We read with great interest the article recently published in "Heart"
on the current use of anticoagulation for non-valvar atrial fibrillation
[1].
This article analyses the use of aspirin and anticoagulant treatment
in 313 consecutive patients, presented with chronic atrial fibrillation of
non-valvar etiology, in a single hospital in Northern Italy, from January
1 to June 30 2000. From th...
We read with great interest the article recently published in "Heart"
on the current use of anticoagulation for non-valvar atrial fibrillation
[1].
This article analyses the use of aspirin and anticoagulant treatment
in 313 consecutive patients, presented with chronic atrial fibrillation of
non-valvar etiology, in a single hospital in Northern Italy, from January
1 to June 30 2000. From this cohort, 168 patients with no
contraindications to anticoagulation were identified. These patients were
classified as being at high risk for embolic stroke, hence anticoagulation
was indicated according to recent guidelines.[2] Bo et al. [1] reported
appropriate use of warfarin therapy in only 75 (44%) of patients, with a
substantial proportion (42%) receiving subtherapeutic dosage. Furthermore,
the use of anticoagulation declined with increasing age, despite the
greater net benefit of such use in older patients.
Our group has previously reported on 628 patients presenting with non
-valvar atrial fibrillation in the region of North-Western Greece
(representing mostly rural areas) from March 1 to November 1 1998.[3] We
thought that the similarities in the patient population characteristics,
as well as the inclusion and exclusion criteria, enable a useful
comparison between the two studies.
In our patient population,[3] of the 628 patients, 188 (29.9%) were
excluded from the analysis by criteria similar to those used by Bo et al
[1]. Of the 440 remaining patients, 328 (74.5%) were classified as being
at high risk for embolic stroke, and of them, 95 (29%) were on
anticoagulant therapy, 133 (40.5%) on aspirin and 100 (30.5%) on neither
treatment. In concert with the results reported by Bo et al,[1] a
subtherapeutic dose was given in 50% of our patients, and the use of
anticoagulation declined with increasing age.
We attempted to compare the use of anticoagulation and aspirin in the two
patient cohorts, using chi-square.
Study
Anticoag.
Aspirin
None
Sum
Italian [1]
75
54
39
168
Greek [3]
95
133
100
328
Sum
170
187
139
496
Chi square= 12.42, p<_0.01 p="p"/> This comparison reinforces the conclusions drawn by Bo et al.[1]
Anticoagulation treatment for non-valvar atrial fibrillation is
substantially underused, especially in older patients, with therapeutic
doses being achieved in only approximately half of the patients.
Furthermore, these limitations appear even more prominent in rural areas,
most likely due to additional difficulties in monitoring international
normalized ratio (INR) values, compared to urban areas.
References
(1) Bo S, Ciccone G, Scaglione L, Taliano C, Piobbici M, Mereletti F,
Pagano G. Warfarin for non-valvar atrial fibrillation: still underused in
the 21st century? Heart 2003;89:553-554.
(2) Scottish Intercollegiate Guidelines Network (SIGN). Antithrombotic
therapy. A national guideline. Edinburgh: SIGN, 1999, SIGN publication
number 36.
(3) Patsouras D, Vakalis I, Giogakas V, Kitsanou M, Sioros L,
Oikonomidis K, Goudevenos J. Status of anticoagulation therapy for
patients with atrial fibrillation in north-western Greece. Hellenic J
Cardiol (Athens) 1998;39:237-245.
I thank John Polito for his lengthy reply to my article. I will try
to discuss some of his points as far as I understand them.
Firstly, no, my article is not a "commercial" for nicotine
replacement! If anything it is a "commercial" for specialist psychological
support. My intention was to present the data and these indicate that
there is a role for both types of treatment for smokers. The data I...
I thank John Polito for his lengthy reply to my article. I will try
to discuss some of his points as far as I understand them.
