We read the paper by Choi et al with great interest. [1] Clearly NTproBNP (and CRP) appeared to predict perioperative major cardiovascular events (PCME) better than the Revised Cardiac Risk Index (RCRI).
The most traditional way to depict that one predictor is better than other is to use the c-statistic or the area under the ROC curve (AUC). Although the abstract states that NTproBNP and CRP performed better than RCRI by ROC ana...
We read the paper by Choi et al with great interest. [1] Clearly NTproBNP (and CRP) appeared to predict perioperative major cardiovascular events (PCME) better than the Revised Cardiac Risk Index (RCRI).
The most traditional way to depict that one predictor is better than other is to use the c-statistic or the area under the ROC curve (AUC). Although the abstract states that NTproBNP and CRP performed better than RCRI by ROC analysis, the paper does not tell us the actual c-statistic or AUC for either NTproBNP alone or CRP alone. This information would be useful in order to be able to compare directly the c-statistic of NTproBNP (or CRP) alone and RCRI alone. The c-statistic for the NTproBNP alone will help us to judge whether NTproBNP alone is as good as adding NTproBNP to the RCRI which is what the authors advocate. There would need to be a major advantage for combining NTproBNP and the RCRI over using NTproBNP alone for this to become practical reality since combining two separate risk scores is more cumbersome for the practicing clinicians than using either one alone.
Instead of discussing the possibility that NTproBNP could replace the RCRI, the authors present the c-statistic data only for adding NTproBNP (and CRP) to the RCRI. We would urge the authors to now report c-statistic for NTproBNP alone (and CRP alone) so that it can be judged whether we really need to add NTproBNP (or CRP) to the RCRI (as they suggest) or whether NTproBNP (or CRP) can somehow replace the RCRI itself.
1 Choi JH, Cho DK, Song YB, et al. Preoperative NT-proBNP and CRP Predict Perioperative Major Cardiovascular Events in Noncardiac Surgery. Heart 2009.
To the Editor: Ryan et al. report on the efficacy of Dual Chamber
pacemaker implantation in patients with cardio-inhibitory carotid sinus
hypersensitivity (CICSH) and falls in SAFEPACE-2 (Syncope And Falls in the
Elderly- Pacing And Carotid sinus Evaluation)[1]. This study had the
potential to expand on the findings of SAFEPACE-1 [2] and address some of
the weaknesses of the latter with a blinded, multicenter, and less se...
To the Editor: Ryan et al. report on the efficacy of Dual Chamber
pacemaker implantation in patients with cardio-inhibitory carotid sinus
hypersensitivity (CICSH) and falls in SAFEPACE-2 (Syncope And Falls in the
Elderly- Pacing And Carotid sinus Evaluation)[1]. This study had the
potential to expand on the findings of SAFEPACE-1 [2] and address some of
the weaknesses of the latter with a blinded, multicenter, and less select
cohort [3]. However, despite improved external validity, SAFEPACE-2
reports findings at odds with the prior results of SAFEPACE-1 by
demonstrating that the null hypothesis was correct (pacemaker implantation
did not reduce falls in CICSH)[1].
The authors of SAFEPACE-2 are to be applauded for their efforts to
increase the generalizability of their results and for their attention to
detail with regards to data acquisition and analysis. This begs the
question, why the marked difference in findings between the two SAFEPACE
trials [1-2]? While it is true that the cohort in SAFEPACE-2 had more
comorbidity, one wonders whether further review of the trial methodology
will yield another explanation.
The ‘double-blind’ design of SAFEPACE-2 seems difficult to achieve
given the nature of the intervention. Pacemaker insertion requires the
patient to carry a specific pacemaker card and to follow-up at specialized
pacemaker clinics. In contrast, a loop recorder requires specific
education as the patient self-activates the recorder with a hand-held
device. Failure to blind the patients could significantly affect the
primary outcome of self-reported falls, increasing the potential for
recall bias in favor of the intervention. Therefore, this methodological
issue may actually strengthen the author’s findings in SAFEPACE 2 and does
not explain the difference in results between the trials.
