We agree with Dr Al-Mohammad that the classification into the two
study groups (non-reperfusion and reperfusion, respectively) carries some
risk for mis-classification. Nevertheless, grouping done in the present
study was based on cautious evaluation of different clinical and
angiographic parameters as best as possible.[1]
Another point mentioned by Dr Al-Mohammad is the interpretation of
the...
We agree with Dr Al-Mohammad that the classification into the two
study groups (non-reperfusion and reperfusion, respectively) carries some
risk for mis-classification. Nevertheless, grouping done in the present
study was based on cautious evaluation of different clinical and
angiographic parameters as best as possible.[1]
Another point mentioned by Dr Al-Mohammad is the interpretation of
the thallium SPECT images.
Although PET FDG remains the gold standard for the assessment of myocardial viability, SPECT imaging using either thallium or technetium labelled tracers (such as sestamibi) has achieved greater attention for routine use due to lower cost and greater availability. To estimate
myocardial infarct size, in the present study we performed SPECT thallium
imaging >30 minutes after tracer injection at rest with the patients
under full antianginal medication.[2] Dr Al-Mohammad suggests
alternative protocols, such as (72 hours) delayed imaging or thallium re-
injection.
Delayed thallium imaging, especially 72 hours after tracer injection
at rest, is hampered by low myocardial count rates and, thus, poor image
quality. This physical limitation outweighs the potential theoretical
benefits of later imaging.
Thallium re-injection represents today's optimal protocol for
combined assessment of stress induced ischaemia and myocardial viability
with thallium[3]: After "conventional" stress-redistribution imaging
(with tracer injection during stress followed by acquisition of stress and
3-4 hours delayed redistribution images), a third set of images is
performed after re-injection of thallium at rest. These "re-injection
images" significantly improve the diagnostic reliability of viability
assessment, as documented by clinicopathologic studies.[4] Thallium rest
re-injection after rest imaging, however, should not provide any
additional information on myocardial viability.
Thomas J Dengler Hugo A Katus
Department of Cardiology
University of Heidelberg
Heidelberg, Germany
References
(1) Licka M, Zimmermann R, Zehelein J, Dengler TJ, Katus HA , Kübler
W. Troponin T concentrations 72 hours after myocardial infarction as a
serological estimate of infarct size. Heart 2002;87:520-524
(2) Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM,
Grunwald MA, Levy D, Lytle BW, O'Rourke RA, Schafer WP, Williams SV.
ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic
stable angina: executive summary and recommendations. A Report of the
American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on Management of Patients with Chronic
Stable Angina). Circulation 1999;99:2829-2848
(3) Dilsizian V, Rocco T P, Freedman N M, Leon M B, Bonow R O. Enhanced
detection of ischemic but viable myocardium by the reinjection of thallium
after stress-redistribution imaging. N Engl J Med 1990;323:141-6.
(4) Zimmermann R, Mall G, Rauch B, Zimmer G, Gabel M, Zehelein J, Bubeck
B, Tillmanns H, Hagl S, Kübler W. Residual thallium-201 activity in
irreversible defects as marker of myocardial viability.
Clinicopathological study.Circulation 1995;91: 1016-1021.
I read with interest the study by Licka et al. published in a recent
issue of Heart.[1] The authors classified 37 consecutive patients with
acute myocardial infarction (AMI) into two groups, according to the
results of "induced" re-canalisation. Such classification is not always
correct when it relies on delayed angiography in the patients treated
either conservatively or with a thrombolytic...
I read with interest the study by Licka et al. published in a recent
issue of Heart.[1] The authors classified 37 consecutive patients with
acute myocardial infarction (AMI) into two groups, according to the
results of "induced" re-canalisation. Such classification is not always
correct when it relies on delayed angiography in the patients treated
either conservatively or with a thrombolytic agent. Both re-occlusion of
initially re-canalised arteries,[2,3] and spontaneous re-canalisation of
initially occluded arteries,[4,5] are well recognised phenomena. Those two
possibilities could lead to misclassification.
