At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a
simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happenin...
At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a
simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happening from previous ischemia, from present reperfusion and from ischemia that is present in the micro-
vasculature despite reperfusion. There were multiple reference articles that were quoted which again use the term" reperfusion injury" (2-4) adding to the impression that reperfusion is the "only" culprit, which in-fact, is playing a “partial” role.
From the available experimental data, we totally agree that “reperfusion associated injury” is real and proven. As agreed by authors in their article, reperfusion is only a part of this problem (while, in fact, it is the solution to the problem of coronary ischemia). It helps to have a proper terminology for this complex phenomenon so that whole gamut of the problem is reflected in the terminology rather than a part. We strongly feel that a proper terminology makes a huge difference in proper understanding, especially when a complex phenomenon is involved.
“Myocardial ischemia and reperfusion injury” (5) may be one terminology close this phenomenon than “reperfusion injury”, as it implies that the injury is happening both from ischemia and reperfusion rather than reperfusion alone.
A most appropriate terminology, we feel, is “Reperfusion Micro-vascular Ischemia (RMI)”(6) as coined by Spears et al , which signifies that the injury is caused by ischemia, reperfusion and persistent micro-vascular dysfunction despite reperfusion, rather than “reperfusion injury” alone.
References:
1. Basso C, Thiene G The pathophysiology of myocardial reperfusion: a pathologist's perspective Heart (British Cardiac Society). Nov 2006;92(11):1559-1562
2. Ambrosio G, Tritto I Reperfusion injury: experimental evidence and clinical implications American heart journal. Aug 1999;138(2 Pt 2):S69-75
3. Kloner RA Does reperfusion injury exist in humans? Journal of the American College of Cardiology. Feb 1993;21(2):537-545
4. Maxwell SR, Lip GY Reperfusion injury: a review of the pathophysiology, clinical manifestations and therapeutic options International journal of cardiology. Jan 31 1997;58(2):95-117
6. Spears JR, Prcevski P, Xu R, Li L, Brereton G, DiCarli M, Spanta A, Crilly R, Lavine S, vander Heide R Aqueous oxygen attenuation of reperfusion microvascular ischemia in a canine model of myocardial infarction Asaio J. Nov-Dec 2003;49(6):716-720
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undul...
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undulating phenotype” of the cardiac abnormalities is a feature of LVHT, not exclusively found in children, but also in adults.[3]
With interest we recognized that the applied diagnostic criteria are a fruitful combination of Jenni’s and our criteria. Recently we proposed to classify LVHT cases fulfilling both criteria as “definite” and fulfilling
either criterion as “probable” LVHT.[4] How was “dilated”, “hypertrophic” and “combined” phenotype defined?
It is well known that TDI parameters and measurements are influenced by the type of the echocardiographic machine.[5] Did the authors observe different results when using different machines? Were interobserver variability studies performed regarding registration of the TDI signals?
Were there any correlations between heart rate or blood pressure and the parameters measured by TDI?
We miss information about the gender of the included patients, and results of the 2-D and M-mode echocardiographic measurements, like left ventricular wall thickness or enddiastolic diameter. Why were these
parameters not included in the calculation of the Cox model? It cannot be excluded that conventional 2-D and M-mode echocardiographic parameters are predictors for prognosis of equal emphasis as TDI parameters.
According to which protocol were the follow-up investigations performed?
How to explain the discrepancy of patient recruitment starting in January 1999 and the maximal follow-up duration of 132 months? How many thromboembolic events occurred during follow-up?
How to explain the threefold increased mortality in the presented cohort compared to the 5.3% mortality/year as observed in adults?[2]
In the two patients with dysmorphic features, which genetic syndrome was diagnosed? Did these two patients also present with skeletal muscle abnormalities? At least in adults, LVHT is frequently associated with neuromuscular disorders. How many of the included 56 patients were seen by a neurologist, and in how many was a neurological disorder detected?
Interestingly, in 4 patients LVHT affected the interventricular septum.
Septal LVHT is extremely rare, thus it would be of interest to have more information about these patients.
