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
The clinical presentation which simulates ST-segment elevation myocardial infarction(STEMI)(1) is one of the most deceptive manifestations of dissecting aortic aneurysm(DAA), deserving detailed analysis notwithstanding its infrequent(2)(3)(4) occurrence. In Zhu et al DAA was prevalent in only 0.5% of 1576 subjects with suspected STEMI(2). Conversely, Kosuge et al documented a 4%(9 patients) prevalence of ST segment elevation among 233 subjects with confirmed DAA(3). In Hirata et al ST segment elevation was prevalent in 8.2% of 159 subjects with type A aortic dissection(4). When ST segment elevation occurs as a manifestation of DAA, there is a high prevalence of involvement of the inferior leads, exemplified by 6 of the 9 patients in Kosuge et al(3)., and seven of the 13 cases in Hirata et al(4)., arguably because type A aortic dissection is more likely to compromise the ostium of the right coronary artery than the ostium of the left coronary artery(5). In view of the life-threatening nature of DAA clinicians should not rely only on clinical decision rules to raise the index of suspicion. The rationale for a more open-minded approach is that clinical decision rules such as the AAD risk score tend to emphasise typical symptoms, such as the "tearing" character of the back pain(1), almost to the total exclusion of less typical symptoms such as nonspecific back pain, the latter typically radiating from a retrosternal chest pain. For example, a literat...
The clinical presentation which simulates ST-segment elevation myocardial infarction(STEMI)(1) is one of the most deceptive manifestations of dissecting aortic aneurysm(DAA), deserving detailed analysis notwithstanding its infrequent(2)(3)(4) occurrence. In Zhu et al DAA was prevalent in only 0.5% of 1576 subjects with suspected STEMI(2). Conversely, Kosuge et al documented a 4%(9 patients) prevalence of ST segment elevation among 233 subjects with confirmed DAA(3). In Hirata et al ST segment elevation was prevalent in 8.2% of 159 subjects with type A aortic dissection(4). When ST segment elevation occurs as a manifestation of DAA, there is a high prevalence of involvement of the inferior leads, exemplified by 6 of the 9 patients in Kosuge et al(3)., and seven of the 13 cases in Hirata et al(4)., arguably because type A aortic dissection is more likely to compromise the ostium of the right coronary artery than the ostium of the left coronary artery(5). In view of the life-threatening nature of DAA clinicians should not rely only on clinical decision rules to raise the index of suspicion. The rationale for a more open-minded approach is that clinical decision rules such as the AAD risk score tend to emphasise typical symptoms, such as the "tearing" character of the back pain(1), almost to the total exclusion of less typical symptoms such as nonspecific back pain, the latter typically radiating from a retrosternal chest pain. For example, a literature search of STEMI-like DAA over the period 2000-February 2020 disclosed 4 patients(5)(6)(7)(8) in whom ST segment elevation in the inferior leads was associated with a clinical presentation which included back pain(with concurrent chest pain), and a clinically detectable murmur of aortic regurgitation, all three stigmata, namely, inferior lead ST segment elevation, back pain, and an aortic regurgitant murmur, deserving to be recognised as "red flags" for DAA in a patient with a clinical presentation which includes electrocardiographic ST segment elevation. None of these 4 patients described the back pain as being "tearing" in character. On the basis of that omission the clinicians who managed those patients initially attributed both the associated chest pain and the ST segment elevation solely to acute myocardial infarction(AMI)(5)(6)(7)(8).
The occurrence of focal neurological signs in a patient with ST segment elevation should also be recognised as a "red flag" for DAA. Over the period 2000-2020 a literature search of STEMI-like DAA disclosed 5 patients in whom inferior ST segment elevation occurred in conjunction with focal neurological symptoms comprising hemiparesis(9), right upper limb pain(10), left arm numbness(11), flaccid paraparesis(12), and paraparesis(13), respectively. One of these patients had nonspecific back pain as well(13).
In conclusion, the occurrence of ST segment elevation in one or more of the inferior leads II,III,AVF(with or without concurrent ST segment elevation in other leads) should raise the index of suspicion for DAA(3)(4), especially when such an occurrence is associated with back pain of any description, and/or clinically detectable aortic regurgitation.
I have no funding and no conflict of interest.