The second and more important problem is the interpretation of the
resting thallium SPECT perfusion defects following AMI. The authors
suggested these defects reflect the infarct size.[1] Thallium, however, is
known to re-distribute into an initial defect, when the supplying vessel
is tightly stenosed. Re-distribution suggests the presence of reversible
ischaemia, and not just an infarct.[6,7]
Even if delayed imaging was undertaken, the defects may still over-
estimate the scar size.[8] This can be overcome by either obtaining an
even later image (up to 72 hours); or by adding a second smaller thallium
dose (re-injection) to the imaging protocol to increase the thallium
available for uptake.[9]
Therefore, a perfusion defect on the resting thallium images could
potentially reflect: a transmural scar, a non-transmural scar, viable
hypoperfused myocardium and viable stunned myocardium.
Finally, another way of positively identifying the scarred part
within a perfusion defect in the early phase following a myocardial
infarction is to combine the resting thallium scan with simultaneous
imaging with an infarct avid tracer, such as antimyosin.(10)
The above points do not however deny the importance of the study by
Licka et al.[1] In particular their demonstration of two patterns of the
bi-phasic troponin T release; and the "potential" absence of an effect of
re-perfusion on the height of the enzyme peak.
Dr. A. Al-Mohammad, MD, MRCP
Consultant Cardiologist
References
(1) Licka M, Zimmermann R, Zehelein J, Dengler T J, Katus H A, Kubler
W. Troponin T concentrations 72 hours after myocardial infarction as a
serological estimate of infarct size. Heart 2002;87:520-524.
(2) Johnson TL, Topol EJ. Early, complete infart vessel patency:
Arriving at a gold standard for future clinical investigation in
myocardial reperfusion. Journal of Thrombosis & Thrombolysis
1997;4(2):259-266.
(3) Hackett D, Andreotti F, Haider AW, Brunelli C, Shahi M, Fussell A, et al. Effectiveness and safety of a single intravenous bolus injection of
tissue-type plasminogen activator in acute myocardial infarction. Am J of
Cardiol 1992;69(17):1393-1398.
(4) Munkvad S, Gram J, Jespersen J, Grande P. Reduction of infarct
size estimated enzymatically in patients with acute myocardial infarction
after treatment with recombinant tissue-type plasminogen activator or
after spontaneous coronary recanalisation: A randomised, placebo-
controlled study. Fibrinolysis 1990;4(2):95-99.
(5) Timmis AD, Griffin B, Crick JCP, Nelson DJ, Sowton E. The effects
of early coronary patency on the evolution of myocardial infarction: A
prospective arteriographic study. Br Heart J 1987;58(4):345-351.
(6) Liu P, Kiess M C, Okada R D, Block P C, Strauss H W, Pohost G M,
et al. The persistent defect on exercise thallium imaging and its fate
after myocardial revascularization: Does it represent scar or ischemia? Am
Heart J 1985;110:996-1001.
(7) Cloninger K G, DePuey E G, Garcia E V, Roubin G S, Robbins W L,
Nody A, et al. Incomplete re-distribution in delayed thallium-201 single
photon emission computed tomographic (SPECT) images: An overestimation of
myocardial scarring. J Am Coll Cardiol 1988;12:955-63.
(8) Yang L D, Berman D S, Kiat H, Ressen K J, Friedman J D, Rozanski A et al. The frequency of late reversibility in SPECT thallium-201 stress
redistribution studies. J Am Coll Cardiol 1989;15:334-40.
(9) Dilsizian V, Rocco T P, Freedman N M, Leon M B, Bonow R O.
Enhanced detection of ischemic but viable myocardium by the reinjection of
thallium after stress-redistribution imaging. N Engl J Med 1990;323:141-6.
(10) Khaw B A, Yasuda T, Gold H K, Leinbach R C, Johns J A, Kanke M,
et al. Acute myocardial infarct imaging with indium-111-labeled monoclonal
antimyosin Fab. J Nucl Med 1987;28:1671-8.
