1Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinuora, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan
Address correspondence and reprint requests to: Seigo Okada, M.D., Ph.D.
Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinoura, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan. Tel: 81-93-641-5111; Fax: 81-93-642-1868; E-mail: sokada0901@gmail.com; ORCID: 0000-0002-9150-1913
Dear Editor:
We read the article by Charla et al.1 with great interest. The authors conducted a phase-contrast magnetic resonance study during biphasic ventilation (BPV) in 10 patients aged 20–34 years who had Fontan circulation and 10 matched control subjects. BPV resulted in significant pulmonary blood flow and cardiac output augmentations in the Fontan group, which suggests the importance of “thoracic pump” in Fontan patients without a subpulmonary ventricle. We appreciate the authors’ efforts to assess the efficacy and feasibility of noninvasive external ventilation for Fontan patients. This is a thoughtfully conducted study, but some issues must be further discussed.
First, the authors mentioned that the study was the first to describe the impact of BPV in the Fontan population. However, we...
1Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinuora, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan
Address correspondence and reprint requests to: Seigo Okada, M.D., Ph.D.
Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinoura, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan. Tel: 81-93-641-5111; Fax: 81-93-642-1868; E-mail: sokada0901@gmail.com; ORCID: 0000-0002-9150-1913
Dear Editor:
We read the article by Charla et al.1 with great interest. The authors conducted a phase-contrast magnetic resonance study during biphasic ventilation (BPV) in 10 patients aged 20–34 years who had Fontan circulation and 10 matched control subjects. BPV resulted in significant pulmonary blood flow and cardiac output augmentations in the Fontan group, which suggests the importance of “thoracic pump” in Fontan patients without a subpulmonary ventricle. We appreciate the authors’ efforts to assess the efficacy and feasibility of noninvasive external ventilation for Fontan patients. This is a thoughtfully conducted study, but some issues must be further discussed.
First, the authors mentioned that the study was the first to describe the impact of BPV in the Fontan population. However, we previously described the efficacy of BPV for failing Fontan circulation in a 16-year-old male patient with hypoplastic left heart syndrome who presented protein-losing enteropathy and plastic bronchitis (PB).2 He underwent rehabilitation using an RTX respirator (Medivent Ltd., London, UK) with the vibration mode set at −10/+10 cm H2O for 3 minutes, followed by the cough mode set at −9/+18 for 1 minute, three times for 12 minutes per session.3 The brief period of BPV increased the stroke volume without changing the heart rate. After the start of the BPV, the PB, hypoalbuminemia, and congestive symptoms all improved. No signs of recurrent circulatory failure have since been observed. As the management strategy for the complex pathophysiology of Fontan circulation is not yet established, their and our results suggest that BPV can be an effective treatment and preventive rehabilitation for failing Fontan circulation.
Second, several Fontan patients were likely to have no significant pulmonary blood flow and cardiac output augmentations during BPV.1 In the practical setting of BPV, it is important for a cuirass to fit the patient’s chest. Thereby, we wonder whether overweight or obesity is a risk factor of ineffective BPV. Do you have data regarding the relationship between body mass index and augmentation of pulmonary blood flow during BPV in your cohort? Pulmonary arterial size is an important determinant of pulmonary circulation in Fontan patients. A recent report has shown that pulmonary arterial size expressed as Nakata index is an independent predictor of functional clinical status in adult Fontan patients.4 Thus the relationship between pulmonary arterial size and augmentation of pulmonary blood flow during BPV should also be addressed.
1. Charla P, Karur GR, Yamamura K, et al. Augmentation of pulmonary blood flow and cardiac output by non-invasive external ventilation late after Fontan palliation. Heart Published Online First: 06 July 2020. doi: 10.1136/heartjnl-2020-316613
2. Okada S, Muneuchi J, Nagatomo Y, et al. Successful Treatment of Protein-Losing Enteropathy and Plastic Bronchitis by Biphasic Cuirass Ventilation in a Patient with Failing Fontan Circulation. Int Heart J 2018;59:873-6.
3. Pediheart Podcast 49: Surveillance of the Fontan Patient + Novel Ventilation Approaches for the Fontan Patient. Available from: https://podcasts.apple.com/us/podcast/pediheart-podcast-49-surveillance-... (accessed July 18, 2020).
4. Ridderbos FS, Bonenkamp BE, Meyer SL, et al. Pulmonary artery size is associated with functional clinical status in the Fontan circulation. Heart 2020;106:233-9.
We read with interest the review of non-infective endocarditis by Hurrell et al. [1] and would like to report our experience. We recently reported the case of an asymptomatic, hypertensive 36-year-old man who was found to have a mobile structure attached to the posterior mitral valve leaflet causing moderate eccentric regurgitation on routine echocardiography [2]. Extensive workup was only notable for strongly positive cardiolipin IgG and IgM antibodies and lupus anticoagulant suggesting a diagnosis of antiphospholipid antibody (APLA) syndrome. We referred the patient for surgical intervention (excision and mitral valve repair with a bovine pericardial patch) and this also allowed us to achieve a diagnosis. Histological features were typical of nonbacterial thrombotic endocarditis (NBTE) with fibrin deposits, inflammatory cells and erythrocytes and confirmed an underlying diagnosis of primary APLA syndrome.
The association of APLA syndrome with or without autoimmune disease increases prothrombotic tendency and these patients therefore have a higher likelihood of NBTE which can remain clinically silent. We therefore propose that transthoracic echocardiography should be used as a screening and surveillance tool for NBTE in all patients who are found to have primary or secondary APLA syndrome and potentially in patients with autoimmune disease and hypercoaguable states. We also emphasize consideration of a histological diagnosis when there is diagn...
We read with interest the review of non-infective endocarditis by Hurrell et al. [1] and would like to report our experience. We recently reported the case of an asymptomatic, hypertensive 36-year-old man who was found to have a mobile structure attached to the posterior mitral valve leaflet causing moderate eccentric regurgitation on routine echocardiography [2]. Extensive workup was only notable for strongly positive cardiolipin IgG and IgM antibodies and lupus anticoagulant suggesting a diagnosis of antiphospholipid antibody (APLA) syndrome. We referred the patient for surgical intervention (excision and mitral valve repair with a bovine pericardial patch) and this also allowed us to achieve a diagnosis. Histological features were typical of nonbacterial thrombotic endocarditis (NBTE) with fibrin deposits, inflammatory cells and erythrocytes and confirmed an underlying diagnosis of primary APLA syndrome.
The association of APLA syndrome with or without autoimmune disease increases prothrombotic tendency and these patients therefore have a higher likelihood of NBTE which can remain clinically silent. We therefore propose that transthoracic echocardiography should be used as a screening and surveillance tool for NBTE in all patients who are found to have primary or secondary APLA syndrome and potentially in patients with autoimmune disease and hypercoaguable states. We also emphasize consideration of a histological diagnosis when there is diagnostic uncertainty – tissue is the issue. Continued anticoagulation is particularly important in NBTE, irrespective of aetiology and even after surgical resection, because of the high incidence of associated embolic and vaso-occlusive events. In fact, the diagnosis is usually reached at post-mortem.
