The case described by Blommaert et al makes
interesting reading. Inadvertent left ventricular (LV) pacing following
attempted placement of a lead in the right ventricle (RV) is a known
occurrence. It is vital to recognise the problem to institute appropriate therapeutic
measures, realising however that often right bundle branch block (RBBB)
pattern results from normal RV pacing. It would however be in...
The case described by Blommaert et al makes
interesting reading. Inadvertent left ventricular (LV) pacing following
attempted placement of a lead in the right ventricle (RV) is a known
occurrence. It is vital to recognise the problem to institute appropriate therapeutic
measures, realising however that often right bundle branch block (RBBB)
pattern results from normal RV pacing. It would however be interesting to
point out the following points, if only for a purely academic exercise.
First, it is obviously important in such cases to study the 12 lead ECG
as it is known that even normal RV pacing can lead to right bundle branch
block (RBBB) patterns on the ECG, which can often be corrected by
placement of leads V1 and V2 1 interspace lower than normal. The FRONTAL QRS AXIS and the PRECORDIAL transition are important determinators of the
site of the lead.[1]
Thus, a frontal QRS axis from 0 to -90 and a precordial QRS tansition
by lead V3 points to a lead which is still sited in the RV septum/apex
pacing with a positive predictive accuracy of 95%, often necessitating no
further intervention. If however, the QRS tansition is after V4, it is
more likely to be in the posterior LV or a coronary vein.
A frontal QRS axis from -90 to -180 localises the lead to the LV in
practically all cases. A precordial transition by V3 results from a pacing
site in the distal anterior LV or the LV apex. A precordial transition
after V3 results from pacing lead in the inferior LV.
A frontal QRS axis from 90 to 180 results from pacing in the
anterior/anterolateral LV.
Second, a 12 lead ECG and a frontal and lateral x ray (or fluoroscopic
position of the lead post implant) are vital for early detection of
malpositioned leads. A posterior loop of the lead in the LAO view or a
more superior course in the AP view (as it courses across the RA-LA-LV)
are important pointers.
Third, it would be interesting to know about the ECG of the reported
patient immediately following the implant, as it would have probably
helped make the diagnosis right away (RBBB pattern, frontal QRS axis to
the right, and precordial transition after V4 localising it to be in the
LV)
Aditya Kapoor
Reference
(1) Coman JA, Trohman RG. Incidence and electrocardiographic
localisation of safe right bundle branch block configurations during
permanent ventricular pacing. Am J Cardiol 1995;76:781-4.
We have read the interesting comments of Dr Kapoor concerning left
ventricular pacing and discriminating ECG patterns.
In our short case report,[1] we could not, by lack of space, include
the different ECG tracings nor discuss the complete differential
diagnosis. The subject remains nevertheless extremely important with
respect to the precise diagnosis and the therapeutic measures we have...
We have read the interesting comments of Dr Kapoor concerning left
ventricular pacing and discriminating ECG patterns.
In our short case report,[1] we could not, by lack of space, include
the different ECG tracings nor discuss the complete differential
diagnosis. The subject remains nevertheless extremely important with
respect to the precise diagnosis and the therapeutic measures we have to
consider.
We agree totally with most of the comments of Dr Kapoor and we take the
opportunity to discuss more in detail some aspects of this particular
case.
Of course, we all know that a certain percentage of right ventricle
leads may exhibit a right bundle branch bloc pattern when located at the
septal part of the right ventricle. To differentiate it from a left
ventricar site, the orientation of the QRS in the frontal plane or its
axis, is a major determinant. If we analyse carefully the tracings in the
peripheral leads we may observe the following important aspects: in lead
I, the QRS has a QS pattern, indicating without any doubt a left lateral
location of the pacing origin. A QS morphology in lead I is
characteristic of such a location and can never be observed in a right
septal pacing, except maybe in the high right ventricular outflow tract.
In this latter situation however, the QRS has a left bundle branch block
pattern.
We may thus state that the sole presence of a QS pattern in lead I is
specific of left ventricular pacing. The correlation of this is the
presence of a positive R wave in lead III which can only be seen when
pacing starts at the left lateral or the anterior wall.
