Möller and colleagues interpret their case-crossover study as
demonstrating that sexual activity is causally associated with triggering
acute myocardial infarction.[1] The moderate relative risk of about 2-fold
reported, was derived from five acute myocardial infarctions occurring in
399 people having sex about once a week, equivalent to increasing the risk
of a heart attack from 0.26 percent per year...
Möller and colleagues interpret their case-crossover study as
demonstrating that sexual activity is causally associated with triggering
acute myocardial infarction.[1] The moderate relative risk of about 2-fold
reported, was derived from five acute myocardial infarctions occurring in
399 people having sex about once a week, equivalent to increasing the risk
of a heart attack from 0.26 percent per year to 0.52 percent per year,
equivalent to 1 event for every 20,000 sexual acts. While this relative
risk might cause concern to the risk averse, the estimated risk is
trivial. Furthermore, the possible long-term benefits of more frequent
sexual intercourse in halving mortality among men having sex at least once
a week compared with those who have sex less often than once a month was
not considered by Möller.[2] For every 1000 middle-aged men participating
in frequent sexual intercourse, 8 would avoid dying each year. The acute
myocardial infarctions that would be expected to be triggered in these men
over the course of a year is about 2.6 per 1000, equivalent to no more
than 3 events, of which perhaps no more than half would be fatal. Even if
the "protective" effect of frequent sexual intercourse is generated, at
least in part, by confounding[2], these data illustrate that any harmful
influence of sexual activity is minor, and can be swamped by the
confounding produced by factors associated with what is a relatively
modest level of desire coupled with available opportunities for sex. If,
as may be the case, even some of the "protective" influence seen in the
Caerphilly study is real, then frequent sexual intercourse is clearly of
net overall benefit.
In health promotion terms, sexual intercourse might be considered to
be a form of moderate activity, as it uses (on average) only half the
energy of vigorous forms of physical activity.[3] Given the increased
evidence that health benefits accrue from even moderate levels of physical
activity, perhaps a more popular message would be to substitute sex for
more boring forms of physical activity three times a week.
Shah Ebrahim, Professor of Epidemiology of Ageing
George Davey Smith, Professor of Clinical Epidemiology
Department of Social Medicine, University of Bristol, BS8 2PR
References
(1) Möller J, Ahlbom A, Hulting J, Diderichsen F, de Faire U,
Reuterwall C, Hallqvist J. Sexual activity as a trigger of myocardial
infarction. A case-crossover analysis in the Stockholm Heart Epidemiology
Programme (SHEEP). Heart 2001;86:387-390
(2) Davey Smith G, Frankell S, Yarnell J. Sex and death: are they
related? Findings from the Caerphilly cohort study. BMJ 1997;315:1641-5
(3) Tofler GH, Mittleman MA, Muller JE. Physical activity and the
triggering of myocardial infarction: the case for regular exercise. Heart
1996;75:323-5
In the report by Palka et al,[1] and in previous such reports [2,3]
the phenotypic variation seen in supposedly genetically identical
monozygotic (MZ) twins with hypertrophic cardiomyopathy (HCM) is
interpreted as a measure of the importance of environmental influences.
However, although environmental factors undoubtedly contribute to the
phenotype in HCM, there is substantial evidence that d...
In the report by Palka et al,[1] and in previous such reports [2,3]
the phenotypic variation seen in supposedly genetically identical
monozygotic (MZ) twins with hypertrophic cardiomyopathy (HCM) is
interpreted as a measure of the importance of environmental influences.
However, although environmental factors undoubtedly contribute to the
phenotype in HCM, there is substantial evidence that discordance between
MZ twins in fact has a genetic component. MZ twins develop from a
separation of the embryonic cells at any point from the two-cell stage up
until as late as day 8 when the primordial streak has already started to
form.[4] The timing of the separation has consequences for the genetic
composition of each twin, as the cells become more heterogeneous with time
with respect to the mitochondria they carry [5] and the pattern of
methylation, and hence potential gene expression, they display.[6]
Mitochondria are inherited through the maternal line only and contain
their own genome which encodes a subset of mitochondrial proteins. During
mitosis mitochondria can segregate unequally between the daughter cells.
Where the oocyte contains a mixed population of mitochondrial DNA variants
somatic mosaicism can arise, one consequence of which is that one MZ twin
may inherit a different complement of mitochondrial DNA than the other.
