The “Heartline Online” description (Heart 2007;93:773-774) of the
results of
our iron reduction study (JAMA 2007;297:603-610) is only partially
correct.
Indeed, analysis of the entire cohort showed no difference in outcomes for the primary endpoint, all cause mortality, and the secondary endpoint,
combined endpoint of death plus non-fatal myocardial infarction and
stroke.
However, analysis accord...
The “Heartline Online” description (Heart 2007;93:773-774) of the
results of
our iron reduction study (JAMA 2007;297:603-610) is only partially
correct.
Indeed, analysis of the entire cohort showed no difference in outcomes for the primary endpoint, all cause mortality, and the secondary endpoint,
combined endpoint of death plus non-fatal myocardial infarction and
stroke.
However, analysis according to randomization variables at entry showed
potentially important interactions between iron reduction and several of
these
variables, notably age. Figure 3 showed a graded effect of age for both
the
primary and secondary endpoints that was statistically significant (p for
interaction = 0.0038) for the secondary endpoint. Age analyzed as a
continuous variable was significantly related to outcome for both the
primary
(p = 0.04) and secondary (p = 0.001) endpoints (figure 4). Analysis of the youngest age quartile showed that iron reduction significantly reduced the primary (p=0.02) and secondary (p=0.001) endpoints. We concluded that
“iron reduction appeared to improve outcome to a significantly greater
extent
in younger compared to older patients,” an effect that likely represented
benefit in earlier disease.
Partial disclosure of these data, as in “Heartline Online”, has the
effect of
stifling future investigation into what may be an effective and low-cost
strategy for disease prevention.
Thank you for the positive response to our paper on spinal cord stimulation for treatment of patients with refractory angina pectoris.(1)
At the time when we performed the study and wrote the report, we were not aware of your scientific letter dealing with heart rate variability and spinal cord stimulation.(2) Otherwise we would certainly have discussed it in our paper....
Thank you for the positive response to our paper on spinal cord stimulation for treatment of patients with refractory angina pectoris.(1)
At the time when we performed the study and wrote the report, we were not aware of your scientific letter dealing with heart rate variability and spinal cord stimulation.(2) Otherwise we would certainly have discussed it in our paper.
Your study supports our findings in showing that “LF spectral components were significantly diminished in the absence of perceived paraesthesia with SCS.” We are pleased to learn that there is additional data supporting the hypothesis that spinal cord stimulation, even at a level below the sensory threshold, elicits positive effects in patients with refractory angina pectoris.
Sincerely,
Heinz Theres, MD
Stephan Eddicks, MD
References
1. Eddicks S, Maier-Hauff K, Schenk M et al. Thoracic spinal cord stimulation improves functional status and relieves symptoms in patients with refractory angina pectoris: the first placebo-controlled randomised study. Heart. 2007;93:585-590.
2. Moore R, Groves D, Nolan J et al. Altered short term heart rate variability with spinal cord stimulation in chronic refractory angina: evidence for the presence of procedure related cardiac sympathetic blockade. Heart. 2004;90:211-212.
In his editorial on ‘Alternative treatments for angina,’ Dr Lanza makes no mention of the value of rehabilitation, especially patient and carer education,
in improving quality of life. Given the central role of patient education in [refractory] angina management, this requires comment.
Damaging misconceptions are common in angina sufferers and their carers, and education is a potent and critica...
In his editorial on ‘Alternative treatments for angina,’ Dr Lanza makes no mention of the value of rehabilitation, especially patient and carer education,
in improving quality of life. Given the central role of patient education in [refractory] angina management, this requires comment.
Damaging misconceptions are common in angina sufferers and their carers, and education is a potent and critically important intervention that can have profound effects on understanding, behaviour and quality of life (1,2). It
is for this reason that both the ESC and the AHA/ACC/ACIP/ASM stable angina management guidelines recommend a continuous process of identifying and
clarifying misconceptions throughout care (3,4). Similarly it is why the ESC Refractory Angina Study Group came to the same conclusion (5). It is perhaps because rehabilitation and patient education is not regarded as ‘treatment’ that this most important aspect of good clinical care is so often neglected.
