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.
This is a really important and interesting article. I would like to congratulate the authors with their work.
I do have one question with regard to figure 3B. The numbers needed to treat to harm (NNTH) in this table seem to have counterintuitive values, for instance see the value from the direct thrombin inhibitor, which is listed as 153, with a corresponding OR of harm of 2.63. This NNTH value is more or less equal to that of aspirin, which has a listed NNTH of 155, however, its corresponding OR for harm is much lower, namely 1.07. Similarly, the point estimate of the NNTH for standard dose Xa is 270 which is higher than that listed for low dose Xa inhibitor (187), while the respective ORs for harm show that standard-dose Xa inhibitor has a higher odds for harm. I realize that there is a possible logical explanation for these counterintuitive results, namely that the base rates of the placebo/observation condition vary significantly, but that would not be expected. Could the authors elaborate on this? Thank you very much in advance.
This is our response to a concern raised by a reader regarding the estimates and credible intervals of those numbers needed to treat to harm presented in our article titled “Extended treatment of venous thromboembolism: a systematic review and network meta-analysis.”
First, we confirm that data published in the Journal are valid and correct.
We also like to thank the reader to point it out as a number needed (either for benefit or harm) derived from an effect estimate that crosses the unity has been intuitively challenging to visualize (Hutton JL. Br J Haematol. 2009;146:27-30). Because it is given by the reciprocal of the absolute risk difference, a number needed can never include zero but straddles plus and minus infinity ∞ when the absolute risk difference include zero. By the frequentist approach based on inverting the confidence interval of the absolute risk difference, it represents that the number needed encompasses two disjoint regions: one from upper confidence interval to plus ∞ and the other from lower confidence interval to minus ∞ (Altman DG. BMJ. 1998;317:1309-12). Some had argued that for those non-significant results, a number needed should be presented as a single number without its confidence interval as it includes the possibility of no benefit or harm (McQuay HJ. Ann Intern Med. 1997;126:712-20). Other had suggested that it should not be reported when being non-significant (McAlister FA. CMAJ. 2008;179:549-53).
This is our response to a concern raised by a reader regarding the estimates and credible intervals of those numbers needed to treat to harm presented in our article titled “Extended treatment of venous thromboembolism: a systematic review and network meta-analysis.”
First, we confirm that data published in the Journal are valid and correct.
We also like to thank the reader to point it out as a number needed (either for benefit or harm) derived from an effect estimate that crosses the unity has been intuitively challenging to visualize (Hutton JL. Br J Haematol. 2009;146:27-30). Because it is given by the reciprocal of the absolute risk difference, a number needed can never include zero but straddles plus and minus infinity ∞ when the absolute risk difference include zero. By the frequentist approach based on inverting the confidence interval of the absolute risk difference, it represents that the number needed encompasses two disjoint regions: one from upper confidence interval to plus ∞ and the other from lower confidence interval to minus ∞ (Altman DG. BMJ. 1998;317:1309-12). Some had argued that for those non-significant results, a number needed should be presented as a single number without its confidence interval as it includes the possibility of no benefit or harm (McQuay HJ. Ann Intern Med. 1997;126:712-20). Other had suggested that it should not be reported when being non-significant (McAlister FA. CMAJ. 2008;179:549-53).
Our analyses with the Bayesian approach based on probability derived a number needed from the posterior distribution of the reciprocal of the absolute risk difference. Mathematically, its distribution stretches from minus ∞ to plus ∞ and can be bi-modal (as the probability of a number needed being zero is zero) (Thabane L. Biostatistics. 2003;4:365-70). The median of a number needed falls within its credible interval.
We also provided the estimates of the absolute risk difference in Supplementary table 3. When using them by the frequentist approach, the number needed to treat to harm (95% credible interval) is 4560 (-368, 110), 95 (16, 3461), 87(23, 348), 805 (-381, 56), 363 (-854, 56), and 184 (-1103, 17) for aspirin, low-intensity vitamin K antagonist, standard-intensity vitamin K antagonist, low-dose factor Xa inhibitor, standard-dose factor Xa inhibitor, and direct thrombin inhibitor, respectively.
We opted for presenting all numbers needed with their credible intervals by the Bayesian approach. However, neither the frequentist approach nor the Bayesian approach is ideal when reporting non-significant results. It should take extra caution when using and interpreting a number needed derived from an effect estimate that crosses the unity.
