The corollary to the association of incident heart failure and an
increase in serum gamma glutamyl transferase(GGT)(1) is that fluctuations
in the severity of heart failure might, also, have the potential to
trigger fluctuations in blood levels of this parameter. Fluctuations in
serum GGT levels(including restoration to the normal range) also occur
during the course of the natural history of choledocholithiasis(CDL), eve...
The corollary to the association of incident heart failure and an
increase in serum gamma glutamyl transferase(GGT)(1) is that fluctuations
in the severity of heart failure might, also, have the potential to
trigger fluctuations in blood levels of this parameter. Fluctuations in
serum GGT levels(including restoration to the normal range) also occur
during the course of the natural history of choledocholithiasis(CDL), even
when calculi are still retained within the common bile duct(CBD)(2). The
latter phenomenon is a confounding factor for identification of CDL when
the latter co-exists with congestive heart failure(CHF), as might well be
the case in patients of mean age 56.5 years(3).In the latter study 6.8% of
73,064 patients with a discharge diagnosis of uncomplicated CDL were also
documented as having coexisting CHF(3). In the same study there were 15,
121 patients in whom CDL had been complicated by the development of
cholangitis. Coexisting CHF was documented in 12.5% of those 15,121
patients with complicated CDL(cCDL). Acute pancreatitis was documented in
the other 38,953 patients with cCDL. Congestive heart failure coexisted
with cCDL in 6.8% of patients in the latter subgroup. The transition from
uncomplicated CDL to cCDL is one which ocurs at the rate of 0.8% per
year(3), clearly signifying that CDL is a "ticking time bomb" which, in
CHF patients, mandates a heightened index of suspicion, not only for
coexisting CDL,but also for cCDL. Given the fact that coexisting CHF was
more prevalent in choangitis patients than in patients with acute
pancreatitis(12.5% vs 6.8%) it may well be that even more vigilance is
required for stigmata of cholangitis, such as increased levels of
inflammatory markers, and unexplained pyrexia, in CHF patients with raised
serum GGT than in counterparts with normal GGT. What also needs to be
recognised is that, even when GGT has reverted to the normal range, the
occasional patient with cholangitis may still have retained CBD
calculi(2).
References
(1)Wang Y., Tuomilehto J., Jousilahti P et al
Serum gamma-glutamyl transferase and the risk of heart failure in men and
women in Finland
Heart 2013;99:163-167
(2)Jolobe OMP
Limitations of gammaglutamyl transaminase as an indicator of biliary
obstruction(letter)
European Journal of Internal Medicine 2012;23:e75
(3) Kummerow KL., Shelton J., Phillips S et al
Predicting complicated choledocholithiasis
Journal of Surgical research 2012;177:70-74
To the Editor,
We read with interest the paper by Itagaki et al in Heart (1). The
authors investigate the impact of bilateral internal mammary artery (BIMA)
use in 1 526 360 isolated coronary artery bypass operations on inhospital
mortality and deep sternal wound infection (DSWI). While there is survival
benefit with BIMA, it was associated with higher incidence of DSWI but
only in patients with chronic complications of d...
To the Editor,
We read with interest the paper by Itagaki et al in Heart (1). The
authors investigate the impact of bilateral internal mammary artery (BIMA)
use in 1 526 360 isolated coronary artery bypass operations on inhospital
mortality and deep sternal wound infection (DSWI). While there is survival
benefit with BIMA, it was associated with higher incidence of DSWI but
only in patients with chronic complications of diabetes mellitus. This
finding correlates with those of the Arterial Revascularisation Trial
where half the patients requiring sternal reconstruction in the BIMA group
had diabetes (2). By harvesting the IMA in a skeletonised fashion (3) ,
longer conduits are obtained, the risks of kinking are reduced. Moreover,
a beneficial reduction in sternal wound infection has been observed with
this effect being more evident in diabetic patients undergoing BIMA
grafting (4). Furthermore, since diabetic patients present with coronary
artery disease earlier and have poorer outcomes with vein grafts or when
treated with percutaneous coronary interventions; pure IMA
revascularization offers the best prospective in terms of outcomes and can
be performed using BIMA (3).
Would the authors comment on the impact of harvesting technique, sternal
wound closure technique and perioperative blood sugar control on DSWI in
this huge series of patients?
References:
1. Itagaki S, Cavallaro P, Adams DH, Chikwe J. Bilateral internal mammary
artery grafts, mortality and morbidity: an analysis of 1 526 360 coronary
bypass operations. Heart (2013). doi:10.1136/heartjnl-2013-303672
2. Taggart DP, Altman DG, Gray AM, et al; ART Investigators. Randomized
trial to compare bilateral vs. single internal mammary coronary artery
bypass grafting: 1-year results of the Arterial Revascularisation Trial
(ART). Eur Heart J. 2010;31:2470-81.