Firstly, no, my article is not a "commercial" for nicotine
replacement! If anything it is a "commercial" for specialist psychological
support. My intention was to present the data and these indicate that
there is a role for both types of treatment for smokers. The data I cite
in support of pharmacotherapy come from independent and authoratitive
sources (NICE, Cochrane, WHO, UK & US Clinical Guidelines). The main
gist of what I wrote concerned the need to encourage doctors and others to
intervene with smokers by referring them to specialist smoking cessation
clinics where intensive behavioural/psychological support can be provided
alongside pharmacotherapy. As a clinical psychologist who has specialised
in treating smokers for 17 years I know only too well the importance of
helping smokers develop new skills and behaviours to protect against
relapse back to smoking.
Mr Polito disputes the evidence from the Cochrane Review Group and
the US Guidelines showing that adding NRT to any level of behavioural
support is better than that level of behavioural support given alone. He
reaches this conclusion by assuming that using NRT (or placebo) in RCT's
in some way diffuses or undermines the behavioural support and diminishes
it’s effectiveness. This is certainly not my experience, either in
conducting trials or in clinical practice. Behavioural support
concentrates on aspects of quitting smoking not related to NRT use. It has
to, because we know only to well that NRT only partially relieves tobacco
withdrawal symptoms and craving. It does not remove the need for the
smoker to make a concerted effort to modify their behaviour and
cognitions. If it were the case that behavioural support was reduced when
combined with NRT in trials this should apply equally to both active and
placebo groups, so that any additional effect of NRT can still be
accurately delineated. Over many trials this has been found to be of
substantial clinical value.
Mr Polito also forgets that some NRT trials have been conducted
without a placebo using behavioural therapy alone as the control group. In
these trials the behavioural support was clearly not focussed on NRT, and
Cochrane report that these trials give results similar to those with
placebo. One area where we do not have a strong evidence base is in
comparing brief behavioural support plus NRT with more intensive
behavioural support alone. Perhaps this is what Mr Polito was alluding to?
Although I am sure these two treatments would give similar success rates
(see Figure 1, bars 3 & 4), this comparison is of little interest,
because we know we can do even better in the intensive support group by
adding NRT or bupropion (see Figure 1 bar 5).
Mr Polito is incorrect in saying that on ceasing NRT use nicotine
withdrawal symptoms “peak in intensity”. This would only be the case if
NRT was discontinued during the first week or so, when tobacco withdrawal
symptoms are at their peak. Many smokers stopping smoking using the
nicotine patch, for instance, simply forget to use it after a few weeks.
If this caused an upsurge in withdrawal symptoms they would soon remember
to use it again! If stopping using NRT is associated with an increase in
withdrawal symptoms, then we might expect this to be reflected in higher
relapse rates when people come off NRT, which is not the case. The large
scale CEASE trial compared relapse rates in an abrupt NRT patch cessation
arm compared to a gradual nicotine weaning arm and there was no suggestion
of a differential relapse rate subsequently.
Contrary to Mr Polito's view that having a small dose of nicotine in
a placebo patch would diminish the likelihood of quitting, I believe the
opposite has been found in trials. In the dose-ranging trials I have seen,
the very low doses did as well, if not better, than pure placebos.
My article concerned clinician-supported treatment for smokers, not
self-help OTC NRT. These scenarios differ considerably. The latter does
not include the type of behavioural support, which my article makes clear,
is essential to increase success rates. The California study to which Mr
Polito refers has already been seriously and vociferouly questioned in
JAMA and elsewhere for its use of self-selected smokers as well as on
several other methodological grounds. Regardless of the interpretation of
those findings, it is a single study, in one unique population. I give
more weight to evidence from the meta-analysis of OTC NRT studies to which
he refers. These do not show NRT “generating a 93% midyear relapse rate”,
but rather that NRT enables a 7% success rate. This is very much in line
with the 5% additional success rate due to NRT that my 12-month success
rate graph (see Figure 1) would suggest by subtracting the brief advice alone
(bar 2) from the brief advice plus NRT (bar 3). Furthermore, the majority
of these smokers did not stop for any length of time, so cannot be
regarded as having “relapsed”. For those who did have a substantial period
of abstinence followed by relapse, this cannot have been due to NRT, or
there would be no 7% excess benefit from NRT.
