Sir, in their elegant evaluation of primary angioplasty vs
thrombolysis cost-effectiveness,
Wailoo and Coll. conclude that primary angioplasty-based care is highly
likely to be costeffective,
particularly if patients are admitted directly to the cardiac catheter
laboratory 1.
These conclusions will certainly trigger the opening of new
catheterization laboratories
across the UK and elsewhere as well. As a consequence, the...
Sir, in their elegant evaluation of primary angioplasty vs
thrombolysis cost-effectiveness,
Wailoo and Coll. conclude that primary angioplasty-based care is highly
likely to be costeffective,
particularly if patients are admitted directly to the cardiac catheter
laboratory 1.
These conclusions will certainly trigger the opening of new
catheterization laboratories
across the UK and elsewhere as well. As a consequence, the manoeuvre will
increase not
only the number of primary angioplasties being performed, but also and
above all the
number of cardiac catheterization procedures performed for reason other
than treating
myocardial infarction 2.
We believe that shifting the strategy model from thrombolysis to primary
angioplasty
implies costs far exceedings those calculated in their sensitivity
analysis by Wailoo and
Coll.
1. Wailoo A, Goodacre S, Sampson F, Alava MnHn, Asseburg C, Palmer S, Sculpher M,
Abrams K, de Belder M, Gray H. Primary angioplasty versus thrombolysis for acute
ST-elevation myocardial infarction: an economic analysis of the National Infarct
Angioplasty project
10.1136/hrt.2009.167130. Heart. 2010;96:668-672.
2. Nallamothu BK, Rogers MAM, Chernew ME, Krumholz HM, Eagle KA, Birkmeyer JD.
Opening of Specialty Cardiac Hospitals and Use of Coronary Revascularization in
Medicare Beneficiaries
10.1001/jama.297.9.962. JAMA. 2007;297:962-968.
Paolo Alboni et al concluded that the patient's tolerance of intravenous
administration of flecainide or propafenone does not seem to predict
adverse effects during out-of-hospital self administration of these drugs
(1). However, it is important to note that the number of patients in the
study were only 122 with a 5% incidence of major adverse effects.
Patients without structural heart disease would benefit from propafeno...
Paolo Alboni et al concluded that the patient's tolerance of intravenous
administration of flecainide or propafenone does not seem to predict
adverse effects during out-of-hospital self administration of these drugs
(1). However, it is important to note that the number of patients in the
study were only 122 with a 5% incidence of major adverse effects.
Patients without structural heart disease would benefit from propafenone
or flecainide (2) but in this current study, the left atrial diameter
ranged from 35-45mm. This could have contributed to the high incidence of
adverse events.
A previous study defined enlarged left atrium as diameter >38mm in
women (56%) and >42mm in men (38%) with p<0.01 (3).
Also the author rightly pointed out that the pharmacodynamic effects of
oral vs intravenous forms of flecainide and propafenone work differently
(4). Hence, evaluating the effects of both drugs in the same study may not
give the best results.
References
1. Alboni P, Botto GL, et al. Intravenous administration of flecanide or
propafenone in patients with recent-onset atrial fibrillation does not
predict adverse effects during "pill-in-the- pocket" treatment. Heart 2010;96:546-549
2. Naccarelli GV, Wolbrette DL, et al. Old and new antiarrhythmic drugs
for converting and maintaining sinus rhythm in atrial fibrillation:
comparative efficacy and results of trials. Am J Cardiol. 2003 Mar
20;91(6A):15D-26D
3. Gerdts E, Oikarinen L, et al. Correlated of Left Atrial Size in
Hypertensive Patients with Left Ventricular Hypertrophy (LIFE) Study.
Hypertension 2002;39:739-743
4. Alp NJ, Bell JA, Shahi M. Randomised double blind trial of oral versus
intravenous flecanide for the conversion of acute atrial fibrillation.
Heart 2000;84:37-40
Our ischaemic cardiopathy study group have read with interest the article written by Lawesson et al (1).