3. Al-Attar N, Nataf P. Multiple extensive coronary artery stenting: does
it compromise future surgical revascularization? Curr Opin Cardiol.
2007;22:529-33.
4. Saso S, James D, Vecht JA, et al. Effect of skeletonization of the
internal thoracic artery for coronary revascularization on the incidence
of sternal wound infection. Ann Thorac Surg. 2010;89:661-70.
I read with interest the recent papers and editorial concerning
elevated levels of troponin in chronic obstructive pulmonary disease
(COPD) (references - 1: S?yseth V et al, Acute exacerbation of COPD is
associated with fourfold elevation of cardiac troponin T, Heart 2013;99:2
122-126; 2: Stone IS et al, Raised troponin in COPD: clinical
implications and possible mechanisms, Heart doi:10.1136/heartjnl-2012-
302969; and...
I read with interest the recent papers and editorial concerning
elevated levels of troponin in chronic obstructive pulmonary disease
(COPD) (references - 1: S?yseth V et al, Acute exacerbation of COPD is
associated with fourfold elevation of cardiac troponin T, Heart 2013;99:2
122-126; 2: Stone IS et al, Raised troponin in COPD: clinical
implications and possible mechanisms, Heart doi:10.1136/heartjnl-2012-
302969; and 3: Neukamm AMC et al, High-sensitivity cardiac troponin T
levels are increased in stable COPD, Heart heartjnl-2012-303429Published
Online First: 12 January 2013 doi:10.1136/heartjnl-2012-303429). The
authors proffered a variety of possible mechanisms which could account at
least in part for the troponin rises detected in instances of both acute
exacerbation of COPD and stable COPD, but appear to have overlooked the
possibility of right ventricular myocardial necrosis and inflammation
thought secondary to increased right ventricular stretch and strain - as
described by myself and co-workers in a previous article (4: Orde MM et
al, Myocardial pathology in pulmonary thromboembolism, Heart 2011;97:1695-
1699). As alluded to in that paper, we are also aware of instances in
which similar right ventricular myocardial necroinflammatory changes were
identified in the absence of pulmonary thromboembolism (PTE), but in which
there were other potential causes of increased right ventricular strain.
COPD in both stable and acute guises would of course have such potential,
by way of hypoxic pulmonary vasoconstriction and increased right
ventricular afterload. Indeed, perhaps rather fortuitously, routine
autopsy histology undertaken by myself only today - on a case with
clinically significant COPD and marked pathological changes of chronic
bronchitis and emphysema but only mild coronary artery disease -
demonstrated quite florid changes identical with those previously
described by us in instances of PTE. This proposed hypothesis explaining
the elevated levels of cardiac biomarkers detected in COPD sufferers seems
entirely plausible, and there is a sound evidence base to suggest that
this mechanism is indeed operative in such instances.
To the Editor, we read with interest Ball et al's article exploring
the prevalence of mild cognitive impairment (MCI) in patients with chronic
atrial fibrillation (AF)[1]. This study suggests that MCI is highly
prevalent (50 to 65%), among older, hospitalized patients with AF. This is
valuable research, highlighting the much-overlooked association between
cognitive impairment (CI) and AF. We feel however, that the prevalen...
To the Editor, we read with interest Ball et al's article exploring
the prevalence of mild cognitive impairment (MCI) in patients with chronic
atrial fibrillation (AF)[1]. This study suggests that MCI is highly
prevalent (50 to 65%), among older, hospitalized patients with AF. This is
valuable research, highlighting the much-overlooked association between
cognitive impairment (CI) and AF. We feel however, that the prevalence
rates reported may over-state the true prevalence of MCI in older adults
with AF. In this case, MCI was classified using a cut-off score of less
than 26 (or 24) on the Montreal Cognitive Assessment (MoCA), in patients
deemed not to have dementia following routine evaluation by hospital
clinical teams. While the authors of the article acknowledge that the MoCA
is a screening test and that further assessment is required to determine a
diagnosis of MCI, using the MoCA as a single cognitive screen presents
other challenges that need to be addressed.
Firstly, our experience of using the MoCA to identify CI in a memory
clinic setting is that it over-estimates CI in older adults with less time
in formal education, irrespective of their subtype of CI. Among a sample
of patients with memory loss attending our clinic, 50%(30/60) with normal
cognition screened positive on the MoCA compared to 13% using a new rapid
screen for MCI, the Quick MCI screen (Qmci)[2] and only 3% on the Mini-
Mental. Adjusting for age and education, the MoCA misclassified
38.5%(10/26) of those <75 with >12 years education. An acute
hospital admission, given the increased likelihood of delirium, is likely
to exaggerate this misclassification.
