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.
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
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
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.
Given the fact that some of the patients studied by Chou et al were characterised by the coexistence of , at least, four CHADS2 parameters, namely, Congestive heart failure, Hypertension, Age 75 or more, and Diabetes(1), it is to be expected that some of those patients will have stenotic cerebrovascular disease(both intracranial and extracranial)(2). In the latter study of 780 subjects presenting with stroke in the presence of nonvalvular atrial fibrillation(NVAF), concomitant cerebrovascular stenosis of 50% or more was identified in 231 patients. Multivariate analyses showed that CHADS2 score was an independent predictor of concomitant cerebral atherosclerosis(Odds Ratio 3.121; 95% Confidence Interval 1.770 to 5.504), and also a predictor of the presence of proximal stenosis at the symptomatic artery(OR, 3.043; 95% CI 1.458 to 6.350)(2).
When the CHADS2 score is associated with coronary heart disease(CHD) , as might have been the case in 1475 of the heart failure patients studied by Chou et al(1), CHADS2 predicts stroke in the total absence of NVAF(3). In the latter study, over a period of 5821 person-years of follow up, 40 out of 916 non anticoagulated patients with stable CHD and no NVAF suffered an ischaemic stroke/transient ischaemic attack. Compared with those with low(0-1) CHADS2 scores, those with progressively higher CHADS2 scores had a stepwise significant increase in rates of stroke/TIA(3). This increase in stroke rate might, arguably, hav...
Given the fact that some of the patients studied by Chou et al were characterised by the coexistence of , at least, four CHADS2 parameters, namely, Congestive heart failure, Hypertension, Age 75 or more, and Diabetes(1), it is to be expected that some of those patients will have stenotic cerebrovascular disease(both intracranial and extracranial)(2). In the latter study of 780 subjects presenting with stroke in the presence of nonvalvular atrial fibrillation(NVAF), concomitant cerebrovascular stenosis of 50% or more was identified in 231 patients. Multivariate analyses showed that CHADS2 score was an independent predictor of concomitant cerebral atherosclerosis(Odds Ratio 3.121; 95% Confidence Interval 1.770 to 5.504), and also a predictor of the presence of proximal stenosis at the symptomatic artery(OR, 3.043; 95% CI 1.458 to 6.350)(2).
When the CHADS2 score is associated with coronary heart disease(CHD) , as might have been the case in 1475 of the heart failure patients studied by Chou et al(1), CHADS2 predicts stroke in the total absence of NVAF(3). In the latter study, over a period of 5821 person-years of follow up, 40 out of 916 non anticoagulated patients with stable CHD and no NVAF suffered an ischaemic stroke/transient ischaemic attack. Compared with those with low(0-1) CHADS2 scores, those with progressively higher CHADS2 scores had a stepwise significant increase in rates of stroke/TIA(3). This increase in stroke rate might, arguably, have been attributable to left atrial dysfunction and its associated risk of concomitant left atrial prothrombotic milieu, given the fact that the study of 970 subjects(of whom only 35 had atrial fibrillation) showed that high CHADS2 score was associated with the lowest quartile of left atrial functional index (Odds Ratio 2.34, p=0.001)(4)
The association of older age and hypertension, also documented in the recent study(1), confers increased risk of carotid artery stenosis(CAS)(5). Given the fact that smoking also confers increased risk of CAS(5), it would be useful to ascertain the proportion of smokers in the study by Chou et al(1). Furthermore, according to the retrospective study of 3,435 NVAF patients who underwent carotid sonography, the prevalence of carotid plaques increased significantly with the increase in CHA2DS2-Vasc score(P for trend < 0.001). Multivariate logistic regression analysis showed that, for each 1 point increase in the CHA2DS2-Vasc score, there was a 37% increase in the prevalence of carotid plaques(6). Given the predictive power of CHADS2 for IS even in the absence of NVAF(3), the above observation could be extrapolated to heart failure patients who have a high CHADS2 score in the absence of NVAF. Occult paroxysmal atrial fibrillation(PAF), a parameter also not evaluated by Chou et al(1), may coexist with CAS, thereby compounding the risk of IS. The association of PAF and CAS was documented in a study which showed that CAS was prevalent in 13.5% of PAF patients of mean age 69(7).
