We agree that the lack of drug specificity indicates that other
factors, such as those relating to underlying depression, may explain the
associations we have found with myocardial infarction. If amelioration of
depression reduces the risk of myocardial infarction, then, yes,
antidepressants may reduce the risk of later MI. Our data indicate that
people with remaining time on antidepressants for a l...
We agree that the lack of drug specificity indicates that other
factors, such as those relating to underlying depression, may explain the
associations we have found with myocardial infarction. If amelioration of
depression reduces the risk of myocardial infarction, then, yes,
antidepressants may reduce the risk of later MI. Our data indicate that
people with remaining time on antidepressants for a longer period than 28
days do have a lower point estimate risk of MI, however the confidence
intervals for these risk estimates crossed 1.
Why should lipid lowering drugs be associated with an increased risk
of developing peripheral neuropathies [1,2]? For the same reason that
rapid glycaemic control might be [3]? That would imply that fatty acids can
be used as a substrate for oxidative phosphorylation in the brain just as
it is peripherally and the current view is that it cannot. The brain can
use glucose and in some circumstances ket...
Why should lipid lowering drugs be associated with an increased risk
of developing peripheral neuropathies [1,2]? For the same reason that
rapid glycaemic control might be [3]? That would imply that fatty acids can
be used as a substrate for oxidative phosphorylation in the brain just as
it is peripherally and the current view is that it cannot. The brain can
use glucose and in some circumstances ketone bodies but it is claimed not
fatty acids.
What almost every in vitro biochemical experiment has done has been
to buffer pH and gas with 95% O2 and 5% CO2. [That is a highly abnormal
state]. What is more the liver has been excluded and hence the opportunity
for recycling anaerobic metabolites and maintaining ATP resynthesis by
anaerobic glycolysis. [The same applies to almost every in vitro
experiment that has been performed on the heart]. In any event the brain
[and even the heart] contains large amounts of lipid [4] a significant
portion of which must exist in mobile pools.
Might a lipid shift increase the efficiency of ATP resynthesis during
reductive stress in the brain just as it has been proposed to do
peripherally? Being highly diffusable ketone bodies might operate a
particularly effective shuttle analogous to that proposed in the lactate
shuttle hypothesis. If so might lipid lowering drugs compromise this in
patients exposed to some degree of reductive stress and who might have
become dependent upon this source of nutrient for efficient neurological
energy metabolism as proposed might be the case in diabetics?
References
1. Corrao G, Zambon A, Bertu L, Botteri E, Leoni O, Contiero P. Lipid
lowering drugs prescription and the risk of peripheral neuropathy: an
exploratory case-control study using automated databases.
J Epidemiol Community Health. 2004 Dec;58(12):1047-51.
2. G Corrao, A Zambon, L Bertù, E Botteri, O Leoni, and P Contiero
Lipid lowering drugs prescription and the risk of peripheral neuropathy:
an exploratory case-control study using automated databases
Heart 2005; 91: 560.
3. Grounds for abandoning "diabetes" as a diagnosis?
Richard G Fiddian-Green (9 March 2005) eLetter re: M K S Leow and J
Wyckoff
Under-recognised paradox of neuropathy from rapid glycaemic control
Postgrad Med J 2005; 81: 103-107.
4. Isabelle Carriéa,b, Michel Clémenta, Dominique de Javelb,
Henriette Francèsa, and Jean-Marie Bourrea Specific phospholipid fatty
acid composition of brain regions in mice: effects of n;–3 polyunsaturated
fatty acid deficiency and phospholipid supplementation Journal of Lipid
Research, Vol. 41, 465-472, March 2000.
The article using a FE model described the biomechanics of plaque
rupture, which is very interesting. However, there are a few points that I
disagree.
Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it....
The article using a FE model described the biomechanics of plaque
rupture, which is very interesting. However, there are a few points that I
disagree.
Firstly, the geometries were used with two sharp angles in the
shoulder regions, which will cause errors for FEA simulation. Special
method needs to use in this regions for correct results, while the authors
didn’t do anything with it.
Secondly, in figure 4a and figure 4b, the results showed maximal stress
actually in the opposite side of the plaque, which is in grey. This is not
in the shoulder region which is in red. This is due to the very thin
fibrous in that region.
Thirdly, figure 4c doesn’t prove anything, and it possibly is wrong. Thin
fibrous cap does result in high stress concentration in the thin fibrous
region. The result shows the stress only increases in the other parts of
the fibrous cap but not in the shoulders, which seems incorrect.