Secondly, the diagnosis of MCI itself is under scrutiny given the lack of
consensus in developing cut-offs for its defining characteristic, namely
the presence of CI without social and functional impairment. Presenting
functional data, rather than stating that subjects were living
independently, would provide context for the MoCA scores. Furthermore, the
diagnostic criteria for MCI related to cerebrovascular disease are even
less clearly defined[3], than MCI relating to Alzheimer's dementia. The
MoCA has particularly poor specificity in these circumstances, resulting
in high false positive rates, which improve after application of age and
education adjusted cut-offs[4]. Presenting the prevalence of CI, both MCI
and dementia, among similar age and education-matched hospital patients is
necessary to give additional context to these results. Defining MCI as a
score below a threshold on the MoCA in non-demented persons misses the
complexity and can over-estimate the condition. We agree with the authors
that cognitive screening is important in persons with AF but reiterate
that caution is needed in diagnosing vascular MCI in this fashion.
References
1. Ball J, Carrington M J, Stewart S, on behalf of the SAFETY
investigators. Mild cognitive impairment in high-risk patients with
chronic atrial fibrillation: a forgotten component of clinical management?
Heart doi:10.1136/heartjnl-2012-303182
2. O'Caoimh R, Gao Y, McGlade C, Healy L, Gallagher P, Timmons S,
Molloy DW.
Comparison of the quick mild cognitive impairment (Qmci) screen and the
SMMSE in screening for mild cognitive impairment. Age Ageing. 2012
Sep;41(5):624-9.
3. Gorelick PB, Scuteri A, Black SE et al. Vascular contributions to
cognitive impairment and dementia: a statement for healthcare
professionals from the american heart association/american stroke
association. Stroke. 2011 Sep;42(9):2672-713
4. Godefroy O, Fickl A, Roussel M et al. Is the Montreal Cognitive
Assessment Superior to the Mini-Mental State Examination to Detect
Poststroke Cognitive Impairment? A Study With Neuropsychological
Evaluation. Stroke. 2011;42:1712-1716.
We read with interest the recent multicentre UK study by Sandercock
and colleagues1 quantifying prescribed exercise volume and changes in
cardiorespiratory fitness (CRF) involving 950 patients across four UK
outpatient cardiac rehabilitation (CR) centres routinely performing CRF
testing pre- and post-CR and with clinical practice consistent with
professional body guidelines. The authors characterise low volume exercise...
We read with interest the recent multicentre UK study by Sandercock
and colleagues1 quantifying prescribed exercise volume and changes in
cardiorespiratory fitness (CRF) involving 950 patients across four UK
outpatient cardiac rehabilitation (CR) centres routinely performing CRF
testing pre- and post-CR and with clinical practice consistent with
professional body guidelines. The authors characterise low volume exercise
training programmes across the four rehabilitation centres - with patients
receiving a modal value of 8 exercise sessions (range 6-16). This appears
in stark contrast to the international studies outlined in the author's
earlier systematic review and evidence-based guidelines2.
Although CRF improvements varied by rehabilitation centre and testing
protocol (treadmill test protocol was a significant source of the between-
trial heterogeneity), the overall improvement in CRF (0.52 METS) was only
one third the mean estimate reported in their earlier meta-analysis (1.55
METs)2. The authors indicated that if representative of UK services, these
low training volumes and small increases in CRF may partially explain the
reported inefficacy of UK CR to reduce patient mortality and morbidity, as
outlined by the RAMIT group3.
We agree with the assertion that lower exercise training volumes may
be partly responsible for the lower than expected CRF values reported in
the UK centres evaluated. Indeed, the CRF improvements within UK centres
reported by Sandercock and colleagues1 are not consistent with data
observed in our community-based CR investigations (Heartwatch, Leeds
Leisure Services) using submaximal (85% age-predicted maximum heart rate)
exercise testing protocols to evaluate short (3 month) and longer-term (15
month) community-based exercise training in a large, representative sample
of patients with cardiovascular disease. We hereby report unpublished
observations of 139 patients (79% males; mean age 62 (8) years); BMI 28
(4) kg*m-2; 62% on beta-blockers) who undertook 3 months of structured
exercise-based community CR (undertaking a minimum of 2 circuit training
sessions per week). Pre and post-CR exercise testing at the Heartwatch
Centre was conducted on a Marquette treadmill using a specifically
designed 2-minute stage incremental walking protocol4. The oxygen
consumption at stages 5 and 6 (10 to 12 minutes duration) of the protocol
was an estimated 25 to 29 ml?kg-1?min-1. Patients were encouraged to
exercise up to 85% of age-predicted maximum heart rate (220?age) or a
"very hard" rating of perceived exertion (RPE 17) using the Borg scale.
Following 3 months exercise training, surrogate CRF variables including
exercise duration (10.1 ? 2.5 min v 11.5 ? 2.7 min; P=0.0001)
significantly improved. These improvements in submaximal CRF are
consistent with our earlier reported observations5 among 154 non-diabetic
CVD patients (89% male; aged 60 ?9 years; body mass index [BMI], 27?4 kg?m
-2) who completed a further 12 months of exercise training. Self-reported
exercise training compliance rates at 15 months, reported on clinical
reassessment was 2.9 ?0.9 sessions per week. Exercise test results showed
that submaximal treadmill duration increased from 10.1 to 12.2 minutes.
