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Iemura et al's hypothesis that endothelial dysfunction is associated with coronary aneurysms which have regressed after Kawasaki disease (KD) is interesting[1]; however, there are two issues with respect to their study design that need to be considered, in addition to the issues reported before.[2, 3]
(1) Is endothelial dysfunction associated with regressed coronary aneurysms per se late after KD?
Iemura et al's hypothesis that endothelial dysfunction is associated with coronary aneurysms which have regressed after Kawasaki disease (KD) is interesting[1]; however, there are two issues with respect to their study design that need to be considered, in addition to the issues reported before.[2, 3]
(1) Is endothelial dysfunction associated with regressed coronary aneurysms per se late after KD?
Iemura et al showed that acetylcholine-induced vasodilatation is impaired in regressed coronary aneurysms (groups 1 and 2) but there is preserved vasodilatation in patients without coronary involvement during the acute illness of KD (group 3). This could be explained either by the direct effect of the regressed aneurysm or the difference among the study groups (groups 1 and 2 versus group 3). The Kawasaki vasculitis was severe enough to cause coronary aneurysms in some segments during the acute illness.
Although in Fig 1 Iemura et al showed that there is acetylcholine-induced vasoconstriction in the regressed aneurysm, readers might note that the rest of the segments in the right coronary artery without coronary lesions from the onset, including segments remote from the regressed aneurysms, also seem to constrict in response to acetylcholine. This might suggest that the regressed aneurysm per se does not impair endothelial function after KD.
Iemura et al did not present any data analysing the acetylcholine-elicited responses in normal segments from disease onset in groups 1 and 2; therefore the alternative hypothesis remains possible i.e. that coronary segments, regardless of their association with regressed aneurysms, constrict in response to acetylcholine in patients with a history of severe Kawasaki vasculitis. Consistent with this hypothesis, previous reports concluded that endothelial function is impaired in unaffected coronary segments and brachial arteries (usually uninvolved with aneurysms during the acute illness) in patients with severe acute Kawasaki vasculitis in the long term follow up period:
1.5-12.5 years (mean (SE) 6.5 (1.1)) after acute KD in Mitani et al[2]
5.3-17.1 years (median 11.3) after KD in Dhillon et al[4]
16-28 years old (mean 22) at the time of examination in Kamiya et al[5]
1-14 years old (median: 3.5) at the time of examination in Sano et al[6]
(2) Is endothelial function entirely preserved in KD patients without coronary involvement during the acute illness (group 3)?
This is an issue that we did not specifically address in our previous study.[2] Iemura et al showed that coronary arteries normally dilate in response to acetylcholine in patients without coronary lesions during the acute illness (group 3) on the basis of analysing multiple coronary segments.[1] However, in KD patients some coronary segments (ie, proximal segments) are characteristically more susceptible to severe abnormalities than others in terms of morphological, angiographic findings and vasomotor function.[2, 7, 8] Abnormal vasomotor function might be unmasked by specifically focusing on some "susceptible" segments in group 3, as we did in uninvolved proximal coronary segments in patients with coronary aneurysms in other segments.[2] An alternative hypothesis that some susceptible segments are associated with impaired acetylcholine-induced vasodilatation even in group 3 remains to be tested.
Iemura et al's conclusion might not be consistent with a previous report showing that endothelial function is impaired in KD patients without aneurysms in any segment during the acute illness.[4] This inconsistency remains to be addressed.
References
1. Iemura M, Ishii M, Sugimura T, et al. Long term consequences of regressed coronary aneurysms after Kawasaki disease: vascular wall morphology and function. Heart 2000;83:307-11.
2. Mitani Y, Okuda Y, Shimpo H, et al. Impaired endothelial function in epicardial coronary arteries after Kawasaki disease. Circulation 1997;96:454-61.
3. Mitani Y. Coronary endothelial dysfunction after Kawasaki disease. J Am Coll Cardiol 2000;35:821-3
4. Dhillon R, Clarkson P, Donald AE, et al. Endothelial dysfunction late after Kawasaki disease. Circulation 1996;94:2103-6.
5. Kamiya Y, Onouchi Z, Hamaoka K. Arteriosclerosis long after Kawasaki disease: endothelial function. Acta Cardiol Paediat Jpn 1997;13:252 (Japanese).
6. Sano T, Tagawa T, Itagaki Y, et al. Endothelial dysfunction after Kawasaki vasculitis. Jpn Circ J 1999;63:338 (Japanese).