The benefits of regular exercise are non deniable with reduction in all cause, cardiovascular and cancer mortality (1,2,3). Endurance exercise with increase in cardiac output results in dilatation of left ventricular cavity size and eccentric hypertrophy with low normal ejection fraction that is a dilated cardiomyopathy phenocopy. The ability to distinguish true pathology from physiological remodelling remains a difficult area for cardiologists. Frequently asymptomatic athletic individuals are referred to the cardiology service with abnormal resting 12 lead ECGs. They must be appropriately investigated. The dimema for the investigating cardiologist is to determine the healthy athlete from the athlete with DCM. An erroneous diagnosis of DCM in an athlete may lead to unnecessary disqualification from sport, unnecessary pharmacotherapy and a decline in physical and psychological well being as well as implications for life insurance. Millar et al study adds vital information to the field (4). It is reassuring that the study reported that none of the athletes with a physiologically increased LV size and borderline or low resting LV ejection fraction (grey-zone participants) had replacement fibrosis of the left ventricular myocardium on cardiac MRI. In addition, the authors have reported that functional assessment of the heart by stress echocardiography can discriminate between DCM and DCM phenocopy with high sensitivity and specificity. This study will likely be a game...
The benefits of regular exercise are non deniable with reduction in all cause, cardiovascular and cancer mortality (1,2,3). Endurance exercise with increase in cardiac output results in dilatation of left ventricular cavity size and eccentric hypertrophy with low normal ejection fraction that is a dilated cardiomyopathy phenocopy. The ability to distinguish true pathology from physiological remodelling remains a difficult area for cardiologists. Frequently asymptomatic athletic individuals are referred to the cardiology service with abnormal resting 12 lead ECGs. They must be appropriately investigated. The dimema for the investigating cardiologist is to determine the healthy athlete from the athlete with DCM. An erroneous diagnosis of DCM in an athlete may lead to unnecessary disqualification from sport, unnecessary pharmacotherapy and a decline in physical and psychological well being as well as implications for life insurance. Millar et al study adds vital information to the field (4). It is reassuring that the study reported that none of the athletes with a physiologically increased LV size and borderline or low resting LV ejection fraction (grey-zone participants) had replacement fibrosis of the left ventricular myocardium on cardiac MRI. In addition, the authors have reported that functional assessment of the heart by stress echocardiography can discriminate between DCM and DCM phenocopy with high sensitivity and specificity. This study will likely be a game changer in the investigation of athletic remodelling and may reduce the requirement to ask athletic individuals to decondition and refrain from their sport.
1. Parry-Williams, G., Sharma, S. The effects of endurance exercise on the heart: panacea or poison?. Nat Rev Cardiol 17, 402–412 (2020).
2. Fiuza-Luces, C. et al. Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors. Nat. Rev. Cardiol. 15, 731–743 (2018).
3. Pedisic, Z. et al. Is running associated with a lower risk of all-cause, cardiovascular and cancer mortality, and is the more the better? A systematic review and meta-analysis. Br. J. Sports Med.
4.Millar LM, Fanton Z, Finocchiaro G, et al Differentiation between athlete’s heart and dilated cardiomyopathy in athletic individuals Heart 2020;106:1059-1065.
For the sake of completeness, the approach to narrow complex tachycardia(1), and the differential diagnosis of that disorder, should also include the entity of fascicular ventricular tachycardia, in which the duration of the QRS complex does not exceed 120 ms during ventricular tachycardia(VT)(2)(3). There are 3 subtypes, namely, left posterior fascicular VT with right bundle branch(RBBB) morphology and left axis deviation, left anterior fascicular VT with RBBB pattern and right axis deviation, and upper septal fascicular VT with a narrow QRS and normal axis configuration(2).
Talib et al evaluated 10 patients aged 14-66 with upper septal ventricular tachycardia in whom there was no structural heart disease, and in whom the QRS duration amounted to < 120 ms during VT. In 8 instances VT could be terminated by administration of verapamil. In the other 2 instances no attempt had been made to terminate the episodes of VT with that drug. In the verapamil-responsive subjects, the episodes of VT were characterised by QRS duration amounting to 75 ms, 90 ms(two patients), 93 ms, 96 ms, 105 ms, 115 ms, and 118 ms, respectively. In 4 patients precordial QRS configuration during VT was identical to QRS configuration during sinus rhythm. In the other four, QRS configuration was of the RBBB subtype during VT(3).
Narrow complex VT can also be a manifestation of coronary artery disease, but, in this context, there appears to be no involvement of the His-Purki...
For the sake of completeness, the approach to narrow complex tachycardia(1), and the differential diagnosis of that disorder, should also include the entity of fascicular ventricular tachycardia, in which the duration of the QRS complex does not exceed 120 ms during ventricular tachycardia(VT)(2)(3). There are 3 subtypes, namely, left posterior fascicular VT with right bundle branch(RBBB) morphology and left axis deviation, left anterior fascicular VT with RBBB pattern and right axis deviation, and upper septal fascicular VT with a narrow QRS and normal axis configuration(2).
Talib et al evaluated 10 patients aged 14-66 with upper septal ventricular tachycardia in whom there was no structural heart disease, and in whom the QRS duration amounted to < 120 ms during VT. In 8 instances VT could be terminated by administration of verapamil. In the other 2 instances no attempt had been made to terminate the episodes of VT with that drug. In the verapamil-responsive subjects, the episodes of VT were characterised by QRS duration amounting to 75 ms, 90 ms(two patients), 93 ms, 96 ms, 105 ms, 115 ms, and 118 ms, respectively. In 4 patients precordial QRS configuration during VT was identical to QRS configuration during sinus rhythm. In the other four, QRS configuration was of the RBBB subtype during VT(3).
Narrow complex VT can also be a manifestation of coronary artery disease, but, in this context, there appears to be no involvement of the His-Purkinje system, although the underlying mechanism has yet to be fully elucidated(4). In the latter example, a 54 year old man had a previous history of ST segment inferior myocardial infarction characterised by right coronary artery occlusion. One month later he experienced an episode of tachycardia (ventricular rate 140 beats/min) characterised by QRS duration amounting to 120 ms and atrioventricular dissociation(4).
Of all the patients with narrow complex VT the ones most likely to be confused with supraventricular tachycardia are the ones described by Talib et al, in whom QRS duration amounted to < 120 ms during VT. In some of those patients diagnostic confusion would have been compounded by the fact that QRS configuration was the same during sinus rhythm and VT. In those with RBBB during VT a potential diagnostic trap would be attribution of RBBB to rate-dependent aberrant conduction.