Finally, thank you for letting us clarify this.
Kang-Ling Wang and Marc Carrier
General Clinical Research Center, Taipei Veterans General Hospital, Taipei, Taiwan
Department of Medicine, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada
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
On reading Dobson et al’s enlightening article we were saddened but not surprised to hear that nationally, there were no cardiology LTFT trainees training in electrophysiology (EP). Of course, it remains unclear as the relationship here: do trainees planning LTFT avoid EP, or do EP trainees fear reducing their hours will prove challenging?
Either way, this represents a great shame for both trainees and subspecialty. For trainees, the fulfilment of electrophysiological problem-solving and skilful intervention should be accessible to all regardless of hours worked. For the subspecialty, a growth in diversity of electrophysiologists as well as flexible working seems very sensible to ensure the continued growth of the subspecialty and its long-term sustainability. Ongoing initiatives by the BCS, BHRS, EHRA and others continue to advocate for a diverse and flexible workforce in EP, and we applaud these efforts.
Given the fact that high-grade carotid artery stenosis(CAS)(50% or more stenosis) is an independent risk factor for stroke in patients with coexisting nonvalvular atrial fibrillation(NVAF)(1), the optimum management of NVAF patients who have symptomatic CAS should be included among the key outstanding research questions enumerated by the authors of the recent review(2). In one study high-grade CAS was prevalent in 12%-14% of NVAF patients aged 71-80(3).. When high-grade CAS gives rise to amaurosis fugax , transient ischaemic attack(TIA), or stroke, the urgent priority is to mitigate the risk of subsequent occurrence of disabling stroke. That priority should prevail irrespective of presence or absence of coexisting NVAF. Strategies to mitigate that risk include initiation of dual antiplatelet therapy(4)(5) followed by interventional treatment of the CAS itself(6).
For patients in whom symptomatic CAS coexists with NVAF, when the latter is associated with a CHA2DS2-Vasc score that justifies oral anticoagulation to mitigate the risk of cardioembolis stroke , coprescription of oral anticoagulants has to be included in the management strategy. Furthermore after interventional treatment of symptomatic CAS, secondary prevention of neurological events(including stroke) necessitates long term antithrombotic medication with aspirin(5). Concurrently , in the presence of coexisting NVAF, long term primary prevention of cardioembolic stroke necessitates long...
Given the fact that high-grade carotid artery stenosis(CAS)(50% or more stenosis) is an independent risk factor for stroke in patients with coexisting nonvalvular atrial fibrillation(NVAF)(1), the optimum management of NVAF patients who have symptomatic CAS should be included among the key outstanding research questions enumerated by the authors of the recent review(2). In one study high-grade CAS was prevalent in 12%-14% of NVAF patients aged 71-80(3).. When high-grade CAS gives rise to amaurosis fugax , transient ischaemic attack(TIA), or stroke, the urgent priority is to mitigate the risk of subsequent occurrence of disabling stroke. That priority should prevail irrespective of presence or absence of coexisting NVAF. Strategies to mitigate that risk include initiation of dual antiplatelet therapy(4)(5) followed by interventional treatment of the CAS itself(6).
For patients in whom symptomatic CAS coexists with NVAF, when the latter is associated with a CHA2DS2-Vasc score that justifies oral anticoagulation to mitigate the risk of cardioembolis stroke , coprescription of oral anticoagulants has to be included in the management strategy. Furthermore after interventional treatment of symptomatic CAS, secondary prevention of neurological events(including stroke) necessitates long term antithrombotic medication with aspirin(5). Concurrently , in the presence of coexisting NVAF, long term primary prevention of cardioembolic stroke necessitates long term oral anticoagulation. Future research should address the issue of the optimum choice of oral anticoagulant to be coprescribed with aspirin so as to optimise stroke prevention concurrently with mitigation of the risk of iatrogenic bleeding.
For all these issues to be fully addressed the minimum requirement is that the work-up of all older(?aged 60 or more) NVAF patients should include carotid arty sonography, and the incorporation of high-grade CAS(if present) in the CHA2DS2-Vasc score.
I have no funding and no conflict of interest.
