We use cookies to improve our service and to tailor our content and advertising to you.More infoYou can manage your cookie settings via your browser at any time. To learn more about how we use cookies, please see our cookies policy.
We read the study of Wei-Shiang Lin et al.[1] with a great interest. In their large-scale cohort retrospective study, they found that traumatic intracranial hemorrhage was associated with an increased risk of atrial fibrillation (AF) and hypothesized that inflammation and/or secondary cardiac insult due to the traumatic brain injury (TBI) may cause AF. Nevertheless, several points should be discussed. First, acute inflammation is well-known to be related to AF in trauma patients. The risk of new-onset AF is reasonably expected to occur at the acute phase following the trauma. This point has already been previously demonstrated to occur during the days following cardiac surgery or septic shock onset.[2] In the same way, cardiac insult occurs at the very early phase of TBI and the consecutive cardiac systolic dysfunction was reported to be reversible within the first week after the trauma. [3] In this perspective, how to explain that the risk of AF persists one year after the trauma? It would be very helpful if the authors could provide data on the delay between the day of trauma and the day of new-onset AF. Furthermore, inflammation and cardiac dysfunction are related to the TBI severity and it would be valuable to know whether the more severe TBI patients are more prone to develop AF than mild or moderate TBI. Finally, in their statistical model, the authors have taken into account comorbidities which are also known to favor AF. But others factors, such as sepsis and relat...
We read the study of Wei-Shiang Lin et al.[1] with a great interest. In their large-scale cohort retrospective study, they found that traumatic intracranial hemorrhage was associated with an increased risk of atrial fibrillation (AF) and hypothesized that inflammation and/or secondary cardiac insult due to the traumatic brain injury (TBI) may cause AF. Nevertheless, several points should be discussed. First, acute inflammation is well-known to be related to AF in trauma patients. The risk of new-onset AF is reasonably expected to occur at the acute phase following the trauma. This point has already been previously demonstrated to occur during the days following cardiac surgery or septic shock onset.[2] In the same way, cardiac insult occurs at the very early phase of TBI and the consecutive cardiac systolic dysfunction was reported to be reversible within the first week after the trauma. [3] In this perspective, how to explain that the risk of AF persists one year after the trauma? It would be very helpful if the authors could provide data on the delay between the day of trauma and the day of new-onset AF. Furthermore, inflammation and cardiac dysfunction are related to the TBI severity and it would be valuable to know whether the more severe TBI patients are more prone to develop AF than mild or moderate TBI. Finally, in their statistical model, the authors have taken into account comorbidities which are also known to favor AF. But others factors, such as sepsis and related medications are of major concerns in increasing inflammation and the risk of new-onset AF.[4] Especially, TBI patients are particularly at risk to develop sepsis in the course of disease, mainly ventilator-associated pneumonia amongst the more severe TBI patients. We think these factors should be mentioned and included in the Cox regression model.
1 Lin W-S, Lin T-C, Hung Y, et al. Traumatic intracranial haemorrhage is in association with an increased risk of subsequent atrial fibrillation. Heart Br Card Soc Published Online First: 7 April 2017. doi:10.1136/heartjnl-2016-310451
2 Meierhenrich R, Steinhilber E, Eggermann C, et al. Incidence and prognostic impact of new-onset atrial fibrillation in patients with septic shock: a prospective observational study. Crit Care Lond Engl 2010;14:R108. doi:10.1186/cc9057
3 Chaikittisilpa N, Krishnamoorthy V, Lele AV, et al. Characterizing the relationship between systemic inflammatory response syndrome and early cardiac dysfunction in traumatic brain injury. J Neurosci Res Published Online First: 2 June 2017. doi:10.1002/jnr.24100
4 Launey Y, Lasocki S, Asehnoune K, et al. Impact of Low-Dose Hydrocortisone on the Incidence of Atrial Fibrillation in Patients With Septic Shock. J Intensive Care Med 2017;:885066617696847. doi:10.1177/0885066617696847
We have read the article by dr. Ghannam with interest. We appreciate their summary of the available data on anticoagulant treatment in special patient populations. However, with the rapidly increasing evidence in this field, some recent relevant studies were not mentioned.
For instance, in patients undergoing cardioversion, the authors suggest treatment with VKA or rivaroxaban, based on the statement that this is the only available NOAC studied prospectively in this setting. Last year, the data of the ENSURE-AF with edoxaban were presented, which provide similar evidence for the use of edoxaban in this setting (1). Furthermore, the recently published EMANATE-AF study adds solid evidence for the use of apixaban in this setting (2).
Similarly, in patients undergoing catheter ablation, the RE-CIRCUIT study published earlier this year provides very reassuring prospective data on the uninterrupted use of dabigatran in patients undergoing catheter ablation (3), yet this is not mentioned in the article. At the ESC in 2017, the data of the RE-DUAL PCI study provide insight in different strategies on how to combine dabigatran with single or dual antiplatelet therapy in patients undergoing percutaneous coronary interventions (4). Similar data for rivaroxaban were described in the PIONEER study (5), and the results of the ongoing AUGUSTUS study with apixaban are expected within the next years.
In summary, the very large number of patients studied...
We have read the article by dr. Ghannam with interest. We appreciate their summary of the available data on anticoagulant treatment in special patient populations. However, with the rapidly increasing evidence in this field, some recent relevant studies were not mentioned.
For instance, in patients undergoing cardioversion, the authors suggest treatment with VKA or rivaroxaban, based on the statement that this is the only available NOAC studied prospectively in this setting. Last year, the data of the ENSURE-AF with edoxaban were presented, which provide similar evidence for the use of edoxaban in this setting (1). Furthermore, the recently published EMANATE-AF study adds solid evidence for the use of apixaban in this setting (2).
Similarly, in patients undergoing catheter ablation, the RE-CIRCUIT study published earlier this year provides very reassuring prospective data on the uninterrupted use of dabigatran in patients undergoing catheter ablation (3), yet this is not mentioned in the article. At the ESC in 2017, the data of the RE-DUAL PCI study provide insight in different strategies on how to combine dabigatran with single or dual antiplatelet therapy in patients undergoing percutaneous coronary interventions (4). Similar data for rivaroxaban were described in the PIONEER study (5), and the results of the ongoing AUGUSTUS study with apixaban are expected within the next years.
