It is with great interest to read a recent article of " Evidence of
the role of short-term exposure to ozone on ischaemic cerebral and cardiac
events: the Dijon Vascular Project (DIVA)" by Henrotin et al.1 They
detailed addressed the analysis procedure and considerations and presented
findings on the relationship of air pollution and ischaemic cerebral and
cardiac events in a large population-based setting. However, a few...
It is with great interest to read a recent article of " Evidence of
the role of short-term exposure to ozone on ischaemic cerebral and cardiac
events: the Dijon Vascular Project (DIVA)" by Henrotin et al.1 They
detailed addressed the analysis procedure and considerations and presented
findings on the relationship of air pollution and ischaemic cerebral and
cardiac events in a large population-based setting. However, a few
methodological considerations need to be further discussed.
The human body is affected by the thermal environment, which is not
only air temperature and rain. A potential environment risk factor is, in
fact, influenced by many different climatic factors such as air
temperature, air humidity, vapor pressure, wind speed, cloud cover,
radiation flux, etc. Thus, meteorological conditions adjusted in the model
may not be appropriate from an epidemiological point of view since the
assumption was based on a significant association between climactic
variables and ischaemic cerebral and cardiac events. Yet, this was not
clearly addressed in the article in firstly evaluating if the association
existed.2 If there is no association, is it still appropriate to "adjust"
meteorological conditions for air pollution assessment? In addition, when
considering meteorological variables, wind speed, cloud cover, radiation
flux, etc also have certain influences on human beings besides air
temperature and humidity. Is it appropriate to ignore in the assessment?
Finally, sex difference examination is recommended since females may be
more sensitive to the environmental change than males.
Given that conflicting results exist worldwide, a suggestion is to
have a physically equivalent temperature (PET) by combining all the
relevant climatic variables to be adjusted when assessing the relationship
of air pollution and cardiovascular disease.3, 4 This may give a more
precise indication close to human experience in exposing to the weather.
No doubt, future studies are needed to firstly confirm the association of
PET and cardiovascular events and then with the effect of air pollution
before clinical practice can be made.
Patients eligible for the TAVI intervention are old (>75), face a
high mortality risk and generally have multiple comorbidities [1]. Health
care consumption of this group of patients can therefore expected to be
high [2,3]. As a consequence, life extension in this group would probably
result in additional health care consumption in so-called life years
gained. Health care consumption in life years gained could be due...
Patients eligible for the TAVI intervention are old (>75), face a
high mortality risk and generally have multiple comorbidities [1]. Health
care consumption of this group of patients can therefore expected to be
high [2,3]. As a consequence, life extension in this group would probably
result in additional health care consumption in so-called life years
gained. Health care consumption in life years gained could be due to
treatment of a large variety of diseases related to old age and/or
consumption of long-term care due to disabilities.
In the article by Watt et al. [4] only a limited set of cost
categories is included, which results in too favourable estimates of the
cost effectiveness of TAVI. Current NICE guidelines do not advocate the
inclusion of medical costs in life years gained of diseases not directly
related to the intervention under study [5]. Ignoring costs that are
relevant for the NHS is difficult to defend using scientific arguments [6-
8]. It also results in favoring interventions that primarily increase
length of life over interventions that mainly improve quality of life [9].
Broadening the perspective beyond the NHS, as Watts et al. suggest, would
probably result in even less favourable cost effectiveness estimates as
the target group of TAVI does not participate in the labour market anymore
and therefore consumes more than they produce [9]. While there may be
uncomfortable implications of including more cost categories that warrant
discussion, this can never be a reason to exclude foreseeable costs.
References
1. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve
implantation for aortic stenosis in patients who cannot undergo surgery.
New Engl J Med 2010; 363: 1597-607
2. Yang Z, Norton EC, Stearns SC.J Gerontol B Psychol Sci Soc Sci.
2003 Jan;58(1):S2-10.Longevity and health care expenditures: the real
reasons older people spend more.
3. Basu A, Arondekar BV, Rathouz PJ.Scale of interest versus scale of
estimation: comparing alternative estimators for the incremental costs of
a comorbidity. Health Econ. 2006 Oct;15(10):1091-107.
