I read with great interest the study by Little et al. (1)
investigating the effect of acute blood pressure change on hemodynamic
parameters of aortic stenosis (AS). Their implication that "differences in
haemodynamics should be considered as a potential explanation for a change
in AS severity independent of disease progression" should be stressed not
only in clinical practice, but as well in prospect...
I read with great interest the study by Little et al. (1)
investigating the effect of acute blood pressure change on hemodynamic
parameters of aortic stenosis (AS). Their implication that "differences in
haemodynamics should be considered as a potential explanation for a change
in AS severity independent of disease progression" should be stressed not
only in clinical practice, but as well in prospective studies assessing
the effect of medical treatment of AS.
I would like to call attention to the coincidence of chronic blood
pressure change in essential arterial hypertension with calcific AS, which
may be much more frequent than previously reported. According to our data
(2), hypertension was found in more than two thirds of 225 patients with
nonrheumatic severe AS at the time of evaluation for surgery. Such a high
percentage, however, should not be a surprise, as it is similar to the
prevalence in the general population of corresponding age and gender (3).
Within last decade, vasodilators have become common part of
antihypertensive medication in clinical practice (2, 4), though their good
tolerance in patients with AS has been demonstrated prospectively only
recently (5).
To conclude, in patients with AS arterial hypertension is frequent, should
be actively sought after, and carefully controlled.
References
1. Little SH, Chan KL, Burwash IG. Impact of blood pressure on the Doppler echocardiographic assessment of severity of aortic stenosis. Heart
2007;93:848-855.
2. Linhartová K, Filipovský J, Èerbák R, et al. Severe aortic
stenosis and its association with hypertension: analysis of clinical and
echocardiographic parameters. Blood Pressure 2007;16:122-128.
3. Hajjar I, Kotchen A. Trends in prevalence, awareness, treatment,
and control of hypertension in the United States, 1988-2000. JAMA
2003;290:199-206.
4. Rosenhek R, Rader F, Loho N, et al. Statins but not angiotensin-
converting enzyme inhibitors delay progression of aortic stenosis. Circulation, 2004;110:1291-1295.
5. Jimenez-Candil J, Bermejo J, Yotti R, et al. Effects of
angiotensin converting enzyme inhibitors in hypertensive patients in
aortic stenosis: a drug withdrawal study. Heart 2005;91:1311-8.
Breidthardt et al. (1) found that acute decompensated
heart failure (HF) patients presenting to their Emergency Department with
prolonged QRS interval (>=120 ms) showed higher long-term mortality.
This is a pathophysiologically plausible finding: after initially
representing a marker of diseased myocardium, prolonged QRS may itself
subsequently contribute to disease progression. (2) Nevertheless,...
Breidthardt et al. (1) found that acute decompensated
heart failure (HF) patients presenting to their Emergency Department with
prolonged QRS interval (>=120 ms) showed higher long-term mortality.
This is a pathophysiologically plausible finding: after initially
representing a marker of diseased myocardium, prolonged QRS may itself
subsequently contribute to disease progression. (2) Nevertheless, we cannot
totally agree with the clinical implication the authors make regarding use
of this particular ECG measure for clinical management of acute HF.
The concept that QRS measurement could help guide rapid intensive care
modalities is very attractive. However, patients with prolonged QRS
interval at the time of admission to the Emergency Department did not show
significant differences in 30-day mortality (P=0.27) or length of hospital
stay (P=0.32). Therefore, the present study provides little direct
evidence that prolonged QRS interval at presentation affects outcome in
the acute phase of HF, and further studies will be needed to address this
question.
Patients presenting with prolonged QRS did show remarkably higher 2-year
mortality (59% vs. 37%, P=0.004). However, attribution of part or all of
this excess risk to the acute phase may imply some overinterpretation. We
do not know how much of this excess risk can be attributed to acute phase
occurrences, and how much may result from subsequent effects of QRS
prolongation on progression of chronic HF. This consideration implicitly
raises the question of whether QRS prolongation could help guide
management of the chronic phase of HF (of note, admission ECGs would not
be an appropriate measure to address this question since QRS duration can
vary significantly during hospitalization, particularly after achievement
of a compensated euvolemic state(3). In this regard, we previously reported
that time-related changes in QRS duration during chronic HF seems to
provide incremental independent prognostic information as compared with
single measurements. (4, 5) To better interpret the findings of the present
study, it would be interesting to know if prolonged QRS interval at the
time of hospital discharge also appeared to be associated with worse long-
term outcome.
References
1. Breidthardt T, Christ M, Matti M, et al. QRS and QTc interval
prolongation in the prediction of long-term mortality of patients with
acute destabilised heart failure. Heart (British Cardiac Society)
2007;93(9):1093-7.
2. Grines CL, Bashore TM, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional abnormalities in isolated left bundle branch block. The effect
of interventricular asynchrony. Circulation 1989;79(4):845-53.
3. Aranda JM, Carlson ER, Pauly DF, et al. QRS duration variability
in patients with heart failure. The American journal of cardiology
2002;90(3):335-7.