It is of great concern that this oversight seems to characterise each point of the patient’s journey. The AHA/ACC guidance has observed that, “…healthcare providers tend to focus on diagnostic and therapeutic interventions, often overlooking critically important aspects of high-
quality care. Chief among these neglected areas is the education of patients.”(4)
This point was vividly illustrated in an editorial on the British Cardiac Intervention Society website in 2001, when it was observed that, “The under-provision of cardiologists, out-patient facilities, hospital beds, cardiac catheterisation laboratories, and importantly, IT personnel and hardware in the average UK intervention centre frequently results in the patient arriving on the day of the procedure, having never been seen previously, and in many cases, not having met the interventional cardiologist before arriving in the catheterisation laboratory.”(6)
It may be that clinicians do not put much store in clinical guidelines, however authoritative, but what is intriguing about this failure to educate patients is
that it is not simply a minor clinical governance issue. Education is a decisive intervention for patients with angina and has the force of law. The requirement to ensure that patients are fully informed has been a necessary
element of valid consent for decades but as recently as 2001, the BMA consent working party was able to conclude that “current awareness of the relevant ethical and legal principles relating to consent among the medical profession is largely inadequate” (7). In order to clarify the guidance on consent, the Parliamentary Ombudsman and the President of the Society of Cardiac Surgeons produced a joint recommendation on consent practice which emphasises the need to ensure full disclosure of facts (8). The
joint statement reflects the trend away from the notion that doctors can decide what it is necessary for the patient to know, towards the North American standard of disclosing what a ‘prudent patient’ would wish to take into
account in making a decision about treatment. More recently the GMC’s update of ‘Good Medical Practice’ makes explicit the requirement to ensure that patients fully understand their condition to enable them to be full and active participants in the decision-making process (9).
In our experience many of the problems encountered by refractory angina patients and their carers are iatrogenic, arising from a deficient ‘education’ process, often involving many different healthcare professionals over many
years. The perceived referral criterion for specialist refractory angina management is when no further intervention is possible, and this point in the
patient’s career marks a significant moment when patients views about their condition can be adversely influenced by poorly communicated information.
We frequently meet patients who, having been told that further revascularisation is not feasible, erroneously believe that their lives are threatened by their stable angina. The terms in which this message is delivered to patients often involve such colourful phrases as: ‘I am sorry but your narrowings are just too far gone and there is nothing more that can be done’; ‘he’s a walking time bomb’; ‘you must take things very easy’; 'the artery is hanging by a thread.’
Much of our work involves treating the damaging consequences of cardiac misconceptions with individually targeted education. Careful dissection of angina patients’ beliefs and misconceptions about their condition is
rewarding for health professionals and benefits patients in terms of quality of life, frequency and duration of hospital admissions and frequency and severity of pain. The alternative to patient education raises for doctors
the risk that they may be open to challenge for having given treatment to patients who have given consent on the basis of fundamental misconceptions about the nature of their condition.
References
1. Health related quality of life of patients with refractory angina before and one year after enrolment onto a refractory angina program. Moore RK et al. Eur J Pain. 2005 Jun;9(3):305-10
2. A Brief Cognitive-Behavioral Intervention Reduces Hospital Admissions in Refractory Angina Patients. Moore RK et al. J Pain Symptom Manage. 2007 Mar;33(3):310-316
5. The problem of chronic refractory angina Report
from the ESC Joint Study Group on the Treatment of Refractory Angina Mannheimer al. European Heart Journal (2002) 23, 355–370
8. Parliamentary and Health Service Ombudsman, and the President of the Society of Cardiothoracic Surgeons of Great Britain and Ireland a joint report. ‘Consent in cardiac surgery: a good practice guide to agreeing and
recording consent’ May 2005 www.ombudsman.org.uk/improving_services/best_practice/cardiac05/index.html
Eddicks and colleagues’ placebo controlled study of spinal cord stimulation in refractory angina is important and interesting work which shows for the first time that patient appreciation of the sensation of spinal cord stimulation is not necessary to achieve clinical benefit.
The article gives the impression that no previous work had been carried out investigating sub-sensory threshold Spinal...
Eddicks and colleagues’ placebo controlled study of spinal cord stimulation in refractory angina is important and interesting work which shows for the first time that patient appreciation of the sensation of spinal cord stimulation is not necessary to achieve clinical benefit.
The article gives the impression that no previous work had been carried out investigating sub-sensory threshold Spinal Cord Stimulation (SCS) applied clinically to refractory angina patients and that, before their work, the
possibility of therapeutic effect of SCS applied at sub-sensory threshold levels could only be deduced from animal studies. This requires clarification.
