Takeda et al. have observed that degree of mitral lateral annular
excursion in mild to moderate aortic stenosis is very close to that in
control group. In this study, both lateral and septal side of mitral
annulus have shown a consistent decrease in long axis excursion with
disease progression. Aortic stenosis may lead to physiological hypertrophy
in early stages of the disease as discussed in hy...
Takeda et al. have observed that degree of mitral lateral annular
excursion in mild to moderate aortic stenosis is very close to that in
control group. In this study, both lateral and septal side of mitral
annulus have shown a consistent decrease in long axis excursion with
disease progression. Aortic stenosis may lead to physiological hypertrophy
in early stages of the disease as discussed in hypertrophy session at the
4th annual meeting of the working group on echocardiography of the ESC.[1]
In a similar way, we have observed that mitral annular circumferential and
longitudinal axis functions are in normal limits as compared to much
lower function in cardiomyopathic patients using real-time 3-dimensional
echocardiography and complex reconstruction methodology in patients with
secondary LV hypertrophy caused by aortic stenosis.[2] In those patients,
left ventricular systolic function had been preserved.
Takeda et al. have shown that long axis excursion is independently related
to both LV mass index and the grade of aortic stenosis. They have
explained that both pathophysiological changes as a result of LV
hypertrophy and increased afterload as a result of aortic stenosis may
together contribute to changes in systolic function in aortic stenosis.
These observations can support that aortic stenosis possibly results in
physiological hypertrophy before existing LV dysfunction.
On the other hand, it is well known that hypertension and cardiomyopathy
are associated with pathological hypertrophy.[3] I believe, this
comprehensive study by Takeda et al. is an important step to predict the
stages of the disease process and aortic stenosis may be the unique
example of physiological hypertrophy conversion to pathological one with
development of LV dysfunction.
Note: I noticed that there may be a discordance between a sentence
and the referred number. In the discussion part, the second sentence is
about wall stress relief in patients with aortic stenosis after the valve
replacement, while marked reference (19th) is related to left ventricular
dysfunction after MI.
References
(1) 4th Annual and plenary meeting of the working group on echocardiography
of the European Society of Cardiology, 2000.
(2) Yalçin F, Tsujino H, Greenberg N, Bauer F, Farias CA, Shiota T,
Lever H, Thomas JD. Real-time three-dimensional echocardiographic
evaluation of mitral annular characteristics in myocardial hypertrophy.
Europ Heart J 1999:291;P1599.
(3) Vinereanu D, Florescu N, Sculthorpe N,. Tweddel AC, Stephens MR, Fraser AG. Differentiation between pathologic and physiologic left
ventricular hypertrophy by tissue doppler assessment of lon-axis function
in patients with hypertrophic cardiomyopathy or systemic hypertension and
in athletes. Am J Cardiol 2001; 88:53-8.
McKenna and Behr´s recommendation that offspring of carriers of mutations
causing hypertrophic cardiomyopathy (HCM) should have regular evaluation
“during puberty and early adulthood” could be read as suggesting that
evaluation for carrier status is not necessary before puberty. This would
be a pity as there is now good evidence arguing for echo...
McKenna and Behr´s recommendation that offspring of carriers of mutations
causing hypertrophic cardiomyopathy (HCM) should have regular evaluation
“during puberty and early adulthood” could be read as suggesting that
evaluation for carrier status is not necessary before puberty. This would
be a pity as there is now good evidence arguing for echocardiographic
screening of children of affected parents at a much earlier age. McKenna
and Behr quote an annual incidence of sudden death from 2-4% in children
diagnosed before 14 years of age, but neglected to point out that some of
the children in these studies received drug therapy. The only complete
geographically based cohort study of childhood hypertrophic cardiomyopathy
published to date in fact demonstrates a higher mortality in untreated
patients, with an annual mortality of 6.6% when heart-failure related
deaths are included, and that even completely asymptomatic children had a
3.5% annual mortality in sudden death.[1] In relation to timing for family
screening the majority (6/10) of sudden deaths occurred in the pre-
pubertal and early pubertal age of 9-13 years.[1] An expanded follow-up
study including 122 patients from six centres with a geographical referral
pattern confirms that a majority of unexpected sudden deaths occur in the
8-11 years age band.[2] Such an age distribution of sudden deaths in
childhood suggests that family screening should take place well before the
offspring reaches 8 years of age, and probably before the child starts
school. Using relative rather than absolute wall-thickness for screening
greatly increases the possibility of diagnosing the abnormal phenotype.