Mr Polito may see the efficacy of NRT as an emperor without clothes,
but I would ask him to take a longer and less emotive look at all the
evidence. The first essential point to realise is that NRT is not the
emperor in the field of smoking cessation, nor has anyone tried to pretend
that it is. NRT is just one useful component which adds a modest, but
worthwhile boost to the likelihood of success.
On his next point I can agree. If a smoker can get access to
professional counselling support (with or without NRT) , as all smokers
now can in the UK, this will give them by far the best chance of success
and I would not advise a smoker to make a self-help attempt with OTC NRT
if they are prepared to attend a formal behavioural treatment programme.
Unfortunately, many smokers are not prepared to attend these even when
they are readily accessible - at least not initially - so the real
question is whether they are better off with OTC NRT or nothing. The
balance of evidence still remains firmly in favour of the former, although
we cannot be comfortable about the fact that so many choose to take this
route when there are far better options, at least in the UK. I also agree
that the more active, knowledgeable, and engaged physicians are, then the
more success they will achieve. Finally although there are many online
cessation sites, these are of very mixed quality and have not yet been
adequately evaluated so I would not recommend them as the best evidenced-
based sources. As with all things WWW, one has to be discriminating, and
the unwary can easily be misled.
We read the recent published paper by Mueller and co-workers.[1]
They demonstrate convincingly that the neutrophil count is a strong
predictor for future coronary events in patients with acute coronary
syndromes. Smoking habits, however, may to some extent confound their
results.[2] To verify the assumption we want to publish this scientific
note.
We read the recent published paper by Mueller and co-workers.[1]
They demonstrate convincingly that the neutrophil count is a strong
predictor for future coronary events in patients with acute coronary
syndromes. Smoking habits, however, may to some extent confound their
results.[2] To verify the assumption we want to publish this scientific
note.
Neutrophil granulocytes are a well-recognised risk factor for
coronary heart disease [3] closely related to smoking.[2] The neutrophils
are increased in conjunction with acute myocardial infarctions (MI) [3]
and predictive for coronary recurrence.[1] Before elective coronary
angiography we measured neutrophil counts in 74 patients with stable
angina pectoris (Table 1, see below). All participants were males and below 75 years
of age. Patients with an acute MI within the previous 3 months were
disqualified, as were individuals with unstable angina pectoris, rheumatic
arthritis or diabetes mellitus. At blood sampling, 11 individuals were
smokers whereas the remainder (n=63) did not smoke. In this homogeneous
cohort smokers had enhanced neutrophil counts (4.8 ± 1.5(SD) x 1012/L) as
compared with non-smokers (3.4 ± 1.1(SD) x 1012/L). The difference is highly
significant (p<_0.001. consequently="consequently" in="in" conjunction="conjunction" with="with" the="the" data="data" provided="provided" by="by" mueller="mueller" i="i"/>et al.[1] our results show a possible
pathophysiological mechanism explaining the deleterious effects of smoking
in male coronary heart disease patients. A leukocyte mediated
hypercoagulable state and subsequent neutrophil microvascular plugging
could offer tenable explanations. Thus, longitudinal measurements of the
neutrophil count could provide the physician with additional arguments
when persuading patients with coronary heart disease to stop smoking.
References
(1) Mueller C, Neumann FJ, Perruchoud AP, Buettner HJ. White blood cell
count and long time mortality after non-ST elevation acute coronary
syndrome treated with very early revascularisation. Heart 2003:89:389-392.
(2) Zalokar JB, Richard JL, Claude JR. Leukocyte count, smoking, and
myocardial infarction. N Engl J Med 1981:304:465-468.
(3) Danesh J, Collins R, Appleby P, Peto R. Association of fibrinogen, C-
reactive protein, albumin, or leukocyte count with coronary heart disease.
Meta-analyses of prospective studies. JAMA 1998:279:1477-1482.
(4) Järemo P, Hansson G, Nilsson O. Elevated inflammatory parameters are
associated with lower platelet density in acute myocardial infarctions
with ST-elevation. Thromb Res 2000:100:471-478.