These short and longer term improvements in CRF to graded walking
represented an additional 2-minute stage of the incremental walking
protocol4, corresponding to a 1.0 MET improvement in CRF.
We also feel that the methods used to estimate exercise training
volumes and the impact this may have on exercise prescription may also be
contributory factors in many UK-based CR programmes. The prescription of
an appropriate exercise dose should be predicated on a clear appreciation
of patient requirements and their physical characteristics including the
degree of cardiac dysfunction and level of skeletal muscle wastage.
Exercise intensity thresholds should be high enough to be effective but
should be titrated within appropriate safety margins. Therefore, CRF
should be assessed as accurately possible in cardiac populations. In the
UK, there has arguably been a historical over-reliance on exercise
prescription derived from indirect, submaximal assessments of exercise
capacity, such as the incremental shuttle walk test (ISWT) and/or 6-minute
walk tests (6-MWT) in patients undertaking CR. This observation was
clearly evident in the recent publication by Dr Sandercock and colleagues1
who reported the use of these assessment modalities in four audited
centres (treadmill and cycle ergometry were also used in two centres).
Many UK centres will then use performance from submaximal tests to inform
exercise training prescription relying solely on using predicted heart
rate training zones and/or ratings of perceived exertion. Clearly,
submaximal exercise test protocols do not rigorously evaluate the
integrity of the cardiorespiratory system (a primary purpose of the
exercise test). Therefore, it is possible that patient effort may be more
variable in submaximal, self-paced tests such as the 6-MWT. Consequently,
the widespread practice of submaximal exercise testing in the UK may be
one of the reasons why CR programmes appear to be less effective.
In Europe and North America there is a much greater focus on "gold
standard" techniques, including maximal exercise testing with metabolic
gas exchange (cardiopulmonary exercise testing) which provide the
preferred method for assessing CRF and prescribing exercise training in
CR. Exercise prescription may be fine-tuned on the ventilatory anaerobic
threshold or respiratory compensation point. There is overwhelming
evidence indicating the superior prognostic value of ventilatory markers
including peak oxygen uptake, VE/VCO2 slope, and exertional oscillatory
ventilation, amongst others, especially in lower functional capacity
groups such as chronic heart failure6. Ventilatory markers are rarely
assessed and are seldom considered during exercise prescription in the
majority of CR programmes in the UK.
Under certain circumstances, there may be a requirement to assess
individual responses to exercise with submaximal testing protocols. For
example, if the assessment of exercise capacity is undertaken outside a
hospital setting (sporting or community centre); if a medical doctor is
not available to supervise the maximal test; or when a large number of
patients require assessment over a short time frame. If maximal exercise
testing is to become more pervasive in the UK there will be a requirement
for an initial capital outlay on equipment (though existing testing
systems may be under-utilised in many Trusts around the country), and
there will be a need for specialist staff training and on-going consumable
costs. However, we should not lose perspective over the major objectives
of CR, the Cinderella of cardiology services, and bear in mind the
apparent under-prescription of exercise that seems to be common practice
in UK centres. UK-based CR should not be run on a shoe-string budget. It
has been long-established that increasing CRF reduces mortality and
morbidity in secondary prevention settings7. There is a pressing need to
adopt a more evidence-based approach to exercise prescription in patients
undertaking CR in the UK.
Dr Lee Ingle & Professor Sean Carroll
Department of Sport, Health & Exercise Science
University of Hull
Kingston-upon-Hull HU6 7RX
United Kingdom
References:
1. Sandercock GR, Cardoso F, Almodhy M, Pepera G. Cardiorespiratory
fitness changes in patients receiving comprehensive outpatient cardiac
rehabilitation in the UK: a multicentre study. Heart. 2012 Nov 24. [Epub
ahead of print].
2. Sandercock G, Hurtado V, Cardoso F. Changes in cardiorespiratory
fitness in cardiac rehabilitation patients: A meta-analysis. Int J
Cardiol. 2011; [Epub ahead of print].
3. West RR, Jones DA, Henderson AH. Rehabilitation after myocardial
infarction trial (RAMIT): multi-centre randomised controlled trial of
comprehensive cardiac rehabilitation in patients following acute
myocardial infarction. Heart 2012; 98(8):637-44.
4. Lehmann G, Schmid S, Ammer R, Sch?mig A, Alt E. Evaluation of a
new treadmill exercise protocol. Chest1997;112(1):98-106.
5. Carroll S, Tsakirides C, Hobkirk J, Moxon JW, Moxon JW, Dudfield
M, Ingle L. Differential improvements in lipid profiles and Framingham
recurrent risk score in patients with and without diabetes mellitus
undergoing long-term cardiac rehabilitation. Arch Phys Med Rehabil
2011;92(9):1382-7.
