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.
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
We appreciate the kind comments of Dr Mitani regarding
our article in the March 2000 issue of Heart and for
sharing their experiences with us.[1]
In group 1 and 2 patients who had regressed coronary aneurysm after Kawasaki disease, there was significantly more vascular constriction with acetylcholine and poorer dilatation with isosorbide
dinitrate at the regressed site, than in group 3 patient...
We appreciate the kind comments of Dr Mitani regarding
our article in the March 2000 issue of Heart and for
sharing their experiences with us.[1]
In group 1 and 2 patients who had regressed coronary aneurysm after Kawasaki disease, there was significantly more vascular constriction with acetylcholine and poorer dilatation with isosorbide
dinitrate at the regressed site, than in group 3 patients
who had no coronary artery lesions after Kawasaki disease.
Fourteen patients in group 1 and group 2 in the acute stage
of illness had coronary artery lesions on one side of the
coronary artery but no coronary artery lesion on the
opposite side.
We also evaluated the vascular function of
these sites (n = 19) using intracoronary infusion of
acetylcholine chloride and isosorbide. The mean (SD)
change in the coronary artery diameter after infusion of
acetylcholine was 12.5 (3.0)% in group 1 and 2, and
11.3 (5.6)% in group 3. The mean (SD) change in the
coronary artery diameter after infusion of isosorbide
dinitrate was 17.3 (9.5)% in group 1 and 2, and 18.0
(8.2)% in group 3. There was no significant difference in
responses to the infusion of either acetylcholine or
isosorbide dinitrate between these two groups.
These
findings suggested that such coronary arteries had finctionally normal
endothelium and smooth muscle even in
patients with a history of severe Kawasaki vasculitis.
The coronary arteries in group 3 patients had normal
responses to the infusion of either acetylcholine or
isosorbide dinitrate, according to the analysis of multiple
coronary artery segments involving proximal coronary artery
segments. We assessed differences in responses to the
infusion of acetylcholine or isosorbide dinitrate
between proximal coronary artery segments and distal
coronary artery segments in group 3 patients and in controls. The mean (SD) change in the coronary artery
diameter after infusion of acetylcholine was 11.9 (3.5)% at
the proximal artery coronary segments and 12.8 (4.0)% at
the distal coronary artery segments in group 3. The mean
(SD) change in the coronary artery diameter after infusion
of isosorbide dinitrate was 16.8 (4.2)% at the proximal
coronary artery segments and 17.1 (8.0)% at the distal
coronary artery segments in group 3.
These results
suggested that there was no significant difference in
responses to the infusion of either acetylcholine or
isosorbide dinitrate between the proximal coronary artery
segments and the distal coronary artery segments in group 3
patients. Similar findings were found in the control
patients.
In a new study,[2] we investigated
the vascular morphology of the coronary artery, in 6
Kawasaki disease patients who had completely normal first
coronary angiography findings, using intravascular
ultrasound imaging; we found no differences in wall
morphology between the proximal coronary artery segments
and the distal coronary artery segments.
From the basis of our studies, we conclude that long-term
persistent coronary aneurysms and regressed coronary
aneurysms after Kawasaki disease exhibit vascular
dysfunction.[1-5] These patients should be counseled to
avoid potential risk factors for atherosclerosis, and they
should be advised that long-term follow-up is needed into
adulthood. However, patients with normal coronary arteries after
Kawasaki disease had no significant difference from the
controls in response to either acetylcholine or isosorbide
dinitrate infusion. These findings suggested that such
coronary arteries had normal function of the endothelium
and smooth muscle even in the long term.
References
(1) Iemura M, Ishii M, Sugimura T, Akagi T, Kato H. Long-
term consequences of regressed coronary aneurysms after
Kawasaki Disease: vascular wall morphology and function.
Heart 2000;83:307-11.
(2) Ishii M, Hashino K, Iemura M, Yamakawa R, Muta H, Himeno
W, Akagi T, Kato H. Long-term consequences of coronary
aneurysms after Kawasaki disease: vascular wall morphology
and endothelium function (abstract). J Am Coll Cardiol 2000;35:513A.