First of all, the occurrence of ST-elevation myocardial infarction in young women is rare and the tobacco nocive role is well established in the medical literature. However, we would like to emphasize that smoking in women is growing nowadays. According to World Health Organization, there are 1,2 billion smokers around the wo...
Our ischaemic cardiopathy study group have read with interest the article written by Lawesson et al (1).
First of all, the occurrence of ST-elevation myocardial infarction in young women is rare and the tobacco nocive role is well established in the medical literature. However, we would like to emphasize that smoking in women is growing nowadays. According to World Health Organization, there are 1,2 billion smokers around the world, in which 200 million are women (2,3). Even with this, in the article, the women are not having infarctions more often. Regarding this, we would like to know the position of the authors on the following questions judged relevant by our group: first, what is the prevalence of early coronary diseases in the first grade relatives of these women? And second, knowing that the use of drugs or vasoactive substances and having AIDS are related to the occurrence of myocardial infarction in youngs, we ask if these factors were present in the studied female population.
REFERENCES
1.Lawesson SS, Stenestrand U, Lagerqvist B et al. Gender perspective on risk factors, coronary lesions and long-term outcome in young patients with ST-elevation myocardial infarction. Heart 2010;96:453-459
2.Choudhury L, Marsh JD. Myocardial infarction in young patients. Am J Med 1999;107:254e61.
3.World Health Organization (WHO). Tobbaco Free Iniciative. http://www.who.int/tobacco/en
With great interest we have read the article by Politi et al(1) on
revascularisation of patients with ST-elevation myocardial infarction and
multivessel disease. The authors are to be complimented with the largest
randomised trial on this subject, with the longest follow-up.
However, we question whether this study is the 'justification for
complete revascularisation at the time of primary angioplasty', as the
p...
With great interest we have read the article by Politi et al(1) on
revascularisation of patients with ST-elevation myocardial infarction and
multivessel disease. The authors are to be complimented with the largest
randomised trial on this subject, with the longest follow-up.
However, we question whether this study is the 'justification for
complete revascularisation at the time of primary angioplasty', as the
paper is labeled by the accompanying Editorial. Apart from the
considerable imbalance in patient numbers, which remains unexplained,
there are several other major concerns.
First, there is no mentioning of routine non-invasive testing for
ischemia after discharge in the COR group, as is currently advocated by
the guidelines(2). Thus, it is not clear if the additional PCI procedures
in the COR group were unexpected events or a result of planned non-
invasive testing. All these events were considered MACEs in the COR group,
while planned revascularisations in the SR group were not.
Second, testing for ischemia is relevant since 40% of non-culprit
lesions do not produce ischemia, as we demonstrated in a recent randomised
trial of FFR-guided early (7.5 days) additional revascularisation versus
culprit-only revascularisation(3). Also, we found that after 6 months
death and MI had occurred only in the early treatment group. This
underlines that early additional treatment is probably not without risk,
while benefit is not to be expected in a considerable number of patients.
Third, the importance of complete revascularisation is emphasized in
the discussion, but it is not clear in how many patients of the CR or SR
group this was actually achieved. Since more complex lesions are to be
expected in a population with multivessel disease, in which for instance
about 30% of the patients have a CTO, this is a relevant question. It has
been suggested that the presence of a CTO is the only independent factor
that determines the additional risk in patients with multivessel
disease(4).
For now, it seems that staged PCI of non-culprit lesions guided by
ischemia testing is still the most reasonable treatment strategy for
patients with multivessel disease and STEMI. We agree with the authors
that clearly more research is needed to define the optimal treatment in
these patients.
References
1. A randomised trial of target-vessel versus multi-vessel
revascularisation in ST-elevation myocardial infarction: major adverse
cardiac events during long-term follow-up. Politi L, Sgura F, Rossi R, et
al. Heart 2010 96: 662-667.
2. Management of acute myocardial infarction in patients presenting
with persistent ST-segment elevation: the Task Force on the Management of
ST-Segment Elevation Acute Myocardial Infarction of the European Society
of Cardiology. Van de Werf F, Bax J, Betriu A, et al. Eur Heart J 2008
Dec;29(23):2909-45.