Aortic aneurysms in children are occurring extremely infrequently.
Most wellknown is maybe the annulo-aortic ectasia, often associated with
Marfan's Syndrome. In the described patient Marfan's syndrome or other
associated connective tissue disorders have been excluded. Genetic
investigation of the patient have not been indicative of eventual yet
unrecognized connective tissue disorders.
Aortic aneurysms in children are occurring extremely infrequently.
Most wellknown is maybe the annulo-aortic ectasia, often associated with
Marfan's Syndrome. In the described patient Marfan's syndrome or other
associated connective tissue disorders have been excluded. Genetic
investigation of the patient have not been indicative of eventual yet
unrecognized connective tissue disorders.
Degenerative aneurysm forming are predominantly located in the
descending aorta, but in the patholigic tissue evaluation no evidence of
the presence of either atheromatous canges or deficiencies of smooth
cells, elastin or collagen have been encounterd.
Rheumatic disease and pre-existing syphylitic exposure have been
excluded. Patients previous history reports a mild hypertension, not
requiring pharmacotherapeutic intervention. Patient was an avid trampolin
jumper, but in absence of a clearcut traumic incident. The day before
admission patient had a near fall during ice-skating.
Associated cardiac abnormalities have been excluded, the aortic valve
was not bicuspid and functioned well on surgical inspection, although
secondary aortic insufficiency was present and required in a later state
aortic valve replacement.
The most likely cause might be chronic traumatic transection with a
periaortic hematoma in communication with the ascending aorta.
The follow-up of the patient has been complicated by a gradual
distension of the residual original aortic tissue. This required complete
replacement of the aortic arch, aortic valve and re-implantation of the
carotid arteries. The patiernt is on anti-hypertensive medication and uses
anti-coagulative therapy.
The prognosis of the patient is questionable despite the excellent
surgical result. Re-occurrence of the distention and extension into the
descending aorta carries the additional risk of paraplegia and renal
dysfunction.
Non-inflammatory and non-traumatic aneurysms in children in the first
decade of life are most infrequent and it was therefore important that
connective tissue disorders, congenital heart disease and hypertension
were excluded in the case reported by Noordzij et al.[1] For these images
in cardiology to be of educational value, it is important that all
essential features should be considered. A...
Non-inflammatory and non-traumatic aneurysms in children in the first
decade of life are most infrequent and it was therefore important that
connective tissue disorders, congenital heart disease and hypertension
were excluded in the case reported by Noordzij et al.[1] For these images
in cardiology to be of educational value, it is important that all
essential features should be considered. A further possibility is that
the aneurysm could have been associated with severe aortic valve disease
(stenosis, incompetence or severe sclerosis) such as to produce a murmur
and thrill. These signs could have been masked by the poor cardiac state
of the child with hypertension, extensive mural thrombosis and the large
mediastinal haematoma. On surgical replacement of the ascending aorta
with prosthesis, it is surprising the aortic valve was not inspected.
Although rheumatic and syphilitic aortic stenoses usually occur in older
subjects, a sclerotic or an incompetent aortic valve or a small
ventricular septal defect could produce such a lesion.[2,3] Another
possibility is the presence of an as yet unrecognized connective tissue
disorder.
The cervical segments of the internal carotid and vertebral arteries
are usually not referred to as cerebral vessels. To do so is misleading
especially to the young.
References
(1) Noordzij M, Hanlo-Ploeger E, Meijboom EJ. Ruptured thoracic aneurysm in
a 10 year old boy. Heart 2002;87:404.
The 'Viewpoint' presented by Harrison and Mayet [1] reiterates long-
established observations on the difficulties in arranging elective DC
cardioversion based on the need for a CCU bed and several different team
members to be in the same place at the same time as a suitably prepared
(fasted, appropriately anticoagulated and stable) patient.
The practice of arranging 'elective' admission to CCU i...