6. Arena R, Myers J, Williams MA, et al. Assessment of functional
capacity in clinical and research settings: A scientific statement from
the American Heart Association Committee on Exercise, Rehabilitation, and
Prevention of the Council on Clinical Cardiology and the Council on
Cardiovascular Nursing Circulation. 2007;116: 329-343.
7. Vanhees L, Fagard R, Thijs L, Amery A. Prognostic value of
training-induced change in peak exercise capacity in patients with
myocardial infarcts and patients with coronary bypass surgery. Am J
Cardiol 1995; 15; 76(14):1014-9.
To the Editor, we read with interest Ball et al's article exploring
the prevalence of mild cognitive impairment (MCI) in patients with chronic
atrial fibrillation (AF)[1]. This study suggests that MCI is highly
prevalent (50 to 65%), among older, hospitalized patients with AF. This is
valuable research, highlighting the much-overlooked association between
cognitive impairment (CI) and AF. We feel however, that the prevalen...
To the Editor, we read with interest Ball et al's article exploring
the prevalence of mild cognitive impairment (MCI) in patients with chronic
atrial fibrillation (AF)[1]. This study suggests that MCI is highly
prevalent (50 to 65%), among older, hospitalized patients with AF. This is
valuable research, highlighting the much-overlooked association between
cognitive impairment (CI) and AF. We feel however, that the prevalence
rates reported may over-state the true prevalence of MCI in older adults
with AF. In this case, MCI was classified using a cut-off score of less
than 26 (or 24) on the Montreal Cognitive Assessment (MoCA), in patients
deemed not to have dementia following routine evaluation by hospital
clinical teams. While the authors of the article acknowledge that the MoCA
is a screening test and that further assessment is required to determine a
diagnosis of MCI, using the MoCA as a single cognitive screen presents
other challenges that need to be addressed.
Firstly, our experience of using the MoCA to identify CI in a memory
clinic setting is that it over-estimates CI in older adults with less time
in formal education, irrespective of their subtype of CI. Among a sample
of patients with memory loss attending our clinic, 50%(30/60) with normal
cognition screened positive on the MoCA compared to 13% using a new rapid
screen for MCI, the Quick MCI screen (Qmci)[2] and only 3% on the Mini-
Mental. Adjusting for age and education, the MoCA misclassified
38.5%(10/26) of those <75 with >12 years education. An acute
hospital admission, given the increased likelihood of delirium, is likely
to exaggerate this misclassification.
Secondly, the diagnosis of MCI itself is under scrutiny given the lack of
consensus in developing cut-offs for its defining characteristic, namely
the presence of CI without social and functional impairment. Presenting
functional data, rather than stating that subjects were living
independently, would provide context for the MoCA scores. Furthermore, the
diagnostic criteria for MCI related to cerebrovascular disease are even
less clearly defined[3], than MCI relating to Alzheimer's dementia. The
MoCA has particularly poor specificity in these circumstances, resulting
in high false positive rates, which improve after application of age and
education adjusted cut-offs[4]. Presenting the prevalence of CI, both MCI
and dementia, among similar age and education-matched hospital patients is
necessary to give additional context to these results. Defining MCI as a
score below a threshold on the MoCA in non-demented persons misses the
complexity and can over-estimate the condition. We agree with the authors
that cognitive screening is important in persons with AF but reiterate
that caution is needed in diagnosing vascular MCI in this fashion.
Rahman et al report on the utility of FDG/CT imaging in a case of large vessel arteritis, presenting as a P.U.O in a patient with severe aortic regurgitation and a dilated left ventricle.
It would be of interest to know what the
mechanism of the Aortic valve incompetence was? Was there any congenital valvular abnormality or evidence of aortic annular dilatation? And if so was this related to the arteritis?
Finally the authors d...
Rahman et al report on the utility of FDG/CT imaging in a case of large vessel arteritis, presenting as a P.U.O in a patient with severe aortic regurgitation and a dilated left ventricle.
It would be of interest to know what the
mechanism of the Aortic valve incompetence was? Was there any congenital valvular abnormality or evidence of aortic annular dilatation? And if so was this related to the arteritis?
Finally the authors do not comment on the subsequent natural history of the aortic regurgitation and left Ventricular geometry (if any) following management with steroids?
Dear Editors:
We are writing in regards to the paper entitled " Increased left
ventricular trabeculation in highly trained athletes: do we need more
stringent criteria for the diagnosis of left ventricular non-compaction in
athletes?" that is published in the February 2012 issue of Heart. We would
like to congratulate the authors for a very interesting and quite unique
study that has revealed a controversial question of no...