(1) Salmasi MY., Al Saadi N., Hartley P et al
The risk of misdiagnosis in acute thoracic aortic dissection: a review of current guidelines
Heart 2020 doi:10.1136/heartjnl-2019-316322
(2) Zhu Q-y., Tai S., Tang L et al
STEMI could be the primary presentation of acute aortic dissection
Amer J Emerg Med 2017;35:1713-1717
(3) Kosuge M., Uchida K., Imoto K et al
Frequency and implications of ST-T abnormalities on hospital admission electrocardiograms in patients with typeA aortic dissection
Am J Cardiol 2013;112L424-429
(4) Hirata K., Wake M., Kyushima M., Takahashi T et al
Electrocardiographic changes in patients with tyoe A acute aortic dissection. Incidence, patterns and underlying mechniasms in 159 cases
Journal of Cardiology 2010;56:147-153
(5)Palmiera M., Ribeiro HYU., Lira YC et al
Aortic aneurysm with complete atrioventricular block and acute coronary syndrome
BMC Research Notes 2016;9:257
(6) Hawatmeh A., Arqoub AA., Isbitan A., Shamoon F
A case of ascending aortic dissection mimicking acute myocardial infarction and complicated with pericardial tamponade
Cardiovasc Diagn Ther 2016;6:166-171
(7) Tsigkas G., Kasimis G., Theodoropoulos K et al
A successfully thrombolysed acute inferior myocardial infarction due to type A aortic dissection with lethal consequence: the importance of early cardiac echocardiography
Journal of Cardiothoracic surgery 2011;6:101
(8)Fernandez-Jimenez R., Vivas D., de Agustin HA et al
Acute aortic dissection with ongoing right coronary artery and aortic valave involvement
Int J Cardiol 2012;161:e34-e36
(9) Cook J., Aeschlimann S., Fuh A., Kohmoto T., Chang SM
Aortic dissection presenting as concomitant stroke and STEMI
J Human Hypertens 2007;21:818-821
(10) Doksoz A., Ozturk MT., Salha W., Taraktas M., Soydemir H
A case of aortic dissection complicating right subclavian artery occlussion and mimicking inferior myocardial, infarction
Emerg Case Rep 2011;8:40-42
(11) Al-Saad AA., Odunukan OW., Patton JN
Ascending aortic dissection presented as inferior myocardial infarction: a clinical and diagnostic mimicry
BMJ Case Rep 2016;doi:1136/bcr-2016-217543
(12) Tarver K., Kindier H., Lythall D
Extensive aortic dissection presenting as acute inferior myocardial infarction
Heart 2016;doi:10.1136/hrtjnl 2006.097444
(13) Abrams E., Allen A., Lahham S
Aortic dissection with subsequent hemorrhagic tamponade diagnosed with point of care ultrasound in a patient presenting with STEMI
Clin Pract Vases Emerg Med 2019;3:103-105
Release of troponin after exercise stress test in hypertrophic cardiomyopathy
Pawel Petkow Dimitrow1, Renata Rajtar-Salwa2, Tomasz Tokarek2
1 2nd Department of Cardiology, Jagiellonian University Medical College, Kraków, Poland
2 Department of Cardiology and Cardiovascular Interventions, University Hospital, Krakow, Poland
Correspondence to: Paweł Petkow Dimitrow, 2nd Department of Cardiology, Jagiellonian University Medical College, Jakubowskiego 2 Str., 30-688 Krakow, Poland, e-mail: dimitrow@mp.pl, tel. 0048 12 400 22 50
Recently Cramer et al. demonstrated very important observation on troponin level increase after exercise in patients with hypertrophic cardiomyopathy (HCM) [1]. Several concerns regarding to methodology of their study should be explained. Authors decided to perform only one measurement of troponin level at 6 hours after end of exercise. In our opinion, sampling after 6, 12, 18 and 24 hours after exercise provide more adequate profile of troponin level and allow to monitor possible post-exercise ischemia. Furthermore, data on prevalence of silent myocardial ischemia (only troponin increase) should be provided. In our study [2] painless ischemia detected by troponin measurement after normal daily physical activity was present in 25% of HCM patients. In another study [3], among HCM patients monitored by HOLTER ECG during normal daily physical activity, maximum heart rate was higher in th...