If the authors assume that TDI is influenced by LVHT, why did they choose movement of the basal parts of the ventricle for registration, where no LVHT is located, and not the midventricular or apical parts of the left
ventricle, where LVHT is usually located? Which explanation do the authors have for their observation of decreased velocities as assessed by TDI in LVHT? Did the velocities change in patients with undulating phenotype in
accordance with improvements in left ventricular systolic function?
In conclusion, before assessing TDI parameters as useful parameters to predict outcome of patients with LVHT, information about other echocardiographic findings and extracardiac comorbidities is necessary.
References
1. McMahon CJ, Pignatelli RH, Nagueh SF, Lee VV, Vaughn W, Valdes SO, Kovalchin JP, Jefferies JL, Dreyer WJ, Denfield SW, Clunie S, Towbin JA, Eidem BW Left ventricular noncompaction cardiomyopathy in children: Characterization of clinical status using tissue Doppler-derived indices of left ventricular diastolic relaxation Heart 2006 Nov 29;ePub
2. Stöllberger C, Winkler-Dworak M, Blazek G, Finsterer J Prognosis of left ventricular hypertrabeculation/noncompaction is dependent on cardiac
and neuromuscular comorbidity Int J Cardiol 2006; in press
3. Stöllberger C, Keller H, Finsterer J Disappearance of left ventricular hypertrabeculation/noncompaction after biventricular pacing in a patient with myopathy J Card Fail 2006; in press
4. Finsterer J, Stöllberger C Definite, probable , and possible left ventricular hypertrabeculation/noncompcation Int J Cardiol 2006; in press
5. Kjaergaard J, Korinek J, Belohlavek M, Oh JK, Sogaards Hassager C Accuracy, reproducibility, and comparability of Doppler tissue imaging by two high-end ultrasound systems J Am Soc Echocardiogr 2006;19:322-8
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction
(MI) patients (17 with major depressive disorder [MDD]) and reported that
two items from the Beck Depression Inventory (BDI) related to sadness and
loss of interest formed an effective screening tool for post-MI
depression. The sensitivity and specificity results reported by Huffman et
al. are, in fact, highly similar to those repo...
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction
(MI) patients (17 with major depressive disorder [MDD]) and reported that
two items from the Beck Depression Inventory (BDI) related to sadness and
loss of interest formed an effective screening tool for post-MI
depression. The sensitivity and specificity results reported by Huffman et
al. are, in fact, highly similar to those reported for two other existing
brief depression screens, the PHQ-2 [2], which was validated in a sample
of 580 primary care patients (41 with MDD), and a similar 2-item screen
[3], which was validated in a sample of 1,024 patients with coronary heart
disease (CHD) (224 with MDD). The validation study for the CHD screen
included a comparison to the PHQ-2 and found identical areas under the
curve (a measure of overall accuracy) of 0.84 for both instruments and
sensitivities and specificities that were very similar to those reported
by Huffman et al.when a cutoff of 1 or greater was used for each
instrument. Notably, these two screening tools and the screening tool
proposed by Huffman et al. each include slightly differently worded
versions of 2 items: an item about mood and an item about anhedonia, the
two core symptoms of a DSM-IV diagnosis of MDD.
Is it beneficial to continue to look for “new” and slightly different
versions of brief depression screening tools? The authors of a literature
synthesis of case-finding instruments for identifying depression in
primary care concluded that it is not [4]. They found 16 case-finding
instruments of 1-30 items that all had adequate performance
characteristics in primary care and found very few differences between
instruments (although there were significant differences within
instruments across studies) . In their words, “the search for a better
mousetrap has not led to an instrument with superior performance
characteristics.” Furthermore, the proliferation of new instruments with
no notable improvement in performance has the potential to create
confusion, but not better options, for clinicians and researchers.
While the search for “a better mousetrap” is not likely to add much
to the clinical care of MI patients, a simple mousetrap is clearly
desirable for use in acute cardiac care, since MI patients are generally
cared for by cardiovascular specialists whose focus is not on depression
and who often do not have the expertise to diagnose or treat this
condition. However, the question is not whether a few simple questions
can improve rates of recognition of depression in busy cardiac units.