(3) Yamakawa R, Ishii M, Sugimura T, Akagi T, Eto G, Iemura
M, Tsutsumi T, Kato H. Coronary endothelial dysfunction
after Kawasaki disease: evaluation by intracoronary
injection of acetylcholine. J Am Coll Cardiol 1998;31:1074-
80.
(4) Sugimura T, Kato H, Inoue O, et al. Vasodilatory
response of the coronary arteries after Kawasaki disease:
evaluation by intracoronary injection of isosorbide
dinitrate. J Pediatr 1992;121:684-8.
(5) Sugimura T, Kato H, Inoue O, Fukuda T, Sato N, Ishii M,
Takagi J, Akagi T, Maeno Y, Kawano T, Takagishi T, Sasaguri
Y. Intravascular ultasound of coronary arteries in
children: assessment of the wall morphology and the lumen
after Kawasaki disease. Circulation 1994;89:258-65.
We read with interest the article by Kubler et al[1]
concerning 3 patients with platypnoea-orthodeoxia syndrome. As reported,
this syndrome is infrequent and the diagnosis can be difficult. It
is characterised by dyspnoea and arterial hypoxaemia induced by upright
position that resolved by recumbency. This is usually the consequence of
right-to-left shunt at the atrial level. Such shunting is frequent in...
We read with interest the article by Kubler et al[1]
concerning 3 patients with platypnoea-orthodeoxia syndrome. As reported,
this syndrome is infrequent and the diagnosis can be difficult. It
is characterised by dyspnoea and arterial hypoxaemia induced by upright
position that resolved by recumbency. This is usually the consequence of
right-to-left shunt at the atrial level. Such shunting is frequent in
patients with congenital heart defects when there is high pulmonary artery
pressure and patent foramen ovale/atrial septal defect (PFO/ASD) but
usually there is no postural change for both dyspnoea and hypoxaemia.
More
surprisingly are the normal right-sided pressures associated with this
syndrome. Moreover, due to the high prevalence of PFO in the "normal" population
(between 25 and 33%) we might expect to observe more and
more patients with this syndrome.
In our experience, this syndrome is not extremely rare; we
collected 18 patients with similar symptoms (10 female and 8
male, meand (SD) age 71 (6) years).[2] Most of them presented with
variable dyspnoea on exercise and/or hypoxaemia. In fact, the postural
character was present in only 55% of our
group, and can be masked when the patient cannot be weaned off the
ventilator! Some of the patients had a history of stroke or
paradoxical embolism (27%).
It is possible that the concept of platypnoea
-orthodeoxia may be too restrictive. In this population, the first
diagnosis advocated is usually pulmonary embolism and this has led to
various investigations. In fact, transthoracic but mainly transoesophageal
echocardiography, as reported by Kubler et al is the most common examination to depict the PFO and interatrial right-to-left shunt. In this
setting, cardiac catheterization is not necessary to confirm the
diagnosis. In contrast, we recommend
transcatheter PFO/ASD occlusion instead of surgery. Indeed, a significant
number of patients are quite debilitated or sick and surgical closure would
increase their risk.
The literature describes many devices that have been
successfully used to close such defects. This technique is easy to perform,
does not require general anaesthesia, and provides complete correction. In
our experience, device implantation was performed successfully in all but 1 patient.
Another interest of cardiac catheterization is to reveal
the underlying causes responsible for this interatrial right-to-left
shunting. First, there is frequently a haemodynamic pressure gradient
between both atria favouring a right-to-left shunt noticed in late
diastole or early systole. Also been reported is lower right atrial
pressure or equal to the left atrial pressure. It is probable that
significant amount of blood flow from the inferior vena cava can easily cross a PFO by
kinetic energy without need of a favourable pressure gradient between both
atria. Second, there is frequently a preferential blood flow streaming
from inferior vena cava, or more rarely from superior vena cava,
towards the left atrium through a PFO. In our experience, we have noticed
frequently horizontalization of the atrial septum so that the PFO is
placed directly in line with the blood flow from the inferior vena cava. This can be the
consequence of different causes such as classic pneumonectomy or
lobectomy, cyphoscoliosis, or ascending aorta aneurysm displacing the
atrial septal orientation. The dilatation of ascending aorta due to age
seems to be in our experience the most frequent cause responsible for this
syndrome.