Echocardiographic wall-to-cavity ratios which show very high specificity
and sensitivity for identifying an abnormal phenotype already in young
children are septum-to-cavity ratio >0.26 at any age and/or a systolic
LV-wall-to-cavity ratio >0.63 at ages > 4years of age.[3] The same
ratios, and also diastolic LV wall-to-cavity ratio are more sensitive
measures to monitor any progression of disease in a growing child than the
absolute wall thickness which should of course normally be increasing with
age-related growth.[4] The above considerations therefore would argue for
routine first time echocardiographic screening of offspring to take place
no later than the four to six year age range.
Can treatment improve survival in childhood?
Screening of asymptomatic patients is clearly only worthwhile if high risk
patients can be identified already in childhood, and a treatment that
reduces risk is available. The data from the six centre cohort study shows
that both echocardiographic (including wall-to-cavity ratios) and
electrocardiographic measures of increasing hypertrophy correlates with
risk for childhood death.[1,2] McKenna and Behr qualify their quotation of
the study showing a 5-10 fold reduction in risk of death achieved by high
dose propranolol in childhood HCM[1] by suggesting that HCM associated to
Noonan´s syndrome is likely to have a different risk of sudden death than
familial HCM related to sarcomeric contractile protein mutations. However,
the study in fact clearly shows that the annual sudden death rate in HCM
with Noonan´s syndrome was identical to that in patients with familial or
sporadic HCM.[1] Thus, since the morphological appearance of the myocardium
in HCM associated with Noonan´s syndrome is identical to that of ordinary
familial HCM,[5] and it fits the WHO definition just as well as the HCM seen
with sarcomeric contractile protein mutations, there is no reason to put
HCM associated with Noonan´s syndrome in quotation marks and pretend it is
irrelevant just because we still have not defined the causative mutation.
This is particularly so as there are many kindreds with familial HCM who
also lack the usual sarcomeric protein mutations and some new mutations
described that are unrelated to contractile proteins.[6] McKenna and Behr
have also missed the pertinent finding in this study that propranolol
showed statistically significant protection against risk for fatal outcome
both in HCM associated with Noonan´s syndrome and in HCM not associated
with Noonan´s syndrome, i.e. the effect of propranolol appeared
independent of the type of causative mutation.[1] It is also very clear in
Methods that the non-Noonan HCM group did not include any patients with
secondary HCM; the majority had familial HCM, and a few were new sporadic
mutations not associated with Noonan´s syndrome. The Oxford familial
childhood cases included in this study have all been subject to genetic
evaluation, which has shown a variety of HCM-inducing mutations of
sarcomeric contractile proteins (E. Blair, I. Östman-Smith & H.
Watkins, unpublished data). Thus there is no evidence that the 5-10 fold
reduction in risk conferred by high-dose propranolol in childhood1 is
irrelevant to the mutations encountered in adult familial HCM. The
protection by high dose beta-blockers has now also been confirmed in the
enlarged six centre cohort study with 122 patients, which shows that high-
dose beta-blocker therapy significantly reduces the risk both of sudden
death and of heart-failure related death.[2]
What beta-blocker dose should be employed?