Rather, it is whether cardiovascular specialists can and will use these
screening tools, and how they would perform in their hands under real life
conditions rather than when administered by psychiatrists as in the study
by Huffman, et al.1 In addition, research is needed that attends to
essential, but generally neglected, elements of the screening process,
such as when, where, and how often to screen patients; whether patient
characteristics, such as age, gender, and race, influence the accuracy of
depression screening in the post-MI setting; and, as noted by the authors,
whether serial screening with more than one instrument improves efficiency
and accuracy.
REFERENCES
1. Huffman JC, Smith FA, Blais MA, Beiser ME, Januzzi JL, Fricchione GL. Rapid screening for major depression in post-myocardial infarction patients: an investigation using Beck Depression Inventory II items. Heart 2006;92:1656-60.
2. Kroenke K, Spitzer RL, Williams JB. The Patient Health Questionnaire-2: validity of a two-item depression screener. Med Care 2003;41:1284-92.
3. McManus D, Pipkin SS, Whooley MA. Screening for depression in patients with coronary heart disease (data from the Heart and Soul Study). Am J Cardiol 2005;96:1076-81.
4. Williams JW,Jr, Pignone M, Ramirez G, Perez Stellato C. Identifying depression in primary care: a literature synthesis of case-finding instruments. Gen Hosp Psychiatry 2002;24:225-37.
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral
amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countl...
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral
amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countless times; what proportion of cases result in extravasation injury?
Central line access has many potential complications /
contraindications (e.g. post thrombolysis). If the patient is on ITU and has a central line - great - otherwise the delay and risk involved in inexperienced juniors obtaining central access appear to me to outweigh the tiny risk of extravasation injury; providing the amiodarone is given
through a fresh antecubital fossa venflon.
This Heart article has also been featured in the BMJ and it appears to be a case of a blanket guideline being made on anecdotal evidence.
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by
inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large perip...
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by
inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large peripheral vein.
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone...
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone PCI centres or to create more surgery programs for the sole purpose of supporting PCI. The article of J.
Carlsson et al. (1) from Sweden in this journal supports the first option.
The publication of K. Burton et al. (2) in this journal, which showed that there is no difference in death and myocardial infarction between low and high volume PCI centres in Scotland, is also very interesting in this respect.
However we would like to get some more information on this subject.
On the basis of these data we cannot deduce how safe it was to perform PCI in hospitals without on-site cardiac surgery. In the discussion of the article on page 1671 is mentioned: “Low-volume hospitals are less likely to have on-site surgical facilities.” However no information about this item is given in the methods or/and the results.
All of the 17 417 procedures were performed in six hospitals during 36 hospital years. If possible, we would like to know how many of these six hospitals had cardiac surgery on-site. Further more we can imagine that the use of surgery on-site will have changed over the years; this is why we want to know how many procedures were performed without surgical backup on-site. Finally was there a difference in major complications between hospitals with and without surgical backup on-site?
These data can be of great interest for the ongoing debate whether or not on-site cardiac surgical backup is still necessary for PCI. From a health care point of view, access to the best therapy for the greatest numbers of patients is an important goal. There is no doubt that, on the field, PCI has proven to be the best therapy in ST-elevation myocardial infarction (3, 4). Legitimating of hospitals to perform PCIs without cardiac surgery on-site, will improve access and could thereby lower mortality. Recommendations on this topic are given in literature by
experts working in Europe as well in North America (5, 6). It is in the best interest of our patients and the society, to stop the discussion between the haves and the have nots and to stop recommending against PCI in hospitals without surgical backup on-site.
References
1. Carlsson J, James SN, Stahle E, et al. Outcome of percutaneous coronary intervention in hospitals with and without on-site cardiac surgery standby. Heart published online first 15 September 2006.
2. Burton KR, Slack R, Oldroyd KG, et al. Hospital volume of throughput and periprocedural and medium-term adverse events after percutaneous coronary intervention: retrospective cohort study of all 17 417 procedures undertaken in Scotland, 1997-2003. Heart 2006; 92: 1667-1672.
3. Stenestrand U, Lindbäck J, Wallentin L. Long-term outcome of primary percutaneous coronary intervention vs. prehospital and in-hospital thrombolysis for patients with ST-elevation myocardial infarction. JAMA 2006; 296: 1749-1756.
4. Clemmensen P, Jurlander B. Primary PCI for ST elevation AMI saves lives and money-what more do we want? Editorial. Scand Cardiovasc J 2005; 39: 264-266.