4. Grigioni F, Boriani G, Magelli C, Branzi A. QRS interval time-
related changes and prognosis in heart failure. The American journal of
cardiology 2003;91(4):514.
5. Grigioni F, Carinci V, Boriani G, et al. Accelerated QRS widening
as an independent predictor of cardiac death or of the need for heart
transplantation in patients with congestive heart failure. J Heart Lung
Transplant 2002;21(8):899-902.
Lin et al. report an observational study in 52 patients investigating
whether upgrading an ICD, implanted predominantly for secondary prevention
to CRT-D, can reduce arrhythmias.[1] They failed to detect an effect of
CRT on arrhythmias during a mean follow up of 14 months. The CARE-HF
extension study suggested that reduction in sudden death with CRT might be
a late phenomenon occurring only after one...
Lin et al. report an observational study in 52 patients investigating
whether upgrading an ICD, implanted predominantly for secondary prevention
to CRT-D, can reduce arrhythmias.[1] They failed to detect an effect of
CRT on arrhythmias during a mean follow up of 14 months. The CARE-HF
extension study suggested that reduction in sudden death with CRT might be
a late phenomenon occurring only after one or more year of therapy and
after extensive left ventricular remodelling.[2] There are number of
disturbing aspects to this report. Pharmacological therapy at baseline was
far from optimal and appeared to deteriorate after device upgrade
suggesting that the investigators had focussed on device therapy to the
detriment of pharmacological care. Many of the patients selected were in
NYHA stage II. Currently, it is not known if such patients benefit from
CRT; the results of the REVERSE, RAFT and MADIT-CRT trials are awaited.[3]
Almost two-thirds of patients were in AF, a group of patients in whom the
evidence of benefit for CRT is not clear.
Although the mean ejection fraction increased in Lin’s study, LV
dimension was unchanged, suggesting that reverse remodelling had not taken
place, perhaps due to the selection of patients unable to benefit and
neglect of pharmacological therapy. In turn, this may have been
responsible for the lack of an observed effect on ventricular
tachyarrhythmias.
Finally, this was not a randomised controlled trial. It is not
unlikely that arrhythmias worsen with longer duration of follow-up as
heart disease progresses and therefore the apparent lack of effect of CRT
may be deceptive. In conclusion, this was not a fair test of the
hypothesis that guideline-indicated CRT associated with high quality
pharmacological care reduces arrhythmias in patients with heart failure.
References
1. Lin G, Rea RF, Hammill SC, et al. Effect of cardiac
resynchronisation therapy on occurence of ventricular arrhythmia in
patients with implantable cardioverter defibrillators undergoing upgrade
to cardiac resynchronisation therapy devices. Heart, 2007.
doi:10.1136/hrt.2007.118372.
2. Cleland JGF, Daubert JC, Erdmann E, at al. on behalf of The
Cardiac Resynchronisation-Heart Failure (CARE-HF) Study Investigators. Longer-term effects of cardiac resynchronisation therapy on mortality in
heart failure [the CArdiac REsynchronisation-Heart Failure (CARE-HF) trial
extension phase]. European Heart Journal, 2006. 27: p. 1928-1932.
3. Cleland JGF, Nasir M, Tageldien A. Cardiac resynchronization
therapy or atrio-biventricular pacing—what should it be called? Nature
Clinical Practice Cardiovascular Medicine, 2007. 4: p. 90-101.
Dr. Wahl and colleagues studied the short and long-
term safety and efficacy of percutaneous closure of patent foramen ovale
(PFO) for prevention of paradoxical embolization using fluoroscopic
guidance only (1). While we command their technical skills, we disagree
that using fluoroscopy only is the safest and most efficient approach to
percutaneous PFO closure. The authors correctly note that to dat...
Dr. Wahl and colleagues studied the short and long-
term safety and efficacy of percutaneous closure of patent foramen ovale
(PFO) for prevention of paradoxical embolization using fluoroscopic
guidance only (1). While we command their technical skills, we disagree
that using fluoroscopy only is the safest and most efficient approach to
percutaneous PFO closure. The authors correctly note that to date there
are no randomized controlled trials that have shown improvement in hard
clinical endpoints with PFO closure. This is an elective procedure that is
frequently performed in young patients (mean age in their study 51) that
have little to no co-morbidities. Therefore, any imaging guidance that
minimizes the risk associated with this procedure should be utilized. The
authors state “none of these complications could have been avoided by
additional echocardiographic guidance”; however, they never had a
ultrasound guided comparison group. Additionally, they did not use balloon
inflation prior to closure, which provides information not only about the
size but also of the shape and quality of septal tissue. They report
embolization of devices in 1% (5 patients), upsizing of the device in 5%,
and residual shunt in 27% of patients with larger devices. Furthermore, 14
patients (3%) underwent repeat intervention and 2 patients had erosions.
Although the complication rates are small they are substantial
considering the relatively healthy population that undergoes this
procedure. The authors are very experienced; however, we believe that
advocating closure of PFOs by only fluoroscopic guidance is dangerous and
to some extent irresponsible. Specially, when the rate of complications by
ultrasound guided approach as reported by Du et al and Bruch et al has
been 0% with 100% closure at 6 months (2,3).