7. Naoe S, Takahashi K, Masuda H, et al. Kawasaki disease: with the particular emphasis on arterial lesions. Acta Pathol Jpn 1991;41:785-97.
8. Kato H, Sugimura T, Akagi T, et al. Long-term consequences of Kawasaki disease: a 10-21 year follow-up study of 594 patients. Circulation 1996;94:1379-85
Kurbaan and Sutton provide a balanced view of the role of pacing in
vasovagal syncope[1] - a common but complex and challenging medical
condition.
However, we feel that attention should be drawn to the methodological
problems that bedevil interpretation of the North American Vasovagal
Pacemaker Study (VPS).[2] This was not a randomised study of cardiac
pacing, but rather a randomised trial...
Kurbaan and Sutton provide a balanced view of the role of pacing in
vasovagal syncope[1] - a common but complex and challenging medical
condition.
However, we feel that attention should be drawn to the methodological
problems that bedevil interpretation of the North American Vasovagal
Pacemaker Study (VPS).[2] This was not a randomised study of cardiac
pacing, but rather a randomised trial of pacemaker prescription and
implantation. The control group did not undergo an operation with
subsequent reprogramming to an "inactive" mode, and so did not receive the
attendant medical follow-up afforded the paced group.
Recent data from a trial examining the role of cardiac pacing in
hypertrophic cardiomyopathy have clearly demonstrated the profound placebo
effect of pacemaker implantation[3] on both symptoms and objective
echocardiographic evidence of outflow tract obstruction. These
improvements were apparent despite programming the pacemaker to an
inactive mode. There is no direct evidence from the North American study
that it was appropriate pacemaker therapy that was the cause of the
reduction in symptoms seen in the paced group. Patients were highly
selected and very symptomatic, with an imbalance in symptom burden between
the 2 arms that would favour pacing (median number of lifetime episodes 14
paced versus 35 non-paced). The only way to address these issues
satisfactorily would be by implanting systems in all patients, and blindly
randomising groups to "active" or "inactive" pacing.
For the present we agree that "there are limitations to the benefits
of pacing in vasovagal syncope", particularly in young patients whom would
be subject to a lifelong burden of cardiac pacing with its inevitable
complications. Several alternative approaches are available, and should
be tried first. Leaving aside pharmacological treatment,[4] simple
orthostatic training[5] has demonstrated a greater reduction in symptom
burden than that seen in the North American VPS. This technique is both
simple and proved to be extremely effective: over a median follow-up of 18
months, spontaneous syncope was seen in 0% versus 56% in the trained and
control group respectively.
Until further randomised data become available, pacemaker
implantation should be regarded as a last resort in vasovagal syncope.
Dr Adrian Morley-Davies
Senior Registrar, Department of Cardiology
Glasgow Royal Infirmary, Glasgow G31 2ER, UK
Dr J Byrne
Specialist Registrar in Cardiology, Department of Cardiology
Western Infirmary, Glasgow
References
1. Kurbaan AS, Sutton R. Pacing for vasovagal syncope. Heart 1999;
82:649-50.
2. Connolly SJ, Sheldon RS, Roberts R. The North American Vasovagal
Pacemaker Study: A randomised trial of permanent cardiac pacing for the
prevention of vasovagal syncope. JACC 1999; 33:16-20.
3. Linde C, Gadler F, Kappenberger L, Ryden L. Placebo effect of
pacemaker implantation in obstructive hypertrophic cardiomyopathy. Am J
Cardiol 1999; 83:903-7.
5. Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A.
Usefulness of a tilt-training program for the prevention of refractory
neurocardiogenic syncope in adolescents: a controlled study. Circulation
1999; 100:1798-801.
We share many of the reservations that Morley-Davies and Byrne have
regarding the North American Vasovagal Pacemaker Study (VPS).[1] However,
this study should be considered in the context of the other available data
supporting the role of pacing in selected patients. We also are
interested in the study by Di Girolamo et al[2] suggesting a benefit for
orthostatic training in those with neurocardio...
We share many of the reservations that Morley-Davies and Byrne have
regarding the North American Vasovagal Pacemaker Study (VPS).[1] However,
this study should be considered in the context of the other available data
supporting the role of pacing in selected patients. We also are
interested in the study by Di Girolamo et al[2] suggesting a benefit for
orthostatic training in those with neurocardiogenic (vasovagal) syncope.
However, they do not classify the tilt test induced haemodynamic responses
seen in their population. In those with vasovagal syncope the different
haemodynamic collapse patterns seen on tilt testing[3] may have a very
useful role in identifying not only those who may benefit from pacing but
also those in whom pacing may be inappropriate even as a 'last resort'.