Although McKenna and Behr list beta-blockers as first line medical
therapy, they give no guidelines in relation to dose. The data from the
above studies suggest that conventional doses of beta-blockers (equivalent
to 1-4 mg/kg BW of propranolol/day) do not protect against sudden death,
in agreement with previous reports, whereas doses >5 mg/kg/day do
protect.[1,2] Likewise, adult HCM patients treated with an average
propranolol dose of 6 mg/kg day, titrated by finding a dose that blocked
the effects of a standardised isoprenaline infusion, have a low annual
mortality of 0.5%.[7] Our experience is that the best way to identify the
appropriate dose for an individual is to use 24 Holter ECG to assess the
efficacy of beta-receptor blockade. Some young individuals with
particularly severe HCM will need up to 20 mg/kg BW/day to achieve
effective beta-blockade.[1] Why should really effective beta-receptor
blockade be so important? There are experimental data in mice that show
that over-expression of the cardiac beta-adrenoceptor G-protein adenyl
cyclase pathway results in a late developing HCM that can be prevented by
propranolol therapy.[8] Interestingly, over-expression of this pathway also
potentiates and accelerates cardiomyopathy due to alpha-myosin heavy chain
mutations,[9] i.e. significantly worsens the clinical disease expression in
our closest animal model to contractile protein HCM in humans. In humans
we know that subjects with clinically overt HCM have increased activity of
their cardiac sympathetic nerves,[10] so it would seem that this could
initiate a vicious cycle of progressive hypertrophy, as occurs in the
mice. The fact that so many different mutations in at least nine different
genes encoding contractile proteins, and one affecting AMP-activated
protein kinase, can cause essentially the same phenotype argues strongly
for the fact that the hypertrophy that is the essential definition of
disease expression is a secondary compensatory response, either directly
from a trophic effect of increased sympathetic nervous activity,[11,12] or
secondary to inability to maintain normal ATP levels.[6] Either way,
effective beta-receptor blockade could have a crucial role in modifying
disease-expression, either by protecting against the trophic effects of
noradrenaline, or by improving ATP-conservation. That beta-blocker therapy
can reduce compensatory hypertrophy has been shown in several experimental
models.[13,14] Thus the efforts at modifying disease progression must
proceed in parallel to efforts at protecting high risk patients from
sudden death with ICDs, because progressive disease with severe
hypertrophy can lead to heart failure, both early due to impaired
diastolic filling, and late due to dilated, fibrotic endstage.
References
(1) Östman-Smith I, Wettrell G, Riesenfeld T. A cohort study of
childhood hypertrophic cardiomyopathy: improved survival following high-
dose beta-adrenoceptor antagonist treatment. J Am Coll Cardiol
1999;34:1813-22.
(2) Östman-Smith I, Wettrell G, Keeton B, Riesenfeld T, Holmgren D,
Ergander U. Risk factors for disease-related death in childhood
hypertrophic cardiomyopathy. Cardiol Young 2001;11 Suppl. 1:31.
(3) Devlin AM, Östman-Smith I. Diagnosis of hypertrophic cardiomyopathy and
screening for the phenotype suggestive of gene carriage in familial
disease: a simple echocardiographic procedure. J Med Screen 2000;7:82-90.
(4) Östman-Smith I, Devlin AM. A simple method for assessing the regression
or progression of ventricular hypertrophy in the growing child and adult:
the value of left ventricular wall-to-cavity ratios. Eur J
Echocardiography 2001;2:22-30.
(5) Burch M, Mann JM, Sharland M, Shinebourne EA, Patton MA, McKenna WJ.
Myocardial disarray in Noonan syndrome. Br Heart J 1992;68M:586-8.
(6) Blair E, Redwood C, Ashrafian H, Oliveira M, Broxholme J, Kerr B, et
al. Mutations in the gamma(2) subunit of AMP-activated protein kinase
cause familial hypertrophic cardiomyopathy: evidence for the central role
of energy compromise in disease pathogenesis. Hum Mol Genet 2001;10:1215-
20.
(7) Canedo MI, Frank MJ. Therapy of hypertrophic cardiomyopathy: medical or
surgical? clinical and pathophysiologic considerations. Am J Cardiol
1981;48:383-8.
(8) Asai K, Yang GP, Geng YJ, Takagi G, Bishop S, Ishikawa Y, et al. Beta-
adrenergic receptor blockade arrests myocyte damage and preserves cardiac
function in the transgenic G(s)alpha mouse. J Clin Invest 1999;104:551-8.