In summary, the very large number of patients studied in phase III studies, the increasing number of data from phase IV studies, and the ongoing prospective studies in specific patient situations continue to provide new data on anticoagulation therapy in situations where this was never available before. This increasing knowledge is likely to further advance the field, and algorithms as presented in this article should reflect which choices are based on clear contra-indications, and which suggestions are based on current absence of specific data, where recommendations may change based on the availability of new data.
Sincerely,
(1) Lancet. 2016 Oct 22;388(10055):1995-2003. doi: 10.1016/S0140-6736(16)31474-X. Epub 2016 Aug 30.
(2) Ezekowitz MD, et al. Late Breaking Clinical Trials 2. Presented at: European Society of Cardiology Congress; August 26-30, 2017; Barcelona, Spain
(3) Calkins H, Willems S, Gerstenfeld EP, Verma A, Schilling R, Hohnloser SH, Okumura K, Serota H, Nordaby M, Guiver K, Biss B, Brouwer MA, Grimaldi M; RE-CIRCUIT Investigators. N Engl J Med. 2017 Apr 27;376(17):1627-1636. doi: 10.1056/NEJMoa1701005. Epub 2017 Mar 19.
(4) Cannon CP, Bhatt DL, Oldgren J, Lip GYH, Ellis SG, Kimura T, Maeng M, Merkely B, Zeymer U, Gropper S, Nordaby M, Kleine E, Harper R, Manassie J, Januzzi JL, Ten Berg JM, Steg PG, Hohnloser SH; RE-DUAL PCI Steering Committee and Investigators.
(5) Gibson CM, Mehran R, Bode C, Halperin J, Verheugt FW, Wildgoose P, Birmingham M, Ianus J, Burton P, van Eickels M, Korjian S, Daaboul Y, Lip GY, Cohen M, Husted S, Peterson ED, Fox KA. N Engl J Med. 2016 Dec 22;375(25):2423-2434. doi: 10.1056/NEJMoa1611594. Epub 2016 Nov 14.
To the Editor,
We read with interest the work presented by Cahill et al. [1] in which the authors evaluate the impact of antibiotic prophylaxis to prevent bacteremia and infective endocarditis in patients undergoing dental procedures. The analysis was performed based on 36 studies, including 21 bacteremia studies, five case controls and cohort studies, and 10 time trend studies.
It is generally well established that dental cares cause bacteremia, and that most are due to streptococcal strains [1,2]. It is, consequently, reasonable to think that prescribing antibiotics before dental cares decreases the incidence of such bacteremia. Globally, the discordant results between the different kinds of studies analyzed in the paper by Cahill et al. [1] are clearly insufficient to conclude that antibiotic prophylaxis prevents bacteremia due to streptococci. In our view, this observation can be explained by the fact that dental care is not the only cause of streptococcal bacteremia. Indeed, such bacteremia are extremely common, and it has been demonstrated that they can occur after chewing and after brushing in patients with periodontitis (cumulatively in 25% and 20% of cases, respectively) [2]. It is, therefore, fairly unlikely that bacteremias due to dental cares are more responsible for endocarditis than other kinds of bacteremias. In practice, this implies that the only reasonable antibiotic prophylaxis to prevent almost every bacteremia due to oral streptococci wou...
To the Editor,
We read with interest the work presented by Cahill et al. [1] in which the authors evaluate the impact of antibiotic prophylaxis to prevent bacteremia and infective endocarditis in patients undergoing dental procedures. The analysis was performed based on 36 studies, including 21 bacteremia studies, five case controls and cohort studies, and 10 time trend studies.
It is generally well established that dental cares cause bacteremia, and that most are due to streptococcal strains [1,2]. It is, consequently, reasonable to think that prescribing antibiotics before dental cares decreases the incidence of such bacteremia. Globally, the discordant results between the different kinds of studies analyzed in the paper by Cahill et al. [1] are clearly insufficient to conclude that antibiotic prophylaxis prevents bacteremia due to streptococci. In our view, this observation can be explained by the fact that dental care is not the only cause of streptococcal bacteremia. Indeed, such bacteremia are extremely common, and it has been demonstrated that they can occur after chewing and after brushing in patients with periodontitis (cumulatively in 25% and 20% of cases, respectively) [2]. It is, therefore, fairly unlikely that bacteremias due to dental cares are more responsible for endocarditis than other kinds of bacteremias. In practice, this implies that the only reasonable antibiotic prophylaxis to prevent almost every bacteremia due to oral streptococci would be lifetime treatment with penicillin or ampicillin [3]. However, even doing so, it would be impossible to prevent all infective endocarditis, as the authors observe[1].
The main limitation of the study by Cahill et al. [1] is that it did not include negative controls for bacteremia and that the frequency of bacteremia was measured only after dental care rather than after different day-to-day situations. This is an important methodological error which makes it an unreasonable basis for justifying particular conclusions.
Thus, and for the reasons mentioned above, there is still no evidence that dental prophylaxis during dental care changes the incidence of infective endocarditis [4], and this is the only reasonable conclusion of this study.
References
[1] Cahill TJ, Harrison JL, Jewell P, Onakpoya I, Chambers JB, Dayer M, et al. Antibiotic prophylaxis for infective endocarditis: a systematic review and meta-analysis. Heart 2017;103:937–44. doi:10.1136/heartjnl-2015-309102.
[2] Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation. J Clin Periodontol 2006;33:401–7. doi:10.1111/j.1600-051X.2006.00924.x.
[3] Diene SM, Abat C, Rolain J-M, Raoult D. How artificial is the antibiotic resistance definition? Lancet Infect Dis 2017;17:690. doi:10.1016/S1473-3099(17)30338-9.
[4] Million M, Grisoli D, Griffiths K, Raoult D. Antibiotic prophylaxis of endocarditis. Lancet Infect Dis 2016;16:773–4. doi:10.1016/S1473-3099(16)30084-6.
We have read with great interest the paper “Chocolate intake and risk of clinically apparent atrial
fibrillation: the Danish Diet, Cancer, and Health Study” by Elizabeth Mostofsky and coworkers [1] and we found their conclusion of importance with a view to clinical prevention.
With reference to the findings reported in the paper, we would like to make the following contribution to the discussion. In a recent analysis performed on 650 healthy women in pre-menopausal age (age range 45-54 years) chocolate intake was higher in women in the low quartile of adherence to Mediterranean Diet (low Med Score). This subgroup of women showed a lower ABI index compared to women with higher Med Score. The analysis of sources of antioxidants showed a greater intake from fruit and vegetables in the higher quartiles of Med Score. Coffee and tea were similarly distributed among the quartiles of Med Score [2]. Analysis from diet recall had the major limitation of missing data regarding out-of-mealtime snacking and drinking.