Fourthly, in figure 5a, maximal stress decreases when degree of stenosis
increases. This is due to the lumen is decreased with large stenosis, and
this results in less loading (pressure) applied on the lumen wall. This
certainly decreases the maximal stress on the fibrous cap. The same lumen
areas should be chosen when comparing the stenosis effect.
Finally, the finite element method needs to be refined for this
model. The FEM actually affected the results (including figure 7), and
resulted incorrect conclusion.
The lack of difference between the size of the effects associated
with tricyclic and selective serotonin reuptake inhibitor antidepressants
points to some intrinsic characteristic of the underlying depressive
disorder which determined the increased risk of myocardial infarction.
Actually, these antidepressants may even have reduced the risk of
myocardial infarction later.
We thank Dr Brenes for his interest in our case report and for his
insightful comments. We agree that there is more than one possible
explanation for the variation in QRS morphology, and that his may well be
correct. However, in our experience, this degree of respiratory variation
of QRS morphology is unusual during monomorphic VT, and this prompted us to
seek an alternative explanation.
We thank Dr Brenes for his interest in our case report and for his
insightful comments. We agree that there is more than one possible
explanation for the variation in QRS morphology, and that his may well be
correct. However, in our experience, this degree of respiratory variation
of QRS morphology is unusual during monomorphic VT, and this prompted us to
seek an alternative explanation.
Our main purpose in submitting this case was rather to highlight the
unusual cause for the monomorphic ventricular tachycardia itself.
We thank Corea F et al. for highlighting the inconsistency between
the current clinical practice and guidelines in the use of oral
anticoagulation for stroke prevention in patients with atrial fibrillation
(AF). The purpose of our study was to determine the clinical implication
of transient and non-sustained atrial arrhythmias detected by the
pacemaker [1]. Our findings suggest that device detected...
We thank Corea F et al. for highlighting the inconsistency between
the current clinical practice and guidelines in the use of oral
anticoagulation for stroke prevention in patients with atrial fibrillation
(AF). The purpose of our study was to determine the clinical implication
of transient and non-sustained atrial arrhythmias detected by the
pacemaker [1]. Our findings suggest that device detected atrial
arrhythmias was associated with a 1.5 fold increase in major
cardiovascular event, especially stroke.
In this retrospective analysis, the reasons for under-utilization of
anticoagulation in patients with AF could not be clearly determined.
However, there are several potential explanations for a relatively low
percentage of our Chinese AF patients treated with anticoagulation at
baseline and during follow-up. First, current guidelines [2, 3] have not
specifically addressed the use of anticoagulation based on device detected
transient atrial arrhythmias. However, based on our data [1] and recent
studies by Glotzer TV et al. [4], the presence of device detected AF
episodes, irrespectively of symptoms, was associated with an increase risk
of stroke. Anticoagulation therapy should be considered in those high risk
patients with AF detected by the implantable device. The future
application of wireless remote monitoring for atrial arrhythmias using
implantable device may further enhance early detection of AF for the use
of anticoagulation in high risk patients [5]. Second, most of the current
data regarding the use of anticoagulation for prevention of
thromboembolism in AF are on Caucasians population (97%) [2, 3].
Furthermore, Chinese population has a higher prevalence of hemorrhagic
stroke than Caucasians population [6]. As a result, the safety and
efficacy of anticoagulation therapy for prevention of thromboembolic event
in Chinese population remain unclear. Lastly, the utilization of
anticoagulation in Chinese population is further confounded by the lower
dose requirement [7] and a high prevalence of herbal intake [8].
Therefore, more studies are needed to evaluate the optimal use of
anticoagulation for stroke prevention in Chinese patients with AF.
References:
1. Tse HF, Lau CP. Prevalence and clinical implications of atrial
fibrillation episodes detected by pacemaker in patients with sick sinus
syndrome. Heart. 2005;91:362-4.
2. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for
the management of patients with atrial fibrillation: executive summary; a
report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines and Policy Conferences (Committee to
Develop Guidelines for the Management of Patients With Atrial
Fibrillation) developed in collaboration with the North American Society
of Pacing and Electrophysiology. Circulation 2001;104,2118-2150.
3. Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ.
Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference
on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:429S-456S.