I have no funding and no conflict of interest
References
(1)Shah RL., Badhwar N
Approach to narrow complex tachycardia: non-invasive guide to interpretation and management
Heart 2020;106:772-783
((2)Ramprakash B., Jaishankar S., Rao H., Narasimhan C
Catheter ablation of fascicular ventricular tachycardia
Indian Journal Pacing and Electrophysiology www.ipej.org 193-201
(3)Talib AK., Nogami A., Nishiuchi S et al
Verapamil-sensitive upper septal idiopathjic left ventricular tachycardia
JACC;Clinical Electrophysiology 2015;1:369-380
(4)Sakamoto T., Fujiki A., Nakatani Y. et al
Narrow QRS ventricular tachycardia from the posterior mitral annulus without involvement of the His-Purkinje system in a patient with prior inferior myocardial infarction
Heart Vessels 2010;25;170-173
The authors (Nazir et al) of the review of CT fractional flow reserve published in Heart are to be congratulated on very well balanced and well written review of this relatively new technology (1).
We would like to raise a couple of points regarding imaging stress tests functioning as a gatekeeper to invasive coronary angiography after a stenosis is identified on CTCA. A recent survey of UK cardiologists identified imaging stress tests as the most common approach to assess the functional significance of a moderate stenosis (50-70%) on CTCA, with only 2% electing to use CT-FFR (2). The current increase in the use of CT-FFR is because it is nationally funded. Importantly, stress echocardiography is a very low cost test with a national tariff of £177, which compares favourably with the new reduced tariff for CT-FFR of £530. With time, this may be re-balance in favour of CT-FFR if the tariff drops further, particularly given the attraction of a single patient episode and with an anticipated growth of cardiac CT in line with NICE recommendations.
It is important to remind readers that the PLATFORM (3) trial compared CTCA plus CT-FFR versus the standard of care in patients with stable chest pain. The patients were divided into an invasive sub-study (n=380) and a non-invasive sub-study (n=204) and the end point of the study was reduction of invasive coronary angiography that showed no obstructive CAD. In the non-invasive sub-study there was no difference in the r...
The authors (Nazir et al) of the review of CT fractional flow reserve published in Heart are to be congratulated on very well balanced and well written review of this relatively new technology (1).
We would like to raise a couple of points regarding imaging stress tests functioning as a gatekeeper to invasive coronary angiography after a stenosis is identified on CTCA. A recent survey of UK cardiologists identified imaging stress tests as the most common approach to assess the functional significance of a moderate stenosis (50-70%) on CTCA, with only 2% electing to use CT-FFR (2). The current increase in the use of CT-FFR is because it is nationally funded. Importantly, stress echocardiography is a very low cost test with a national tariff of £177, which compares favourably with the new reduced tariff for CT-FFR of £530. With time, this may be re-balance in favour of CT-FFR if the tariff drops further, particularly given the attraction of a single patient episode and with an anticipated growth of cardiac CT in line with NICE recommendations.
It is important to remind readers that the PLATFORM (3) trial compared CTCA plus CT-FFR versus the standard of care in patients with stable chest pain. The patients were divided into an invasive sub-study (n=380) and a non-invasive sub-study (n=204) and the end point of the study was reduction of invasive coronary angiography that showed no obstructive CAD. In the non-invasive sub-study there was no difference in the rate of invasive coronary angiography between imaging stress tests and CTCA plus CT-FFR. In the invasive sub-study, CTCA plus CT-FFR reduced the rate of invasive coronary angiography as only patients found to have significant stenosis on CTCA and positive CT-FFR went on to have an invasive coronary angiogram, while in the invasive arm all patients had to undergo invasive coronary angiogram ± invasive FFR.
Finally, the ISCHAEMIA trial (4) would suggest that following CT assessment of the coronary arteries and exclusion of left main stem disease, further investigation to assess significance of coronary stenoses is not necessarily required should symptoms be controlled on optimal medical therapy.
1. Nazir MS, Mittal TK, Weir-McCall J, et al Opportunities and challenges of implementing computed tomography fractional flow reserve into clinical practice Heart Published Online First: 19 June 2020. doi: 10.1136/heartjnl-2019-315607
2. Fyyaz S, Papachristidis A, Byrne J, Alfakih K. Opinions on the expanding role of CTCA in patients with stable chest pain and beyond: a UK survey. The British Journal of Cardiology. 2018;25:107-9 doi: 10.5837/bjc.2018.019
3. Hlatky MA, De Bruyne B, Pontone G, et al. PLATFORM Investigators. Quality-of-Life and Economic Outcomes of Assessing Fractional Flow Reserve With Computed Tomography Angiography: PLATFORM. J Am Coll Cardiol 2015;66:2315-2323.
4. Maron DJ, Hochman JS, Reynolds HR, Bangalore S, O’Brien SM, Boden WE, et al. Initial Invasive or Conservative Strategy for Stable Coronary Disease. New England Journal of Medicine. 2020.
A review of comparative incidence of infective endocarditis in bioprosthetic vs mechanical valves (1) can only be complete if there is a clear statement of the criteria for the diagnosis of infective endocarditis. An important characteristic of prosthetic valve endocarditis is that "the diagnosis[of endocarditis] is more difficult in the presence of a prosthetic valve when compared with a native valve" due to the fact that "the Duke criteria have been shown to be less helpful in prosthetic valve endocarditis because of lower sensitivity in this setting"(2). Furthermore,
the diagnostic accuracy of some imaging modalities is suboptimal in prosthetic valve endocarditis(3). According to the latter review , among patients with suspected prosthetic valve endocarditis sensitivity of transthoracic echocardiography can be as low as 17%-36%. For transoesophageal echocardiography(TOE) that parameter increases to 82-96%, the latter statistic comparable to the sensitivity associated with 18 Fluorodeoxyglucose positron emission tomography/CT(PET/CT). Also in the context of prosthetic valve endocarditis, TOE and PET/CT also have comparable specificities in the range 80-96%(3). The major limitation of TOE is that it is invasive and also operator dependent. By contrast PET/CT not only increases the sensitivity of the modified Duke criteria from 70% to 97%(without affecting specificity) but that modality also identifies metastatic septic embol...
A review of comparative incidence of infective endocarditis in bioprosthetic vs mechanical valves (1) can only be complete if there is a clear statement of the criteria for the diagnosis of infective endocarditis. An important characteristic of prosthetic valve endocarditis is that "the diagnosis[of endocarditis] is more difficult in the presence of a prosthetic valve when compared with a native valve" due to the fact that "the Duke criteria have been shown to be less helpful in prosthetic valve endocarditis because of lower sensitivity in this setting"(2). Furthermore,
the diagnostic accuracy of some imaging modalities is suboptimal in prosthetic valve endocarditis(3). According to the latter review , among patients with suspected prosthetic valve endocarditis sensitivity of transthoracic echocardiography can be as low as 17%-36%. For transoesophageal echocardiography(TOE) that parameter increases to 82-96%, the latter statistic comparable to the sensitivity associated with 18 Fluorodeoxyglucose positron emission tomography/CT(PET/CT). Also in the context of prosthetic valve endocarditis, TOE and PET/CT also have comparable specificities in the range 80-96%(3). The major limitation of TOE is that it is invasive and also operator dependent. By contrast PET/CT not only increases the sensitivity of the modified Duke criteria from 70% to 97%(without affecting specificity) but that modality also identifies metastatic septic emboli(3). The caveat is that false positives may occur soon after prosthetic valve implantation(due to reactive inflammatory activity) whereas false negatives may be attributable to previous antibiotic therapy or attributable to small vegetations(3). Further support for PET/CT comes from a study of 303 subjects who underwent PET/CT evaluation for suspected aortic valve endocarditis and for suspected infection of ascending aortic prostheses . 141 had bioprosthetic valves, and 10 had mechanical valves. 115 had native valves. The rest had ascending aortic prostheses. Among the 188 with an eventual diagnosis of either prosthetic valve endocarditis or an ascending aortic implant infection the sensitivity, specificity, and positive and negative predictive values of PET/CT amounted to 93%, 90%, 89%, and 94%, respectively. Among the 115 subjects with native valve endocarditis the corresponding values were 22%, 100%, 100%, and 66%(4).