The 'Viewpoint' presented by Harrison and Mayet [1] reiterates long-
established observations on the difficulties in arranging elective DC
cardioversion based on the need for a CCU bed and several different team
members to be in the same place at the same time as a suitably prepared
(fasted, appropriately anticoagulated and stable) patient.
The practice of arranging 'elective' admission to CCU in the face of
growing emergency admission rates to this specialist resource remains -
anecdote would have it - widespread yet serves patients particularly
poorly. A small series reported from York [2] in the late 1990s suggested
that redesigning the system was safe and effective provided the
appropriate protocols and safeguards were in place. Patients certainly
fared better with less cancellations, less waiting around for a CCU bed to
become available only to have an emergency admission remove the
anaesthetist from availability etc. The cardioversion procedure itself was
undertaken by a senior CCU nurse and the only doctor required to be
present was the anaesthetist (although the medical juniors could attend as
available for teaching and to gain experience). With a regular
'cardioversion slot' timetabled weekly, the anaesthetist and
'cardioversion nurse', together with staff on the elective (day case) ward
to which patients were admitted and the procedure performed, were able to
timetable their activities to ensure that the procedures took place as
planned. The experience of all concerned - patients and hospital personnel
- was improved, with waiting times significantly reduced.
A further benefit of the redesigned service was the introduction of
information materials for patients and family members prior to the
procedure, alongside improvements in anticoagulation management and
preparation (bloods, consent etc) on the day of the procedure.
Elective cardioversion rarely requires a cardiologist to be present
(in the majority of cases the 'operator' is a CCU nurse, under the
'supervision' of a middle grade often much less experienced in the
procedure. The York paper [2] discusses the competencies required to
safely perform cardioversion, adapted from published guidelines of the
ACC/AHA.
References
(1) Harrison SJ, Mayet J Physician administered sedation for DC
cardioversion. Heart 2002;88:117-118.
(2) Quinn T Early experience of nurse-led elective DC cardioversion. Nursing in Critical Care 1998;3:59-62.
I wish the current editor of Heart would heed the pledge made eight years ago by his predecessor that "authors and speakers must spell out all acronyms at the first mention".[1] The authors of the above article defined all the abbreviations and acronyms except the most important one - PREVENIR!
The exponential growth of acronyms of cardiologic trials should be resisted.[2] But the resistance...
I wish the current editor of Heart would heed the pledge made eight years ago by his predecessor that "authors and speakers must spell out all acronyms at the first mention".[1] The authors of the above article defined all the abbreviations and acronyms except the most important one - PREVENIR!
The exponential growth of acronyms of cardiologic trials should be resisted.[2] But the resistance has met little success; the number of trial acronyms has exploded from 245 in 1992 [3] to over 3600 in 2002,[4] a 15-fold increase in a decade. Authors and editors should be reminded that few readers are allowed the luxury of reading a whole article in a modern cardiology journal without the frequent and disruptive interruption caused by unexplained acronyms.[5]
Burchell said in 1985: "I shall not be the cavalier accoucheur of an acronym or the uncritical promoter of a new one".[6] If we have to invent a new acronym, let us at least explain it at the first mention.
Tsung O. Cheng, MD
Professor of Medicine
George Washington University
Washington, DC, USA
References
(1) Cheng TO (and Editor's Note). Acronym aggravation. Br Heart J 1994;71:107-109.
(2) Cheng TO: Acronymophilia: The exponential growth of the use of acronyms should be resisted. Br Med J1994;309:683-684.
(3) Cheng TO. Acronyms of major cardiologic trials. Am J Cardiol 1992;70:1512-1514.
(4) Cheng TO, Julian D. Acronyms of cardiologic trials - 2002. Int J Cardiol, in press.
(5) Cheng TO. Acronymania, acronymophilia and acronymophobia. Br J Cardiol 1998;5:624-625.
(6) Burchell HB. Thoughts on eponyms. Int J Cardiol 1985;8:229-234.