At first glance, the difference may be explained by the lack of
statistical power in SAFEPACE-2. It is true that SAFEPACE 2 is
underpowered to detect a difference of 20% in the number of patients who
fell, however it is almost fully powered to detect a difference of 40%.
This was the power criteria used in SAFEPACE 1 [2]. Therefore, lack of
statistical power also does not fully explain the difference in results
between the trials.
One methodological issue which may account for the different trial
results is the ‘randomization to implantation’ time. The overall relative
risk (RR) for falls with pacemaker implantation in SAFEPACE-2 was 0.79
(95% Confidence Interval [CI], 0.4-1.5), but was 0.23 (95% CI, 0.15-0.32)
when comparing patients before and after device implantation [1]. The
latter RR suggests that device implantation made a difference to fall
rates and raises the possibility that the overall result was obscured by a
prolonged ‘randomization to implantation’ time. Given the multicenter
nature of this trial it seems likely that this time was longer in SAFEPACE
-2 than the single centre SAFEPACE-1. Therefore, it seems possible that
inclusion of fall data prior to device implantation (the intervention)
obscured the result of SAFEPACE-2 and may partially explain the difference
in results between the two SAFEPACE trials.
Reporting the mean and median time from ‘randomization to
implantation’, and exclusion of the pre-implantation fall data from the
analysis may help shed more light on this important issue.
John W. McEvoy M.B., M.R.C.P.I.
The Johns Hopkins Hospital
600 N. Wolfe Street
Baltimore, Maryland 21287
Jmcevoy1@jhmi.edu
1. Ryan D, Steen N, Seifer C, Kenny RA. Carotid Sinus Syndrome and
falls, should we pace? A multi-centre, randomised control trial (Safepace
2). Heart 2009.
2. Kenny RA, Richardson DA, Steen N, Bexton RS, Shaw FE, Bond J. Carotid
sinus syndrome: a modifiable risk factor for nonaccidental falls in older
adults (SAFE PACE). J Am Coll Cardiol 2001;38(5):1491-6.
3. McAnulty JH. Carotid sinus massage in patients who fall: will it define
the role of pacing? J Am Coll Cardiol 2001;38(5):1497.
To the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1The study showed the presence of abnormal
longitudinal left ventricular strain in patients with aortic stenosis and concentric left...
To the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1The study showed the presence of abnormal
longitudinal left ventricular strain in patients with aortic stenosis and concentric left ventricular hypertrophy. Similar observations of reduced (less
negative) peak longitudinal strain have been made in hypertensive-hypertrophic
heart disease,2 heart failure with a normal
ejection fraction (HFNEF),3, 4
and other causes of pathological left ventricular hypertrophy5, 6, 7
Further, abnormalities of midwall
circumferential shortening have been shown in hypertensive-hypertrophic left
ventricular disease2 and in HFNEF.8Wang also showed a trend to reduced
circumferential strain from -20% to -15% in HFNEF.3The effect of myocardial disease on
circumferential strain appears to be slightly less marked than that on
longitudinal strain.3In addition, there is significantly reduced radial
strain in HFNEF despite the apparent normal radial ‘function’ and ejection
fraction.3, 4
An increase in end-diastolic wall thickness may explain the combination
of reduced myocardial shortening and yet a normal ejection fraction. This can be understood by considering a cube
of myocardium 9 x 9 x 9 mm as a non-compressible elastomer.If circumferential and longitudinal strain
are both normal (-20%) then radial strain (i.e. relative wall thickening) is +56%
and absolute wall thickening is 5.1 mm (see Table). When there is left ventricular hypertrophy
with an end-diastolic wall thickness of 13 mm and circumferential and
longitudinal strain are reduced (-15%), radial strain is also significantly reduced
(38%) but absolute wall thickening remains almost identical at 5.0 mm (see
Table).Therefore, it is important to
differentiate between absolute and relative radial thickening.