4. Watt M, Mealing S, Eaton J, Piazza N, Moat N, Brasseur P, Palmer
S, Busca R, Sculpher M.Cost-effectiveness of transcatheter aortic valve
replacement in patients ineligible for conventional aortic valve
replacement. Heart. 2012 Mar;98(5):370-6. Epub 2011 Nov 10.
5. ISPOR. Pharmacoeconomic Guidelines Around The World. Available at:
http://www.ispor.org/PEguidelines/index.asp. Accessed 08/18, 2011.
6. Rappange DR, van Baal PH, van Exel NJ, Feenstra TL, Rutten FF,
Brouwer WB. Unrelated medical costs in life-years gained: should they be
included in economic evaluations of healthcare interventions?
Pharmacoeconomics 2008;26(10):815-830.
7. Meltzer D. Response to "Future costs and the future of cost-
effectiveness analysis". J.Health Econ. 2008 Jul;27(4):822-825.
8. Feenstra TL, van Baal PH, Gandjour A, Brouwer WB. Future costs in
economic evaluation. A comment on Lee. J.Health Econ. 2008 Dec;27(6):1645-
9; discussion 1650-1.
9. Meltzer D. Accounting for future costs in medical cost-
effectiveness analysis. J.Health Econ. 1997 Feb;16(1):33-64.
It was with interest that we read the featured correspondence from
Rajani et al (ref). We entirely agree with their assertion that there is
a growing need for multi-modality cardiac imagers and acknowledge their
concerns about the lack of structured "in-programme" training
opportunities, such as cardiac imaging fellowships, to support this
requireme...
It was with interest that we read the featured correspondence from
Rajani et al (ref). We entirely agree with their assertion that there is
a growing need for multi-modality cardiac imagers and acknowledge their
concerns about the lack of structured "in-programme" training
opportunities, such as cardiac imaging fellowships, to support this
requirement.
As an initial step, The British Society of Cardiovascular Imaging (BSCI)
has recently followed the lead of the British Society of Cardiovascular
Magnetic Resonance (BSCMR) in producing detailed competency frameworks for
cardiac CT, incorporating competency based assessment tools such as Mini
CEX, DOPS and CbD to support the evolving cardiac imaging curricula
produced by the respective Royal Colleges. This, in conjunction with
other training frameworks, will hopefully allow a structure for more
formalised imaging training in the UK.
As is noted by Rajani et al some deaneries have started delivering
dedicated training in cardiovascular imaging and indeed the BSCI is now
running twice yearly core training days in cardiovascular CT, open to all
trainees and consultants alike as part of the overall cardiac imaging
training run with the Royal Society of Medicine. These conferences are
delivered essentially at cost to recognise and to provide for the growing
requirement for dedicated multi-modality imaging training for radiologists
and cardiologists alike.
As a next step, the BSCI, in conjunction with London STC in cardiology and
head of radiology training in London, have set up six formal, structured,
in-programme fellowships in cardiac CT that are to be launched imminently.
This model has previously been developed and successfully delivered for
CMR colleagues in London and it provides aspirant trainees the opportunity
to gain on-site experience at established centres of excellence. This
hands-on training is supported by a monthly lecture series to cover the
didactic training and knowledge components of the advanced curriculum. At
the core of this endeavour is to provide high quality training in cardiac
imaging within the current constraints of the curriculum, to equip
trainees with the skills required to be able to lead and direct cardiac
imaging services in the future. It is our hope that this model may be
able to be reproduced across other regions and also across the wider remit
of cardiac imaging modalities.
There are however significant hurdles to be overcome. Firstly cardiac
imagers must seek to both work and train collaboratively. They must start
engaging with each other, regardless of chosen specialty, from the outset
and bring their differing skills and approaches to each other to enhance
the service delivered by all. Secondly, there is a clear requirement for
these individual training opportunities to be brought together as true
multi-modality imaging fellowships. Thirdly, if the four main cardiac
imaging societies (BNCS, BSCI, BSCMR and BSE) could sign up to a formal
concordat ensuring joint advertising of training opportunities, running
joint or concurrent meetings and providing a forum to develop advanced
subspecialty "in programme" fellowships, open to all cardiac imagers at
affordable costs, this would be a major step towards making cardiac
imaging training more robust and comprehensive. Very few cardiac imagers
practice in isolation from other cardiac imaging modalities and a broad
understanding of complementary techniques is fundamental to high quality
care. The formation of the British Cardiac Society Imaging Council has
been an important initial step and would seem the obvious vehicle to
facilitate these goals.