The consensus is that pacing is of the greatest benefit in those with a
predominantly bradycardiac (cardioinhibitory) response on tilt testing.
Furthermore, the population in Di Girolamo et al's study[2] is not
comparable to that in VPS and most other studies of pacing in vasovagal
syncope. The former's population were all adolescents (mean age 16
years), whereas much older patients were recruited into VPS (mean age 43
years). Our experience suggests that many adolescents will over time
'grow out of' their fainting episodes. Hence, in the majority of cases
our advice to this group is simply reassurance.
Since the beginning of 1997 we have run a prospective register of the
all tilt tests that we have undertaken including the management suggested.
Up until December 1999 over 600 patients had been tilted. Of these 186
were under 35 years of age. Only 5 (2.7%) of these young patients have
been paced. In each cases multiple non-pacing strategies (though not
orthostatic training) were attempted prior to offering pacing.
In selected patients with vasovagal syncope pacing offers excellent
symptomatic relief, enabling a return to normal life.
Dr A S Kurbaan
Department of Cardiology, London Chest Hospital,
London E2 9SX, UK
Dr R Sutton
Department of Cardiology, Royal Brompton Hospital,
London SW3 6NP, UK
References
1. Connolly SJ, Sheldon R, Roberts RS, Gent M on behalf of the
Vasovagal Pacemaker Study investigators. The North American Vasovagal
Pacemaker Study (VPS). A randomised trial of permanent cardiac pacing for
the prevention of vasovagal syncope. J Am Coll Cardiol 1999;33:16-20.
2. Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A.
Usefulness of a tilt training program for the prevention of refractory
neurocardiogenic syncope in adolescents: a controlled study. Circulation
1999;100:1798-1801
3. Kurbaan AS, Franzén A-C, Bowker TJ, Williams TR, Kaddoura S,
Petersen MEV, Sutton R. Usefulness of tilt test induced patterns of heart
rate and blood pressure using a two stage protocol with glyceryl
trinitrate provocation in patients with syncope of unknown origin. Am J
Cardiol 1999;84:695-670.
We thank Dr. Pocar and his colleagues for contributing their
experience with another case of cardiocutaneous fistula [1], which
confirms several points that we and others have previously discussed [2]
[3] [4]. The clinical presentation of cardiocutaneous fistula is usually
slow and indolent but may rapidly deteriorate. Therefore, when this
diagnosis is established elective operation should be perfo...
We thank Dr. Pocar and his colleagues for contributing their
experience with another case of cardiocutaneous fistula [1], which
confirms several points that we and others have previously discussed [2]
[3] [4]. The clinical presentation of cardiocutaneous fistula is usually
slow and indolent but may rapidly deteriorate. Therefore, when this
diagnosis is established elective operation should be performed without
undue delay, to excise the fistulous tract and remove the infected foreign
bodies. With medical therapy alone the infection cannot be eradicated. The
natural progression of the disease may lead to catastrophic hemorrhage and
grim outcome, as occurred in the case illustrated by Pocar M, et al. [1]
and previous reports [3]. Meticulous surgical technique should always be
employed during left ventricular aneurysm repair to prevent this rare but
serious complication.
Peter G. Danias, MD, PhD
Cardiology Division, Department of Medicine
Beth Israel Deaconess Medical Center and Harvard Medical School
330 Brookline Avenue, Boston, Massachusetts 02215, USA
Dr. Danias is partially supported by the Clinical Investigator Training
Program: BIDMC - Harvard/MIT Health Sciences and Technology - Pfizer Inc.
References
1. Pocar M, Donatelli F, Grossi, A. Cardiocutaneous fistula following
left ventricular aneurysmectomy. Heart Rapid Response, 17 May 2000.
We read the case report by Elliott et al (1) with great interest
and would like to add to their findings. In three of five consecutive
patients undergoing percutaneous septal ablation (PTSMA) for hypertrophic
cardiomyopathy (HCM) they observed left ventricular cavity opacification
during selective injection of the first septal perforator with the
contrast agent Optison.
We read the case report by Elliott et al (1) with great interest
and would like to add to their findings. In three of five consecutive
patients undergoing percutaneous septal ablation (PTSMA) for hypertrophic
cardiomyopathy (HCM) they observed left ventricular cavity opacification
during selective injection of the first septal perforator with the
contrast agent Optison.