References
(1) Chang Y-J., Ryu S-J., Lin S-K
Carotid artery stenosis in ischemic stroke patients with nonvalvular atrial fibrillation
Cerebrovascular Diseases 2002;13:16-20
(2) Stroke and thromboembolism in atrial fibrillation
Heart 2019
(3) Kanter MC., Tegeler CH., Pearce LA., Weinberger J., Feinberg WM., Anderson DC et al
Carotid stenosis in aptients with atrial fibrillation
Arch Intern Med 1994;154:1372-1377
(4) Batchelder A., Hubter J., Cairns V., Sandford R., Munshi A., Naylor AR
Dual antiplatelet therapy prior to expedited carotid surgery reduces recurrent events prior to surgery without significantly increasing peri-operative bleeding complications
Eur J Vasc Endovasc Surg 2015;50:412-419
(5) Ricotta JJ., AbuRahma A., Ascher E., Eskandari M., Faries P., Lal BK
Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease
J Vasc Surg 2011;54:e1-e31
(6)Brott TG., Hobson RW., Howard G., Roubin GS., Clark WM., Brooks W et al
Stenting versus endarterectomy for treatment of carotid artery stenosis
N Engl J Med 2010;363:11-23
Echocardiography has been shown to generate decisive diagnostic information when pulmonary embolism(PE) presents atypically with paradoxical cerebral embolism in the absence of concurrent PE-related stigmata such as dyspnoea, chest pain, or haemoptysis(1)(2), and also in those cases where the atypical presentation is one which simulates ST segment elevation myocardial infarction(STEMI) in the absence of paradoxical coronary artery embolism(3).
The following are some anecdotal report which exemplify the diagnostic role of echocardiography:-
A 32 year old man presented with a stroke , but no concurrent breathlessness or clinical signs of deep vein thrombosis(DVT). Transthoracic echocardiography(TTE) revealed intracardiac thrombus and also a thrombus in the main pulmonary artery. A subsequent Doppler examination revealed a DVT in the right lower limb(1).
In another report, a 55 year old man presented with a stroke and no concurrent breathlessness. However, he had a blood pressure of 70/40 mm Hg and an elevated serum troponin of 0.07 ng/ml(normal < 0.03 ng/ml). TTE revealed a "positive bubble study" which was followed up with a transoesopahageal echocardiogram(TOE) which showed a patent foramen ovale(PFO). A subsequent Duplex study revealed right lower limb DVT.. His management included intracardiac surgery, which revealed biatrial thrombus straddling a patent foramen ovale. An extensive pulmonary thrombus was also discovered(...
Echocardiography has been shown to generate decisive diagnostic information when pulmonary embolism(PE) presents atypically with paradoxical cerebral embolism in the absence of concurrent PE-related stigmata such as dyspnoea, chest pain, or haemoptysis(1)(2), and also in those cases where the atypical presentation is one which simulates ST segment elevation myocardial infarction(STEMI) in the absence of paradoxical coronary artery embolism(3).
The following are some anecdotal report which exemplify the diagnostic role of echocardiography:-
A 32 year old man presented with a stroke , but no concurrent breathlessness or clinical signs of deep vein thrombosis(DVT). Transthoracic echocardiography(TTE) revealed intracardiac thrombus and also a thrombus in the main pulmonary artery. A subsequent Doppler examination revealed a DVT in the right lower limb(1).
In another report, a 55 year old man presented with a stroke and no concurrent breathlessness. However, he had a blood pressure of 70/40 mm Hg and an elevated serum troponin of 0.07 ng/ml(normal < 0.03 ng/ml). TTE revealed a "positive bubble study" which was followed up with a transoesopahageal echocardiogram(TOE) which showed a patent foramen ovale(PFO). A subsequent Duplex study revealed right lower limb DVT.. His management included intracardiac surgery, which revealed biatrial thrombus straddling a patent foramen ovale. An extensive pulmonary thrombus was also discovered(2).
Echocardiography also has a role in identifying hitherto unsuspected PE in a patient who presents with an electrocardiogram(ECG) simulating ST segment elevation myocardial infarction(STEMI). One such patient was a 63 year old man who was admitted with cardiac arrest in the context of multiple risk factors for acute myocardial infarction and previous placement of a coronary artery stent. His ECG showed marked ST segment elevation(simulating the "tombstone" pattern) in the anterior leads, but coronary coronary angiography did not reveal any coronary artery occlusion in the epicardial arteries, and the left anterior descending artery stent was patent. A bedside echocardiogram was performed "emergently", and it revealed a dilated right ventricle, thereby raising a suspicion of massive pulmonary embolism. This provisional diagnosis was validated by pulmonary angiography. Pulmonary embolectomy was performed, but the patient subsequently died(3).