While such a difference in mitochondrial DNA is often of only theoretical
relevance, it would be of particular importance in HCM. Not only do many
of the mitochondrial DNA mutation syndromes display HCM-like features, but
common variants in mtDNA are associated with susceptibility to
cardiomyopathy [7] and co-inheritance of mitochondrial variants with
sarcomeric mutations produces a much more extreme phenotype .[8] These
findings can be explained by the recent recognition that perturbations of
myocardial energetics play a central role in HCM pathogenesis.[9]
DNA methylation plays a recognised role in regulation of gene
expression, and important changes in the methylation of genes occur during
embryogenesis. In particular the male gametic genome is first demethylated
[10] and then selectively re-methylated in a step wise fashion up to the
stage of the blastocyst.[5] Hence, some of the observed discordance
between MZ twins can also be due to separation of a heterogeneously
methylated group of cells, with discordant patterns of gene expression.
It is through these epigenetic modifying phenomena that we may begin
to explain the differences in phenotypic expression of HCM, not only in MZ
twins but also that seen within and between pedigrees containing the same
causal mutant gene.
References
(1) Palka P, A Lange, DJ Burstow. Different presentation of
hypertrophic cardiomyopathy in monozygotic twins. Heart 2003;89(7):751.
(2) Reid JM, AB Houston, E Lundmark. Hypertrophic
cardiomyopathy in identical twins. Br Heart J 1989;62(5):384-8.
(3) Ko YL et al. Idiopathic hypertrophic cardiomyopathy in
identical twins. Morphological heterogeneity of the left ventricle. Chest1992;102(3):783-5.
(4) Gringras, P. and W. Chen, Mechanisms for differences in monozygous
twins. Early Hum Dev 2001;64(2):105-17.
(5) Youssoufian H, RE Pyeritz. Mechanisms and consequences of somatic mosaicism in humans. Nat Rev Genet 2002;3(10):748-58.
(6) Singh SM, B Murphy, R O'Reilly. Epigenetic contributors
to the discordance of monozygotic twins. Clin Genet 2002;62(2):97-103.
(7) Khogali SS et al. A common mitochondrial DNA variant
associated with susceptibility to dilated cardiomyopathy in two different
populations. Lancet 2001;357(9264):1265-7.
(8) Arbustini E. et al. Coexistence of mitochondrial DNA and beta
myosin heavy chain mutations in hypertrophic cardiomyopathy with late
congestive heart failure. Heart 1998;80(6):548-58.
(9) Blair E. 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(11):1215-20.
(10) Mayer W et al. Demethylation of the zygotic paternal genome. Nature 2000;403(6769):501-2.
Bosi and colleagues [1] suggested that significant volume
load of the heart as a result of chronic anaemia in young adults with beta
thalassaemia major is the main culprit of the so-called 'beta thalassaemic
cardiomyopathy'. Their findings, based on echocardiographic assessment of
left ventricular function, were similar to those reported
previously.[2,3] Nonetheless, the role of arterial dysfunction in th...
Bosi and colleagues [1] suggested that significant volume
load of the heart as a result of chronic anaemia in young adults with beta
thalassaemia major is the main culprit of the so-called 'beta thalassaemic
cardiomyopathy'. Their findings, based on echocardiographic assessment of
left ventricular function, were similar to those reported
previously.[2,3] Nonetheless, the role of arterial dysfunction in the
pathogenesis of myocardial contractile dysfunction has likewise been
ignored.
The fact that both the end systolic meridional and circumferential
wall stress were increased in their patients would suggest an elevated
left ventricular afterload. The importance of optimal ventriculo-arterial
interaction in enhancing mechanical efficiency of the heart cannot be
overemphasized. Unexpectedly, the systemic vascular resistance, which
reflects the static vascular load, was significantly lower in their
patients than controls. Furthermore, the significance of the pulsatile
vascular load has not been discussed.
We have previously shown that teenagers and young adults with beta-
thalassaemia major have arterial endothelial dysfunction and increased
arterial stiffness.[4] The increase in arterial stiffness, relating
probably to structural alteration as a result of iron overload and
endothelial dysfunction, and increased wave reflection as a result of a
faster pulse wave velocity increase the pulsatile afterload. Interaction
between left ventricular ejection and systemic arterial impedance may thus
render less favorable as the impedance modulus may no longer be the least
at where the flow harmonics are highest.[5]
Our previous findings support the view of a multi-factorial etiology
of LV failure in patients with beta-thalassaemia major.[6] Apart from
myocardial iron deposition, myocarditis and immunogenetic profile,
arterial dysfunction is also contributory.
References
(1) Bosi G, Crepaz R, Gamberini MR, et al. Left ventricular
remodelling, and systolic and diastolic function in young adults with b
thalassaemia major: a Doppler echocardiographic assessment and correlation
with haematological data. Heart 2003;89:762-766.