We hope that publication in Heart of 3 cases of platypnoea-orthodeoxia will heighten awareness of this complication. When this
syndrome is suspected, we strongly recommend transoesophageal echocardiography
with contrast study to depict the interatrial right-to-left shunt and propose transcatheter PFO occlusion. The true incidence of
this syndrome remains to be established and a registry of the complication
would be of interest.
F GODART
C REY
Department of Paediatric Cardiology
CHRU de Lille, 59037 Lille cedex
France
(2) Godart F, Rey C, Prat A, et al. Atrial right-to-left shunting causing
severe hypoxaemia despite normal right-sided pressures. Report of 11
consecutive cases corrected by percutaneous closure. Eur Heart J 2000;21:483-9.
I read with interest this case report from Hirooka and colleagues.[1]
Myocardial contrast echocardiography (MCE) allows the assessment of
myocardial perfusion, however, several technical issues remain unresolved
and artifacts are quite common.
It is highly debatable whether the perfusion defect shown represents
myocardial ischemia due to systolic compression of the LAD septal
branches. If that w...
I read with interest this case report from Hirooka and colleagues.[1]
Myocardial contrast echocardiography (MCE) allows the assessment of
myocardial perfusion, however, several technical issues remain unresolved
and artifacts are quite common.
It is highly debatable whether the perfusion defect shown represents
myocardial ischemia due to systolic compression of the LAD septal
branches. If that were the case, the bottom right picture also shows a
perfusion defect in the basal and mid-portion of the contra-lateral wall,
which cannot be explained by the angiographic findings and more likely
represents an artifact commonly seen in the basal portions of the LV.
Destruction of the microbubbles due to vigorous myocardial contraction may
explain the findings.
It is possible that MCE, due to its sampling rate, may allow us to
assess phasic changes in myocardial blood volume (MBV).[2] However, from
the physiologic standpoint, it is difficult to conceive that
autoregulation of the coronary microcirculation is absent and systolic
compression of the LAD septal branches would simultaneously cause such
dramatic reduction of MBV.
MCE is an emerging technique with great clinical potential for the
assessment of myocardial perfusion. At the current stage of the MCE
technology, and to facilitate its progress and acceptance within the
cardiology community, caution must be exercised to avoid conclusions,
especially when based upon a case report.
References
(1) Hirooka K, Masakazu Y, Miyatake K. Visualisation of systolic
myocardial perfusion defect induced by septal squeezing. Heart
2000;84:482.
(2) Kaul S, Jayaweera AR. Coronary and myocardial blood volumes:
noninvasive tools to assess the coronary microcirculation? Circulation
1997;96:719–24.
Fruhwald FM and their colleagues mentioned about ANP synthesis from
the atrium in their lecture.
Most of the ANP is synthesized in the myocites of atrium and the synthesis
is prominent in the right atrium than the left. Another location of the
ANP synthesis is the ventricles. The highest ANP expression is in the
intrauterine period, it declines after birth and reaches to the adult
levels of 1-2% of atriu...
Fruhwald FM and their colleagues mentioned about ANP synthesis from
the atrium in their lecture.
Most of the ANP is synthesized in the myocites of atrium and the synthesis
is prominent in the right atrium than the left. Another location of the
ANP synthesis is the ventricles. The highest ANP expression is in the
intrauterine period, it declines after birth and reaches to the adult
levels of 1-2% of atrium.[1] Ventricular expression increases with volume
overload,increased pressure or both.[2] Also, it has been shown that, ANP
can be released from the ventriculs in dilated cardiomyopathy as
well.[3] As the heart failure progresses, the atrial ANP synthesis and the
gene expression decreases, but the expression continous from the ventricle.[4]
BNP has been mentioned another good predictor of heart failure in the
literature. However, Wei et al, reported that, the plasma levels of BNP
remains the same in the early stages of heart failure.[6] Therefore, in
this study ANP has been decleared by early predictor of heart failure in
the asymptomatic stage.
(3) Yasue H, Obata K, Okumura K, Kurose M, Ogawa H, Matsuyama K, Jougasaki
M: Increased secretion of atrial natriuretic polypeptide from the left
ventricule in patients with dilated cardiomyopathy. J Clin Invest 1989;83:46-51.