Comment:-
"Emergent" echocardiography should, arguably, be a routine component of the "workup" of a patient presenting with crytpogenic stroke, so as to mitigate the risk of missed diagnosis of PE-related paradoxical cerebral embolism.
Likewise, given the increasing awareness of the entity of PE presenting with an ECG simulating STEMI in the absence of paradoxical coronary artery embolism(4), the work up of such patients should routinely include TTE, with the specific aim of identifying stigmata of PE.
References
(1) Kumar T., Budnur SC., Mahadevappa NC., Singla V
Paradoxical embolism via patent foramen ovale
BMJ case Rep 2013;doi 10.1136/bcr-2013-009818
(2)dada R., dada J., Abdelsalam M., Agrawal Y
Thrombus straddling a patent foramen ovale, pulmonary embolism and paradoxical embolism: a rare trifata
BMJ case Reports 2018;doi:10.1136/bcr-2018-227505
(3)Ghatak A., Alsulaimi A., Acosta YM., ferreira A
Acute pulmonary embolism masquerading as acute myocardial infarction
Proc Bayl Univ Med Cent 2015;28:69-70
(4)Villablanca PA., Vlismas PP., Alexandrovich T., Omondi A., Gupta T et al
Case report and systematic review of pulmonary embolism mimicking ST elevation myocardial infarction
Vascular 2019;27:90-97
The focus on left atrial dimensions in the risk stratification of patients with atrial fibrillation(AF) and also in those without AF(1), is a timely departure from the prevailing preoccupation with AF-related risk stratification strategies such as the CHA2 DS2-Vasc score which do not include evaluation of left atrial function(2), notwithstanding the hypothesis that the predictive ability of the CHADS2 index to stratify stroke risk may be mechanistically linked to severity of left atrial dysfunction(3). In the latter study left atrial functional index(LAFI) was the parameter utilised to evaluate left atrial function. Regression analysis showed that mean LAFI significantly(p < 0.001) decreased across tertiles of CHADS2(42.8, 37.8, 36.7). After adjustment for age, sex, race, and other parameters , high CHADS2 remained significantly associated with the lowest quartile of LAFI(Odds Ratio 2.34). For every point increase in CHADS2 the LAFI decreased by 4 %. Secondary analyses using CHA2 DS2 Vasc score replicated these results(3). In view of these observations LAFI is a potential modality to risk stratify nonvalvular atrial fibrillation(NVAF) subjects such as those with CHA2DS2 Vasc score of zero , who might otherwise be ineligible for thromboprophylaxis with oral anticoagulants. LAFI could even be utilised to evaluate eligibility for thromboprophylaxis in patients with excessive atrial ectopic activity or short-run atrial tachyarrhythmis, given the fact that each...
The focus on left atrial dimensions in the risk stratification of patients with atrial fibrillation(AF) and also in those without AF(1), is a timely departure from the prevailing preoccupation with AF-related risk stratification strategies such as the CHA2 DS2-Vasc score which do not include evaluation of left atrial function(2), notwithstanding the hypothesis that the predictive ability of the CHADS2 index to stratify stroke risk may be mechanistically linked to severity of left atrial dysfunction(3). In the latter study left atrial functional index(LAFI) was the parameter utilised to evaluate left atrial function. Regression analysis showed that mean LAFI significantly(p < 0.001) decreased across tertiles of CHADS2(42.8, 37.8, 36.7). After adjustment for age, sex, race, and other parameters , high CHADS2 remained significantly associated with the lowest quartile of LAFI(Odds Ratio 2.34). For every point increase in CHADS2 the LAFI decreased by 4 %. Secondary analyses using CHA2 DS2 Vasc score replicated these results(3). In view of these observations LAFI is a potential modality to risk stratify nonvalvular atrial fibrillation(NVAF) subjects such as those with CHA2DS2 Vasc score of zero , who might otherwise be ineligible for thromboprophylaxis with oral anticoagulants. LAFI could even be utilised to evaluate eligibility for thromboprophylaxis in patients with excessive atrial ectopic activity or short-run atrial tachyarrhythmis, given the fact that each of those arrhythmias is an independent risk factor for ischemic stroke(4)(5).