Dear Editors:
We are writing in regards to the paper entitled " Increased left
ventricular trabeculation in highly trained athletes: do we need more
stringent criteria for the diagnosis of left ventricular non-compaction in
athletes?" that is published in the February 2012 issue of Heart. We would
like to congratulate the authors for a very interesting and quite unique
study that has revealed a controversial question of non compacted
myocardium in sport cardiology and added more insight into the diagnostics
of this pathology. Gati et al. demonstrated that athletes displayed a
higher prevalence of increased LV trabeculation compared with controls;
however only a small proportion of athletes (0.9%) revealed reduced
systolic function and marked repolarisation changes in association with
echocardiographic criteria for LVNC raising the possibility of an
underlying cardiomyopathy, but without adverse events in follow-up
period.[1] However, ethnicity plays an important role, since left
ventricular (LV) trabeculation may be more pronounced in ethnic African
than in Caucasian (European) athletes, leading to possible incorrect
diagnosis of left ventricular non-compaction cardiomyopathy (LVNC). [1, 2]
Although isolated noncompaction of the ventricular myocardium was first
reported two decades ago, this congenital malformation may be often
overlooked, delayed, or misinterpreted in general population as
hypertrophic cardiomyopathy, endocardial fibroelastosis, dilative
cardiomyopathy, restrictive cardiomyopathy, apical thrombosis, or
endomyocardial fibrosis. In most of patients noncompacted ventricular
myocardium involves only the left ventricle and in a smaller proportion
both ventricles are involved. [3,4] Echocardiogram is the diagnostic
procedure of choice and diagnosis is based on established criteria by
Jenni et al, [4] additional diagnostic tools in suspected patients are
still necessary: contrast echocardiography and cine-magnetic resonance
imaging, showing a double-layered appearance on four-chamber view in short
-axis plane and marked trabeculations as well as intratrabecular recesses
in one or more ventricular segments. [5] Clinical presentation and
prognosis can vary from mild to severe heart failure, occurrence of
ventricular tachycardia, cardioembolic events, syncopa and even sudden
cardiac death. [3,4]
The main problem in evaluation of patients with noncompacted
cardiomyopathy is a risk stratification and prevention of adverse clinical
outcomes including sudden cardiac death, due to ventricular tachycardia
and the need for implantable cardioverter defibrillator. Thus this
problem is more complex in athletes. Since left ventricular diastolic
function in LVNC was assessed just in a few echocardiographic studies,
we suggest evaluation of diastolic function by tissue Doppler imaging in
these situations since athletes have "super normal" diastolic function.
[3,6] New studies indicated that the tissue Doppler evaluation of the
mitral annulus could help in risk stratification of patients with poor
prognosis and left ventricular systolic function deterioration, but the
similar investigations of athletes with LVNC still missing. [6]
We suggest that cardiologists and echosonographers should be very careful
in early diagnosis of noncompaction in athletes, especially in cases of
positive family history for cardiomyopathies and ventricular artrhythmias.
Best regards,
Marija Zdravkovic, MD, PhD, Assistant Proffesor, University Hospital
Medical Center Bezanijska kosa, Faculty of Medicine, University of
Belgrade,Belgrade, Serbia
Mirjana Krotin, MD, PhD, Full Proffesor, University Hospital Medical
Center Bezanijska kosa, Faculty of Medicine, University of Belgrade,
Belgrade, Serbia
Goran Koracevic, MD, PhD, Proffesor, Clinic for Cardiology, Faculty of
Medicine, University of Nis, Nis, Serbia
Sergej Prijic, MD, BSc, Institute for Mother and Child, Belgrade, Serbia
Dragan Lovic, MD, BSc, Serbian Society for Hypertension, Nis, Serbia
Olivera Markovic, MD, PhD, Assistant Proffesor, University Hospital
Medical Center Bezanijska kosa, Faculty of Medicine, University of
Belgrade, Belgrade, Serbia
Branka Filipovic, MD, PhD, Assistant Proffesor, University Hospital
Medical Center Bezanijska kosa, Faculty of Medicine, University of
Belgrade, Belgrade, Serbia
References:
1.Gati S, et al. Increased left ventricular trabeculation in highly
trained athletes: do we need more stringent criteria for the diagnosis of
left ventricular non-compaction in athletes? Heart. 2013 Feb 7.
2.Luijkx T, et al. Ethnic differences in ventricular hypertrabeculation
on cardiac MRI in elite football players. Neth Heart J. 2012 ;20(10): 389-
95.
3. Espinola-Zavaleta N, et al. Non-compacted cardiomyopathy: clinical-
echocardiographic study. Cardiovasc Ultrasound 2006; 4: 35.
4. Jenni R, et al. Echocardiographic and pathoanatomical characteristics
of isolated left ventricular non-compaction: a step towards classification
as a distinct cardiomyopathy. Heart 2001; 86: 666-71.
5.Yousef ZR, et al. Left ventricular non-compaction: clinical features
and cardiovascular magnetic resonance imaging.BMC Cardiovasc Disord. 2009
;9:37.
6. Fazio G, et al. Left ventricular non-compaction cardiomyopathy in
children: is segmental fibrosis the cause of tissue Doppler alterations
and of EF reduction? Int J Cardiol 2009; 132: 278-80.