(9) Hardt SE, Geng YJ, Montagne O, Asai K, Hong C, Yang GP, et al.
Accelerated cardiomyopathy in mice with overexpression of cardiac
G(s)alpha and a missense mutation in the alpha-myosin heavy chain.
Circulation 2002;105:614-20.
(10) Brush JE, Eisenhofer G, Garty M, Stull R, Maron BJ, Cannon RO, et al.
Cardiac norepinephrine kinetics in hypertrophic cardiomyopathy.
Circulation 1989;79:836-844.
(11) Östman-Smith I. Cardiac sympathetic nerves as the final common pathway
in the induction of adaptive cardiac hypertrophy. Clin Sci 1981;61:265-
272.
(12) Östman-Smith I, Wettrell G. Pathophysiology of hypertrophic
cardiomyopathy. Lancet 2000;355:928.
(13) Östman-Smith I. Reduction by oral propranolol treatment of left
ventricular hypertrophy secondary to pressure-overload in the rat. Br J
Pharmacol 1995;116:2703-9.
(14) Östman-Smith I. Reduction by beta-adrenoceptor blockade of hypoxia-
induced right heart hypertrophy in the rat. Br J Pharmacol 1995;116:2698-
702.
I read with great interest the paper by Y Matsumura1 et al.[1] On
face value the paper appears good. However, I am concerned about the
increasing number of papers on Doppler Tissue Imaging (DTI) appearing in
leading medical journals. DTI is a clear case of misuse of technology. It
could turn out to be the 'Philadelphia Experiment' in cardiology. Doppler
is best suited to study the direction of free m...
I read with great interest the paper by Y Matsumura1 et al.[1] On
face value the paper appears good. However, I am concerned about the
increasing number of papers on Doppler Tissue Imaging (DTI) appearing in
leading medical journals. DTI is a clear case of misuse of technology. It
could turn out to be the 'Philadelphia Experiment' in cardiology. Doppler
is best suited to study the direction of free moving objects. In the case
of echocardiology it is mainly to study free moving blood cells (blood
flow). It is the direction of motion that is important. The velocity
measurements are secondary. A comparison of flow Doppler (color flow
mapping – CFM) and DTI will make things clear.
CFM allows us to 'see' what we cannot see with ultrasonic 'eyes'
hence its value is great. In DTI we see more or less what we already see
by B-mode hence its value is marginal. In CFM the anatomic landmarks are
intact as the colour is superimposed on the B-mode image. In DTI the B-
mode is eliminated and the entire 'picture' is Doppler information
resulting in a fuzzy image. It is difficult to determine the different
anatomic regions on DTI.
Doppler studies are primarily for the study of the direction of
motion. The 'red shift' in astronomy for example shows the stars moving
away from us indicating an expanding universe. Calculation of velocities
is supplementary. In blood flow there is a definite direction of flow and
Doppler can detect any aberration in this. An example is the circuit of
pulmonary veins – left atrium – left ventricle – aorta. Suitably directed
Doppler interrogation can study and detect any deviation in this circuit.
In flow Doppler the projectile motion of free moving blood cells are
studied. Blood flow is simple and suitable for Doppler study. At the
current interrogation points there is a unique unidirectional flow in one
part of the cardiac cycle. For example in mitral valve Doppler
interrogation, the unique directional signal is obtained only in diastole.
If there is a signal in systole it becomes abnormal. In DTI the to- and-
fro motion (systole and diastole) of a tethered interconnected syncytium
of myocytes is imaged. Such information is useless. This can be even
otherwise seen and analysed by B-mode imaging.