Achieving the vision set by Rajani et al will require significant
cooperation by cardiac imagers in the broadest sense. There will no doubt
be significant challenges along the way but by achieving this goal we will
be a stronger community both nationally and internationally but most
importantly locally for our patients.
Acknowledgements:
Dr Ed Nicol is a London cardiology SpR and trainee representative on the
BSCI Executive and Education Committees
Dr Stephen Harden is a consultant cardiac radiologist in Southampton,
chairs the BSCI Education Sub-committee and is a regional training lead in
Radiology
Dr Roger W Bury is a consultant cardiac radiologist in Blackpool and the
President of the BSCI.
The potential cost-effectiveness (CE) of adopting innovative
procedures within a publically funded healthcare system is a recurring
issue.[1] Trans-catheter aortic valve insertion (TAVI) is not currently
provided by the devolved National Health Service (NHS) in Scotland,
although a single high quality randomised controlled clinical trial (RCT)
has demonstrated that TAVI is a clinically effective intervention for
reducin...
The potential cost-effectiveness (CE) of adopting innovative
procedures within a publically funded healthcare system is a recurring
issue.[1] Trans-catheter aortic valve insertion (TAVI) is not currently
provided by the devolved National Health Service (NHS) in Scotland,
although a single high quality randomised controlled clinical trial (RCT)
has demonstrated that TAVI is a clinically effective intervention for
reducing the risk of death in older patients with severe aortic stenosis
considered unfit for standard surgery.[2] The recently published CE
analysis of TAVI reports an incremental CE ratio (ICER) of 16,000 [pounds
sterling] per quality adjusted life year (QALY) gained, which falls below
the ICER thresholds applied by the National Institute for Health and
Clinical Excellence (NICE) in the UK.[1]
The science-consultancy company 'Oxford Outcomes' constructed their
CE model based on New York Heart Association (NYHA) category data obtained
in the original RCT.[2] This involved adopting a rather convoluted
approach of indirectly estimating EQ-5D (EuroQol) values ('utilities')
based on data concerning the relationship between NHYA categories and EQ-
5D in patients with heart failure, and on UK population norms that are now
almost 20 years old.[1] Given that individual patients in the original RCT
had their EQ-5D values measured directly (at baseline, one, six and 12
months) it is not clear why 'Medtronic' (the TAVI-device manufacturer who
funded both the original RCT and the CE analysis) did not release the ED-
5D data to 'Oxford Outcomes'. Other important clinical values are derived
from a 'literature review' and estimates made by a 'clinical steering
group'. Unfortunately making an informed judgement about the validity of
these values is difficult as the literature search strategy is not
described and membership of the 'steering group' is not reported.
Historically the assessment of CE in the cardiovascular arena has
predominantly related to drug therapies, but the approach is now
increasingly being applied to cardiovascular devices.[3] Unfortunately CE
studies, with their heavy reliance on statistical modelling based on
multiple assumptions, have a poor track record of providing unbiased
information for healthcare decision making. In a previous systematic
review of almost 500 CE studies, industry-sponsored studies were 2-3 times
more likely to report favourable results compared to non-industry funded
analyses.[4] This may be because the biomedical industry regards the
undertaking and reporting of CE analyses as a marketing tool, rather than
as an independent scientific endeavour.[3] Consequently clinicians and
policy-makers need to be both cautious and critical in assessing this type
of study. In our opinion a further replication of these CE findings are
required using the EQ-5D data from the original trial.
[1] Watt M, Mealing S, Eaton J, et al. Cost-effectiveness of
transcatheter aortic valve replacement in patients ineligible for
conventional aortic valve replacement. Heart 2012;98:370-6.
[2] Leon MB, Smith CR, Mack M, et al. PARTNER Trial Investigators.
Transcatheter aortic-valve implantation for aortic stenosis in patients
who cannot undergo surgery. N Engl J Med 2010;363:1597-607.
[3] Tarricone R, Drummond M. Challenges in the clinical and economic
evaluation of medical devices: the case of transcatheter aortic valve
implantation. J Med Marketing 2011;11:221-229.