(2) Lewis SB, Rachmilewitz AE, Amitai N, et al. Left ventricular function
in b-thalassemia and the effect of multiple transfusion. Am Heart J 1978;96:636-645.
(3) Kremastinos DT, Tsiapras DP, Tsetos GA, et al. Left ventricular
diastolic Doppler characteristics in beta-thalassemia major. Circulation 1993;88:1127-1135.
(4) Cheung YF, Chan GCF, Ha SY. Arterial stiffness and endothelial function
in patients with beta-thalassaemia major. Circulation 2002;106;2561-2566.
(5) Nichols WW, O'Rourke MF. Vascular impedance. In McDonalds's Blood
Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th
ed. London: Edward Arnold; 1998:54-97, 243-293.
(6) Jessup M, Manno CS. Diagnosis and management iron-induced heart disease
in Cooley's anemia. Ann N Y Acad Sci 1998;850:242-250.
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular
mechanisms involved in the inflammatory mechanisms and haemostatic factors
leading to coronary atherosclerosis. They also describe the role of
chronic infection in this process.[1] However, they omit an important
factor that is common to the majority of patients su...
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular
mechanisms involved in the inflammatory mechanisms and haemostatic factors
leading to coronary atherosclerosis. They also describe the role of
chronic infection in this process.[1] However, they omit an important
factor that is common to the majority of patients suffering from this
condition – current or previous cigarette smoking.
We have undertaken an investigation into the relationship between
smoking habit, notably quantitative measurement of nicotine intake and
factors involved in the formation of the plaque and the inflammatory
process. Due to ‘social desirability bias’ associated with smoking
patients frequently under-report or deny their smoking habit. It would
seem therefore that the greater the clinical impact of smoking the greater
the patient guilt enhancing the likelihood of denial.
To improve the accuracy of information about smoking a 6-minute point
-of-care test to detect nicotine metabolites (including cotinine), called
SmokeScreen® was developed.[2] The easy to use colorimetric urine test
can provide qualitative, semi-quantitative and quantitative measurements
of nicotine intake. With this test we undertook an audit of smoking habits
of 154 new patients attending a large inner-city hospital cardiology
outpatient clinic, comparing the test identification of smoking with self-
completed questionnaire of current smoking habit. The results identified
112 (72.7%) as non-smokers, 30 (19.5%) as confessed smokers and 12 (7.8%)
as ‘smoking deceivers’.
We followed this with another study of the same population (n=85, 33
smokers and 52 never-smokers) to examine the interaction of smoking with
risk factors associated coronary artery disease, as assessed by a
biochemical screen and a blood count. Interestingly, none of the
parameters measured in the biochemical screen, such as cholesterol, HDL
and triglycerides; urea and electrolytes and liver function tests were
associated with smoking habit or quantitative assessment of nicotine
intake. Whereas white blood cell count (WBC) was significantly higher in
smokers (p=0.002), in particular neutrophils (p=0.01) and eosinophils
(p=0.02). Lymphocytes, monocytes and basophiles were higher but failed to
reach significance. Quantitative assessment of nicotine intake of the
smokers further revealed a positive correlation with WBC (p<_0.0001 neutrophils="neutrophils" p0.001="p0.001" eosinophils="eosinophils" p0.004="p0.004" and="and" lymphocytes="lymphocytes" p0.02="p0.02" with="with" monocytes="monocytes" approaching="approaching" significance="significance" p="p"/> It would seem from this pilot study that smoking or the amount of
tobacco consumed doesn’t influence the biochemical risk factors for
coronary artery disease, such as cholesterol and HDL, but does increase
many of the cellular factors which Tousoulis et al. identified as
contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]
We suggest that identification of smokers, feedback from the point-of-care
test and subsequent advice on smoking cessation could have a significant
impact on reducing many of the risk factors associated with coronary
atherosclerosis and lower cardiovascular events and mortality.
References
(1) Tousoulis D, Davies G, Stefanadis, Toutouzas P, Ambrose JA.
Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart 2003;89:993-997.
(2) Cope GF, Nayyar P, Holder R, Gibbons J, Bunce R. A simple near-patient
test for nicotine and its metabolites in urine to assess smoking habit. Clin Chim Acta 1996;256:135-149.
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack,
and surgery. Symathetic denervation is involved in such cases. Prolonged T
wave inversion would indicate the change in repolarization related to the
sympathetic...
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack,
and surgery. Symathetic denervation is involved in such cases. Prolonged T
wave inversion would indicate the change in repolarization related to the
sympathetic activation. The discrepancy between remarkable ST elevation and
mild elevation of myocardial enzymes would indicate myocardial stunning with
sympathetic denervation. Although some Japanese docotrs call such a clinical
state ampulla cardiomyopathy, it is contoversial. Apical thrombus has
firstly described all over the world.[2]
References
(1) Barrera-Ramirez CF, Jimenez-Mazuecos JM, Alfonso F. Apical thrombus associated with left ventricular apical ballooning. Heart 2003;89:927.