5. Montalescot G, Anderson HR, Antoniucci D, et al. Summary of recommendations on percutaneous coronary intervention for the reperfusion of acute ST elevation myocardial infarction. Heart 2004; 90: 676-677.
6. Ting HT, Raveendram G, Lennon RJ, et al. A total of 1,007 percutaneous coronary interventions without onsite cardiac surgery. Acute and long term outcomes. J Am Coll Cardiol 2006; 47: 1713-21.
Conflict of interest/financial disclosure: There are no conflicts of interest and no financial disclosures.
Antoon. E. Weyne M.D., F.A.C.C.(1), Johan F. Vandenbogaerde M.D.(1), Philippe G. Dejaegher M.D.(1), Robert Van den Oever M.D.(2)
(1) Department of Cardiology, AZ Groeninge, Kortrijk, Belgium
(2) Director Health Policy, LCM, Brussels
Amiodarone is frequently used in the intensive care units. Very often
it is used to treat atrial fibrillation in septic patients. As Russel and
Saltissi mentioned in the case report we also give first a bolus of
amiodarone followed by an maintainance infusion over 23 hours.
It is advised in the BNF that amiodaorne has to be given through the
central line. In the intensive Care Unit we follow this stri...
Amiodarone is frequently used in the intensive care units. Very often
it is used to treat atrial fibrillation in septic patients. As Russel and
Saltissi mentioned in the case report we also give first a bolus of
amiodarone followed by an maintainance infusion over 23 hours.
It is advised in the BNF that amiodaorne has to be given through the
central line. In the intensive Care Unit we follow this strictly
especially if a maintenance infusion has to be started. As a consequence
there are incidences where central line is inserted only to start
amiodarone infusion.
We read with interest the recent article published by Iliodromitis et. al.(1), but do not agree with the conclusions drawn by the authors.
The study appears to be under-powered to draw meaningful conclusions as to the therapeutic value of remote ischaemic preconditioning, and certainly the size of the study precludes a subgroup analysis of the role of statins. The authors do not state the actual number...
We read with interest the recent article published by Iliodromitis et. al.(1), but do not agree with the conclusions drawn by the authors.
The study appears to be under-powered to draw meaningful conclusions as to the therapeutic value of remote ischaemic preconditioning, and certainly the size of the study precludes a subgroup analysis of the role of statins. The authors do not state the actual number of patients that had
troponin release or the individual values of troponin in the patients studied. It is possible that a single, large troponin value in the remote ischaemic preconditioning group may have skewed the results.
It is recognised that troponin can be detected in approximately one third of patients following percutaneous intervention (2,3). Selvanayagam et. al (2). have demonstrated by cardiac MR, that troponin release reflects either a down stream microembolisation injury or side branch occlusion at the site of stent implantation. Troponin release correlated with stent length. The published study by Iliodromitis et. al. implanted short stents to treat simple, single vessel disease. They excluded lesions with side branch involvement and therefore it is surmised that the injury in these study patients would only be micro-embolic. It could be inferred that the incidence of troponin release in this study should be a
lot lower than a third of the patients. In addition, failure to demonstrate protection by remote ischaemic preconditioning could be explained by the inclusion of a large proportion of patients with diabetes, a group where ischaemic preconditioning is thought to be less effective (4). There was also a high incidence of nitrate use in the
control arm which has been shown to have preconditioning-mimetic properties (5).
In such a small study, the incidence of a type II error must be high.
It may be that remote ischaemic preconditioning does not protect from the microembolic injury that occurs during stenting, as the authors conclude.
Preconditioning is thought to only be protective if there is reperfusion (6) and the microembolic injury may not be a an ischaemia-reperfusion injury. However, this small study cannot draw this conclusion, and an appropriately powered study is required.
References
1. Iliodromitis EK, Kyrzopoulos S, Paraskevaidis IA, et al.
Increased C- reactive protein and cardiac enzyme levels after coronary stent implantation. Is there protection by remote ischemic preconditioning? Heart 2006.
2. Selvanayagam JB, Porto I, Channon K, et al.
Troponin elevation after percutaneous coronary intervention directly represents the extent of irreversible myocardial injury: insights from cardiovascular magnetic resonance imaging. Circulation 2005;111(8):1027-32.