[4] Bell CM, Urbach DR, Ray JG, Bayoumi A, Rosen AB, Greenberg D,
Neumann PJ. Bias in published cost effectiveness studies: systematic
review. BMJ 2006;332:699-703.
To the editor: With great interest we have read the paper on
hypertrophic cardiomyopathy by ten Berg et al.1 As the paper has an
educational aim, we would like to address some minor misconceptions that
could have major implications.
Genotyping in HCM to establish a molecular diagnosis in HCM patients
can indeed probably not be used to guide prognosis or therapy. However, it
has been proven to be a more cost-effe...
To the editor: With great interest we have read the paper on
hypertrophic cardiomyopathy by ten Berg et al.1 As the paper has an
educational aim, we would like to address some minor misconceptions that
could have major implications.
Genotyping in HCM to establish a molecular diagnosis in HCM patients
can indeed probably not be used to guide prognosis or therapy. However, it
has been proven to be a more cost-effective strategy than cardiac
screening to identify relatives at risk.2 This is mainly due to the
inability of ECG and echocardiography to exclude a future risk of HCM -
which is possible by genotyping-, because contrary to what the authors
state hypertrophy in relatives often develops after adolescence. Studies
in HCM mutation carriers have shown that disease penetrance increases with
age and a significant subset of carriers develops hypertrophy well into
adulthood.3 4 Unfortunately the misconception that hypertrophy does not
develop after adolescence is still around leading to inappropriate cardiac
care and sometimes even sudden cardiac death, because relatives are
incorrectly discharged from cardiac follow-up.
The incomplete and age dependent disease penetrance together with the
clinical heterogeneity of the disease also explain why many HCM patients
do not know of any affected relatives. The latter is therefore probably
not due to sporadic mutation and more complex patterns of inheritance as
the authors suggest. With today's knowledge the main causal genetic defect
arises seldom de novo and is usually inherited in an autosomal dominant
way. Individuals without the disease-causing mutation therefore do not
have an increased risk of developing HCM and carriers do. Clinical
heterogeneity and disease penetrance, however, are likely to be influenced
by genetic modifiers, which still need to be identified. Hopefully, future
genetic research in HCM will enable us to better predict the phenotype and
prognosis in the individual HCM patient or carrier of a disease-causing
mutation.
References
1. ten Berg J, Steggerda RC, Siebelink HM. Myocardial disease: the
patient with hypertrophic cardiomyopathy. Heart 2010;96:1764-72.
2. Wordsworth S, Leal J, Blair E, et al. DNA testing for hypertrophic
cardiomyopathy: a cost-effectiveness model. Eur Heart J 2010;31:926-35.
3. Niimura H, Bachinski LL Sangwatanaroj S, et al. Mutations in the
gene for cardiac myosin binding protein C and late-onset familial
hypertrophic cardiomyopathy. N Engl J Med 1998;338:1248-57.
4. Christiaans I, Birnie E, van Langen IM, et al. The yield of risk
stratification for sudden cardiac death in hypertrophic cardiomyopathy
Myosin-Binding Protein C gene mutation carriers: focus on predictive
screening. Eur Heart J 2010;31:842-8.
In their recent editorial in this Journal Theodoraki and Bouloux [1]
question the cut-off values employed in our article on the association
between circulating androgens and mortality risk in heart failure (HF).[2]
While we (according to our local Central Hospital Laboratory) defined
androgen deficiency by total testosterone values <180 ng/dl for
patients >50 years and 260 ng/dl for younger patients, and by free
te...
In their recent editorial in this Journal Theodoraki and Bouloux [1]
question the cut-off values employed in our article on the association
between circulating androgens and mortality risk in heart failure (HF).[2]
While we (according to our local Central Hospital Laboratory) defined
androgen deficiency by total testosterone values <180 ng/dl for
patients >50 years and 260 ng/dl for younger patients, and by free
testosterone values <9 ng/dl, Theodoraki and Bouloux - referencing
Wang et al. [3] - suggest a more liberal and age-independent cut-off value
for total testosterone (<230 ng/dl), but a more restrictive cut-off
level for free testosterone (<6.5 ng/dl). If these alternative cut-off
levels were applied to our data, prevalence of androgen deficiency defined
by total testosterone would hardly be affected (15 instead of 9%), while
it would be markedly reduced if defined by free testosterone (from 79 to
51%). Since we performed all survival analyses using continuous rather
than categorized variables, however, these considerations do not affect
the main finding of our study, namely the lacking association between
androgen levels and mortality risk after adjustment for important
confounders. We agree, however, that reaching a consensus on both
standardized testosterone measurement and definition of (possibly age-
dependent) cut-off values is mandatory in order to establish direct
comparability between studies.