(2) Tetsuya Sato et al. Extensive myocardial stunning showing transient regression of prolonged T wave inversion and prolonged sympathetic
denervation. Internal Med 2001;40:312-319.
I read with great interest the article by Jenni and colleagues [1], and the accompanying editorial by Varnava [2]. I agree with them that this entity is deserving of more attention, but if it is to be accorded special
status within the group of cardiomyopathies, then I would suggest that much more work needs to be done to establish the phenotype.
Thus, Jenni et al [1] argue that the non-compacted layer o...
I read with great interest the article by Jenni and colleagues [1], and the accompanying editorial by Varnava [2]. I agree with them that this entity is deserving of more attention, but if it is to be accorded special
status within the group of cardiomyopathies, then I would suggest that much more work needs to be done to establish the phenotype.
Thus, Jenni et al [1] argue that the non-compacted layer of the myocardium needs to be twice as thick as the compact layer to justify the diagnosis. They also indicate, however, that the bilaminar arrangement is not uniformly distributed throughout the left ventricular walls. The
autopsied examples they show in Figure 4 illustrate the problems which might arise in applying their definition. To my eyes, the heart illustrated in Figure 4B at no site shows a non-compacted layer twice as thick as the compact layer.
Indeed, the trabeculations at the apical part
of the ventricle look relatively normal, with most of the ventricular wall seemingly having a compact appearance. There is then a further problem in that, in the normal heart, the compact myocardium is of no more than 1-2mm
thickness at the apical thin point. Have the team from Zurich taken this into account when making their correlations? And why did they not measure the thickness of the compact and non-compact layers in their autopsy
specimens, in this way providing objective rather than subjective evidence to establish this important phenotype?
I am not meaning to devalue the importance of their work, since this is by far the largest and best documented series establishing the existence of this diagnostic entity. But we need to establish whether it is the trabeculations themselves which are abnormal, or the ventricular myocardium related to the origins of the papillary muscles of the mitral valve. In fact, in all the examples shown, the area of maximal non-compaction is at the site of the origins of the papillary muscles from the lateral ventricular wall. And, as is shown by Figure 3, this is the site of maximal abnormality in all seven patients in which echo-pathological
correlations were made.
This feature is also worthy of consideration by Varnava [2], who uses the beautiful illustrations by my friend David Sedmera to illustrate the points made. To the best of my knowledge, however, there is no evidence as yet to substantiate the claim that the entity represents "an arrest in cardiac embryogenesis". In this age of evidence-based medicine, one had rather hoped we had passed the stage of using speculative armchair embryology to support scientific data. Examination of Sedmera's scanning electron microscopic preparations shows that the normal process of
compaction is confined largely to the apex and the mid-anterior ventricular wall, findings which do not correlate well with the observations of Jenni et al [1] for isolated left ventricular non-compaction.
(1) Jenni R, Oeschslin E, Schneider J, Attenhoffer Jost C, and Kaufmann P A. Echocardiographic and pathoanatomical characteristics of isolated left
ventricular non-compaction: a step towards classification as a distinct
cardiomyopathy. Heart 2001; 86:666-671.
(2) Varnava A M. Isolated left ventricular non-compaction: a distinct cardiomyopathy? Editorial. Heart 2001; 86:599-600.
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a
protocol for earlier sit up and mobilisation after routine transfemoral
cardiac catheterisation in contemporary practice. Patients were
randomised to be mobilised after 2½ hours or 4½ hours bed rest. The
authors report that a significant reduction in...
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a
protocol for earlier sit up and mobilisation after routine transfemoral
cardiac catheterisation in contemporary practice. Patients were
randomised to be mobilised after 2½ hours or 4½ hours bed rest. The
authors report that a significant reduction in the duration of bed rest
was achieved in the early mobilisation protocol group with no adverse
effect on vascular complications. They also report that early
mobilisation was associated with a reduction in pain and discomfort,
although this data is not presented. On this basis, the authors call into
question the role of alternative arterial access sites for diagnostic
cardiac catheterisation.