In response to Tammy Vehige et al,[1] we had recognised that our findings may
be controversial, but these were rigorously evaluated by ourselves and
others before publication. However, to put it in context, it is one study
amongst a particular population of healthy, middle-aged men of whom about
40% appeared to be doing enough vigorous intensity activity to confer
cardiovascular benefit. The pape...
In response to Tammy Vehige et al,[1] we had recognised that our findings may
be controversial, but these were rigorously evaluated by ourselves and
others before publication. However, to put it in context, it is one study
amongst a particular population of healthy, middle-aged men of whom about
40% appeared to be doing enough vigorous intensity activity to confer
cardiovascular benefit. The paper itself urges caution in extrapolating
the findings to other populations, but recommends that the findings should
be rigorously checked in other similar studies.
Reference
(1) Vehige TM et al. General Exercise Recommendation
[electronic response to Yu S et al. What level of physical activity protects against premature cardiovascular
death? The Caerphilly study] heartjnl.com 2003 http://heart.bmjjournals.com/cgi/eletters/89/5/502#150
In response to Dr Buckley [1] we agree that data on cardiovascular
fitness would have been a useful addition to our study but resources in
terms of staff and equipment precluded this possibility. In an ideal
study, both cardiovascular fitness and questionnaire data would be
obtained in parallel and in a long term cohort study habitual physical
activity should be re-assessed at intervals.
In response to Dr Buckley [1] we agree that data on cardiovascular
fitness would have been a useful addition to our study but resources in
terms of staff and equipment precluded this possibility. In an ideal
study, both cardiovascular fitness and questionnaire data would be
obtained in parallel and in a long term cohort study habitual physical
activity should be re-assessed at intervals.
Reference
(1) Buckley JP. Some key weakness in this study [electronic response to Yu S et al. What level of physical activity protects against premature cardiovascular death? The Caerphilly study] heartjnl.com 2003 http://heart.bmjjournals.com/cgi/eletters/89/5/502#154
Is this abstract yet another nicotine commercial urging physicians to deprive patients of another of their diminishing windows of opportunity to
begin allowing their reward pathways to sense the arrival of nicotine-free
blood serum? I want to share a bit of contrary patient cessation counsel
but first some background on why.
I question this abstract's broad assertion that the "[use] of
...nicoti...
Is this abstract yet another nicotine commercial urging physicians to deprive patients of another of their diminishing windows of opportunity to
begin allowing their reward pathways to sense the arrival of nicotine-free
blood serum? I want to share a bit of contrary patient cessation counsel
but first some background on why.
I question this abstract's broad assertion that the "[use] of
...nicotine replacement therapy ... in combination with behavioural
support achieves higher cessation rates than either component alone and is
the most effective way of helping smokers to stop." I do so because I have
yet to read a single NRT study in which any abrupt cessation behavioural
program went head-to-head with NRT behavioural support, that was obviously
designed to foster successful nicotine delivery device transfer followed
by gradual nicotine weaning.
Yes, psychological crave trigger reconditioning is common to both
groups but which NRT study focused its behavioural and knowledge lessons
on the immediate needs of nicotine dependent humans using nicotine-free
placebos? Not only are abrupt cessation and delivery device transfer
needs different, many critical lessons are in direct conflict.
In which NRT studies were placebo group recovery expectations fueled
by assurance that within 72 hours of ceasing the use of all nicotine that
their nicotine withdrawal symptoms would peak in intensity and begin
easing-off, as their brain reward pathways began adjusting to the arrival
and presence of 100% nicotine-free blood serum?[1] What recovery
expectations conditioning was employed?
Why would an NRT study designed, funded and supported by a
pharmaceutical company warn heavy caffeine users in the placebo group that
unless they cut their caffeine intake by roughly one-half that their blood
serum caffeine level would skyrocket to 203% of baseline within 24 hours
of quitting?[2] What motive was there to stress the importance of
reestablishing normal regular eating patterns or share simple blood-sugar
stabilization techniques, due to abrupt cessation ending nicotine induced
adrenaline releases that pumped stored fats and sugar into the blood with
each puff? [3]
To the contrary, there was zero pharmaceutical or academic economic
incentive to design studies focusing on enhancing placebo group
performance. In fact, imagine depriving newly recovering alcoholics of
their daily bottle and then forcing each to use a placebo bottle
containing the alcohol equivalent of just one drink a day. Could such
practices alter the duration, intensity and/or outcome of recovery?