Current guidelines advocate testosterone replacement only in
"symptomatic" patients with repeatedly "low" testosterone levels.[4] HF,
like any chronic illness, profoundly affects sex steroid metabolism, and
better understanding of underlying pathologies is warranted to disentangle
the cause-effect relations in this situation. Theodoraki and Bouloux build
their line of arguments on two small trials on testosterone therapy in
patients with HF, which were considered positive as they improved
patients' symptoms. However, the authors omit to comment on the liberal
inclusion criteria not demanding established testosterone deficiency (in
both studies prevalence of androgen deficiency <30%), and on the very
high drop-out rate in one study. We would conclude that liberal
testosterone therapy in patients with HF is presently not justified since
conclusive evidence of benefit is lacking, pathophysiology is ill
understood, and important safety concerns are unresolved.[4, 5]
1 Theodoraki A, Bouloux PM. Low sex hormones in heart failure.
Heart;96:496-7.
2 Guder G, Frantz S, Bauersachs J, et al. Low circulating androgens
and mortality risk in heart failure. Heart;96:504-9.
3 Wang C, Nieschlag E, Swerdloff R, et al. ISA, ISSAM, EAU, EAA and
ASA recommendations: investigation, treatment and monitoring of late-onset
hypogonadism in males. Int J Impot Res 2009;21:1-8.
4 Bhasin S CG, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS,
Montori VM. Testosterone Therapy in Men with Androgen Deficiency
Syndromes: An Endocrine Society Clinical Practice Guideline. J Clin
Endocrinol Metab 2010;Jun;95(6)::2536-59.
5 Basaria S, Coviello AD, Travison TG, et al. Adverse events
associated with testosterone administration. N Engl J Med;363:109-22.
In their Viewpoint article, Warner et al hypothesized that the
administration of aspirin to patients who are treated with potent
antagonists of the platelet P2Y12 receptors might increase cardiovascular
risk.1 The authors' hypothesis is based on the observation that P2Y12
antagonists inhibit the platelet production of thromboxane A2 (TxA2)
(which would render the use of aspirin superfluous), and on the
consideration tha...
In their Viewpoint article, Warner et al hypothesized that the
administration of aspirin to patients who are treated with potent
antagonists of the platelet P2Y12 receptors might increase cardiovascular
risk.1 The authors' hypothesis is based on the observation that P2Y12
antagonists inhibit the platelet production of thromboxane A2 (TxA2)
(which would render the use of aspirin superfluous), and on the
consideration that aspirin may cause adverse effects. It is my opinion
that there is no evidence yet to suggest that aspirin is superfluous or
even detrimental when administered in combination with P2Y12 antagonists.
In fact, the inhibition of TxA2 production by P2Y12 antagonists in
monotherapy is incomplete and may be insufficient to inhibit the TxA2-
dependent component of thrombus formation. The clinical relevance of
effective TxA2 inhibition is demonstrated by the extremely good efficacy
of aspirin in patients with acute coronary syndromes (ACS),2 which, in my
opinion, was underestimated by Warner et al.1 I think that the real
question is not whether or not aspirin should be associated with P2Y12
antagonists, but, rather, what is the best dose of aspirin to be used in
association. We recently showed that inhibition of the platelet P2Y12
receptor potentiates the anti-platelet effect of prostacyclin and
hypothesized that this effect may substantially contribute to the
antithrombotic efficacy of P2Y12 antagonists.3 Since aspirin, at high
doses, inhibits the endothelial production of prostacyclin, it can be
hypothesized that, the higher the dose of aspirin used in combination with
P2Y12 antagonists, the lower will be the prostacyclin-dependent
antithrombotic activity of P2Y12 antagonists.3 The results of the PLATO
trial, which showed that high-dose aspirin tended to be less effective
than low-dose aspirin in ACS patients treated with the potent P2Y12
antagonist ticagrelor,1 are compatible with our hypothesis and with the
suggestion by Warner et al that high-dose aspirin may be more detrimental
when associated with potent P2Y12 antagonists.1 However, the results of
the CURRENT OASIS-7 trial, which showed that high dose-aspirin was more
effective than low-dose aspirin in combination with high-dose clopidogrel
(but not with standard dose clopidogrel) oppose it.4 Therefore, the issue
of the best dose of aspirin to be associated to P2Y12 antagonists can only
be settled by the results of properly designed experimental studies.