In 2004, we published the findings of a study in Heart in which we evaluated the effect of full therapeutic, half therapeutic (sub sensory threshold) and zero (placebo) voltages of spinal cord stimulation in refractory angina
patients who, like the patients in Eddicks’ study, had all benefited from spinal cord stimulation (1).
Our study showed that full (sensory) therapeutic voltage and half (sub-sensory) therapeutic voltage SCS both brought about a significant reduction in cardiac sympathetic drive (as measured by low frequency heart rate variability) compared to that brought about by zero(placebo) voltage SCS.
From this we deduced that analgesia in refractory angina patients is brought about at least in part by SCS producing cardiac sympathetic blockade. We postulated that, “prolonged stimulation at this lower level could offer lessening in the total ischaemic burden and possibly altered arrhythmia thresholds for this patient group.”
References
1. Altered short term heart rate variability with spinal cord stimulation in chronic refractory angina: evidence for the presence of procedure related cardiac sympathetic blockade. R Moore, D Groves, J Nolan, D Scutt, J Pumprla, MR Chester Heart 2004;90:211-212
I read with interest the case report of a papillary fibroelastoma with heavily calcified bicuspid aortic valve, coronary artery disease and 2nd degree heart block. The authors mention this is the first case of a papillary fibroelastoma presenting with conduction block. While this may be true, it is evident that heavy calcification of a bicuspid aortic valve is a much more common and likely cause of con...
I read with interest the case report of a papillary fibroelastoma with heavily calcified bicuspid aortic valve, coronary artery disease and 2nd degree heart block. The authors mention this is the first case of a papillary fibroelastoma presenting with conduction block. While this may be true, it is evident that heavy calcification of a bicuspid aortic valve is a much more common and likely cause of conduction block in this patient, as is the possibility of AV nodal ischaemia in the setting of proven coronary artery disease. Hence the papillary fibroelastoma is likely to only be a coincidental finding in this case report.
In the article “Can atrioventricular septal defects exist with intact
structures?”, the authors seem not to know that a similar case was
described on a fetus and published in 2002[1].
This case was diagnosed through the prenatal ultrasound screening of
a supposed partial AVSD which led to the discovery of a Down Syndrome
(DS). The parents asked for a termination of pregnancy and a fetal
pa...
In the article “Can atrioventricular septal defects exist with intact
structures?”, the authors seem not to know that a similar case was
described on a fetus and published in 2002[1].
This case was diagnosed through the prenatal ultrasound screening of
a supposed partial AVSD which led to the discovery of a Down Syndrome
(DS). The parents asked for a termination of pregnancy and a fetal
pathological examination. The standardized examination of the heart[2]
showed no defect (neither atrial nor ventricular) and a normal mitral left
atrioventricular valve. The pathologist, who also practised fetal
ultrasonography (US), thought of sectioning this heart in the plane of the
US four chamber view. There, instead of the normal offsetting, the septal
leaflets of the atrioventricular valves were found to be at the same level
of the crux of the heart. This we called: the Linear insertion of the
atrioventricular valves (LIAVV) without defect[1].
This case became the index case of an anatomical series of 52 hearts
of DS fetuses. 23 out of 41 examinable hearts were “supposed normal”
because without any associated defect. After a standardized complementary
four chamber view section[3], 16 out of these 23 DS fetal hearts (70%)
showed a LIAVV. This result was highly significant (p<10-6) compared
with the controls showing a 100% normal offsetting.
A further anatomical series of 213 fetal hearts confirmed these
data[4]. 63% LIAVV without defect were found among 113 “supposed normal”
DS hearts
None of our “supposed normal”DS hearts ever showed any trileaflet left
atrioventricular valve, unlike the 4 DS postnatal cases described in the
article. Moreover, we noticed[4] some ballooning of the septal tricuspid
leaflet and/or a particular aspect of the membranous septum. This one was
more often losangic than triangular, and in a few cases, it was so thin
that it looked like a spontaneously prenatally closed VSD.
We previously defined the apex and the two inferior pulmonary veins
as the most reliable hallmarks of an “optimal” fetal four chamber view
through echo-anatomical correlations. These hallmarks are reproducible in
the Fetal pathology complementary section[3] and in the routine US
screening as well[4]. The histological study enabled us to find the best
US incidence and settings able to emphasize the crux of the heart in order
to search for LIAVV without defect cases[4,5].