In conclusion, for the sake of completeness, it would be useful to ascertain the proportion of smokers in the study by Chou et al(1). Documentation of PAF, left atrial functional index, and carotid artery sonography would also be useful indicators of the relative contributions of left atrial cardiomyopathy and CAS to IS prevalence in heart failure.
I have no funding and no conflict of interest
References
(1)Chou Y-L., Liou J-T., Cheng C-C., Tsai M-C., Lin W-S., Cheng S-M et al
The association of ischaemic stroke in patients with heart failure without atrial flutter/fibrillation
Heart 2019;doi:10.1136/heartjnl 2019-315646
(2) Kim DY., Cha MJ., Kim J., Lee DH., Lee HS., Nam CM., Nam HS et al
Increases in cerebral atherosclerosis according to CHADS2 scores in patients with stroke with nonvalvular atrial fibrillation#
STROKE 2011;42:930-934
(3) Welles CC., Whooley MA., Na B., Ganz P., Schiller NB., Turakhia MP
The CHADS2 score predicts ischemic stroke in the absence of atrial fibrillation among patients with coronary heart disease:Data from the Heart and Soul Study
Am Heart J 2011;162:555-561
(4)Azarbal F., Welles CC., Wong JM., Whooley MA., Schiller MB., Turakhia MP
Association of CHADS2, CHADS2-Vasc, R2CHADS2 scores with left atrial dysfunction in patients with coronary heart disease(from the Heart and Soul Study)
Am J Cardiol 2014;113;1166-1172
(5)Woo SY., Joh JH., Han S-A., Park H-C
Prevalence and risk factors for atherosclerotic carotid stenosis and plaque. A population-based screening study
Medicine 2017;96:4(e5999)
(6) Shang L., Zhao Y., Shao M., Sun H., Feng M., Li Y et al
The association of CHA2DS2-Vasc score and carotid plaque in patients with nonvalvular atrial fibrillation
LOS one 2019;14(2);e0210945
(7) Gu Y., Feng L., Xu Y., Zhao Y
Co-prevalence of carotid stenosis and coronary artery disease in Chinese patients with paroxysmal atrial fibrillation
Journal of International Medical Research 2014;42:1294-1300
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
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.
In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
Firstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wal...
In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
Firstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wall (3). However, we hold the opinion that these aneurysms mostly arise as a ‘de novo’ phenomenon in apparently normal or mildly affected coronary segments (and hence not associated with severe necrotizing vasculitis at the onset), and might potentially be associated with dysfunctional vascular healing in the long-term (potential under-healing due to prolonged steroid use for KD or other purposes, diabetes, etc).
Secondly, as analogous to progressive aortic remodeling in connective tissue disease, an over-healing process leading to excessive vascular remodeling in the long-term (largely through genetically determined and enhanced actions of certain profibrotic substances including transforming growth factor-beta (TGF-ß) (1), ,etc.and certain enzymes including matrix metalloproteinase-9 (MMP-9)) has been previously reported in KD, and might also serve as an alternative mechanism of late CAA evolution (4-6) particularly in coronary segments with pre-existing mild vasculitis as well.
Thirdly, based on potential favorable impact of captopril on prevention of classical early CAA formation (through inhibition of MMP-9) (5), blockade of renin-angiotensin system might also be indicated indefinitely in the presence of high-risk features (persistently high levels of profibrotic mediators and MMP-9, etc.) for prevention of late CAA evolution.
Lastly, even though late CAA, reportedly appears to have a more favorable prognosis (3) (due to its smaller size and low incidence of intramural thrombus formation, etc as compared with classical CAA), close supervision of long-term changes in coronary morphology (even in the presence of normal or near-normal coronary arteries at 6 weeks) may also be indicated in high-risk patients for timely initiation of further management strategies (anticoagulation, etc.). Interestingly, since late CAAs might be associated with progressive arterial remodeling involving intima and media layers (4,6), they may possibly be more prone to specific complications including spontaneous coronary artery dissection (SCAD) in comparison to classical CAAs with substantial multi-layer necrosis.
In conclusion, late CAA formation in KD might be regarded as an under-recognized phenomenon with important implications, and might constitute a significant portion of idiopathic coronary aneurysms on routine coronary imaging regardless of confirmed KD history. However, further insights of this phenomenon still remain to be established.