Harding, Boon and Flapan review the role of antiplatelet agents in
patients with non-ST elevation acute coronary syndrome.[1] Whilst their
strategy for using glycoprotein (GP) IIb/IIIa antagonists is supported by
abundant clinical trial data, their recommendations regarding clopidogrel
are based on the results of a single randomised study [2] and therefore
lack authority. We would suggest, on the b...
Harding, Boon and Flapan review the role of antiplatelet agents in
patients with non-ST elevation acute coronary syndrome.[1] Whilst their
strategy for using glycoprotein (GP) IIb/IIIa antagonists is supported by
abundant clinical trial data, their recommendations regarding clopidogrel
are based on the results of a single randomised study [2] and therefore
lack authority. We would suggest, on the basis of our own interpretation
of the CURE data, that the role of clopidogrel in treating patients with
acute coronary syndrome remains unclear, and question the validity of
making firm recommendations on the basis of limited trial evidence.
Although the CURE study reported a highly significant reduction in
the composite primary end-point after nine months follow-up (relative risk
(RR) 0.80; p<_0.001 this="this" was="was" largely="largely" due="due" to="to" a="a" _23="_23" _="_" relative="relative" reduction="reduction" in="in" myocardial="myocardial" infarction="infarction" with="with" no="no" significant="significant" death="death" or="or" stroke.="stroke." from="from" the="the" clinicians="clinicians" perspective="perspective" absolute="absolute" appears="appears" less="less" impressive.="impressive." thus="thus" treating="treating" _100="_100" patients="patients" clopidogrel="clopidogrel" for="for" _9="_9" months="months" would="would" prevent="prevent" approximately="approximately" _1.5="_1.5" non-fatal="non-fatal" infarctions="infarctions" mi="mi" at="at" cost="cost" of="of" _2.5="_2.5" minor="minor" and="and" _1="_1" major="major" bleeding="bleeding" complications="complications" _5="_5" sustain="sustain" an="an" despite="despite" treatment.="treatment." whilst="whilst" recognising="recognising" limitations="limitations" subgroup="subgroup" analysis="analysis" number="number" observations="observations" are="are" worthy="worthy" comment.="comment." first="first" categorised="categorised" as="as" high="high" risk="risk" appear="appear" benefit="benefit" than="than" those="those" low="low" intermediate="intermediate" risk.="risk." second="second" associated="associated" most="most" striking="striking" history="history" previous="previous" revascularisation.="revascularisation." majority="majority" whom="whom" there="there" revascularisation="revascularisation" _82="_82" study="study" population="population" treatment="treatment" terms="terms" primary="primary" end-point="end-point" relatively="relatively" modest="modest" rr="rr" _0.9.="_0.9." p="p"/> In PCI Cure [3] the event rate (cardiovascular death, MI, or repeat
revascularisation) 30 days after percutaneous coronary intervention (PCI)
was reduced from 6.4 % in the placebo group to 4.5 % in the treatment group
but confidence intervals for relative risk were wide (RR 0.7, 95 % CI 0.50
-0.97; p= 0.03). Furthermore the restricted use of GP IIb/IIIa
antagonists, in a study where 80% of patients received an intracoronary
stent, limits the applicability of these results to current clinical
practice where these agents are used routinely as adjunct therapy during
urgent coronary intervention.
Although the early event rate during the time preceding PCI was lower
in the clopidogrel arm of the study, this was largely due to a reduction
in refractory ischaemia and the absolute reduction in MI was just 1.5 % (RR
0.68, 95 % CI: 0.47-0.99; p0.04). This early treatment benefit should be
interpreted in the context of a relatively long delay from initial
presentation to PCI (median 10 days in PCI CURE) and timely intervention
may be the most effective strategy for reducing early ischaemic events.
In summary, it may be premature to recommend the routine use of
clopidogrel in addition to aspirin for the treatment of patients with
acute coronary syndrome. Cost effectiveness [4] and the potential for
bleeding complications may weigh against its modest efficacy in an area
where aspirin and GP IIb/IIIa antagonists are already firmly established
therapies.
efernecs
(1) Harding SA, Boon NA, Flapan AD. Antiplatelet treatment in
unstable angina: aspirin, clopidogrel, glycoprotein IIb/IIIa antagonist,
or all three? Heart 2002;88: 11-14.