3. Harris BM, Nageh T, Marsden JT, Thomas MR, Sherwood RA.
Comparison of cardiac troponin T and I and CK-MB for the detection of minor myocardial damage during interventional cardiac procedures. Ann Clin Biochem 2000;37 (Pt 6):764-9.
4. Ishihara M, Inoue I, Kawagoe T, et al.
Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction. J Am Coll Cardiol 2001;38(4):1007-11.
5. Leesar MA, Stoddard MF, Dawn B, Jasti VG, Masden R, Bolli R.
Delayed preconditioning-mimetic action of nitroglycerin in patients undergoing coronary angioplasty. Circulation 2001;103(24):2935-41.
6. Murry CE, Jennings RB, Reimer KA.
Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986;74(5):1124-36.
We read with interest the recent editorial by Siotia and Gunn [1] which emphasised the need and growing enthusiasm for risk scoring for percutaneous coronary intervention (PCI). This editorial focuses on the recent publication by Wu and colleagues from New York of a risk model to predict in-hospital mortality following PCI [2]. This particular risk model was based on 46,090 patients undergoing PCI between 2...
We read with interest the recent editorial by Siotia and Gunn [1] which emphasised the need and growing enthusiasm for risk scoring for percutaneous coronary intervention (PCI). This editorial focuses on the recent publication by Wu and colleagues from New York of a risk model to predict in-hospital mortality following PCI [2]. This particular risk model was based on 46,090 patients undergoing PCI between 2002 and 2003, and is clearly the largest study of its kind. However, it only examines in-hospital mortality as an outcome and does not include other important
complications following PCI, such as Q-wave myocardial infarction (MI), emergency coronary artery bypass graft (CABG) surgery, and cerebrovascular accidents.
We have recently published a risk model for PCI which was based on 9,914 patients undergoing PCI between 2002 and 2003 using registry data from the North West Quality Improvement Programme (NWQIP) [3]. Although the NWQIP model was based on a sample size one quarter of that available
in the New York model, it examined outcomes of in-hospital mortality, Q-wave MI, emergency CABG, and cerebrovascular accidents.
We share Siotia and Gunn's enthusiasm to establish risk scoring in PCI and hope that in 2007 this will be possible for all interventional cardiologists. As with all risk models, the NWQIP model will have limitations and more work will be required to examine its applicability in other health care systems and with continuing changes in PCI practice.
However, what the NWQIP model does offer is a contemporary risk model for PCI in a UK setting, which uses variables which are part of the minimum dataset for the British Cardiovascular Interventional Society, which is currently submitted to the Central Cardiac Audit Database (CCAD) [4].
Currently the NWQIP model is being validated to see how applicable it might be to other hospitals outside of the north west of England; preliminary results look good. Recent analyses using PCI data available on the CCAD database showed promising preliminary results (David Cunningham, personal communication); the NWQIP algorithm appears to be predictive for all MACE occurrences within 30 days, although more detailed analysis will be required to confirm these early findings.
The intervention unit at the Royal Bournemouth Hospital recently assessed their first 1013 cases and concluded that the NWQIP model was a powerful tool to assess interventional performance. Dr Witherow concludes
that the NWQIP model provides an up to date, simple, practical scoring system and should be used to its full potential by as many centres as possible [5].
Competing interests: ADG, MJ, and RHS are all members of NWQIP and were involved in developing the NWQIP risk model for PCI.
References
[1] Siotia A, Gunn J
Risk scoring for percutaneous coronary intervention: let's do it! Heart 2006;92(11):1539-40
[2] Wu C, Hannan EL, Walford G, Ambrose JA, Holmes DR Jr, King SB 3rd, Clark LT, Katz S, Sharma S, Jones RH
A risk score to predict in-hospital mortality for percutaneous coronary interventions. J Am Coll Cardiol 2006;47(3):654-60
[3] Grayson AD, Moore RK, Jackson M, Rathore S, Sastry S, Gray TP, Schofield I, Chauhan A, Ordoubadi FF, Prendergast B, Stables RH
North West Quality Improvement Programme in Cardiac Interventions. Multivariate prediction of major adverse cardiac events after 9914 percutaneous coronary interventions in the north west of England. Heart 2006;92(5):658-63
[4] Central Cardiac Audit Database. Coronary heart disease audit supported by the Central Cardiac Audit Database. www.ccad.org.uk (accessed 19 Oct 2006)
[5] Witherow FN
What is 'high risk' PCI? Heart Online, 1 Sep 2006 (eLetters: Heart 2006;92(5):658-63)
We note Dorman et al's comments regarding our paper (1). We agree that risk scores should not be used in isolation to determine either the management or triage of patients. Although, in our study, no patient with a
score of 0 experienced a major cardiac event within thirty days, the confidence interval includes a rate of up to 1.5%. A recent prospective evaluation of the TIMI score used in a simila...