Further studies were required to establish the feasibility of the US
screening of this marker and its diagnostic value for the detection of DS.
So, we induced a prospective ultrasonographic study. Previously trained
physicians studied the crux of the heart in all the routine 2nd and 3rd
trimester prenatal screening they practised on low risk pregnancies.
Reliable results will be soon submitted for publication.
References
1. Fredouille C, Piercecchi-Marti M-D, Liprandi A et al. Linear insertion of atrioventricular valves without septal defect; a new anatomical landmark for Down’s syndrome?
Fetal Diagn Ther 2002 ; 17 : 188-92. Erratum in: Fetal Diagn Ther. 2002 ;17(5):292.
2. Fredouille C. Diagnosis of a fetal cardiac malformation. Fetal heart.
Ann Pathol.1997. Sep; 17(4):300-5.
3. Fredouille C, Morice JE, Delbecque K, et al. New foetopathological section of the heart. Correlated to the ultrasonographic 4 Chamber view in fetuses.
Ann Pathol. 2006 Feb;26(1):60-5.
4. Fredouille C, Baschet N, Morice JE, et al. Linear insertion of the atrioventricular valves without defect
Arch Mal Coeur Vaiss. 2005 May;98(5):549-55.
5. Develay-Morice J-E. Settings in Fredouille C, Develay-Morice J-E. Fetal
Heart Ultrasound. How Why and When.
Elsevier-Churchill Livingstone 2007 page 77 in print
We read with great interest Kessels et. al's article on magnetic
resonance imaging (MRI) of epicardial adipose tissue (EAT), a well
established cardiovascular risk factor [1].
EAT in vivo is shown in Fig. 1.
Though MRI is the gold standard for
viewing EAT, echocardiography is a more cost-effective and routinely
conducted me...
We read with great interest Kessels et. al's article on magnetic
resonance imaging (MRI) of epicardial adipose tissue (EAT), a well
established cardiovascular risk factor [1].
EAT in vivo is shown in Fig. 1.
Though MRI is the gold standard for
viewing EAT, echocardiography is a more cost-effective and routinely
conducted method that can also be used to view EAT (Fig. 2) [2].
EAT
assessed by echocardiography is reliable [2]. EAT is associated with
anthropometric and clinical parameters of the metabolic syndrome [3],
atrial dilation and diastolic function [4] in morbidly obese patients, and
with insulin insensitivity and left ventricular mass in uncomplicated
obesity [5].
References
1. Kessels K, Cramer MJ, Velthuis B. Epicardial adipose tissue imaged by magnetic resonance imaging: an important risk marker of cardiovascular
disease. Heart. 2006; 92: 962.
2. Iacobellis G, Assael F, Ribaudo MC, Zappaterreno A, Alessi G, Di Mario U, Leonetti F. Epicardial fat from echocardiography: a new method
for visceral adipose tissue prediction. Obes Res. 2003; 11: 304-10.
3. Iacobellis G, Ribaudo MC, Assael F, Vecci E, Tiberti C, Zappaterreno A, Di Mario U, Leonetti F. Echocardiographic epicardial adipose tissue is related to anthropometric and clinical parameters of metabolic syndrome: a new indicator of cardiovascular risk. 2003; 88: 5163-8.
4. Iacobellis G, Leonetti F, Singh N, Sharma AM. Relationship of epicardial adipose tissue with atrial dimensions and diastolic function in morbidly obese subjects. Int J Cardiol. 2007 115:272-3
5. Iacobellis G, Ribaudo MC, Zappaterreno A, Vecci E, Tiberti C, Di Mario U, Leonetti F. Relationship of insulin sensitivity and left ventricular mass in uncomplicated obesity. Obes Res. 2003; 11:518-24.
Complete AV block can occur more than 3 years after percutaneous
closure of perimembranous ventricular septal defect in children Anita Dumitrescu, Geoffrey K Lane, James L Wilkinson, TH Goh, Daniel J Penny, Andrew M Davis
There have been increasing concerns about the potential for
atrioventricular block after transcatheter closure of perimembranous
ventricular septa...