Fungal endocarditis, for which prosthetic valve implantation is also a risk factor, poses additional challenges because there are no diagnostic criteria specific to fungal endocarditis. Potential imaging modalities in this context include PET/CT, complemented by magnetic resonance imaging of the head in patients who have embolic phenomena, and abdominal computed tomography for suspected intra abdominal emboli(5).
Although it is an important caveat that PET/CT is expensive and not widely available, and that preprocedural fasting and dietary regimes still have to be optimised(6) , the reality is the the use of PET/CT has highlighted the recognition that there is a huge potential for underdiagnosis of prosthetic valve endocarditis with the use of less expensive but more widely available technologies, thereby undermining any attempts to evaluate the prevalence of prosthetic valve endocarditis, let alone its prevalence in subgroups of prosthetic valve recipients.
I have no funding and no conflict of interest
References
(1) Anantha-Naranayan M., Reddy YNV., Sundaram V et al
Endocarditis risk with bioprosthetic and mechanical valves: systematic review and meta-analysis
Heart doi 10.1136/heartjnl-2020-316718
(2)Bruun NE., Habib G., Thuny F., Sogaard P
Cardiac imaging in infectious endocarditis
Eur heart J 2014;35:624-632
(3)Ivanovic B., Trifunovic D., Matic S., et al
Prosthetic valve endocarditis- A trouble or a challenge?
Journal of Cardiology 2019;73:126-133
(4) de Camargo RA., Bitencourt MS., Monaghetti JC et al
The role of 18 Fluorodeoxyglucose positron emission tomography/computed tomography in the diagnosis of left-side endocarditis: native vs prosthetic valves endocarditis
Clinical Infectious Diseases 2020;70:583-595
(5)Pasha A., Lee JZ., Low S-W., et al
Fungal endocarditis : Update on diagnosis and management
Am J Med 2016;129:1037-1043
(6) Sanbuceti G., Morbelli S., Orengo AM., Bauckneht M., Marini C
18F-Fkuorodeoxyglucose imaging of inflammation Ready to represent a stndard in diagnosing endocarditis?
Circ Cardiovasc Imaging 2017;10:e006185
Regardless of the conclusions of the authors regrading thromboembolic risk(1), atrial fibrillation patients with CHA2DS2 Vasc score of zero or 1 cannot be pronounced to be at truly low risk of stroke unless coexisting high-grade carotid artery stenosis(CAS) has been ruled out. According to one study, among patients with nonvalvular atrial fibrillation(NVAF) who are older than 70 years, the frequency of high grade carotid stenosis(stenosis of 50% or more) is 12% in men and 11% in women(2). High-grade CAS, in turn, is an important risk factor for stroke. Potentially modifiable risk factors for CAS-related stroke include smoking, hypertension, diabetes mellitus, and hyperlipidaemia(3). According to an observational study of subjects with asymptomatic high-grade CAS, progression of the severity of CAS can be mitigated by optimally controlling those risk factors(4). Accordingly, the management of NVAF subjects with CHA2DS2 Vasc score of zero or 1 should include screening for CAS, and optimal control of hypertension, diabetes, and low density lipoprotein levels, over and above cessation of smoking, in the event of a diagnosis of coexisting high-grade CAS. There is also a diagnostic advantage from awareness of the coexistence of high-grade CAS in a patients with zero or 1 CHA2DS2 Vasc score. If such a patient experiences an ischaemic stroke characterised by a cerebral infarct ipsilateral to the high-grade CAS the appropriate management would be prompt prescription o...
Regardless of the conclusions of the authors regrading thromboembolic risk(1), atrial fibrillation patients with CHA2DS2 Vasc score of zero or 1 cannot be pronounced to be at truly low risk of stroke unless coexisting high-grade carotid artery stenosis(CAS) has been ruled out. According to one study, among patients with nonvalvular atrial fibrillation(NVAF) who are older than 70 years, the frequency of high grade carotid stenosis(stenosis of 50% or more) is 12% in men and 11% in women(2). High-grade CAS, in turn, is an important risk factor for stroke. Potentially modifiable risk factors for CAS-related stroke include smoking, hypertension, diabetes mellitus, and hyperlipidaemia(3). According to an observational study of subjects with asymptomatic high-grade CAS, progression of the severity of CAS can be mitigated by optimally controlling those risk factors(4). Accordingly, the management of NVAF subjects with CHA2DS2 Vasc score of zero or 1 should include screening for CAS, and optimal control of hypertension, diabetes, and low density lipoprotein levels, over and above cessation of smoking, in the event of a diagnosis of coexisting high-grade CAS. There is also a diagnostic advantage from awareness of the coexistence of high-grade CAS in a patients with zero or 1 CHA2DS2 Vasc score. If such a patient experiences an ischaemic stroke characterised by a cerebral infarct ipsilateral to the high-grade CAS the appropriate management would be prompt prescription of an antiplatelet agent, followed by urgent carotid endarterectomy or carotid artery stenting
I have no conflict of interest
References
(1) Verbrugge FH., Martin A., Siegel D et al
Impact of oral anticoagulation in patients with atrial fibrillation at very low thromboembolis risk
Heart 2020;106;845-851
(2) Kanter MC., Tegler CH., Pearce LA et al
Carotid stenosis in patients with atrial fibrillation
Arch Intern Med 1994;154:1327-1377
(3) Woo SY., Joh JH., Han S-A., Park H-C
Prevalence and risk factors for atherosclerotic carotid stenosis and plaque
Medicine 2017;96:4
(4) Shah Z., Massoomi R., Thapa R., Wani M et al
Optimal medical management reducews risk of disease progression and iscemic events in asymptomatic carotid stenosis patients: A long-term follow-up study
Cerebrovascular Diseases 2017;44:150-159
(5) Brott TG., Hobson RW., Howard G et al
Stenting versus endarterectomy for treatment of carotid artery stenosis
N Engl J Med 2010;363:11-23
Given the fact that high-sensitivity cardiac troponin is a parameter prevalent, not only in acute myocardial infarction(AMI)(1), but also in close mimics of AMI such as pulmonary embolism(PE)(2) and dissecting aortic aneurysm(DAA)(3), respectively, it is now time for action to be taken to include point-of-care transthoracic echocardiography(TTE) in the algorithm for triaging patients who present with the association of chest pain and an electrocardiogram simulating ST segment elevation myocardial infarction(STEMI). PE subgroups with STEMI-like presentation and DAA subgroups with STEMI-like presentation are each likely to have subsets of subjects with TTE stigmata unique to PE(4) and to DAA(5), respectively, which enable them to be differentiated from subjects with AMI, thereby mitigating the risk of inappropriate percutaneous coronary intervention. When patients with suspected AMI are triaged towards the observation zone that should also be an opportunity to elicit stigmata that might favour a diagnosis of either PE or DAA. For PE those stigmata can be elicited by invoking the Wells clinical decision rule(6), and also by specifically looking for clinical stigmata of deep vein thrombosis(7), and even triggering a Doppler scan of the lower limbs(7), and where appropriate, the upper limbs as well.