Three dimensional modelling demonstrates that ejection
fraction is principally determined by both myocardial shortening (strain) and
end-diastolic wall thickness independently of loading conditions.9The normal absolute wall thickening in
presence of reduced strain results in the normal ejection fraction.9, 10End-diastolic wall thickness and strain are the
determinants of absolute wall thickening; absolute wall thickening is the main
determinant of left ventricular ejection fraction in a curvilinear manner.10
An individual’s resting metabolic requirements demand a
reasonably normal stroke volume (SV) in stable heart failure regardless of
ejection fraction.10Ejection fraction is merely the ratio of gross
SV and end-diastolic volume (where, gross SV = net SV + valvular regurgitant
volume). If the numerator is relatively fixed
the denominator must change; accordingly the relationship between ejection
fraction and end-diastolic volume is reciprocal even in heart failure.11Three-dimensional modelling suggests thatthe
end-diastolic volume may be physiologically regulated by the need to have an
appropriate net stroke volume to satisfy the physiological needs of peripheral tissues
in health (e.g. growth, pregnancy) and in heart disease.10
An increase in end-diastolic wall thickness with normal
shortening must lead to an increased absolute thickening; in order for the
absolute wall thickening to remain normal, myocardial shortening must be
reduced.Myocardial strain has to be
reduced proportionally to the degree of concentric hypertrophy otherwise the
ejection fraction and stroke volume will be inappropriately increased.
Hypertrophic left ventricular disease occurs in numerous
conditions including hypertension, aortic stenosis,
hypertrophic cardiomyopathy, HFNEF, Fabry disease and amyloid.Each condition can be explained by the
combination of abnormal myocardial shortening and increased end-diastolic wall
thickness determining the absolute myocardial thickening and ejection
fraction.The end-diastolic volume being
adjusted to normalise net stroke volume for the given ejection fraction.10
These proposals explain the geometric findings in
hypertrophic heart disease regardless of the cause.A normal ejection fraction does not equate to
normal deformation or even normal systolic function.The term ‘global systolic function’ is
meaningless, misleading and should be abandoned.
Table
Normal peak strain
-20%
Abnormal peak strain
-15%
Abnormal strain
-10%
End-diastolic thickness (mm)
9
13
17
21
9
13
17
21
9
13
17
21
End-systolic thickness (mm)
14
20
27
33
13
19
25
31
13
18
24
29
Radial strain (%)
56
56
56
56
38
38
38
38
23
23
23
23
Absolute wall thickening
(mm)
5.1
7.3
9.6
11.8
3.5
5.0
6.5
8.1
2.1
3.1
4.0
4.9
DH MacIver
Taunton
& Somerset Hospital, Taunton, UK.
Correspondence to: Dr DH MacIver
Conflict of interest: None.
1Cramariuc
D, Gerdts E, Davidsen ES, et al. Myocardial deformation in aortic valve stenosis
- relation to left ventricular geometry. Heart
2009:hrt.2009.172569.
2Shimizu
G, Hirota Y, Kita Y, et al. Left ventricular midwall mechanics in systemic
arterial hypertension. Myocardial function is depressed in pressure-overload
hypertrophy. Circulation 1991;83:1676-84.
3Wang
J, Khoury DS, Yue Y, et al. Preserved left ventricular twist and
circumferential deformation, but depressed longitudinal and radial deformation
in patients with diastolic heart failure. Eur
Heart J 2008;29:1283-9.
4Tan
YT, Wenzelburger F, Lee E, et al. The pathophysiology of heart failure with
normal ejection fraction: exercise echocardiography reveals complex
abnormalities of both systolic and diastolic ventricular function involving
torsion, untwist, and longitudinal motion. J
Am Coll Cardiol 2009;54:36.
5Nagueh
SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects
myocardial abnormalities in patients with hypertrophic cardiomyopathy and
provides a novel means for an early diagnosis before and independently of
hypertrophy. Circulation 2001;104:128-30.
6Weidemann
F, Breunig F, Beer M, et al. Improvement of cardiac function during enzyme
replacement therapy in patients with Fabry disease. A prospective strain rate
imaging study. Circulation 2003;108:1299-301.
7Koyama
J, Ray-Sequin PA, Falk RH. Longitudinal myocardial function assessed by tissue
velocity, strain, and strain rate tissue Doppler echocardiography in patients
with AL (primary) cardiac amyloidosis. Circulation
2003;107:2446-52.
