In a response letter Cope et al. stated that smoking or the amount of
tobacco consumed did not influence the biochemical risk factors for
coronary artery disease such as cholesterol and HDL, but increased many of
the cellular factors which we have reported in the recent review article
as contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]...
In a response letter Cope et al. stated that smoking or the amount of
tobacco consumed did not influence the biochemical risk factors for
coronary artery disease such as cholesterol and HDL, but increased many of
the cellular factors which we have reported in the recent review article
as contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]
We agree with Dr Cope regarding the possible relationship of smoking with
inflammatory process associated with the development of coronary
atherosclerosis and acute coronary thrombosis. However, the underlining
mechanisms remain obscure.
Therefore, we have examined whether chronic smoking is associated
with increased thrombosis and inflammatory process. We also investigated
the role of oxidative stress and the impact of antioxidant vitamins in
chronic smokers. We found that smoking is related with abnormalities in
thombosis/fibrinolysis system, such as increased levels of von Willebrand
factor (vWF), plasminogen activator inhibitor 1 (PAI-1) and increased PAI-
1/tPA ratio. These changes are partly reversible by high-dose antioxidant
treatment with vitamins C (2g/day) plus E (800IU/day) for a short period
of 4 weeks administration.[2] Furthermore, we have also shown that this
combination of antioxidants also decrease the expression of several
inflammatory markers such as interleukins 1b and 6, vascular cell adhesion
molecule and intercellular adhesion molecule.[3]
This beneficial effect of antioxidants reflects the possible role of
oxidative stress as a connective link between smoking, inflammatory
process and thrombosis/fibrinolysis system. It is widely believed, that
oxygen free radicals produced as a result of smoking, lead to both,
oxidative inactivation of endothelium-derived nitric oxide and direct
oxidative damage of endothelial cells. This phenomenon may increase the
release of endothelium-derived components of thrombosis/fibrinolysis
system and trigger a generalized vascular inflammatory process, associated
with increased risk for atherothrombosis.
The findings of Cope et al. and our observations indicate that smoking may
indirectly lead to increased risk for coronary atherosclerosis and acute
coronary syndromes, by affecting the inflammatory process and
thrombosis/fibrinolysis system.
References
(1) Tousoulis D, Davies GJ, Stefanadis C, Toutouzas P, Ambrose JA.
Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart
2003;89:993-997.
(2) Antoniades C, Tousoulis D, Tentolouris C, et al. Effects of Antioxidant Vitamins C and E on Endothelial Function and
Thrombosis/Fibrinolysis System in Smokers. Thromb/Haemost 2003;85:190-6
(3) Tousoulis D, Antoniades C, Tentolouris C, et al. Antioxidant
Vitamins C and E Administration in Smokers: Effects on Endothelial
Function and Adhesion Molecules. Atherosclerosis 2003; in press.
I would like to point out that Maisch and Ristic's recomendations [1]
on the duration of treatment and the use of adjuvant steroids in
tuberculous pericarditis are not consistent with the best available
evidence. They advise treatment for '9-12 months' with anti-tuberculous
drugs. In a recent systematic review of clinical trials of antituberculous
chemotherapy in patients with tuberculous pericarditis,...
I would like to point out that Maisch and Ristic's recomendations [1]
on the duration of treatment and the use of adjuvant steroids in
tuberculous pericarditis are not consistent with the best available
evidence. They advise treatment for '9-12 months' with anti-tuberculous
drugs. In a recent systematic review of clinical trials of antituberculous
chemotherapy in patients with tuberculous pericarditis, we found no
evidence that treatment for 9 months or more was any better than treatment
for the standard duration of 6 months.[2] Thus, the current
recommendation is that these patients should be treated with stanrd
antituberculous chemotherapy for 6 months.[3]
Furthermore, a meta-analysis of trials of the the effectiveness of
adjuvant steroids in tuberculous pericarditis showed promising but
inconclusive results.[4] These trials included very small numbers of
patients with HIV infection, and the potentially harmful side effects of
steroid use in immunocompromised patients has not been examined adequately.[5] Therefore, the routine use of adjuvant steroids in all patients with
tuberculous pericarditis (as recommended by Maisch and Rustic) is not
supported by current best evidence. The effectiveness and safety of
adjuvant corticosteroids in tuberculous pericarditis remains to be
established in large, well-designed placebo-controlled trials that involve
adequate numbers of HIV postive patients.[2,3,4].