We treated a 61 year old man with a long history
of HCM and limiting breathlessness depsite maximal medical therapy with
PTSMA. His peak resting intraventricular gradient, measured using a double
-lumen pitail catheter, was 134 mmHg with a post-ectopic gradient of 165
mmHg. With a 2.0 by 20 mm balloon inflated, initial injection of the
echocardiographic contrast agent Levovist (Schering AG, Germany)
selectively into the first septal perforator showed opacification of the
basal septum as demonstrated on transoesophageal echocardiography. Using
appropriate technical considerations 2.5 ml of alcohol was then injected
into this artery. The ballon was left inflated in the septal perforator
for 15 minutes and subsequently deflated. Following this the resting
gradient was negligible but a peak provokable gradient of 105 mmHg was
obtained. In view of this further ablation was planned and the adjacent
second septal perforator was selectively instrumented. Levovist injection
into this artery however resulted in echocardiographic enhancement of the
mid septum distal to the site of flow acceleration.It was therefore
decided not to proceed further with this artery and we returned to the
original septal perforator.
Repeat echocardiographic contrast injection
through a shorter balloon (2.0 by 15mm) produced clear opacification of
the left ventricular cavity.
In view of the safety considerations raised
by Elliott el al (1)regarding the sytemic effects of alcohol we elected
not to proceed further with the procedure.
This case adds to the findings documented previously (1). It demonstrates
that this phenomenon occurs with both Optison and Levovist contrast
agents. The mechanism however is not clear although a number of
possibilities are raised by Elliott et al (1). Interestingly in our
patient left ventricular opacification occurred only after the first
alcohol injection whereas in those cases discussed previously
opacification occurred prior to alcohol injection. This could relate to
our subsequent choice of a shorter balloon (the same size as used in the
cases described by Elliott et al (1)) which may increase the number of
septal sub-branches exposed to the contrast agent. Alternatively it may
relate to the toxic effects of alcohol on the vasculature.
Mechanisms
aside, our findings and those documented previously suggest that caution
may be appropriate for the injection of alcohol where this phenomenon is
observed.
1 Elliott PM, Brecker SJ, McKenna WJ. Left ventricular
opacification during selective intracoronary injection of
echocardiographic contrast in patients with hypertrophic cardiomyopathy. Heart 2000;83:e7
We have read with great interest the short case in cardiology
reported by E Zakynthinos et al (1) in the March 2000 edition of Heart. The ECG
recordings after acute ingestion of amitriptyline are remarkable,
especially the ST segment elevation in the precordial leads V1 - V3, 6 to
100 hours after admission in the intensive care unit.
The ECG pattern resembles markedly the ones described in...
We have read with great interest the short case in cardiology
reported by E Zakynthinos et al (1) in the March 2000 edition of Heart. The ECG
recordings after acute ingestion of amitriptyline are remarkable,
especially the ST segment elevation in the precordial leads V1 - V3, 6 to
100 hours after admission in the intensive care unit.
The ECG pattern resembles markedly the ones described in the Brugada
syndrome (2). Thus this case could represent a specific effect of the
ionic action of tricyclic agents with selective blockade of the sodium
channels (3,4), mimicking temporarily a Brugada pattern, as an acquired
phenomenon in an otherwise electrically normal myocardium.
Another mechanism could be an unmasking effect of amitriptyline
similar to that of other sodium channel blockers which revealed a silent
dysfunction of the sodium channels in a "concealed" Brugada Syndrome (5).
This has, in our opinion, to be discussed and verified by means of a
pharmacological test with ajmaline (5), at distance of the acute event.
The apparent absence of threatening arrhythmias in the presence of such a
high concentration of amitriptyline is however an argument pleading
against this hypothesis.
In the same issue of Heart, R P Steeds et al (6) report a case of
abnormal ventricular conduction following dothiepin overdose with images
resembling an acute myocardial infarction. The ST segment elevation in
leads V1-V3 is however somewhat different and less suggestive of a Brugada
Syndrome. Nevertheless, the ionic mechanism of intoxication could be the
same, though occurring in an electrically otherwise normal myocardium.
Similarly in this case, an ajmaline pharmacological test could be
appropriate to ensure the integrity of sodium ionic channels. A genetic
study would be also advocated in these two cases.
L DE ROY, MD
C SCAVEE, MD
J MUCUMBITSI, MD
D BLOMMAERT, MD
Department of Cardiology, Arrhythmia Unit
University of Louvain
B 5530 YVOIR Belgium
References
1. E. Zakynthinos, T. Vassilakopoulos, C. Roussos, S Zakynthinos.
Abnormal atrial and ventricular repolarisation resembling myocardial
injury after tricyclic antidepressant drug intoxication. Heart 2000;83:353-354.