The published data does not support this viewpoint. Firstly, the
early mobilisation protocol still required 2½ hours of bed rest. There is
extensive published evidence that bed rest after medical procedures has
few benefits and a wide range of adverse effects.[2] The combination of
back pain related to bed rest and groin pain related to femoral puncture
and pressure haemostasis delays mobilisation and return to normal activity
after discharge in at least one third of patients.[3] Secondly, despite
studying only a selected low risk group of patients (only some elective
patients with chest pain undergoing diagnostic angiography were eligible
for the study. Patients with a difficult femoral puncture, those
undergoing percutaneous revascularisation, receiving adjunctive
antithrombotic therapy or with previously treated peripheral vascular
disease were excluded) haematomas re-bleeding and vaso-vagal reactions
were common. Indeed this study suggests that these problems occur in 15-
20% of these low risk patients. In contrast to this, we have recently
reported on a series of 1000 consecutive transradial cases, in which a
third of the study subjects had major risk factors for vascular
complications.[4] Patients undergoing diagnostic angiography or
percutaneous intervention were mobilised immediately, removing the
potential for adverse effects from bed rest. Avoiding a groin puncture
will facilitate a rapid return to normal activity after discharge. In
this high risk population the incidence of both major and minor vascular
complications was less than 1%. The data from the North Staffordshire
series is entirely compatible with other published case series and
randomised trials, which consistently show that use of the transradial
access site is associated with short mobilisation and discharge times, a
reduction in procedure costs and vascular complications, and a consistent
improvement in patient quality of life when compared to the femoral access
site.[5-7]
In our view the data presented (a 2½ hour period of bed rest and 15-
20% incidence of access site problems) strengthens the case for selecting
the radial artery (no bed rest and less than 1% incidence of access site
problems) in the majority of patients undergoing routine diagnostic
cardiac catheterisation.
References
(1) Pollard SD, Munks K, Wales C, Crossman DC, Cumberland DC, Oakley
GDG, Gunn J. Position and mobilisation post-angiography study. (PAMAS): a
comparison of 4.5 hours and 2.5 hours bed rest. Heart 2003;89:447-448.
(2) Allen C, Glasziou P, Del Mar C. Bed rest: a potentially harmful
treatment needing more careful evaluation. Lancet 1999;354:1229-1233.
(3) Foulger V. Patients’ views of day-case cardiac catheterisation.
Professional Nurse 1997;12:478-480.
(4) Eccleshall SC, Banks M, Carroll R, Jaumdally R, Fraser D, Nolan J.
Implementation of a diagnostic and interventional transradial programme:
resource and organisational implications. Heart 2003;89:561-562.
(5) Eccleshall S, Muthusamy T, Nolan J. The transradial access site
for cardiac procedures: a clinical perspective. Stent 1999;2(3):74-9.
(6) Al-Allaf K, Eccleshall S, Kaba R, et al. Arterial access for
cardiac procedures utilising the percutaneous transradial approach. Br J
Cardiol 2000;7:548-52.
(7) Kiemeneij F, Laarman GJ, Odekerken D et al. A randomised
comparison of percutaneous transluminal coronary angioplasty by the
radial, brachial and femoral approaches: the Access study. J Am Coll
Cardiol 1997;29(6):1269-75.
Barakat and colleagues' observations are clinically important.
Our work on the performance of the Rose angina questionnaire in a multi-
ethnic study of a community based sample of 1509 adults from European,
Indian, Pakistani and Bangladeshi ethnic groups corroborates and
complements, their observations.[1]
European men and women mostly reported chest pain in Rose
Questionnaire (definite angina c...
Barakat and colleagues' observations are clinically important.
Our work on the performance of the Rose angina questionnaire in a multi-
ethnic study of a community based sample of 1509 adults from European,
Indian, Pakistani and Bangladeshi ethnic groups corroborates and
complements, their observations.[1]
European men and women mostly reported chest pain in Rose
Questionnaire (definite angina criteria) qualifying sites i.e. sternum or
left chest and left arm. In contrast, there were substantial numbers of
South-Asian respondents with left-sided chest pain but without left-sided
arm pain. This pattern was particularly clear in Indians. Right-sided
chest pain was commoner in Pakistanis and the pattern of pain was diffuse
in Bangladeshis of both sexes, in whom left chest pain was never combined
with left arm pain. Our published diagrams on chest pain site illustrate
these points.[1]
The‘classical’ elements of the history were less frequent in South
Asians than in Europeans, while ‘atypical’ features were most common in
Pakistanis and Bangladeshis. Bangladeshis with chest pain mostly failed to
report the other features required for definite angina on the Rose
Questionnaire. Our paper raised the possibility of systematic differences
between ethnic groups in the site of reported chest pain. We wrote that
firm conclusions must await confirmation from further studies. With the
observations of Barakat et al, this area is shown to be epidemiologically
and clinically important. It is likely that Barakat et al's findings
apply not just to Bangladeshis but to other South Asian populations.