4. Glotzer TV, Hellkamp AS, Zimmerman J, Sweeney MO, Yee R, Marinchak
R, Cook J, Paraschos A, Love J, Radoslovich G, Lee KL, Lamas GA; MOST
Investigators. Atrial high rate episodes detected by pacemaker diagnostics
predict death and stroke: report of the Atrial Diagnostics Ancillary Study
of the MOde Selection Trial (MOST). Circulation. 2003;107:1614-9.
6. Ayala C, Croft JB, Greenlund KJ, Keenan NL, Donehoo RS, Malarcher
AM, Mensah GA. Sex differences in US mortality rates for stroke and stroke
subtypes by race/ethnicity and age, 1995-1998. Stroke. 2002;33:1197-201.
7. Gan GG, Teh A, Goh KY, Chong HT, Pang KW. Racial background is a
determinant factor in the maintenance dosage of warfarin. Int J Hematol.
2003;78:84-6.
8. Wong RS, Cheng G, Chan TY. Use of herbal medicines by patients
receiving warfarin. Drug Saf. 2003;26:585-8.
In the article entitled “An unusual case of ventricular tachycardia”
published in the February issue of this journal, the authors report a case
of ventricular tachycardia that occurred following placement of a Hickman
catheter that reverted to sinus tachycardia upon catheter removal. The
authors concluded that the variation of the QRS morphologies, resulting in
the episode of ventricular tachycardia,...
In the article entitled “An unusual case of ventricular tachycardia”
published in the February issue of this journal, the authors report a case
of ventricular tachycardia that occurred following placement of a Hickman
catheter that reverted to sinus tachycardia upon catheter removal. The
authors concluded that the variation of the QRS morphologies, resulting in
the episode of ventricular tachycardia, was due to variable degrees of QRS
fusion.
We question the validity of the authors’ conclusion for the following
reasons. Firstly, there is a significant difference in the heart rates
between the two ECGs: 135 bpm in the ventricular tachycardia and 112
during sinus rhythm. Secondly, in the case of true ventricular fusion
beats, changes in QRS morphology should be accompanied by changes in T
wave morphology which was not evident on the ECGs. Thirdly, as noted in
the rhythm tracing (lead II), there is a clear sequential pattern of the
morphologic variations related to the inspiratory and expiratory phases of
respiration. The respiratory rate is 18 p.m. Such variations are also
seen, to a lesser degree, on the ECG with sinus tachycardia, at the time
when the patient is breathing at a slower rate.
We, therefore, conclude that the morphologic variations in QRS in the
article are related to variations in respiratory activity and are not the
result of fusion.
In his recent review on the question of whether the relationship
between patent foramen ovale and stroke is a causal one, Amarenco supports
his scepticism of a paradoxical embolism mechanism by writing firstly that
a Valsalva maneouvre is "mandatory" to allow paradoxical embolism, and
secondly that the prevalence of prothrombotic mutations in patients with
PFO and stroke is lower than that found in th...
In his recent review on the question of whether the relationship
between patent foramen ovale and stroke is a causal one, Amarenco supports
his scepticism of a paradoxical embolism mechanism by writing firstly that
a Valsalva maneouvre is "mandatory" to allow paradoxical embolism, and
secondly that the prevalence of prothrombotic mutations in patients with
PFO and stroke is lower than that found in the deep venous thrombosis
population. Both of these are spurious. In the first instance, there are
well documented situations in which vigorous right to left shunting occurs
in the absence of a valsalva maneouvre, such as in patients with
platypnoea orthodeoxia. In the second, there are a number of explanations
for why the prevalence of prothrombotic mutations may be lower in those
with stroke and PFO than in those with DVT, including the possibility that
the thromboses that cross a PFO and cause stroke may simply be a
particular subgroup of thromboses.
Cardioembolic stroke according to many data available is one of the
major killers in cerebrovascular diseases. When age-adjusted to the
European population cardioembolism have the highest incidence rates,
higher case fatalities as well as recurrence rates [1].
The (under)use of oral anticoagulants in AF subjects is the cornerstone of
many guidelines [2,4].
Cardioembolic stroke according to many data available is one of the
major killers in cerebrovascular diseases. When age-adjusted to the
European population cardioembolism have the highest incidence rates,
higher case fatalities as well as recurrence rates [1].
The (under)use of oral anticoagulants in AF subjects is the cornerstone of
many guidelines [2,4].
According to the latest available World Survey of Cardiac Pacing report,
despite health care authorities budget reductions, the total amount of PM
implants increased worldwide. Taking into account data regarding EU and US
more than 7.000 PMs in 1997 were implanted. In 2001 over the same
countries involved in the project, more than 9.000 devices were positioned
[5].