References
(1) Maisch B, Ristic AD. Practical aspects of the management of pericardial
disease. Heart 2003;89:1096-1103.
(2) Mayosi BM, Ntsekhe M, Volmink JA, Commerford PJ. Tuberculous
pericarditis treatment (Cochrane Review). In The Cochrane Library, Issue
4, 2001. Oxford: Update Software.
(3) Mayosi BM, Volmink JA, Commerford PJ. Pericardial disease: an evidence
based approach to diagnosis and treatment. In Evidence Based Cardiology, 2nd edition, Yusuf S, Cairns JA, Camm
AJ, Fallen EL, Gersh BJ, (Eds). London:
BMJ Books, 2002:735-48.
(4) Ntsekhe M, Wiysonge C, Volmink J, Commerford PJ, Mayosi BM. Adjuvant
corticosteroids for tuberculous pericarditis: promising, but not proven.
QJM 2003;96:593-599.
(5) Elliott AM, Halwaiindi B, Bagshawe A, et al. Use of prednisolone in the
treatment of HIV-positive tuberculosis patients. QJM 1992;85:855-60.
We read with great interest the report discussing the management
strategies of low pressure giant pulmonary artery aneurysms.[1] As these
cases are uncommon, the natural history ill defined, and management
controversial, we wish to further contribute to the literature, discussing
two adult cases of giant low pressure pulmonary artery aneurysms, one
presenting with and the other without symptoms.
We read with great interest the report discussing the management
strategies of low pressure giant pulmonary artery aneurysms.[1] As these
cases are uncommon, the natural history ill defined, and management
controversial, we wish to further contribute to the literature, discussing
two adult cases of giant low pressure pulmonary artery aneurysms, one
presenting with and the other without symptoms.
Case 1 is a 38-year-old man with no prior cardiac history including
heart murmurs, which presented with a chronic cough, chest pains, and
exertional dyspnea. He had an unremarkable physical examination, but chest
radiograph suggested enlargement of the pulmonary artery. Transthoracic
echocardiography revealed a normal appearing pulmonary valve with trivial
regurgitation, and aneurysmal dilatation of the proximal pulmonary artery.
Computed tomography confirmed a 9 cm pulmonary artery aneurysm of the main
pulmonary artery. Because of his symptoms, he underwent surgical repair
with a 28 mm intervascular graft. The pulmonary valve was found to be
trileaflet, and the pulmonary artery was free of intimal tear or
calcification. At 6 months’ follow up, his symptoms have completely
resolved.
Case 2 is a 60-year-old female with isolated congenital pulmonary
stenosis who underwent a Brock valvotomy at age 16 for severe valvar
stenosis. She has been followed over the last 3 years for severe pulmonary
regurgitation and a pulmonary artery aneurysm. She is asymptomatic with a
preserved functional capacity on stress testing. Transthoracic
echocardiography shows severe pulmonary regurgitation, and severe right
ventricular enlargement with normal systolic function. Computed tomography
confirmed a 6.1 cm pulmonary artery aneurysm involving the main pulmonary
artery and proximal branches. Because of her lack of symptoms, preserved
right ventricular function and exercise capacity, she continues to be
conservatively managed with regular follow up.
The series by Veldtman [1] reports survival of four patients with low
pressure giant pulmonary artery aneurysms to a median age of 52 years,
with the oldest being 64 years. Our second case provides further
confirmation of the potential for late survival with a conservative
management strategy. None of the reported patients in the series [1] had
pulmonary hypertension, intracardiac shunts, systemic vasculitides, or
connective tissue disorders, similar to our two patients. Should this
patient profile be present in the setting of an asymptomatic giant
pulmonary artery aneurysm, we agree that a conservative approach can be
adopted. Careful clinical and echocardiographic follow up is indicated to
detect evidence of right ventricular dysfunction from chronic volume
overload, which seems to be the most common indication prompting surgical
intervention.