8Vinch
C, Aurigemma G, Simon H, et al. Analysis of left ventricular systolic function
using midwall mechanics in patients > 60 years of age with hypertensive
heart disease and heart failure. Am J
Cardiol 2005;96:1299-303.
9MacIver
DH, Townsend M. A novel mechanism of heart failure with normal ejection
fraction. Heart 2008;94:446-9.
10MacIver
DH. Is remodeling the dominant compensatory mechanism in both chronic heart
failure with preserved and reduced left ventricular ejection fraction? Basic Res Cardiol 2009:Online first DOI:
10.1007/s00395-009-0063-x.
11MacIver
DH. Surgical ventricular reconstruction: an oversimplified hypothesis? N Engl J Med 2009;361:529-32.
November 11, 2009
Editor, Heart
British Medical Journal
Dear Sir:
I am writing to comment on the excellent article by Bhaskaran et al in Heart[1], and especially on the editorial by David Newby [2] that commented on this paper. In my opinion, Dr. Newby has missed the most important conclusion of the Bhaskaran paper.
Dr. Newby’s editorial was focused mainly on the cardiac effects of fine particulate pollution, and included a...
November 11, 2009
Editor, Heart
British Medical Journal
Dear Sir:
I am writing to comment on the excellent article by Bhaskaran et al in Heart[1], and especially on the editorial by David Newby [2] that commented on this paper. In my opinion, Dr. Newby has missed the most important conclusion of the Bhaskaran paper.
Dr. Newby’s editorial was focused mainly on the cardiac effects of fine particulate pollution, and included a graph of data from Beijing, China.
However, it seems to me that a far more important contribution of the Bhaskaran paper was the observation of an “ozone protective effect” in several parts of the world. The authors pointed out that this effect is probably due to some pollutant that is negatively correlated with ozone, and cites my previous paper[3] suggesting that the effect could be due to unsuspected methyl nitrite (MN) in the air. This hypothesis has a high degree of plausibility because it is known that MN, unlike ozone, is rapidly destroyed by sunlight and so would be negatively correlated with ozone. To the best of my knowledge, this ozone protective effect is totally inexplicable unless an unknown pollutant, such as MN, is present.
If Dr. Newby’s point of view is to be accepted, then presumably he must argue that fine particulate pollution is also the cause of the ozone protective effect. However, that hypothesis has been thoroughly discredited in another paper [4]. In that paper I showed that fine particulate matter can not explain the negative ozone associations in any parts of the world in which there is published evidence for the negative effects. I particularly showed that explanation is extremely unlikely in Hong Kong, China.
Hence, I feel that the most important contribution of the Bhaskaran paper is to alert the world to the possible existence of a very important toxic pollutant whose presence has escaped attention. Most desperately needed is funding for research to identify MN in engine exhaust. To date, such funding has not been available in the United States.
Sincerely,
Professor Peter M. Joseph, Ph.D.
School of Medicine
University of Pennsylvania
Philadelphia, PA, USA
email = joseph@rad.upenn.edu
REFERENCES
1. Bhaskaran K, Hajat S, Haines A, Herrett E, Wilkinson P, Smeeth L. Effects of air pollution on the incidence of myocardial infarction. Heart 2009;95:1746-1759.
2. Langrish JP, Mills NL, Newby DE. Heat and haze: a forecast for myocardial infarction? Heart 2009;95:1721-1722.
3. Joseph PM. Paradoxical ozone associations could be due to methyl nitrite from combustion of methyl ethers or esters in engine fuels. Environ Int 2007;33:1090-106.
4. Joseph PM. Can fine particulate matter explain the paradoxical ozone associations? Environ Int 2008;34:1185-91.
Dear Sir,
We enjoyed the recent paper in Heart by Rana et 1, but were concerned that the sample was composed of approximately 80% of individuals with intermediate or high-risk of having an event, which impaired the diagnostic and prognostic accuracy of the assessed test. The markers used reflect the biological state of elevated risk of an adverse outcome in the studied subjects that is secondary to the interaction of risk-factor...