In Mediterranean countries, wine is a strong antioxidant source and the synergistic effect of drinking wine during meals and antioxidant bioavailability is well known. We clearly understand that nutritional habits in Northern Europe differ from Mediterranean ones. However, we would like to underline that in a Mediterranean lifestyle characterized by high intake of antioxidants,...
We have read with great interest the paper “Chocolate intake and risk of clinically apparent atrial
fibrillation: the Danish Diet, Cancer, and Health Study” by Elizabeth Mostofsky and coworkers [1] and we found their conclusion of importance with a view to clinical prevention.
With reference to the findings reported in the paper, we would like to make the following contribution to the discussion. In a recent analysis performed on 650 healthy women in pre-menopausal age (age range 45-54 years) chocolate intake was higher in women in the low quartile of adherence to Mediterranean Diet (low Med Score). This subgroup of women showed a lower ABI index compared to women with higher Med Score. The analysis of sources of antioxidants showed a greater intake from fruit and vegetables in the higher quartiles of Med Score. Coffee and tea were similarly distributed among the quartiles of Med Score [2]. Analysis from diet recall had the major limitation of missing data regarding out-of-mealtime snacking and drinking.
In Mediterranean countries, wine is a strong antioxidant source and the synergistic effect of drinking wine during meals and antioxidant bioavailability is well known. We clearly understand that nutritional habits in Northern Europe differ from Mediterranean ones. However, we would like to underline that in a Mediterranean lifestyle characterized by high intake of antioxidants, chocolate represents only a small percentage with a low impact on total antioxidant intake. [3]
Moreover, It is well known that chocolate bars contain a low level of caffeine. In a previous report on hypertensive patients we found that those who reduced coffee intake had a higher chocolate bar consumption which affected total caffeine intake [3]. Due to the controversial results of the effect of caffeine on atrial fibrillation, we cannot therefore exclude the potential effects of this on arrhythmias [4].
Anna Vittoria Mattioli MD PhD, Alberto Farinetti MD, Antonio Manenti MD.
Surgical, Medical and Dental Department of Morphological Sciences related to Transplant, Oncology and Regenerative Medicine
University of Modena and Reggio Emilia (Italy)
1. Mostofsky E, Berg Johansen M, Tjønneland A, Chahal HS, Mittleman MA, Overvad K. Chocolate intake and risk of clinically apparent atrial fibrillation: the Danish Diet, Cancer, and Health Study. Heart 2017;0:1–5. doi:10.1136/heartjnl-2016-310357.
2. Mattioli AV, Pennella S, Manenti A, Migaldi M, Farinetti A. Mediterranean Diet and antioxidants intake: relationship with asymptomatic peripheral arterial disease in a population of pre-menopausal women. Abstract presented at ESC Congress August 2016
3. Mattioli AV, Farinetti A, Miloro C, Pedrazzi P, Mattioli G. Influence of coffee and caffeine consumption on atrial fibrillation in hypertensive patients. Nutr Metab Cardiovasc Dis. 2010 Feb 16. [Epub ahead of print] doi:10.1016/j.numecd.2009.11.003
4. Bhave PD, Hoffmayer K. Caffeine and atrial fibrillation: friends or foes? Heart. 2013 Oct;99(19):1377-8. doi: 10.1136/heartjnl-2013-304543.
The study of Olmos et al., on prediction of in-hospital mortality in patients with active infective endocarditis undergoing cardiac surgery, is of great interest.1
Indeed, this topic is fascinating because it is complicated to make a choice in so dramatic and not so rare situation.
To help with this decision-making, the authors proposed a model for predicting hospital mortality: a classic multivariate logistic regression model.
However, the editorial published with this article evokes in the title a new method: machine learning.2 Machine learning, which is a field of artificial intelligence, has already been used for predicting hospital mortality after elective cardiac surgery.3 This study aimed at comparing a machine learning model, a classic logistic regression model and EuroSCORE II on a cohort including 6,520 patients. The comparison of these models was based on ROC curves and decision curve analysis (DCA).4 Whatever the method of comparison, machine learning model was more accurate than other models.
Our experience in this area probably allows us to make some comments on this editorial. Considering, the increase of studies comparing machine learning with logistic regression, it is now known that supervised machine learning algorithms improve the prediction of post-operative mortality. However, the size of the cohort used in the present study makes it difficult to apply machine learning algorithms. Indeed, this cohort comprised 671 patients who...
The study of Olmos et al., on prediction of in-hospital mortality in patients with active infective endocarditis undergoing cardiac surgery, is of great interest.1
Indeed, this topic is fascinating because it is complicated to make a choice in so dramatic and not so rare situation.
To help with this decision-making, the authors proposed a model for predicting hospital mortality: a classic multivariate logistic regression model.
However, the editorial published with this article evokes in the title a new method: machine learning.2 Machine learning, which is a field of artificial intelligence, has already been used for predicting hospital mortality after elective cardiac surgery.3 This study aimed at comparing a machine learning model, a classic logistic regression model and EuroSCORE II on a cohort including 6,520 patients. The comparison of these models was based on ROC curves and decision curve analysis (DCA).4 Whatever the method of comparison, machine learning model was more accurate than other models.
Our experience in this area probably allows us to make some comments on this editorial. Considering, the increase of studies comparing machine learning with logistic regression, it is now known that supervised machine learning algorithms improve the prediction of post-operative mortality. However, the size of the cohort used in the present study makes it difficult to apply machine learning algorithms. Indeed, this cohort comprised 671 patients who had cardiac surgery, with a cohort of derivation containing only 424 patients (300 discharged alive and 124 died after surgery). This cohort was probably too small for efficient use of machine learning algorithms. However, it would have been interesting to fit a machine learning model in this field. Moreover, the fact that this database is spread over 18 years compromises the validity of this model in 2017.
In conclusion, this article and the accompanying editorial very well illustrate the current problem of artificial intelligence in medicine: how to find reliable data in sufficient quantities?
References
1 Olmos C, Vilacosta I, Habib G, et al. Risk score for cardiac surgery in active left-sided infective endocarditis. Heart 2017; 10.1136/heartjnl-2016-311093.