Reference
(1) Veldtman GR, Dearani JA, Warnes CA. Low pressure giant pulmonary artery
aneurysms in the adult: natural history and management strategies. Heart
2003;89:1067-1070.
The article by Androne et al.[1] describing the improvement in heart
rate recovery after maximal exercise in patients with chronic heart
failure when treated with pyridostigmine, supports the recent concept that
cholinergic stimulation may have a protective role in cardiovascular
disease.[2] We have prompted to investigate this possibility, since
depressed heart rate variability[3] and baroref...
The article by Androne et al.[1] describing the improvement in heart
rate recovery after maximal exercise in patients with chronic heart
failure when treated with pyridostigmine, supports the recent concept that
cholinergic stimulation may have a protective role in cardiovascular
disease.[2] We have prompted to investigate this possibility, since
depressed heart rate variability[3] and baroreflex sensitivity,[4] both
used as indices of parasympathetic function, has been shown to be
independent risk markers for death in chronic heart failure.
We have described previously several aspects of the oral
administration of pyridostigmine bromide, an indirect cholinomimetic
agent, in healthy volunteers, such as the effect on heart rate variability [5] and the response to physical [6] and mental stress.[7,8] Contrary to
the statement by Andone et al,[1] we have demonstrated that
pyridostigmine did blunt the heart rate response to physical exercise, an
effect previous reported by others,[9] and to mental stress. Our
unpublished data with patients with chronic heart failure during exercise
reveal that pyridostigmine causes submaximal bradycardia and increased
oxygen pulse, a variable calculated by the ratio between oxygen uptake and
heart rate that is proportional to stroke volume, suggesting an
improvement in cardiac dynamics during physical effort. Unfortunately, our
findings could not be compared to those by Androne et al.[1] in this
respect, since they did not report data on oxygen pulse.
We have just published [10] results from a ramdomized, double-blind,
cross-over study where pyridostigmine reduced ventricular ectopic activity
and increased heart rate variability in patients with chronic heart
failure. This study together with that of Androne (1) may not contitute
enough evidence to support the proposal for large-scale clinical trials to
test the hypothesis that selective enhancement of parasympathetic activity
will improve outcome,[11] but do certainly point to a new and promising
perspective concening the therapeutic management of patients with chronic
heart failure.
References
(1) Androne AS, Hryniewicz K, Goldsmith R, Arwady A, Katz SD.
Acetylcholinesterase inhibition with pyridostigmine improves heart rate
recovery after maximal exercise in patients with chronic heart failure.
Heart 2003;89(8):854-8.
(2) Nobrega ACL, Castro RRT. Parasympathetic dysfunction as a risk
factor in myocardial infarction: what is the treatment? Am Heart J
2000;140(4):E23
(3) Nolan J, Batin PD, Andrews R, et al. Prospective study of heart
rate variability and mortality in chronic heart failure: results of the
United Kingdom heart failure evaluation and assessment of risk trial (UK-
heart).
Circulation 1998;98(15):1510-6.
(4) Mortara A, La Rovere MT, Pinna GD, et al. Arterial baroreflex
modulation of heart rate in chronic heart failure: clinical and
hemodynamic correlates and prognostic implications. Circulation
1997;96(10):3450-8.
(5) Nobrega AC, dos Reis AF, Moraes RS, Bastos BG, Ferlin EL, Ribeiro
JP. Enhancement of heart rate variability by cholinergic stimulation with
pyridostigmine in healthy subjects. Clin Auton Res 2001;11(1):11-7.
(6) Serra SM, Costa RV, Bastos BG, Santos KB, Ramalho SH, da Nobrega
AC. Exercise stress testing in healthy subjects during cholinergic
stimulation after a single dose of pyridostigmine. Arq Bras Cardiol
2001;76(4):279-84
(7) Nobrega AC, Carvalho AC, Santos KB, Soares PP. Cholinergic
stimulation with pyridostigmine blunts the cardiac responses to mental
stress. Clin Auton Res 1999;9(1):11-6.