Myocardial motion is very complex and not amenable to Doppler
studies. In the cardiac motion there are translational, rotational and
deformational movements. Doppler interrogation at one point will represent
the resultant of all these movements. At a particular point we can never
predict the resultant vector. Even if known, the resultant is accurately
recorded only if it is in the line of the Doppler beam. This is due to the
inherent problem of directional bias. Besides many tissues near the heart
move – due to transmitted cardiac motion, vessel pulsation, respiratory
motion and involuntary muscle movements. All these cause false Doppler
shifts.[2]
In flow Doppler there are definite 'points of interrogation', which
are the normal and abnormal orifices. In DTI there are no such definite
points. While in flow Doppler higher velocities are studied, DTI is used
to study lower velocities i.e. to study hypo functioning myocardial
segments. Lower velocities are difficult to appreciate. The higher
velocities are easier to appreciate with the help of aliasing and
variance. Hypo function is difficult to analyse. The derivations from flow
Doppler allows us to get orifice size, amount of flow and pressure
gradients, which are clinically of great importance. Thus Doppler studies
are best suited to study flow.
Doppler Tissue Imaging has been a disappointing modality in clinical
echocardiology. This is due to the basic flaw in the application of the
principles of Doppler. Doppler is best suited for flow studies and
applying it to tissue motion is ridiculous. In flow Doppler we suppress
the tissue 'noise' and display flow.[2] In DTI it is the other way round.
It is like suppressing the PQRST in an electrocardiogram and displaying
the 'noise'. Besides DTI is ultra sensitive and so the information
gathered is almost useless (too many false positive information). In fact
excellent cardiac waveforms can be obtained by placing the sample volume
even outside the cardiac region! Once the foundation of a modality is
wrong, all derivations tend to be wrong.
It is time to look at Doppler tissue imaging on more realistic terms.
As a new modality of imaging it appears exciting. But its real clinical
utility is doubtful. DTI does not give any additional information over the
conventional modalities. In fact due to the above-mentioned deficiencies
it could give misleading information. Making diagnostic decisions based
on this faulty application of technology would be unacceptable to the
scientific cardiologist.
Dr. George Thomas
Senior Consultant
Department of Cardiology
Indira Gandhi Co-operative Hospital & The Co-operative Medical College
Kochi
India
References
(1) Y Matsumura, P M Elliott, M S Virdee, P Sorajja, Y Doi W J
McKenna. Left ventricular diastolic function assessed using Doppler tissue
imaging in patients with hypertrophic cardiomyopathy: relation to symptoms
and exercise capacity. Heart 2002;87:247-251
(2) Maslak SH, Freund JG. Color Doppler Instrumentation. In: Vascular
Imaging by Color Doppler and Magnetic resonance. Lanzer P (Ed), Springer-
Verlag Berlin Heidelberg; 1991: 87-123
In their study, Jenni et al describe the echocardiographic characteristics
of a relatively rare cardiomyopathy, isolated ventricular non-compaction.
As stated by the authors, this is a disease entity that is difficult to
diagnose during life, and the improvement in image quality of modern
echocardiography will probably allow to improve its early detection. In
the last two years, our group diagno...
In their study, Jenni et al describe the echocardiographic characteristics
of a relatively rare cardiomyopathy, isolated ventricular non-compaction.
As stated by the authors, this is a disease entity that is difficult to
diagnose during life, and the improvement in image quality of modern
echocardiography will probably allow to improve its early detection. In
the last two years, our group diagnosed ventricular non compaction by
magnetic resonance (MR)imaging in several patients in whom no suspicion of
this disease existed after routine echocardiography and cardiac
catheterisation. Even in retrospect, it was impossible to detect the
abnormalities described by Jenni et al in several of these patients. MR
however clearly showed localised thickening of the left ventricular wall
("spongy myocardium" with intramyocardial caverns and excessive
trabeculation. Dynamic MR demonstrated the high speed expulsion of blood
from the caverns during systole which was not visible on color doppler.
In our series of 7 patients, the reason for referral was heart
failure in 4 and ventricular arrhythmias in 1. One patient was examined
because he was the father of a baby with heart failure and proven non
compaction. Surprisingly, in 2 other patients, typical signs of
ventricular non compaction were found even though the referral diagnosis
was myocardial infarction or atrial septal defect. The MR characteristics
were increased thickness of parts of the left ventricle of 1.3 up to 1.7
cm in diastole and an irregular endocardial surface with increased
trabeculation. In all cases, the thickening was seen in the apex and part
of the lateral wall. Basal portions of the ventricle were always normal.
