The excellent article by Oliver-Williams and co-authors (1) provides
strong evidence to link miscarriages, the most prevalent major
complication of pregnancy, the commonest situation in women's life, with
coronary heart disease (CHD), the leading cause of death in women.
The relationship between miscarriage and cardiovascular risk should
be attributed to certain risk factor...
The excellent article by Oliver-Williams and co-authors (1) provides
strong evidence to link miscarriages, the most prevalent major
complication of pregnancy, the commonest situation in women's life, with
coronary heart disease (CHD), the leading cause of death in women.
The relationship between miscarriage and cardiovascular risk should
be attributed to certain risk factors shared by the two multifactorial
disorders, thrombophilia holding a prominent position. Acquired
thrombophilia is adequately discussed in the article. Recent attention has
been focused on inherited thrombophilic factors that may predispose to
pregnancy complications, including pregnancy loss. The genetic
heterogeneity of several loci, including coagulation factors V (FVL-R506Q)
and II (FII-G20210A), strongly associated with venous and modestly with
arterial thrombosis (2), and platelet glycoproteins Ia (GpIa-C807T) and
IIIa (GpIIIa-PlA1/PlA2) which influence thrombosis exclusively in the
arterial side, have been studied in women with miscarriages (3).
Clinically significant relative risks are mainly related to the
accumulation of risk alleles acting synergistically (4). The postulated
pathogenetic mechanisms include abnormal placentation and reduced
perfusion of the intervillous space.
Albeit the majority of miscarriages are considered to be sporadic,
the important corollary of this study is that women with a history of even
one miscarriage are at 50% higher risk of CHD. The authors also report a
twofold risk for women with recurrent miscarriages, implying a "dose-
response relationship". However, some women may have experienced only one
fetal loss because they had only one pregnancy, but still have a higher
burden of risk factors, compared with those with recurrent miscarriages.
High-risk women would be expected to have an increased incidence of
miscarriages in younger age (age is an established risk factor for
miscarriage) or miscarry earlier in pregnancy (3) (the accumulation of
risk factors contributing to an acceleration of the biological processes
of the disorder). A potential explanation of the aforementioned finding
could be that every fetal loss per se increases cardiovascular risk,
potentially via endothelial stimulation or dysfunction, hence these women
should be considered for relevant evaluation (e.g. FDA approved
Lipoprotein-associated phospholipase A2 and/or flow mediated dilatation).
These results support respective screening in women with at least one
miscarriage to identify individual risk factors in order to provide
personalized treatment for successful completion of next pregnancy and
early prevention of future cardiovascular events
Nikolaos Vlachadis M.D.(1),
Vassileios Tsamadias B.Sc.(1),
Emmanouel Economou Ph.D.(2)
(1) Research Fellow
(2) Assistant Professor of Pharmacogenetics
Clinical Laboratory of Therapeutic Individualization,
Second Department of Obstetrics and Gynaecology,
National and kapodistrian University of Athens, Medical School, Aretaieio
Hospital,
76 Vasilissis Sofias Avenue, 115 28, Athens, Greece
References
1)Oliver-Williams CT, Heydon EE, Smith GC, Wood AM. Miscarriage and
future maternal cardiovascular disease: a systematic review and meta-
analysis. Heart. 2013 Mar 28. [Epub ahead of print] doi:10.1136/heartjnl-
2012-303237
2)de Moerloose P, Boehlen F. Inherited thrombophilia in arterial
disease: a selective review. Semin Hematol. 2007;44:106-113
3)Gerhardt A, Scharf RE, Mikat-Drozdzynski B, Kr?ssel JS, Bender HG,
Zotz RB. The polymorphism of platelet membrane integrin alpha2beta1
(alpha2807TT) is associated with premature onset of fetal loss. Thromb
Haemost. 2005;93:124-9.
4)Coulam CB, Jeyendran RS, Fishel LA, Roussev R. Multiple
thrombophilic gene mutations rather than specific gene mutations are risk
factors for recurrent miscarriage. Am J Reprod Immunol. 2006;55:360-368.
In their recently published elegant article (1), Padfield GJ et al
have reported potential cardiovascular effects of tumor necrosis
factor alpha (TNF-alpha) antagonism i...