(2) The CURE investigators. Effects of clopidogrel in addition to
aspirin in patients with acute coronary syndromes without ST segment
elevation. N Engl J Med 2001;345: 494-502.
(3) Metha SR, Yusuf S, Peters RJG et al. Effects of pre-treatment
with clopidogrel and aspirin followed by long-term therapy in patients
undergoing percutaneous coronary intervention. Lancet 2001; 358: 527-33
(4) Gaspoz J-M, Coxson PG, Goldman PA et al. Cost effectiveness of
aspirin, clopidogrel, or both for secondary prevention of coronary heart
disease. N Engl J Med 2002; 346: 1800-6.
We thank Professor Underwood for his erudite and pertinent comments.
We agree totally with his final comment, but is the situation truly
unbroken? Surely the question to be debated is whether the next generation
of doctors should have to struggle, as did the current one, with a system
of nomenclature that Professor Underwood agrees is illogical? At least the
anatomists, who instigated the current dilemma,...
We thank Professor Underwood for his erudite and pertinent comments.
We agree totally with his final comment, but is the situation truly
unbroken? Surely the question to be debated is whether the next generation
of doctors should have to struggle, as did the current one, with a system
of nomenclature that Professor Underwood agrees is illogical? At least the
anatomists, who instigated the current dilemma, had an excuse, since they
removed the heart before re-orientating it, and then describing it in the
"valentine" position. Those involved with tomographic imaging have no such
excuse, since they see the heart in the context of the body. The crucial
point made by Professor Underwood, with which we agree completely, is that
"posterior" has been abused for far too long to be reincarnated in its
attitudinally correct form. We accept his criticism that it was
inappropriate of us to use this adjective to describe that part of the
left ventricle closest to the spine, even though it is truly posterior!
His alternatives, or "parietal", would all be preferable. He accepts our
suggestion for describing the diaphragmatic surface of the heart as being
inferior, and this adjective is also used in the statement from the
American Heart Association [1] to which he drew our attention. Presumably,
Professor Underwood agrees with us that the artery irrigating this part of
the heart is best described as being inferior and interventricular, rather
than posterior and descending? Although the American statement uses the
term "inferior" in appropriate fashion, sadly it falls from grace when
using "anterior". According to the American statement, "anterior" is
opposite to "inferior", which is manifestly not the case. The appropriate
adjective for the quadrant of left ventricle closest to the head is
"superior". Thus, although the American statement avoids inappropriate use
of "posterior", it falls from grace in its attitudinally inappropriate use
of "anterior". If Professor Underwood, and all those who accept the use of
logical names, join us in our quest for improvement, then perhaps our
American cousins can be persuaded to engage in further constructive
dialogue, and to remove the remaining illogical aspects of their proposed
terminology, as proved possible with the nomenclature previously used by
electrophysiologists.[2]
References
(1) American Heart Association Writing Group on Myocardial
Segmentation and Registration for Cardiac Imaging. Standardized Myocardial
Segmentation and Nomenclature for Tomographic Imaging of the Heart.
Circulation 2002;105:539-47
(2) Cosio FC, Anderson RH, Kuck K, et al. Living anatomy of the
atrioventricular junctions. A guide to electrophysiological mapping. A
consensus statement from the Cardiac Nomenclature Study Group, Working
Group of Arrhythmias, European Society of Cardiology, and the Task Force
on Nomenclature from NASPE.
Circulation 1999;100:e31-7.
Professor Dargie's closely argued Editorial is to be welcomed in
advising caution in accepting the recommendations of the Consensus
Document which offers a redefinition of myocardial infarction.[1] I
strongly support his recommendation that we should continue to use the
present way until more robust evidence supports change. There should be no
problem with the use of troponins as one part of the risk stra...
