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.
I commend Azevedo and colleagues(1) for testing the ACC/AHA stages of heart failure.(2) Although these stages are theoretically appealing, they are challenging to use in practice. I am, however, concerned about the criteria used to differentiate asymptomatic and symptomatic structural
abnormalities. The authors use a narrow definition of heart failure symptoms: shortness of breath and edema. Many heart...
I commend Azevedo and colleagues(1) for testing the ACC/AHA stages of heart failure.(2) Although these stages are theoretically appealing, they are challenging to use in practice. I am, however, concerned about the criteria used to differentiate asymptomatic and symptomatic structural
abnormalities. The authors use a narrow definition of heart failure symptoms: shortness of breath and edema. Many heart failure patients do not experience these hallmark signs, but suffer instead from unexplained fatigue, exercise intolerance, early satiety, or confusion. I also question the authors’ use of the Rotterdam study approach(3) to classifying heart failure, which requires the presence of at least two signs and/or symptoms. I am left wondering if it is appropriate to label a person as having Stage B heart failure if in fact s/he has symptoms other than shortness of breath and edema or a single symptom. Heart failure patients are known to have poor symptom recognition ability.(4) In particular, they may minimize or deny subtle signs and symptoms,(5) fail to recognize non-specific and progressive symptoms,(6) or fail to connect symptoms with a
disease process.(7) The strict definition of “symptomatic” used by these investigators may grossly underestimate the number of Stage C heart failure patients. As it stands, this important population study has identified an alarmingly large cohort of persons with heart failure. I
fear the proportion of Stage C heart failure may be even greater than that found by these investigators.
The definitional nuances of the boundaries between Stage B heart failure and Stage C heart failure is a challenge faced by everyone seeking to identify Stage B heart failure patients. Can researchers exclude subjects from Stage C just because the symptoms they experience are not the hallmark signs? To what extent must we inquire about previous and current symptoms to improve the probability that we have appropriately labeled a subject as having Stage B or C heart failure? I believe that the
essence of what separates stage B and C heart failure patients is symptom naivety. Thus, the assessment of symptoms must be inclusive and precise.
Regarding this matter, the scientific letter by Azevedo et al. was neither.
Respectfully,
Christopher S. Lee, RN, MSN, CCRN
University of Pennsylvania Predoctoral Fellow
University of Pennsylvania School of Nursing
Philadelphia, Pennsylvania
United States of America
References
1. Azevedo A, Bettencourt P, Dias P, Abreu-Lima C, Hense HW, Barros H.
Population based study on the prevalence of the stages of heart
failure.
Heart 2006;92:1161-3.
2. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG,
Jessup M, Konstam MA, Mancini DM, Michl K, Oates JA, Rahko PS, Silver MA,
Stevenson LW, Yancy CW, Antman EM, Smith SC, Jr., Adams CD, Anderson JL,
Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Jacobs AK, Nishimura R,
Ornato JP, Page RL, Riegel B.
ACC/AHA 2005 Guideline Update for the
Diagnosis and Management of Chronic Heart Failure in the Adult: a report
of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Writing Committee to Update the 2001
Guidelines for the Evaluation and Management of Heart Failure): developed
in collaboration with the American College of Chest Physicians and the
International Society for Heart and Lung Transplantation: endorsed by the
Heart Rhythm Society.
Circulation 2005;112:e154-235.
3. Mosterd A, Hoes AW, de Bruyne MC, Deckers JW, Linker DT, Hofman A,
Grobbee DE.
Prevalence of heart failure and left ventricular dysfunction
in the general population; The Rotterdam Study.
Eur Heart J 1999;20:447-55.
4. Jurgens CY.
Somatic awareness, uncertainty, and delay in care-
seeking in acute heart failure.
Res Nurs Health 2006;29:74-86.
5. Goldberg LR, Jessup M.
Stage B heart failure: management of
asymptomatic left ventricular systolic dysfunction. Circulation 2006;113:2851-60.
6. Jurgens CY, Fain JA, Riegel B.
Psychometric Testing of the Heart
Failure Somatic Awareness Scale.
J Cardiovasc Nurs 2006;21:95-102.
7. Horowitz CR, Rein SB, Leventhal H.
A story of maladies,
misconceptions and mishaps: effective management of heart failure.