These different criteria in relation with pacing sites have been
learned from pacemaping during ablation procedures for ventricular
tachycardias and more recently from left ventricular pacing in congestive
heart failure. They are logical and correlate well with the observations
of Coman et al.[2]
Mapping have learned us also that the transition in the precordial
leads discriminates more between an apical or a basal position of the
lead. A late transition (>V4), as in our case, indicates a more basal
position. This has been confirmed during the surgical intervention. On
the contrary, an earlier transition is characteristic of a more apical
site.
With respect to the X ray imaging, in the LAO view, a left
ventricular lead is not seen more posteriorly but more laterally, pointing
to the location of the left ventricle and distinguishing it from a right
ventricular position. It is in the lateral view or in the RAO view that
we may see a posterior course of a left ventricular lead.
Finally we may confirm that the ECG recordings just after the implant
had exactly the same pattern as the one we reported. Unfortunately, at
that time, the diagnosis has not been made.
L De Roy
D Blommaert
J Mucumbitsi
University of Louvain
Cliniques Universitaires - UCL - Mont-Godinne Belgium
References
(1) Blommaert D, Mucumbitsi J, De Roy L. Ventricular pacing and right
bundle branch block morphology: diagnosis and management. Heart
2000;83:666.
(2) Coman JA, Trohman RG. Incidence and electrocardiographic
localisation of safe right bundle branch block configuration during
permanent ventricular pacing. Am J Cardiol 1995;76:781-4.
Dr Gavaliatsis points out the severe limitations that we still face
in the exact diagnosis of monogenic diseases causing ventricular
arrhythmias, like Brugada syndrome and the long QT syndrome. In Brugada
syndrome it seems that we have a pharmacologic challenge (iv flecainide,
ajmaline or procainamide) to unmask the phenotype. Unfortunately, that is
not so in the long QT syndrome. But even with the ph...
Dr Gavaliatsis points out the severe limitations that we still face
in the exact diagnosis of monogenic diseases causing ventricular
arrhythmias, like Brugada syndrome and the long QT syndrome. In Brugada
syndrome it seems that we have a pharmacologic challenge (iv flecainide,
ajmaline or procainamide) to unmask the phenotype. Unfortunately, that is
not so in the long QT syndrome. But even with the pharmacologic challenge
I agree with Dr Gavaliatsis that there may exist a problem of sensitivity
and specificity in the diagnosis that will only be uncovered by exact
knowledge of the genotype. But we need more than genetic analysis to make
the correct correlations.
It starts with
1. The correct clinical
diagnosis (something no that easy sometimes, particularly in the long QT
syndrome), it continues by 2. Showing a change in the genetic code - for
instance in the gene SCN5A encoding for the human cardiac sodium channel -
and ends by 3. Expressing the mutation to show its functional
consequences.
Of course, the diagnostic chain is only closed at the time
that the functional consequences of the mutation turn out to make sound
pathophysiologic sense, that is, they correlate with the clinical
diagnosis and the known consequences of the disease. Mutation "hunters"
seem to forget more and more frequently step 3. They report results that
rather confuse instead of clarifying the many scientific questions that
still remain. Publication of "mutations" without functional analysis to
exclude among others, polymorphisms and non-significant changes in DNA
sequences should be avoided by all serious scientific journals.
The points by Dr Gavaliatsis are well taken but a simple answer will
not become available instantaneously. Meanwhile it remains the duty of the
physician to protect patients with a Brugada phenotype against sudden
death. It is a matter of medical phylosophy: When we do not know the
patient should not become the victim of our ignorance. Implanting a
defibrillator too much is not nice, but seeing a young individual succumb
suddenly to ventricular fibrillation because a defibrillator was not
implanted is much worse.
In the July 2000 issue of Heart, in an Editorial by Brugada,[1]
about a paper by Viskin et al,[2] it is stated:
"The most important conclusion of the study by Viskin and colleagues is,
however, that patients with syncope of unknown origin should be
pharmacologically tested for Brugada syndrome, a suggestion made by the
authors on the basis of their results."
In the July 2000 issue of Heart, in an Editorial by Brugada,[1]
about a paper by Viskin et al,[2] it is stated:
"The most important conclusion of the study by Viskin and colleagues is,
however, that patients with syncope of unknown origin should be
pharmacologically tested for Brugada syndrome, a suggestion made by the
authors on the basis of their results."
However, in the conclusions of the Abstract by Viskin et al, it is stated:
"A definite Brugada sign is a specific marker for arrhythmic risk. However,
less than obvious ECG abnormalities have little diagnostic value, as a
'questionable' Brugada sign was observed in 1% of healthy controls. In
this series of concecutive patients with idiopathic ventricular
fibrillation, most had normal ECGs".