With their exceptionally poor knowledge about heart disease and
diabetes,[2] their economic deprivation, the significant clustering of
cardiovascular risk factors,[3] and atypical presentation of pain
associated with coronary heart disease, Bangladeshis are in particular
jeopardy.
References
(1) Fischbacher CM, Bhopal R, Unwin N, White M, Alberti
KG. The performance of the Rose angina questionnaire in South Asian and
European origin populations: a comparative study in Newcastle Int J
Epidemiol 2001;54:786.
(2) Rankin J, Bhopal R. Understanding of heart disease and diabetes
in a South Asian community: cross sectional study testing the `snowball'
sample method. Pub Health 2001;115:253-260.
(3) Bhopal, R S, Unwin N, White M. et al. heterogeneity of coronary
heart disease risk factors in Indian, Pakistani, Bangladeshi and European
origin populations: cross sectional study. BMJ 1999;319:215-220.
In normal hearts the left ventricle has only up to 3 trabeculations and is less trabeculated than the right ventricle [1]. In 1990, however, it was first described that in rare cases >3 trabeculations occur in
the left ventricle (Non-compaction, isolated left ventricular abnormal trabeculation, hypertrabeculation) [2]. The trabeculations consist of myocardium, show the same echogenicity, move synchronously w...
In normal hearts the left ventricle has only up to 3 trabeculations and is less trabeculated than the right ventricle [1]. In 1990, however, it was first described that in rare cases >3 trabeculations occur in
the left ventricle (Non-compaction, isolated left ventricular abnormal trabeculation, hypertrabeculation) [2]. The trabeculations consist of myocardium, show the same echogenicity, move synchronously with the heart and have echocardiographically to be differentiated from thrombi and
intramural haematoma [3]. Hypertrabeculation occurs with or without cardiac malformations in dilated as well as in normally sized hearts, commonly associated with heart failure and ECG abnormalities [4,5,6]. A considerable number of patients with left ventricular hypertrabeculation
were found to suffer from neuromuscular disorders like Becker’s muscular dystrophy [7], metabolic myopathy [8], myotonic dystrophy [9], Barth syndrome [10], infantile epilepsy-encephalopathy syndrome [11], Roifman syndrome [12], and skeletal abnormalities like Melnick-Needles syndrome [13] and nail-patella syndrome [14]. Hypertrabeculation can be familial and can develop during lifetime [15]. Hypertrabeculation seems frequently
overlooked, and considerable overlap exists between the diagnosis of apical hypertrophic cardiomyopathy, left ventricular involvement of right ventricular dysplasia and endocardial fibroelastosis. To bridge the gap between ignorance and knowledge Jenni at al. propose “clear cut echocardiographic criteria” for “isolated ventricular non-
compaction” and, furthermore, suggest that the WHO classification of cardiomyopathies should include non-compaction as a distinct
cardiomyopathy [16]. Unfortunately, their suggestions might create more confusion than understanding.
1. The term “isolated – without coexisting cardiac abnormalities” is misleading, since it ignores the finding of decreased left ventricular function or left ventricular wall thickening in nearly all patients with
hypertrabeculation [4,5,6]. Additionally, hypertrabeculation may have the same pathogenetic background in both these forms.
2. The term “noncompaction” suggests that the pathogenesis of the abnormality is known and due to an disturbed compaction process of the myocardium. A scientific proof, however, that this abnormality results
from an embryonic defect in the compaction process of the myocardium, is still lacking. On the contrary, development of hypertrabeculations in a normally compacted left ventricle in adulthood has been described [15].
3. The given definition “numerous, excessively prominent trabeculations” is not clear cut as it does not give a number above which the phenomenon is abnormal. On the contrary, we suggest the anatomically confirmed
definition of >3 trabeculations within one imaging plane, apically from the insertion of the papillary muscles, as a practically useful diagnostic criterion when performing echocardiography, but also magnetic resonance imaging or computed tomography [1,4,7].
4. The definition of hypertrabeculation based on the relation between volume recessuses and volume of trabeculations is weak, as volume and depth of the recessuses are difficult to assess echocardiographically and
might be dependent on the hemodynamic status of the patient. Similarly, the ratio between non-compaction and compaction layer >2 is also dependent at which location and volume status measurements are performed.
5. Since the follow-up studies of patients with hypertrabeculation are rare and conflicting data are available about the embolic risk of patients with hypertrabeculation, the general recommendation for oral
anticoagulation in all patients with hypertrabeculation does not seem to be justified [5,6,7]. Overlooking patients with hypertrabeculation over 6 years we did not find an increased rate of stroke or embolism in them.