Soc Sci Med 2004;58:631-43.
We read with interest the article by Conway Morris et al.(1) on the utility of the ‘front door’ TIMI risk score. The authors suggest that the TIMI score may be used to risk stratify patients with undifferentiated chest pain presenting to the emergency department and further state that patients with low scores (0 or 1) are at low risk of further cardiac events. Whilst the TACTICS-TIMI 18 investigators sugg...
We read with interest the article by Conway Morris et al.(1) on the utility of the ‘front door’ TIMI risk score. The authors suggest that the TIMI score may be used to risk stratify patients with undifferentiated chest pain presenting to the emergency department and further state that patients with low scores (0 or 1) are at low risk of further cardiac events. Whilst the TACTICS-TIMI 18 investigators suggested that patients with low TIMI risk score (0-2) could be safely managed without course to
immediate invasive investigation(2), the authors’ interpretation is in conflict with their own data and other published data(3). In their study, 137 patients experienced a major cardiac event within 30 days, and nearly a quarter (n=30: 22%) of these patients had a front door TIMI risk score of only 0 or 1, classifying them as low risk. Our own data on patient’s presenting with acute coronary syndrome showed that even the lowest risk cases with a negative troponin and a TIMI score of less than or equal to three had significant obstructive coronary artery disease and underwent revascularisation in 38% of cases.(3)
These findings highlight the false reassurance that can be taken if scoring systems are used in isolation from traditional clinical judgement.
For instance, an obese 60 year old male diabetic with lifelong smoking history but no other conventional risk factors, presenting with classical crescendo angina associated with dynamic biphasic anterior ECG changes
will have a front door TIMI score of 1 before troponin levels are measured. Using a TIMI risk stratification model, it may be falsely concluded that this man is at low risk of serious major cardiac events; more worryingly, the patient may even be discharged without recourse to further investigation or follow-up if the initial troponin measurement is normal.
Whilst the TIMI risk score has a well-defined role in the stratification of patients with non-ST segment elevation myocardial infarction (for which purpose it was derived and designed), there is a need to place it firmly in the context of a carefully-taken history that critically assesses the nature of the chest pain as well as an individual patient’s predisposing ischaemic risk factors.
Yours sincerely,
Dorman SH, Johnson TW, West NEJ
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. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med. 2001; 344: 1879–1887
3. Johnson TW, Dorman SH, West NEJ.
Conventional bedside methods of risk stratification in acute coronary syndromes do not predict need for revascularization in a ‘real-world’ population. Eur Heart Journal (2006) 27 (abstract supplement), p.672
We read with great interest the article by Nayar et al (1) on the concept of increased myxomatous tissue of the mitral valve serving as nidus for development of rheumatic heart disease. In developing countries, the morbidity and mortality related to rheumatic heart disease continues
unabated. At our institution, we perform a large number of autopsies and many have rheumatic heart disease.(2)...
We read with great interest the article by Nayar et al (1) on the concept of increased myxomatous tissue of the mitral valve serving as nidus for development of rheumatic heart disease. In developing countries, the morbidity and mortality related to rheumatic heart disease continues
unabated. At our institution, we perform a large number of autopsies and many have rheumatic heart disease.(2) Besides, we also receive a large number of rheumatic mitral and/or aortic valvectomies. We disagree with the authors on two issues. Firstly, we strongly feel that the absence or
presence of increased ground substance or ‘myxomatous tissue’ is largely related to the degree of valvar incompetence. We have observed that valvar incompetence induces accumulation of ground substance, the quantity of
which is directly proportional to the degree of regurgitation. The authors have not cor-related the amount of myxoid tissue with the type of dysfunction i.e. pure stenosis, stenosis with regurgitation or pure
regurgitation. Secondly, if anti-streptococcal antibodies were supposed to cross-react with the hyaluronic acid in the valves, then the immune complexes should elicit an inflammatory reaction, which should be followed by reactive fibrosis. Hence the ground substance should decrease and not increase.