2 Donal E, Flecher E, Tattevin P. Machine learning to support decision-making for cardiac surgery during the acute phase of infective endocarditis. Heart Published Online First: 8 May 2017. doi:10.1136/heartjnl-2017-311512
3 Allyn J, Allou N, Augustin P, et al. A Comparison of a Machine Learning Model with EuroSCORE II in Predicting Mortality after Elective Cardiac Surgery: A Decision Curve Analysis. PloS One 2017;12:e0169772. doi:10.1371/journal.pone.0169772
4 Fitzgerald M, Saville BR, Lewis RJ. Decision curve analysis. JAMA 2015;313:409–10. doi:10.1001/jama.2015.37
To the Editor,
The timely retrospective US cohort study by Alonso et al.1 assessed the risk of hospitalisations for liver injury after initiation of oral anticoagulation in patients with non-valvular atrial fibrillation, an unresolved safety issue so far.
This study has key merits. First, it demonstrates the importance of conducting analytical research following safety signals emerging from spontaneous reporting systems2, to confirm or refute the drug-related hypothesis; this allows actual risk assessment and avoids unnecessary alarm, sometimes generated by pharmacovigilance analyses which do not recognize the limits of detected signals.
Second, it provides a significant contribution to the debate on targeted patients’ selection when prescribing DOACs. In fact, the authors found that hospitalization rates for liver injury were lower among DOAC initiators as compared to patients starting warfarin, with rivaroxaban and dabigatran associated with highest and lowest risk, respectively. They conclude that “dabigatran may be considered a safer option” in patients susceptible of liver complications. In this vulnerable population, our proposal when initiating DOAC administration is to early monitor hepatic enzymes (i.e., within the first month of therapy) and, subsequently, on a yearly basis, especially for rivaroxaban users.3
Although this study contributes to allay concern on the hepatotoxicity potential of DOACs, a residual aspect deserves attention. The...
To the Editor,
The timely retrospective US cohort study by Alonso et al.1 assessed the risk of hospitalisations for liver injury after initiation of oral anticoagulation in patients with non-valvular atrial fibrillation, an unresolved safety issue so far.
This study has key merits. First, it demonstrates the importance of conducting analytical research following safety signals emerging from spontaneous reporting systems2, to confirm or refute the drug-related hypothesis; this allows actual risk assessment and avoids unnecessary alarm, sometimes generated by pharmacovigilance analyses which do not recognize the limits of detected signals.
Second, it provides a significant contribution to the debate on targeted patients’ selection when prescribing DOACs. In fact, the authors found that hospitalization rates for liver injury were lower among DOAC initiators as compared to patients starting warfarin, with rivaroxaban and dabigatran associated with highest and lowest risk, respectively. They conclude that “dabigatran may be considered a safer option” in patients susceptible of liver complications. In this vulnerable population, our proposal when initiating DOAC administration is to early monitor hepatic enzymes (i.e., within the first month of therapy) and, subsequently, on a yearly basis, especially for rivaroxaban users.3
Although this study contributes to allay concern on the hepatotoxicity potential of DOACs, a residual aspect deserves attention. The authors acknowledge the fact that concerns/awareness about liver toxicity could have potentially resulted in selective prescribing towards DOACs of patients at higher hepatic risk, but did not discuss the resulting channeling bias. Notably, warfarin initiators were older, had higher CHA2DS2-VASc and HAS-BLED scores and higher prevalence of comorbidities, as compared to DOACs users. Therefore, it is plausible that this phenomenon generated confounding, which was not fully captured despite extensive adjustment strategies.4 Therefore, we believe that this first important piece of evidence cannot stand alone when it comes to selecting a given oral anticoagulant.
We encourage additional observational studies to replicate these findings, especially in different contexts, such as the European scenario and in patients with venous thromboembolism, which might be more prone to develop liver injury.3 Hopefully, collaborative multidisciplinary consortia will fill the mechanistic and clinical gaps to establish actual drug-event relationship and support risk stratification.
REFERENCES
1 Alonso A, MacLehose RF, Chen LY et al. Prospective study of oral anticoagulants and risk of liver injury in patients with atrial fibrillation. Heart 2017 Jan 5. pii: heartjnl-2016-310586. doi: 10.1136/heartjnl-2016-310586. [Epub ahead of print]
2 Raschi E, Poluzzi E, Koci A et al. Liver injury with novel oral anticoagulants: assessing post-marketing reports in the US Food and Drug Administration adverse event reporting system. Br J Clin Pharmacol 2015;80:285-93.
3 Raschi E, Bianchin M, Ageno W et al. Adverse events associated with the use of direct-acting oral anticoagulants in clinical practice: beyond bleeding complications. Pol Arch Med Wewn 2016;126:552-61.
4 Gorst-Rasmussen A, Lip GY, Bjerregaard Larsen T. Rivaroxaban versus warfarin and dabigatran in atrial fibrillation: comparative effectiveness and safety in Danish routine care. Pharmacoepidemiol Drug Saf 2016;25:1236-44.
We congratulate McDowell et al. on their educational and interesting case report.1 However, we would like to comment on their use of the term ‘near-drowning’. This, and other confusing and older terms which caused inconsistencies in the literature, have been abandoned by organisations such as the International Liaison Committee on Resuscitation (ILCOR) and the World Health Organisation (WHO) who recommend a more structured and clearer way of reporting drowning incidents.2,3 For several years now, drowning has been defined as ‘a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident’. 2,3 We would thus recommend that the authors and readers of your journal follow ILCOR and WHO recommendations, and simply use the term ‘drowning’ irrespective of the patient outcome. While this may seem pedantic, we do believe that it will assist with standardisation in drowning research and literature.
References
1. McDowell K, Carrick D, Weir R. Heart Published Online First: 18 may 2017. doi:10.1136/heartjnl-2016-311043.
2. Idris AH, Berg RA, Bierens J, Bossaert L, Branche CM, Gabrielli A, Graves SA, Handley AJ, Hoelle R, Morley PT, Papa L, Pepe...
We congratulate McDowell et al. on their educational and interesting case report.1 However, we would like to comment on their use of the term ‘near-drowning’. This, and other confusing and older terms which caused inconsistencies in the literature, have been abandoned by organisations such as the International Liaison Committee on Resuscitation (ILCOR) and the World Health Organisation (WHO) who recommend a more structured and clearer way of reporting drowning incidents.2,3 For several years now, drowning has been defined as ‘a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident’. 2,3 We would thus recommend that the authors and readers of your journal follow ILCOR and WHO recommendations, and simply use the term ‘drowning’ irrespective of the patient outcome. While this may seem pedantic, we do believe that it will assist with standardisation in drowning research and literature.