6. Facing all the uncertainties and open questions regarding genetics, pathogenesis, aetiology, clinical manifestations and prognosis of left ventricular hypertrabeculation, there is a need to collect all the
available data. Unfortunately, Jenni at al. have completely ignored any indications reported in the literature about an association of non-compaction with systemic disorders.
In conclusion, our present knowledge about left ventricular hypertrabeculation is too poor to recommend it to the WHO as a distinct cardiomyopathy. Left ventricular hypertrabeculation may be due to a frustrated attempt of an impaired myocardium due to an inborn error to
hypertrophy, that either manifests congenitally or in adulthood. Instead of creating unnecessary borders and ignoring valuable contributions there is a need to concentrate on common research about hypertrabeculation. Too many questions are awaiting an answer.
References
(1) Boyd M T, Seward J B, Tajik A J, et al. Frequency and location of prominent left ventricular trabeculations at autopsy in 474 normal human hearts: Implications for evaluation of mural thrombi by two-dimensional
echocardiography. J Am Coll Cardiol 1987; 9:323-6.
(2) Chin T K, Perloff J K, Williams R G, et al. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation 1990; 82:507-13.
(3) Stöllberger C, Finsterer J, Waldenberger F R, et al. Intramyocardial hematoma mimicking abnormal left ventricular trabeculation. J Am Soc Echocardiogr 2001; 14:1030-2.
(4) Stöllberger C, Finsterer J, Blazek G. Isolated left ventricular abnormal trabeculation: Follow-up and association with neuromuscular disorders. Can J Cardiol 2001; 17:163-8.
(5) Oechslin E, Attenhofer Jost C H, Rojas J R, et al. Long-term follow-up of 34 adults with isolated left ventricular noncompaction: a distinct cardiomyopathy. J Am Coll Cardiol 2000; 36:493-500.
(6) Ichida F, Hamamichi Y, Miyawaki T, et al. Clinical features of isolated noncompaction of the ventricular myocardium. J Am Coll Cardiol 1999; 34:233-40.
(7) Stöllberger C, Finsterer J, Blazek G, et al. Left ventricular non-compaction in a patients with Becker’s muscular dystrophy. Heart 1996; 76:380.
(8) Finsterer J, Stöllberger C. Hypertrabeculated left ventricle in mitochondriopathy. Heart 1998; 80:632.
(9) Finsterer J, Stöllberger C, Wegmann R, et al. Left ventricular hypertrabeculation in myotonic dystrophy type 1. Herz 2001; 26:287-90.
(10) Bleyl S B, Mumford B R, Thompson V, et al. Neonatal, lethal noncompaction of the left ventricular myocardium is allelic with Barth syndrome. Am J Hum Genet 1997; 61:868-72.
(11) Hussein A, Schmaltz A A, Trowitzsch E. Isolated abnormality of the myocardium in 3 children. Klin Pädiatr 1999; 211:175-8.
(12) Mandel K, Grunebaum E, Benson L. Noncompaction of the myocardium associated with Roifman syndrome. Cardiol Young 2001; 11:240-3.
(13) Wong J A, Bofinger M K. Noncompaction of the ventricular myocardium in Melnick-Needles syndrome. Am J Med Genet 1997; 71:72-5.
(14) Finsterer J, Stöllberger C, Wanschitz J, et al. Nail-patella syndrome associated with respiratory chain disorder. Eur Neurol 2001; 46:92-5.
(15) Finsterer J, Stöllberger C, Blazek G, et al. Cardiac involvement in myotonic dystrophy, Becker muscular dystrophy and mitochondrial myopathy: A five-year follow-up. Can J Cardiol 2001; 17:1061-9.
(16) Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and pathoanatomical characteristics of isolated left ventricular non-compaction: a step towards classification as a distinct cardiomyopathy.
Heart 2001; 86:666-71.
On 24 June the National Institute of Clinical Excellence (NICE)
issued their Appraisal consultation document: coronary artery
stents.[1] With the proviso that ‘the decision to use a bare metal
stent or drug-eluting stent (DES) will depend on the anatomy of
the target vessel for stenting and the severity of the disease’
(presumably reflecting issues of deliverability of the stent
platforms on offer), t...
On 24 June the National Institute of Clinical Excellence (NICE)
issued their Appraisal consultation document: coronary artery
stents.[1] With the proviso that ‘the decision to use a bare metal
stent or drug-eluting stent (DES) will depend on the anatomy of
the target vessel for stenting and the severity of the disease’
(presumably reflecting issues of deliverability of the stent
platforms on offer), the key point was that a ‘DES is
recommended .. [when] .. the target artery is less than 3mm in
diameter or the lesion to be stented is longer than 20mm.’