2. P Brugada, J Brugada. Right bundle-branch block persistent ST segment
elevation and sudden cardiac death: a distinct clinical and
electrocardiographic syndrome. A multicenter report J Am Coll Cardiol 1992;20:1391-1396.
3. MJ Barber, CF Starmer, AO Grant. Blockade of cardiac sodium channels by
amitriptyline and diphenylhydantoïne.Evidence for two use-dependent binding sites. Circ Res 1991;69:677-96.
4. C Nau, M Seaver, SY Wang, GK Wang. Block of human heart hH1 sodium
channels by amitriptyline.J Pharmacol Exp Ther 2000;292:1015-23.
5. R Brugada, J Brugada, C Antzelevitch, G E Kirsch, D Potenza, J A
Towbin, P Brugada: Sodium channel blockers identify risk for sudden death
in patients with ST segment elevation and right bundle branch block but
structurally normal hearts. Circulation 2000;101:510-515.
6. R P Steeds, R Muthusamy: Abnormal ventricular conduction following
dothiepin overdose simulating acute myocardial infarction. Heart 2000;83:289.
We read with great interest the review "Cardiocutaneous fistula"
published by Dr. Danias and co-workers. At our Institution, we encountered
a similar case, concerning a 72-year-old female, who developed this
complication eleven months after coronary bypass sugery and linear
resection of an anteroapical left ventricular aneurysm; the postoperative
course had been complicated by mediastinitis necessit...
We read with great interest the review "Cardiocutaneous fistula"
published by Dr. Danias and co-workers. At our Institution, we encountered
a similar case, concerning a 72-year-old female, who developed this
complication eleven months after coronary bypass sugery and linear
resection of an anteroapical left ventricular aneurysm; the postoperative
course had been complicated by mediastinitis necessitating surgical
debridement and irrigation with 0.5% povidone-iodine until removal of
chest tubes. Initially, the patient presented mimicking subacute
endocarditis and subsequently developed the fistulous tract from the
cardiac apex through the chest wall. As stated by others [1] [2] [3] there
was no tendency to spontaneous healing, and bleeding was only mild and
transient, resembling chronic fistula secondary to chronic sternal
osteomyelitis; cultures were negative. Elective operation was not planned
because of poor general state and relative paucity of symptoms. Conditions
gradually declined until, during hospitalization, massive hemorrhage
ensued; no hemodynamic instability was observed during compressive
maneuvers. Emergency operation was accomplished through re-sternotomy
after institution of moderately hypothermic (28 °C) cardiopulmonary bypass
through the femoral vessels. Cooling was continued during dissection of
extremely dense adhesions and fragile tissues to obtain complete exposure
the left ventricle, avoiding free dissection of the great vessels; the
defect was repaired during circulatory arrest (20 °C) removing all foreign
material and infected tissue along with two chronically eroded costal
segments. The patient died on the fourth postoperative day in multi-organ
failure.
It is difficult to give guidelines, but some points should be
stressed:
High-risk surgery is probably the only therapeutic option and should
be planned electively avoiding life-saving emergency operations.
In our case, infection was not secondary to chest wall erosion due to
prosthetic material (a theoretical possibility previously stated by others
[3]). Mediastinitis may represent the inital cause, but also a consequence
of implantation of contaminated prosthetic material during aneurysmectomy.
The role of extensive use of prosthetic material (in particular,
Teflon felt) outside the heart is unclear, but may be important. This
specifically applies to patients undergoing left ventricular aneurysm
repair, who often present additional risk factors for infection (advanced
age, associated heart failure, longer cardiopulmonary bypass times, etc).
In case of postoperative mediastinitis should extracardiac Teflon be
replaced with autologous pericardium? This is a very difficult issue, due
to the different extensiveness of surgical options, but may be important
in the development of fistulae/pseudaneurysms of the heart/great vessels.
In case of extensive use of prosthetic material, removal should probably
be considered.
Re-sternotomy [1] may not be the optimal approach for repair. If
operation involves the left ventricle alone, an anterior thoracotomy
through the 5th or 6th intercostal space [4] is more appealing and less
cumbersome, despite the necessity of extrathoracic cannulation, deep
hypothermia and low-flow bypass/circulatory arrest. Sternotomy may prolong
surgery rather than represent a more expeditious technique. We reccomend
to avoid re-sternotomy whenever possible, especially in case of previous
mediastinitis.