Transesophageal echocardiography has certain limitations in the
catheterization laboratory, intracardiac echocardiography (ICE) was
introduced in 2000, it is easy to use, and its safety and efficacy has
been validated in multiple studies (4). During the procedure, ICE can
evaluate adequate device sizing and positioning in relation to septum
primum, secundum and aorta (Figure 1); as well as the mechanism of
residual shunt (e.g. multiple holes, Figure 2). It is also very useful in
the infrequent situation where transseptal puncture for a tunneled PFO is
necessary. Therefore, given the minimum associated risk and the
preponderance of the information that is provided by intraprocedural ICE
we feel that this modality should be an integral part of percutaneous PFO
closure.
References
1. Wahl A, Kunz M, Moschovitis A, et al.
Long-Term Results after
Fluoroscopy Guided Closure of Patent Foramen Ovale for Secondary
Prevention of Paradoxical Embolism.
Heart 2007.
2. Bruch L, Parsi A, Grad MO, et al.
Transcatheter closure of interatrial
communications for secondary prevention of paradoxical embolism: single-
center experience. Circulation 2002;105(24):2845-8.
3. Du ZD, Cao QL, Joseph A, et al.
Transcatheter closure of patent foramen
ovale in patients with paradoxical embolism: intermediate-term risk of
recurrent neurological events. Catheter Cardiovasc Interv 2002;55(2):189-
94.
4. Brochet E, Aubry P, Juliard JM, et al. [Intracardiac echography]. Arch Mal Coeur Vaiss 2007;100(1):52-60.
Antibiotic Prophylaxis to Prevent Infective Endocarditis should be given to Patients with Valvular or Structural Heart Disease Prior to Dental Treatment: Results of a National Survey Amongst UK Cardiologists and Cardiac Surgeons
Dear Editor,
Recently published guidelines suggesting that antibiotic prophylaxis
(ABP) should not be given prior to dental treatment to patients with
valvular or structural h...
Antibiotic Prophylaxis to Prevent Infective Endocarditis should be given to Patients with Valvular or Structural Heart Disease Prior to Dental Treatment: Results of a National Survey Amongst UK Cardiologists and Cardiac Surgeons
Dear Editor,
Recently published guidelines suggesting that antibiotic prophylaxis
(ABP) should not be given prior to dental treatment to patients with
valvular or structural heart disease who are considered to be at risk of
infective endocarditis (IE)1,2 have been firmly opposed by ourselves3-6
on the grounds that such a change of policy is not evidenced-based, that
it is contrary to the view of cardiologists and cardiac surgeons in
Europe7,8 and because ABP is safe and cost-effective.
Our reasons for advocating ABP are based on an understanding of the
pathogenesis of IE, animal experimentation, case reports and the vast
experience of clinical practice over the last 50 years worldwide rather
than on specific randomised, controlled clinical trial data. Moreover,
experience of the destructive cardiac complications and the devastating
embolic and vasculitic complications of IE, the need for prolonged in-
hospital (and often prolonged ITU) care and the requirement for high doses
of parenteral antibiotics, a high morbidity and mortality and the not
infrequent need for cardiac surgery, demand that clinicians do everything
in their power to prevent the development of IE.
However, there are some medical personnel who demand hard, clinical
trial evidence of benefit of ABP before holding to what is currently
considered to be standard practice and they dismiss case reports and case
series as unacceptable evidence for supporting the case for continued ABP.
In our view this is unreasonable.
Although it was our personal opinion that only a minority of cardiac
specialists within the UK held the “no ABP” stance, we performed a
national survey amongst UK cardiologists and cardiac surgeons in order to
firmly establish their views on the subject and on the importance of case
reports associating IE with invasive procedures and bacteraemia.
Between February – April 2007, 830 cardiologists and cardiac surgeons
practising in the UK were sent a questionnaire by e-mail and/or post.
Table 1 shows the 4 questions that were asked. 523 replies were
received.
Table 2 shows the responses to the questions.
Of the questions that were answered:
Q1.
94.2% of the cardiac specialists felt that patients with
valvular, congenital or other structural heart disease and considered to
be at moderate risk of IE should receive ABP prior to dental treatment.
Q2.
83.3% took the view that case reports of IE following invasive
procedures constituted “evidence” of an association between the two
events, sufficient enough to warrant ABP prior to these procedures for
those individuals considered to be at risk because of their heart disease.
Q3.
74.6% of respondents felt that evidence of bacteraemia following
invasive diagnostic or interventional procedures constituted sufficient
evidence to highlight these procedures for ABP in patients considered at
moderate risk for IE.
Q4.
Finally, 95.8% of cardiac specialists were of the opinion that it
was unsafe to recommend that patients with valvular, congenital or other
structural heart disease and considered to be at moderate risk of IE
should not receive ABP prior to dental treatment.