For DAA the "red flags" to look for include interarm blood pressure difference(8), the murmur of aortic regurgitation(9), and mediastinal widening(10)(11), the...
Given the fact that high-sensitivity cardiac troponin is a parameter prevalent, not only in acute myocardial infarction(AMI)(1), but also in close mimics of AMI such as pulmonary embolism(PE)(2) and dissecting aortic aneurysm(DAA)(3), respectively, it is now time for action to be taken to include point-of-care transthoracic echocardiography(TTE) in the algorithm for triaging patients who present with the association of chest pain and an electrocardiogram simulating ST segment elevation myocardial infarction(STEMI). PE subgroups with STEMI-like presentation and DAA subgroups with STEMI-like presentation are each likely to have subsets of subjects with TTE stigmata unique to PE(4) and to DAA(5), respectively, which enable them to be differentiated from subjects with AMI, thereby mitigating the risk of inappropriate percutaneous coronary intervention. When patients with suspected AMI are triaged towards the observation zone that should also be an opportunity to elicit stigmata that might favour a diagnosis of either PE or DAA. For PE those stigmata can be elicited by invoking the Wells clinical decision rule(6), and also by specifically looking for clinical stigmata of deep vein thrombosis(7), and even triggering a Doppler scan of the lower limbs(7), and where appropriate, the upper limbs as well.
For DAA the "red flags" to look for include interarm blood pressure difference(8), the murmur of aortic regurgitation(9), and mediastinal widening(10)(11), the latter a simple strategy that can even distinguish between haemoptysis attributable to PE and haemoptysis attributable to DAA(11).
I have no conflict of interest and no funding
References
(1) Chapman AR., Mills NL
High-sensitivity cardiac troponin and the early ruleout of myocardial infarction: time for action
Heart 2020 Vol 0: No 0
(2) Kaeberich A., Seeber V., Jimenez D et al
Age-adjusted high-sensitivity troponin T cut-off value for risk stratification of pulmonary embolism
Eur Respir J 2015;45:1323-1331
(3) Gawinecka J., Schobrath F., von Eckardstein A
Acute aortic dissection;pathogenesis and diagnosis
Swiss Medical Weekly 2017;147:w14489
(4) Shy BD., Gutierrez., Strayer RJ
Bedside ultrasound to evaluate pulmonary embolism masquerading as ST elevation myocardial infarction(STEMI)
Journal of Emergency Medicine 2015;49:703-704
(5) Chenkin J
Diagnosis of aortic dissection presenting as ST-elevation myocardial infarction using point-of care ultrasound
Journal of Emergency Medicine 2017;53:880-884
(6) Wells PS., Anderson DR., Rodger M et al
Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: Increasing the model's utility with simpliRED-D-dimer
Thromb Haemost 2000;83:416-420
(7) Bozorgi A., Rahnamoun Z
Pulmonary thromboembolism initially mistaken for inferior STEMI
Herz 2013;38:553-555
(8) Phowthongkum P
Acute aortic dissection mimics acute inferoposterior wall myocardial infarction in a Marfan syndrome patient
BMJ Case Rep 2010;bcr08.2009.2155
(9) Cai J., Cao Y., Yuan KY., Zhu Y-S
Inferior myocardial infarction secondary to aortic dissection associated with bicuspud aortic valve
Journal of Cardiovascular Disease Research 2012;3:138-142
Al-Whaibi K., Al-Dhuhli H., Diputado T., Alzadjali N
Acute cardiovascular emergency: Missed killer in the emergency room
Oman Medical Journal 2008;23:112-115
(11) Li SW and Osman M
Thoracic aortic aneurysm(TAA) a diagnostic dilemna in a patient with haemoptysis
M-JEM 2017;2:23-27
ACUTE AUTOIMMUNE REACTION: AN OBSCURE MECHANISM OF COVID-19-RELATED MYOCARDIAL INJURY ?
Kenan YALTA, MD a
Ertan YETKIN, MD b
Gokay TAYLAN, MD a
Tulin YALTA, MD c
a Trakya University, Cardiology Department, Edirne, TURKEY
b Istinye University, Liv Hospital, Cardiology Department, Istanbul, TURKEY
c Trakya University, Pathology Department, Edirne, TURKEY
Acute myocardial injury has been suggested as an important prognostic factor in Covid-19 patients (1-3). In their recently published article (1), Wei JF, et al. have demonstrated a significant association of acute myocardial injury (defined as elevation of high sensitive troponin-T (hs-TnT) levels) with older age, pre-existing cardiovascular disease, disease severity (and hence; general frailty) and adverse prognosis in Covid-19 patients . The authors have principally attributed this injury to certain factors including systemic inflammation, hypoxemia and direct myocardial invasion by the viral agent (1). However, as described below, an acute autoimmune reaction triggered by the virus might also be considered as an alternative mechanism of myocardial injury par...
ACUTE AUTOIMMUNE REACTION: AN OBSCURE MECHANISM OF COVID-19-RELATED MYOCARDIAL INJURY ?