Conflict of interest: None
REFERENCES:
1- Newburger JW, Takahashi M, Burns JC. Kawasaki Disease. J Am Coll Cardiol. 2016 ;67(14):1738-49.
2- Brogan P, Burns JC, Cornish J, et al. Lifetime cardiovascular management of patients with previous Kawasaki disease. Heart 2019;0:1–10. doi:10.1136/heartjnl-2019-315925
3- Tsuda E, Kamiya T, Ono Y, et al. Dilated coronary arterial lesions in the late period after Kawasaki disease. Heart. 2005; 91(2): 177-82.
4- Suzuki A, Miyagawa-Tomita S, et al. Remodeling of coronary artery lesions due to Kawasaki disease: comparison of arteriographic and immunohistochemical findings. Jpn Heart J. 2000 ;41(3):245-56.
5- Inoue N, Takai S, Jin D, et al. Effect of angiotensin-converting enzyme inhibitor on matrix metalloproteinase-9 activity in patients with Kawasaki disease. Clin Chim Acta. 2010; 411(3-4): 267-9.
6- Toyono M, Shimada S, Aoki-Okazaki M, et al. Expanding coronary aneurysm in the late phase of Kawasaki disease. Pediatr Int. 2012; 54(1): 155-8.
Some of the risk factors for atrial fibrillation(AF) mentioned by the authors, such as hypertension, diabetes, sleep apnoea, older age, and lack of exercise, respectively(1), are also risk factors for myocardial stiffness(2)(3)(4)(5)(6). Myocardial stiffness, in turn, is a risk factor for atrial remodeling in the canine heart(7), and a parameter associated with paroxysmal AF in structurally normal human hearts(8). What is more, exercise has been shown to be capable of reversing myocardial stiffness, both in animals(9), and in human subjects(10).
In the more specific context of left atrial stiffness, obesity has emerged as a risk factor for left atrial stiffness(11)(12). Among patients with obesity, hypertension, and diabetes, respectively, a link has been hypothesised between the twin entities of left ventricular stiffness and depressed atrial compliance, on the one hand, and the development of myocardial fibrosis.(12) . The authors of the latter hypothesis proposed that obesity, hypertension and diabetes generated a systemic proinflammatory state which culminated in the emergence of the coexistence of stiff cardiomyocytes and interstitial fibrosis(12). Furthermore, in a study where the assumption was made that the existence of low voltage areas was a surrogate for left atrial fibrosis, the presence of a left atrial low voltage burden exceeding 10% was shown to be associated with significantly(p < 0.0001) higher left atrial stiffness index((LASI)(13)....
Some of the risk factors for atrial fibrillation(AF) mentioned by the authors, such as hypertension, diabetes, sleep apnoea, older age, and lack of exercise, respectively(1), are also risk factors for myocardial stiffness(2)(3)(4)(5)(6). Myocardial stiffness, in turn, is a risk factor for atrial remodeling in the canine heart(7), and a parameter associated with paroxysmal AF in structurally normal human hearts(8). What is more, exercise has been shown to be capable of reversing myocardial stiffness, both in animals(9), and in human subjects(10).
In the more specific context of left atrial stiffness, obesity has emerged as a risk factor for left atrial stiffness(11)(12). Among patients with obesity, hypertension, and diabetes, respectively, a link has been hypothesised between the twin entities of left ventricular stiffness and depressed atrial compliance, on the one hand, and the development of myocardial fibrosis.(12) . The authors of the latter hypothesis proposed that obesity, hypertension and diabetes generated a systemic proinflammatory state which culminated in the emergence of the coexistence of stiff cardiomyocytes and interstitial fibrosis(12). Furthermore, in a study where the assumption was made that the existence of low voltage areas was a surrogate for left atrial fibrosis, the presence of a left atrial low voltage burden exceeding 10% was shown to be associated with significantly(p < 0.0001) higher left atrial stiffness index((LASI)(13). The relationship between left atrial stiffness and AF is exemplified by the observation that patients with a burden of left atrial low voltage areas(LA-LVA) exceeding 10% had a significantly(p=0.0002) higher prevalence of non-paroxysmal AF than counterparts without LV-LVA(13). Furthermore, meta-analysis has confirmed that left atrial stiffness is a risk factor for recurrence of AF in patients undergoing radiofrequency catheter ablation(14). Arguably in view of these observations(12)(13(14) the hypothesis has emerged that "atrial fibrosis is a disease process that triggers the initiation and maintenance of the syndrome of AF"(15). Accordingly lifestyle modification is mandatory, not only for treatment of atrial fibrillation(1) but also , as far as is practicable, for its prevention.