3. Non-culprit lesions detected during primary PCI: treat invasively
or follow the guidelines? Dambrink JHE, Debrauwere JP, van 't Hof AWJ, et
al. Eurointervention 2010; 5:968-975.
4. Impact of multivessel coronary disease on long-term mortality in
patients with ST-elevation myocardial infarction is due to the presence of
a chronic total occlusion. Van der Schaaf RJ, Vis MM, Sjauw KD, et al. Am
J Cardiol 2006;98:1165-1169.
To the editor: I would like to thank Dr Lerman for his reply to our
measurement question [1]. I am acutely aware of Dr Lerman's fantastic
research pedigree and the excellent ground breaking work produced by the
Mayo clinic group, which swamps my paltry contribution to this area.
However, My specific question in the previous letter [2] was not related
to the ability of the IVUS-VH classification tree to determine plaque...
To the editor: I would like to thank Dr Lerman for his reply to our
measurement question [1]. I am acutely aware of Dr Lerman's fantastic
research pedigree and the excellent ground breaking work produced by the
Mayo clinic group, which swamps my paltry contribution to this area.
However, My specific question in the previous letter [2] was not related
to the ability of the IVUS-VH classification tree to determine plaque
characteristics accurately, as I feel that this has been previously well
investigated (as cited in your reply)[3-5] The question was more related
to your own inter-observer variability of IVUS-VH necrotic core analyses.
For example: The Thoraxcenter group have published the limits of
agreement around the measurement of necrotic core area [6]. They have
quoted an inter-observer range between 0.16mm2 and -0.20mm2. This is a
potential swing of 0.36mm2 of necrotic core across individual analyses
between operators. Although this inter-observer variability appears very
good, Rodriguez-Granillo do state in their discussion that "Overall, the
inter-catheter and inter-observer differences shown might provide
boundaries over which changes are statistically significant.The inter-
observer relative difference in plaque CSA measurements was 10%, This can
aid investigators to perform precise power calculations for longitudinal
studies"
The differences quoted in necrotic core within your study[7] was 0.13
(IQR 0.03-0.33) mm2 versus 0.0 (IQR 0.0-0.07) mm2, p<0.001. This
difference in real terms could be calculated as 0.13mm2 (IQR 0.03-0.26)
which is within Rodriguez-Granillo's range for simple inter-observer
variability (0.36mm2).
In short, is it possible that changes in necrotic core between the
groups with and without endothelial dysfunction (in your paper) were
simply a factor of inherent measurement variability? The absolute values
are very small and I appreciate this is difficult when studying coronary
segments with minimal disease.
I must apologise for forcing this debate to a conclusion, however
this measurement issue does have an effect on my own work in this area and
also future pharmacological and clinical trials using necrotic core as a
potential endpoint.
Best Wishes
Dr SW Murray
References
1. Amir Lerman Endothelial dysfunction and necrotic core plaques.
Heart 2010 96:551
2. Murray SW,Palmer ND Segmental coronary endothelial dysfunction in
patients with minimal atherosclerosis. Heart 2010;96:550.
3. Nasu K, Tsuchikane E, Katoh O, et al. Accuracy of in
vivo coronary plaque morphology assessment:a validation study of in vivo
virtual histology compared with in vitro histopathology. J Am Coll Cardiol
2006;47:2405e12.
4. Granada JF, Wallace-Bradley D, Win HK, et al. In vivo plaque
characterization using intravascular ultrasound virtual histology in a
porcine model of complex coronary lesions. Arterioscler Thromb Vasc Biol
2007;27:387e93.
5. Nasu K, Tsuchikane E, Katoh O, et al. Plaque
characterisation by virtual histology intravascular
ultrasound analysis in patients with type 2 diabetes.
Heart 94;2008:429e33.