References
1. Heart valve structure: a predisposing factor for rheumatic heart disease.
Nayar S, Nayar PG, Cherian KM Heart 2006; 91: 1151 e2
2. Rheumatic heart disease in the past decade: an autopsy analysis.
Deshpande J, Vaideeswar P, Amonkar G, Vasandani S Indian Heart J 2002; 54: 676-80
We were pleased to read the innovative and compelling work by Dr. Agnoletti and colleagues [1]. The authors have eloquently (via surgical procedures) revealed the importance of right-to-left shunting (through an
inter-atrial communication) on arterial oxyhemoglobin saturation during resting and exercise conditions. They have also provided convincing evidence of the detrimental effects of an inter-atrial s...
We were pleased to read the innovative and compelling work by Dr. Agnoletti and colleagues [1]. The authors have eloquently (via surgical procedures) revealed the importance of right-to-left shunting (through an
inter-atrial communication) on arterial oxyhemoglobin saturation during resting and exercise conditions. They have also provided convincing evidence of the detrimental effects of an inter-atrial septal defect on exercise capacity. We would also like to acknowledge that a significant proportion (50-70%) of highly trained athletes exhibit desaturation (i.e.,exercise-induced arterial hypoxemia (EIAH)) during exercise conditions [2,3]. In some instances, this desaturation occurs quite early into exercise reaching levels similar to that observed by Dr. Agnoletti et al. In our work [4] and that of others [5] approximately 10-15% of highly trained athletes (who are screened via echocardiography) are diagnosed a patent
foramen ovale. It is likely that a patent foramen ovale, which is present in 10-25% of the general population, often goes undiagnosed in highly trained endurance athletes. We propose that the presence of inter-atrial septal defects may explain (in part) the marked and early desaturation
observed in some highly trained athletes. It is also clear (as supported by the present work of Dr. Agnoletti et al.) that the presence of an inter-atrial communication and significant right-to-left shunting can have marked effects on exercise tolerance and capacity (in sedentary and highly
trained individuals).
We also support Dr. Agnoletti and colleagues’ statements regarding the importance of standard exercise testing for the identification of patients who can benefit from the closure of an inter-atrial communication. We respectfully would also like to extend these findings to
the screening of significant inter-atrial communications. We believe that an incremental exercise test with the concurrent monitoring of arterial oxyhemoglobin saturation may be a valuable and relatively inexpensive methodology for the screening of significant inter-atrial communication in asymptomatic and symptomatic populations. This appears to be particularly salient for individuals that exhibit early (e.g., less than 50% of maximum) and severe (e.g. ≤88%) reductions in arterial oxyhemoglobin saturation during incremental exercise.
In summary, we congratulate the authors for their detailed evaluation of the effects of inter-atrial septal defects on arterial oxyhemoglobin saturation and exercise capacity. This work provides a glimpse into a potential mechanism responsible (in part) for the early and marked EIAH observed in a subset of highly trained individuals.
References
1 Agnoletti G, Boudjemline Y, Ou P, et al. Right to left shunt through interatrial septal defects in patients with congenital heart disease: results of interventional closure. Heart 2006;92:827-31.
2 Richards JC, McKenzie DC, Warburton DE, et al. Prevalence of exercise-induced arterial hypoxemia in healthy women. Med Sci Sports Exerc 2004;36:1514-21.
4 Esch BTA, Scott JM, Haykowsky MJ, et al. Diastolic ventricular interactions in endurance athletes during lower body positive and negative pressure. Med Sci Sports Exerc 2006;38:s18.
5 Stickland MK, Welsh RC, Haykowsky MJ, et al. Intra-pulmonary shunt and pulmonary gas exchange during exercise in humans. J Physiol 2004;561:321-9.
Given the fact that patients with subnormal left ventricular ejection fractions frequently have co-existing diastolic dysfunction(1)the therapeutic benefits resulting from blockade of the renin-angiotensin-aldosterone system(RAAS)in studies enrolling heart failure(HF) patients
with subnormal left ventricular ejection fraction(LVEF)(2)(3)might, arguably, be attributable, at least in part, to amelioration of...