I have no funding and no conflict of interest
References
(1`) Middeldorp ME., Ariyaratnam J., Lau D., Sanders P
Lifestyle modification for treatment of atrial fibrillation
Heart 2019 doi:10.1136/heartjnl-2019-315327
(2)Cvijic M., Bezy S., Petrescu A et al
Interplay of cardiac remodelling and myocardial stiffness in hypertensive heart disease: a shear wave imaging study using high-frame rate echocardiography
Eur Heart J Cardiovasc Imaging 2019;Epub ahead of print. doi:10.1093/ehjci/jez205
(3)Benech JC., Benech N., Zambrana AI et al
Diabetes increases stiffness of live cardiomyocytes measured by atomic force microscopy nanoindentation
Am J Physiol Cell Physiol 2014;307:C910-C919
(Farre N., Otero J., Falcones B et al
Intermittent hypoxia mimicking sleep apnea increases passive stiffness of myocardial extracellular matrix. A multiscale study
Frontiers in Physiology doi:10.3389/phys.2018.01143
(5) Lieber SC., Aubry N., Pain J et al
Aging increases stiffness of cardiac myocytes measured by atomic force microscopy nanoindentation
Am J Physiol Heart Circ Physiol 2004;287:I1645-I1651
(6) Lalande S., Mueller PJ., Chung CS
The link between exercise and Titin passive stiffness
Exp Physiol 2017;102;1055-1066
(7) Zakeri R., Moulay G., Chai Q et al
Left atrial remodeling and atrioventricular coupling in a canine model of early heart failure with preserved ejection fraction
Circ Haert Fail 2016;9:doi:10.1161/CIRCHEARTFAILURE:115;003238
(8)Uetake S., Maruyama M., Yamamoto T et al
Left ventricular stiffness estimated by diastolic wall strain is associated with paroxysmal atrial fibrillation in structurally normal hearts
Clinical Cardiology 2016;39:728-732
(9) Slater RE., Strom JG., Granzier H
Effect of exercise on passive myocardial stiffness in mice with diastolic dysfunction
J Mol Cell Cardiol 2017;108:24-33
(10) Howden EJ., Sarma S., Lawley JS et al
Reversing the cardiac effects of sedentary aging in middle age .A randomized controlled trial
circulation 2018;137:1549-1560
(11) Mahfouz RA., Gomma A., Goda M., safwat M
Relation of left atrial stiffness to insulin resistance in obese children: Doppler strain imaging study
Echocardiography 2018;32:1157-1163
(12) Paulus WJ., Tschope C
A novel paradigm for heart failure with preserved ejection fraction
JACC 2013;62:263-271
(13)Kishima H., Mine T., Fukuhara E., Ashida K., Ishihara M
The association between left atrial stiffness and low-grade areas of left atrium in patients with atrial fibrillation
Heart and Vessels 2019;34;1830-1838
(14) de Oliveira Correia E., dos Santos Barbetta l., da Silva CMP., Mesquita ET
Left atrial stiffness A predictor of atrial fibrillation recurrence after radiofrequency catheter ablation. A systematic review and meta-analysis
Arq Bras Cardiol 2019;112:501-508
(15) gal P., Marrouche NF
Magnetic resonance imaging of atrial fibrosis : redefining atrial fibrillation to a syndrome
Eur Heart J 2017;38;14-19
We have read with interest the review published by Goldsweig et al of predictors of readmission after transcatheter aortic valve replacement (TAVR) (1). We agree that identifying factors linked with a higher rate of readmission is of utmost importance. In this review, several clinical and procedural factors have been identified as predictors of adverse events after TAVR. However, the potential value of biomarkers for risk stratification in this setting has also been suggested in the literature. Several biomarkers have been tested for prognostic purposes; among them, we would like to highlight the role of Carbohydrate Antigen 125 (CA125). CA125 is a glycoprotein released by the mesothelial cells in response to increased hydrostatic pressures and/or inflammatory stimuli (2). Their levels are elevated in up to two-thirds of decompensated patients and correlated to parameters of clinical and echocardiographic congestion including pulmonary artery and right atrial pressures. Interestingly, its changes after discharge are strongly associated with the risk of adverse clinical events (2). In the setting of TAVR, baseline (pre-implant) CA125 levels were independent predictors of death and MACE (death, myocardial infarction, stroke, and readmission), even after adjusting for well-established prognostic factors, in an observational study (3). Interestingly, increases of CA125 at any time in the follow-up after TAVR were independently related to events, suggesting its usefulness not...