6.Gaston A. Rodriguez-Granillo, Sophia Vaina, Hector M. Garcia-Garcia
et al Reproducibility of intravascular ultrasound radiofrequency data
analysis: implications for the design of longitudinal studies The
International Journal of Cardiovascular Imaging (2006) 22: 621-631
7. Lavi S, Bae JH, Rihal CS et al Segmental coronary endothelial
dysfunction in patients with minimal atherosclerosis is associated with
necrotic core plaques. Heart 2009;95:525-30
We have read with interest the article written by Piscione et al1
related with direct stenting. The authors have performed a meta-analysis
of 24 randomised controlled trials of direct stenting vs. stenting with
predilatation and the conclusion is a 23 % reduction in the odds of
myocardial infarction. In our opinion, direct stenting should be the
approach of choice in all the susceptible cases because this important
bene...
We have read with interest the article written by Piscione et al1
related with direct stenting. The authors have performed a meta-analysis
of 24 randomised controlled trials of direct stenting vs. stenting with
predilatation and the conclusion is a 23 % reduction in the odds of
myocardial infarction. In our opinion, direct stenting should be the
approach of choice in all the susceptible cases because this important
benefit is not associated with an increase in mortality, restenosis or
stent expansion2 3, and also direct stenting saves time and reduces
significantly procedural costs. In the current context with a strict
reduction in economical resources every approach directed to reduce costs
should always be attempted. A typical case of direct stenting can usually
be performed with one guiding catheter, one coronary wire and one stent.
In our country the use of one balloon will represent aproximately 28 % of
the cost of the procedure if the stent is bare metal and 20 % if is a drug
eluting stent. Few actions in medicine allow us to save such percentage
with the same or even better results. Stent dislodgment is extremely
unfrequent with the current stent designs and there are guiding catheters
dedicated to accomplish active intubation that facilitates direct
stenting. Moreover, if postdilatation needs to be performed to complete
the procedure, new balloons which can be inflated up to 40 atmospheres can
be found in the market. We believe that there are not arguments to perform
predilatation if direct stenting is potentially possible.
REFERENCES
1. Piscione F, Piccolo R, Cassese S, Galasso G, D'Andrea C, De Rosa
R et al. Is direct stenting superior to stenting with predilation in
patients treated with percutaneous coronary intervention? Results from a
meta-analysis of 24 randomised controlled trials. Heart 2010;96:588-94.
2. Le Breton H, Boschat J, Commeau P, Brunel P, Gilard M, Breut C et
al. Randomised comparison of coronary stenting with and without balloon
predilatation in selected patients. Heart 2001;86:302-8.
3. Lopez-Palop R, Pinar E, Lozano I, Carrillo P, Cortes R, Saura D
et al. Comparison of intracoronary ultrasound expansion parameters in
coronary stents implanted with or without balloon predilatation. A
randomized intravascular ultrasound study. Rev Esp.Cardiol 2004;57:403-11.
Editor, we read with great interest the article "NICE evaluation of
transmyocardial laser revascularisation and percutaneous laser
revascularisation for refractory angina [1].
The authors described a variety of treatment options for patients
suffering from refractory angina pectoris (RAP). However, a very
important, evolving innovation is missing: coronary sinus intervention
(CSI).
Editor, we read with great interest the article "NICE evaluation of
transmyocardial laser revascularisation and percutaneous laser
revascularisation for refractory angina [1].
The authors described a variety of treatment options for patients
suffering from refractory angina pectoris (RAP). However, a very
important, evolving innovation is missing: coronary sinus intervention
(CSI).
Coronary venous intervention (CVI) and CSI for the treatment of
ischemic heart disease were introduced more than 60 years ago [2]. CVI and
CSI means ligation or narrowing of the coronary sinus or other components
of the coronary venous system. Sixty years ago CVI, CSI like
transmyocardial laser revascularisation (TMR) was a major chest surgery
requires general anesthesia and lateral thoracotomy. This raises the
question of whether a patient with a jeopardized myocardium can survive
such a major operation.
In the mid-1990s, we invented the first percutaneous intravenous
coronary sinus reducer stent (CSRS). The CSRS is the implementation of
what we've called the upside-down strategy. When impaired coronary blood
flow can't be restored with input improvement, restriction of coronary
output remains an option and instead of forcing pressure to enlarge a
coronary artery the CSRS restricts a coronary sinus.