References
1. McDowell K, Carrick D, Weir R. Heart Published Online First: 18 may 2017. doi:10.1136/heartjnl-2016-311043.
2. Idris AH, Berg RA, Bierens J, Bossaert L, Branche CM, Gabrielli A, Graves SA, Handley AJ, Hoelle R, Morley PT, Papa L, Pepe PE, Quan L, Szpilman D, Wigginton JG, Modell JH, American Heart Association. Recommended guidelines for uniform reporting of data from drowning: the "Utstein style". Circulation 2003;108:2565-74.
3. van Beeck E, Branche C, Szpilman D, Modell J, Bierens J. A new definition of drowning: towards documentation and prevention of a global public health problem. Bull World Health Organ 2005;83:853-6.
We read with interest the Editorial on the recently updated National Institute for Health and Care Excellence (NICE) guidance for the assessment of suspected stable angina (1). The authors raise some salient points regarding the importance of careful history taking, the vexed question of the exercise ECG and the relative merits of the myriad non-invasive tests for diagnosing coronary artery disease (CAD). However, we believe they have adopted an unnecessarily alarmist tone in their criticisms and feel obliged to respond to several issues.
Although they suggest that the assessment of pretest probability (PTP) has been disregarded, this process has merely been made implicit rather than explicit. The guidelines emphasise the pivotal importance of the clinical history and, in the setting of suspected angina, the nature of the presenting symptoms is the dominant predictor of CAD. Existing risk tables (2) show that either typical or atypical angina essentially guarantees a PTP of CAD ≥ 10%, the threshold warranting further investigation in the earlier NICE guideline. The residual clinical risk seen in patients with non-anginal symptoms is best addressed through cardiovascular screening approaches with an emphasis of lifestyle modification and primary prevention.
Second, in arguing against the cost-effectiveness of the new approach, the authors imply that NICE are recommending “universal CTCA” which is incorrect. Non-anginal chest pain occurs in 40-60% of patients pre...
We read with interest the Editorial on the recently updated National Institute for Health and Care Excellence (NICE) guidance for the assessment of suspected stable angina (1). The authors raise some salient points regarding the importance of careful history taking, the vexed question of the exercise ECG and the relative merits of the myriad non-invasive tests for diagnosing coronary artery disease (CAD). However, we believe they have adopted an unnecessarily alarmist tone in their criticisms and feel obliged to respond to several issues.
Although they suggest that the assessment of pretest probability (PTP) has been disregarded, this process has merely been made implicit rather than explicit. The guidelines emphasise the pivotal importance of the clinical history and, in the setting of suspected angina, the nature of the presenting symptoms is the dominant predictor of CAD. Existing risk tables (2) show that either typical or atypical angina essentially guarantees a PTP of CAD ≥ 10%, the threshold warranting further investigation in the earlier NICE guideline. The residual clinical risk seen in patients with non-anginal symptoms is best addressed through cardiovascular screening approaches with an emphasis of lifestyle modification and primary prevention.
Second, in arguing against the cost-effectiveness of the new approach, the authors imply that NICE are recommending “universal CTCA” which is incorrect. Non-anginal chest pain occurs in 40-60% of patients presenting to chest pain clinics in the United Kingdom (3, 4), creating the opportunity for many more individuals to be discharged without further investigation. In addition, the Scottish COmputed Tomography of the Heart (SCOT-HEART) trial (3) did not demonstrate an overall increase in invasive coronary angiograms or revascularisation rates, perhaps reflecting a more nuanced response to coronary disease in the modern era.
Third, although correct in noting the borderline statistical significance of the reduction in fatal and non-fatal myocardial infarction after 1.7 years follow-up of the SCOT-HEART trial (3), the primary pre-specified timeframe for reporting this outcome is 5 years, with final results due early 2018.
Finally, the authors will be pleased to learn that we will shortly present a comprehensive analysis of the clinical impact of the revised NICE guidelines when applied to the SCOT-HEART trial population, addressing the questions and allaying the concerns raised in this Editorial.
References:
1. Cremer PC, Nissen SE. The National Institute for Health and Care Excellence update for stable chest pain: poorly reasoned and risky for patients. Heart. 2017:heartjnl-2017-311410.
2. European Society of Cardiology Task Force. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013;34(38):2949-3003.
3. The SCOT-HEART investigators. CT coronary angiography in patients with suspected angina due to coronary heart disease (SCOT-HEART): an open-label, parallel-group, multicentre trial. The Lancet. 2015;385(9985):2383-91.
4. McKavanagh P, Lusk L, Ball PA, Verghis RM, Agus AM, Trinick TR, Duly E, Walls GM, Stevenson M, James B, Hamilton A, Harbinson MT, Donnelly PM. A comparison of cardiac computerized tomography and exercise stress electrocardiogram test for the investigation of stable chest pain: the clinical results of the CAPP randomized prospective trial. Eur Heart J Cardiovasc Imaging. 2015;16(4):441-8.
The article by Wouters and colleagues (1) presents an exhaustive overview on how QALYs can be used in cost-effectiveness analysis. In this framework, the authors also mention the incremental cost-effectiveness ratio (ICER), which is the parameter typically employed to express the results of a cost-effectiveness study. The article, however, does not discuss the net monetary benefit (NMB), which is another parameter employed to express the results of a cost-effectiveness study.
The incremental cost (deltaC) and the incremental effectiveness (deltaE) are the two main parameters of pharmacoeconomics and cost-effectiveness analysis, along with the willingness-to-pay threshold (lambda). The decision rule (e.g. in the case of a favourable pharmacoeconomic result) is (deltaC/deltaE)<lambda (Equation 1), if based on the ICER, or (deltaE x lambda - deltaC) > 0 (Equation 2), if based on the NMB. Likewise, an unfavourable pharmacoeconomic result is when (deltaC/deltaE)>lambda or when (deltaE x lambda - deltaC) < 0; NMB is defined as deltaE x lambda - deltaC, while ICER is defined as deltaC/deltaE.
Despite its apparent complexity, most part of pharmacoeconomic methodology is described by the two simple equations reported above (i.e. Equations 1 and 2), but whether the ICER or the NMB is the best parameter for the purposes of pharmacoeconomic decision-making remains on open question.
The study by Cowper et al evaluating new versus old oral antic...
The article by Wouters and colleagues (1) presents an exhaustive overview on how QALYs can be used in cost-effectiveness analysis. In this framework, the authors also mention the incremental cost-effectiveness ratio (ICER), which is the parameter typically employed to express the results of a cost-effectiveness study. The article, however, does not discuss the net monetary benefit (NMB), which is another parameter employed to express the results of a cost-effectiveness study.