Believe it or not, the odds ratio victories in many NRT studies employed
placebo devices that administered small amounts of nicotine.[4-6] I
have repeatedly, in both private and public, sought reference to any study
examining the impact of placebo nicotine doctoring but without reply.[7]
In the last eight months, OTC NRT's efficacy credibility has taken a
serious beating yet millions are still being spent marketing "clean-
nicotine" as a stand-alone recovery chemical. In September, we were told
that "NRT appears no longer effective in increasing long-term successful
cessation in California smokers."[8] November brought word that NRT
benefits provided under Minnesota health insurance plans did not "result
in higher rates of quitting smoking."[9] In March we were shocked when
the first ever OTC NRT meta-analysis revealed that the cornerstone of
worldwide cessation policy - OTC NRT - was generating a 93% midyear
smoking relapse rate.[10]
Now that all can see that the emperor has no clothes, those marketing
NRT are giving lip service to the need to combine costly OTC NRT with
lengthy gradual weaning behavioural programs. As they slowly retreat into
the sanctuary of the early NRT studies I pray that those researchers who
have maintained the independence to do so will begin to examine and
question the protocols and content upon which NRT's early conclusions
rest.
As for giving counsel to patients, I couldn't agree more with
Sutherland's conclusion that most physicians are missing a golden
opportunity to motivate smoking patients to commence nicotine dependency
recovery. My concern is when the advice given is to go out and purchase
alterative nicotine delivery devices that carry a 93% chance of early
failure.
A three-second comment like, "Ms. Jones, you need to quit smoking,"
does little more than remind her of the obvious, while leaving her with
nothing of substance. I strongly encourage physicians to spend a couple
of hours exploring the content offered at a few of the wonderful online
cessation education sites. Print those articles, tips and recommendations
that you find interesting, hand them to patients, and then stand back and
watch the magic unfold.
Yes, knowledge is power but how do you peak a patient's interest in
learning? What did ignorant in-the-dark cessation attempts, the patch,
gum, hypnosis or acupuncture teach them? As a doctor you may want to
build a skyscraper but if you don’t know how it can prove rather
challenging. Try something like this to motivate interest in learning.
"Ms. Jones, have you ever done any reading on how your brain reward
pathways are chemically addicted to nicotine, or on the timing and phases
that each nicotine addict must go through in order to once again adjust to
functioning comfortably without nicotine?" "Ms. Jones, there really are
instructions that came with your addiction and I'm a bit surprised that
you have not yet taken the time to read them." "I’ve printed a few
articles that I’d like you to read."
For patients with access to the internet, take the extra step and
actually hand them a list of internet addresses that you've found worthy
of their time. In less than two minutes you'll have given them both hope
and quality guidance!
(2) Swanson, JA, et al. The impact of caffeine use on tobacco
cessation and withdrawal.
Addict Behav 1997;22(1):55-68.
(3) Andersson K, et al. Changes in circulating lipid and
carbohydrate metabolites following systemic nicotine treatment in healthy
men. Int J Obes Relat Metab Disord 1993;17(12):675-80.
(4) Sanderskov J, et al. Nicotine patches in smoking cessation, a
randomized trial among over-the-counter customers in Denmark. Am J
Epidemiol 1997;145:309-18.
(5) Campbell, et al. Transdermal nicotine plus support in patients
attending hospital with smoking-related diseases: a placebo-controlled
study. Respir Med 1996;90(1):47-51.
(6) Ahluwalia JS, et al. Smoking cessation among inner-city African
Americans using the nicotine transdermal patch, Journal of General
Internal Medicine (JGIM) 1998; 13(1):1-8.