Kenan YALTA, MD a
Ertan YETKIN, MD b
Gokay TAYLAN, MD a
Tulin YALTA, MD c
a Trakya University, Cardiology Department, Edirne, TURKEY
b Istinye University, Liv Hospital, Cardiology Department, Istanbul, TURKEY
c Trakya University, Pathology Department, Edirne, TURKEY
Acute myocardial injury has been suggested as an important prognostic factor in Covid-19 patients (1-3). In their recently published article (1), Wei JF, et al. have demonstrated a significant association of acute myocardial injury (defined as elevation of high sensitive troponin-T (hs-TnT) levels) with older age, pre-existing cardiovascular disease, disease severity (and hence; general frailty) and adverse prognosis in Covid-19 patients . The authors have principally attributed this injury to certain factors including systemic inflammation, hypoxemia and direct myocardial invasion by the viral agent (1). However, as described below, an acute autoimmune reaction triggered by the virus might also be considered as an alternative mechanism of myocardial injury particularly in a specific subgroup of Covid-19 patients, and might have potential implications:
Firstly; autoimmune myocardial injury in Covid-19 patients might, paradoxically, be considered as a sign of immunocompetence, and might more likely emerge in apparently healthy and relatively young patients, yet; with a genetic propensity for autoimmune diseases. Moreover, occurence of this phenomenon might not necessarilly be associated with pulmonary disease severity as well. Within this context, potential autoimmune reaction in Covid-19 patients might be susbstantiated by a recent report suggesting a potential link between covid-19 infection and Kawasaki disease (KD) (4) (a multisystemic disease renowned for its genetic and potentially autoimmune basis (5)). Moreover, autoimmunity was recently suggested to account for the evolution of interstitial pneumonia in genetically susceptible covid-19 patients (6). Accordingly, we would like to have information regarding co-existing autoimmune diseases (that might create a proclivity for autoimmune myocardial injury) particularly in those with elevated hs-TnT in the study (1)
Secondly; covid-19-related autoimmune myocardial injury might be due to a variety of molecular mechanisms (including cross reaction, bystander activation, etc. in genetically susceptible subjects (7)), and might be expected to arise particularly during the late course or even after convalescence period of the infection. Importantly, this autoimmune reaction should not be confused with another late presenting phenomenon namely ‘cytokine release syndrome’ (CRS) (2,3) that is well known to arise more likely in fragile subjects (with a deficiency of early cellular immune response to combat the virus), and has a poor prognosis. Accordingly, we wonder whether there were very late presentations of acute myocardial injury (suggestive of an autoimmune reaction) in the study (1).
Thirdly; the degree and extent of autoimmune reaction, if any, to the viral pathogen (possibly also involving other organ systems including vascular structures, etc.) might exclusively determine the prognosis in Covid-19 cases with minimal or no pulmonary findings. In particular, myocardial involvement might be expected to be transient and mild (as analogous to the setting of other acute autoimmune conditions including KD (5)). However, certain immunomodulatory strategies (similar to those in KD (5)) might speed up myocardial recovery, and might improve the prognosis in particular cases suffering acute heart failure.
In summary, autoimmune myocardial injury in covid-19 patients might serve as an important; yet overlooked mechanism of elevated cardiac biomarkers , particularly in apparently healthy and robust subjects regardless of their pulmonary disease severity. However, further implications of this phenomenon still needs to be established in the clinical setting.
Conflict of Interest: None
REFERENCES:
1- Wei JF, Huang FY, Xiong TY, et al. Acute myocardial injury is common in patients with covid-19 and impairs their prognosis. Heart. 2020 Apr 30. pii: heartjnl-2020-317007. doi: 10.1136/heartjnl-2020-317007. [Epub ahead of print].
2- Cheng R, Leedy D. COVID-19 and acute myocardial injury: the heart of the matter or an innocent bystander ? Heart. 2020 Apr 30. pii: heartjnl-2020-317025. doi: 10.1136/heartjnl-2020-317025. [Epub ahead of print].
3- Kang Y, Chen T, Mui D, et al. Cardiovascular manifestations and treatment considerations in covid-19. Heart. 2020 Apr 30. pii: heartjnl-2020-317056. doi: 10.1136/heartjnl-2020-317056. [Epub ahead of print].
4- Jones VG, Mills M, Suarez D, et al. COVID-19 and Kawasaki disease: Novel virus and novel case. Hosp Pediatr. doi.10.1542/hpeds.2020-0123
5- McCrindle BW, Rowley AH, Newburger JW, et al. American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; Council on Cardiovascular Surgery and Anesthesia; and Council on Epidemiology and Prevention. Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation. 2017; 135(17): e927-e999.
6- Caso F, Costa L, Ruscitti P , et al. Could Sars-coronavirus-2 trigger autoimmune and/or autoinflammatory mechanisms in genetically predisposed subjects? Autoimmun Rev. 2020 May;19(5):102524. doi: 10.1016/j.autrev.2020.102524. Epub 2020 Mar 24.
7- Smatti MK, Cyprian FS, Nasrallah GK, et al. Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms. Viruses. 2019 Aug 19;11(8). pii: E762. doi: 10.3390/v11080762.
Among the underlying causes of recurrent pericarditis which require specific treatment strategies (1) mention must also be made of recurrent pericarditis attributable to coeliac disease(2)(3), and recurrent pericarditis attributable either to Type 2 autoimmune endocrinopathy(4) or to hypoadrenalism(5).
Faizallah et al reported 3 patients aged 40, 40, and 56, respectively, with recurrent pericarditis attributable to coeliac disease. The first patient presented with a temperature of 38.5 degrees Celsius, pericardial friction rub, and macrocytic anaemia attributable to folate deficiency. Pericardiocentesis yielded blood stained fluid that tested negative on bacteriological and M tuberculosis culture. Viral studies were negative and there were no malignant cells in the pericardial fluid. He responded well to reducing doses of corticosteroid therapy. However, it was only after a relapse of pericarditis that he had a duodenal biopsy, the latter an evaluation which revealed histological stigmata of coeliac disease. He was subsequently managed with a gluten-free diet(GFD), concurrently with an attempt to taper off the corticosteroid treatment. In spite of two subsequent relapses, corticosteroid treatment was eventually permanently terminated without any further relapse of pericarditis. The second patient was on GFD as well as a small dose of prednisolone at the time of publication of the report. The third patient, characterised by two episodes of pericarditi...
Among the underlying causes of recurrent pericarditis which require specific treatment strategies (1) mention must also be made of recurrent pericarditis attributable to coeliac disease(2)(3), and recurrent pericarditis attributable either to Type 2 autoimmune endocrinopathy(4) or to hypoadrenalism(5).
Faizallah et al reported 3 patients aged 40, 40, and 56, respectively, with recurrent pericarditis attributable to coeliac disease. The first patient presented with a temperature of 38.5 degrees Celsius, pericardial friction rub, and macrocytic anaemia attributable to folate deficiency. Pericardiocentesis yielded blood stained fluid that tested negative on bacteriological and M tuberculosis culture. Viral studies were negative and there were no malignant cells in the pericardial fluid. He responded well to reducing doses of corticosteroid therapy. However, it was only after a relapse of pericarditis that he had a duodenal biopsy, the latter an evaluation which revealed histological stigmata of coeliac disease. He was subsequently managed with a gluten-free diet(GFD), concurrently with an attempt to taper off the corticosteroid treatment. In spite of two subsequent relapses, corticosteroid treatment was eventually permanently terminated without any further relapse of pericarditis. The second patient was on GFD as well as a small dose of prednisolone at the time of publication of the report. The third patient, characterised by two episodes of pericarditis, was successfully managed solely on a GFD, and had remained free of relapses thereafter(2).
Recurrent pericarditis was also reported by Laine and Holt in a 63 year old patient with coeliac disease(3). That patient experienced two episodes of pericarditis, each characterised by pleuritic pain in association with a pericardial friction rub(4).