The incremental cost (deltaC) and the incremental effectiveness (deltaE) are the two main parameters of pharmacoeconomics and cost-effectiveness analysis, along with the willingness-to-pay threshold (lambda). The decision rule (e.g. in the case of a favourable pharmacoeconomic result) is (deltaC/deltaE)<lambda (Equation 1), if based on the ICER, or (deltaE x lambda - deltaC) > 0 (Equation 2), if based on the NMB. Likewise, an unfavourable pharmacoeconomic result is when (deltaC/deltaE)>lambda or when (deltaE x lambda - deltaC) < 0; NMB is defined as deltaE x lambda - deltaC, while ICER is defined as deltaC/deltaE.
Despite its apparent complexity, most part of pharmacoeconomic methodology is described by the two simple equations reported above (i.e. Equations 1 and 2), but whether the ICER or the NMB is the best parameter for the purposes of pharmacoeconomic decision-making remains on open question.
The study by Cowper et al evaluating new versus old oral anticoagulants in patients with atrial fibrillation (2) is a typical ICER-based cost-effectiveness analysis in which the ICER of apixaban versus warfarin is compared against a willingness-to-pay threshold. This analysis can be taken as an example for comparing ICER vs NMB.
In one of the base-case analyses of the study by Cowper et al, QALYs per patient were 7.94 for apixaban and 7.54 for warfarin, while pharmacological costs per patient were $22,934 and $4,392, respectively. These data yielded, for apixaban versus warfarin, an ICER of $46,355 per QALY gained, a value that remains within the willingness-to-pay threshold of $50,000 per QALY gained and is therefore considered favourable (or “high value care”). As pointed our by Hlatky (3), in interpreting a specific ICER value, more than a single willingness-to-pay threshold is frequently considered (e.g. the threshold between $50,000 and $150,000 or the threshold above $150,000), and this allows us to better understand a pharmacoeconomic result expressed on the basis of an ICER.
In the methodology of pharmacoeconomics, the net monetary benefit (NMB) plays a role similar to that of ICER, but some differences are important.
Firstly, the ICER –by definition- has always an incremental nature and consequently the absolute cost-effectiveness ratio (calculated for a single treatment in the absence of any comparison) makes little sense and, for this reason, is rarely employed. In contrast, the NMB can be calculated for a single treatment in the absence of any comparison (absolute NMB) or can conversely be calculated as an incremental parameter [according to the equation: (incremental NMB) = (incremental QALYs per patient) x (willingness-to-pay threshold) – (incremental cost per patient)]. Another feature of NMB is that the incremental NMB for the comparison of A vs B can be estimated as the absolute NMB calculated for A minus the absolute NMB calculated for B. In this sequence of calculations, calculating the absolute NMB makes sense because the absolute NMB (separately calculated for the experimental treatment and for the control treatment) represents an intermediate step in the calculation of the incremental NMB (Table 1)
The values of absolute NMB for apixaban and warfarin (Table 1) are, respectively, 374,066 and $372,608 per patient (calculated according to Equation 2). Hence, the incremental NMB for apixaban vs warfarin is simply the difference of the above two values, i.e. $1,458 per patient.
References
1. Wouters OJ, Naci H, Samani NJ. QALYs in cost-effectiveness analysis: an overview for cardiologists. Heart. 2015 Dec;101(23):1868-73.
2. Cowper PA, Sheng S, Lopes RD, Anstrom KJ, Stafford JA, Davidson-Ray L, Al-Khatib SM, Ansell J, Dorian P, Husted S, McMurray JJ, Steg PG, Alexander JH, Wallentin L, Granger CB, Mark DB. Economic Analysis of Apixaban Therapy for Patients With Atrial Fibrillation From a US Perspective: Results From the ARISTOTLE Randomized Clinical Trial. JAMA Cardiol. 2017 Mar 29. doi:10.1001/jamacardio.2017.0065. [Epub ahead of print]
3. Hlatky MA. Are Novel Anticoagulants Worth Their Cost? JAMA Cardiol. 2017 Mar 29. doi: 10.1001/jamacardio.2017.0126. [Epub ahead of print]
Table 1. Cost-effectiveness of apixaban vs warfarin in atrial fibrillation: base-case analysis reported by Cowper et al. (2)
___________________________________________________
a) STARTING VALUES
Apixaban: QALYs per patient = 7.94, cost per patient = $22,934
Warfarin: QALYs per patient = 7.54, cost per patient = $4,392
Sawhney et al. reported that nurse-led, physician-directed moderate sedation during cardiac electrophysiology procedures is safe (1). All of the patients undergoing cardiac electrophysiological (EP) procedures and cardiac implantable electronic device (CIED) implantation during the last 12 years were moderately sedated. Since this study is a retrospective study, we could not comprehend why all patients were sedated despite the fact that routine sedation during all cardiac EP procedures and all CIED implantation is not recommended.
Moreover, as mentioned in the article, sedation is a continuum and it is not always possible to predict how individual patients will respond. Therefore, a gradual increase of doses of the sedatives during sedation may be needed which may possibly increase the procedure duration. Did authors ascertain any prolongation of the procedures due to sedative administration?
Furthermore, sedation may diminish arrythmia induction during EP procedures, particularly in patients with catecholamine-sensitive ventricular tachycardias (2). Did authors have any data questioning this issue?
As a conclusion, the aim of sedation is to diminish the anxiety and to relieve the pain during the procedure. Therefore, using moderate sedation selectively in patients with anxiety or hyperalgesia may be more practical and rational rather than its routine use due to the fact that as mentioned in the article, researches and audit demonstrate continued avoidabl...
Sawhney et al. reported that nurse-led, physician-directed moderate sedation during cardiac electrophysiology procedures is safe (1). All of the patients undergoing cardiac electrophysiological (EP) procedures and cardiac implantable electronic device (CIED) implantation during the last 12 years were moderately sedated. Since this study is a retrospective study, we could not comprehend why all patients were sedated despite the fact that routine sedation during all cardiac EP procedures and all CIED implantation is not recommended.
Moreover, as mentioned in the article, sedation is a continuum and it is not always possible to predict how individual patients will respond. Therefore, a gradual increase of doses of the sedatives during sedation may be needed which may possibly increase the procedure duration. Did authors ascertain any prolongation of the procedures due to sedative administration?