Most importanly, in the Results, it is stated: "Six patients received
intravenous ajmaline or procainamide and 26 patients received oral
treatment with class 1A drugs (mainly quinidine but also disopyramide)
following the diagnosis of idiopathic ventricular fibrillation. Class 1A
drugs did not unmask a Brugada sign in any patient".
Furthermore, in the Discussion, it is stated:
"It should be noted,
however, that the specificity of ST elevation following class 1 drug
administration is not at all clear. This point cannot be overemphasised in
view of anecdotal reports suggesting that ECG features indistinguishable
from a Brugada sign may apper in patients without documented or suspected
ventricular arrhythmias following administration of class 1C drugs".
After all these, and not very convincingly, in an Addendum, based on Brugada et al data,[3] it is stated:
"This new evidence underscores the need for systematic performance of a 'flecainide challenge' in
patients with idiopathic ventricular fibrillation and apparently normal
ECG, and in patients with questionable symptoms and a questionable
Brugada sign".[2]
I also "question the validity of pharmacological testing for the
Brugada syndrome".[4]
I also "agree that genetics will provide a definitive diagnosis".[4]
(1) Brugada P. Brugada syndrome: an electrocardiographic diagnosis
not to be missed. Heart 2000;84:1-2.
(2) Viskin S, Fish R, Eldar M, et al. Prevalence of the Brugada sign
in idiopathic ventricular fibrillation and healthy controls. Heart 2000;84:31-6.
(3) Brugada R, Brugada J, Antzelevitch C, et al. Sodium channel
blockers identify risk for sudden death in patients with ST-segment
elevation and right bundle branch block but structurally normal hearts.
Circulation 2000;101:510-15.
(4) Wilde AAM, Priori SG. Brugada syndrome and sudden death. [Letter
and Reply]. Eur Heart J 2000;21:1483-4.
The August 2000 issue of Heart contained our article
entitled "Incidence, recurrence, and case fatality rates for myocardial
infarction in southwestern France, 1985 to 1993".[1] This work was the
last version of the presentation and the interpretation of data carefully
collected for 10 years.
The Editorial in the same issue written[2] by Simon Capewell and John McMurray
concerning our article is...
The August 2000 issue of Heart contained our article
entitled "Incidence, recurrence, and case fatality rates for myocardial
infarction in southwestern France, 1985 to 1993".[1] This work was the
last version of the presentation and the interpretation of data carefully
collected for 10 years.
The Editorial in the same issue written[2] by Simon Capewell and John McMurray
concerning our article is a brilliant and exhaustive synthesis of the
problem. However, when reading the Editorial, it seems that data from the
Toulouse MONICA team are not consistent with data already published by
this group[3] or by the MONICA Programme.[4]
The first inconsistency we should eliminate concerns the
establishment of exceptionally low coronary mortality rates in France.
Since 1994,[5] the MONICA Project has shown that, even after correcting
routine mortality statistics, coronary heart disease mortality rates in
France were among the lowest. Hence, we do not understand the interest of
publications[6] based on data other than standardised data such as MONICA
data.
The second inconsistency concerns potential contradictions between
works already published by the Toulouse MONICA team.[3] After reading
both articles, it appears that data do not concern identical cases of
acute coronary heart disease. Indeed, according to the princeps work of
1994[5] in our intermediate work published in 1995[3] we used the MONICA
definition 2 whereas in the most recent work[1] and in the final report
of the international MONICA project[4] definition 1 had been chosen.
Definition 1 is more representative of epidemiological reality whereas
definition 2 is more representative of in-hospital cardiological reality.
After a 10-year long discussion within the MONICA cooperation, definition
1 was selected since it was the widest and the most exhaustive but
probably including acute coronary disease events that were not myocardial
infarction.
The third inconsistency concerns the difference between results
published by the International MONICA Project[4] and the results
presented in Heart.[1] Both works being based on the same data, it seems
coherent to find identical results. These final results are reported in
our article in Heart.[1] After reading the Lancet's proofs,[4] it
was obvious that a line inversion had occurred between Strasbourg and
Toulouse data and this error was immediately corrected.