Complete AV block can occur more than 3 years after percutaneous
closure of perimembranous ventricular septal defect in children Anita Dumitrescu, Geoffrey K Lane, James L Wilkinson, TH Goh, Daniel J Penny, Andrew M Davis
There have been increasing concerns about the potential for
atrioventricular block after transcatheter closure of perimembranous
ventricular septal defect, which has, again, been emphasized in your most
current issue by Ian Sullivan’ article “Transcatheter closure of
perimembranous ventricular septal defect: is the risk of hear block too
high a price?” The complication was previously highlighted in a clinical
series recently published by Walsh et al1 in your journal, however in all
these patients who developed heart block after closure of perimembranous
VSD (pmVSD) this had occurred within 10 days of the procedure.
In a retrospective study we have reviewed all patients who have had
percutaneous closure of pmVSD at our institution. This had been initiated
because we had recently encountered two instances of very late onset
complete atrioventricular block (cAVB) 24 months and 39 months after
successful and uncomplicated percutaneous closure of perimembranous
ventricular septal defect (pmVSD) using the asymmetrical Amplatzer
perimembranous ventricular septal defect occluder (AGA Medical, Golden
Valley, Minnesota, USA). The retrospective analysis of our total
collective of 36 patients who had interventional pmVSD closure
demonstrated 3 patients who developed atrioventricular (AV) block
requiring permanent pacemaker implantation. One patient developed cAVB
within 6 days of closure and presented with recurrent syncopal episodes
and hypotensive seizures. He underwent implantation of a permanent
pacemaker and later AV conduction normalised.
One patient presented with tiredness at 24 months and was found to be
in 2:1 AV block with periods of cAVB. Our most recent patient presented
with intermittent cAVB 39 months post procedure and reported non-specific
mild symptoms of tiredness and dizziness for the past five months only
after focused interrogation. Holter monitor showed frequent periods of AV
block with 2:1 conduction, Mobitz type II and intermittent cAVB (figure).
The longest pause was 9.6 seconds. Both patients had permanent pacemakers
implanted, their conduction has not normalised since. Because of the late
onset and severity of symptoms we have not attempted steroid therapy2. The
incidence of cAVB in our patient cohort is 8.3% compared with reports in
published data of 1-5% after percutaneous closure of pmVSD1,3,4.
Following the first instance of late cAVB we ceased our program of
interventional pmVSD closure and alerted all families with children who
have had the procedure performed, detailing the clinical manifestations of
cAVB. Apart from the routinely performed pre-and post interventional
Holter monitoring, we have now recalled all patients for regular ECG and
Holter monitors.
Incidents of late onset of cAVB in children following interventional
closure of pmVSD have been reported over the past few years5 and very late
onset has been rarely reported after surgical closure6,7.
It is important to alert all those who look after these patients to
the unpredictability and relatively high incidence of the very late onset
of this potentially fatal complication and to recommend that all patients
who have had the procedure have their AV conduction followed carefully. It
is time for all units performing this procedure to consider whether it is
ever indicated with the currently available device.
References
1. Walsh MA, Bialkowski J, Szkutnik M, Pawelec-Wojtalik M, Bobkowski W, Walsh KP. Atrioventricular block after transcatheter closure of
perimembranous ventricular septal defects. Heart. 2006 Sep;92(9):1295-7.Epub 2006 Jan 31
2. Yip WC, Zimmerman F, Hijazi ZM. Heart block and empirical therapy after transcatheter closure of
perimembranous septal defect. Catheter Cardiovasc Interv.2005;66(3):436-41
3. Masura J, Gao W, Gavora P, et al. Percutaneous closure of perimembranous ventricular septal defects
with the eccentric Amplatzer device: multicenter follow-up study. Pediatr Cardiol 2005;26:216-9
4. Arora R, Trehan V, Kumar A, et al. Transcatheter closure of congenital ventricular septal defects:
experience with various devices. J Interv Cardiol 2003;16:83-91
5. Butera G, Chessa M, Carminato M, Drago M, Negura D, Piazza L. Late complete atrioventricular block after percutaneous closure
of a perimembranous ventricular septal defect. Catheterization and Cardiovascular interventions. Volume 67,
Issue 6, Pages 938-941
6. Fukuda T, Nakamura Y, Iemura J, Oku H. Onset of complete atrioventricular block 15 years after
ventricular septal defect surgery. Pediatric Cardiology 2002;23:80-3
7. Roos-Hesslink JW, Meijboom FJ, Spitaels SEC, van Domburg R, van Rijen EHM, Utens EMWJ, Bogers AJJC, Simoons ML. Outcome of patients after surgical closure of ventricular septal
defect at young age: longitudinal follow-up of 22-34
years. European Heart Journal 2004;25:1057-1062.