Dear Sir,
We enjoyed the recent paper in Heart by Rana et 1, but were concerned that the sample was composed of approximately 80% of individuals with intermediate or high-risk of having an event, which impaired the diagnostic and prognostic accuracy of the assessed test. The markers used reflect the biological state of elevated risk of an adverse outcome in the studied subjects that is secondary to the interaction of risk-factors such as smoking, diabetes mellitus and dyslipidemia that can affect the endothelium 2,3,4.
1. Rana JS, Cote M, Despres JP, Sandhu MS, Talmud PJ, Ninio E, et al.
Inflammatory biomarkers and the prediction of coronary events among people at intermediate risk: the EPIC-Norfolk prospective population study. Heart 2009;95(20):1682-7.
2. Koskinen J, Kahonen M, Viikari JS, Taittonen L, Laitinen T, Ronnemaa T, et al. Conventional cardiovascular risk factors and metabolic syndrome in predicting carotid intima-media thickness progression in young adults: the cardiovascular risk in young Finns study. Circulation 2009;120(3):229-36.
3. Kalra L, Iveson E, Rambaran C, Sherwood R, Chowienczyk P, Ritter J, et al. Homocysteine, migration and early vascular impairment in people of African descent. Heart 2008;94(9):1171-4.
4. De Michele M, Iannuzzi A, Salvato A, Pauciullo P, Gentile M, Iannuzzo G, et al. Impaired endothelium-dependent vascular reactivity in patients with familial combined hyperlipidaemia. Heart 2007;93(1):78-81.
We read with great interest the work by Luckie et al., recently
published in this Journal. (1) It's known that for patients who suffer
from infiltrative, obstructive or bleeding carcinomas, or for high rupture
risk aneurismal disease, a prompt surgical procedure may represent
“survival”, and that in case of revascularization requirement, currently
available options, either bare-metal or drug-eluting stent or plain-old
ba...
We read with great interest the work by Luckie et al., recently
published in this Journal. (1) It's known that for patients who suffer
from infiltrative, obstructive or bleeding carcinomas, or for high rupture
risk aneurismal disease, a prompt surgical procedure may represent
“survival”, and that in case of revascularization requirement, currently
available options, either bare-metal or drug-eluting stent or plain-old
balloon angioplasty, might put back surgical procedure, according to the
mandatory antiplatelet therapy time window. (2) In the section “Stents
with pro-healing surfaces” of their manuscript, the Authors reported our
preliminary data regarding a pilot study of percutaneous revascularization
with a new type of “pro-healing” stent, followed by a short-term dual
antiplatelet therapy, and subsequent urgent or life-saving surgery few
days after stent deployment. Recently, we published as a full-length
manuscript, (3) final data regarding 30 consecutive patients treated with
this stenting strategy, with optimal acute procedural result. According to
an average antiplatelet therapy time of 12.2±3.9 days, patients included
underwent surgery 10 to 22 days after coronary stent deployment (average
17.2±3.9 days). No cardiac event has been reported in the perioperative
period up to 30-days follow-up after surgery. Clearly, we did not
randomize or match this population with a comparison group because it
would not be possible to perform surgical procedure, as soon as we did.
(2) Although based on a small sample size, our findings suggest that the
“pro-healing” stent should be safe and feasible for patients candidate for
upcoming major surgery who need a previous revascularization. Further
registries are needed to confirm the safety and furthermore the mid- and
long term efficacy of this stent that is racking up among interventional
cardiologists, especially in this specific subset of patients. In this
respect, we completely agree with Authors regarding the importance of a
timely identification of patients who could have an high surgical
probability within next months after revascularization. (4) We firmly
believe that such patients could take a great advantage from this stenting
strategy!
References
1. Luckie M, et al. Non-cardiac surgery and antiplatelet therapy
following coronary artery stenting. Heart 2009; 95: 1303-1308
2. Poldermans D, et al., Guidelines for pre-operative cardiac risk
assessment and perioperative cardiac management in non-cardiac surgery:
The Task Force for Preoperative Cardiac Risk Assessment and Perioperative
Cardiac Management in Non-cardiac Surgery of the European Society of
Cardiology (ESC) and endorsed by the European Society of Anaesthesiology
(ESA). Eur Heart J. 2009 Aug 27. [Epub ahead of print]
3. Piscione F, et al. A new approach to percutaneous coronary
revascularization in patients requiring undeferrable non-cardiac surgery.