Furthermore, sedation may diminish arrythmia induction during EP procedures, particularly in patients with catecholamine-sensitive ventricular tachycardias (2). Did authors have any data questioning this issue?
As a conclusion, the aim of sedation is to diminish the anxiety and to relieve the pain during the procedure. Therefore, using moderate sedation selectively in patients with anxiety or hyperalgesia may be more practical and rational rather than its routine use due to the fact that as mentioned in the article, researches and audit demonstrate continued avoidable morbidity and mortality from sedation.
Kind Regards
REFERENCES
1) Sawhney V, Bacuetes E, Wray M, et al. Moderate sedation in cardiac electrophysiology laboratory: a retrospective safety analysis. Heart. 2017 Mar 1. pii: heartjnl-2016-310676. doi: 10.1136/heartjnl-2016-310676.
2) EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhytmias. Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. Europace. 2009 Jun;11(6):771-817. doi: 10.1093/europace/eup098.
We read the study of Wei-Shiang Lin et al.[1] with a great interest. In their large-scale cohort retrospective study, they found that traumatic intracranial hemorrhage was associated with an increased risk of atrial fibrillation (AF) and hypothesized that inflammation and/or secondary cardiac insult due to the traumatic brain injury (TBI) may cause AF. Nevertheless, several points should be discussed. First, acute inflammation is well-known to be related to AF in trauma patients. The risk of new-onset AF is reasonably expected to occur at the acute phase following the trauma. This point has already been previously demonstrated to occur during the days following cardiac surgery or septic shock onset.[2] In the same way, cardiac insult occurs at the very early phase of TBI and the consecutive cardiac systolic dysfunction was reported to be reversible within the first week after the trauma. [3] In this perspective, how to explain that the risk of AF persists one year after the trauma? It would be very helpful if the authors could provide data on the delay between the day of trauma and the day of new-onset AF. Furthermore, inflammation and cardiac dysfunction are related to the TBI severity and it would be valuable to know whether the more severe TBI patients are more prone to develop AF than mild or moderate TBI. Finally, in their statistical model, the authors have taken into account comorbidities which are also known to favor AF. But others factors, such as sepsis and relat...
Show MoreDear Editor,
We have read the article by dr. Ghannam with interest. We appreciate their summary of the available data on anticoagulant treatment in special patient populations. However, with the rapidly increasing evidence in this field, some recent relevant studies were not mentioned.
Show MoreFor instance, in patients undergoing cardioversion, the authors suggest treatment with VKA or rivaroxaban, based on the statement that this is the only available NOAC studied prospectively in this setting. Last year, the data of the ENSURE-AF with edoxaban were presented, which provide similar evidence for the use of edoxaban in this setting (1). Furthermore, the recently published EMANATE-AF study adds solid evidence for the use of apixaban in this setting (2).
Similarly, in patients undergoing catheter ablation, the RE-CIRCUIT study published earlier this year provides very reassuring prospective data on the uninterrupted use of dabigatran in patients undergoing catheter ablation (3), yet this is not mentioned in the article. At the ESC in 2017, the data of the RE-DUAL PCI study provide insight in different strategies on how to combine dabigatran with single or dual antiplatelet therapy in patients undergoing percutaneous coronary interventions (4). Similar data for rivaroxaban were described in the PIONEER study (5), and the results of the ongoing AUGUSTUS study with apixaban are expected within the next years.
In summary, the very large number of patients studied...
To the Editor,
Show MoreWe read with interest the work presented by Cahill et al. [1] in which the authors evaluate the impact of antibiotic prophylaxis to prevent bacteremia and infective endocarditis in patients undergoing dental procedures. The analysis was performed based on 36 studies, including 21 bacteremia studies, five case controls and cohort studies, and 10 time trend studies.
It is generally well established that dental cares cause bacteremia, and that most are due to streptococcal strains [1,2]. It is, consequently, reasonable to think that prescribing antibiotics before dental cares decreases the incidence of such bacteremia. Globally, the discordant results between the different kinds of studies analyzed in the paper by Cahill et al. [1] are clearly insufficient to conclude that antibiotic prophylaxis prevents bacteremia due to streptococci. In our view, this observation can be explained by the fact that dental care is not the only cause of streptococcal bacteremia. Indeed, such bacteremia are extremely common, and it has been demonstrated that they can occur after chewing and after brushing in patients with periodontitis (cumulatively in 25% and 20% of cases, respectively) [2]. It is, therefore, fairly unlikely that bacteremias due to dental cares are more responsible for endocarditis than other kinds of bacteremias. In practice, this implies that the only reasonable antibiotic prophylaxis to prevent almost every bacteremia due to oral streptococci wou...
Chocolate intake and risk of atrial fibrillation
Dear Editor,
We have read with great interest the paper “Chocolate intake and risk of clinically apparent atrial
fibrillation: the Danish Diet, Cancer, and Health Study” by Elizabeth Mostofsky and coworkers [1] and we found their conclusion of importance with a view to clinical prevention.
With reference to the findings reported in the paper, we would like to make the following contribution to the discussion. In a recent analysis performed on 650 healthy women in pre-menopausal age (age range 45-54 years) chocolate intake was higher in women in the low quartile of adherence to Mediterranean Diet (low Med Score). This subgroup of women showed a lower ABI index compared to women with higher Med Score. The analysis of sources of antioxidants showed a greater intake from fruit and vegetables in the higher quartiles of Med Score. Coffee and tea were similarly distributed among the quartiles of Med Score [2]. Analysis from diet recall had the major limitation of missing data regarding out-of-mealtime snacking and drinking.
Show MoreIn Mediterranean countries, wine is a strong antioxidant source and the synergistic effect of drinking wine during meals and antioxidant bioavailability is well known. We clearly understand that nutritional habits in Northern Europe differ from Mediterranean ones. However, we would like to underline that in a Mediterranean lifestyle characterized by high intake of antioxidants,...
The study of Olmos et al., on prediction of in-hospital mortality in patients with active infective endocarditis undergoing cardiac surgery, is of great interest.1
Show MoreIndeed, this topic is fascinating because it is complicated to make a choice in so dramatic and not so rare situation.
To help with this decision-making, the authors proposed a model for predicting hospital mortality: a classic multivariate logistic regression model.
However, the editorial published with this article evokes in the title a new method: machine learning.2 Machine learning, which is a field of artificial intelligence, has already been used for predicting hospital mortality after elective cardiac surgery.3 This study aimed at comparing a machine learning model, a classic logistic regression model and EuroSCORE II on a cohort including 6,520 patients. The comparison of these models was based on ROC curves and decision curve analysis (DCA).4 Whatever the method of comparison, machine learning model was more accurate than other models.