Given the fact that patients with subnormal left ventricular ejection fractions frequently have co-existing diastolic dysfunction(1)the therapeutic benefits resulting from blockade of the renin-angiotensin-aldosterone system(RAAS)in studies enrolling heart failure(HF) patients
with subnormal left ventricular ejection fraction(LVEF)(2)(3)might, arguably, be attributable, at least in part, to amelioration of diastolic dysfunction. This would account for the fact that RAAS blockade continues to be beneficial even in the presence of intact sytolic function regardless of whether "stand alone" diastolic dysfunction gives rise to clinically overt HF(4)(5) or whether "stand alone" diastolic dysfunction is associated only with a limitation in treadmill exercise time(6).
Accordingly, the therapeutic nihilism currently associated with the management of diastolic dysfunction should be replaced by the assumption that the therapeutic benefits of RAAS blockade are applicable across the entire spectrum of left ventricular ejection fractions.
References
(1) Abhayaratna WP., Marwick TH., Smith WT., Becker NG
Characteristics of left ventricular diastolic dysfunction in the community: an echocardiographic survey
Heart 2006:92:1259-64
(2) The SOLVD Investigators Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure
New England Journal of Medicine 1991:325:293-302
(3) Pitt B., Zannad F., Remme WJ., et al
The effect of spironolactone on morbidity and mortality in patients with severe heart failure
New England Journal of Medicine 1999:341:709-17
(4)Yusuf S., Pfeffer MA., Swedberg K., et al
Effects of candesartan in patients with chronic heart failure and preserved left ventricular ejection fraction: teh CHARM-Preserved Trial
Lancet 2003:362:777-81
(5) Sueta CA., Russo A., Schenck A., Brown DW., Simpson RJ
Effect of angiotensin-converting inhibitor or angiotensin receptor blocker on one-year survival in patients >_ 65 years hospitalised with a left ventricular ejection fraction >_ 50%
American Journal of Cardilogy 2003:91:363-5
(6)Little WC., Zile MR., Klein A., et al
Effect of losartan and hydrochlorothiazide on exercise tolerance in exertional hypertension and left ventricular diastolic function
American Journal of Cardiology 2006:98:383-5
In the April edition of Heart, the North West Quality Improvement Programme (NWQIP) produced a multivariate prediction model to assess the risk of major adverse cardiac events (MACE) in patients undergoing percutaneous coronary revascularisation.(1) The risk score was based on
the outcomes of 9914 patients undergoing PCI in the four PCI centres in the northwest of England. From the data, a formula was pro...
In the April edition of Heart, the North West Quality Improvement Programme (NWQIP) produced a multivariate prediction model to assess the risk of major adverse cardiac events (MACE) in patients undergoing percutaneous coronary revascularisation.(1) The risk score was based on
the outcomes of 9914 patients undergoing PCI in the four PCI centres in the northwest of England. From the data, a formula was produced that could be used to calculate the risk of MACE in a set of patients undergoing PCI using seven variables, namely age, female sex, cerebrovascular disease, cardiogenic shock, priority, left main stem lesion and vein graft lesion.
It follows that any centre can use this scoring system and produce a meaningful risk adjusted comparison of MACE to the four centres of the NWQIP.
The intervention unit at the Royal Bournemouth Hospital was opened in April 2005 and performed over 1000 PCI’s in the first year. As a district general cardiac centre without surgical cover on site it was important to
assess the performance of the unit in a manner that allowed for casemix, and this multivariate prediction model provides the ideal tool. To assess the odds of MACE in our patient group we used the multivariate prediction
model to risk assess each patient and then took the percentage mean and standard error to derive an overall risk of MACE in our first 1013 cases.
The average risk of MACE in these cases was 1.6 ± 0.1% which suggests that our unit is performing cases of higher risk than performed in the original paper. This is compared to an actual MACE rate of 0.4% (3 deaths, 1 Q-wave
MI, 0 CVA’s and 0 emergency CABG referrals) which also suggests our complication rate is far better than expected. These results are very reassuring and proves that ‘high risk’ complex PCI can be performed in centres with ‘off-site’ surgical cover with excellent results and shows that “guidelines to assist in appropriate patient selection” (2) are unnecessary provided experienced operators are delivering the service.
