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
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.
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 read with interest the report of McMahon and colleagues (Heart 2001;86:e1) regarding a case of rapid regression of primary pulmonary hypertension in a 14 month old child. Although the authors describe this as spontaneous regression, the patient underwent two months of continuous nitric oxide therapy prior to resolution of her disease. This case may in fact be similar to our previously reported series of four i...
We read with interest the report of McMahon and colleagues (Heart 2001;86:e1) regarding a case of rapid regression of primary pulmonary hypertension in a 14 month old child. Although the authors describe this as spontaneous regression, the patient underwent two months of continuous nitric oxide therapy prior to resolution of her disease. This case may in fact be similar to our previously reported series of four infants with severe primary pulmonary hypertension who were treated with prolonged
inhaled nitric oxide and heparin therapy (1). Three out of four patients had long term reduction in pulmonary artery pressures that have been sustained in up to 62 months of follow up. The demonstrated ability of inhaled nitric oxide to decrease vascular smooth muscle proliferation, reduce hypoxic lung vessel remodeling and inhibit platelet aggregation may be useful in long-term therapy of primary pulmonary hypertension in children and warrants further prospective study.
(1) Atz, A M, and Wessel, D L. Inhaled nitric oxide and heparin for infantile primary pulmonary hypertension Lancet 1998; 351:1701
Fatigue, a frequent complaint in patients with congestive heart failure (CHF), is associated with poor exercise tolerance. Coats in his article enumerated the patho-physiological mechanisms of fatigue in patients with CHF, which includes anaerobic metabolism, de-conditioning of
skeletal muscles, malfunction of endothelial vasodilator as well as vasoconstrictor systems, role of tumor necrosis factor-alpha and other mediators...
Fatigue, a frequent complaint in patients with congestive heart failure (CHF), is associated with poor exercise tolerance. Coats in his article enumerated the patho-physiological mechanisms of fatigue in patients with CHF, which includes anaerobic metabolism, de-conditioning of
skeletal muscles, malfunction of endothelial vasodilator as well as vasoconstrictor systems, role of tumor necrosis factor-alpha and other mediators like norepinephrine. The author also emphasized the central role of these factors in limiting exercise and urged the importance of antineurohormonal and metabolic treatments in the management of fatigue in CHF.
Depression is being increasingly reported in patients with CHF. Fatigue is a common symptom in depression and manifests as loss of energy accompanied by other neuro-vegetative signs and symptoms. Koenig, 2 in 1998, found a 36.5% prevalence of major depression in elderly patients with CHF. In a recent prospective study among 374 patients with CHF, 35.3% had a Beck Depression Inventory Score of 10 or higher while 13.9% had major depression.3 There is growing evidence that major depression
causes neuro-hormonal changes such as activation of inflammatory response systems and is observed as increased production of pro-inflammatory cytokines like tumor necrosis factor and interleukins.4 In addition, depression is also known to alter cardiac autonomic balance through adrenergic mechanisms causing significant impairment of heart rate variability and myocardial contractility.5 These factors acting together can worsen fatigue and anergia in patients with an already compromised heart.
We believe that, in CHF while the above mentioned pathophysiological mechanisms play a significant role in causing fatigue through peripheral 'histo-toxic' mechanisms, the role of depression as a central cause of fatigue should not be underestimated. Depression may have an additive
effect in causing a sense of fatigue in patients with CHF. Exercise training regimens have been shown to improve exercise tolerance in such patients. Its therapeutic benefits are also seen in patients with depression. When designing optimal strategies to improve symptoms in
patients with CHF, one should also consider the interplay of
pathophysiological mechanisms of depression and CHF in addition to the complex mechanisms1 determining exercise capacity. Timely recognition and aggressive management of depressive symptoms will be as important as the antineurohomonal and metabolic treatments and may be pivotal in improving the sense of well being in patients with CHF.
References:
(1) Coats A J S. What causes the symptoms of heart failure? Heart 2001; 86(5):574-578.
(2) Koenig H G. Depression in hospitalized older patients with congestive heart failure. Gen Hosp Psychiatry 1998; 20:29-43
(3) Jiang W, Alexander J, Christopher E, et al. Relationship of depression to increased risk of mortality and rehospitalization in patients with congestive heart failure Arch Intern Med 2001; 161:1849-1856.
(4) Mikova O, Yakimova R, Bosmans E, Kenis G, Maes M. Increased serum tumor necrosis factor alpha concentrations in major depression and multiple sclerosis. European Neuropsychopharmacology 2001; 11(3):203-208.
(5) Carney R M, Freedland K E, Stein P K, Skala J A, Hoffman P, Jaffe A S. Change in heart rate and heart rate variability during treatment for depression in patients with coronary heart disease. Psychosomatic Medicine 2000; 62(5):639-47.