REFERENCES
1. Warner TD, Armstrong PCJ, Curzen NP, Mitchell JA. Dual
antiplatelet therapy in cardiovascular disease: does aspirin increase
clinical risk in the presence of potent P2Y12 receptor antagonists? Heart
2010;96:1693-1694.
2. ISIS-2 (Second International Study of Infarct Survival) Collaborative
Group. Randomised trial of intravenous streptokinase, oral aspirin, both,
or neither among 17,187 cases of suspected acute myocardial infarction:
ISIS-2. Lancet.1988;2:349-60.
3. Cattaneo M, Lecchi A. Inhibition of the platelet P2Y12 receptor for
adenosine diphosphate potentiates the antiplatelet effect of prostacyclin.
J Thromb Haemost. 2007;5:577-82.
4. CURRENT-OASIS 7 Investigators, Mehta SR, Bassand JP, Chrolavicius S,
Diaz R, Eikelboom JW, Fox KA, Granger CB, Jolly S, Joyner CD, Rupprecht
HJ, Widimsky P, Afzal R, Pogue J, Yusuf S. Dose comparisons of clopidogrel
and aspirin in acute coronary syndromes. N Engl J Med. 2010;363:930-42.
Changqing Yang
Guoxin Fan, Xiaolong Qi, Shisheng He,
Tongji Hospital, Tongji University School of Medicine Shanghai China
TO THE EDITOR: We take great interest in the paper (1) by Nijjer et al with regard to instantaneous wave-free ratio (iFR) assessing improvement in coronary haemodynamics after percutaneous coronary intervention (PCI). However, we have some concerns about the invasive, pressure-only index, iFR.
Changqing Yang
Guoxin Fan, Xiaolong Qi, Shisheng He,
Tongji Hospital, Tongji University School of Medicine Shanghai China
TO THE EDITOR: We take great interest in the paper (1) by Nijjer et al with regard to instantaneous wave-free ratio (iFR) assessing improvement in coronary haemodynamics after percutaneous coronary intervention (PCI). However, we have some concerns about the invasive, pressure-only index, iFR.
iFR, a novel resting index without hyperemia, is calculated over five heartbeats as the ratio of distal to proximal coronary pressures during the diastolic. The assumption is that the resistance during a particular part of diastole will be as low as the average resistance during the complete heart cycle in hyperemia and not be influenced by adenosine infusion.2
Nevertheless, assumption is assumption, whilst numerical equation makes sense. Fluid-dynamics equation elucidates that iFR is able to predict the severity of stenosis (e.g. a 70% long LAD stenosis) only when friction is the predominant cause of energy loss within the stenosis.(2) That is to say, a short 50% left main stenosis, in which separation and turbulent flow are responsible for the energy loss, creates a negligible resting gradient with an extremely large hyperemic gradient. In the recent Resolve registry (3), a poor correlation was found between iFR and fractional flow reserve (FFR). Only if iFR was <_0.82 as="in=" _24="of=" the="_1539="_1539"" patients="patients" could="could" hyperemia="hyperemia" be="be" omitted="omitted" to="to" achieve="achieve" a="a" _95="_95" certainty="certainty" making="making" correct="correct" decision="decision" whether="whether" or="or" not="not" revascularize.="revascularize." so="so" our="our" question="question" raised="raised" again="again" is="is" ifr="ifr" equivalent="equivalent" ffr="ffr" _4="_4" it="it" even="even" instantaneously="instantaneously" measured="measured" name="name" suggests="suggests" totally="totally" independent="independent" pharmacological="pharmacological" vasodilatation="vasodilatation" because="because" calculated="calculated" an="an" average="average" value="value" and="and" strongly="strongly" influenced="influenced" by="by" hyperemia.2="hyperemia.2" we="we" really="really" appreciate="appreciate" this="this" prospective="prospective" observational="observational" study="study" applying="applying" assess="assess" improvement="improvement" coronary="coronary" haemodynamics="haemodynamics" after="after" pci.="pci." found="found" that="that" change="change" intervention="intervention" _0.20="_0.20" _0.21="_0.21" was="was" similar="similar" _0.22="_0.22" _0.15="_0.15" p="p" surely="surely" based="based" on="on" data="data" presented="presented" might="might" used="used" objectively="objectively" document="document" following="following" pci="pci" manner="manner" ffr.1="ffr.1" however="however" may="may" have="have" highly="highly" variable="variable" measurement="measurement" clinical="clinical" practice="practice" almost="almost" unachievable="unachievable" create="create" true="true" resting="resting" condition="condition" obscure="obscure" determine="determine" what="what" extent="extent" some="some" present.="present."/>