Release of troponin after exercise stress test in hypertrophic cardiomyopathy
Pawel Petkow Dimitrow1, Renata Rajtar-Salwa2, Tomasz Tokarek2
1 2nd Department of Cardiology, Jagiellonian University Medical College, Kraków, Poland
2 Department of Cardiology and Cardiovascular Interventions, University Hospital, Krakow, Poland
Correspondence to: Paweł Petkow Dimitrow, 2nd Department of Cardiology, Jagiellonian University Medical College, Jakubowskiego 2 Str., 30-688 Krakow, Poland, e-mail: dimitrow@mp.pl, tel. 0048 12 400 22 50
Recently Cramer et al. demonstrated very important observation on troponin level increase after exercise in patients with hypertrophic cardiomyopathy (HCM) [1]. Several concerns regarding to methodology of their study should be explained. Authors decided to perform only one measurement of troponin level at 6 hours after end of exercise. In our opinion, sampling after 6, 12, 18 and 24 hours after exercise provide more adequate profile of troponin level and allow to monitor possible post-exercise ischemia. Furthermore, data on prevalence of silent myocardial ischemia (only troponin increase) should be provided. In our study [2] painless ischemia detected by troponin measurement after normal daily physical activity was present in 25% of HCM patients. In another study [3], among HCM patients monitored by HOLTER ECG during normal daily physical activity, maximum heart rate was higher in the troponin positive as compared to troponin negative group (139±9 vs. 125±8 [bpm], p<0.05). Similar association was observed in current exercise study [1]. However, peak exercise left ventricular outflow tract gradient (LVOTG ) was not evaluated [1] despite previously reported association with elevated troponin level [4].
To provide more individualised and comprehensive recommendations with regard to exercise intensity in HCM some additional study should be performed with improved methodology including described above criteria.
References:
1. Cramer GE, Gommans DHF, Dieker H, et al. Exercise and myocardial injury in hypertrophic cardiomyopathy. Heart Published Online First: 30 January 2020. doi: 10.1136/heartjnl-2019-315818
2. Gębka A, Rajtar-Salwa R, Dziewierz A, Dimitrow P. Painful and painless myocardial ischemia detected by elevated level of high-sensitive troponin in patients with hypertrophic cardiomyopathy. Adv Interv Cardiol. 2018; 14: 195-198.
3. Hładij R, Rajtar-Salwa R, Petkow Dimitrow P. Associaton of elevated troponin levels with increased heart rate and higher frequency of nonsustained ventricular tachycardia in hypertrophic cardiomyopathy. Pol Arch Intern Med. 2017; 126: 445-447.
4. Rajtar-Salwa R, Gębka A, Dziewierz A, Dimitrow PP. Hypertrophic Cardiomyopathy: The Time-Synchronized Relationship between Ischemia and Left Ventricular Dysfunction Assessed by Highly Sensitive Troponin I and NT-proBNP. Dis Markers. 2019: 6487152.
ACUTE OR PRE-EXISTING CORONARY SLOW FLOW IN TAKOTSUBO CARDIOMYOPATHY: DOES IT MATTER ?
Kenan YALTA, MD a
Tulin YALTA, MD b
Muhammet GURDOGAN, MD a
aTrakya University, Cardiology Department, Edirne, TURKEY
b 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: 0090505657985
In the setting of takotsubo cardiomyopathy (TTC), coronary microvascular dysfunction has been mostly considered as a causative factor (1,2). In their recently published article (1), Montone RA et al have demonstrated, for the first time, the prognostic value of coronary slow flow (CSF) phenomenon in TTC patients. Of note, as we previously discussed, on a theoretical basis, the particular prognostic value of CSF phenomenon in these patients (3), we feel now pleased to notice that this theory has been fully confirmed by a well-designed study (1). Nevertheless, we would like to make a few comments on this issue:
Firstly; temporal emergence of CSF phenomenon might possibly matter in TTC as well. Accordingly; an acutely evolving CSF pattern (due to severe adrenergic discharge (1)) as compared with a sole pre-existing one (emerging long before the index TTC as part of generalized...
ACUTE OR PRE-EXISTING CORONARY SLOW FLOW IN TAKOTSUBO CARDIOMYOPATHY: DOES IT MATTER ?
