognition and treatment of device pocket related complications
Heart Rhythm Case Reports 2017;3:40-42
[6] Patel N., McDonald ML., Bradford NS et al
AngioVac debulking in endocarditis patients with large, device-related vegetations
The Journal of Innovations in Cardiac Rhythm Management 2018;9:3291-3296
[7]Sarvat B., Sarria JC
Implantable cardioverter-defibrillator infection due to Scetosporium apiospermum
Journal of Infection 2007;55:e109-e113
[8]Dilsizian V., Budde RPJ., Chen W et al
Best practice for imaging cardiac device-related infections and endocarditis
A JACC Cardiovascular imaging expert panel statement
JACC Cardiovascular Imaging 2022;15:891-911
[9]Cautela J., Alessandrini S., Carmmiller S et al
Diagnostic yield of FDG positron emission tomography/computed tomography in patients with CEID infection: a pilot study
Europace 2013;15:252-257
It is, indeed, a truism that poor rates blood pressure(BP) control are, in part, attributable to clinical inertia, whereby therapy is not escalated when BP is uncontrolled[1]. However, the criterion for escalation of antihypertensive therapy utilised by the authors, namely, a BP amounting to 140/90 mm Hg or more[1], is inappropriate, given the fact that the goal BP most likely to mitigate the risk of incident hypertension-related atrial fibrillation(AF) and hypertension-related congestive heart failure(CHF), respectively, is a goal BP amounting to < 120/80 mm Hg[2],[3]. In principle, that goal BP can be achieved by ultralow-dose quadruple combination therapy either on its own or in combination with lifestyle antihypertensive strategies such as regular exercise[4] and low-salt diet with or without abstinence from alcohol[5]. The younger the patient the more compelling the requirement to attain a BP amounting to < 120/80 mm Hg because it is theoretically possible that the longer the duration of suboptimal blood pressure the greater the long term risk of AF, CHF, and, arguably, hypertension-related vascular dementia[6].
Attainment of optimum goal BP crucially depends on accurate measurement of both "office" and home blood pressures[7],[8], and both those goals are predicated on the use of well-validated blood pressure monitors[8]. However, the minimum requirement for ultimate success in the control of BP is an honest conversation between doctor...
It is, indeed, a truism that poor rates blood pressure(BP) control are, in part, attributable to clinical inertia, whereby therapy is not escalated when BP is uncontrolled[1]. However, the criterion for escalation of antihypertensive therapy utilised by the authors, namely, a BP amounting to 140/90 mm Hg or more[1], is inappropriate, given the fact that the goal BP most likely to mitigate the risk of incident hypertension-related atrial fibrillation(AF) and hypertension-related congestive heart failure(CHF), respectively, is a goal BP amounting to < 120/80 mm Hg[2],[3]. In principle, that goal BP can be achieved by ultralow-dose quadruple combination therapy either on its own or in combination with lifestyle antihypertensive strategies such as regular exercise[4] and low-salt diet with or without abstinence from alcohol[5]. The younger the patient the more compelling the requirement to attain a BP amounting to < 120/80 mm Hg because it is theoretically possible that the longer the duration of suboptimal blood pressure the greater the long term risk of AF, CHF, and, arguably, hypertension-related vascular dementia[6].
Attainment of optimum goal BP crucially depends on accurate measurement of both "office" and home blood pressures[7],[8], and both those goals are predicated on the use of well-validated blood pressure monitors[8]. However, the minimum requirement for ultimate success in the control of BP is an honest conversation between doctor and patient about the goals of treatment. The patient should be told that achievable treatment goals include mitigation of risk of hypertension-related AF and, hence, AF-related stroke, and mitigation of risk of hypertension-related CHF. The doctor can then proceed to spell out their role, which consists of checking the "office" BP and instigating regular ambulatory blood pressure measurements, as well as titrating antihypertensive medication on the basis of all the available blood pressure readings, including home blood pressure readings. The role of the patient is to do home blood pressure checks, to comply with medication and to adhere to a lifestyle which is compliant with good BP control.
That might well be the most cost-effective strategy for hypertension control.