All physicians and surgeons, general practitioners and dentists who
have clinical responsibility for patients who have a previous history of
IE, structural cardiac abnormalities or a prosthetic heart valve that puts
them at increased risk of developing IE as a result of a procedure that
gives rise to bacteraemia should take note of the results of this survey
and offer such patients ABP in an attempt to prevent IE. This practice
should continue until there is incontrovertible evidence that it is
totally ineffective or harmful to our patients. Dentists and other
colleagues are likely to find themselves unsupported by cardiologists and
cardiac surgeons if their patient develops IE as a result of the wilful
omission of ABP.
Following the publication of the BSAC guidelines and the editorial by
Martin in the British Dental Journal,9 some medical and dental
practitioners have claimed to be unsure as to “what to do”. The National
Institute for Clinical Excellence is planning to develop and publish NICE
Guidelines on the “ABP for IE” issue. In the light of this survey, that
the overwhelming consensus amongst cardiologists and cardiac surgeons in
the UK is in favour of continuing to offer ABP to cardiac patients “at-
risk”, it is unthinkable that any alternative advice will be proposed.
Yours faithfully,
David R Ramsdale BSc MB ChB MD FRCP, Consultant Cardiologist.
Nick D Palmer MB BS MD MRCP, Consultant Cardiologist.
John A C Chalmers BSc MB ChB FRCS, Consultant Cardiac Surgeon.
The Cardiothoracic Centre,
Thomas Drive,
Liverpool, UK
L14 3PE
REFERENCES
1. Gould FK, Elliott TSJ, Foweraker J et al. Guidelines for the prevention of endocarditis: report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother
2006;57:1035-42.
2. Wilson W, Taubert KA, Gewitz M et al. Prevention of Infective Endocarditis. Guidelines from The American Heart Association. Circulation 2007 Apr 19; [Epub ahead of print].
3. Ramsdale DR and Palmer ND. Antimicrobial prophylaxis for endocarditis: emotion or science? Heart Online. 7th February 2007.
4. Chalmers JAC and Pullan DM. Antimicrobial prophylaxis for endocarditis: emotion or science? Heart Online. 7th February 2007.
6.Ramsdale DR, Egred M, Palmer ND and Chalmers JAC. Prevention of Infective Endocarditis. Guidelines from The American Heart Association 2007. Criticism of Guidelines and Writing Group’s response. http://www.americanheart.org/presenter.jhtml?identifier=3044644
7. Ramsdale DR and Turner-Stokes L on behalf of the Advisory Group of the British Cardiac Society Clinical Practice Committee and the RCP Clinical Effectiveness and Evaluation Unit (2004). Prophylaxis and
treatment of infective endocarditis in adults: a concise guide. Clin Med 2004;4:545-50.
8. The Task Force on Infective Endocarditis of the European Society
of Cardiology. Guidelines on Prevention, Diagnosis and Treatment of
Infective Endocarditis. Executive Summary. Eur Heart J 2004;25:267-276.
9. Martin M. A victory for science and common sense. The new guidelines on antimicrobial prophylaxis for infective endocarditis. Br Dent J 2006;200:471.
O'Flaherty and colleagues (1) have identified a worrying change in
the hitherto improving CHD mortality data in England and Wales that has
occurred despite record spending on coronary revascularisation. They
correctly propose that the health intervention measures, as recommended by
Wanless (2) and supported by the National Heart Forum (3) and NICE (4),
should be urgently implemented in an attempt to p...
O'Flaherty and colleagues (1) have identified a worrying change in
the hitherto improving CHD mortality data in England and Wales that has
occurred despite record spending on coronary revascularisation. They
correctly propose that the health intervention measures, as recommended by
Wanless (2) and supported by the National Heart Forum (3) and NICE (4),
should be urgently implemented in an attempt to prevent premature death
especially in young socially disadvantaged adults.
What 0'Flaherty and colleagues fail to address is the funding issue.
As Wanless hints in his report, the most logical and theoretically least
challenging way to fund the expansion of effective preventative
interventions is to redeploy resources from wasteful and expensive
practices that are unproven or whose cost/benefit balance cannot be
justified.
PCT commissioners have a duty to optimise the effectiveness of NHS
resources and should urgently review their blank cheque approach to
palliative percutaneous coronary intervention (PCI). The Courage trial (5)
confirmed that PCI does not improve prognosis and is only marginally
superior to optimal drug treatment in ameliorating symptoms in low-risk
stable angina patients. Griffin et al., (6) confirmed the suspicions
first raised following the RITA-2 study (7), that the high cost of PCI
cannot be justified. These data, coupled with concerns over late drug
eluting stent (DES) thrombosis and the controversy around the
inappropriate implantation of DES in unlicensed situations have combined
to change practice in the US where manufacturers have recently reported a
more than 40% slump in DES sales.
When the QALY cost of preventative measures (£20-£400) (4) are
compared to PCI (£47,000) (6) the case for redeploying resources becomes
overwhelming, especially when the effectiveness of preventative measures
take account of their ability to reduce the need for expensive
revascularisation procedures.