The ultimate risk factor for left atrium-related cadiogenic thromboembolism is the documentation of a prothrombotic state in the left atrium and left atrial appendage(LAA), but this entails the use of an invasive strategy, namely, trans oesophageal echocardiography(TOE)(6). Recourse to this modality could be circumvented if a correlation cloud be shown to exist between LAFI and LAA abnormalities such as smoke, sludge, and thrombus. Already, the CHA2DS2 Vasc score has been shown to be significantly associated with TOE risk factors for thromboembolism(7). The next step is also to explore the potential association between LAFI and TOE risk factors for thrromboembolism .
Given the fact that echocardiographically documented left atrial strain has been shown to predict a prothrombotic state in patients with NVAF(8) it would also be worthwhile to explore a potential relationship between LAFI and left atrial strain, not only in NVAF ,but also in subjects with excessive atrial ectopic activity and in subjects with short-run atrial tachyarrhythmia. Furthermore, given the fact that atrial fibrosis(documented by late gadolinium enhancement magnetic resonance imaging[LGE-MRI]) has been shown to predict occurrence of incident atrial fibrillation in non-AF subjects of mean age 49(9), it might be informative to explore a correlation between LAFI and the extent and distribution of atrial fibrosis.
In conclusion, if LAFI proves to be significantly correlated with parameters of the prothrombotic state and also correlated with the extent and distribution of left atrial fibrosis, it might be the modality of choice for stratification of risk of left atrial-related cardiogenic thromboembolism either in NVAF or in patients with excessive atrial ectopic activity or short-run atrial tachyarrhytmia.
References
(1) Froehlich L., Meyre P., Aeschbacher S et al
Left atrial dimensions and cardiovascular outcomes in patients with and without atrial fibrillation: A systematic review and meta analysis
Heart 2019;doi:10.1136/heartjnl 2019-315174
(2) Lip GYH., Nieuwlaat R., Oisters R
Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach
CHEST 2010;137:263-272
(3)Azarbal F., Welles C., Wong JM et al
Association of CHA2DS2-Vasc and RCHADS2 scores with atrial dysfunction in patients with coronary heart disease(from the Heart and Soul Study)
Am J Cardiol 2014;113:1166-1172
(4) Marinheiro R., Parreira L., Amador P et al
Excessive atrial ectopic activity as an independent risk factor for ischemic stroke
Int J Cardiol 2017;240:226-230
(5) Yzamada S., Lin C-Y., Cahng S-L et al
Risk of stroke in patients with short-run atrial tachyarrhythmia
STROKE 2017;48:3232-3238
(6)Dinh T., Baur LH., Pisters R et al
Aspirin versus vitamin K antagonist treatment guided by transoesophageal echocardiography in patients with atrial fibrillation: a pilot study
Heart 2014;100;563-558
(7) Willens HJ., Gomez-Marin O., Nelson K et al
Correlation of CHADS2 and CHA2 DS2 Vasc scores with transesophageal echocardiography irisk factors for thromboembolism in a multi-ethnic United States population with nonvalvular atrial fibrillation
Journal of the American Society of echocardiography 2013;26:175-184
(8) Kupczynska K., Michalski BW., Miskowicc D et al
Association between left atrial function assessed by speckle-tracking echocardiography and the presence of atrial appendage thrombus in aptients with atrial fibrillation
Anatoll J cardiol 2017;18:15-22
(9) Siebramair J., Suksaranjit P., McGann CJ et al
Atrial fibrosis in non-atrial fibrillation individuals and prediction of atrial fibrillation by use of late gadolinium enhancement magbetic resonance imaging
J cardiovasc Electophysiol 2019;30:550-556
Given the fact that acute myocardial infarction(AMI)(1), left bundle branch block(LBBB)(2), and pulmonary embolism(PE), are all age-related disorders, the authors of the recent study correctly highlighted the importance of including PE in the differential diagnosis of the association of suspected AMI and LBBB(2). For the purpose of identifying those patients who are most likely to have AMI the authors proposed the use of serum troponin as a rule-in criterion during the first 3 hours of hospital admission . By implication the inclusion of PE in the differential diagnosis should be deferred for at least 3 hours, and only activated in patients who do not have a raised serum troponin level.