Recurrent pericarditis is also a feature of autoimmune endocrinopathy. Examples of this phenomenon were documented in patients with primary hypoadrenalism as well as in patients with primary hypothyroidism(4). Hypoadrenalism-related pericarditis may also be associated with life-threatening cardiac cardiac tamponade(5). In the latter report the patient was a 44 year old woman with unequivocal hypoadrenalism(5). The only uncertainty was whether hypoadrenalism primary or secondary(5). Accordingly, at the very least, the work-up of recurrent pericarditis should include evaluation for coeliac disease and evaluation for endocrinopathy.
I have no funding, and no conflict of interest.
References
(1)Cacoub P., Marques C
Acute recurrent pericarditis: from pathophysiology towards new treatment strategy
Heart doi: 10.1136/heartjnl-2019-316481
(2)Faizallah R., Costello FC., Lee FI., Walker R
Adult celiac disease and recurrent pericarditis
Digestive Diseases and Sciences 1982;27:728-730
*3)Laine LA., Holt KM
Recurrent pericarditis and celiac disease
JAMA 1984;252:doi:10.100/jama.1984.03350220074036
(4)Tucker WS., Niblack GD., McLean RH et al
Serositis with autoimmune endocrinopathy: Clinical and Immunogenetic features
Medicine 1987;66:138-147
(5)Manthri S., Bandaru S., Ibrahim A., Mamillapalli C
Acute pericarditis as a presentation of adrenal insufficiency
Cureus 2018;10;e2474 DOI 10.7759/cureus 2474
Biphasic ventilation for failing Fontan physiology
Seigo Okada1, MD, PhD, Jun Muneuchi1, MD, PhD, Mamie Watanabe1, MD
1Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinuora, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan
Address correspondence and reprint requests to: Seigo Okada, M.D., Ph.D.
Department of Pediatrics, Japan Community Healthcare Organization, Kyushu Hospital, 1-8-1, Kishinoura, Yahatanishiku, Kitakyushu, Fukuoka, 806-8501, Japan. Tel: 81-93-641-5111; Fax: 81-93-642-1868; E-mail: sokada0901@gmail.com; ORCID: 0000-0002-9150-1913
Dear Editor:
Show MoreWe read the article by Charla et al.1 with great interest. The authors conducted a phase-contrast magnetic resonance study during biphasic ventilation (BPV) in 10 patients aged 20–34 years who had Fontan circulation and 10 matched control subjects. BPV resulted in significant pulmonary blood flow and cardiac output augmentations in the Fontan group, which suggests the importance of “thoracic pump” in Fontan patients without a subpulmonary ventricle. We appreciate the authors’ efforts to assess the efficacy and feasibility of noninvasive external ventilation for Fontan patients. This is a thoughtfully conducted study, but some issues must be further discussed.
First, the authors mentioned that the study was the first to describe the impact of BPV in the Fontan population. However, we...
TO THE EDITOR:
We read with interest the review of non-infective endocarditis by Hurrell et al. [1] and would like to report our experience. We recently reported the case of an asymptomatic, hypertensive 36-year-old man who was found to have a mobile structure attached to the posterior mitral valve leaflet causing moderate eccentric regurgitation on routine echocardiography [2]. Extensive workup was only notable for strongly positive cardiolipin IgG and IgM antibodies and lupus anticoagulant suggesting a diagnosis of antiphospholipid antibody (APLA) syndrome. We referred the patient for surgical intervention (excision and mitral valve repair with a bovine pericardial patch) and this also allowed us to achieve a diagnosis. Histological features were typical of nonbacterial thrombotic endocarditis (NBTE) with fibrin deposits, inflammatory cells and erythrocytes and confirmed an underlying diagnosis of primary APLA syndrome.
Show MoreThe association of APLA syndrome with or without autoimmune disease increases prothrombotic tendency and these patients therefore have a higher likelihood of NBTE which can remain clinically silent. We therefore propose that transthoracic echocardiography should be used as a screening and surveillance tool for NBTE in all patients who are found to have primary or secondary APLA syndrome and potentially in patients with autoimmune disease and hypercoaguable states. We also emphasize consideration of a histological diagnosis when there is diagn...
The benefits of regular exercise are non deniable with reduction in all cause, cardiovascular and cancer mortality (1,2,3). Endurance exercise with increase in cardiac output results in dilatation of left ventricular cavity size and eccentric hypertrophy with low normal ejection fraction that is a dilated cardiomyopathy phenocopy. The ability to distinguish true pathology from physiological remodelling remains a difficult area for cardiologists. Frequently asymptomatic athletic individuals are referred to the cardiology service with abnormal resting 12 lead ECGs. They must be appropriately investigated. The dimema for the investigating cardiologist is to determine the healthy athlete from the athlete with DCM. An erroneous diagnosis of DCM in an athlete may lead to unnecessary disqualification from sport, unnecessary pharmacotherapy and a decline in physical and psychological well being as well as implications for life insurance. Millar et al study adds vital information to the field (4). It is reassuring that the study reported that none of the athletes with a physiologically increased LV size and borderline or low resting LV ejection fraction (grey-zone participants) had replacement fibrosis of the left ventricular myocardium on cardiac MRI. In addition, the authors have reported that functional assessment of the heart by stress echocardiography can discriminate between DCM and DCM phenocopy with high sensitivity and specificity. This study will likely be a game...
Show MoreFor the sake of completeness, the approach to narrow complex tachycardia(1), and the differential diagnosis of that disorder, should also include the entity of fascicular ventricular tachycardia, in which the duration of the QRS complex does not exceed 120 ms during ventricular tachycardia(VT)(2)(3). There are 3 subtypes, namely, left posterior fascicular VT with right bundle branch(RBBB) morphology and left axis deviation, left anterior fascicular VT with RBBB pattern and right axis deviation, and upper septal fascicular VT with a narrow QRS and normal axis configuration(2).
Show MoreTalib et al evaluated 10 patients aged 14-66 with upper septal ventricular tachycardia in whom there was no structural heart disease, and in whom the QRS duration amounted to < 120 ms during VT. In 8 instances VT could be terminated by administration of verapamil. In the other 2 instances no attempt had been made to terminate the episodes of VT with that drug. In the verapamil-responsive subjects, the episodes of VT were characterised by QRS duration amounting to 75 ms, 90 ms(two patients), 93 ms, 96 ms, 105 ms, 115 ms, and 118 ms, respectively. In 4 patients precordial QRS configuration during VT was identical to QRS configuration during sinus rhythm. In the other four, QRS configuration was of the RBBB subtype during VT(3).
Narrow complex VT can also be a manifestation of coronary artery disease, but, in this context, there appears to be no involvement of the His-Purki...
The authors (Nazir et al) of the review of CT fractional flow reserve published in Heart are to be congratulated on very well balanced and well written review of this relatively new technology (1).
We would like to raise a couple of points regarding imaging stress tests functioning as a gatekeeper to invasive coronary angiography after a stenosis is identified on CTCA. A recent survey of UK cardiologists identified imaging stress tests as the most common approach to assess the functional significance of a moderate stenosis (50-70%) on CTCA, with only 2% electing to use CT-FFR (2). The current increase in the use of CT-FFR is because it is nationally funded. Importantly, stress echocardiography is a very low cost test with a national tariff of £177, which compares favourably with the new reduced tariff for CT-FFR of £530. With time, this may be re-balance in favour of CT-FFR if the tariff drops further, particularly given the attraction of a single patient episode and with an anticipated growth of cardiac CT in line with NICE recommendations.