Marco Pocar, MD - Francesco Donatelli, MD - Adalberto Grossi, MD
Istituto di Malattie dell'apparato cardiovascolare e respiratorio -
Università degli Studi di Milano
Divisione di Cardiochirurgia - IRCCS, Ospedale Maggiore Policlinico -
Via Francesco Sforza, 35 - 20122 Milano, Italy
References
1 McHenry MC, Longworth DL, Rehm SJ, et al. Infection of the cardiac
suture line after left ventricular surgery. Am J Med 1988;85:292-300.
2 Stanford W, Reuben CF, Flemma RJ, et al. Management of long-standing
cardiocutaneous fistulas after resection of left ventricular aneurysms. J
Thorac Cardiovasc Surg 1980;79:789-792.
3 Deuvaert FE, Wellens F, De Paepe J, at al. Cardiocutaneous fistula
after left ventricular anuerysm repair. Case report and review of the
literature. J Cardiovasc Surg (Torino) 1984;25:560-562.
4 Wellens F, Vanermen H. Treatment of the infected cardiac suture line.
J Cardiac Surg 1988;3:109-118.
I would like to acknowledge the interesting work published by Coulden
et al [1] in the February 2000 edition of the journal. The concept of
noninvasive arterial wall imaging with MR is an exciting new field with
numerous potential implications, including atherosclerotic plaque
characterisation. However, I would like to raise a few questions about the
selection of MR imaging parameters.
I would like to acknowledge the interesting work published by Coulden
et al [1] in the February 2000 edition of the journal. The concept of
noninvasive arterial wall imaging with MR is an exciting new field with
numerous potential implications, including atherosclerotic plaque
characterisation. However, I would like to raise a few questions about the
selection of MR imaging parameters.
Firstly, I was interested to note that the resolution is different in
all 3 axes. Although a characteristic of 2-D imaging is a loss of z-axis
resolution (slice thickness), previous work in animal models [2] [3] [4]
and humans [5] [6] has generally been with the same resolution in the x-
and y- axes allowing homogeneity of the resolution within the artery wall
and thus the atherosclerotic plaque.
Secondly, using a slice thickness of 3-mm with an image interval of
1.5-mm means that one third of the arterial wall and associated
atherosclerosis is missed. Although consecutive imaging without gaps leads
to cross excitation, one may interleave slices or if more than one
acquisition is performed, acquire alternating slices, to obtain MR images
of the entire arterial segment of interest without this interference.
Finally, the authors note the previously reported utility of T2-
weighted imaging for the characterisation of atherosclerotic plaque [6]
and yet use T1-weighted imaging in their study. Although for the purpose
of documenting arterial plaque burden and vessel wall remodelling T1-
weighted imaging is adequate, data on the relative contribution of
fibrotic and lipidic components to the atherosclerotic process and how
this influences the angioplasty process would be of great interest. I do
appreciate, however, that given the number of patients studied (n=4), and
the need for probably at least two imaging sequences (i.e. T1 and T2
weighted) to discern all components of complex human atherosclerotic
lesions, [6] conclusions regarding these concepts would be limited in this
study.
References
1. Coulden RA, Moss H, Graves MJ, et al. High resolution magnetic
resonance imaging of atherosclerosis and the response to balloon
angioplasty. Heart 2000;83:188-91.
2. Worthley SG, Helft G, Fuster V, et al. Serial in vivo MRI documents
arterial remodeling in experimental atherosclerosis. Circulation
2000;101:586-9.
3. Skinner MP, Yuan C, Mitsumori L, et al. Serial magnetic resonance
imaging of experimental atherosclerosis detects lesion fine structure,
progression and complications in vivo. Nat Med 1995;1:69-73.
4. McConnell MV, Aikawa M, Maier SE, et al. MRI of rabbit atherosclerosis
in response to dietary cholesterol lowering. Arterioscler Thromb Vasc Biol
1999;19:1956-9.
5. Yuan C, Beach KW, Smith LH, Jr., et al. Measurement of atherosclerotic
carotid plaque size in vivo using high resolution magnetic resonance
imaging. Circulation 1998;98:2666-71.
6. Toussaint JF, LaMuraglia GM, Southern JF, et al. Magnetic resonance
images lipid, fibrous, calcified, hemorrhagic, and thrombotic components
of human atherosclerosis in vivo. Circulation 1996;94:932-8.
Cowie et al(1) reported high case fatality rates in a population-based
cohort of patients with incident heart failure between 1995 and 1996.