In their recently published elegant article (1), Padfield GJ et al
have reported potential cardiovascular effects of tumor necrosis
factor alpha (TNF-alpha) antagonism in patients with non-ST elevation
acute myocardial infarction (NSTEMI). In this first in human study, the
authors have demonstrated that a single dose of etanercept (a TNF-
alpha antagonist) infusion might blunt systemic inflammatory response ,
but might appear to enhance platelet aggregation along with its
neutral effects on fibrinolytic and peripheral vasomotor functions in
these patients at 24 hr after infusion suggesting that TNF alpha
antagonism should not be regarded as a promising therapeutic strategy
in the setting of acute myocardial infarction (AMI) (1). We also agree
that currently, this strategy should be regarded with caution in the
setting of acute coronary syndromes (ACS) . However, based on the multi
-faceted nature of systemic inflammation and its detrimental effects,
modulation of cytokine response in conditions with heightened systemic
inflammation might be associated with favorable outcomes including
suppression of life-threatening arrhythmias,etc. particularly in the
setting of ACSs. Therefore; regarding the study by Padfield GJ et al (1),
it is still too early to conclude that TNF-alpha antagonism appears to
be totally useless in AMI patients solely based on its adverse
effects on platelet aggregation.
In the recent years, there has been growing interest towards the
potential link between systemic inflammation and arrhythmogenesis
particularly in the setting of atrial fibrillation (AF) (2). AMI, an
important trigger of inflammatory response, is regarded as an important
cause of acute arrhythmogenesis leading to significant morbidity and
mortality. Arrhythmias in the setting of AMI are generally attributable
to a variety of factors including ongoing ischemia (due to ischemia at
a distance or in infarct zone), congestive heart failure, peri-infarct
scar tissue, electrolyte imbalance, and sympathetic discharge, etc.
(3). Interestingly, it was previously suggested that enhanced
inflammatory response might potentially have a role in the genesis of
malign ventricular arrhythmias and sudden cardiac death during or after
an AMI (3,4). Consistent with this, a previous clinical study comprising
patients with ACSs suggested a potential link between TNF-alpha and
reduced hear t rate variability (HRV) (5), a well known index of
arrhythmogenesis and sudden cardiac death (SCD). Moreover, it was
previously suggested in a viewpoint article that TNF-alpha might be
regarded as a novel substrate of ischemic ventricular fibrillation
(VF), and inhibition of secretion and expression of TNF-alpha in the
ischemic myocardium might therefore serve as a therapeutic option for
ischemic VF (6). However, in conditions with modest inflammation
including ACSs, it seems plausible that TNF-alpha may not be regarded as
the sole actor, but may only serve as a contributor to other
arrhythmogenic substrates including peri-infarct scar tissue, ongoing
ischemia, electrolyte imbalance etc. possibly through reduction in
arrhythmia threshold in atrial and ventricular tissues. Mechanistically,
defective calcium handling and prolongation in action potential duration
(APD) were previously suggested as potential mechanisms regarding TNF-
alpha mediated arrhythmogenesis in myocardial tissue (6).
Therefore; based on current literature (2-6), it is of possibility
that TNF-antagonism during early AMI (when the inflammatory response is
the highest) may be considered as a promising approach for the
prevention of a variety of supraventricular and ventricular arrhythmias
in the hospital setting , and hence might potentially improve in-
hospital prognosis and reduce the need for anti-arrhythmics and/or
implantable cardioverter defibrillator (ICD) therapy, etc. in AMI
patients. Within this context, even though the study by Padfield GJ et
al (1) was not spesifically designed for the investigation of clinical end
-points, we wonder whether etanercept use might have an influence on
arrhythmic end-points in AMI patients. The authors may want to make
clear whether there were any significant differences in terms of
arrhythmic events and arrhythmic mortality between etanercept and
placebo groups in an effort to uncover any potential anti-arrhythmic
benefit of TNF-antagonism, and to suggest a potential therapeutic
implication of etanercept, if any, with regards to arrhythmia prevention
in AMI patients in the hospital setting. However, future studies are
still warranted to further investigate the potential role of anti-
inflammatory agents in the management of arrhythmias in the setting of
ACSs.