It was interesting to read the novel approach to transseptal puncture
guided by intracardiac echocardiography describe by Szili-Torok et al. [1]
There is no doubt about its efficacy to accurately pinpoint the site of
puncture. In this era of high technology, many new devices are designed
for easier and safer procedures. But they are not uniformly affordable
especially in third world countries.
It was interesting to read the novel approach to transseptal puncture
guided by intracardiac echocardiography describe by Szili-Torok et al. [1]
There is no doubt about its efficacy to accurately pinpoint the site of
puncture. In this era of high technology, many new devices are designed
for easier and safer procedures. But they are not uniformly affordable
especially in third world countries.
In our technique of transseptal catheterization without needle
puncture of the septum,[2] we probed the fossa prior to puncture with the
needle in group I (n=25). Needle puncture was resorted to after 120
seconds when this failed. In another 30 patients, left atrium was entered
directly through traditional puncture (group II). There was reduction in
the time taken for puncture: 84.7+27.5 sec in group I and 116.1+37.9 sec
in group II, p<_0.02. fluoroscopy="fluoroscopy" time="time" was="was" also="also" less="less" _51.219.6="_51.219.6" sec="sec" in="in" group="group" i="i" vs="vs" _73.622.3="_73.622.3" ii="ii" p0.03.="p0.03." p="p"/> All our patients underwent balloon mitral valvulopasty. The risk of
injury with needle tip was avoided by
(a) keeping the needle tip well
inside the sheath throughout the procedure, (b) proper positioning of the
sheath tip, (c) application of gentle and controlled pressure which was
less than the force used for standard needle puncture, (d) allowing only 2
to 3 mm of the tip of the sheath to enter left atrium after probing and
(e) further advancement of sheath only after confirmation of left atrial
entry. It may be emphasised that if gentle pressure failed, probing was
never done with force.
Comparing our technique with that of Szili-Torok et al [1], it is
seen that fossa was visualized and penetration of the needle seen by the
ultrasound catheter in 100% of patients in the latter series. By our
method, 90% of the patients had successful left atrial entry. Thus, 90%
had visualization of catheter entry into left atrium by the naked eye.
Echocardiographic contrast material applied in the left atrium was seen in
all by Szili-Torok et al [1], while radiographic contrast medium was seen
in all our patients. It must be emphasized that unlike their series, we
did not use a needle to enter left atrium. As in our series, their
patients also showed the characteristic jump of the needle onto the fossa
(by fluoroscopy). All procedures were successful and without
complications. This was also demonstrated in our technique.
Our technique is easy as well as inexpensive. It may be applied in
standard as well as difficult cases of puncture where the anatomy of the
septum is altered which is usual in mitral stenosis. [3] The biggest
advantage is that it avoids needle puncture with has potential
complications. [4] Transseptal catheterization without needle puncture is
feasible at very low costs.
References
(1) Szili-Torok T, Kimman GP, Theuns D, Res J, Roelandt JRTC, Jordaens
LJ. Transseptal left heart catheterisation guided by intracardiac
echocardiography. Heart 2001;86:e11.
(2) Krishnamoorthy KM, Dash PK. Transseptal catheterization without
needle puncture. Scandinavian Cardiovasc J 2001;35:1-2.
(3) Clugston R, Lau FYK, Ruiz C. Transseptal catheterisation update
1992. Cathet Cardiovasc Diagn 1992;26:266-274.
4. Baim DS. Percutaneous approach, including Transseptal and apical
puncture. In: Baim DS, Grossman W, ed. Cardiac catheterisation,
angiography and intervention, 5th ed, Baltimore, Williams and Wilkins,
1996:78.
Acknowledgements:
Grateful acknowledgement are due to Taylor and Francis for their
permission to reproduce data from table 1 of the article: Krishnamoorthy
KM, Dash PK. Transseptal catheterization without needle puncture.
Scandinavian Cardiovasc J 2001;35:1-2.
With reference to the report by Liistro and Colombo in the August
issue of Heart entitled ‘Late acute thrombosis after paclitaxel eluting
stent implantation' (Heart 2001 86 262-265 ), I feel it is important that
readers be aware that not all paclitaxel–eluting stents, nor the trials
testing them, are the same.
There is currently a great deal of research interest into drug-eluting
stents and...
With reference to the report by Liistro and Colombo in the August
issue of Heart entitled ‘Late acute thrombosis after paclitaxel eluting
stent implantation' (Heart 2001 86 262-265 ), I feel it is important that
readers be aware that not all paclitaxel–eluting stents, nor the trials
testing them, are the same.
There is currently a great deal of research interest into drug-eluting
stents and paclitaxel, as indicated by the authors, is a good drug
candidate since it can be loaded onto stents and influences smooth muscle
cell activity through stabilisation of microtubules, inhibiting mitosis.
It undoubtedly also has effects on endothelial cells and since re-endothelialisation is an important reparative process following
percutaneous coronary intervention then any delayed endothelialisation of
the stent will add to the risk of stent thrombosis.