On dynamic imaging (gradient echo sequence) blood was seen to be expulsed
from caverns in the thickened myocardium. On T1 weighted spin echo
imaging, the thickened myocardium had a peculiar aspect comparable to the
echo finding of Jenni : the endocardial part of the myocardium showed an
important increase in signal intensity in comparison with the epicardial
part of the muscle the normal myocardium and the normal myocardiyum. This
is typical for imaging of slowly flowing blood : the spin echo images were
made in mid diastole, a part of the heart cycle with less movement of
blood in these caverns.
On the basis of these findings, we would suggest to incorporate an MR
study in suspected cases of heart failure cardiomyopathy, apical
hypertrophy, and important ventricular arrhythmias. Larger cooperative
studies are needed to further delineate the role of MR in this difficult
diagnosis.
We read with great interest the article by Toivonen who has shed
light on the difficulties encountered in applying heart rate correction
formulae for the QT interval.
We studied the QT-RR relationship in 130 term born infants during sleep
and tested the appropriateness of different heart rate correction
formulae(Bazett, Hodges, Fridericia and Framingham) used to compute the
QTc intervals derive...
We read with great interest the article by Toivonen who has shed
light on the difficulties encountered in applying heart rate correction
formulae for the QT interval.
We studied the QT-RR relationship in 130 term born infants during sleep
and tested the appropriateness of different heart rate correction
formulae(Bazett, Hodges, Fridericia and Framingham) used to compute the
QTc intervals derived from the electrocardiogram recorded in healthy
infants undergoing routine polysomnography. We tested the behaviour of
these formulae at the physiologically higher heart rates encountered in
infants.
With increasing heart rate and younger age the Bazett and Hodges formulae
overcorrects the QTc whereas the Fridericia and Framingham formulae
undercorrect. As already pointed out, there is strong dependence of these
formulae on heart rate or RR Interval, with no single formula providing a
linear relationship. However, the Hodges formula correlated best with the
RR interval and displayed the least scatter of the formulae tested. In
infants,in the setting of a borderline prolonged QTc Bazett interval, the
Hodges formula may be a useful adjunct in clinical decision-making.
The question about how we should manage an asymptomatic individual
with Brugada syndrome (BS) is not easy to answer. In the case reported,
the patient has remained asymptomatic for years (first ECG in 1987) but
despite of this, he is carrier of a disease with demonstrated association
with arrhythmic death, sometimes the first manifestation in this
population. Also, sudden death (SD) related to the syn...
The question about how we should manage an asymptomatic individual
with Brugada syndrome (BS) is not easy to answer. In the case reported,
the patient has remained asymptomatic for years (first ECG in 1987) but
despite of this, he is carrier of a disease with demonstrated association
with arrhythmic death, sometimes the first manifestation in this
population. Also, sudden death (SD) related to the syndrome is higher in
symptomatic families. In other genetically determined diseases, a family
history of SD is a predictive risk factor of SD. This has not been proven
in BS.[1]
There is no doubt that symptomatic patients must be protected with an
implantable cardioverter defibrillator (ICD). Asymptomatic individuals,
either with spontaneously abnormal ECG as the case discussed, or with
abnormal ECG after administration of drugs, should undergo an
electrophysiologic study (EPS). If inducible, then an ICD should be
recommended. HV measurement is of interest as up to 50% of BS have a
prolonged HV reflecting conduction disturbances.[2] Pharmacologic testing
with an intravenous sodium channel blocker should be performed in
patient's relatives for screening of possible carriers of the disease.
There is a 100% correlation between the results of the test and the
genotype.[3]
New data on asymptomatic individuals with a follow up of 3 years have
been recently presented.[4] A total of 16 SDs occurred in 190 asymptomatic
patients with BS (111 had spontaneously abnormal ECG and 79 had abnormal
ECG after administration of an antiarrhythmic drug). All SDs occurred in
the group with spontaneously abnormal ECG. EPS was performed in 136
subjects, of these, 45 were inducible and 91 were not. Six SDs occurred in
inducible patients (6/45, 13.33%) and 1 SD in those not inducible (1/91,
1.09%). In 9 patients with SD no EPS was performed. Therefore, inducible
patients with spontaneously abnormal ECG have an increased risk of SD
(13.33%) compared to those not inducible (1%). But still risk does exist
in this latter group. There is also the limitation of the 9 SDs in
individuals in whom EPS was not performed.