The interest and the relevance of the publication of our results in
Heart was to show that exceptions to the message conveyed by the Lancet
do exist. We agree with the fact that in most centres, the decrease in
coronary heart disease mortality is due to a decrease in the number of
acute coronary heart disease events. In some centres, such as Toulouse,
the decrease in case fatality rates is accountable for the decrease of
coronary heart disease mortality. When we used the term "acute management"
to explain the decrease in coronary heart disease mortality in Toulouse,
the authors of the Editorial should have understood that it was an
extensive definition of myocardial infarction therapy during its acute
phase including pre-hospital management, the disease severity and a very
effective treatment provided in some highly performing regional hospitals.
The originality of our message is to assess a fundamental epidemiological
rule: variability in relation to person, place and time.
Jean Ferrières MD, MSc, FESC
on behalf of the Toulouse MONICA team
References
(1) Marques-Vidal P, Ruidavets JB, Cambou JP, et al. Impact of incidence,
recurrence and case-fatality rates of myocardial infarction in coronary
heart disease mortality in Southwestern France, 1985-1993. Heart
2000;84:171-5.
(2) Capewell S, McMurray J. Coronary heart disease trends in France and
elsewhere [editorial]. Heart 2000;84:121-2.
(3) Ferrières J, Cambou JP, Ruidavets JB, et al. Trends in acute myocardial
infarction prognosis and treatment in Southwestern France between 1985 and
1990 (The MONICA Project-Toulouse). Am J Cardiol
1995;75:1202-5.
(4) Tunstall-Pedoe H, Kuulasmaa K, Mähönen M, et al, for the WHO MONICA
(monitoring trends and determinants in cardiovascular disease) Project.
Contribution of trends in survival and coronary-event rates to changes in
coronary heart disease mortality: 10 year results from 37 WHO MONICA
Projects populations. Lancet 1999;353:1547-57.
(5) Tunstall-Pedoe H, Kuulasmaa K, Amouyel P, et al. Myocardial infarction
and coronary deaths in the World Health Organization MONICA Project.
Registration procedures, event rates, and case-fatality rates in 38
populations from 21 countries in four continents. Circulation 1994;90:583-612.
(6) Law M, Wald N. Why heart disease mortality is low in France: the time
lag explanation. BMJ 1999;318:1471-6.
Neurobiological features of fetal and infant markers of adult heart
diseases are suggested by short-term laboratory experience demonstrating
that adult female speech production is sufficient to influence infant
speech production occurring in the silent intervals between the adult's
vocalizations on the order of 3 s and is linked to increased coherence of
EEG gamma-band activity associated with the...
Neurobiological features of fetal and infant markers of adult heart
diseases are suggested by short-term laboratory experience demonstrating
that adult female speech production is sufficient to influence infant
speech production occurring in the silent intervals between the adult's
vocalizations on the order of 3 s and is linked to increased coherence of
EEG gamma-band activity associated with the execution of more complex
tasks leading to the evolution of language. Infant speech production
involves linguistic processing and associative learning through increases
in effective connectivity between distinct cortical systems, and
spontaneous patterned activity in the developing cortex may establish long
-range neuronal connections. This hypothesis is supported by reports that:
variations in maternal care in the rat promote hippocampal synaptogenesis
and spatial learning and memory through systems known to mediate
experience-dependent neural development; and the entrainment of intrinsic
gamma-frequency oscillators (30 Hz to 50 Hz or broader, centered on 40 Hz)
in involved in processes associated with encoding into sensory memory and
the cellular level (synaptic potentiation) and at the cognitive level.
It is also supported by studies demonstrating that: the microvascular
response to the onset of neural activity is delayed consistently by
several seconds; language discrimination by human newborns may be
influenced by hearing rhythmic aspects of speech while in the womb, a
period in development during which exposure may have a more profound
effect on the organization of the brain than does learning after birth;
the replaying to the fetus of the mother's recording of a nursery rhyme
leads to notable temporal-lobe activation; and by the remarkable neural
plasticity that is inherent in reproduction itself, particularly during
late pregnancy and the postpartum period increasing the reliability of
synaptic transmission, which contributes to attention, perception and
information processing.
Therefore, exploration of pathways and mechanisms in the evolution of
heart diseases through an interaction between fetomaternal environment and
individual genotype may be facilitated by monitoring temporal features of
expressive activity to clarify the role of the central nervous and its
effect on the microvasculature.