Our experience in this area probably allows us to make some comments on this editorial. Considering, the increase of studies comparing machine learning with logistic regression, it is now known that supervised machine learning algorithms improve the prediction of post-operative mortality. However, the size of the cohort used in the present study makes it difficult to apply machine learning algorithms. Indeed, this cohort comprised 671 patients who...
To the Editor,
Show MoreThe timely retrospective US cohort study by Alonso et al.1 assessed the risk of hospitalisations for liver injury after initiation of oral anticoagulation in patients with non-valvular atrial fibrillation, an unresolved safety issue so far.
This study has key merits. First, it demonstrates the importance of conducting analytical research following safety signals emerging from spontaneous reporting systems2, to confirm or refute the drug-related hypothesis; this allows actual risk assessment and avoids unnecessary alarm, sometimes generated by pharmacovigilance analyses which do not recognize the limits of detected signals.
Second, it provides a significant contribution to the debate on targeted patients’ selection when prescribing DOACs. In fact, the authors found that hospitalization rates for liver injury were lower among DOAC initiators as compared to patients starting warfarin, with rivaroxaban and dabigatran associated with highest and lowest risk, respectively. They conclude that “dabigatran may be considered a safer option” in patients susceptible of liver complications. In this vulnerable population, our proposal when initiating DOAC administration is to early monitor hepatic enzymes (i.e., within the first month of therapy) and, subsequently, on a yearly basis, especially for rivaroxaban users.3
Although this study contributes to allay concern on the hepatotoxicity potential of DOACs, a residual aspect deserves attention. The...
Sir,
We congratulate McDowell et al. on their educational and interesting case report.1 However, we would like to comment on their use of the term ‘near-drowning’. This, and other confusing and older terms which caused inconsistencies in the literature, have been abandoned by organisations such as the International Liaison Committee on Resuscitation (ILCOR) and the World Health Organisation (WHO) who recommend a more structured and clearer way of reporting drowning incidents.2,3 For several years now, drowning has been defined as ‘a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident’. 2,3 We would thus recommend that the authors and readers of your journal follow ILCOR and WHO recommendations, and simply use the term ‘drowning’ irrespective of the patient outcome. While this may seem pedantic, we do believe that it will assist with standardisation in drowning research and literature.
References
1. McDowell K, Carrick D, Weir R. Heart Published Online First: 18 may 2017. doi:10.1136/heartjnl-2016-311043.
Show More2. Idris AH, Berg RA, Bierens J, Bossaert L, Branche CM, Gabrielli A, Graves SA, Handley AJ, Hoelle R, Morley PT, Papa L, Pepe...
We read with interest the Editorial on the recently updated National Institute for Health and Care Excellence (NICE) guidance for the assessment of suspected stable angina (1). The authors raise some salient points regarding the importance of careful history taking, the vexed question of the exercise ECG and the relative merits of the myriad non-invasive tests for diagnosing coronary artery disease (CAD). However, we believe they have adopted an unnecessarily alarmist tone in their criticisms and feel obliged to respond to several issues.
Show MoreAlthough they suggest that the assessment of pretest probability (PTP) has been disregarded, this process has merely been made implicit rather than explicit. The guidelines emphasise the pivotal importance of the clinical history and, in the setting of suspected angina, the nature of the presenting symptoms is the dominant predictor of CAD. Existing risk tables (2) show that either typical or atypical angina essentially guarantees a PTP of CAD ≥ 10%, the threshold warranting further investigation in the earlier NICE guideline. The residual clinical risk seen in patients with non-anginal symptoms is best addressed through cardiovascular screening approaches with an emphasis of lifestyle modification and primary prevention.
Second, in arguing against the cost-effectiveness of the new approach, the authors imply that NICE are recommending “universal CTCA” which is incorrect. Non-anginal chest pain occurs in 40-60% of patients pre...
The article by Wouters and colleagues (1) presents an exhaustive overview on how QALYs can be used in cost-effectiveness analysis. In this framework, the authors also mention the incremental cost-effectiveness ratio (ICER), which is the parameter typically employed to express the results of a cost-effectiveness study. The article, however, does not discuss the net monetary benefit (NMB), which is another parameter employed to express the results of a cost-effectiveness study.
The incremental cost (deltaC) and the incremental effectiveness (deltaE) are the two main parameters of pharmacoeconomics and cost-effectiveness analysis, along with the willingness-to-pay threshold (lambda). The decision rule (e.g. in the case of a favourable pharmacoeconomic result) is (deltaC/deltaE)<lambda (Equation 1), if based on the ICER, or (deltaE x lambda - deltaC) > 0 (Equation 2), if based on the NMB. Likewise, an unfavourable pharmacoeconomic result is when (deltaC/deltaE)>lambda or when (deltaE x lambda - deltaC) < 0; NMB is defined as deltaE x lambda - deltaC, while ICER is defined as deltaC/deltaE.
Despite its apparent complexity, most part of pharmacoeconomic methodology is described by the two simple equations reported above (i.e. Equations 1 and 2), but whether the ICER or the NMB is the best parameter for the purposes of pharmacoeconomic decision-making remains on open question.
The study by Cowper et al evaluating new versus old oral antic...
Show MoreSawhney et al. reported that nurse-led, physician-directed moderate sedation during cardiac electrophysiology procedures is safe (1). All of the patients undergoing cardiac electrophysiological (EP) procedures and cardiac implantable electronic device (CIED) implantation during the last 12 years were moderately sedated. Since this study is a retrospective study, we could not comprehend why all patients were sedated despite the fact that routine sedation during all cardiac EP procedures and all CIED implantation is not recommended.
Show MoreMoreover, as mentioned in the article, sedation is a continuum and it is not always possible to predict how individual patients will respond. Therefore, a gradual increase of doses of the sedatives during sedation may be needed which may possibly increase the procedure duration. Did authors ascertain any prolongation of the procedures due to sedative administration?
Furthermore, sedation may diminish arrythmia induction during EP procedures, particularly in patients with catecholamine-sensitive ventricular tachycardias (2). Did authors have any data questioning this issue?
As a conclusion, the aim of sedation is to diminish the anxiety and to relieve the pain during the procedure. Therefore, using moderate sedation selectively in patients with anxiety or hyperalgesia may be more practical and rational rather than its routine use due to the fact that as mentioned in the article, researches and audit demonstrate continued avoidabl...
Pages