It is a fact that asymptomatic individuals may become symptomatic
during follow up and at present we don't know how to identify them.
Actually all symptomatic patients were carriers of the disease and
asymptomatic until the moment they developed the first symptoms. Efforts
should be made to find out predictive markers of SD in this subgroup. But,
no matter the result of the EPS, the threshold for ICD implantation should
be low in asymptomatic patients with a malignant family history. No deaths
have occurred in patients implanted with an ICD. Some questions still
remain. Is previous syncope predictive of SD? Being the peak incidence of
symptoms around the fourth decade of life, is there a higher risk in
younger patients as compared to the older ones? Is the magnitude of the ST
segment elevation related to the occurrence of arrhythmias? Also, taking
into account the data presented before, it seems that individuals with
spontaneously abnormal ECG are at higher risk than those with abnormal ECG
only after drug challenge. Does the fact that up to 40% of symptomatic
patients normalise the ECG during follow up have any predictive value?
Finally, we would like to discuss the study carried out by Hermida et
al.,[5] pointed in the article as showing 0% cardiovascular mortality of
asymptomatic patients with BS over a follow up of 49 months. In this
study, diagnosis of BS was made on the basis of the ECG pattern (ST
segment elevation of at least 0.1 mm in leads V1-V3). Prevalence was found
to be 6.1% (61 of 1000 subjects analysed) much higher than the prevalence
reported by other studies. Only 1 of the 61 individuals exhibited a coved-
type ST segment elevation (shown in the publication), characteristic of BS
and similar to the first cases reported in 1992. This subject had a
history of unexplained syncopes and resulted inducible in the EPS. The
other 60 individuals had an ECG with a saddle back-type ST segment
elevation (one of these is also shown in the article, and looks only
"suspicious" of BS). As the authors say, probably not all the subjects
with saddle back-type ST segment elevation had BS (early repolarization
may show a similar pattern). These individuals should have been exposed to
pharmacological testing to confirm or exclude the diagnosis. It seems
reasonable to think that an overestimation of BS occurred in the study
population, so the lack of mortality can be related to the fact that only
a small number of the subjects really had BS.
References
(1) Brugada P, Brugada R, Brugada J. Sudden death in high risk family
members: Brugada syndrome. Am J Cardiol 2000;86(suppl):40K-43K.
(2) Brugada P, Brugada J. Right bundle branch block, persistent ST elevation
and sudden cardiac death: a distinct clinical and electrocardiographic
syndrome. J Am Coll Cardiol 1992;20:1391-6.
(3) Brugada J, Brugada R, Wang Q, et al. Unmasking of genotype and phenotype
abnormalities by administration of class I antiarrhythmic drugs in
patients with sudden death (abstract). Eur Heart J 1998;19:557.
(4) Brugada J, Brugada R, Antzelevitch C, et al. Arrhythmic events in
patients with right bundle branch block and ST segment elevation in right
precordial leads (abstract). Eur Heart J 2001;22:17.
(5) Hermida J, Lemoine J, Bou Aoun F, et al. Prevalence of the Brugada
syndrome in an apparently healthy population. Am J Cardiol 2000;86:91-4.
Most cases of bacterial endocarditis of oral origin are not caused by dental procedures, but rather by poor oral health and hygiene. Poor oral
hygiene leading to inflamed gingiva is susceptible for bleeding. 38.5% of
patients are bacteriemic after toothbrushing or oral irrigation [1].
Gunthered concluded that in hypothetical month ending with a dental
extraction, the number of bacteriemic insults...
Most cases of bacterial endocarditis of oral origin are not caused by dental procedures, but rather by poor oral health and hygiene. Poor oral
hygiene leading to inflamed gingiva is susceptible for bleeding. 38.5% of
patients are bacteriemic after toothbrushing or oral irrigation [1].