(8) Sant'anna ID, Sousa EB, Moraes AV, Loures DL, Mesquita ET,
Nobrega AC. Cardiac function during mental stress: cholinergic modulation
with pyridostigmine in healthy subjects. Clin Sci (Lond) 2003;105(2):161-
5.
(9) Wenger B, Quigley MD, Kolka MA. Seven-day pyridostigmine
adminstration and thermoregulation during rest and exercise in dry heat.
Aviat Space Environ Med 1993;64(10):905-11.
(10) Behling A, Moraes RS, Rohde LE, Ferlin EL, Nobrega ACL, Ribeiro
JP. Cholinergic stimulation with pyridostigmine reduces ventricular
arrhythmia and enhances heart rate variability in heart failure. Am Heart
J 2003;146(3):494-500.
(11) Sueta CA. Heart rate variability in chronic heart failure:
target for therapy? Am Heart J 2003;146(3):385-7.
Barakat and colleagues' observations are clinically important.
Our work on the performance of the Rose angina questionnaire in a multi-
ethnic study of a community based sample of 1509 adults from European,
Indian, Pakistani and Bangladeshi ethnic groups corroborates and
complements, their observations.[1]
European men and women mostly reported chest pain in Rose
Questionnaire (definite angina c...
Barakat and colleagues' observations are clinically important.
Our work on the performance of the Rose angina questionnaire in a multi-
ethnic study of a community based sample of 1509 adults from European,
Indian, Pakistani and Bangladeshi ethnic groups corroborates and
complements, their observations.[1]
European men and women mostly reported chest pain in Rose
Questionnaire (definite angina criteria) qualifying sites i.e. sternum or
left chest and left arm. In contrast, there were substantial numbers of
South-Asian respondents with left-sided chest pain but without left-sided
arm pain. This pattern was particularly clear in Indians. Right-sided
chest pain was commoner in Pakistanis and the pattern of pain was diffuse
in Bangladeshis of both sexes, in whom left chest pain was never combined
with left arm pain. Our published diagrams on chest pain site illustrate
these points.[1]
The‘classical’ elements of the history were less frequent in South
Asians than in Europeans, while ‘atypical’ features were most common in
Pakistanis and Bangladeshis. Bangladeshis with chest pain mostly failed to
report the other features required for definite angina on the Rose
Questionnaire. Our paper raised the possibility of systematic differences
between ethnic groups in the site of reported chest pain. We wrote that
firm conclusions must await confirmation from further studies. With the
observations of Barakat et al, this area is shown to be epidemiologically
and clinically important. It is likely that Barakat et al's findings
apply not just to Bangladeshis but to other South Asian populations.
With their exceptionally poor knowledge about heart disease and
diabetes,[2] their economic deprivation, the significant clustering of
cardiovascular risk factors,[3] and atypical presentation of pain
associated with coronary heart disease, Bangladeshis are in particular
jeopardy.
References
(1) Fischbacher CM, Bhopal R, Unwin N, White M, Alberti
KG. The performance of the Rose angina questionnaire in South Asian and
European origin populations: a comparative study in Newcastle Int J
Epidemiol 2001;54:786.
(2) Rankin J, Bhopal R. Understanding of heart disease and diabetes
in a South Asian community: cross sectional study testing the `snowball'
sample method. Pub Health 2001;115:253-260.
(3) Bhopal, R S, Unwin N, White M. et al. heterogeneity of coronary
heart disease risk factors in Indian, Pakistani, Bangladeshi and European
origin populations: cross sectional study. BMJ 1999;319:215-220.
We thank Dr Cheung for the interesting observations [1]concerning
our paper.[2]
They suggest - on the basis
of their study,[3] that an arterial
dysfunction (probably due to iron overload) could contribute to the
pathogenesis of the so-called “Thalassemic cardiomyopathy” causing an
increase of arterial stiffness and, consequently, an increase of the
pulsatile pressure if the ventricular systoli...