It is important to remind readers that the PLATFORM (3) trial compared CTCA plus CT-FFR versus the standard of care in patients with stable chest pain. The patients were divided into an invasive sub-study (n=380) and a non-invasive sub-study (n=204) and the end point of the study was reduction of invasive coronary angiography that showed no obstructive CAD. In the non-invasive sub-study there was no difference in the r...
Show MoreA review of comparative incidence of infective endocarditis in bioprosthetic vs mechanical valves (1) can only be complete if there is a clear statement of the criteria for the diagnosis of infective endocarditis. An important characteristic of prosthetic valve endocarditis is that "the diagnosis[of endocarditis] is more difficult in the presence of a prosthetic valve when compared with a native valve" due to the fact that "the Duke criteria have been shown to be less helpful in prosthetic valve endocarditis because of lower sensitivity in this setting"(2). Furthermore,
Show Morethe diagnostic accuracy of some imaging modalities is suboptimal in prosthetic valve endocarditis(3). According to the latter review , among patients with suspected prosthetic valve endocarditis sensitivity of transthoracic echocardiography can be as low as 17%-36%. For transoesophageal echocardiography(TOE) that parameter increases to 82-96%, the latter statistic comparable to the sensitivity associated with 18 Fluorodeoxyglucose positron emission tomography/CT(PET/CT). Also in the context of prosthetic valve endocarditis, TOE and PET/CT also have comparable specificities in the range 80-96%(3). The major limitation of TOE is that it is invasive and also operator dependent. By contrast PET/CT not only increases the sensitivity of the modified Duke criteria from 70% to 97%(without affecting specificity) but that modality also identifies metastatic septic embol...
Regardless of the conclusions of the authors regrading thromboembolic risk(1), atrial fibrillation patients with CHA2DS2 Vasc score of zero or 1 cannot be pronounced to be at truly low risk of stroke unless coexisting high-grade carotid artery stenosis(CAS) has been ruled out. According to one study, among patients with nonvalvular atrial fibrillation(NVAF) who are older than 70 years, the frequency of high grade carotid stenosis(stenosis of 50% or more) is 12% in men and 11% in women(2). High-grade CAS, in turn, is an important risk factor for stroke. Potentially modifiable risk factors for CAS-related stroke include smoking, hypertension, diabetes mellitus, and hyperlipidaemia(3). According to an observational study of subjects with asymptomatic high-grade CAS, progression of the severity of CAS can be mitigated by optimally controlling those risk factors(4). Accordingly, the management of NVAF subjects with CHA2DS2 Vasc score of zero or 1 should include screening for CAS, and optimal control of hypertension, diabetes, and low density lipoprotein levels, over and above cessation of smoking, in the event of a diagnosis of coexisting high-grade CAS. There is also a diagnostic advantage from awareness of the coexistence of high-grade CAS in a patients with zero or 1 CHA2DS2 Vasc score. If such a patient experiences an ischaemic stroke characterised by a cerebral infarct ipsilateral to the high-grade CAS the appropriate management would be prompt prescription o...
Show MoreGiven the fact that high-sensitivity cardiac troponin is a parameter prevalent, not only in acute myocardial infarction(AMI)(1), but also in close mimics of AMI such as pulmonary embolism(PE)(2) and dissecting aortic aneurysm(DAA)(3), respectively, it is now time for action to be taken to include point-of-care transthoracic echocardiography(TTE) in the algorithm for triaging patients who present with the association of chest pain and an electrocardiogram simulating ST segment elevation myocardial infarction(STEMI). PE subgroups with STEMI-like presentation and DAA subgroups with STEMI-like presentation are each likely to have subsets of subjects with TTE stigmata unique to PE(4) and to DAA(5), respectively, which enable them to be differentiated from subjects with AMI, thereby mitigating the risk of inappropriate percutaneous coronary intervention. When patients with suspected AMI are triaged towards the observation zone that should also be an opportunity to elicit stigmata that might favour a diagnosis of either PE or DAA. For PE those stigmata can be elicited by invoking the Wells clinical decision rule(6), and also by specifically looking for clinical stigmata of deep vein thrombosis(7), and even triggering a Doppler scan of the lower limbs(7), and where appropriate, the upper limbs as well.
Show MoreFor DAA the "red flags" to look for include interarm blood pressure difference(8), the murmur of aortic regurgitation(9), and mediastinal widening(10)(11), the...
ACUTE AUTOIMMUNE REACTION: AN OBSCURE MECHANISM OF COVID-19-RELATED MYOCARDIAL INJURY ?
Kenan YALTA, MD a
Ertan YETKIN, MD b
Gokay TAYLAN, MD a
Tulin YALTA, MD c
a Trakya University, Cardiology Department, Edirne, TURKEY
b Istinye University, Liv Hospital, Cardiology Department, Istanbul, TURKEY
c Trakya University, Pathology Department, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
Acute myocardial injury has been suggested as an important prognostic factor in Covid-19 patients (1-3). In their recently published article (1), Wei JF, et al. have demonstrated a significant association of acute myocardial injury (defined as elevation of high sensitive troponin-T (hs-TnT) levels) with older age, pre-existing cardiovascular disease, disease severity (and hence; general frailty) and adverse prognosis in Covid-19 patients . The authors have principally attributed this injury to certain factors including systemic inflammation, hypoxemia and direct myocardial invasion by the viral agent (1). However, as described below, an acute autoimmune reaction triggered by the virus might also be considered as an alternative mechanism of myocardial injury par...
Show MoreAmong the underlying causes of recurrent pericarditis which require specific treatment strategies (1) mention must also be made of recurrent pericarditis attributable to coeliac disease(2)(3), and recurrent pericarditis attributable either to Type 2 autoimmune endocrinopathy(4) or to hypoadrenalism(5).
Show MoreFaizallah et al reported 3 patients aged 40, 40, and 56, respectively, with recurrent pericarditis attributable to coeliac disease. The first patient presented with a temperature of 38.5 degrees Celsius, pericardial friction rub, and macrocytic anaemia attributable to folate deficiency. Pericardiocentesis yielded blood stained fluid that tested negative on bacteriological and M tuberculosis culture. Viral studies were negative and there were no malignant cells in the pericardial fluid. He responded well to reducing doses of corticosteroid therapy. However, it was only after a relapse of pericarditis that he had a duodenal biopsy, the latter an evaluation which revealed histological stigmata of coeliac disease. He was subsequently managed with a gluten-free diet(GFD), concurrently with an attempt to taper off the corticosteroid treatment. In spite of two subsequent relapses, corticosteroid treatment was eventually permanently terminated without any further relapse of pericarditis. The second patient was on GFD as well as a small dose of prednisolone at the time of publication of the report. The third patient, characterised by two episodes of pericarditi...
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