References
1. O'Flaherty M E, Ford E S, Allender S, Scarborough P, Capewell S. Coronary heart disease trends in England and Wales from 1984 to 2004: concealed leveling of mortality rates among young adults Heart published online 19 Jul 2007; doi:10.1136/hrt.2007.118323
3. The National Heart Forum And The UKPHA Submission To: HM Treasury Review: Securing Good Health for the Whole Population by Derek Wanless. December 2003. LS\WANLESS\7791
4. NICE Public Health Intervention Guidance no.2 http://www.nice.org.uk/page.aspx?o=PhysicalActivityandEnv
5. Boden et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease. N Engl J Med 2007; 356:1503-1516
6. Griffin et al. Cost effectiveness of clinically appropriate decisions on alternative treatments for angina pectoris: prospective
observational study. BMJ 2007;334:624(24 March)
7. Sculpher MJ, Smith DH, Clayton T, Henderson R, Buxton MJ, Pocock SJ, et al. Coronary angioplasty versus medical therapy for angina. Eur Heart J 2002;23:1291-300
McMahon et al reported in a recent article a reduction of TD
velocities in children with noncompaction of the left ventricle, compared
with normal controls. The authors concluded their work saying that the
reduction of lateral mitral Ea velocity helps to predict children with
LVNC who are at risk of adverse clinical outcomes including death and need
for cardiac transplantation. In a precedent report...
McMahon et al reported in a recent article a reduction of TD
velocities in children with noncompaction of the left ventricle, compared
with normal controls. The authors concluded their work saying that the
reduction of lateral mitral Ea velocity helps to predict children with
LVNC who are at risk of adverse clinical outcomes including death and need
for cardiac transplantation. In a precedent report our group reported a
strong correlation between pathological tissue Doppler and reduction of
ejection fraction. In our report the tissue Doppler analysis was performed
segment by segment, and a correlation had been ob served only in patients
with a low EF.
Noncompaction of the ventricular myocardium (LVNC) is a rare
congenital cardiomyopathy resulting from an arrest in normal
endomyocardial embryogenesis; it is characterized by a thin compacted
epicardial and an extremely thickened endocardial layer with prominent
trabeculations and deep intertrabecular recesses (1-6). In this rare
cardiomyopathy clinical presentation and outcome is variable, but heart
failure, arrhythmias and sudden cardiac death are described like common
clinical findings (1-6). Unfortunately the pathophysiological mechanisms
are unknown. In 2002 Jenni et al. (7) reported a microvascular dysfunction
in 12 patients affected by non compaction: areas of restricted myocardial
perfusion have been documented by scintigraphy, suggesting a reduction of
Coronary flow reserve (CFR). The decreased of CFR is not confined to
noncompacted segments, but extends to most segments with wall motion
abnormalities, thus global coronary microcirculatory dysfunction could be
associated with IVNC (7-12). McMahon et al (1) reported in a recent
article a reduction of TD velocities in children with noncompaction of the
left ventricle, compared with normal controls. In a precedent report our
group reported a strong correlation between pathological tissue Doppler
and reduction of ejection fraction. In this study we performed a Tissue
Doppler analysis, segment by segment, in a series of 15 children affected
by non-compaction. The bidimensional echocardiogram showed a strong
correlation between systolic function and diastolic dysfunction (2).
Alterations of the diastolic function compared in 7 (49%) patients: in 2
cases, a reduction of the Ea wave was present in all segments. In 3
patients the diastolic dysfunction was limited to apical and lateral
segments. In the last 2 children a reduction of the Ea wave interested
only the apical segments. Every patient with diastolic dysfunction also
presented a severe reduction of the systolic function (less then 40%). In
our opinion the late enhancement can be depend on a CFR, and is the
determinant of the tissue Doppler alterations. So the TD alteration is
associated with EF, and is an indirect index of poor clinical outcome,
like EF (1-12). McMahon et al (1) concluded their work saying that the
reduction of lateral mitral Ea velocity helps to predict children with
LVNC who are at risk of adverse clinical outcomes including death and need
for cardiac transplantation. In our opinion, more then the Em, the EF at
the admission can help to predict the mortality in these patients.
References:
1)McMahon CJ, Pignatelli RH, Nagueh SF, Lee VV, Vaughn W, Valdes SO,
Kovalchin JP, Jefferies JL, Dreyer WJ, Denfield SW, Clunie S, Towbin JA,
Eidem BW Left ventricular non-compaction cardiomyopathy in children:
characterisation of clinical status using tissue Doppler-derived indices
of left ventricular diastolic relaxation Heart. 2007; 93:676-81.
2)Fazio G, Pipitone S, Iacona MA, Marchì S, Mongiovì M, Zito R,
Sutera L, Novo G, Novo S Evaluation of diastolic function by the Tissue doppler in children
affected by non-compaction Int J Cardiol. 2007;116:e60-2.
3)Fazio G, Sutera L, Corrado G, Novo S The chronic heart failure is not so frequent in non-compaction Eur Heart J. 2007; 28:1269.