I have no funding and no conflict of interest
References
[1] Bellows BK., Kazi DS
Ultralow-dose quadruple combination therapy. A cost effective solution for hypertension control
HEART doi.org/10.1136/heartjnl-2023-323007
[2]Soliman EZ., Rahman AKMF., Zhang Z-m et al
Effect of intensive blood pressure lowering on the risk of atrial fibrillation
HYPERTENSION 2020;75:1491-1496
[3]Upadhya B., Rocco M., Lewis CE et al
Effect of intensive blood pressure treatment on heart failure events in the systolic blood pressure reduction intervention trial
Circ Heart Faul 2017 doi.:10.1161/CIRCHEARTFAILURE.116.003613
[4] Jolobe OMP
Regular exercise as an adjunct to antihypertensive therapy
American Journal of Emergency Medicine 2019;37:530-531
[5] Tse Y-H., Tuet C-Y., Lau K-K., Tse H-F
Dietary modification for prevention and control of high blood pressure
Postgrad Med J 2023 doi.org/10.1093postmjqgad021
[6] Li C., Zhu Y., Ma Y et al
Association of cumulative blood pressure with cognitive decline, dementia, and mortality
JACC 2022;79:1321-1335
[7] Johnson KC., Whelton PK., Cushman WC et al
Blood pressure measurement in SPRINT(systolic blood pressure intervention trial)
HYPERTENSION 2018;71:848-857
[8] Cheung AK., Whelton PK., Muntner P et al
International consensus on standardized cliic blood pressure measurement-a call to action
Am J Med drg/10/1016/j.amje,d.2022.12.015
Graham et al. reported the prevalence of anaemia and iron deficiency in patients with cardiovascular disease, aged ≥50 years (1). Prevalence of anaemia in patients with and without heart failure were 46%, and 29%, respectively. In addition, low haemoglobin and transferrin saturation, but not low ferritin, were associated with a worse prognosis. I have two comments.
First, Mahendiran et al. reported that patients with acute coronary syndromes (ACS) and anaemia at admission was significantly associated with 1-year all-cause mortality and cardiovascular events (2). Colombo et al. also conducted a prospective study, with median follow-up of 4.9 years, to investigate the relationship between anaemia and cardiovascular events in patients with ACS (3). The adjusted hazard ratio (95% confidence intervals [CI]) of patients with anaemia at admission against patients without anaemia throughout admission for was 1.51 (1.02-2.25). I suppose that the severity of ACS, including progression of heart failure, may also be closely related to subsequent prognosis.
Second, Graham et al. made an emphasis that anaemia would contribute to a worse prognosis in patients with cardiovascular disease (1). Salisbury et al. reported the risk of in-hospital mortality in relation to anaemia after hospitalization in patients with acute myocardial infarction (4). When the severity of anaemia was classified into three levels of haemoglobin, mild (>11 g/dL), moderate (9-11 g/dL), and severe...
Graham et al. reported the prevalence of anaemia and iron deficiency in patients with cardiovascular disease, aged ≥50 years (1). Prevalence of anaemia in patients with and without heart failure were 46%, and 29%, respectively. In addition, low haemoglobin and transferrin saturation, but not low ferritin, were associated with a worse prognosis. I have two comments.
First, Mahendiran et al. reported that patients with acute coronary syndromes (ACS) and anaemia at admission was significantly associated with 1-year all-cause mortality and cardiovascular events (2). Colombo et al. also conducted a prospective study, with median follow-up of 4.9 years, to investigate the relationship between anaemia and cardiovascular events in patients with ACS (3). The adjusted hazard ratio (95% confidence intervals [CI]) of patients with anaemia at admission against patients without anaemia throughout admission for was 1.51 (1.02-2.25). I suppose that the severity of ACS, including progression of heart failure, may also be closely related to subsequent prognosis.