Survival was 81% at one month, 75% at 3 months, 70% at 6 months, 62% at 12
months and 57% at 18 months. There are few population data that describe
the contemporary survival of patients with heart failure.
Cowie et al(1) reported high case fatality rates in a population-based
cohort of patients with incident heart failure between 1995 and 1996.
Survival was 81% at one month, 75% at 3 months, 70% at 6 months, 62% at 12
months and 57% at 18 months. There are few population data that describe
the contemporary survival of patients with heart failure.
The Linked Morbidity Record Database contains accurate data on all
hospital admissions in Scotland since 1981 and is linked to the Registrar
General's death certificate data. Using this database, we analysed case
fatality in all 66,547 patients admitted to Scottish hospitals for the
first time with a principal diagnosis of heart failure in the period 1986
to 1995.(2) The study by Cowie et al looked at new cases of heart failure
referred to a rapid access clinic as well as those admitted to hospital.
Our results were remarkably consistent with those of Cowie et al. The
median age of our patients was 75 years (compared to 76 in their study)
and men accounted for 47% of our cohort (compared to 54% of theirs). In
1995 unadjusted survival was 81% at 30 days, 73% at three months, 67% at
six months, 58% at one year and 52% at 18 months. Median survival was
only 20 months. Whilst case fatality fell during the period of our study,
it remains high and is substantially greater than that reported in
clinical trials that enrol carefully selected patients.
The data from both these studies highlight the poor prognosis that
patients with heart failure continue to have in the UK. There is still
much room for further improvement in the management of heart failure.
K MacIntyre(1), S Capewell(2), S Stewart(1), JWT Chalmers(3), JJV McMurray(4)
(1) Department of Public Health, University of Glasgow
(2) Department of Public Health, University of Liverpool (3) Information and Statistics Division, Edinburgh
(4) Clinical Research Initiative in Heart Failure, University
of Glasgow
REFERENCES
1. Cowie MR, Wood DA, Coats AJS, Thompson SG, Suresh V, Poole-Wilson PA, Sutton GC. Survival of patients with a new diagnosis of heart failure: a population based study. Heart 2000;83:505-10.
2. MacIntyre K, Capewell S, Livingston M, Chalmers J, Boyd J, Finlayson A, Redpath A, Pell J, Evans C, McMurray JJV. Mortality trends in 86,000 patients admitted with heart failure 1981-1995. Eur Heart J 2000;20(suppl):471.
The excellent review by Ward on the clinical significance of the
bicuspid aortic valve (Heart 2000;83:81-85) is of great
interest and value. The extensive reference list as well put a good bit
of the pertinent bicuspid valve literature in one place. The paper adds
greatly to our knowledge.
However, without critiquing every issue in the paper, there are two
areas in particular I would...
The excellent review by Ward on the clinical significance of the
bicuspid aortic valve (Heart 2000;83:81-85) is of great
interest and value. The extensive reference list as well put a good bit
of the pertinent bicuspid valve literature in one place. The paper adds
greatly to our knowledge.
However, without critiquing every issue in the paper, there are two
areas in particular I would like to discuss. As a pediatric cardiologist
who has been in one division for 40 years, there is considerable natural
history which has been learned, although, perhaps in order to make my
statements I would really have to work in one place for 70 years.
I have seen a huge number of patients with a true bicuspid aortic
valve and I have never seen a patient with a dissecting aneurysm. As Dr.
Ward states, the reason for the reported high incidence of aortic
dissection in the presence of an aortic bicuspid aortic valve is unclear,
particularly since the author states that the bicuspid valve is usually
normally functioning. Although the post bicuspid valve dilatation of the
ascending aorta in the presence of systemic hypertension certainly makes
the environment possible, Dr. Ward’s paper makes no mention as to whether
he has personally seen a patient with dissection. The estimated
incidence of 5% of patients with bicuspid valve having
dissection of the aorta seems very much too high.