Int J Cardiol. 2009 Aug 21. [Epub ahead of print]
4. Vicenzi MN, et al. Coronary artery stenting and non-cardiac surgery – a
prospective outcome study. Br J Anaesth 2006;96:686–93.
To the Editor:
With great interest I read the article by Byrne et al. assessing
antirestenotic efficacy of 3 different rapamycin-eluting stents with
different coating strategies (biodegradable polymer, permanent polymer and
polymer-free stents) at 2 time points after coronary stenting (6 to 8
months and 2 years) [1]. Although the authors suggested delayed late loss
(the difference in in-stent late loss between 6 to 8 mont...
To the Editor:
With great interest I read the article by Byrne et al. assessing
antirestenotic efficacy of 3 different rapamycin-eluting stents with
different coating strategies (biodegradable polymer, permanent polymer and
polymer-free stents) at 2 time points after coronary stenting (6 to 8
months and 2 years) [1]. Although the authors suggested delayed late loss
(the difference in in-stent late loss between 6 to 8 months and 2 years)
was significantly different across the treatment groups, paired
angiographic data was available for only 302 patients (50%) of 605
patients undergoing stenting. Missing was not at random; patients who
underwent revascularization or died were excluded for late follow-up
analysis, which may lead to attrition bias [2]. In fact, late luminal loss
(of selected patients) was similar at 2 year (Figure 4), although target
lesion revascularisation rate (of all patients) seemed to differ at 2 year
(Figure 1). Therefore, it would be of great help if the authors would
provide additional angiographic analysis such as multiple imputation as
well as sensitivity analysis [3].
References
1 Byrne RA, Kufner S, Tiroch K, et al. Randomised trial of three
rapamycin-eluting stents with different coating strategies for the
reduction of coronary restenosis: 2-year follow-up results. Heart
2009;95:1489-94.
2 Juni P, Altman DG, Egger M. Systematic reviews in health care:
Assessing the quality of controlled clinical trials. Bmj 2001;323:42-6.
3 Donders AR, van der Heijden GJ, Stijnen T, et al. Review: a gentle
introduction to imputation of missing values. J Clin Epidemiol
2006;59:1087-91.
To the Editor: We read with great interest the paper published by S
Lavi et al [1] and feel that it is worthy of comment. We admire the
foresight and technical expertise that has gone into creating this study,
to try and prove a worthy concept. However, we do have an issue regarding
the measurement of Necrotic Core in minimal plaques. The authors state
that after selecting the appropriate frames "two independent
investi...
To the Editor: We read with great interest the paper published by S
Lavi et al [1] and feel that it is worthy of comment. We admire the
foresight and technical expertise that has gone into creating this study,
to try and prove a worthy concept. However, we do have an issue regarding
the measurement of Necrotic Core in minimal plaques. The authors state
that after selecting the appropriate frames "two independent
investigators" measured each frame and the results were calculated.
Sections with endothelial dysfunction had larger necrotic core plaques:
0.13 (0.03–
0.33) mm2 vs 0.0 (0.0–0.07), p<0.001 and more dense
calcium: 0.03 (IQR 0.0–0.13) mm2 vs 0.0 (0.0–
0.10) mm2, p<0.01).
The absolute value of these numbers calculated for constituent plaque
area is very small (in keeping with the modest disease) Have the authors
performed intra and inter-observer variability testing to prove that they
are able to reproduce this level of accuracy? Having analysed thousands of
IVUS-VH frames and published work on IVUS-VH variability [2], we are aware
that minimal discrepancies in manual border detection, between operators,
can significantly influence calculated plaque measurements.
If the authors cannot prove from an in-house variability study that
their individual variability measurements are less than the calculated
plaque areas, then their results are invalid. We would be grateful for a
response to this important measurement issue.