Second, Graham et al. made an emphasis that anaemia would contribute to a worse prognosis in patients with cardiovascular disease (1). Salisbury et al. reported the risk of in-hospital mortality in relation to anaemia after hospitalization in patients with acute myocardial infarction (4). When the severity of anaemia was classified into three levels of haemoglobin, mild (>11 g/dL), moderate (9-11 g/dL), and severe (< 9 g/dL), the adjusted odds ratios (95% CIs) of moderate and severe anaemia against no anaemia for in-hospital mortality were 1.38 (1.10-1.73) and 3.39 (2.59-4.44), respectively. Severity of anaemia may be a key factor to assess the in-hospital mortality. Severity of anaemia in patients with ACS would contribute to the increased risk of mortality, and controlling anaemia might relate to subsequent prognosis, which should be examined by interventional studies (5).
References
1. Graham FJ, Friday JM, Pellicori P, et al. Assessment of haemoglobin and serum markers of iron deficiency in people with cardiovascular disease. Heart 2023;109(17):1294-1301.
2. Mahendiran T, Nanchen D, Gencer B, et al. Prognosis of patients with chronic and hospital-acquired anaemia after acute coronary syndromes. J Cardiovasc Transl Res 2020;13(4):618-628.
3. Colombo C, Rebora P, Montalto C, et al. Hospital-acquired anemia in patients with acute coronary syndromes: epidemiology and potential impact on long-term outcome. Am J Med. 2023 Sep 11. doi: 10.1016/j.amjmed.2023.08.012. [Epub ahead of print]
4. Salisbury AC, Amin AP, Reid KJ, et al. Hospital-acquired anemia and in-hospital mortality in patients with acute myocardial infarction. Am Heart J 2011;162(2):300-309.e3.
5. Kang SH, Moon JY, Kim SH, et al. Association of hemoglobin levels with clinical outcomes in acute coronary syndromes in Koreans. Medicine (Baltimore). 2022;101(52):e32579.
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
Over and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
In the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the association of type 1 diabetes and fulminant viral , the latter characterised by ST segment elevation, serum troponin elevation and severe left ventricular systolic dysfunction giving rise to cardiogenic pulmonary oedema[3]. In the latter example parainfluenza-3 was believed to be the underlying cause of both the diabetic decompensation and the severe left ventricular systolic dysfunction[3]. A viral aetiology was also suspected but not serologically proven in a 47 year old patient who experienced a prodrome of fever, vomiting, and diahrroea before she was admitted with severe DKA and pain-free ST segment elevation associted with serum troponin elevation but no angiographically demonstrable coronary occlusion. Endomyocardial biopsy showed a mild accumulation of mononuclear cells in the myocardial interstitium[4].
Diabetic ketoacidosis can also be complicated by the occurrence of pain-free Takotsubo myocarditis with STEMI-like presentation[5][6]]. In both cases coronary angiography did not reveal any coronary occlusion.
The differential diagnosis of pain-free DKA-related STEMI extends to the association of DKA-related hyperkalaemia and ST segment elevation[7],[8]. Only one of the two patients had a raised serum troponin[8]. Both patients had total absence of coronary artery occlusion on coronary angiography. In another severely hyperkalaemic patient(serum potassium 9.0 mmol/l) the ST segment elevation had a Brugada syndrome configuration. Serum troponin peaked at 20.452 mcg/L but no occlusive lesion was documented on coronary angiography[9].
DKA-related ST segment elevation can also occur in patients who are normokalaemic, and have normal serum troponin and no abnormality on coronary angiography[10]. Euglycaemic DKA was the associated feature in the latter patient[10].
Comment
Patients with unrecognised Type 1 STEMI complicated by decompensated CHF incur the double jeopardy of “missing out on coronary reperfusion therapy and also run the risk of inappropriate administration of large volumes of intravenous fluids for the management of DKA-related metabolic decompensation.