Whether dual or single chamber ventricular pacing may have different
relevance over AF recognition, and subsequent stroke risk, have already
been focused [6].
The recent publication of the long term survey on PM patients performed at
Queen Mary Hospital of Hong Kong by Tse made evident that thousands of
normal dwelling PMs patients may have unrecognised AF episodes, not
receiving any adequate antithrombotic prophylaxis [7].
Thus hundreds of potentially preventable ischemic events occur.
Tse showed at baseline how the 28% of AF patients were under oral
anticoagulants, while at the follow up visits such percentage raised to
49%. There were other reasons for not administering anticoagulants ? How
many patients were under aspirin or other antithrombotics ?
In our opinion both new onset AF and contraindications can account only
for a minority of non-prescriptions [6].
Stroke prevention in PM patients can be further optimised: this subjects
are under close follow up, cardiac rhythm can be checked with feasible
procedures thus guidelines needs to be better attended.
We strongly believe that a closer cooperation of cardiologist and the
stroke neurologist is mandatory for implementing strategies to reduce the
burden of stroke.
References
1. Kolominsky-Rabas L, Weber M; Gefeller O; Neundoerfer B, Heuschmann
P Epidemiology of Ischemic Stroke Subtypes According to TOAST Criteria.
Stroke. 2001;32:2735
2. Deplanque D, Corea F, Arquizan C, Parnetti L, Mas JL, Gallai V,
Leys D. Stroke and atrial fibrillation: is stroke prevention treatment
appropriate beforehand? SAFE I Study investigators.Heart. 1999
Nov;82(5):563-9.
3. Deplanque D, Leys D, Parnetti L, Schmidt R, Ferro J, De Reuck J,
Mas JL, Gallai V; SAFE II Investigators. Stroke prevention and atrial
fibrillation: reasons leading to an inappropriate management. Main results
of the SAFE II study. Br J Clin Pharmacol. 2004 Jun;57(6):798-806.
4. Bornstein N, Corea F, Galllai V, Parnetti L. Heart-brain
relationship: atrial fibrillation and stroke. Clin Exp Hypertens. 2002 Oct
-Nov;24(7-8):493-9.
5. Mond HG, Irwin M, Morillo C, Ector H. The world survey of cardiac
pacing and cardioverter defibrillators: calendar year 2001. Pacing Clin
Electrophysiol. 2004 Jul;27(7):955-64.
6. Patel AM, Westveer DC, Man KC, Stewart JR, Frumin HI. Treatment of
underlying atrial fibrillation: paced rhythm obscures recognition. J Am
Coll Cardiol. 2000,Sep;36(3):784-7.
7. Tse HF, Lau CP. Prevalence and clinical implications of atrial
fibrillation episodes detected by pacemaker in patients with sick sinus
syndrome. Heart. 2005 Mar;91(3):362-4.
Dr Osman and colleagues are, of course, correct in their comments
regarding the evolving nature of percutaneous coronary intervention (PCI)
for acute myocardial infarction. However, their comment that the low use
of coronary stents, glycoprotein IIb/IIIa inhibition and thienopyridines
is likely to have influenced the outcome of our study, and hence our
conclusion, is not substantiated by either our...
Dr Osman and colleagues are, of course, correct in their comments
regarding the evolving nature of percutaneous coronary intervention (PCI)
for acute myocardial infarction. However, their comment that the low use
of coronary stents, glycoprotein IIb/IIIa inhibition and thienopyridines
is likely to have influenced the outcome of our study, and hence our
conclusion, is not substantiated by either our own data [1] or by data
from other contemporary trials of infarct angioplasty.
Firstly, plain balloon angioplasty (without stent implantation) was
not associated with hospital mortality in our study and neither was lack
of treatment with a thienopyridine (both of these variables of course
describe the same patient group). PCI without abciximab was also not
associated with hospital mortality. The only univariate or multivariate
predictors of hospital mortality were those described in the manuscript.