References
1. S Lavi, J-H Bae, C S Rihal, et al.
Segmental coronary endothelial dysfunction in
patients with minimal atherosclerosis is associated
with necrotic core plaques. Heart 2009;95:1525–1530.
doi:10.1136/hrt.2009.166017
2. SW Murray, Hamilton C, Perry RA, Palmer ND. Is Volumetric Plaque
Characterisation By Intravascular Ultrasound Based Virtual Histology (IVUS
-VH) Reliable In Serial Studies? An Analysis Of Intra And Inter-observer
Variability In The Culprit Lesion Assessment Of Acute Coronary Syndrome
Patients.Catheterization and Cardiovascular Interventions, May 2009 volume
73, pg 61
We read with interest the comprehensive review article on T2-weighted
(T2w)
cardiovascular magnetic resonance imaging (CMR) by
Edwards, Routledge and Steeds (1). We wish to make one comment for the
sake of clarity and also to bring to the reader’s attention
important new data, which have become available in the meantime and light
up some of the issues raised by the authors. The authors
cite one...
We read with interest the comprehensive review article on T2-weighted
(T2w)
cardiovascular magnetic resonance imaging (CMR) by
Edwards, Routledge and Steeds (1). We wish to make one comment for the
sake of clarity and also to bring to the reader’s attention
important new data, which have become available in the meantime and light
up some of the issues raised by the authors. The authors
cite one of the first reports employing T2w CMR to assess acute myocardial
injury at a very early stage (2) but fail to bring out one key
aspect of that study. We used polyvinyl alcohol foam particles (contour
emboli) rather than ethanol injections to induce therapeutic
infarction in patients undergoing septal artery embolization. As a result,
these ischemic insults were fairly comparable with the clinical
event of atherothrombotic coronary occlusions. Although elevated T2 signal
was not consistently observable within the first 60
minutes after onset of ischemia, it was present on the next day and
remained
elevated for up to 4 weeks. While this study
demonstrated the ability of T2w CMR to identify acute myocardial injury,
the
‘early blind spot’ was possibly related to the
experimental design with embolization of a very small coronary territory.
Furthermore, the impact of such particles on T2 signal was
not investigated, but may have been a confounder.
Recently, Abdel-Aty et al. added a few more pieces to the jigsaw (3):
open-
chest dogs were instrumented with a snare around the 1st
diagonal artery. Ischemia duration was deliberately restricted so as to
avoid
relevant cell destruction (i.e. infarction). While contractility
was immediately affected (reflecting energetic depletion), pathological T2
signal (reflecting tissue oedema) did not visually become
apparent before 28+/-4 minutes after onset of ischemia and was further
increased after reperfusion. The marked increase in T2 signal
was paralleled by a relatively small, yet relevant and significant
increase in
myocardial water content (~ 2%), likely reflecting cellular
rather than interstitial oedema with disruption of cell membranes. This
experiment elucidates the T2w-CMR profile of non-lethal
ischemia in a dog model with some, albeit inherently limited,
transferability
into the human scenario. Moreover, the relationships of
T2 signal with conditions such as stunning, repetitive
ischemia/reperfusion
and peri-ischemic inflammation are still waiting to be
unravelled.
Incremental technical advances in T2w CMR will facilitate that and
are
expected to enhance our understanding of the ischemia-
reperfusion sequence and improve clinical decision-making.
References
1 Edwards NC, Routledge H, Steeds R. T2 Weighted Magnetic Resonance
Imaging to Assess Myocardial Oedema In Ischemic Heart
Disease. Heart. 2009 Aug;95(16):1357-61. Epub 2009 May 15
2 Schulz-Menger J, Gross M, Messroghli D, Uhlich F, Dietz, R,
Friedrich MG.
Cardiovascular Magnetic Resonance of Acute Myocardial
Infarction at a Very Early Stage. J Am Coll Cardiol 42, (3) 2003:513– 8
3 Abdel-Aty H, Cocker M, Meek C, Tyberg JV, Friedrich MG. Edema as a
Very
Early Marker for Acute Myocardial Ischemia: A
Cardiovascular Magnetic Resonance Study. J Am Coll Cardiol 53 (14)
2009:1194 –201
Randomised trials in patients on oral anticoagulation undergoing
coronary stenting
(response to Drs Willem Dewilde and Jurrien m ten Berg)
Dear Sir,
we agree with Dr. Dewilde and Dr. Ten Berg that current
recommendations regarding coronary stenting in patients on oral
anticoagulation (OAC) are not based on randomised controlled trials (RCT)
and congratulate them for addressing this important issue by i...