Wilmshurst et al published their experience of
introducing nurse initiated thrombolysis.[1] They show that door to needle
times (but not outcome) were reduced. Aside from this, the paper raises
important issues about medical training. What the authors demonstrate, is
that if you focus resources and training and follow strict protocol driven
practice, then for a highly specific task you can improve...
Wilmshurst et al published their experience of
introducing nurse initiated thrombolysis.[1] They show that door to needle
times (but not outcome) were reduced. Aside from this, the paper raises
important issues about medical training. What the authors demonstrate, is
that if you focus resources and training and follow strict protocol driven
practice, then for a highly specific task you can improve results. This
is no surprise to anyone and is not a feature of specialist nurses over
doctors.
If adequate junior doctor cover existed for their coronary care unit
then no doubt they could demonstrate the same reduction in door to needle
times. It is frankly insulting for them to say, “doctors failed to
respond speedily even when 'fast' bleeped”. During a busy acute general
medical take there are many sick patients including those having
myocardial infarctions. Many of them are sicker than most infarct
patients and deserve (but sadly don’t always receive) equal treatment and
resources. Simply because large randomised trials exist regarding the
treatment of myocardial infarction does not make it a more important
condition.
With regards to training, I take it that the authors can show that
every junior doctor currently practicing in Shrewsbury Hospital who might
initiate thrombolysis has received identical, documented, accredited and
audited training to the same level as the specialist nurses. If not, why
not? Why should junior doctors face continual comparison of their
performance when they don’t receive adequate training from their Trusts
and Consultants? As doctors become more senior they base their decisions
on their many previous learning opportunities. Each time you thrombolyse
a patient you learn something which you use in future practice. How have
the authors audited the effect on doctors training following their change
in management practice? Can they demonstrate that their doctors retain
the same confidence and skills in managing all aspects of a myocardial
infarction?
The final issue is who should be the “thrombolysis specialist”? If
you believe in such a division of labour, then there is no reason to only
employ senior nursing staff. Why not junior nurses with intensive
training, or technicians trained only to perform thrombolysis? Perhaps
the increase in specialist nurses reflects the attempt of the nursing
profession to change their perceived roles and their desire to not only
raise their low salary but to do less hands on nursing? Because of this,
patients on general wards continue to receive less than adequate care as
there is no one interested in providing the old fashioned, but much
valued, basic care. The glory lies with specialism but at what long-term
price?
At the end of the day, overall quality of practice must remain the
issue. If all staff were adequately trained then standards would improve.
Believing the answer lies in specialist nurses is wishful thinking. I
despair at the thought of turning medicine into a file full of protocols
performed by individual specialist technicians. Of course we can have
technicians who, for example, only insert canulas, diagnose myocardial
infarctions, manage acute exacerbations of COPD, publish audits or even
deploy coronary artery stents. Medicine is much more than this.
Attempting to break every decision a doctor makes into a step in a
protocol, will result in doctors without the overall experience they
desperately want and need, to make the frequent hard, non-evidence based,
decisions of daily clinical life.
Dr Gideon Hirschfield MB BChir MRCP
Reference
(1) Wilmshurst P, Purchase A, Webb C, et al. Improving door to needle times with nurse initiated thrombolysis. Heart 2000;84:262-6.
We agree with Dr Hirschfield that training of doctors is important,
but it must not take precedent over the interests of patients. We could
not continue to delay thrombolysis to patients with myocardial infarction
and thereby increase their mortality rate, so that junior doctors could
have the experience of making a late decision. It may be embarassing for
junior doctors for us to point out that th...
We agree with Dr Hirschfield that training of doctors is important,
but it must not take precedent over the interests of patients. We could
not continue to delay thrombolysis to patients with myocardial infarction
and thereby increase their mortality rate, so that junior doctors could
have the experience of making a late decision. It may be embarassing for
junior doctors for us to point out that they failed to respond when fast
bleeped, but it is a fact. I am afraid that the medical profession has a
long history of covering up poor performance by doctors.