Professor Dargie's closely argued Editorial is to be welcomed in
advising caution in accepting the recommendations of the Consensus
Document which offers a redefinition of myocardial infarction.[1] I
strongly support his recommendation that we should continue to use the
present way until more robust evidence supports change. There should be no
problem with the use of troponins as one part of the risk stratification
of patients with acute coronary ischaemia, but there is a substantial
problem with the label of myocardial infarction for anyone who, in
appropriate clincial circumstances, has an elevated troponin. Even the
consensus document is less than plausible on this point; ’this change in
the definition of MI seems reasonable, because it has been definitively
shown that any amount of cardiac damage, as detected by cardiac troponins,
implies a worsened long-term outcome for the patient.’ An unarguable case
for troponins, but a poor justification for the new label. We cannot
ignore the impact of this label for our patients.
The response in this country, from the evidence of the MINAP database (on
file), using data from the last six months of 2001, has been very
cautious. Of more than 5000 patients having a final diagnosis of definite
infarction, and for whom markers and cardiac enzymes were reported, this
diagnosis was supported by a troponin estimation alone in 14.6 %, both
troponin and creatine kinase in 10.5 %, and by creatine kinase alone in
74.8 %. Where troponin was used the large majority (> 90 %) had a
troponin value of > 20 microgram/L, and by contrast virtually none had
a diagnosis based on the consensus recommendation. Clearly this has not
yet found favour with clinicians.
Professor Dargie's plea for standardisation of troponin assays should not
be ignored, and some acceptance of the reality that change will be slow is
important. A more realistic cut off beyond which the label of myocardial
infarction might be applied will please the pragmatists more that the
purists, but would be welcomed by clinicians. A value of 100 times the
minimum detectable concentration( MDC) might be considered; it has no less
validity than the present cut off point of ten times the MDC used
empirically by some colleagues.
J S Birkhead
Clinical Lead
MINAP
Clinical Effectiveness and Evaluation Unit
Royal College of Physicians
London
Reference
(1) Myocardial infarction redefined - A consensus document of The Joint
European Society of Cardiology/American College of Cardiology Committee
for the Redefinition of Myocardial Infarction. European Heart Journal
2000;21:1502-13.
Dr Cook and Professor Anderson are to be congratulated for pointing
out the illogicality of commonly used nomenclature of the heart in general
and myocardial segments in particular.[1] In the imaging community it
has been clear for some time that the terms used are illogical but we
continue to use them because of the difficulty for any small group of
individuals to effect change, and because of the absenc...
Dr Cook and Professor Anderson are to be congratulated for pointing
out the illogicality of commonly used nomenclature of the heart in general
and myocardial segments in particular.[1] In the imaging community it
has been clear for some time that the terms used are illogical but we
continue to use them because of the difficulty for any small group of
individuals to effect change, and because of the absence of a credible
alternative. It is unfortunate that the American Heart Association did
not take the opportunity to consider this issue in their recent scientific
statement on standardization of myocardial segmentation and nomenclature
for tomographic imaging of the heart.[2]
On a point of information, the term 'inferior' is in widespread use
for the diaphragmatic surface of the heart and the term 'posterior' is
mainly used by echocardiographers or to refer to a certain pattern of
infarction on the ECG. There is not, however, uniform agreement on the
location of the posterior surface of the heart and hence most imagers
refer to 'basal inferior' instead. The term 'posterior' is not included
in the AHA statement.[2]
However, if we are to be more logical then we need a credible
alternative for naming myocardial segments or walls. Cook and Anderson
suggest in their figure 9 that the terms 'septal', 'aortic', 'posterior',
and 'diaphragmatic' should be used. Unfortunately, this proposal has its
limitations because the posterior and diaphragmatic walls may or may not
be correctly described, depending upon the orientation of the heart within
the chest. A more robust system would be independent of cardiac
orientation. In addition, 'posterior' has been abused for too long for it
to be reincarnated in its attitudinally correct form. Perhaps 'lateral'
could be replaced with 'free' but I can think of no better suggestion for
the inferior or diaphragmatic surface.