Kenan YALTA, MD a
Tulin YALTA, MD b
Muhammet GURDOGAN, MD a
aTrakya University, Cardiology Department, Edirne, TURKEY
b 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: 0090505657985
In the setting of takotsubo cardiomyopathy (TTC), coronary microvascular dysfunction has been mostly considered as a causative factor (1,2). In their recently published article (1), Montone RA et al have demonstrated, for the first time, the prognostic value of coronary slow flow (CSF) phenomenon in TTC patients. Of note, as we previously discussed, on a theoretical basis, the particular prognostic value of CSF phenomenon in these patients (3), we feel now pleased to notice that this theory has been fully confirmed by a well-designed study (1). Nevertheless, we would like to make a few comments on this issue:
Firstly; temporal emergence of CSF phenomenon might possibly matter in TTC as well. Accordingly; an acutely evolving CSF pattern (due to severe adrenergic discharge (1)) as compared with a sole pre-existing one (emerging long before the index TTC as part of generalized endothelial dysfunction) might have stronger cardiovascular prognostic implications in the acute course of TTC (3). In contrast, a pre-existing CSF pattern might be associated with a poor long-term prognosis largely driven by the underlying systemic condition. In this context, CSF pattern in the settings of malignancy and neurological disease might have possibly risen as a pre-existing phenomenon in the present study (1).
Secondly; it seems quite challenging to identify whether a CSF pattern in TTC patients appears to be an acute or pre-existing phenomenon (or both) based on a single coronary angiogram (CAG) (unless making a comparison with previous CAG data). However, a sole pre-existing CSF pattern might be relatively mild and diffuse in nature as compared with a sole or superimposed acute CSF in these patients. Accordingly, did the extent and severity of CSF patterns significantly differ between those with acute cardiac complications (mostly arising due to an acute CSF) and those with exclusively long-term events on follow-up (mostly due to the systemic condition (1) associated with pre-existing CSF) ? In particular, potential prediction of an acute or exclusively pre-existing CSF pattern based on angiographic features might help establish further clinical strategies to improve prognosis (for instance; close supervision for expected acute complications or further diagnostic tests (1) for an obscure malignancy, etc.).
Lastly; vasodilator strategies in TTC patients with a CSF pattern (particularly with a predominant acute component) might be of significant benefit (4). Moreover, given the potential association of future TTC recurrences with excessive adrenergic discharge during the index event (2), TTC patients likely to have an acute CSF pattern might need well-known radical measures including sympathetic ganglion blockade, etc for TTC prevention. Accordingly, we wonder their acute and long-term management strategies in TTC patients with a CSF pattern (1).
In summary, CSF pattern might be considered as a prognostic rather than a causative factor in TTC patients (1,3). However, further categories of this phenomenon (acute vs pre-existing) along with their specific implications in these patients still remain to be established.
Conflict of Interest: None
REFERENCES:
1- Montone RA, Galiuto L, Meucci MC, et al. Coronary slow flow is associated with a worse clinical outcome in patients with Takotsubo syndrome. Heart. 2020 Jan 10. pii: heartjnl-2019-315909. doi: 10.1136/heartjnl-2019-315909. [Epub ahead of print]
2- Kawaji T, Shiomi H, Morimoto T, et al. Clinical impact of left ventricular outflow tract obstruction in takotsubo cardiomyopathy. Circ J. 2015; 79(4): 839-46.
3- Yalta K, Yilmaztepe M, Ucar F, et al. Coronary slow flow in the setting of Tako-tsubo cardiomyopathy: A causative factor? An innocent bystander? Or a prognostic sign? Int J Cardiol. 2015; 198:229-31.
4- Yalta K, Sivri N, Yalta T. Neuropeptide Y-induced coronary microvascular dysfunction: a significant contributor to the adverse outcomes in stress cardiomyopathy? Int J Cardiol. 2011; 147(2): 284.