Though there are a few exceptions (such as cardiac and respiratory
arrest and massive haemorrhage), there are few medical emergencies where
patients are sicker than patients with myocardial infarction, as judged by
the effect that delaying treatment has on mortality. Of course there are
some patients who, to the inexperienced, appear sicker, such as a patient
who is toxic with pneumonia. In most of those cases delays in treatment,
while thrombolysis decisions are made has little or no effect on
mortality. A delay in initiating thrombolysis in patients with acute
myocardial infarction will considerably affect mortality. During an acute
medical take in our hospitals there are few occasions when there is a
patient meriting greater priority for attention than patients with
myocardial infarction. In our hospital at the time of our study, there
were at least four junior physicians on duty at any one time. It is
difficult to conceive a situation when one of these would not be available
to deal immediately with a patient with a myocardial infarction, but
delays continued. Regular teaching on the
importance of thrombolysis made no difference to the speed at which junior
doctors attended patients with myocardial infarction, but there was a
dramatic improvement in speed of their attendance once nurses were
authorised to initiate thrombolysis.
We carefully documented the training and experience necessary for our
thrombolysis nurses because they had a novel role and there were clear
legal implications. Junior doctors are legally entitled to give
thrombolytic drugs and their qualifications are laid down in regulations
by the General Medical Council, so the need to document the qualifications
of doctors was unnecessary for our paper. In fact our junior doctors had
more hours of in-house training on thrombolysis than the nurses, if they
elected to attend their protected teaching sessions. Junior doctors expect
to be better trained than their predecessors while spending fewer years
and shorter hours during those years gaining experience. Dr Hirschfield is wrong about
the role of experience in clinical decision making. Though doctors rely
considerably on experience in diagnosis, experience plays a smaller role
in decisions about management. Prescription is based on evidence from
trials, which is published in peer reviewed journals, or conventional
practice, published in textbooks. We hope that the use of antibiotics in
patients with pneumonia is not because each doctor has found out for
himself or herself that to withhold antibiotics in that situation may be
fatal. Trials not "previous learning opportunities" enable us to decide
which patients with myocardial infarction should receive a thrombolytic
drug.
It may reveal more about the motives of junior doctors seeking
specialisation than those of nurses when Dr Hirschfield suggests that
specialisation is due to a desire for better pay, a wish to do less hands-
on work and personal glory. All our thrombolysis nurses are ward based and
do normal nursing duties. Thrombolysis by nurses is when no doctor is
available. The arrangement is now one of cooperation. Many junior doctors
and probably a greater proportion of senior doctors are modest enough to
recognise that they can learn from expert nurses. However in general
extension of the nurses' role owes more to the desire of junior doctors to
delegate less glamorous tasks such as venepuncture, cannulation and
administration of intravenous drugs for their own convenience.
Thrombolysis nurses provide holistic care for patients including
unglamorous basic care.
Our hospital is in a rural area. Some patients with myocardial
infarction travel for over an hour by ambulance before reaching hospital.
To shorten the call to needle time, we have worked with some local general
practitioners to start thrombolysis in the community. We hope eventually
to have paramedic initiated thrombolysis. We have no regrets that we will
not be delaying thrombolysis so that junior doctors can have the
experience of prescribing thrombolysis later than is possible if nurses initiate therapy.
Peter Wilmshurst, Consultant Cardiologist
Carol Webb, Coronary Care Ward Sister
Clare Jowett, Clinical Audit Manager
Chest radiography, to which not even a passing allusion was made in a recent report on misdiagnosis of heart failure,[1] has now been accorded its rightful status in the recognition of this syndrome.[2] Unlike some of the clinical stigmata of pulmonary disease, which have been accorded an importance, in the undergraduate curriculum, disproportionate to their relationship to evidence-based medicine,[3] the radiogra...
Chest radiography, to which not even a passing allusion was made in a recent report on misdiagnosis of heart failure,[1] has now been accorded its rightful status in the recognition of this syndrome.[2] Unlike some of the clinical stigmata of pulmonary disease, which have been accorded an importance, in the undergraduate curriculum, disproportionate to their relationship to evidence-based medicine,[3] the radiographic stigmata of severe chronic left ventricular failure (LVF), although not instilled to the same extent, nevertheless have the merit of having been evaluated for sensitivity, specificity, and positive predictive value, yielding values of 65%, 80%, and 89% respectively, for pulmonary vascular redistribution, and 27%, 87%, and 83%, respectively, for interstitial oedema in the presence of pulmonary capillary wedge pressure > 18 mmHg.[4]
On a 4-point scale of severity, a comparison between clinical and radiographic parameters for LVF generated a concordance which differed by no more than 1 grade, in 94% of instances.[5] Analysis of radiographic parameters also revealed greater interobserver agreement for recognition of interstitial oedema as opposed to pulmonary vascular redistribution (95% vs 74%).[4]
In consequence, this parameter (together with alveolar oedema) deserves recognition in the entirety of its protean manifestations which include, not just the Kerley B lines and "bat's wing" appearance mentioned by the author,[2] but also lower zone "mottled" as well as confluent opacities (some of which may be asymmetrical),[6] and right upper zone opacities (attributable to underlying mitral regurgitation),[6,7] all of which have the potential to be misattributed to pulmonary sepsis.[6]
Overdiagnosis also needs to be avoided, especially in pulmonary embolism (PE), where instead of a positive correlation between clinical and radiographic severity,[5] the degree of breathlessness far outstrips abnormalities (if any) seen on X-ray.