The CSRS is a balloon-expandable stent, hourglass shaped, implanted
by percutaneous transvenous approach through the right internal jugular
vein. It reduces the coronary sinus diameter to 3 mm.
First human study with CSRS began in 2004 [3]. It is a prospective,
open-label, safety feasibility study. The stent was percutaneously
implanted in 15 patients suffering of RAP. All patients were discharged
from hospital one to two days afterward. Six months after implantation,
most of the patients had improved Canadian Cardiovascular Society Scores
(CCSS) compared with baseline (3.07 versus 1.64; P <0.0001).
Improvements were also seen for stress-induced ST-segment depression and
for the extent and severity of myocardial ischemia as shown by either
dobutamine echocardiography or thallium single-photon emission CT. All
these improvements were maintained at 3 years after CSRS implementation
[4].
Further evaluation of CSRS for the treatment of patients with RAP is
ahead but initial findings suggest it may be a safe, feasible,
comfortable, and additional effective option for RAP patients that has to
be mentioned when dealing with RAP.
1. Schofield P M, McNab D. NICE evaluation of transmyocardial laser
revascularisation and percutaneous laser revascularisation for refractory
angina. Heart 2010 Feb;96(4):312-3.
2. Fauteux M. Surgical treatment of angina pectoris: experiences with
ligation of the great cardiac vein and pericoronary neurectomy. Ann Surg.
1946;124:1041-4.
3. Banai S, Ben Muvhar S, Parikh KH et al. Coronary sinus reducer
stent for the treatment of chronic refractory angina pectoris: a
prospective, open-label,
multicenter, safety feasibility first-in-man study. J Am Coll Cardiol.
2007;49:1783-1799.
4. Banai S, Schwartz M, Sievert H et al. Long-term follow-up to
evaluate the safety of the Neovasc Reducer a device-based therapy for
chronic refractory angina. J Am Coll Cardiol. 2010;55;A98.E927.
Editor, I read the recent publication by Uno et al [1]. Uno et al concluded that adiponectin is an indicator of LV diastolic dysfunction in patients with HCM [1]. There are some points to be concerned before using this conclusion. First, only 26 cases were investigated in this work and this might be a weakness in statistical analysis. Second, there are several practical concerns on the measurement of adiponectin starting from samp...
Editor, I read the recent publication by Uno et al [1]. Uno et al concluded that adiponectin is an indicator of LV diastolic dysfunction in patients with HCM [1]. There are some points to be concerned before using this conclusion. First, only 26 cases were investigated in this work and this might be a weakness in statistical analysis. Second, there are several practical concerns on the measurement of adiponectin starting from sample collection to intralaboratory analysis [2 - 3]. Indeed, a more favorable method for determination of adiponectin seems to be a latex particle-enhanced turbidimetric immunoassay with an automated analyzer [3]. Whether the inferences are well controlled by Uno et al is still questionable.
References 1. Unno K, Shibata R, Izawa H, Hirashiki A, Murase Y, Yamada T, Kobayashi M, Noda A, Nagata K, Ouchi N, Murohara T. Adiponectin acts as a positive indicator of left ventricular diastolic dysfunction in patients with hypertrophic cardiomyopathy. Heart. 2010 Mar;96(5):357-61. 2. Tanita T, Miyakoshi H, Nakano Y. Performance of ELISA for specific measurement of high-molecular-weight (HMW) adiponectin. J Immunol Methods. 2008 Apr 20;333(1-2):139-46. 3. Nishimura A, Sawai T. Determination of adiponectin in serum using a latex particle-enhanced turbidimetric immunoassay with an automated analyzer. Clin Chim Acta. 2006 Sep;371(1-2):163-8.
Shaw D and Conway DI (1) correctly identify that a fact neither proved nor disproved lies at the heart of both Pascalââ¬â¢s wager and the National Institute of Clinical Excellence (NICE) guidance in relation to the use of antibiotic (abx) prophylaxis for infective endocarditis (IE) . The no lose argument is no match winner for NICE because cardiologists are all too keenly aware that antibiotics kill as sure...