We read with interest Bellenger et als description of the
determination of fractional flow reserve (FFR) to guide treatment of side
branch arteries following provisional stenting across a bifurcation. The
use of pressure wires to guide treatment of main vessel narrowings (1) and
ambigious stenoses in multi-vessel disease (2) and ACS (3) is established.
We read with interest Bellenger et als description of the
determination of fractional flow reserve (FFR) to guide treatment of side
branch arteries following provisional stenting across a bifurcation. The
use of pressure wires to guide treatment of main vessel narrowings (1) and
ambigious stenoses in multi-vessel disease (2) and ACS (3) is established.
Based on their preliminary findings, that there is a poor correlation
between the angiographic degree of nipping by quantitative coronary
angiography (QCA) and the FFR in the side branches after stenting the main
vessel, the authors called for a randomised controlled trial to determine
whether FFR-directed treatment of side branch nipping improves clinical
and angiographic outcome following PCI at bifurcations.
Given that such side branches may be relatively small (2.3 +/-0.2mm
in the current study) we question the assertion that a QCA stenosis
>50% would trigger treatment by many interventionists. FFR
determination encompasses the interaction between the degree of anatomic
stenosis and the area of myocardium perfused by the vessel.
This goes some
way in accounting for the occurrence of haemodynamically significant
obstruction in only a minority of vessels (3/14) in the current study.
Indeed others have shown that in larger side branches (> 2.5mm) where
QCA-assessed stenosis is >75% following main vessel stenting, a greater
proportion will demonstrate functional significance (38% vs 27% in vessels
< 2.5mm), although the overall occurrence of functionally significant
stenoses remains small (4). Further, were treatment of the side branch to
be undertaken, it is as likely to involve POBA as a second stent procedure
(5). The authors own findings would suggest that a strategy of treating
only the main vessel is sufficient, achieving a "functionally adequate
result" in the majority of cases (79%). Therefore the extra cost incurred
by routine use of a pressure wire in this situation might prove difficult
to justify if, as the authors concur, the likelihood of a functionally
significant lesion is "infrequent". In their small pilot study, none of
the lesions measuring less than 50% by QCA were associated with a FFR less
than 0.75.
Undoubtedly deferring treatment of side branches will prevent
unnecessary coronary interventions and their related complications -
whether routine use of a pressure wire is required to achieve this is
debateable.
References
1. Bech GJW, De Bruyne B, Pijls NHJ, et al. Fractional Flow Reserve
to Determine the Appropriateness of Angioplasty in Moderate Coronary
Stenosis : A Randomized Trial. Circulation. 2001; 103(24):2928-2934.
2. Berger A, Botman K-J, MacCarthy PA, et al. Long-Term Clinical
Outcome After Fractional Flow Reserve-Guided Percutaneous Coronary
Intervention in Patients With Multivessel Disease. JACC. 2005; 46(3):438-442.
3. Joshua J. Fischer X. Outcome of patients with acute coronary
syndromes and moderate coronary lesions undergoing deferral of
revascularization based on fractional flow reserve assessment. Catheterization and Cardiovascular Interventions. 2006; 68(4):544-548.
4. Koo B-K, Kang H-J, Youn T-J, et al. Physiologic Assessment of
Jailed Side Branch Lesions Using Fractional Flow Reserve. JACC. 2005; 46(4):633-637.
5. Pan M, de Lezo JS, Medina A, et al. Rapamycin-eluting stents for
the treatment of bifurcated coronary lesions: A randomized comparison of a
simple versus complex strategy. Am Heart J. 2004; 148(5):857-864.
Drs. Ince and Nienaber (1) provided an excellent and interesting review of the diagnosis and management of patients with aortic dissection.
Long-term follow-up was stressed as being of prime importance for these
patients, particularly the ongoing monitoring of aortic size parameters.
In addition, although not specifically mentioned in their review, one must
pay careful attention to the family...
Drs. Ince and Nienaber (1) provided an excellent and interesting review of the diagnosis and management of patients with aortic dissection.
Long-term follow-up was stressed as being of prime importance for these
patients, particularly the ongoing monitoring of aortic size parameters.