Radiographic abnormalities common to heart failure and PE include pleural effusions which, in heart failure, are reported (sic) more likely to be either bilateral (73%) or right sided (19%), than left sided (9%),[8] a preferential distribution not documented in PE.
References
(1) Caruana L, Petrie MC, Davie AP, McMurray JJV. Do patients with suspected heart failure and preserved left ventricular systolic function suffer from "diastolic heart failure" or from misdiagnosis? A prospective study. BMJ 2000;321:215-19.
(2) Struthers AD. The diagnosis of heart failure. Heart 2000;84:334-8.
(3) McAlister FA, Strauss SE, Sackett DL, on behalf of the CARE-COAD Group. Why we need large, simple studies of the clinical examination: the problem and proposed situation. Lancet 1999;354:1721-4.
(4) Butman SM, Ewy GA, Standen JR, Kern KB, Hahn E. Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible venous distention. J Am Coll Cardiol 1993;22:969-74.
(5) Forrester JS, Diamond GA, Swan HJC. Correlative classification of clinical and hemodynamic function after acute myocardial infarction. Am J Cardiol 1977;39:137-45.
(6) Fraser RS, Colman N, Muller NL, Pare PD. Pulmonary edema. In: Diagnosis of Diseases of the Chest. 4th ed, Vol III. WB Saunders Company: Philadelphia, London, Toronto, Montreal, Sydney, Tokyo. pp 1946-2017.
(7) Brander L, Kloeter U, Henzen C, Briner V, Stulz P. Right-sided pulmonary oedema. Lancet 1999;354:1440.
(8) Weiss JM, Spodick DH. Laterality of pleural effusions in congestive heart failure. Am J Cardiol 1984;53:951.
The study by Hetmanski investigates the use of plasma BNP to detect
low left ventricular ejection fraction in a cohort of patients in the
community on frusemide.[1] The study showed a poor, albeit statistically
significant, correlation between plasma BNP and left ventricular ejection
fraction. The area under the receiver operating curve for BNP was only
0.587, and the authors conclude that the "accuracy o...
The study by Hetmanski investigates the use of plasma BNP to detect
low left ventricular ejection fraction in a cohort of patients in the
community on frusemide.[1] The study showed a poor, albeit statistically
significant, correlation between plasma BNP and left ventricular ejection
fraction. The area under the receiver operating curve for BNP was only
0.587, and the authors conclude that the "accuracy of BNP concentrations
to provide a measure of left ventricular ejection fraction and help
diagnose heart failure is not as good as previously reported".[1]
This study correctly acknowledges that primary care patients in whom
there is a clinical suspicion of heart failure differ in several important
aspects from patients in clinical trials: they tend to be elderly,
commonly have comorbid conditions, and the symptoms of heart failure are
frequent and often mild, making diagnosis difficult. However, this study
has several important limitations.
The first problem is that of patient selection. Although the
community setting is relevant and topical, we question the authors'
assumption that the majority of patients prescribed loop diuretics in
primary care would have the clinical syndrome of heart failure. Loop
diuretics are widely used in hypertension and for the empirical treatment
of ankle swelling of uncertain cause. Little is known about the prevalence
of heart failure in patients prescribed loop diuretics, but it may not
differ significantly from age-matched community controls. The presence of
echocardiographic left ventricular systolic dysfunction in community-based
patients treated with loop diuretics in previous reports varies from 26%[2]
to 41%.[3]
Secondly, of the 1425 patients prescribed diuretics identified from
practice registers and invited to take part in the study, only 653 (46%)
consented and underwent echocardiography and BNP measurement. It may be
possible that the patients with heart failure in the original cohort did
not take part in the study.