We note Dorman et al's comments regarding our paper (1). We agree that risk scores should not be used in isolation to determine either the management or triage of patients. Although, in our study, no patient with a
score of 0 experienced a major cardiac event within thirty days, the confidence interval includes a rate of up to 1.5%. A recent prospective evaluation of the TIMI score used in a similar population demonstrated a 1.7% event rate in the 0 score group (2). Low risk clearly does not equate to no risk.
This is the reason that we suggested the TIMI score, and its ‘front door’ modification be used to inform triage decisions, not make them. Equally, we would not advocate immediate discharge on the basis of the score but rather
appropriate further investigation such as early cardiac marker determination, chest pain unit observation or provocative testing. As with all tools, they are only useful as an adjunct to clinical judgement and are no substitute for review by a doctor.
At present Emergency Department inappropriate discharge rate ranges from 6-16% (3), and we believe that use of risk stratification tools may reduce this by helping identifying those at higher risk whilst not leading to high
rates of admission for low risk patients.
References
1. Conway Morris A, Caesar D, Gray S and Gray A.
TIMI risk score accurately risk stratifies patients with undifferentiated chest pain presenting to an emergency department. Heart 2006;92:1333-1334
2. Chase M. Robey JL. Zogby KE. Sease KL et al. Prospective validation of the Thrombolysis in Myocardial Infarction Risk Score in the emergency department chest pain population. Ann Emerg Med 2006. 48(3):252-9
3. Goodacre SW, Nicholl J, Dixon S, et al.
Randomised controlled trial and economic evaluation of a chest pain observation unit compared with routine care. BMJ 2004;328:254–9.
Dear Editor,
At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happenin...
Dear Editor,
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undul...
Dear Editor,
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction (MI) patients (17 with major depressive disorder [MDD]) and reported that two items from the Beck Depression Inventory (BDI) related to sadness and loss of interest formed an effective screening tool for post-MI depression. The sensitivity and specificity results reported by Huffman et al. are, in fact, highly similar to those repo...
Dear Editor,
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countl...
Dear Editor,
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large perip...
Dear Editor,
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone...
Dear Editor,
Amiodarone is frequently used in the intensive care units. Very often it is used to treat atrial fibrillation in septic patients. As Russel and Saltissi mentioned in the case report we also give first a bolus of amiodarone followed by an maintainance infusion over 23 hours. It is advised in the BNF that amiodaorne has to be given through the central line. In the intensive Care Unit we follow this stri...
Dear Editor,
We read with interest the recent article published by Iliodromitis et. al.(1), but do not agree with the conclusions drawn by the authors. The study appears to be under-powered to draw meaningful conclusions as to the therapeutic value of remote ischaemic preconditioning, and certainly the size of the study precludes a subgroup analysis of the role of statins. The authors do not state the actual number...
Dear Editor,
We read with interest the recent editorial by Siotia and Gunn [1] which emphasised the need and growing enthusiasm for risk scoring for percutaneous coronary intervention (PCI). This editorial focuses on the recent publication by Wu and colleagues from New York of a risk model to predict in-hospital mortality following PCI [2]. This particular risk model was based on 46,090 patients undergoing PCI between 2...
Dear Editor,
We note Dorman et al's comments regarding our paper (1). We agree that risk scores should not be used in isolation to determine either the management or triage of patients. Although, in our study, no patient with a score of 0 experienced a major cardiac event within thirty days, the confidence interval includes a rate of up to 1.5%. A recent prospective evaluation of the TIMI score used in a simila...
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