Gunthered concluded that in hypothetical month ending with a dental
extraction, the number of bacteriemic insults arising from “physiologic”
sources (eg, toothbrushing and chewing ) is almost 1000 times more than
those arising from dental extraction [2]. Al-Karaawi et al showed that,
non-prophylaxis procedures (eg, dental examination, polishing teeth, local
anesthetic infiltration) present a similar risk of cumulative bacteremia
with the prophylaxis procedures (eg, scaling, multiple extractions,
mucoperiosteal surgery) [3]. On the other hand, many of the infected
patients in studies were shown to be taking antibiotic prophylaxis for the
dental procedures. At this point, the problem is that it is possible that
the prophylaxis failed to be successful, or the patients had contracted
endocarditis before or after dental procedure because of poor oral
hygiene.
As a conclusion, although prophylaxis is obligative, we hypothesize and
suggest that it is more important to encourage the patients with cardiac
abnormalities to maintain a high level of oral health.
References
(1) Roberts GJ, Holzel HS, Sury MRJ, Simmons NA, Gardner P, Longhurst P.
Dental bacteremia in children. Pediatr Cardiol 1997;18(1):24-7
(2) Guntheroth WG, How important are dental procedures as a cause of
infective endocarditis? Am J Cardiol 1984 ;54(7):797-801
(3) Al-Karaawi ZM, Lucas VS, Gelbier M, Roberts GJ. Dental procedures
inchildren with severe congenital heart disease: a theoretical analysis of
prophylaxis and non-prophylaxis procedures. Heart 2001;85:66-68
Dear Editor
Takeda et al. have observed that degree of mitral lateral annular excursion in mild to moderate aortic stenosis is very close to that in control group. In this study, both lateral and septal side of mitral annulus have shown a consistent decrease in long axis excursion with disease progression. Aortic stenosis may lead to physiological hypertrophy in early stages of the disease as discussed in hy...
Dear Editor
Optimal age for screening for familial HCM.
McKenna and Behr´s recommendation that offspring of carriers of mutations causing hypertrophic cardiomyopathy (HCM) should have regular evaluation “during puberty and early adulthood” could be read as suggesting that evaluation for carrier status is not necessary before puberty. This would be a pity as there is now good evidence arguing for echo...
I read with great interest the paper by Y Matsumura1 et al.[1] On face value the paper appears good. However, I am concerned about the increasing number of papers on Doppler Tissue Imaging (DTI) appearing in leading medical journals. DTI is a clear case of misuse of technology. It could turn out to be the 'Philadelphia Experiment' in cardiology. Doppler is best suited to study the direction of free m...
Dear Editor
In their study, Jenni et al describe the echocardiographic characteristics of a relatively rare cardiomyopathy, isolated ventricular non-compaction. As stated by the authors, this is a disease entity that is difficult to diagnose during life, and the improvement in image quality of modern echocardiography will probably allow to improve its early detection. In the last two years, our group diagno...
Dear Editor
We read with great interest the article by Toivonen who has shed light on the difficulties encountered in applying heart rate correction formulae for the QT interval.
We studied the QT-RR relationship in 130 term born infants during sleep and tested the appropriateness of different heart rate correction formulae(Bazett, Hodges, Fridericia and Framingham) used to compute the QTc intervals derive...
Dear Editor
The question about how we should manage an asymptomatic individual with Brugada syndrome (BS) is not easy to answer. In the case reported, the patient has remained asymptomatic for years (first ECG in 1987) but despite of this, he is carrier of a disease with demonstrated association with arrhythmic death, sometimes the first manifestation in this population. Also, sudden death (SD) related to the syn...
Dear Editor
Most cases of bacterial endocarditis of oral origin are not caused by dental procedures, but rather by poor oral health and hygiene. Poor oral hygiene leading to inflamed gingiva is susceptible for bleeding. 38.5% of patients are bacteriemic after toothbrushing or oral irrigation [1].
Gunthered concluded that in hypothetical month ending with a dental extraction, the number of bacteriemic insults...
Pages