Randomised trials in patients on oral anticoagulation undergoing
coronary stenting
(response to Drs Willem Dewilde and Jurrien m ten Berg)
Dear Sir,
we agree with Dr. Dewilde and Dr. Ten Berg that current
recommendations regarding coronary stenting in patients on oral
anticoagulation (OAC) are not based on randomised controlled trials (RCT)
and congratulate them for addressing this important issue by initiating
this WOEST trail (NCT00769938). While the WOEST trial compares a triple
therapy with a therapy consisting of OAC + clopidogrel, a second RCT is
ongoing (ISAR-TRIPLE, NCT00776633) which evaluates the length of
clopidogrel therapy (6 weeks versus 6 months) after drug eluting stent
placement in patients on OAC + aspirin.
These randomized trials will answer unresolved questions regarding
ischemic and bleeding complications in this high risk population. In the
future, we hope that the recommendations can be based on the results of
these RCT’s.
Albert Schömig, MD, Nikolaus Sarafoff, MD and Melchior Seyfarth, MD
References
WOEST (What is the Optimal antiplatelet and anticoagulant therapy in
patients with oral anticoagulation and coronary StenTing,
clinicaltrials.gov: NCT00769938)
ISAR-TRIPLE (Testing of a six-week versus a six-month clopidogrel
treatment Regimen In Patients with concomitant aspirin and oraL
anticoagulant therapy following drug-Eluting stenting, clinicaltrials.gov:
NCT00776633)
To the Editor: Ryan et al. report on the efficacy of Dual Chamber pacemaker implantation in patients with cardio-inhibitory carotid sinus hypersensitivity (CICSH) and falls in SAFEPACE-2 (Syncope And Falls in the Elderly- Pacing And Carotid sinus Evaluation)[1]. This study had the potential to expand on the findings of SAFEPACE-1 [2] and address some of the weaknesses of the latter with a blinded, multicenter, and less se...
To the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1 The study showed the presence of abnormal longitudinal left ventricular strain in patients with aortic stenosis and concentric left...
We read with great interest the work by Luckie et al., recently published in this Journal. (1) It's known that for patients who suffer from infiltrative, obstructive or bleeding carcinomas, or for high rupture risk aneurismal disease, a prompt surgical procedure may represent “survival”, and that in case of revascularization requirement, currently available options, either bare-metal or drug-eluting stent or plain-old ba...
To the Editor: With great interest I read the article by Byrne et al. assessing antirestenotic efficacy of 3 different rapamycin-eluting stents with different coating strategies (biodegradable polymer, permanent polymer and polymer-free stents) at 2 time points after coronary stenting (6 to 8 months and 2 years) [1]. Although the authors suggested delayed late loss (the difference in in-stent late loss between 6 to 8 mont...
To the Editor: We read with great interest the paper published by S Lavi et al [1] and feel that it is worthy of comment. We admire the foresight and technical expertise that has gone into creating this study, to try and prove a worthy concept. However, we do have an issue regarding the measurement of Necrotic Core in minimal plaques. The authors state that after selecting the appropriate frames "two independent investi...
To the Editor:
We read with interest the comprehensive review article on T2-weighted (T2w) cardiovascular magnetic resonance imaging (CMR) by Edwards, Routledge and Steeds (1). We wish to make one comment for the sake of clarity and also to bring to the reader’s attention important new data, which have become available in the meantime and light up some of the issues raised by the authors. The authors cite one...
Randomised trials in patients on oral anticoagulation undergoing coronary stenting (response to Drs Willem Dewilde and Jurrien m ten Berg)
Dear Sir,
we agree with Dr. Dewilde and Dr. Ten Berg that current recommendations regarding coronary stenting in patients on oral anticoagulation (OAC) are not based on randomised controlled trials (RCT) and congratulate them for addressing this important issue by i...
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