We have read with interest the review published by Goldsweig et al of predictors of readmission after transcatheter aortic valve replacement (TAVR) (1). We agree that identifying factors linked with a higher rate of readmission is of utmost importance. In this review, several clinical and procedural factors have been identified as predictors of adverse events after TAVR. However, the potential value of biomarkers for risk stratification in this setting has also been suggested in the literature. Several biomarkers have been tested for prognostic purposes; among them, we would like to highlight the role of Carbohydrate Antigen 125 (CA125). CA125 is a glycoprotein released by the mesothelial cells in response to increased hydrostatic pressures and/or inflammatory stimuli (2). Their levels are elevated in up to two-thirds of decompensated patients and correlated to parameters of clinical and echocardiographic congestion including pulmonary artery and right atrial pressures. Interestingly, its changes after discharge are strongly associated with the risk of adverse clinical events (2). In the setting of TAVR, baseline (pre-implant) CA125 levels were independent predictors of death and MACE (death, myocardial infarction, stroke, and readmission), even after adjusting for well-established prognostic factors, in an observational study (3). Interestingly, increases of CA125 at any time in the follow-up after TAVR were independently related to events, suggesting its usefulness not only to identify higher-risk patients before the procedure but also as a tool to anticipate events during follow-up (3). Moreover, CA125 showed to be a useful tool for improving risk stratification beyond EuroSCORE and natriuretic peptides (4; 5). Additionally, this biomarker offers some important logistic advantages. First, CA125 levels, conversely to natriuretic peptides, are not influenced by common confounders in TAVR patients such as renal dysfunction and age. Second, their wide availability and low cost make feasible its implantation in daily clinical practice.
In summary, we believe biomarkers may improve clinical evaluation in TAVR decision-making work out, adding valuable information to identify patients with worse prognosis after TAVR in which the procedure could be dismissed (considered as futile) or postposed after medical treatment optimization. Following TAVR, biomarkers may also play a relevant role in clinical monitoring. All these assumptions must be confirmed in prospective further studies.
References
1. Goldsweig A, Aronow HD. Identifying patients likely to be readmitted after transcatheter aortic valve replacement. Heart. 2019 Oct 24. pii: heartjnl-2019-315381.
2. Núñez J, Miñana G, Núñez E, Chorro FJ, Bodí V, Sanchis J. Clinical utility of antigen carbohydrate 125 in heart failure. Heart Fail Rev. 2014 Sep;19(5):575-84.
3. Husser O, Núñez J, Núñez E, Holzamer A, Camboni D, Luchner A et al. Tumor marker carbohydrate antigen 125 predicts adverse outcome after transcatheter aortic valve implantation. JACC Cardiovasc Interv. 2013 May;6(5):487-96.
4. Husser O, Núñez J, Burgdorf C, Holzamer A, Templin C, Kessler T et al. Improvement in Risk Stratification in Transcatheter Aortic Valve Implantation Using a Combination of the Tumor Marker CA125 and the Logistic EuroSCORE. Rev Esp Cardiol. 2017 Mar;70(3):186-193.
5. Rheude T, Pellegrini C, Schmid H, Trenkwalder T, Mayr NP, Joner M et al. Comparison of Carbohydrate Antigen 125 and N-Terminal Pro-Brain Natriuretic Peptide for Risk Prediction After Transcatheter Aortic Valve Implantation. Am J Cardiol. 2018 Feb 15;121(4):461-468.
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:
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...