(7) Polito JR. OTC NRT 93% Midyear Relapse Rate [electronic response to Hughes JR et al. A meta-analysis of the efficacy of over-the-counter nicotine replacement] tobaccocontrol.com 2003 http://tc.bmjjournals.com/cgi/eletters/12/1/21#88
(8) Pierce, JP, et al. Impact of Over-the-Counter Sales on
Effectiveness of Pharmaceutical Aids for Smoking Cessation. JAMA
2002;288:1260-1264.
(9) Boyle RG, et al. Does insurance coverage for drug therapy
affect smoking cessation? Health Affairs (Millwood). 2002 Nov-
Dec;21(6):162-8.
We read with interest the article by Bouvy and colleagues [1] and the accompanying editorial by Professor Cowie.[2] We would like to congratulate the investigators in attempting to construct a prognostic rule for patients with chronic heart failure. This is a neglected area in heart failure research.
We have recently completed 5-year follow up of a study with the specific aim of identifying independe...
We read with interest the article by Bouvy and colleagues [1] and the accompanying editorial by Professor Cowie.[2] We would like to congratulate the investigators in attempting to construct a prognostic rule for patients with chronic heart failure. This is a neglected area in heart failure research.
We have recently completed 5-year follow up of a study with the specific aim of identifying independent predictors of mortality in patients with mild to moderate chronic heart failure.[3,4] Using over 2000 patient years of follow up and 201 deaths we have constructed our own prognostic index.[5] This index integrates abnormalities of cardiac autonomic and electrical function, metabolic disturbances and abnormalities of cardiac size.
The report by Bouvy et al. has a number of problems, which one should bear in mind before the results are incorporated into clinical practice. As the authors acknowledge the study cohort is a highly selected group of patients taking part in a study not designed to evaluate variables in predicting outcome in chronic heart failure. The variables employed were not selected a priori and this should be recognised as a potential source of bias. Furthermore, this may account for the very impressive C statistic of 0.80 for the model described.
Before one can apply a prognostic rule clinicians should know the exact characteristics of the population in question. Bouvy et al do not present data describing the whole population, markers of heart failure severity such as mean frusemide dose, cardiothoracic ratio and echocardiographic variables are an important part of patient characterisation. Furthermore, renal insufficiency is part of the index yet the authors do not clearly define what they mean by this.
As the authors also admit the prognostic index requires validation in a separate cohort. To give the reader an idea of its internal validity and potential transportability Bouvy et al. should have performed ‘bootstrapping’ [5] or a similar technique.
In conclusion we agree that development of prognostic indices is an important goal for patients with chronic heart failure, and Bouvy et al. have made a commendable attempt at this. However, further details of their study and prospective validation in an adequately powered trial, in a clearly defined population needs to be performed before clinicians can consider transfering the proposed model into clinical practice.
References
(1) Bouvy ML, Heerdink ER, Leufkens HGM, Hoes AW. Predicting mortality in patients with heart failure: a pragmatic approach. Heart 2003;89:605-609.
(2) Cowie MR. Estimating prognosis in heart failure: time for a better approach. Heart 2003;89:587-588.
(3) Kearney MT, Fox KA, Lee AJ et al. Predicting death due to progressive heart failure in patients with mild-to-moderate chronic heart failure. J Am Coll Cardiol 2002;40:1801-8.
(4) Kearney MT, Zaman A, Eckberg DL et al. Cardiac size, autonomic function, and 5-year follow-up of chronic heart failure patients with severe prolongation of ventricular activation. J Card Fail 2003;9:93-9.
(5) Kearney MT, Nolan J, Lee AJ et al. A prognostic index to predict long-term mortality in patients with mild to moderate chronic heart failure stabilised on angiotensin converting enzyme inhibitors. Eur J Heart Fail; in press
Recently a reporter from the Arizona Republic wrote an article that cited your study[1] on vigorous exercise. The author stated that "a half-hour brisk walk every day may make you feel better, but it is not enough to ward off premature death from heart trouble."
As a public health specialist it concerns me that we are sending
mixed messages to the public. In the United States approximately 60% of...