Thirdly, recent studies have demonstrated that BNP levels are
decreased by frusemide.[4-7] A major part of the therapeutic regimen used
in the BNP-guided treatment trial by Troughton et al[7] was an increase in
diuretic therapy to decrease the BNP level. Therefore, the influence of
diuretic therapy on BNP will impair the performance of BNP as a diagnostic
test in the study by Hetmanski et al.[1] The diagnostic efficacy of BNP
measurement performed during the first presentation of patients with
symptoms is still unknown.
Fourthly, there is confusion between the identification of left
ventricular systolic dysfunction and the diagnosis of the clinical
syndrome of heart failure. We believe that the goal of a diagnostic test
in the community is to aid recognition of the clinical syndrome of heart
failure so that appropriate further investigations, treatment and follow-
up can be instituted. This still remains the potential value of a
biochemical diagnostic tool such as BNP. BNP could well complement, rather
than replace, echocardiographic assessment of the left ventricle.[8] Left
ventricular systolic dysfunction on echo overlaps with but is not
synonymous with the clinical syndrome of heart failure. This study, by
using an arbitrary left ventricular ejection fraction (LVEF) cut-off of
40%, will have missed many patients with the clinical syndrome of heart
failure including those with diastolic dysfunction, an important
consideration in the community and in elderly patients.[9] Echocardiograhic
assessment of the LV in this study depends on an arbitrary LV ejection
fraction cut-off to "rule in" or "rule out" left ventricular systolic
dysfunction. Any chosen level of LVEF cut-off - usually adopted from
mechanistic clinical trials - will have a unique ROC curve reflecting the
changing relationship between diagnostic sensitivity and specificity at
any particular level of LVEF. In reality, improved recognition of the
clinical syndrome of heart failure may prove more useful.
Community studies of the effectiveness of BNP measurement for the
diagnosis of the clinical syndrome of heart failure are still needed.
These studies must be carefully conducted randomised controlled trials
which recognise the contribution of heart failure with preserved systolic
function in this group and utilise a pragmatic definition of the syndrome
of heart failure appropriate for primary care.
Dr SP Wright
Research Fellow in Cardiovascular Medicine
Department of Medicine
Dr RN Doughty
New Zealand National Heart Foundation BNZ Senior Fellow
Department of Medicine
Dr A Pearl
Research Fellow
Department of General Practice and Primary Health Care
School of Medicine and Health Sciences
University of Auckland
Private Bag 92019, Auckland, New Zealand
References
(1) Hetmanski D, Sparrow N, Curtis S, Cowley A. Failure of plasma
brain natriuretic peptide to identify left ventricular systolic
dysfunction in the community. Heart 2000;84:357-60.
(2) Francis C, Caruana L, Kearney P, Love M, Sutherland G, Starkey I, et
al. Open access echocardiography in management of heart failure in the
community. BMJ 1995;310:634-6.
(3) Wheeldon N, MacDonald T, Flucker C, McKendrick A, McDevitt D, Struthers
A. Echocardiography in chronic heart failure in the community. Quart J Med 1993;86:17-23.
(4) Murdoch D, McDonagh T, Byrne J, Blue L, Farmer R, Morton J. Titration
of vasodilator therapy in chronic heart failure according to plasma brain
natriuretic peptide concentration. Am Heart J 1999;138:1128-32.
(5) Northridge D, Newby D, Rooney E, Norrie J, Dargie H. Comparison of the
short-term effects of candoxatril, an orally active neutral endopeptidase
inhibitor, and frusemide in the treatment of patients with chronic heart
failure. Am Heart J 1999;138:1149-57.
(6) Kelly R, Struthers A. Risk assessment of left ventricular systolic
dysfunction: drug treatment might be contaminating factor [letter]. BMJ
2000(321):111.
(7) Troughton R, Frampton C, Yandle T, Espiner E, Nicholls M, Richards A.
Treatment of heart failure guided by plasma aminoterminal natriuretic
peptide (N-BNP) concentrations. Lancet 2000;355:1126-30.
(8) Struthers A. Further defining the role for natriuretic peptide levels
in clinical practice [editorial]. Eur Heart J 1999;20:712-4.
(9) Tresch D, McGough M. Heart failure with normal systolic function: a
common disorder in older people. J Am Geriatr Soc 1995;43:1035-42.
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