We thank Dr Cheung for the interesting observations [1]concerning
our paper.[2]
They suggest - on the basis
of their study,[3] that an arterial
dysfunction (probably due to iron overload) could contribute to the
pathogenesis of the so-called “Thalassemic cardiomyopathy” causing an
increase of arterial stiffness and, consequently, an increase of the
pulsatile pressure if the ventricular systolic pump function remains
within normal ranges.
We wish to underline that, even in the presence of an increased impedence
of the proximal arterial bed, the systemic vascular resistance (totally
considered) could be reduced in a high cardiac output state due to the
significant chronic anemia. This seems confirmed in our patients, in whom
the afterload was increased because of an unfavourable mass/volume ratio.
Anyway, as suggested by Cheung et al, an increased pulsatile
vascular load might play an additional role in increasing the afterload.
We obviously agree with the multifactorial pathogenesis of this
"cardiomyopathy", but we think that the iron overload play an important
role. Unfortunately, in our group of patients with a quite preserved left
ventricular systolic pump function, we have found only a weak correlation
between ferritin levels and EF% of the left ventricle. Being aware that
the conventional endocardial indexes may overestimate the myocardial fibre
shortening (an effect proportional to wall thickness) we have calculated
(data not published) stress/velocity indexes at midwall level
demonstrating a reduced contractility in 13% of our patients. So, more
detailed information on the myocardial function in thalassemic patients
affected by dilated and hypertrophic ventricles are needed. Doppler tissue
imaging with strain and strain/rate imaging at different stages of the
disease could probably give more information.
References
(1) Cheung YF. Arterial dysfunction contributes to 'beta-thalassaemia cardiomyopathy' [electronic response to Bosi G et al. Left ventricular remodelling, and systolic and diastolic function in young adults with ß thalassaemia major: a Doppler echocardiographic assessment and correlation with haematological data] heartjnl.com 2003
(2) Bosi G, Crepaz R, Gamberini MR, Fortini M, Scarcia S, Bonsante E, Pitscheider W, Vaccari M. Left ventricular remodelling, and systolic and diastolic function in young adults with ß thalassaemia major: a Doppler echocardiographic assessment and correlation with haematological data. Heart 2003;89:762-766.
(3) Cheung YF, Chan GC, Ha SY. Arterial stiffness and endothelial function in patients with beta-thalassemia major. Circulation 2002 Nov 12;106(20):2561-6.
On 24 June the National Institute of Clinical Excellence (NICE)
issued their Appraisal consultation document: coronary artery
stents.[1] With the proviso that ‘the decision to use a bare metal
stent or drug-eluting stent (DES) will depend on the anatomy of
the target vessel for stenting and the severity of the disease’
(presumably reflecting issues of deliverability of the stent
platforms on offer), t...
On 24 June the National Institute of Clinical Excellence (NICE)
issued their Appraisal consultation document: coronary artery
stents.[1] With the proviso that ‘the decision to use a bare metal
stent or drug-eluting stent (DES) will depend on the anatomy of
the target vessel for stenting and the severity of the disease’
(presumably reflecting issues of deliverability of the stent
platforms on offer), the key point was that a ‘DES is
recommended .. [when] .. the target artery is less than 3mm in
diameter or the lesion to be stented is longer than 20mm.’
We applaud the NICE philosophy of selective DES implantation
in a resource-hungry health service. It must be appreciated by
interventional cardiologists, however, that this guideline will
reduce, but not abolish, restenosis. As we recently argued,[2]
there is a law of diminishing returns with DESs; escalating
numbers (and, therefore, costs) would be required to squeeze the
last few % points of restenosis out of the system. Clearly, NICE
have grasped this reality and are endorsing a policy of scientific
rationing, the science providing some targeting of the few DESs
permitted to the lesions most likely to restenose.