Secondly, Osman et al. refer to "outcomes" when our study is based on
survival in particular. Although stenting confers some advantage, there is
currently no evidence that it improves the chance of survival. In the
stent-PAMI (Primary Angioplasty in Myocardial Infarction) trial [2], there
was no reduction in one month mortality in the group receiving coronary
stent(s) compared to those receiving angioplasty alone. In fact,
numerically more patients died in the stent arm by one month of follow up
(3.5% versus 1.8%, p=0.15). The only significant difference in one month
outcomes was in a reduction in target vessel revascularisation in the
stent arm (1.3% versus 3.8%, p=0.02). Despite this, there was no
difference in the incidence of the combined clinical endpoint of death,
reinfarction, disabling stroke or target vessel revascularisation at one
month. By six months, the incidence of this composite (primary endpoint)
was lower in the stent arm (12.6% versus 20.1%, p<_0.01 almost="almost" exclusively="exclusively" due="due" to="to" less="less" target="target" revascularisation="revascularisation" in="in" the="the" stent="stent" arm="arm" _7.7="_7.7" versus="versus" _17.0="_17.0" p0.001="p0.001" and="and" with="with" a="a" persistent="persistent" numeric="numeric" excess="excess" of="of" deaths="deaths" _4.2="_4.2" _2.7="_2.7" p="p" similarly="similarly" cadillac="cadillac" comparison="comparison" angioplasty="angioplasty" stenting="stenting" or="or" without="without" abciximab="abciximab" acute="acute" myocardial="myocardial" infarction="infarction" trial="trial" _3="_3" incidence="incidence" _30="_30" day="day" mortality="mortality" each="each" four="four" groups="groups" balloon="balloon" alone="alone" was="was" statistically="statistically" same.="same." fact="fact" numerically="numerically" more="more" patients="patients" died="died" _="_" than="than" arm.="arm." these="these" trials="trials" were="were" not="not" powered="powered" detect="detect" early="early" differences="differences" mortality.="mortality."/> Thirdly, the ADMIRAL (Abciximab before Direct Angioplasty and
Stenting in Myocardial Infarction Regarding Acute and Long-Term Follow-up)
trial [4] in which patients with STEMI were randomised to receive
abciximab or placebo prior to primary angioplasty with stenting,
demonstrated a statistically significant difference in the incidence of
the primary composite endpoint of death, reinfarction, or urgent
revascularization of the target vessel at 30 days favouring the abciximab
arm (6% versus 14.6%, p=0.01). The trial did not (and could not, because
of inadequate power) demonstrate a reduction in mortality at 30 days.
Similarly, although Osman cites the trial by Brener et al. [5] for showing
clear benefit with the addition of glycoprotein IIb/IIIa inhibition, we
must be clear about exactly what those benefits were. There was no benefit
in terms of 30 day mortality, nor was there a reduction in the incidence
of reinfarction by 30 days. The principle benefit seen by 30 days was a
reduction in the incidence in urgent target vessel revascularisation.
Fourthly, there are no data in the current literature to indicate
that the addition of a thienopyridine prior to or after primary PCI for
STEMI, in any dose, has any effect on early mortality. The CREDO
(Clopidogrel for the Reduction of Events during Observation) trial [6]
provides some information on the addition of clopidogrel in patients
undergoing contemporary PCI, but these were not patients with STEMI and
they were certainly not in cardiogenic shock. There was no statistically
significant reduction at 28 days in the incidence of death, MI or target
vessel revascularisation in the clopidogrel group compared to placebo
(6.8% versus 8.3%, p=0.23) and certainly no mortality benefit. Even
amongst those receiving clopidogrel loading more than 6hrs before
intervention, there was no significant reduction in mortality. Arbitrarily
delaying intervention in cardiogenic shock for such a weak benefit could
hardly be justified and none of the patients we treated who were referred
from other centres took six hours from referral to the time of
angioplasty. It is doubtful whether the paper by Angiolillo et al. [7], in
which 50 patients with stable coronary artery disease undergoing elective
PCI were randomised to receive either 300mg or 600mg of clopidogrel prior
to PCI and underwent assessment of platelet aggregation and activation, is
relevant to the current discussion.
The principle point of interest in our study is whether the presence
of particular patient characteristics can be used to determine the
likelihood of the natural history of cardiogenic shock complicating acute
myocardial infarction being altered by emergency transfer and attempted
PCI. Once a catheter-based revascularisation strategy is started, there is
very little evidence that procedural or pharmacological "niceties" play a
significant role in affecting hospital mortality. Although current
patients are likely to receive stents as well as additional anti-platelet
agents, we should be clear about what is known and what is not known about
these strategies.
AGC Sutton, MA de Belder
References
1. Sutton AGC, Finn P, Hall JA et al. Predictors of outcome after
percutaneous treatment for cardiogenic shock. Heart 2005; 91: 339-344.
2. Grines CL, Cox DA, Stone GW et al. Coronary angioplasty with or
without stent implantation for acute myocardial infarction. N Eng J Med
1999;341:1949-56.