Sovari and Dudley write in their editorial [1] that "Despite ... a
central role for ROS [reactive oxygen species] in many cardiovascular
disorders including AF, clinical trials have not shown an impressive
result with using general ROS scavengers [2]." In their editorial
focused
on AF [1], this statement is misleading in two ways.
First, at least four studies have reported that vitamin C decreas...
Sovari and Dudley write in their editorial [1] that "Despite ... a
central role for ROS [reactive oxygen species] in many cardiovascular
disorders including AF, clinical trials have not shown an impressive
result with using general ROS scavengers [2]." In their editorial
focused
on AF [1], this statement is misleading in two ways.
First, at least four studies have reported that vitamin C decreases the
incidence of AF [3-6], but all of them are ignored in the editorial and
the
sentence above. In a case control study, Carnes et al. [3] found that
16% (7/43) of vitamin C participants, but 35% (15/43) of control
participants had AF after CABG, which gives P = 0.027 (1-tail mid-P
values [7]). In an RCT, Korantzopoulos et al. [4] found that one week
after a successful cardioversion, AF recurred in 5% (1/22) of vitamin C
participants, but in 36% (8/22) of control participants, which gives P
= 0.0057. In an RCT, Eslami et al. [5] found that 4% (2/50) of vitamin
C
participants, but 26% (13/50) of control participants had AF after
CABG, which gives P = 0.0011. In an RCT, Papaoulidis et al. [6] found
that 45% (38/85) of vitamin C participants, but 61% (52/85) of control
participants had AF after CABG, which gives P = 0.017. The four
P(1-tail) values can be combined by using the Fisher's combined
probability test [8], which gives chi-square (8 df) = 39.3
corresponding to P = 0.000005 for the overall test on whether vitamin C
groups differ from control groups in these four studies. If the pooling
of P-values is restricted to the three RCTs, the chi-square (6 df) =
32.1 corresponding to P = 0.00002 so that the conclusions do not depend
on the case control study [3]. Thus, four studies, three of which are
RCTs, give very strong evidence that
vitamin C prevents AF after CABG or after a successful cardioversion,
yet - as noted above - all these studies are ignored in the editorial
discussing antioxidants and AF [1].
Second, Sovari and Dudley refer to the Sesso et al. trial [2] as an
evidence against antioxidants in treating or preventing AF although the
Sesso study
does not report any data about AF. Furthermore, given that there are
dozens of RCTs on antioxidants, picking a single study is misleading.
There were only 1661 deaths in the Sesso et al. study [2], whereas
there were 3571 deaths in the ATBC Study which examined the effects of
vitamin E supplementation [9]. Therefore, the ATBC Study has much
greater statistical power to examine possible variations in vitamin E
effect between
subgroups. In the ATBC Study, there was strong evidence that vitamin E
effect was heterogeneous: vitamin E decreased mortality by 41%
among older males who had dietary vitamin C intake over the median [9].
Among
2,284 ATBC Study participants with dietary vitamin C intakes above the
median who smoked less than a pack of cigarettes per day, the survival
curves of vitamin E and no-vitamin E participants diverged at 71 years
and vitamin E extended lifespan by 2 years at the upper limit of the
follow-up age span [10]. It is not clear whether this effect of vitamin
E is partly explained by an influence on AF incidence, or whether the
effect of vitamin E is fully independent of AF. In any case, these
findings refute Sovari and Dudley's argument that the large antioxidant
RCTs are unanimously negative.
References
1. Sovari AA, Dudley SC. Antioxidant therapy for atrial fibrillation:
lost in translation? Heart 2012;98:1615-6. http://dx.doi.org/10.1136/heartjnl-2012-302328
2. Sesso HD, et al. Vitamins E and C in the prevention of
cardiovascular disease in men: the Physicians' Health Study II
randomized controlled trial. JAMA 2008;300:2123-33.http://dx.doi.org/10.1001/jama.2008.600
3. Carnes CA, et al. Ascorbate attenuates atrial pacing-induced
peroxynitrite formation and electrical remodeling and decreases the
incidence of postoperative atrial fibrillation. Circ Res
2001;89:E32-8. http://circres.ahajournals.org/content/89/6/e32
4. Korantzopoulos P, et al. Oral vitamin C administration reduces early
recurrence rates after electrical cardioversion of persistent atrial
fibrillation and attenuates associated inflammation. Int J Cardiol
2005;102:321-6. http://www.ncbi.nlm.nih.gov/pubmed/15982504
5. Eslami M, et al. Oral ascorbic acid in combination with
beta-blockers is more effective than beta-blockers alone in the
prevention of atrial fibrillation after coronary artery bypass
grafting. Tex Heart Inst J 2007;34:268-74. http://www.ncbi.nlm.nih.gov/pubmed/17948074
6. Papoulidis P, et al. The role of ascorbic acid in the prevention of
atrial fibrillation after elective on-pump myocardial revascularization
surgery. Interact Cardiovasc Thorac Surg 2011;12:121-4. http://dx.doi.org/10.1510/icvts.2010.240473
7. Lydersen S, et al. Recommended tests for association in 2 x 2
tables. Stat Med 2009;28:1159-75. http://www.ncbi.nlm.nih.gov/pubmed/19170020
8. Fisher RA. A method for combining P-values (1925). http://en.wikipedia.org/wiki/Fisher's_method
9. Hemila H, Kaprio J. Modification of the effect of vitamin E
supplementation on the mortality of male smokers by age and dietary
vitamin C. Am J Epidemiol 2009;169:946-53. http://dx.doi.org/10.1093/aje/kwn413
10. Hemila H, Kaprio J. Vitamin E may affect the life expectancy of
men, depending on dietary vitamin C intake and smoking. Age Ageing
2011;40:215-20. http://dx.doi.org/10.1093/ageing/afq178
This is invaluable work in a very complex clinical situation. The
scenario of increasing shortness of breath and chest tightness is a common
occurance in people with chronic obstructive pulmonary disorder. This
usually leads to a clinical suspicion of a cardiac event and in quite a
few cases the tropnin levels are done and found to be high. The correct
interpretation in these cases is of paramount significance as manageme...