What are the implications of the NICE guidelines? Applying
them to our institution reveals that a DES would be used in about
34% of lesions. This would reduce our clinical recurrence (re-
PCI) rate - the only restenosis parameter a centre not performing
routine follow-up angiography can count – from 9% to 5.1%. A
considerable disadvantage of the NICE system would be that no
stents of certain important and commonly used sizes would be
permitted, such as 3 x16mm, 3 x 18mm or any stent of 3.5mm
calibre, even if the target lesion is a long stenosis in the proximal
left anterior descending artery of a diabetic patient. If, instead,
we allotted DES according to our recommended system, based
upon a matrix of restenosis risk,[2] we find that a 34% DES rate
would yield an almost identical overall institutional recurrence
risk (5.2%), with the advantage that we would have DES
available for the sizes and indications mentioned above. Stock
control would also be simpler (important if the DES in question
has a limited shelf life) because rarely used sizes would not be
stocked.
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a
protocol for earlier sit up and mobilisation after routine transfemoral
cardiac catheterisation in contemporary practice. Patients were
randomised to be mobilised after 2½ hours or 4½ hours bed rest. The
authors report that a significant reduction in...
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a
protocol for earlier sit up and mobilisation after routine transfemoral
cardiac catheterisation in contemporary practice. Patients were
randomised to be mobilised after 2½ hours or 4½ hours bed rest. The
authors report that a significant reduction in the duration of bed rest
was achieved in the early mobilisation protocol group with no adverse
effect on vascular complications. They also report that early
mobilisation was associated with a reduction in pain and discomfort,
although this data is not presented. On this basis, the authors call into
question the role of alternative arterial access sites for diagnostic
cardiac catheterisation.
The published data does not support this viewpoint. Firstly, the
early mobilisation protocol still required 2½ hours of bed rest. There is
extensive published evidence that bed rest after medical procedures has
few benefits and a wide range of adverse effects.[2] The combination of
back pain related to bed rest and groin pain related to femoral puncture
and pressure haemostasis delays mobilisation and return to normal activity
after discharge in at least one third of patients.[3] Secondly, despite
studying only a selected low risk group of patients (only some elective
patients with chest pain undergoing diagnostic angiography were eligible
for the study. Patients with a difficult femoral puncture, those
undergoing percutaneous revascularisation, receiving adjunctive
antithrombotic therapy or with previously treated peripheral vascular
disease were excluded) haematomas re-bleeding and vaso-vagal reactions
were common. Indeed this study suggests that these problems occur in 15-
20% of these low risk patients. In contrast to this, we have recently
reported on a series of 1000 consecutive transradial cases, in which a
third of the study subjects had major risk factors for vascular
complications.[4] Patients undergoing diagnostic angiography or
percutaneous intervention were mobilised immediately, removing the
potential for adverse effects from bed rest. Avoiding a groin puncture
will facilitate a rapid return to normal activity after discharge. In
this high risk population the incidence of both major and minor vascular
complications was less than 1%. The data from the North Staffordshire
series is entirely compatible with other published case series and
randomised trials, which consistently show that use of the transradial
access site is associated with short mobilisation and discharge times, a
reduction in procedure costs and vascular complications, and a consistent
improvement in patient quality of life when compared to the femoral access
site.[5-7]
In our view the data presented (a 2½ hour period of bed rest and 15-
20% incidence of access site problems) strengthens the case for selecting
the radial artery (no bed rest and less than 1% incidence of access site
problems) in the majority of patients undergoing routine diagnostic
cardiac catheterisation.
References
(1) Pollard SD, Munks K, Wales C, Crossman DC, Cumberland DC, Oakley
GDG, Gunn J. Position and mobilisation post-angiography study. (PAMAS): a
comparison of 4.5 hours and 2.5 hours bed rest. Heart 2003;89:447-448.
(2) Allen C, Glasziou P, Del Mar C. Bed rest: a potentially harmful
treatment needing more careful evaluation. Lancet 1999;354:1229-1233.
(3) Foulger V. Patients’ views of day-case cardiac catheterisation.
Professional Nurse 1997;12:478-480.
(4) Eccleshall SC, Banks M, Carroll R, Jaumdally R, Fraser D, Nolan J.
Implementation of a diagnostic and interventional transradial programme:
resource and organisational implications. Heart 2003;89:561-562.
(5) Eccleshall S, Muthusamy T, Nolan J. The transradial access site
for cardiac procedures: a clinical perspective. Stent 1999;2(3):74-9.