4) Fazio G, Corrado G, Pizzuto C, Zachara E, Rapezzi C, Sulafa AK,
Sutera L, Stollberger C, Sormani L, Finsterer J, Benatar A, Di Gesaro G,
Novo G, Cavusoglu Y, Baumhakel M, Drago F, Carerj S, Pipitone S, Novo S. Supraventricular arrhythmias in noncompaction of left ventricle: Is this a
frequent complication? Int J Cardiol. 2007; [Epub ahead of print]
5)Fazio G, Corrado G, Zachara E, Rapezzi C, Sulafa AK, Sutera L,
Pizzuto C, Stollberger C, Sormani L, Finsterer J, Benatar A, Di Gesaro G,
Cascio C, Cangemi D, Cavusoglu Y, Baumhakel M, Drago F, Carerj S, Pipitone
S, Novo S. Ventricular tachycardia in non-compaction of left ventricle: is
this a frequent complication? Pacing Clin Electrophysiol. 2007; 30:544-6
6) Fazio G, Sutera L, Vernuccio F, Fazio M, Vernuccio D, Pizzuto C,
Di Gesaro G, Cascio C, Novo S Heart failure and cardiomyopathies: a case report G Ital Cardiol. 2007; 8:129-32
7) Jenni R, Wyss CA, Oechslin EN, Kaufmann PA Isolated ventricular noncompaction is associated with coronary
microcirculatory dysfunction. J Am Coll Cardiol. 2002; 39:450-4
8) Hamamichi Y, Ichida F, Hashimoto I, Uese KH, Miyawaki T, Tsukano
S, Ono Y, Echigo S, Kamiya T Isolated noncompaction of the ventricular myocardium: ultrafast computed
tomography and magnetic resonance imaging. Int J Cardiovasc Imaging. 2001;17:305-14
9) Sato Y, Matsumoto N, Matsuo S, Kunimasa T, Yoda S, Tani S,
Kasamaki Y, Kunimoto S, Saito S. Myocardial perfusion abnormality and necrosis in a patient with isolated
noncompaction of the ventricular myocardium: Evaluation by myocardial
perfusion SPECT and magnetic resonance imaging. Int J Cardiol. 2007; [Epub ahead of print]
10) Jassal DS, Nomura CH, Neilan TG, Holmvang G, Fatima U, Januzzi J,
Brady TJ, Cury RC. Delayed enhancement cardiac MR imaging in noncompaction of left
ventricular myocardium. J Cardiovasc Magn Reson. 2006;8:489-91
11) Korcyk D, Edwards CC, Armstrong G, Christiansen JP, Howitt L,
Sinclair T, Bargeois M, Hart H, Patel H, Scott T Contrast-enhanced cardiac
magnetic resonance in a patient with familial isolated ventricular non-
compaction. J Cardiovasc Magn Reson. 2004;6:569-76
12) Soler R, Rodríguez E, Monserrat L, Alvarez N MRI of subendocardial perfusion deficits in isolated left ventricular
noncompaction. J Comput Assist Tomogr. 2002; 26:373-5
A recent study in Heart by Edwards and colleagues found an
interesting association between rheumatoid factor (RF) and ischaemic heart
disease [1]. We examined independently the related issue of the role of
systemic inflammation in relation to clinical outcome in a forthcoming
study [2]. This subsequent study reports an association between systemic
inflammation, as measured by C-reactive protein (CRP...
A recent study in Heart by Edwards and colleagues found an
interesting association between rheumatoid factor (RF) and ischaemic heart
disease [1]. We examined independently the related issue of the role of
systemic inflammation in relation to clinical outcome in a forthcoming
study [2]. This subsequent study reports an association between systemic
inflammation, as measured by C-reactive protein (CRP), and all cause
mortality (n = 22,982). We also found a weak association with heart
disease but the study was, we believe, statistically underpowered to
properly evaluate this outcome. In light of the findings reported by
Edwards and colleagues, here we report supplementary data from a sub-group
of subjects from the CRP [2] study where data were available
characterising RF (n = 3,588). The objective of this report was to
characterise survival over a four year period from first CRP observation
in this sub-groups of subjects where RF data were also available.
Details of the data source and the general methods were published
elsewhere [2]. In brief, data were routine data from hospital, record-
linked sources in Cardiff and the Vale of Glamorgan. A Cox proportional
hazards model (CPHM) was developed using SPSS for Windows v14. We
evaluated a number of potential model covariates including age, sex, prior
disease (cancer, diabetes, vascular disease), general morbidity at
baseline (total days in hospital in year prior to first CRP observation),
and CRP itself. RF was measured in IU/ml and included in the model as a
continuous variable following logarithmic transformation.
The mean age of the 3,588 evaluable subjects was 62 years and 33%
were female. The CPHM of survival determined a strong association between
RF and survival (hazard ratio [HR] for log RF = 1.229; p = 0.008).
Furthermore, CRP (log transformed), was also included simultaneously in
this statistical model (HR = 1.495; p < 0.001) in preference to other
factors such as a history of diabetes and cancer. As expected, age and
being male also increased risk of death in the CPHM. The association
between RF and all cause mortality is illustrated in figure 1.