DKA patients with hyperkalaemia related ST elevation and serum troponin elevation run the risk of mistaken diagnosis of type 2 acute myocardial infarction
Clinicians must be vigilant for both types of eventualities in DKA patients presenting with pain-free ST segment elevation
I have no funding and no conflict of interest
References
[1]Kumar A., Sanghera A., Sanghera B et al
Chest pain symptoms during myocardial infarction in patients with and without diabetes: a systematic review and meta-analysis
Heart doi. 10.1136/heartjnl-2022-322289
[2]Baral N., Montalbano A., KhanA., Qureshi M., Luitel P
Silent myocardial infarction and acute multiorgan failure in a COVID-19 patient: A case report
J Nepal Med Assoc 2021;59:1048-1051
[3]Ohara N., Kaneko M., Kuwano H et al
Fulminant Type 1 diabetes mellitus and fulminant viral myocarditis: A case report and literature review
Int Heart J 2015;56:239-244
[4]Hiramatsu S., Komori K., Mori E et al
A case of fulminant type 1 diabetes mellitus accompoanied by myocarditis
Endocrine Journal 2011;58:553-557
[5]Patel KKHP., Soe HM
Association of diabetic ketoacidosis with Takotsubo cardiomyopathy
CHEST doi:https://doi.org/10.1016/chest.2020.08.283
[6] Gordon A., LaCapra G., Roberti R
DKA-induced Takotsubo cardiomyopathy in patient with known HOCM
Case Reports in Critical Care 2017 doi.org/10.1155/2017/4287125
[7]Ziakas A., Basangiannis C., Stiliadis I
Pseudoinfarction pattern in a patient with hyperkalaemia, diabetic ketoacidosis and normal coronary vessels: a case report
Journal of Medical Case Reports 2020;4:115
[8]Sharma E., Dagal S., Sharma P., Ghimire DKC., Dahal S
A case of pseudo infarction pattern in diabetic ketoacidosis
A diagnostic and therapeutic dilemma
Cardiol Res 2018;9:250-252
[9] Pfirman KS., Donley CJ., Fryman EB., Champaneria SU., Gatewood WT
Brugada pattern manifesting during hyperkalaemia, diabetic ketoacidosis, and acute alcohol intoxication
American Journal of Case Reports 2021;22;e932048
[10]Jay DR., Henry TD., Sharkey SW
Acute inferior myocardial infarction or Not?
JAMA Internal Medicine 2022;182:224-225
I have known this for years. A silent heart attack is relatively more common in a patient with diabetes than in a patient without diabetes. However this then leads to the medical myth that patients with diabetes mostly get silent ischaemia, leading to possible over-investigation of patients with diabetes and non-cardiac pain. It should thus be part of teaching that most patients with diabetes still get typical chest pain during a heart attack - I have long used a 80/20 vs 90/10 rule, the % of patients who have chest pain during a heart attack/do not have chest pain, diabetics vs non-diabetics.
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
Over and above the scenario cited by the authors, where the presence of Roth spots became a "red flag" for infective endocarditis(IE)[1], clinicians also need to take note of endogenous endophthalmitis as a "red flag" for IE, both in the context of native valve IE, and in the context of intracardiac device-related IE.
Endophthalmitis and native valve infective endocarditis:-
Awareness of endophthalmitis as a manifestation of IE is of heightened value when IE presents in the absence of a cardiac murmur, so-called "silent" infective endocarditis. In one patient with silent IE , Roth spots were identified in the same eye that was affected by endogenous endophthalmitis[2]. In another patient with silent IE initial transthoracic echocardiography(TTE) did not disclose any vegetations. Ten days later, however, transoesophageal echocardiography(TOE) disclosed the presence of vegetations[3]. The clinical course of another patient with silent IE was characterised by non diagnostic initial TTE, and nondiagnostic TOE on day 12. On day 31, however, TOE showed severe aortic regurgitation and what appeared to be a vegetation on the aortic valve. Intraoperatively, however, what had previously appeared to be a vegetation proved to be a destroyed non coronary valve tip[4].
Endophthalmitis and infective endocarditis attributable to intracardiac devices:-
Endogenous endophthalmitis is also a red flag for infective endocarditis attr...