(6) Al-Allaf K, Eccleshall S, Kaba R, et al. Arterial access for
cardiac procedures utilising the percutaneous transradial approach. Br J
Cardiol 2000;7:548-52.
(7) Kiemeneij F, Laarman GJ, Odekerken D et al. A randomised
comparison of percutaneous transluminal coronary angioplasty by the
radial, brachial and femoral approaches: the Access study. J Am Coll
Cardiol 1997;29(6):1269-75.
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack,
and surgery. Symathetic denervation is involved in such cases. Prolonged T
wave inversion would indicate the change in repolarization related to the
sympathetic...
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack,
and surgery. Symathetic denervation is involved in such cases. Prolonged T
wave inversion would indicate the change in repolarization related to the
sympathetic activation. The discrepancy between remarkable ST elevation and
mild elevation of myocardial enzymes would indicate myocardial stunning with
sympathetic denervation. Although some Japanese docotrs call such a clinical
state ampulla cardiomyopathy, it is contoversial. Apical thrombus has
firstly described all over the world.[2]
References
(1) Barrera-Ramirez CF, Jimenez-Mazuecos JM, Alfonso F. Apical thrombus associated with left ventricular apical ballooning. Heart 2003;89:927.
(2) Tetsuya Sato et al. Extensive myocardial stunning showing transient regression of prolonged T wave inversion and prolonged sympathetic
denervation. Internal Med 2001;40:312-319.
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular
mechanisms involved in the inflammatory mechanisms and haemostatic factors
leading to coronary atherosclerosis. They also describe the role of
chronic infection in this process.[1] However, they omit an important
factor that is common to the majority of patients su...
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular
mechanisms involved in the inflammatory mechanisms and haemostatic factors
leading to coronary atherosclerosis. They also describe the role of
chronic infection in this process.[1] However, they omit an important
factor that is common to the majority of patients suffering from this
condition – current or previous cigarette smoking.
We have undertaken an investigation into the relationship between
smoking habit, notably quantitative measurement of nicotine intake and
factors involved in the formation of the plaque and the inflammatory
process. Due to ‘social desirability bias’ associated with smoking
patients frequently under-report or deny their smoking habit. It would
seem therefore that the greater the clinical impact of smoking the greater
the patient guilt enhancing the likelihood of denial.
To improve the accuracy of information about smoking a 6-minute point
-of-care test to detect nicotine metabolites (including cotinine), called
SmokeScreen® was developed.[2] The easy to use colorimetric urine test
can provide qualitative, semi-quantitative and quantitative measurements
of nicotine intake. With this test we undertook an audit of smoking habits
of 154 new patients attending a large inner-city hospital cardiology
outpatient clinic, comparing the test identification of smoking with self-
completed questionnaire of current smoking habit. The results identified
112 (72.7%) as non-smokers, 30 (19.5%) as confessed smokers and 12 (7.8%)
as ‘smoking deceivers’.
We followed this with another study of the same population (n=85, 33
smokers and 52 never-smokers) to examine the interaction of smoking with
risk factors associated coronary artery disease, as assessed by a
biochemical screen and a blood count. Interestingly, none of the
parameters measured in the biochemical screen, such as cholesterol, HDL
and triglycerides; urea and electrolytes and liver function tests were
associated with smoking habit or quantitative assessment of nicotine
intake. Whereas white blood cell count (WBC) was significantly higher in
smokers (p=0.002), in particular neutrophils (p=0.01) and eosinophils
(p=0.02). Lymphocytes, monocytes and basophiles were higher but failed to
reach significance. Quantitative assessment of nicotine intake of the
smokers further revealed a positive correlation with WBC (p<_0.0001 neutrophils="neutrophils" p0.001="p0.001" eosinophils="eosinophils" p0.004="p0.004" and="and" lymphocytes="lymphocytes" p0.02="p0.02" with="with" monocytes="monocytes" approaching="approaching" significance="significance" p="p"/> It would seem from this pilot study that smoking or the amount of
tobacco consumed doesn’t influence the biochemical risk factors for
coronary artery disease, such as cholesterol and HDL, but does increase
many of the cellular factors which Tousoulis et al. identified as
contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]
We suggest that identification of smokers, feedback from the point-of-care
test and subsequent advice on smoking cessation could have a significant
impact on reducing many of the risk factors associated with coronary
atherosclerosis and lower cardiovascular events and mortality.