However, in view of the fact that elevation in serum troponin may be a feature in the presentation of PE(4), and also in view of the fact that transient LBBB has been reported in a 59 year old patient with PE(5), the latter disorder should be included in the differential diagnosis of the association of acute coronary syndrome and LBBB. In the 59 year old patient who was reported with PE and LBBB, serial troponin levels were 0.38, 0.41, and 1.12 ng/ml(reference range 0-0.04)(5), arguably justifying early coronary angiography(2). That patient had neither pleuritic pain nor breathlessness to raise the index of suspicion for PE. Coronary angiography ruled out coronary artery occlusion, and helical computed tomography revealed extensive PE involving the main branches of both pul...
Given the fact that acute myocardial infarction(AMI)(1), left bundle branch block(LBBB)(2), and pulmonary embolism(PE), are all age-related disorders, the authors of the recent study correctly highlighted the importance of including PE in the differential diagnosis of the association of suspected AMI and LBBB(2). For the purpose of identifying those patients who are most likely to have AMI the authors proposed the use of serum troponin as a rule-in criterion during the first 3 hours of hospital admission . By implication the inclusion of PE in the differential diagnosis should be deferred for at least 3 hours, and only activated in patients who do not have a raised serum troponin level.
However, in view of the fact that elevation in serum troponin may be a feature in the presentation of PE(4), and also in view of the fact that transient LBBB has been reported in a 59 year old patient with PE(5), the latter disorder should be included in the differential diagnosis of the association of acute coronary syndrome and LBBB. In the 59 year old patient who was reported with PE and LBBB, serial troponin levels were 0.38, 0.41, and 1.12 ng/ml(reference range 0-0.04)(5), arguably justifying early coronary angiography(2). That patient had neither pleuritic pain nor breathlessness to raise the index of suspicion for PE. Coronary angiography ruled out coronary artery occlusion, and helical computed tomography revealed extensive PE involving the main branches of both pulmonary arteries(5).
The true prevalence of PE-related LBBB is not known. It might be more prevalent than implied by the occasional anecdote, where it is tachycardia-dependent(5), given the fact that PE, itself, is commonly characterised by sinus tachycardia(6). Conversely, sinus bradycardia is distinctly uncommon in PE(7)(8)(9)(10). Even more unusual is the transient resolution of pre-existing LBBB following the onset of PE, as was the case in a 61 year old man with coexisting deep vein thrombosis(DVT)(11). Accordingly, at the very least, the work-up of an elderly patient with the association of acute coronary syndrome and LBBB should include clinical evaluation for DVT, irrespective of troponin status.
I have no funding and no conflict of interest
References
(1) Sanchis-Gomar F., Perez-Quillis C., Leischik R., Lucia A
Epidemiology of coronary heart disease and acute coronary syndrome
Ann Transl Med 2016;4:256
(2) Nestelberger T., Cullen L., Lindahl B., Reichlin T., Greenslade JH., Giannitsis E., Christ M et al
Diagnosis of acute myocardial infarction in the presence of left bundle branch block
Heart 2019;doi:10.1136/heartjnl-2018-314673
(3) Heit JA., Spencer FA., White RH
The epidemiology of venous thromboembolism
J Thromb Thrombolysis 2016;41:3-14
(4) Lankeit M., Friesen D., Aschoff J., Delias C., HasenfuB G., Katus H et al
Highly sensitive troponin T assay in normotensive patients with acute pulmonary embolism
Eur Heart J 2010;31:1836-1844
(5) Kasmani R., Okoli K., Mohan G., Casey K., Ledrick D
Transient left bundle branch block: an unusual electrocardiogram in acute pulmonary embolism
Am J Med Sc 2009;337:381-382
(6) Raghav KPS., Makkuni P., Figuerdo VM
A review of electrocardiography in pulmonary embolism: recognising pulmonary embolism masquerading as ST-elevation myocardial infarction
Reviews in Cardiovascular Medicine 2011;12:157-163
(7) Khosravi A., Andalib E., Khaledifar A., Hajizadeh M., Nejati M., Behjati M
Pulmonary thromboembolism presenting with recurrent bradycardia and hypotension
National Research Institute of Tuberculosis and Lung Disease, Iran 2017;16:248-250
(8) Larsen TR., Ball TC
Chronic pulmonary embolism in a young athletic woman
Proc Bayl Univ Cent 2015;28:371-374
(9) Lee J-W., Cha S-I., Jung C-Y., Choi W-I., Jeon K-N et al
Clinical course of pulmonary embolism in lung cancer patients
Respiration 2009;78:42-48
(10) Catella P., Wiesel S., Siddiqui A., Chalhoub M
A rare case of pulmonary embolism induced symptomatic bradycardia
American Journal of Respiratory and Critical Care Medicine 2017;195:A5492
(11) Athar SM., Chin BSP., Flint EJ
Transient disappearance of left bundle branch block pattern ; an unusual ECG presentation of acute pulmonary embolism
Postgrad Med J 2002;78:555-558
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...