(4) Satio Y, Nakao K, Nishimura K, Sugawara A, Okumura K, Obata K: Clinical
application of atrial natriuretic polypeptide in patients with congestive
heart failure: Beneficial effects on left ventricular function.
Circulation 1987;76:115-124.
(5) Yoshimura M, Yasue H, Okumura K, Ogawa H, Jougasaki M, Mukoyama M:
Different secretion patterns of atrial natriuretic peptide and brain
natriuretic peptide in patients with congestive heart failure. Circulation 1993;
87:464-469.
(6) Wei CM, Heublein DM, Perrella MA, Lerman A, Rodeheffer RJ, Mc Gregor
CGA, Edwards WD: Natriuretic peptide system in human heart failure.
Circulation 1993;88:1004-9.
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.
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 read with interest the case report by Codispoti et al, depicting
an association of pulmonary atresia and intact inter-ventricular septum
(PAIS) with persistent pulmonary hypertension of the newborn. In our
study of 24 autopsied cases of PAIS, we found four cases (16.7%) with
persistence of fetal circulation. All were a few days old with varying
degrees of ventricular hypoplasia and tricuspid steno...
We read with interest the case report by Codispoti et al, depicting
an association of pulmonary atresia and intact inter-ventricular septum
(PAIS) with persistent pulmonary hypertension of the newborn. In our
study of 24 autopsied cases of PAIS, we found four cases (16.7%) with
persistence of fetal circulation. All were a few days old with varying
degrees of ventricular hypoplasia and tricuspid stenoses. As a protocol
followed at our centre, sections of the lungs (average six) are studied in
all autopsied congenital heart diseases and hence we feel that this
association may not be as uncommon as suggested by the authors.
Taking into consideration the physiology of PAIS, the patent ductus
arteriosus supplies the pulmonary arterial tree in a retrograde fashion
and is responsible for the infrequency of pulmonary arterial hypoplasia
and development of collaterals. However, with persistent pulmonary
hypertension of the newborn, the retrograde blood flow would decrease and
there may even be a right to left shunt at the ductal level. Hence such
neonates will not only have a bad post operative course after correction
as occurred in the authors' case but would also have higher pre-operative
morbidity. It would, therefore, be important to consider them as a subset
of PAIS.
Reference
1. Codispoli M, Burns JE, Haworth SG, Simpson D, Mankad PS. Persistent
pulmonary hypertension of the newborn association with pulmonary atresia
and intact ventricular septum. Heart 1999;82:531-3.
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...
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:
We appreciate the kind comments of Dr Mitani regarding our article in the March 2000 issue of Heart and for sharing their experiences with us.[1]
In group 1 and 2 patients who had regressed coronary aneurysm after Kawasaki disease, there was significantly more vascular constriction with acetylcholine and poorer dilatation with isosorbide dinitrate at the regressed site, than in group 3 patient...
We read with interest the article by Kubler et al[1] concerning 3 patients with platypnoea-orthodeoxia syndrome. As reported, this syndrome is infrequent and the diagnosis can be difficult. It is characterised by dyspnoea and arterial hypoxaemia induced by upright position that resolved by recumbency. This is usually the consequence of right-to-left shunt at the atrial level. Such shunting is frequent in...
I read with interest this case report from Hirooka and colleagues.[1] Myocardial contrast echocardiography (MCE) allows the assessment of myocardial perfusion, however, several technical issues remain unresolved and artifacts are quite common.
It is highly debatable whether the perfusion defect shown represents myocardial ischemia due to systolic compression of the LAD septal branches. If that w...
Dear Editor
Fruhwald FM and their colleagues mentioned about ANP synthesis from the atrium in their lecture. Most of the ANP is synthesized in the myocites of atrium and the synthesis is prominent in the right atrium than the left. Another location of the ANP synthesis is the ventricles. The highest ANP expression is in the intrauterine period, it declines after birth and reaches to the adult levels of 1-2% of atriu...
To the Editor;
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 con...
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 hist...
Dear Editor
We read with interest the case report by Codispoti et al, depicting an association of pulmonary atresia and intact inter-ventricular septum (PAIS) with persistent pulmonary hypertension of the newborn. In our study of 24 autopsied cases of PAIS, we found four cases (16.7%) with persistence of fetal circulation. All were a few days old with varying degrees of ventricular hypoplasia and tricuspid steno...
Pages