This is invaluable work in a very complex clinical situation. The
scenario of increasing shortness of breath and chest tightness is a common
occurance in people with chronic obstructive pulmonary disorder. This
usually leads to a clinical suspicion of a cardiac event and in quite a
few cases the tropnin levels are done and found to be high. The correct
interpretation in these cases is of paramount significance as management
can be quite challenging. Also a wrong presumption of acute coronary
syndrome will lead to unnecessary investigations. Furthermore management
options can be limited because of the respiratory condition. This study
highlights the importance of good clinical assessment in these cases
rather than using the troponin assay as a base for diagnosis.
The corollary to the association of incident heart failure and an increase in serum gamma glutamyl transferase(GGT)(1) is that fluctuations in the severity of heart failure might, also, have the potential to trigger fluctuations in blood levels of this parameter. Fluctuations in serum GGT levels(including restoration to the normal range) also occur during the course of the natural history of choledocholithiasis(CDL), eve...
To the Editor, We read with interest the paper by Itagaki et al in Heart (1). The authors investigate the impact of bilateral internal mammary artery (BIMA) use in 1 526 360 isolated coronary artery bypass operations on inhospital mortality and deep sternal wound infection (DSWI). While there is survival benefit with BIMA, it was associated with higher incidence of DSWI but only in patients with chronic complications of d...
I read with interest the recent papers and editorial concerning elevated levels of troponin in chronic obstructive pulmonary disease (COPD) (references - 1: S?yseth V et al, Acute exacerbation of COPD is associated with fourfold elevation of cardiac troponin T, Heart 2013;99:2 122-126; 2: Stone IS et al, Raised troponin in COPD: clinical implications and possible mechanisms, Heart doi:10.1136/heartjnl-2012- 302969; and...
To the Editor, we read with interest Ball et al's article exploring the prevalence of mild cognitive impairment (MCI) in patients with chronic atrial fibrillation (AF)[1]. This study suggests that MCI is highly prevalent (50 to 65%), among older, hospitalized patients with AF. This is valuable research, highlighting the much-overlooked association between cognitive impairment (CI) and AF. We feel however, that the prevalen...
We read with interest the recent multicentre UK study by Sandercock and colleagues1 quantifying prescribed exercise volume and changes in cardiorespiratory fitness (CRF) involving 950 patients across four UK outpatient cardiac rehabilitation (CR) centres routinely performing CRF testing pre- and post-CR and with clinical practice consistent with professional body guidelines. The authors characterise low volume exercise...
To the Editor, we read with interest Ball et al's article exploring the prevalence of mild cognitive impairment (MCI) in patients with chronic atrial fibrillation (AF)[1]. This study suggests that MCI is highly prevalent (50 to 65%), among older, hospitalized patients with AF. This is valuable research, highlighting the much-overlooked association between cognitive impairment (CI) and AF. We feel however, that the prevalen...
Dear Editors: We are writing in regards to the paper entitled " Increased left ventricular trabeculation in highly trained athletes: do we need more stringent criteria for the diagnosis of left ventricular non-compaction in athletes?" that is published in the February 2012 issue of Heart. We would like to congratulate the authors for a very interesting and quite unique study that has revealed a controversial question of no...
First, at least four studies have reported that vitamin C decreas...
This is invaluable work in a very complex clinical situation. The scenario of increasing shortness of breath and chest tightness is a common occurance in people with chronic obstructive pulmonary disorder. This usually leads to a clinical suspicion of a cardiac event and in quite a few cases the tropnin levels are done and found to be high. The correct interpretation in these cases is of paramount significance as manageme...
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