1 Nijjer SS, et al. Improvement in coronary haemodynamics after percutaneous coronary intervention: Assessment using instantaneous wave- free ratio. Heart. 2013
2. Pijls NH. Fractional flow reserve to guide coronary revascularization. Circ J. 2013; 77: 561-569.
3. A. J. Resolve: A multicenter study to evaluating the diagnostic accuracy of ifr compared to ffr. J Am Coll Cardiol. 2013;
4. Fan GX and Xu YW. Is the instantaneous wave-free ratio equivalent to fractional flow reserve? J Am Coll Cardiol. 2013; 62: 943.
We read with interest the correspondence of Luis Carlos Saiz
regarding our meta-analysis on the effects of antihypertensive treatment
in patients over 65 years of age. The author asserts the INternational
VErapamil SR-Trandolapril STudy (INVEST) trial [1] should not have been
included in the meta-analysis as it did not recruit a predominantly
elderly population.
INVEST enrolled a total of 22,576 patients from 8...
We read with interest the correspondence of Luis Carlos Saiz
regarding our meta-analysis on the effects of antihypertensive treatment
in patients over 65 years of age. The author asserts the INternational
VErapamil SR-Trandolapril STudy (INVEST) trial [1] should not have been
included in the meta-analysis as it did not recruit a predominantly
elderly population.
INVEST enrolled a total of 22,576 patients from 862 sites with the
majority of patients being women (52%) with a mean age of 66 years (in our
analysis one of the inclusion criteria is mean age of 65 years or above).
Approximately one third of patients were older than 70 years and more than
2,000 patients were >85 years old, making this one of the largest
randomized subgroups to be reported among older patients. Therefore, it
was reviewed and included in the ACCF/AHA 2011 expert consensus document
on hypertension in the elderly [2].
Secondary analysis from INVEST trial showed that for patients more
than 70 years old higher systolic blood pressure was associated with less
risk for death, myocardial infarction, or stroke then SBP lower than 130
mmHg [3]. These findings are in accordance with the results of our
sensitivity analysis for patients 70 years old or older, which did not
include the INVEST study. Additionally, the J-curve association between
blood pressure and primary outcomes was similar for those above and below
the age of 65 [4].
We would agree with the author that more data from studies on
exclusively elderly population are required. However, we believe that the
currently available evidence is against author's assertion that the INVEST
trial should have been excluded from the analysis.
References
1. Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al. A calcium
antagonist vs a non-calcium antagonist hypertension treatment strategy for
patients with coronary artery disease. The International Verapamil-
Trandolapril Study (INVEST): a randomized controlled trial. JAMA.
2003;290(21):2805-16.
2. Aronow WS, Fleg JL, Pepine CJ, et al. ACCF/AHA 2011 expert
consensus document on hypertension in the elderly: a report of the
American College of Cardiology Foundation Task Force on Clinical Expert
Consensus Documents. Circulation. 2011;123:2434-2506.
3. Denardo SJ, Gong Y, Nichols WW, et al. Blood pressure and outcomes
in very old hypertensive coronary artery disease patients: an
international verapamil ST-Trandolapril (INVEST) substudy. Am J Med. 18
2010;123:719-26.