References
(1) Tousoulis D, Davies G, Stefanadis, Toutouzas P, Ambrose JA.
Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart 2003;89:993-997.
(2) Cope GF, Nayyar P, Holder R, Gibbons J, Bunce R. A simple near-patient
test for nicotine and its metabolites in urine to assess smoking habit. Clin Chim Acta 1996;256:135-149.
Dear Editor
In a response letter Cope et al. stated that smoking or the amount of tobacco consumed did not influence the biochemical risk factors for coronary artery disease such as cholesterol and HDL, but increased many of the cellular factors which we have reported in the recent review article as contributors to the inflammatory response and to the formation and instability of the atheromatous plaque.[1]...
Dear Editor
I would like to point out that Maisch and Ristic's recomendations [1] on the duration of treatment and the use of adjuvant steroids in tuberculous pericarditis are not consistent with the best available evidence. They advise treatment for '9-12 months' with anti-tuberculous drugs. In a recent systematic review of clinical trials of antituberculous chemotherapy in patients with tuberculous pericarditis,...
Dear Editor
We read with great interest the report discussing the management strategies of low pressure giant pulmonary artery aneurysms.[1] As these cases are uncommon, the natural history ill defined, and management controversial, we wish to further contribute to the literature, discussing two adult cases of giant low pressure pulmonary artery aneurysms, one presenting with and the other without symptoms.
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Dear Editor
The article by Androne et al.[1] describing the improvement in heart rate recovery after maximal exercise in patients with chronic heart failure when treated with pyridostigmine, supports the recent concept that cholinergic stimulation may have a protective role in cardiovascular disease.[2] We have prompted to investigate this possibility, since depressed heart rate variability[3] and baroref...
Dear Editor
Barakat and colleagues' observations are clinically important. Our work on the performance of the Rose angina questionnaire in a multi- ethnic study of a community based sample of 1509 adults from European, Indian, Pakistani and Bangladeshi ethnic groups corroborates and complements, their observations.[1]
European men and women mostly reported chest pain in Rose Questionnaire (definite angina c...
Dear Editor
We thank Dr Cheung for the interesting observations [1]concerning our paper.[2]
They suggest - on the basis of their study,[3] that an arterial dysfunction (probably due to iron overload) could contribute to the pathogenesis of the so-called “Thalassemic cardiomyopathy” causing an increase of arterial stiffness and, consequently, an increase of the pulsatile pressure if the ventricular systoli...
Dear Editor
On 24 June the National Institute of Clinical Excellence (NICE) issued their Appraisal consultation document: coronary artery stents.[1] With the proviso that ‘the decision to use a bare metal stent or drug-eluting stent (DES) will depend on the anatomy of the target vessel for stenting and the severity of the disease’ (presumably reflecting issues of deliverability of the stent platforms on offer), t...
Dear Editor
We were interested to read the recent scientific letter from Pollard et al published in Heart.[1]
The authors evaluated the safety of a protocol for earlier sit up and mobilisation after routine transfemoral cardiac catheterisation in contemporary practice. Patients were randomised to be mobilised after 2½ hours or 4½ hours bed rest. The authors report that a significant reduction in...
Dear Editor
I read the article by Barrera-Ramirez et al. with interest and have some comments.
I think this case is an extensive myocardial stunning induced by emotional stress. Some stunning occured with emotional stress, cerebrovascular attack, and surgery. Symathetic denervation is involved in such cases. Prolonged T wave inversion would indicate the change in repolarization related to the sympathetic...
Dear Editor
We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular mechanisms involved in the inflammatory mechanisms and haemostatic factors leading to coronary atherosclerosis. They also describe the role of chronic infection in this process.[1] However, they omit an important factor that is common to the majority of patients su...
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