The second issue refers to whether or not the patient born with
bicuspid aortic valve and no stenosis is expected to progress to reach
real aortic stenosis as the patient ages in the absence of infective
endocarditis. The accepted knowledge over the years has been that the
elderly with calcific aortic stenosis began with a bicuspid aortic valve,
including the valve with no stenosis to begin with. Evidence for such has
never been documented and perhaps cannot, unless a 100 year prospective
study is planned and funded. The implication of Dr. Ward’s article is not
quite that, for he doesn’t really discuss the patient with bicuspid aortic
valve and no stenosis. He only states, appropriately, that patients with
mild aortic stenosis are expected to progress in adulthood, even patients
with echocardiographic mean gradient of less than 25 mmHg. However, this
does not answer the question as to whether the patients with true bicuspid
aortic valve and no stenosis are expected to progress. In order to
discuss this issue, one needs the physical examination. Is there
a difference in natural history between the patient with true bicuspid
aortic valve with no stenosis and a true bicuspid aortic valve with mild
stenosis? In the early two decades of my 40 years, the diagnosis of
bicuspid aortic valve without stenosis was made by recognizing an aortic
ejection click with no heart murmur. I accept that occasionally an error
can be made in that the presumed aortic ejection click is in actual fact
an unusually loud tricuspid valve component of a normally split first
sound. But in the recent two decades, with echocardiography, confirmation
has been readily available. The patient with a bicuspid aortic valve and
mild aortic stenosis is diagnosed by having the aortic ejection click
plus a normally split second sound and an aortic stenosis murmur at the
second right interspace that is significant but usually stops clearly
before aortic valve closure. The latter will usually have a mean gradient
of less than 25 mmHg in the echo, just as will obviously the patient with
no stenosis. Dr. Ward because of the nature of his review does not
separate these groups. In my 40 years, I have seen many patients with
mild stenosis progress, but I have seen none with no stenosis progress.
In addition, the subgroup of patients with coarctation of the aorta has a
very high incidence of bicuspid valve without stenosis. I have never seen
one of these develop aortic stenosis either.
I realize that 40 years is not 70 years, but since it is unlikely to
be able to find all these patients with no stenosis for an associate to
follow for 30 or 40 more years answering the question for certain at this
time appears unlikely. However, it would be in cumbent upon all of us to
modify what we teach our students and what we advise our families. As far
as we know, the bicuspid aortic valve without stenosis remains without
stenosis.
Sincerely,
Jerome Liebman MD
Division of Pediatric Cardiology
Professor of Pediatrics
Rainbow Babies & Children’s Hospital
Case Western Reserve University
Iemura et al's hypothesis that endothelial dysfunction is associated with coronary aneurysms which have regressed after Kawasaki disease (KD) is interesting[1]; however, there are two issues with respect to their study design that need to be considered, in addition to the issues reported before.[2, 3]
(1) Is endothelial dysfunction associated with regressed coronary aneurysms per se late after KD?
...Dear Editor
Kurbaan and Sutton provide a balanced view of the role of pacing in vasovagal syncope[1] - a common but complex and challenging medical condition.
However, we feel that attention should be drawn to the methodological problems that bedevil interpretation of the North American Vasovagal Pacemaker Study (VPS).[2] This was not a randomised study of cardiac pacing, but rather a randomised trial...
Dear Editor,
We share many of the reservations that Morley-Davies and Byrne have regarding the North American Vasovagal Pacemaker Study (VPS).[1] However, this study should be considered in the context of the other available data supporting the role of pacing in selected patients. We also are interested in the study by Di Girolamo et al[2] suggesting a benefit for orthostatic training in those with neurocardio...
Dear Editor,
We thank Dr. Pocar and his colleagues for contributing their experience with another case of cardiocutaneous fistula [1], which confirms several points that we and others have previously discussed [2] [3] [4]. The clinical presentation of cardiocutaneous fistula is usually slow and indolent but may rapidly deteriorate. Therefore, when this diagnosis is established elective operation should be perfo...
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We treated a 61 year old man with a long hist...
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We have read with great interest the short case in cardiology reported by E Zakynthinos et al (1) in the March 2000 edition of Heart. The ECG recordings after acute ingestion of amitriptyline are remarkable, especially the ST segment elevation in the precordial leads V1 - V3, 6 to 100 hours after admission in the intensive care unit.
The ECG pattern resembles markedly the ones described in...
Dear Editor:
We read with great interest the review "Cardiocutaneous fistula" published by Dr. Danias and co-workers. At our Institution, we encountered a similar case, concerning a 72-year-old female, who developed this complication eleven months after coronary bypass sugery and linear resection of an anteroapical left ventricular aneurysm; the postoperative course had been complicated by mediastinitis necessit...
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To the Editor;
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Dear Editor:
The excellent review by Ward on the clinical significance of the bicuspid aortic valve (Heart 2000;83:81-85) is of great interest and value. The extensive reference list as well put a good bit of the pertinent bicuspid valve literature in one place. The paper adds greatly to our knowledge.
However, without critiquing every issue in the paper, there are two areas in particular I would...
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