I read with interest the super article by Chris Steadman regarding being a clinical director in the NHS. I would add to this article that a particular problem has now become grossly apparent with taking on such a role which is the amount of pension tax that many will find they have to pay in taking such a role on. Previously, leadership and management roles have often attracted a rise in pensionable salary, which was a clear incentive to take them - as per the article, they clearly result in alot of work to the individual and so should be rewarded for this. However with the pension taper which started in 2016 and a low annual allowance, this creates a major problem, with many stories of doctors taking on such roles and receiving a large tax bill as result. How big a bill this may or may not be will depend on the personal circumstances of the individual and the amount of extra pensionable salary the individual trust is offering. For example, under current rules, a £10,000 increase in pensionable pay would result in me doing such a job at a big financial loss in my first year of doing it! Unless the UK government change the pension tax rules, it has created major disincentive for doctors to take on such roles.
APICAL ANEURYSM ? OR TRANSIENT APICAL BALLOONING ? : A POTENTIAL DILEMMA IN RISK-STRATIFICATION OF HYPERTROPHIC CARDIOMYOPATHY
Kenan YALTA, MD a
Muhammet GURDOGAN, MD a
Orkide PALABIYIK, MD b
a,Trakya University, Cardiology Department, Edirne, TURKEY
b Trakya University, Department of Biophysics, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
Left ventricular apical aneurysm (LVAA) formation in the setting of hypertrophic cardiomyopathy (HCM) usually appears to be associated with a significant mid-ventricular obstruction, and is potentially associated with adverse cardiovascular events (1). In their recently published article (1), Ramchand J et al have suggested LVAA as a major risk marker in this setting. Though we fully agree with the authors on this point, we would like to draw attention to certain other conditions including transient LV apical ballooning that might strongly mimick LVAA leading to a potential misdiagnosis in patients with HCM:
Takotsubo cardiomyopathy (TTC) presenting with a transient apical ballooning pattern has been recently suggested to have a pure mechanical basis in certain patients with pre-existing structural heart diseas...
APICAL ANEURYSM ? OR TRANSIENT APICAL BALLOONING ? : A POTENTIAL DILEMMA IN RISK-STRATIFICATION OF HYPERTROPHIC CARDIOMYOPATHY
Kenan YALTA, MD a
Muhammet GURDOGAN, MD a
Orkide PALABIYIK, MD b
a,Trakya University, Cardiology Department, Edirne, TURKEY
b Trakya University, Department of Biophysics, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
Left ventricular apical aneurysm (LVAA) formation in the setting of hypertrophic cardiomyopathy (HCM) usually appears to be associated with a significant mid-ventricular obstruction, and is potentially associated with adverse cardiovascular events (1). In their recently published article (1), Ramchand J et al have suggested LVAA as a major risk marker in this setting. Though we fully agree with the authors on this point, we would like to draw attention to certain other conditions including transient LV apical ballooning that might strongly mimick LVAA leading to a potential misdiagnosis in patients with HCM:
Takotsubo cardiomyopathy (TTC) presenting with a transient apical ballooning pattern has been recently suggested to have a pure mechanical basis in certain patients with pre-existing structural heart disease including hypertensive heart disease and HCM largely attributable to acute increments in intraventricular pressure gradient leading to substantially elavated apical wall stress in these patients (2,3). Interestingly, TTC in this setting might have no preceding overt stressors (emotional, etc.) (3), and might be clinically silent generally with vague symptoms and signs along with a relatively delayed recovery pattern (hence; might potentially arise as a sole incidental finding on cardiac imaging). Nevertheless, there might still exist certain imaging clues to differentiate between true LVAA and transient apical ballooning in the setting of HCM:
Firstly; pronounced wall thinning is mostly present in true LVAA (excluding cases with severe apical hypertrophy at baseline) as opposed to transient apical ballooning that generally presents with normal or increased wall thickness.
Secondly; LVAA generally emerges due to a chronic and significant mid-ventricular gradient (1) leading to progressive structural remodeling in the apex. However, mid-ventricular gradient is relatively mild in the setting of apical ballooning that might have been induced by an abrupt, yet; transient elevation of this mild gradient to excessive levels leading to stunning in apical segments (2,3) usually without any preconditioning to such pressure elevations.
And lastly; late gadolinium enhancement (LGE) on MRI is an expected finding in LVAA (1) while it is relatively rare (and with a low-intensity pattern) in TTC (4) presenting with an apical ballooning pattern.
In summary; transient apical ballooning should also be taken into consideration in HCM patients suggestive of having a LVAA pattern on initial imaging. Therefore, a single echocardiographic examination might not suffice for decision-making for primary implantable cardiac defibrillator (ICD) therapy suggesting detailed and serial examinations along with MRI for absolute confirmation of an irreversible true LVAA in these patients.