This is an incredibly powerful tool to assess interventional performance between units but raises several questions. How should the results be interpreted? If the actual MACE rate in a centre is significantly higher than the risk of MACE then what should be done? The
performance of that unit cannot be blamed on taking on higher risk patients, as the model is risk adjusted. It is likely that any unit with ‘complication overperformance’ should invest in a period of internal audit and reflection perhaps reviewing the cases that resulted in each adverse event. This process may highlight deficiencies in process or operator that may be easily rectifiable. It should be noted that units performing smaller numbers of angioplasty procedures would be more vulnerable to having actual MACE rates that are higher than the MACE risk due to the
generally low MACE event rate for angioplasty. Also centres that generally perform ‘low risk’ PCI e.g. elective cases only, will be vulnerable to disparity between actual MACE and MACE risk due to low MACE events in ‘low risk’ PCI. This will also apply to individual operators whom the authors note will probably not be performing enough procedures to accurately compare MACE risk and true MACE.
One reason our results compare favourably to the PCI centres in the original paper may relate to the fact that our service is consultant based, so the consultant rather than a trainee performs a higher percentage of the PCI’s. Although there were two consultants retraining at our centre during this period of analysis, 66% of cases were performed by a highly trained consultant interventional cardiologist. All consultants involved in PCI training must absorb, into their outcomes, the complications related to the learning curve of their current trainee, so in a centre with a large number of trainees there is naturally going to be an increase in MACE.
In their recent review of risk scoring systems Siota et al, concluded that there was “ a need for an up to date, simple, practical scoring system”.(3) This multivariate prediction model provides just that and
should be used to its full potential by as many centres as possible. As far as we are aware we are the first centre outside the NWQIP to publish our results based on their risk-scoring system.
There is no conflict of interest to declare.
References
1. Grayson AD, Moore RK, Jackson M et al. Multivariate prediction of major adverse cardiac events after 9914 percutaneous coronary interventions in the north west of England. Heart. 2006;92:658-63.
2. Siotia A, Gunn J. Risk scoring for PCI: let's do it! Heart. 2006 Apr 18; [Epub ahead of print]
3. Siota A, Hancock P, Gunn J. Estimating the risk of percutaneous coronary intervention. Br J Cardiol (Acute Interv Cardiol) 2006;13:AIC 39-AIC 45
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...
Dear Editor,
I commend Azevedo and colleagues(1) for testing the ACC/AHA stages of heart failure.(2) Although these stages are theoretically appealing, they are challenging to use in practice. I am, however, concerned about the criteria used to differentiate asymptomatic and symptomatic structural abnormalities. The authors use a narrow definition of heart failure symptoms: shortness of breath and edema. Many heart...
Dear Editor,
We read with interest the article by Conway Morris et al.(1) on the utility of the ‘front door’ TIMI risk score. The authors suggest that the TIMI score may be used to risk stratify patients with undifferentiated chest pain presenting to the emergency department and further state that patients with low scores (0 or 1) are at low risk of further cardiac events. Whilst the TACTICS-TIMI 18 investigators sugg...
Dear Editor,
We read with great interest the article by Nayar et al (1) on the concept of increased myxomatous tissue of the mitral valve serving as nidus for development of rheumatic heart disease. In developing countries, the morbidity and mortality related to rheumatic heart disease continues unabated. At our institution, we perform a large number of autopsies and many have rheumatic heart disease.(2)...
Dear Editor,
We were pleased to read the innovative and compelling work by Dr. Agnoletti and colleagues [1]. The authors have eloquently (via surgical procedures) revealed the importance of right-to-left shunting (through an inter-atrial communication) on arterial oxyhemoglobin saturation during resting and exercise conditions. They have also provided convincing evidence of the detrimental effects of an inter-atrial s...
Dear Editor,
Given the fact that patients with subnormal left ventricular ejection fractions frequently have co-existing diastolic dysfunction(1)the therapeutic benefits resulting from blockade of the renin-angiotensin-aldosterone system(RAAS)in studies enrolling heart failure(HF) patients with subnormal left ventricular ejection fraction(LVEF)(2)(3)might, arguably, be attributable, at least in part, to amelioration of...
Dear Editor,
In the April edition of Heart, the North West Quality Improvement Programme (NWQIP) produced a multivariate prediction model to assess the risk of major adverse cardiac events (MACE) in patients undergoing percutaneous coronary revascularisation.(1) The risk score was based on the outcomes of 9914 patients undergoing PCI in the four PCI centres in the northwest of England. From the data, a formula was pro...
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