Show MoreIt is, indeed, a truism that poor rates blood pressure(BP) control are, in part, attributable to clinical inertia, whereby therapy is not escalated when BP is uncontrolled[1]. However, the criterion for escalation of antihypertensive therapy utilised by the authors, namely, a BP amounting to 140/90 mm Hg or more[1], is inappropriate, given the fact that the goal BP most likely to mitigate the risk of incident hypertension-related atrial fibrillation(AF) and hypertension-related congestive heart failure(CHF), respectively, is a goal BP amounting to < 120/80 mm Hg[2],[3]. In principle, that goal BP can be achieved by ultralow-dose quadruple combination therapy either on its own or in combination with lifestyle antihypertensive strategies such as regular exercise[4] and low-salt diet with or without abstinence from alcohol[5]. The younger the patient the more compelling the requirement to attain a BP amounting to < 120/80 mm Hg because it is theoretically possible that the longer the duration of suboptimal blood pressure the greater the long term risk of AF, CHF, and, arguably, hypertension-related vascular dementia[6].
Show MoreAttainment of optimum goal BP crucially depends on accurate measurement of both "office" and home blood pressures[7],[8], and both those goals are predicated on the use of well-validated blood pressure monitors[8]. However, the minimum requirement for ultimate success in the control of BP is an honest conversation between doctor...
Graham et al. reported the prevalence of anaemia and iron deficiency in patients with cardiovascular disease, aged ≥50 years (1). Prevalence of anaemia in patients with and without heart failure were 46%, and 29%, respectively. In addition, low haemoglobin and transferrin saturation, but not low ferritin, were associated with a worse prognosis. I have two comments.
First, Mahendiran et al. reported that patients with acute coronary syndromes (ACS) and anaemia at admission was significantly associated with 1-year all-cause mortality and cardiovascular events (2). Colombo et al. also conducted a prospective study, with median follow-up of 4.9 years, to investigate the relationship between anaemia and cardiovascular events in patients with ACS (3). The adjusted hazard ratio (95% confidence intervals [CI]) of patients with anaemia at admission against patients without anaemia throughout admission for was 1.51 (1.02-2.25). I suppose that the severity of ACS, including progression of heart failure, may also be closely related to subsequent prognosis.
Second, Graham et al. made an emphasis that anaemia would contribute to a worse prognosis in patients with cardiovascular disease (1). Salisbury et al. reported the risk of in-hospital mortality in relation to anaemia after hospitalization in patients with acute myocardial infarction (4). When the severity of anaemia was classified into three levels of haemoglobin, mild (>11 g/dL), moderate (9-11 g/dL), and severe...
Show MoreOver and above the issues raised by the authors[1], clinicians also need to be aware that pain-free diabetic ketoacidosis(DKA)-related myocardial infarction has the sinister dimension of being a potential harbinger of multiorgan failure, including congestive heart failure(CHF) and acute renal failure(ARF), especially in the context of intercurrent infection[2]. Furthermore, even in the context of severe DKA-related metabolic decompensation, the presence of myocardial infarction-related CHF demands a departure from the usual practice of administration of large amounts of intravenous fluids for the management of DKA. Accordingly, when a 77 year old patient presented with COVID-19 pneumonia, in association with CHF-related pulmonary oedema attributable to Type 1 ST elevation myocardial infarction(STEMI), the latter complicated by left ventricular systolic failure, the metabolic decompensation was managed with intravenous insulin infusion without the concomitant administration of large amounts of intravenous fluids which characterises conventional regimens for management of DKA. STEMI was managed by insertion of a stent in the occluded culprit coronary artery. In spite of subsequent development of ARF temporarily requiring hemodialysis, and in spite of an episode of haematemesis, the patient was eventually successfully discharged to an extended care facility[2].
Show MoreIn the absence of chest pain, the differential diagnosis DKA-related Type 1 STEMI includes the assoc...
I have known this for years. A silent heart attack is relatively more common in a patient with diabetes than in a patient without diabetes. However this then leads to the medical myth that patients with diabetes mostly get silent ischaemia, leading to possible over-investigation of patients with diabetes and non-cardiac pain. It should thus be part of teaching that most patients with diabetes still get typical chest pain during a heart attack - I have long used a 80/20 vs 90/10 rule, the % of patients who have chest pain during a heart attack/do not have chest pain, diabetics vs non-diabetics.
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...
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