3. Stone GW, Grines CL, Cox DA et al. Comparison of angioplasty with
stenting, with or without abciximab, in acute myocardial infarction. N Eng
J Med 2002;346:957-66.
4. Montalescot G, Barragan P, Wittenberg O et al. Platelet
glycoprotein IIb/IIIa inhibition with coronary stenting for acute
myocardial infarction. N Eng J Med 2001;344:1895-903.
5. Brener SJ, Barr LA, Burchenal JEB et al. Randomized, placebo-
controlled trial of platelet glycoprotein IIb/IIIa blockade with primary
angioplasty for acute myocardial infarction. Circulation 1998; 98: 734-
741.
6. Steinhubl SR, Berger PB, Mann JT et al. Early and sustained dual oral
antiplatelet therapy following percutaneous coronary intervention. JAMA
2002; 288(19):2411-20.
7. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, et al. High
clopidogrel loading dose during coronary stenting: effects on drug
response and interindividual variability. Eur Heart J 2004;25:1903-1910.
Dear Editor,
We agree that the lack of drug specificity indicates that other factors, such as those relating to underlying depression, may explain the associations we have found with myocardial infarction. If amelioration of depression reduces the risk of myocardial infarction, then, yes, antidepressants may reduce the risk of later MI. Our data indicate that people with remaining time on antidepressants for a l...
Dear Editor,
Why should lipid lowering drugs be associated with an increased risk of developing peripheral neuropathies [1,2]? For the same reason that rapid glycaemic control might be [3]? That would imply that fatty acids can be used as a substrate for oxidative phosphorylation in the brain just as it is peripherally and the current view is that it cannot. The brain can use glucose and in some circumstances ket...
Dear Editor,
The article using a FE model described the biomechanics of plaque rupture, which is very interesting. However, there are a few points that I disagree.
Firstly, the geometries were used with two sharp angles in the shoulder regions, which will cause errors for FEA simulation. Special method needs to use in this regions for correct results, while the authors didn’t do anything with it....
Dear Editor,
The lack of difference between the size of the effects associated with tricyclic and selective serotonin reuptake inhibitor antidepressants points to some intrinsic characteristic of the underlying depressive disorder which determined the increased risk of myocardial infarction. Actually, these antidepressants may even have reduced the risk of myocardial infarction later.
Dear Editor,
We thank Dr Brenes for his interest in our case report and for his insightful comments. We agree that there is more than one possible explanation for the variation in QRS morphology, and that his may well be correct. However, in our experience, this degree of respiratory variation of QRS morphology is unusual during monomorphic VT, and this prompted us to seek an alternative explanation.
O...
Dear Editor,
We thank Corea F et al. for highlighting the inconsistency between the current clinical practice and guidelines in the use of oral anticoagulation for stroke prevention in patients with atrial fibrillation (AF). The purpose of our study was to determine the clinical implication of transient and non-sustained atrial arrhythmias detected by the pacemaker [1]. Our findings suggest that device detected...
Dear Editor,
In the article entitled “An unusual case of ventricular tachycardia” published in the February issue of this journal, the authors report a case of ventricular tachycardia that occurred following placement of a Hickman catheter that reverted to sinus tachycardia upon catheter removal. The authors concluded that the variation of the QRS morphologies, resulting in the episode of ventricular tachycardia,...
Dear Editor,
In his recent review on the question of whether the relationship between patent foramen ovale and stroke is a causal one, Amarenco supports his scepticism of a paradoxical embolism mechanism by writing firstly that a Valsalva maneouvre is "mandatory" to allow paradoxical embolism, and secondly that the prevalence of prothrombotic mutations in patients with PFO and stroke is lower than that found in th...
Dear Editor,
Cardioembolic stroke according to many data available is one of the major killers in cerebrovascular diseases. When age-adjusted to the European population cardioembolism have the highest incidence rates, higher case fatalities as well as recurrence rates [1]. The (under)use of oral anticoagulants in AF subjects is the cornerstone of many guidelines [2,4].
According to the latest available Wo...
Dear Editor,
Dr Osman and colleagues are, of course, correct in their comments regarding the evolving nature of percutaneous coronary intervention (PCI) for acute myocardial infarction. However, their comment that the low use of coronary stents, glycoprotein IIb/IIIa inhibition and thienopyridines is likely to have influenced the outcome of our study, and hence our conclusion, is not substantiated by either our...
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