Data from this study supports findings from the study by Edwards and
colleagues, and shows that RF not only predicts the likelihood of
ischaemic heart disease but it also predicts the likelihood of all cause
mortality. Furthermore, data from this subgroup of subjects showed that
CRP and RF were independent risk factors for all cause mortality. Thus,
they are likely to represent distinct inflammatory processes that increase
the risk of adverse outcome.
Yours sincerely,
Craig J. Currie
Department of Medicine, School of Medicine, Cardiff University, Cardiff UK
currie@cardiff.ac.uk
Pete Conway
Health Economics, Wyeth Europa Limited, Maidenhead, UK
Chris D. Poole
360° Research Limited, Penarth, UK
Acknowledgement:
This study was funded by Wyeth Europa. PC is a full time employee of Wyeth
Europa.
Figure 1
Four-year risk of death as a function of increasing rheumatoid factor
following standardisation for age, sex and C-reactive protein level.
References
1. Edwards CJ, Syddall H, Goswami R, Goswami P, Dennison EM, Arden NK, Cooper C, on behalf of the Hertfordshire Cohort Study Group. The autoantibody rheumatoid factor may be an independent risk factor for ischaemic heart disease in men. Heart 2007;0:1–5. doi: 10.1136/hrt.2006.097816
2. Poole CD, Conway P, Currie CJ. An evaluation of the association between the first observation and the
longitudinal change in C-reactive protein, and all-cause mortality. Heart 2007 (under final review)
I read with interest, the recent original article by Nallamothu et al. The authors report higher 6-month mortality in both fibrinolysis and PPCI patients (p < 0.001 for both cohorts) with long treatment delays.
For patients who received fibrinolytic therapy, 6-month mortality increased by 0.30% per 10-min delay in door-to-needle time between 30 and 60 min compared with 0.18% per 10-min delay in doo...
I read with interest, the recent original article by Nallamothu et al. The authors report higher 6-month mortality in both fibrinolysis and PPCI patients (p < 0.001 for both cohorts) with long treatment delays.
For patients who received fibrinolytic therapy, 6-month mortality increased by 0.30% per 10-min delay in door-to-needle time between 30 and 60 min compared with 0.18% per 10-min delay in door-to-balloon time between 90 and 150 min for patients undergoing PPCI(1).Boersma E reported on behalf of the ‘The Primary Coronary Angioplasty vs. Thrombolysis Group’that PPCI was associated with significant 37% lower 30-day mortality relative to fibrinolysis[adjusted OR, 0.63; 95% CI (0.42-0.84)], regardless of treatment delay(2).These data convey two important messages.
1. Reiteriates a familiar adage ‘Time is myocardium’ in patients presenting with ST segment Elevation Myocardial Infarction (3).
2. In case of time delay, PPCI yields favorable outcome results than fibrinolysis.
No doubt the preferred treatment of choice for STEMI in the 21st century is PPCI provided when it is delivered rapidly, in high volume centres and by experienced teams(4).However at present the feasibility of ‘PPCI-for-
all’ is constrained by logical, economic and organizational constraints.
Unfortunately in the real world experience time delay is unavoidable due to multiple reasons.STEMI patients are very high risk patients and every effort should be made to deliver the best possible care quickly and effectively in order to minimize the long term morbidity and to reduce
short and long term mortality. A coordinated regional emergency response model as shown by Gross B et al may be the way forward (5).
References
1.Nallamothu B, Fox KA, Kennelly BM,et al. Relationship of treatment delays and mortality in patients undergoing fibrinolysis and primary percutaneous coronary intervention. The Global Registry of Acute Coronary Events. Heart 2007; 0: hrt.2006.112847v1
2.Boersma E. The Primary Coronary Angioplasty vs.Thrombolysis Group. Does time matter? .A pooled analysis of randomized clinical trials comparing primary percutaneous coronary intervention and in-hospital fibrinolysis in acute myocardial infarction patients. Eur Heart J. 2006 Apr;27(7):761-3.
3.Gibson CM. Time is myocardium and time is outcomes. Circulation. 2001 Nov 27;104(22):2632-4.
4.Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction:a quantitative review of 23 randomised trials. Lancet. 2003 Jan 4;361(9351):13-20.
5.Gross BW, Dauterman KW, Moran MG, et al. An approach to shorten time to infarct artery patency in patients with ST-segment elevation myocardial infarction. Am J Cardiol. 2007 May 15;99(10):1360-3. Epub 2007 Apr.
We read with interest the study by Hughes et al (1) that for the first time showed a reduction of Gb3 content in endomyocardial biopsy tissue of patients with Fabry cardiomyopathy after six months agalsidase alfa treatment.
However, it should be point out that this study doesn’t demonstrate the efficacy of enzyme replacement therapy in clearing the Gb3 deposits from the cardiomyocytes, that i...
We read with interest the study by Hughes et al (1) that for the first time showed a reduction of Gb3 content in endomyocardial biopsy tissue of patients with Fabry cardiomyopathy after six months agalsidase alfa treatment.