4. Messerli FH, Mancia G, Conti CR, et al. Dogma disputed: can
aggressively lowering blood pressure in hypertensive patients with
coronary artery disease be dangerous? Ann Intern Med. 2006;144:884-93.
Versteylen et al (1) recently evaluated several area at risk (AAR)
methods in patients with acute ST elevation myocardial infarction (STEMI)
using 4 physiologic principles, and concluded that cardiac magnetic
resonance imaging (CMRI) methods out-perform angiographic methods, which
are better than electrocardiographic (ECG) methods. However this study
utilized the antiquated Aldrich score, rather than the updated ECG inde...
Versteylen et al (1) recently evaluated several area at risk (AAR)
methods in patients with acute ST elevation myocardial infarction (STEMI)
using 4 physiologic principles, and concluded that cardiac magnetic
resonance imaging (CMRI) methods out-perform angiographic methods, which
are better than electrocardiographic (ECG) methods. However this study
utilized the antiquated Aldrich score, rather than the updated ECG index,
described by Wilkins et al (2).
The Aldrich score is based upon the extent of inferior ST elevation
and total number of leads with ST elevation in anterior infarcts. Recent
studies have shown that it is an unstable marker of AAR (3) and correlates
poorly with SPECT imaging (4). The modified score by Wilkins et al (2),
incorporates the number of leads with abnormal Q waves, ST elevation
and/or peaked T waves in anterior infarcts, and the extent of excess Q
wave duration and inferior ST elevation in inferior infarcts. Compared
with the Aldrich score, this method produced better correlations with QRS-
derived final infarct size (2).
To further evaluate the Wilkins method, we compared Aldrich and
Wilkins AAR estimates in 47 acute STEMI patients who had undergone CMRI
with delayed hyperenhancement, and observed the following, as regards
conformity to the 4 physiologic principles proposed by these authors (1):
1. For the concept that AAR is always ? infarct size (IS), the
Wilkins method conformed in 76% of patients, compared to 59% for the
Aldrich score.
2. In patients with transmural infarcts, Bland-Altman plots showed
better agreement between AAR and IS using the Wilkins method (95% CI -
18.42 to 8.125), compared to Aldrich score (95% CI -18.54 to 15.37).
3. Increasing correlation between AAR size and IS was observed with
increasing infarct transmurality for the Wilkins method but not the
Aldrich score.
4. In the correlation of myocardial salvage and mean transmurality,
78% of patients were within the ?30% margin of the inverse 'line of
identity' using the Wilkins method as compared to 60% for the Aldrich
score.
Accordingly, compared with its antecedent ECG index, the Wilkins
method better fulfils the principles outlined by Versteylen et al, perhaps
to degree equivalent to angiographic AAR methods.
References:
1. Versteylen MO, Bekkers SC, Smulders MW, et al. Performance of
angiographic, electrocardiographic and MRI methods to assess the area at
risk in acute myocardial infarction. Heart 2012;98:109-15.
2. Wilkins ML, Maynard C, Annex BH, et al. Admission prediction of
expected final myocardial infarct size using weighted ST-segment, Q wave,
and T wave measurements. J Electrocardiol 1997;30:1-7.
3. Bouwmeester S, van Hellemond IE, Maynard C, et al. The stability of the
ST segment estimation of myocardial area at risk between the prehospital
and hospital electrocardiograms in patients with ST elevation myocardial
infarction. J Electrocardiol 2011;44:363-9.
4. Christian TF, Gibbons RJ, Clements IP, Berger PB, Selvester RH, Wagner
GS. Estimates of myocardium at risk and collateral flow in acute
myocardial infarction using electrocardiographic indexes with comparison
to radionuclide and angiographic measures. J Am Coll Cardiol 1995;26:388-
93.
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Sir,
Cardiac imaging training in the United Kingdom
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Versteylen et al (1) recently evaluated several area at risk (AAR) methods in patients with acute ST elevation myocardial infarction (STEMI) using 4 physiologic principles, and concluded that cardiac magnetic resonance imaging (CMRI) methods out-perform angiographic methods, which are better than electrocardiographic (ECG) methods. However this study utilized the antiquated Aldrich score, rather than the updated ECG inde...
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