Conflict of interest: None
REFERENCES:
1- Ramchand J, Fava AM, Chetrit M, Desai MY. Advanced imaging for risk stratification of sudden death in hypertrophic cardiomyopathy. Heart. 2020 Jan 16. pii: heartjnl-2019-315176. doi: 10.1136/heartjnl-2019-315176. [Epub ahead of print]
2- Yalta K, Yilmaztepe M, Zorkun C. Left Ventricular Dysfunction in the Setting of Takotsubo Cardiomyopathy: A Review of Clinical Patterns and Practical Implications. Card Fail Rev. 2018; 4(1): 14-20.
3- Azzarelli S, Galassi AR, Amico F, et al. Intraventricular obstruction in a patient with tako-tsubo cardiomyopathy. Int J Cardiol. 2007; 121(2): e22-4.
4- Abbas A, Sonnex E, Pereira RS, Coulden RA. Cardiac magnetic resonance assessment of takotsubo cardiomyopathy. Clin Radiol. 2016; 71(1): e110-9.
As a physician dealing with patients with confirmed or suspected Fabry disease, I've read with great interest this editorial. This is a very thought-provoking article, which introduces the process of reclassification of a prevalent variant in the GLA gene associated with the cardiac variant of Fabry disease. I would like to make only a minor correction regarding the nomenclature of the variant mentioned. As written in the article of Valtola et al, the referred variant is c.427G> A and not c.472G> A¹ (transcript NM_000169.2).
1. Valtola K, Nino-Quintero J, Hedman M, et al. Cardiomyopathy associated with the Ala143Thr variant of the α-galactosidase A gene. Heart 2020;:heartjnl-2019-315933. doi:10.1136/heartjnl-2019-315933
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...
The clinical presentation which simulates ST-segment elevation myocardial infarction(STEMI)(1) is one of the most deceptive manifestations of dissecting aortic aneurysm(DAA), deserving detailed analysis notwithstanding its infrequent(2)(3)(4) occurrence. In Zhu et al DAA was prevalent in only 0.5% of 1576 subjects with suspected STEMI(2). Conversely, Kosuge et al documented a 4%(9 patients) prevalence of ST segment elevation among 233 subjects with confirmed DAA(3). In Hirata et al ST segment elevation was prevalent in 8.2% of 159 subjects with type A aortic dissection(4). When ST segment elevation occurs as a manifestation of DAA, there is a high prevalence of involvement of the inferior leads, exemplified by 6 of the 9 patients in Kosuge et al(3)., and seven of the 13 cases in Hirata et al(4)., arguably because type A aortic dissection is more likely to compromise the ostium of the right coronary artery than the ostium of the left coronary artery(5). In view of the life-threatening nature of DAA clinicians should not rely only on clinical decision rules to raise the index of suspicion. The rationale for a more open-minded approach is that clinical decision rules such as the AAD risk score tend to emphasise typical symptoms, such as the "tearing" character of the back pain(1), almost to the total exclusion of less typical symptoms such as nonspecific back pain, the latter typically radiating from a retrosternal chest pain. For example, a literat...
Show MoreRelease of troponin after exercise stress test in hypertrophic cardiomyopathy
Pawel Petkow Dimitrow1, Renata Rajtar-Salwa2, Tomasz Tokarek2
1 2nd Department of Cardiology, Jagiellonian University Medical College, Kraków, Poland
2 Department of Cardiology and Cardiovascular Interventions, University Hospital, Krakow, Poland
Correspondence to: Paweł Petkow Dimitrow, 2nd Department of Cardiology, Jagiellonian University Medical College, Jakubowskiego 2 Str., 30-688 Krakow, Poland, e-mail: dimitrow@mp.pl, tel. 0048 12 400 22 50
Recently Cramer et al. demonstrated very important observation on troponin level increase after exercise in patients with hypertrophic cardiomyopathy (HCM) [1]. Several concerns regarding to methodology of their study should be explained. Authors decided to perform only one measurement of troponin level at 6 hours after end of exercise. In our opinion, sampling after 6, 12, 18 and 24 hours after exercise provide more adequate profile of troponin level and allow to monitor possible post-exercise ischemia. Furthermore, data on prevalence of silent myocardial ischemia (only troponin increase) should be provided. In our study [2] painless ischemia detected by troponin measurement after normal daily physical activity was present in 25% of HCM patients. In another study [3], among HCM patients monitored by HOLTER ECG during normal daily physical activity, maximum heart rate was higher in th...