Shaw D and Conway DI (1) correctly identify that a fact neither proved nor disproved lies at the heart of both Pascalââ¬â¢s wager and the National Institute of Clinical Excellence (NICE) guidance in relation to the use of antibiotic (abx) prophylaxis for infective endocarditis (IE) . The no lose argument is no match winner for NICE because cardiologists are all too keenly aware that antibiotics kill as surely as IE. In relation to Pascal's wager consider the following equation: [harm caused by IE with Abx prophylaxis harm caused by Abx] [harm caused by IE without Abx prophylaxis] The cardiologistââ¬â¢s wager is that this equation is false. Both positions are ultimately based upon belief rather than sufficient empirical evidence because of equipoise in relation to the core fact in play. For cardiologists offering antibiotics is as valid and as strongly based a belief in overall benefit as is the NICE position. Pragmatically the principle should be that NICE should not intervene to alter the status quo where the underlying empirical evidence base is in equipoise. No treatment can be determined to be cost-effective if it is neither proven nor disproven. (2) Indeed in its own guidance upon social value judgements (3) NICE declares its first principle to be that it should not recommend an intervention "if there is no evidence, or not enough evidence, on which to make a clear decision". The effect of the NICE guidance is to implement a de facto clinical trial under the cover of a cost-effectiveness judgement. By purporting to lack the intention to undertake a clinical trial NICE is side-stepping the legal framework for research. (4) The medical duty of care imposes an ethical obligation upon clinicians to pursue the data collection required to interpret the result of the de facto trial in the absence of any other agency being so obliged. (1) Shaw D, Conway DI. Pascalââ¬â¢s Wager, infective endocarditis and the à âno- lose philosophy in medicine. Heart 2010;96:15- 18 doi:10.1136/hrt.2009.186056 (2) Mohindra RK. NICE, drug-eluting stents and the limits of trial data. Heart 2009;95(6):505-506 (3) National Institute For Health And Clinical Excellence. Social Value Judgements. Principles for the development of NICE guidance. 2nd Edition. Para 4.1 www.nice.org.uk/aboutnice/howwework/socialvaluejudgements/socialvaluejudgements.jsp (accessed 13/02/2010 (4) Reg 2 Medicines for Human Use (Clinical Trials) Regulations 2004 SI 2004/103
The statistics of propensity adjustment, that Harjai et al.(1) have
used with some modifications, is a recognised tool to increase the value
of non-experimental data(2,3).
However, these authors have used propensity statistics less
efficiently than other studies in this area have done(2,3). In fact,
propensity statistics has only been introduced by Harjai et al. in their
multivariate regression analysis, but...
The statistics of propensity adjustment, that Harjai et al.(1) have
used with some modifications, is a recognised tool to increase the value
of non-experimental data(2,3).
However, these authors have used propensity statistics less
efficiently than other studies in this area have done(2,3). In fact,
propensity statistics has only been introduced by Harjai et al. in their
multivariate regression analysis, but no 1:1 propensity matching has been
made to identify two patient subgroups of identical size (derived from the
cohorts who continued or discontinued the treatment, respectively) and
compare outcomes between these two matched-pair subgroups.
No specific rules have yet been devised to determine the size of the
cohorts to be included in propensity analyses. Nonetheless, since
propensity studies have less quality of evidence than randomized studies,
one can reasonably assume that the number of patients included in
propensity studies should not be smaller than the number of patients that
one would include in a randomized study aimed at the same question.
In patients receiving percutaneous coronary intervention, the
opportunity to continue clopidogrel at 6 or 12 months is presently matter
of debate. Using non-inferiority power calculations (power=0.80,
alpha=0.05, event frequency around 10%, clinically meaningful relative
risk reduction set at 20%), a total of at least 2,500 patients (1,250 per
arm) would be needed to adequately power a randomized study. Event
frequencies less than 10% would give even larger sample sizes.