In addition, although not specifically mentioned in their review, one must
pay careful attention to the family members of such individuals. (2) Since
many predisposing factors to aortic dissection are inherited, and many of
these genetic conditions have no visible manifestations other than an
intrinsic weakening of the aortic wall, it would seem prudent to evaluate
close kin for the presence of aortic root dilatation. Conditions such as
bicuspid aortic valve, coarctation of the aorta, and the many familial
aortic dissection syndromes including mutations of the transforming growth
factor-beta receptor type II (3) may be etiologic in any given case. The
measurement of aortic root diameters of all close kin will help to avoid
another case of aortic dissection.
References
1. Ince H, Nienaber CA. Diagnosis and management of patients with aortic
dissection. Heart 2007;93:266-70.
2. Fikar CR. Acute aortic dissection in children and adolescents:
diagnostic and after-event follow-up obligation to the patient and family. Clin Cardiol 2006;29:383-6.
3. Pannu H, Fadulu VT, Chang J, et al. Mutations in transforming growth
factor-beta receptor type II cause familial thoracic aortic aneurysms and
dissections. Circulation 2005;112:513-20.
Dear Editor,
The “Heartline Online” description (Heart 2007;93:773-774) of the results of our iron reduction study (JAMA 2007;297:603-610) is only partially correct. Indeed, analysis of the entire cohort showed no difference in outcomes for the primary endpoint, all cause mortality, and the secondary endpoint, combined endpoint of death plus non-fatal myocardial infarction and stroke. However, analysis accord...
Dear Dr. Groves, Dr. Chester, and Editor,
Thank you for the positive response to our paper on spinal cord stimulation for treatment of patients with refractory angina pectoris.(1)
At the time when we performed the study and wrote the report, we were not aware of your scientific letter dealing with heart rate variability and spinal cord stimulation.(2) Otherwise we would certainly have discussed it in our paper....
Dear Editor,
In his editorial on ‘Alternative treatments for angina,’ Dr Lanza makes no mention of the value of rehabilitation, especially patient and carer education, in improving quality of life. Given the central role of patient education in [refractory] angina management, this requires comment.
Damaging misconceptions are common in angina sufferers and their carers, and education is a potent and critica...
Dear Editor,
Eddicks and colleagues’ placebo controlled study of spinal cord stimulation in refractory angina is important and interesting work which shows for the first time that patient appreciation of the sensation of spinal cord stimulation is not necessary to achieve clinical benefit.
The article gives the impression that no previous work had been carried out investigating sub-sensory threshold Spinal...
Dear Editor,
I read with interest the case report of a papillary fibroelastoma with heavily calcified bicuspid aortic valve, coronary artery disease and 2nd degree heart block. The authors mention this is the first case of a papillary fibroelastoma presenting with conduction block. While this may be true, it is evident that heavy calcification of a bicuspid aortic valve is a much more common and likely cause of con...
Dear Editor,
In the article “Can atrioventricular septal defects exist with intact structures?”, the authors seem not to know that a similar case was described on a fetus and published in 2002[1].
This case was diagnosed through the prenatal ultrasound screening of a supposed partial AVSD which led to the discovery of a Down Syndrome (DS). The parents asked for a termination of pregnancy and a fetal pa...
Dear Editor,
We read with great interest Kessels et. al's article on magnetic resonance imaging (MRI) of epicardial adipose tissue (EAT), a well established cardiovascular risk factor [1].
EAT in vivo is shown in Fig. 1.
Though MRI is the gold standard for viewing EAT, echocardiography is a more cost-effective and routinely conducted me...
Dear Editor,
Complete AV block can occur more than 3 years after percutaneous closure of perimembranous ventricular septal defect in children
Anita Dumitrescu, Geoffrey K Lane, James L Wilkinson, TH Goh, Daniel J Penny, Andrew M Davis
There have been increasing concerns about the potential for atrioventricular block after transcatheter closure of perimembranous ventricular septa...
Dear Editor,
We read with interest Bellenger et als description of the determination of fractional flow reserve (FFR) to guide treatment of side branch arteries following provisional stenting across a bifurcation. The use of pressure wires to guide treatment of main vessel narrowings (1) and ambigious stenoses in multi-vessel disease (2) and ACS (3) is established.
Based on their preliminary findings, tha...
Dear Editor,
Drs. Ince and Nienaber (1) provided an excellent and interesting review of the diagnosis and management of patients with aortic dissection.
Long-term follow-up was stressed as being of prime importance for these patients, particularly the ongoing monitoring of aortic size parameters. In addition, although not specifically mentioned in their review, one must pay careful attention to the family...
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