Show MoreACUTE OR PRE-EXISTING CORONARY SLOW FLOW IN TAKOTSUBO CARDIOMYOPATHY: DOES IT MATTER ?
Kenan YALTA, MD a
Tulin YALTA, MD b
Muhammet GURDOGAN, MD a
aTrakya University, Cardiology Department, Edirne, TURKEY
b 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: 0090505657985
In the setting of takotsubo cardiomyopathy (TTC), coronary microvascular dysfunction has been mostly considered as a causative factor (1,2). In their recently published article (1), Montone RA et al have demonstrated, for the first time, the prognostic value of coronary slow flow (CSF) phenomenon in TTC patients. Of note, as we previously discussed, on a theoretical basis, the particular prognostic value of CSF phenomenon in these patients (3), we feel now pleased to notice that this theory has been fully confirmed by a well-designed study (1). Nevertheless, we would like to make a few comments on this issue:
Show MoreFirstly; temporal emergence of CSF phenomenon might possibly matter in TTC as well. Accordingly; an acutely evolving CSF pattern (due to severe adrenergic discharge (1)) as compared with a sole pre-existing one (emerging long before the index TTC as part of generalized...
I read with interest the super article by Chris Steadman regarding being a clinical director in the NHS. I would add to this article that a particular problem has now become grossly apparent with taking on such a role which is the amount of pension tax that many will find they have to pay in taking such a role on. Previously, leadership and management roles have often attracted a rise in pensionable salary, which was a clear incentive to take them - as per the article, they clearly result in alot of work to the individual and so should be rewarded for this. However with the pension taper which started in 2016 and a low annual allowance, this creates a major problem, with many stories of doctors taking on such roles and receiving a large tax bill as result. How big a bill this may or may not be will depend on the personal circumstances of the individual and the amount of extra pensionable salary the individual trust is offering. For example, under current rules, a £10,000 increase in pensionable pay would result in me doing such a job at a big financial loss in my first year of doing it! Unless the UK government change the pension tax rules, it has created major disincentive for doctors to take on such roles.
APICAL ANEURYSM ? OR TRANSIENT APICAL BALLOONING ? : A POTENTIAL DILEMMA IN RISK-STRATIFICATION OF HYPERTROPHIC CARDIOMYOPATHY
Kenan YALTA, MD a
Muhammet GURDOGAN, MD a
Orkide PALABIYIK, MD b
a,Trakya University, Cardiology Department, Edirne, TURKEY
b Trakya University, Department of Biophysics, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
Left ventricular apical aneurysm (LVAA) formation in the setting of hypertrophic cardiomyopathy (HCM) usually appears to be associated with a significant mid-ventricular obstruction, and is potentially associated with adverse cardiovascular events (1). In their recently published article (1), Ramchand J et al have suggested LVAA as a major risk marker in this setting. Though we fully agree with the authors on this point, we would like to draw attention to certain other conditions including transient LV apical ballooning that might strongly mimick LVAA leading to a potential misdiagnosis in patients with HCM:
Show MoreTakotsubo cardiomyopathy (TTC) presenting with a transient apical ballooning pattern has been recently suggested to have a pure mechanical basis in certain patients with pre-existing structural heart diseas...
As a physician dealing with patients with confirmed or suspected Fabry disease, I've read with great interest this editorial. This is a very thought-provoking article, which introduces the process of reclassification of a prevalent variant in the GLA gene associated with the cardiac variant of Fabry disease. I would like to make only a minor correction regarding the nomenclature of the variant mentioned. As written in the article of Valtola et al, the referred variant is c.427G> A and not c.472G> A¹ (transcript NM_000169.2).
1. Valtola K, Nino-Quintero J, Hedman M, et al. Cardiomyopathy associated with the Ala143Thr variant of the α-galactosidase A gene. Heart 2020;:heartjnl-2019-315933. doi:10.1136/heartjnl-2019-315933
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