Recently a reporter from the Arizona Republic wrote an article that cited your study[1] on vigorous exercise. The author stated that "a half-hour brisk walk every day may make you feel better, but it is not enough to ward off premature death from heart trouble."
As a public health specialist it concerns me that we are sending
mixed messages to the public. In the United States approximately 60% of
the population is not even getting 30 minutes of moderate physical
activity. If we tell them that only vigorous activity counts (keeping in
mind that they are not doing moderate activity), is it realistic to think
that they are going to do vigorous activity?
I would appreciate any comments the authors may have.
Reference
(1) S Yu, J W G Yarnell, P M Sweetnam, and L Murray. What level of physical activity protects against premature cardiovascular death? The Caerphilly study. Heart 2003; 89:502-506.
I couldn't help but sit up and take notice of the news this morning, which made reference to this paper on
physical activity and heart disease.[1] Obviously the news reporters are free to say what they like but I am concerned about some key weakness in this study, which has
let the press loose on stating that brisk walking does not help prevent heart disease. It is well known and accepted practice within spo...
I couldn't help but sit up and take notice of the news this morning, which made reference to this paper on
physical activity and heart disease.[1] Obviously the news reporters are free to say what they like but I am concerned about some key weakness in this study, which has
let the press loose on stating that brisk walking does not help prevent heart disease. It is well known and accepted practice within sports medicine and exercise science to
describe exercise intensity in terms relative to an individual's level of fitness and not in absolute terms. The Yu paper only described the activity indexes in absolute terms and thus we have no idea what proportion of the individual participants' aerobic capacity was being challenged in the low to moderate activity categories.
A recent meta-analysis by P Williams [2] did confirm from the evidence that higher intensity aerobic fitness
promoting activity, provided greater prevention of CHD and CVD than did lower to moderate habitual physical activity but that the latter still had a profilactic effect on
CHD/CVD. Furthermore, the work done by Professor Hardman's group and colleagues at Loughborough showed that in middle aged women, brisk walking did result in enhancing
aerobic fitness as well as well as improving healthier levels of serum cholesterol both of which would provide CHD protection.
I was greatly disappointed to see that with
much medical screening of the subjects in the Yu et al. study that they left out an all important fitness test, which is paramount in determining the "intensity threshold" at
which improvements take place. It is quite wholly possible that for many, the habitual physical activity described in absolute terms of intensity may not elicit a level above a
training threshold (e.g. 50% of VO2 max). Aerobic capacity is greatly a function of genetics and gender (which can be independent of levels of physical activity).
As this
study was only done on males, and females tend to have lower aerobic capacities, then this makes for a second weakness of the study; it leaves out 50% of our population. For the unfit person brisk walking may well reqiure the participant to utilise more than 50% of their aerobic capacity, which would thus fit into the moderate to
higher intensity exercise zone that can lead to a training effect and these are the people in most need of taking up the Government's physical activity initiatives. Therefore,
without a description of fitness in the Yu et al. study, we are left with a very big question mark over the differentiation of exercise intensities (Activity Indexes), which were defined.
References
(1) S Yu, J W G Yarnell, P M Sweetnam, and L Murray.
What level of physical activity protects against premature cardiovascular death? The Caerphilly study. Heart 2003;89:502-506.
(2) Williams PT. Physical fitness and activity as separate heart disease risk factors: a meta-analysis.
Med Sci Sports Exerc 2001;33(5):754-61.
1. The questionnaire was modified only in relation to differences in
American and British sports, for example in Britain softball, paddle ball
and raquet ball are rarely played and there is very little hunting for
large game. We included some activities such as mixing cement and we used
approximate equivalents for this activity using a mixer or...
1. The questionnaire was modified only in relation to differences in
American and British sports, for example in Britain softball, paddle ball
and raquet ball are rarely played and there is very little hunting for
large game. We included some activities such as mixing cement and we used
approximate equivalents for this activity using a mixer or at a higher
intensity if done by hand. In particular we did not downgrade any high
intensity codes to moderate intensity codes.