Show MoreThis is a really important and interesting article. I would like to congratulate the authors with their work.
I do have one question with regard to figure 3B. The numbers needed to treat to harm (NNTH) in this table seem to have counterintuitive values, for instance see the value from the direct thrombin inhibitor, which is listed as 153, with a corresponding OR of harm of 2.63. This NNTH value is more or less equal to that of aspirin, which has a listed NNTH of 155, however, its corresponding OR for harm is much lower, namely 1.07. Similarly, the point estimate of the NNTH for standard dose Xa is 270 which is higher than that listed for low dose Xa inhibitor (187), while the respective ORs for harm show that standard-dose Xa inhibitor has a higher odds for harm. I realize that there is a possible logical explanation for these counterintuitive results, namely that the base rates of the placebo/observation condition vary significantly, but that would not be expected. Could the authors elaborate on this? Thank you very much in advance.
This is our response to a concern raised by a reader regarding the estimates and credible intervals of those numbers needed to treat to harm presented in our article titled “Extended treatment of venous thromboembolism: a systematic review and network meta-analysis.”
First, we confirm that data published in the Journal are valid and correct.
We also like to thank the reader to point it out as a number needed (either for benefit or harm) derived from an effect estimate that crosses the unity has been intuitively challenging to visualize (Hutton JL. Br J Haematol. 2009;146:27-30). Because it is given by the reciprocal of the absolute risk difference, a number needed can never include zero but straddles plus and minus infinity ∞ when the absolute risk difference include zero. By the frequentist approach based on inverting the confidence interval of the absolute risk difference, it represents that the number needed encompasses two disjoint regions: one from upper confidence interval to plus ∞ and the other from lower confidence interval to minus ∞ (Altman DG. BMJ. 1998;317:1309-12). Some had argued that for those non-significant results, a number needed should be presented as a single number without its confidence interval as it includes the possibility of no benefit or harm (McQuay HJ. Ann Intern Med. 1997;126:712-20). Other had suggested that it should not be reported when being non-significant (McAlister FA. CMAJ. 2008;179:549-53).
Our analyses with t...
Show MoreGiven 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...
On reading Dobson et al’s enlightening article we were saddened but not surprised to hear that nationally, there were no cardiology LTFT trainees training in electrophysiology (EP). Of course, it remains unclear as the relationship here: do trainees planning LTFT avoid EP, or do EP trainees fear reducing their hours will prove challenging?
Either way, this represents a great shame for both trainees and subspecialty. For trainees, the fulfilment of electrophysiological problem-solving and skilful intervention should be accessible to all regardless of hours worked. For the subspecialty, a growth in diversity of electrophysiologists as well as flexible working seems very sensible to ensure the continued growth of the subspecialty and its long-term sustainability. Ongoing initiatives by the BCS, BHRS, EHRA and others continue to advocate for a diverse and flexible workforce in EP, and we applaud these efforts.
Given the fact that high-grade carotid artery stenosis(CAS)(50% or more stenosis) is an independent risk factor for stroke in patients with coexisting nonvalvular atrial fibrillation(NVAF)(1), the optimum management of NVAF patients who have symptomatic CAS should be included among the key outstanding research questions enumerated by the authors of the recent review(2). In one study high-grade CAS was prevalent in 12%-14% of NVAF patients aged 71-80(3).. When high-grade CAS gives rise to amaurosis fugax , transient ischaemic attack(TIA), or stroke, the urgent priority is to mitigate the risk of subsequent occurrence of disabling stroke. That priority should prevail irrespective of presence or absence of coexisting NVAF. Strategies to mitigate that risk include initiation of dual antiplatelet therapy(4)(5) followed by interventional treatment of the CAS itself(6).