REFERENCES:
1- Padfield GJ, Din JN, Koushiappi E, Mills NL, Robinson SD, Cruden NL,
Lucking AJ, Chia S, Harding SA, Newby DE. Cardiovascular effects of
tumour necrosis factor ? antagonism in patients with acute myocardial
infarction: a first in human study. Heart. 2013 Apr 10. [Epub ahead of
print]. Heart doi:10.1136/heartjnl-2013-303648.
2- Guo Y, Lip GY, Apostolakis S. Inflammation in atrial fibrillation. J Am
Coll Cardiol. 2012 ;60(22):2263-70.
3- Yalta K, Y?lmaz MB, Turgut OO, Tandogan I. Markers of inflammation and
thrombin generation: additional guides in determining the therapeutic
strategy for malign ventricular arrhythmias after an acute myocardial
infarction? Int J Cardiol. 2010; 145(3): 492-3.
4- Elmas E, H?lzer L, Lang S, Popp T, K?lsch T, Wolpert C, Brueckmann M,
Borggrefe M. Enhanced proinflammatory response of mononuclear cells to in
vitro LPS-challenge in patients with ventricular fibrillation in the
setting of acute myocardial infarction. Cytokine. 2008 ;43(2):138-42.
5- Steptoe A, Molloy GJ, Messerli-B?rgy N, Wikman A, Randall G, Perkins-
Porras L, Kaski JC. Fear of dying and inflammation following acute
coronary syndrome. Eur Heart J. 2011; 32(19): 2405-11.
6- Xiao H, Liao YH, Chen ZJ. Tumor necrosis factor-alpha: a new mechanism
of ischemic ventricular fibrillation? Chin Med J (Engl). 2008; 121(18):
1848-51.
I read the publication by Efthymiou et al and was keen to obtain a
few clarifications from the authors.
-I suspect that the vein was harvested by an open technique as opposed an
endo vein harvest which I feel has had an important role to play in the
'pristine' quality noted.
-what medications was the patient on; aspirin etc;
-any co-morbid conditions viz.,hypertension,diabetes etc.,.
-how was the aortotomy managed with the...
I read the publication by Efthymiou et al and was keen to obtain a
few clarifications from the authors.
-I suspect that the vein was harvested by an open technique as opposed an
endo vein harvest which I feel has had an important role to play in the
'pristine' quality noted.
-what medications was the patient on; aspirin etc;
-any co-morbid conditions viz.,hypertension,diabetes etc.,.
-how was the aortotomy managed with the proximal anastomosis in the area
of interest
-what was the nature of the aortic valve-was it Biscupid? This is because
we already have one congenital anomaly.
-how did the RCA look on the pre-operative angiogram; was it a right
dominant system?
-did the vein feel soft as did the aorta?
This is an interesting case and I thank the authors for a succint
presentation.
When the stomach compresses the left atrium this can cause paroxysmal
atrial fibrillation(1), and it can also cause syncope, the latter
associated with deep S waves in Lead I, deep Q waves in lead III, and ST
segement depression in leads V2 to V6(2). In the reported patient with
syncope attributable to left atrial compression(the latter diagnosed by
computed tomography) symptoms were associated with a fall in blood
press...
When the stomach compresses the left atrium this can cause paroxysmal
atrial fibrillation(1), and it can also cause syncope, the latter
associated with deep S waves in Lead I, deep Q waves in lead III, and ST
segement depression in leads V2 to V6(2). In the reported patient with
syncope attributable to left atrial compression(the latter diagnosed by
computed tomography) symptoms were associated with a fall in blood
pressure to 90/60 mm Hg and tachycardia of 130 beats/min. The competing
diagnoses of pulmonary embolism and relevant obstructive coronary heart
disease were ruled out by computed tomography. The episode of syncope was
releived by a short course of cardiac massage, and the "upside down
stomach" which had caused the symptoms was respositioned by hiatoplasty
and fundopexy(2)
References
(1) Temple IP., Schmitt M., Fox DJ
Feeling the squeeze: an unusual cause of atrial fibrillation
Heart 2013;99:752
(2)Zwermann L., Ritter P., Spelberg F et al
Syncope due to a massive upside-down stomach
J Amer Coll Cardiol 2013 doi 10.1016/j.jacc.2012.09.077
To the Editor, we read with interest the editorial by Chambers et al.
exploring the issue of dental surveillance in the UK and its relationship
with infective endocarditis, here referenced1. This editorial highlights
the requirement for comprehensive dental surveillance to detect and manage
poor oral health (a significant risk factor for bacteraemia) as an
essential preventative strategy for infective endocarditis and its...