2. The vigorous activity was usually done on top of light and
moderate intensity activity as Table 3 in the paper makes clear. The
trends for the total activity are significant, particularly for CHD.
3. We combined light and moderate activity only to reduce the number
of tables to 6 instead of 7 as the separate tables showing light or
moderate activity showed no trend whatsoever with increasing activity and
mortality.
4.
Trends were examined with both thirds and fifths of distribution
separately for light and moderate intensity activity and no trends were
detected.
Reference
(1) LaMonte MJ, Adams TD, Yanowitz FG. Lowering CVD risk: walk before we run [electronic response to Yu et al. What level of physical activity protects against premature cardiovascular death? The Caerphilly study] heartjnl.com 2003 http://heart.bmjjournals.com/cgi/eletters/89/5/502#153
Dear Editor
We read with great interest the article recently published in "Heart" on the current use of anticoagulation for non-valvar atrial fibrillation [1].
This article analyses the use of aspirin and anticoagulant treatment in 313 consecutive patients, presented with chronic atrial fibrillation of non-valvar etiology, in a single hospital in Northern Italy, from January 1 to June 30 2000. From th...
Dear Editor
I thank John Polito for his lengthy reply to my article. I will try to discuss some of his points as far as I understand them.
Firstly, no, my article is not a "commercial" for nicotine replacement! If anything it is a "commercial" for specialist psychological support. My intention was to present the data and these indicate that there is a role for both types of treatment for smokers. The data I...
Dear Editor
We read the recent published paper by Mueller and co-workers.[1] They demonstrate convincingly that the neutrophil count is a strong predictor for future coronary events in patients with acute coronary syndromes. Smoking habits, however, may to some extent confound their results.[2] To verify the assumption we want to publish this scientific note.
Neutrophil granulocytes are a well-recogn...
Dear Editor
In response to Tammy Vehige et al,[1] we had recognised that our findings may be controversial, but these were rigorously evaluated by ourselves and others before publication. However, to put it in context, it is one study amongst a particular population of healthy, middle-aged men of whom about 40% appeared to be doing enough vigorous intensity activity to confer cardiovascular benefit. The pape...
Dear Editor
In response to Dr Buckley [1] we agree that data on cardiovascular fitness would have been a useful addition to our study but resources in terms of staff and equipment precluded this possibility. In an ideal study, both cardiovascular fitness and questionnaire data would be obtained in parallel and in a long term cohort study habitual physical activity should be re-assessed at intervals.
Refer...
Dear Editor
Is this abstract yet another nicotine commercial urging physicians to deprive patients of another of their diminishing windows of opportunity to begin allowing their reward pathways to sense the arrival of nicotine-free blood serum? I want to share a bit of contrary patient cessation counsel but first some background on why.
I question this abstract's broad assertion that the "[use] of ...nicoti...
Dear Editor
We read with interest the article by Bouvy and colleagues [1] and the accompanying editorial by Professor Cowie.[2] We would like to congratulate the investigators in attempting to construct a prognostic rule for patients with chronic heart failure. This is a neglected area in heart failure research.
We have recently completed 5-year follow up of a study with the specific aim of identifying independe...
Dear Editor
Recently a reporter from the Arizona Republic wrote an article that cited your study[1] on vigorous exercise. The author stated that "a half-hour brisk walk every day may make you feel better, but it is not enough to ward off premature death from heart trouble."
As a public health specialist it concerns me that we are sending mixed messages to the public. In the United States approximately 60% of...
Dear Editor
I couldn't help but sit up and take notice of the news this morning, which made reference to this paper on physical activity and heart disease.[1] Obviously the news reporters are free to say what they like but I am concerned about some key weakness in this study, which has let the press loose on stating that brisk walking does not help prevent heart disease. It is well known and accepted practice within spo...
Dear Editor
In reply to Michael LaMonte et al.[1]:
1. The questionnaire was modified only in relation to differences in American and British sports, for example in Britain softball, paddle ball and raquet ball are rarely played and there is very little hunting for large game. We included some activities such as mixing cement and we used approximate equivalents for this activity using a mixer or...
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