Two propensity analyses have recently addressed this issue(1,4). The
study by Harjai et al.(1) analyzed 835 patients treated with bare metal
stents and 1024 treated with drug-eluting stents, while Shin's study(4)
examined fewer patients (N=844) treated with drug eluting stents (with an
advantage in that a matched-pair analysis was tried). Both studies suggest
that prolonging clopidogrel beyond 6 or 12 months confers no benefit.
Although these findings have been interpreted this way, it has not
been observed that these studies were largely underpowered to adequately
address this therapeutic problem. Hence, a large-scale randomized study is
still needed in this area. Alternatively, a propensity-score investigation
could be useful provided that at least 3,000 patients are included in the
matched-pair analysis.
References
1. Harjai KJ, Shenoy C, Orshaw P, Boura J. Dual antiplatelet therapy
for more than 12 months after percutaneous coronary intervention: insights
from the Guthrie PCI Registry. Heart. 2009;95(19):1579-86.
2. Mauri L, Silbaugh TS, Garg P, Wolf RE, Zelevinsky K, Lovett A,
Varma MR, Zhou Z, Normand SL. Drug-eluting or bare-metal stents for acute
myocardial infarction. N Engl J Med. 2008;359(13):1330-42.
3. Egorova N, Giacovelli J, Greco G, Gelijns A, Kent CK, McKinsey JF.
National outcomes for the treatment of ruptured abdominal aortic aneurysm:
comparison
of open versus endovascular repairs. J Vasc Surg. 2008;48(5):1092-100.
4. Shin DH, Chae IH, Youn TJ, Cho SI, Kwon DA, Suh JW, Chang HJ, Cho
YS, Chung WY, Choi YJ, Gwon HC, Han KR, Choi DJ. Reasonable duration of
Clopidogrel use after drug-eluting stent implantation in Korean patients.
Am J Cardiol. 2009;104(12):1668-73.
Sir, in their elegant evaluation of primary angioplasty vs thrombolysis cost-effectiveness, Wailoo and Coll. conclude that primary angioplasty-based care is highly likely to be costeffective, particularly if patients are admitted directly to the cardiac catheter laboratory 1. These conclusions will certainly trigger the opening of new catheterization laboratories across the UK and elsewhere as well. As a consequence, the...
Paolo Alboni et al concluded that the patient's tolerance of intravenous administration of flecainide or propafenone does not seem to predict adverse effects during out-of-hospital self administration of these drugs (1). However, it is important to note that the number of patients in the study were only 122 with a 5% incidence of major adverse effects. Patients without structural heart disease would benefit from propafeno...
With great interest we have read the article by Politi et al(1) on revascularisation of patients with ST-elevation myocardial infarction and multivessel disease. The authors are to be complimented with the largest randomised trial on this subject, with the longest follow-up.
However, we question whether this study is the 'justification for complete revascularisation at the time of primary angioplasty', as the p...
To the editor: I would like to thank Dr Lerman for his reply to our measurement question [1]. I am acutely aware of Dr Lerman's fantastic research pedigree and the excellent ground breaking work produced by the Mayo clinic group, which swamps my paltry contribution to this area. However, My specific question in the previous letter [2] was not related to the ability of the IVUS-VH classification tree to determine plaque...
We have read with interest the article written by Piscione et al1 related with direct stenting. The authors have performed a meta-analysis of 24 randomised controlled trials of direct stenting vs. stenting with predilatation and the conclusion is a 23 % reduction in the odds of myocardial infarction. In our opinion, direct stenting should be the approach of choice in all the susceptible cases because this important bene...
Editor, we read with great interest the article "NICE evaluation of transmyocardial laser revascularisation and percutaneous laser revascularisation for refractory angina [1].
The authors described a variety of treatment options for patients suffering from refractory angina pectoris (RAP). However, a very important, evolving innovation is missing: coronary sinus intervention (CSI).
Coronary venous int...
The statistics of propensity adjustment, that Harjai et al.(1) have used with some modifications, is a recognised tool to increase the value of non-experimental data(2,3).
However, these authors have used propensity statistics less efficiently than other studies in this area have done(2,3). In fact, propensity statistics has only been introduced by Harjai et al. in their multivariate regression analysis, but...
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