To the Editor, we read with interest the editorial by Chambers et al.
exploring the issue of dental surveillance in the UK and its relationship
with infective endocarditis, here referenced1. This editorial highlights
the requirement for comprehensive dental surveillance to detect and manage
poor oral health (a significant risk factor for bacteraemia) as an
essential preventative strategy for infective endocarditis and its
potentially life-threatening complications. The authors comment that
"approximately 30% of the population do not attend a dentist regularly"
and correctly focus on the issue of cost as a potential factor in this
relatively poor attendance rate.
This issue has particular significance for the adult congenital heart
disease (ACHD) population, in whom endocarditis occurs more frequently. We
recently conducted an audit project in this group, surveying 50
consecutive ACHD clinic patients and documenting their self-reported
dental attendance in comparison with the NICE recommendation (maximum 2
year intervals between routine appointments)2. Despite 90% of our sample
being registered with a dentist, 20% did not attend for regular dental
reviews at all. A subgroup analysis of patients with highest endocarditis
risk (per the European Society of Cardiology definition3) and special
needs patients (who exhibit dental problems more frequently4) revealed a
similarly inadequate level of dental attendance.
Interestingly, anxiety/dislike of attending the dentist, not cost,
was the most commonly reported barrier to dental care, affecting just over
one third of our sample. Cost was reported by only 17% of patients.
We agree that cost is a significant factor in determining attendance
for dental reviews but, in the congenital heart disease population and
those with special needs, fear and anxiety may be at least as common. It
is our view that for the ACHD population, anxiety relating to dental
visits should be addressed proactively in paediatric clinics.
We strongly concur with Chambers et al that investment in strategies
for the prevention of infective endocarditis would be very worthwhile for
the National Health Service. We would emphasise that additional measures
to improve education and decrease anxiety surrounding dental surveillance
are also needed, especially for the increasing ACHD population, as
demonstrated from our data.
References
1. Chambers JB, Dayer M, Prendergast BD, et al. Beyond the antibiotic
prophylaxis of infective endocarditis: the problem of dental surveillance.
Heart 2013; 99:363-364
2. National Institute for Health and Clinical Excellence. NICE
clinical guideline 19: Dental recall. 2004; Available from:
www.nice.org.uk/CG019NICEguideline
3. European Society of Cardiology. Guidelines on the prevention,
diagnosis and treatment of infective endocarditis. European Heart Journal
2009;30:2369-2413
4. Davies R, Bedi R, Scully C. Oral healthcare for patients with
special needs. BMJ 2000;321:495-8
Dr. Anderson's letter in response to this editorial seems to have
over interpreted the phrase 'naked eye'. I used the phrase, in what I had
hitherto thought was its typical application, as a figure of speech for
visual perception without the aid of a means of a magnification device. I
apologize that I was not aware of the apparently common ironic use of the
phrase in developmental cardiac anatomy....
Dr. Anderson's letter in response to this editorial seems to have
over interpreted the phrase 'naked eye'. I used the phrase, in what I had
hitherto thought was its typical application, as a figure of speech for
visual perception without the aid of a means of a magnification device. I
apologize that I was not aware of the apparently common ironic use of the
phrase in developmental cardiac anatomy.
Dr. Anderson is correct that without specific stains there are no
reliable physical landmarks to identify the majority of the conduction
system. However, with the requisite vital dyes or or post-vital stains
most of the elements of the conventional conduction system in humans can
be observed without magnification aids (eg in the operating room or in the
autopsy suite). Indeed, much of this work is based directly on Anderson's
seminal contributions.
Finally, my description of these structures was intended solely to
indicate that our current conception of the cardiac conduction system, and
of cardiac connectivity in general, is constrained by macroscopic and
microscopic morphology (onto which the surface ECG has been retrofitted)
and would benefit from additional functional annotation. This synergy
between structure and function has not been lost on investigators working
on the 'connectome' in the central nervous system where traditional
neuroanatomy has begun to be revolutionized by cellular resolution
anatomic and physiologic studies. I think a similar effort in cardiology
would be powerful.