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 MoreRegardless 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 MoreAPICAL 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...
Given the fact that some of the patients studied by Chou et al were characterised by the coexistence of , at least, four CHADS2 parameters, namely, Congestive heart failure, Hypertension, Age 75 or more, and Diabetes(1), it is to be expected that some of those patients will have stenotic cerebrovascular disease(both intracranial and extracranial)(2). In the latter study of 780 subjects presenting with stroke in the presence of nonvalvular atrial fibrillation(NVAF), concomitant cerebrovascular stenosis of 50% or more was identified in 231 patients. Multivariate analyses showed that CHADS2 score was an independent predictor of concomitant cerebral atherosclerosis(Odds Ratio 3.121; 95% Confidence Interval 1.770 to 5.504), and also a predictor of the presence of proximal stenosis at the symptomatic artery(OR, 3.043; 95% CI 1.458 to 6.350)(2).
Show MoreWhen the CHADS2 score is associated with coronary heart disease(CHD) , as might have been the case in 1475 of the heart failure patients studied by Chou et al(1), CHADS2 predicts stroke in the total absence of NVAF(3). In the latter study, over a period of 5821 person-years of follow up, 40 out of 916 non anticoagulated patients with stable CHD and no NVAF suffered an ischaemic stroke/transient ischaemic attack. Compared with those with low(0-1) CHADS2 scores, those with progressively higher CHADS2 scores had a stepwise significant increase in rates of stroke/TIA(3). This increase in stroke rate might, arguably, hav...
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
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.
LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS
Kenan YALTA, MD
Muhammet GURDOGAN, MD
Gokay TAYLAN, MD
a,Trakya University, Cardiology Department, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
Show MoreFirstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wal...
Some of the risk factors for atrial fibrillation(AF) mentioned by the authors, such as hypertension, diabetes, sleep apnoea, older age, and lack of exercise, respectively(1), are also risk factors for myocardial stiffness(2)(3)(4)(5)(6). Myocardial stiffness, in turn, is a risk factor for atrial remodeling in the canine heart(7), and a parameter associated with paroxysmal AF in structurally normal human hearts(8). What is more, exercise has been shown to be capable of reversing myocardial stiffness, both in animals(9), and in human subjects(10).
Show MoreIn the more specific context of left atrial stiffness, obesity has emerged as a risk factor for left atrial stiffness(11)(12). Among patients with obesity, hypertension, and diabetes, respectively, a link has been hypothesised between the twin entities of left ventricular stiffness and depressed atrial compliance, on the one hand, and the development of myocardial fibrosis.(12) . The authors of the latter hypothesis proposed that obesity, hypertension and diabetes generated a systemic proinflammatory state which culminated in the emergence of the coexistence of stiff cardiomyocytes and interstitial fibrosis(12). Furthermore, in a study where the assumption was made that the existence of low voltage areas was a surrogate for left atrial fibrosis, the presence of a left atrial low voltage burden exceeding 10% was shown to be associated with significantly(p < 0.0001) higher left atrial stiffness index((LASI)(13)....
We have read with interest the review published by Goldsweig et al of predictors of readmission after transcatheter aortic valve replacement (TAVR) (1). We agree that identifying factors linked with a higher rate of readmission is of utmost importance. In this review, several clinical and procedural factors have been identified as predictors of adverse events after TAVR. However, the potential value of biomarkers for risk stratification in this setting has also been suggested in the literature. Several biomarkers have been tested for prognostic purposes; among them, we would like to highlight the role of Carbohydrate Antigen 125 (CA125). CA125 is a glycoprotein released by the mesothelial cells in response to increased hydrostatic pressures and/or inflammatory stimuli (2). Their levels are elevated in up to two-thirds of decompensated patients and correlated to parameters of clinical and echocardiographic congestion including pulmonary artery and right atrial pressures. Interestingly, its changes after discharge are strongly associated with the risk of adverse clinical events (2). In the setting of TAVR, baseline (pre-implant) CA125 levels were independent predictors of death and MACE (death, myocardial infarction, stroke, and readmission), even after adjusting for well-established prognostic factors, in an observational study (3). Interestingly, increases of CA125 at any time in the follow-up after TAVR were independently related to events, suggesting its usefulness not...
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