The stent used in the trial from which the case report came was however a
very peculiar stent indeed. Firstly the Quanum stent consisted of a
relatively rigid tube with a number of 2 mm polymeric sleeves along its
length. Issues were reportedly raised during the trial by some of the
investigators about lack of side branch access, although there appeared to
be no occlusion of side branches in the patient described.
The use of
polymer bands may also irritate the vessel wall, affect stent apposition
and cause uneven distribution of the drug to the vessel wall as if to
treat only part of the vessel wall and leave intervening segments of the
wall untreated. Additionally, the dose of paclitaxel derivative (Taxane),
which was loaded onto the stent appeared to be huge. According to the
trial investigators [1] as much as 4000ug were loaded into the divided
polymeric sleeve. Published animal data [2], albeit on paclitaxel, rather
than Taxane its derivative, indicates that paclitaxel concentrations of
180ug/stent can cause delayed re-endothelialisation, vessel wall necrosis
and cellular infiltration. While it is difficult to relate the
pathobiological effects of the two agents (paclitaxel and Taxane) the
Principle Investigator (Dr Edorado Grube) has indicated when presenting
the data publicly that he believes that the drug would still be present in
significant amounts at the local site at 6 months. The trial has been
discontinued and the stent is not, I believe, going to be tested in
further trials nor developed clinically.
Other trials have approached the paclitaxel-stent combination differently.
In the ELUTES (Evaluation of Taxol Eluting Stents) we recognised the need
for a dose that needed to be less than suggested by the animal data as
being potentially toxic and that a drug dose was required that was
cytostatic for a short period while the vessel repairs itself from the
trauma of dilatation. In our study the maximum patient stent dose in a 4-dose escalating study design is 1/3 of the dose shown in animals to have
adverse effects on the vessel wall. The stent is a standard laser cut V-flex stent and the drug is applied directly to the abluminal surface of
the stent. There is no polymer covering the stent. Animal data indicates
that at 2 weeks more than 60% of the loaded dose has eluted off the stent.
Enrolment for the ELUTES Trial is complete (n=192) and the angiographic
results will be presented at AHA 2001. Importantly in the context of the
Liistro publication in Heart, the patients were treated with only 3 months
of anti-platelet clopidogrel, and to date there have been no late stent
thromboses with 152 patients completing 6 month follow up.
The ASPECT trial is similar to the ELUTES Study and has been undertaken in
Korea. It also has used a contemporary laser cut slotted tube stent (the
Supra-G) but loaded with slightly more paclitaxel in the maximal dose
group (3.1 ug /mm2stent versus ELUTES 2.7ug/mm2). In the ASPECT study
(reported at TCT 2001) 177 patients were randomised to one of 2 doses of
paclitaxel eluting stent or control. In addition to long-term aspirin,
patients mostly received ticlopidine or clopidogrel. In these patients
there were no late stent thromboses. In a small cohort given for unclear
reasons cilostazole, stent thrombosis occurred in 3 out of 12 patients in
the highest dose paclitaxel treated group.
Therefore, whilst re-endothelialisation is a reasonable consideration
because of the experience with vascular-brachytherapy, the ELUTES and
ASPECT trial do suggest that the actual clinical risk may be minimal when
using a dose of drug considered safe from pre-clinically data, when this
dose of drug is delivered on a standard stent platform and when
appropriate, standard anti-platelet therapy is given. Under these
conditions, the data to date suggest that adequate re-endothelialisation
can be expected before the discontinuation of antiplatelet therapy and
that the risk of adverse events is similar to that of standard coronary
stents.
If successful (by reducing in-stent restenosis) such trials should reduce
the need for repeat procedures in patients and so reduce the gap in early
outcome between coronary surgery and PCI.
A.H.Gershlick (PI The ELUTES trial)
References (1) de la Fuente LM, Miano J Mrad J et al Initial results of the
Quanum drug eluting stent (QuaDS-QP-2) registry (BARDS) in human subjects.
Cath & Cardiovasc. Intervent. 2001; 53 ; 480-488
(2) Heldman AW, Cheng L, Jenkins GM, Heller PF et al. Paclitaxel
stent coating inhibits neointimal hyperplasia at 4 weeks in a porcine
model of coronary restenosis.Circulation 2001 May 8;103(18):2289-95
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
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.
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Dear Editor
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Dear Editor
It was interesting to read the novel approach to transseptal puncture guided by intracardiac echocardiography describe by Szili-Torok et al. [1] There is no doubt about its efficacy to accurately pinpoint the site of puncture. In this era of high technology, many new devices are designed for easier and safer procedures. But they are not uniformly affordable especially in third world countries.
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With reference to the report by Liistro and Colombo in the August issue of Heart entitled ‘Late acute thrombosis after paclitaxel eluting stent implantation' (Heart 2001 86 262-265 ), I feel it is important that readers be aware that not all paclitaxel–eluting stents, nor the trials testing them, are the same. There is currently a great deal of research interest into drug-eluting stents and...
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...
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