As part of their systematic review and meta-analysis, the authors
emphasize the impact of body surface area on athletes heart (1). They
underline the critical importance of reporting anthropometrics and/or
appropriately scaled data in future studies, but conclude that this
approach to analysis is unfortunately rare. We like to refer the
interested reader to our recent comprehensive analysis of the influence of
various ra...
As part of their systematic review and meta-analysis, the authors
emphasize the impact of body surface area on athletes heart (1). They
underline the critical importance of reporting anthropometrics and/or
appropriately scaled data in future studies, but conclude that this
approach to analysis is unfortunately rare. We like to refer the
interested reader to our recent comprehensive analysis of the influence of
various ratiometrically and allometrically scaled body size variables such
as body surface area, fat-free mass and height on left ventricular
dimensions in athletes (2). This study provides gender-specific
echocardiographic data of 1051 healthy adult elite athletes with a mean
training history of 10 years separated by low-, moderate- and high-dynamic
disciplines, the latter of which is also compared to an age-matched
sedentary control group. Appropriate allometric scaling of left
ventricular dimensions eliminated some of the absolute between-group
differences in cardiac dimensions, but in male high-dynamic athletes
cardiac size exceeded a sole influence of body size. The strongest
association between a body size variable and left ventricular dimensions
was found for fat-free mass. We therefore agree with the authors that
cardiac dimensions in elite athletes are substantially influenced by body
size. Appropriate scaling should be a routine part of the cardiovascular
care of elite athletes as it sheds more light on the "gray area" between
physiologic cardiac adaptations to exercise and cardiomyopathy.
References
1. Utomi V, Oxborough D, Whyte GP, et al. Heart Published Online
First: March 9, 2013 doi:10.1136/heartjnl-2012-303465
2. Pressler A, Haller B, Scherr J, et al. Association of body
composition and left ventricular dimensions in elite athletes. Eur J Prev
Cardiol 2012;19:1194-204
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
Sir,
The excellent article by Oliver-Williams and co-authors (1) provides strong evidence to link miscarriages, the most prevalent major complication of pregnancy, the commonest situation in women's life, with coronary heart disease (CHD), the leading cause of death in women.
The relationship between miscarriage and cardiovascular risk should be attributed to certain risk factor...
Kenan YALTA, MD
Nasir SIVRI, MD
Bilal GEYIK, MD
Ertan YETKIN, MD
Trakya ?niversity, Cardiology Department, Edirne, Turkey
Corresponding Author: Kenan Yalta , e-mail: kyalta@gmail.com
In their recently published elegant article (1), Padfield GJ et al have reported potential cardiovascular effects of tumor necrosis factor alpha (TNF-alpha) antagonism i...
I read the publication by Efthymiou et al and was keen to obtain a few clarifications from the authors. -I suspect that the vein was harvested by an open technique as opposed an endo vein harvest which I feel has had an important role to play in the 'pristine' quality noted. -what medications was the patient on; aspirin etc; -any co-morbid conditions viz.,hypertension,diabetes etc.,. -how was the aortotomy managed with the...
When the stomach compresses the left atrium this can cause paroxysmal atrial fibrillation(1), and it can also cause syncope, the latter associated with deep S waves in Lead I, deep Q waves in lead III, and ST segement depression in leads V2 to V6(2). In the reported patient with syncope attributable to left atrial compression(the latter diagnosed by computed tomography) symptoms were associated with a fall in blood press...
To the Editor, we read with interest the editorial by Chambers et al. exploring the issue of dental surveillance in the UK and its relationship with infective endocarditis, here referenced1. This editorial highlights the requirement for comprehensive dental surveillance to detect and manage poor oral health (a significant risk factor for bacteraemia) as an essential preventative strategy for infective endocarditis and its...
Dear Editor
Dr. Anderson's letter in response to this editorial seems to have over interpreted the phrase 'naked eye'. I used the phrase, in what I had hitherto thought was its typical application, as a figure of speech for visual perception without the aid of a means of a magnification device. I apologize that I was not aware of the apparently common ironic use of the phrase in developmental cardiac anatomy....
As part of their systematic review and meta-analysis, the authors emphasize the impact of body surface area on athletes heart (1). They underline the critical importance of reporting anthropometrics and/or appropriately scaled data in future studies, but conclude that this approach to analysis is unfortunately rare. We like to refer the interested reader to our recent comprehensive analysis of the influence of various ra...
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...
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