We applaud the NICE philosophy of selective DES implantation
in a resource-hungry health service. It must be appreciated by
interventional cardiologists, however, that this guideline will
reduce, but not abolish, restenosis. As we recently argued,[2]
there is a law of diminishing returns with DESs; escalating
numbers (and, therefore, costs) would be required to squeeze the
last few % points of restenosis out of the system. Clearly, NICE
have grasped this reality and are endorsing a policy of scientific
rationing, the science providing some targeting of the few DESs
permitted to the lesions most likely to restenose.
What are the implications of the NICE guidelines? Applying
them to our institution reveals that a DES would be used in about
34% of lesions. This would reduce our clinical recurrence (re-
PCI) rate - the only restenosis parameter a centre not performing
routine follow-up angiography can count – from 9% to 5.1%. A
considerable disadvantage of the NICE system would be that no
stents of certain important and commonly used sizes would be
permitted, such as 3 x16mm, 3 x 18mm or any stent of 3.5mm
calibre, even if the target lesion is a long stenosis in the proximal
left anterior descending artery of a diabetic patient. If, instead,
we allotted DES according to our recommended system, based
upon a matrix of restenosis risk,[2] we find that a 34% DES rate
would yield an almost identical overall institutional recurrence
risk (5.2%), with the advantage that we would have DES
available for the sizes and indications mentioned above. Stock
control would also be simpler (important if the DES in question
has a limited shelf life) because rarely used sizes would not be
stocked.
Dear Editor
Möller and colleagues interpret their case-crossover study as demonstrating that sexual activity is causally associated with triggering acute myocardial infarction.[1] The moderate relative risk of about 2-fold reported, was derived from five acute myocardial infarctions occurring in 399 people having sex about once a week, equivalent to increasing the risk of a heart attack from 0.26 percent per year...
Dear Editor
In the report by Palka et al,[1] and in previous such reports [2,3] the phenotypic variation seen in supposedly genetically identical monozygotic (MZ) twins with hypertrophic cardiomyopathy (HCM) is interpreted as a measure of the importance of environmental influences. However, although environmental factors undoubtedly contribute to the phenotype in HCM, there is substantial evidence that d...
Dear Editor
Bosi and colleagues [1] suggested that significant volume load of the heart as a result of chronic anaemia in young adults with beta thalassaemia major is the main culprit of the so-called 'beta thalassaemic cardiomyopathy'. Their findings, based on echocardiographic assessment of left ventricular function, were similar to those reported previously.[2,3] Nonetheless, the role of arterial dysfunction in th...
Dear Editor
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular mechanisms involved in the inflammatory mechanisms and haemostatic factors leading to coronary atherosclerosis. They also describe the role of chronic infection in this process.[1] However, they omit an important factor that is common to the majority of patients su...
Dear Editor
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack, and surgery. Symathetic denervation is involved in such cases. Prolonged T wave inversion would indicate the change in repolarization related to the sympathetic...
I read with great interest the article by Jenni and colleagues [1], and the accompanying editorial by Varnava [2]. I agree with them that this entity is deserving of more attention, but if it is to be accorded special status within the group of cardiomyopathies, then I would suggest that much more work needs to be done to establish the phenotype.
Thus, Jenni et al [1] argue that the non-compacted layer o...
Dear Editor
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a protocol for earlier sit up and mobilisation after routine transfemoral cardiac catheterisation in contemporary practice. Patients were randomised to be mobilised after 2½ hours or 4½ hours bed rest. The authors report that a significant reduction in...
Dear Editor
Barakat and colleagues' observations are clinically important. Our work on the performance of the Rose angina questionnaire in a multi- ethnic study of a community based sample of 1509 adults from European, Indian, Pakistani and Bangladeshi ethnic groups corroborates and complements, their observations.[1]
European men and women mostly reported chest pain in Rose Questionnaire (definite angina c...
In normal hearts the left ventricle has only up to 3 trabeculations and is less trabeculated than the right ventricle [1]. In 1990, however, it was first described that in rare cases >3 trabeculations occur in the left ventricle (Non-compaction, isolated left ventricular abnormal trabeculation, hypertrabeculation) [2]. The trabeculations consist of myocardium, show the same echogenicity, move synchronously w...
Dear Editor
On 24 June the National Institute of Clinical Excellence (NICE) issued their Appraisal consultation document: coronary artery stents.[1] With the proviso that ‘the decision to use a bare metal stent or drug-eluting stent (DES) will depend on the anatomy of the target vessel for stenting and the severity of the disease’ (presumably reflecting issues of deliverability of the stent platforms on offer), t...
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