Therefore, until we have a better proposal we shall need to continue
with our current, if attitudinally incorrect, system. Certainly, it does
not normally lead to any confusion in communication. In the words of many
an engineer, 'if it ain’t broke, don’t fix it'.
References
(1) Cook A C, Anderson R H. Attitudinally correct nomenclature.
Heart 2002;87:503-6.
(2) Cerqueira MD, Weissman NJ, Dilsizian V et al., Standardised
Myocardial Segmentation and Nomenclature for Tomographic Imaging of the
Heart. Circulation 2002;105:539-42.
Dear Editor
We agree with Dr Al-Mohammad that the classification into the two study groups (non-reperfusion and reperfusion, respectively) carries some risk for mis-classification. Nevertheless, grouping done in the present study was based on cautious evaluation of different clinical and angiographic parameters as best as possible.[1]
Another point mentioned by Dr Al-Mohammad is the interpretation of the...
Dear Editor
I read with interest the study by Licka et al. published in a recent issue of Heart.[1] The authors classified 37 consecutive patients with acute myocardial infarction (AMI) into two groups, according to the results of "induced" re-canalisation. Such classification is not always correct when it relies on delayed angiography in the patients treated either conservatively or with a thrombolytic...
Dear Editor
Aortic aneurysms in children are occurring extremely infrequently. Most wellknown is maybe the annulo-aortic ectasia, often associated with Marfan's Syndrome. In the described patient Marfan's syndrome or other associated connective tissue disorders have been excluded. Genetic investigation of the patient have not been indicative of eventual yet unrecognized connective tissue disorders.
Degene...
Dear Editor
Non-inflammatory and non-traumatic aneurysms in children in the first decade of life are most infrequent and it was therefore important that connective tissue disorders, congenital heart disease and hypertension were excluded in the case reported by Noordzij et al.[1] For these images in cardiology to be of educational value, it is important that all essential features should be considered. A...
Dear Editor
The 'Viewpoint' presented by Harrison and Mayet [1] reiterates long- established observations on the difficulties in arranging elective DC cardioversion based on the need for a CCU bed and several different team members to be in the same place at the same time as a suitably prepared (fasted, appropriately anticoagulated and stable) patient.
The practice of arranging 'elective' admission to CCU i...
Dear Editor
I wish the current editor of Heart would heed the pledge made eight years ago by his predecessor that "authors and speakers must spell out all acronyms at the first mention".[1] The authors of the above article defined all the abbreviations and acronyms except the most important one - PREVENIR!
The exponential growth of acronyms of cardiologic trials should be resisted.[2] But the resistance...
Dear Editor
Harding, Boon and Flapan review the role of antiplatelet agents in patients with non-ST elevation acute coronary syndrome.[1] Whilst their strategy for using glycoprotein (GP) IIb/IIIa antagonists is supported by abundant clinical trial data, their recommendations regarding clopidogrel are based on the results of a single randomised study [2] and therefore lack authority. We would suggest, on the b...
Dear Editor
We thank Professor Underwood for his erudite and pertinent comments. We agree totally with his final comment, but is the situation truly unbroken? Surely the question to be debated is whether the next generation of doctors should have to struggle, as did the current one, with a system of nomenclature that Professor Underwood agrees is illogical? At least the anatomists, who instigated the current dilemma,...
Dear Editor
Professor Dargie's closely argued Editorial is to be welcomed in advising caution in accepting the recommendations of the Consensus Document which offers a redefinition of myocardial infarction.[1] I strongly support his recommendation that we should continue to use the present way until more robust evidence supports change. There should be no problem with the use of troponins as one part of the risk stra...
Dear Editor
Dr Cook and Professor Anderson are to be congratulated for pointing out the illogicality of commonly used nomenclature of the heart in general and myocardial segments in particular.[1] In the imaging community it has been clear for some time that the terms used are illogical but we continue to use them because of the difficulty for any small group of individuals to effect change, and because of the absenc...
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