However, it should be point out that this study doesn’t demonstrate the efficacy of enzyme replacement therapy in clearing the Gb3 deposits from the cardiomyocytes, that is a focal issue in the treatment of Fabry disease cardiomyopathy. In fact, it has been recently shown in an experimental model of Fabry disease that after intravenous injection of agalsidase alfa the enzyme is detectable in myocardial capillaries but not in cardiomyocytes (2). In this setting the reduction in Gb3 content in the heart could be interpreted as the result of clearance from other cell types, particularly endothelial cells. In addition blood contamination could be the source of Gb3 changes, since the plasma Gb3 levels decreased of 45% after treatment (1).
In this context, the reduction in myocardial mass could be related to a progression of the disease with increased fibrosis and reduction in myocardial thickness.
Probably, an immunohistochemical demonstration in endomyocardial biopsy tissue of Gb3 cellular distribution and changes after six months of treatment could have been useful in a better understanding of the study results and it’s desirable in future follow-up studies.
References
1. Hughes DA, Elliott PM, Shah J, Zuckerman J, Coughlan G, Brookes J, Mehta AB. Effects of enzyme replacement therapy on the cardiomyopathy of Anderson-Fabry disease: a randomized, double-blind, placebo-controlled clinical trial of agalsidase-alfa. Heart 2007 May 4; [Epub ahead of print].
2. Murray GJ, Anver MR, Kennedy MA, Quirk JM, Schiffmann R. Cellular and tissue distribution of intravenously administered agalsidase alfa. Mol Genet Metab. 2007;90:307-12.
Dear Editor,
I read with great interest the study by Little et al. (1) investigating the effect of acute blood pressure change on hemodynamic parameters of aortic stenosis (AS). Their implication that "differences in haemodynamics should be considered as a potential explanation for a change in AS severity independent of disease progression" should be stressed not only in clinical practice, but as well in prospect...
Dear Editor,
Breidthardt et al. (1) found that acute decompensated heart failure (HF) patients presenting to their Emergency Department with prolonged QRS interval (>=120 ms) showed higher long-term mortality. This is a pathophysiologically plausible finding: after initially representing a marker of diseased myocardium, prolonged QRS may itself subsequently contribute to disease progression. (2) Nevertheless,...
Dear Editor,
Lin et al. report an observational study in 52 patients investigating whether upgrading an ICD, implanted predominantly for secondary prevention to CRT-D, can reduce arrhythmias.[1] They failed to detect an effect of CRT on arrhythmias during a mean follow up of 14 months. The CARE-HF extension study suggested that reduction in sudden death with CRT might be a late phenomenon occurring only after one...
Dear Editor,
Dr. Wahl and colleagues studied the short and long- term safety and efficacy of percutaneous closure of patent foramen ovale (PFO) for prevention of paradoxical embolization using fluoroscopic guidance only (1). While we command their technical skills, we disagree that using fluoroscopy only is the safest and most efficient approach to percutaneous PFO closure. The authors correctly note that to dat...
Antibiotic Prophylaxis to Prevent Infective Endocarditis should be given to Patients with Valvular or Structural Heart Disease Prior to Dental Treatment: Results of a National Survey Amongst UK Cardiologists and Cardiac Surgeons
Dear Editor,
Recently published guidelines suggesting that antibiotic prophylaxis (ABP) should not be given prior to dental treatment to patients with valvular or structural h...
Dear Editor,
O'Flaherty and colleagues (1) have identified a worrying change in the hitherto improving CHD mortality data in England and Wales that has occurred despite record spending on coronary revascularisation. They correctly propose that the health intervention measures, as recommended by Wanless (2) and supported by the National Heart Forum (3) and NICE (4), should be urgently implemented in an attempt to p...
Dear Editor,
McMahon et al reported in a recent article a reduction of TD velocities in children with noncompaction of the left ventricle, compared with normal controls. The authors concluded their work saying that the reduction of lateral mitral Ea velocity helps to predict children with LVNC who are at risk of adverse clinical outcomes including death and need for cardiac transplantation. In a precedent report...
Dear Editor,
A recent study in Heart by Edwards and colleagues found an interesting association between rheumatoid factor (RF) and ischaemic heart disease [1]. We examined independently the related issue of the role of systemic inflammation in relation to clinical outcome in a forthcoming study [2]. This subsequent study reports an association between systemic inflammation, as measured by C-reactive protein (CRP...
Dear Editor,
I read with interest, the recent original article by Nallamothu et al. The authors report higher 6-month mortality in both fibrinolysis and PPCI patients (p < 0.001 for both cohorts) with long treatment delays. For patients who received fibrinolytic therapy, 6-month mortality increased by 0.30% per 10-min delay in door-to-needle time between 30 and 60 min compared with 0.18% per 10-min delay in doo...
Dear Editor,
We read with interest the study by Hughes et al (1) that for the first time showed a reduction of Gb3 content in endomyocardial biopsy tissue of patients with Fabry cardiomyopathy after six months agalsidase alfa treatment.
However, it should be point out that this study doesn’t demonstrate the efficacy of enzyme replacement therapy in clearing the Gb3 deposits from the cardiomyocytes, that i...
Pages