Show MoreFor patients in whom symptomatic CAS coexists with NVAF, when the latter is associated with a CHA2DS2-Vasc score that justifies oral anticoagulation to mitigate the risk of cardioembolis stroke , coprescription of oral anticoagulants has to be included in the management strategy. Furthermore after interventional treatment of symptomatic CAS, secondary prevention of neurological events(including stroke) necessitates long term antithrombotic medication with aspirin(5). Concurrently , in the presence of coexisting NVAF, long term primary prevention of cardioembolic stroke necessitates long...
Echocardiography has been shown to generate decisive diagnostic information when pulmonary embolism(PE) presents atypically with paradoxical cerebral embolism in the absence of concurrent PE-related stigmata such as dyspnoea, chest pain, or haemoptysis(1)(2), and also in those cases where the atypical presentation is one which simulates ST segment elevation myocardial infarction(STEMI) in the absence of paradoxical coronary artery embolism(3).
Show MoreThe following are some anecdotal report which exemplify the diagnostic role of echocardiography:-
A 32 year old man presented with a stroke , but no concurrent breathlessness or clinical signs of deep vein thrombosis(DVT). Transthoracic echocardiography(TTE) revealed intracardiac thrombus and also a thrombus in the main pulmonary artery. A subsequent Doppler examination revealed a DVT in the right lower limb(1).
In another report, a 55 year old man presented with a stroke and no concurrent breathlessness. However, he had a blood pressure of 70/40 mm Hg and an elevated serum troponin of 0.07 ng/ml(normal < 0.03 ng/ml). TTE revealed a "positive bubble study" which was followed up with a transoesopahageal echocardiogram(TOE) which showed a patent foramen ovale(PFO). A subsequent Duplex study revealed right lower limb DVT.. His management included intracardiac surgery, which revealed biatrial thrombus straddling a patent foramen ovale. An extensive pulmonary thrombus was also discovered(...
The focus on left atrial dimensions in the risk stratification of patients with atrial fibrillation(AF) and also in those without AF(1), is a timely departure from the prevailing preoccupation with AF-related risk stratification strategies such as the CHA2 DS2-Vasc score which do not include evaluation of left atrial function(2), notwithstanding the hypothesis that the predictive ability of the CHADS2 index to stratify stroke risk may be mechanistically linked to severity of left atrial dysfunction(3). In the latter study left atrial functional index(LAFI) was the parameter utilised to evaluate left atrial function. Regression analysis showed that mean LAFI significantly(p < 0.001) decreased across tertiles of CHADS2(42.8, 37.8, 36.7). After adjustment for age, sex, race, and other parameters , high CHADS2 remained significantly associated with the lowest quartile of LAFI(Odds Ratio 2.34). For every point increase in CHADS2 the LAFI decreased by 4 %. Secondary analyses using CHA2 DS2 Vasc score replicated these results(3). In view of these observations LAFI is a potential modality to risk stratify nonvalvular atrial fibrillation(NVAF) subjects such as those with CHA2DS2 Vasc score of zero , who might otherwise be ineligible for thromboprophylaxis with oral anticoagulants. LAFI could even be utilised to evaluate eligibility for thromboprophylaxis in patients with excessive atrial ectopic activity or short-run atrial tachyarrhythmis, given the fact that each...
Show MoreGiven the fact that acute myocardial infarction(AMI)(1), left bundle branch block(LBBB)(2), and pulmonary embolism(PE), are all age-related disorders, the authors of the recent study correctly highlighted the importance of including PE in the differential diagnosis of the association of suspected AMI and LBBB(2). For the purpose of identifying those patients who are most likely to have AMI the authors proposed the use of serum troponin as a rule-in criterion during the first 3 hours of hospital admission . By implication the inclusion of PE in the differential diagnosis should be deferred for at least 3 hours, and only activated in patients who do not have a raised serum troponin level.
Show MoreHowever, in view of the fact that elevation in serum troponin may be a feature in the presentation of PE(4), and also in view of the fact that transient LBBB has been reported in a 59 year old patient with PE(5), the latter disorder should be included in the differential diagnosis of the association of acute coronary syndrome and LBBB. In the 59 year old patient who was reported with PE and LBBB, serial troponin levels were 0.38, 0.41, and 1.12 ng/ml(reference range 0-0.04)(5), arguably justifying early coronary angiography(2). That patient had neither pleuritic pain nor breathlessness to raise the index of suspicion for PE. Coronary angiography ruled out coronary artery occlusion, and helical computed tomography revealed extensive PE involving the main branches of both pul...
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