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
While the debate goes on as to whether elevated office readings with white-coat hypertension are diagnostic inaccuracies, or such patients
are at increased risk of development of vascular disease events such as-
stroke, acute coronary syndromes, congestive heart failure, and
hypertensive renal disease; it becomes all the more vital to be attentive
to detect and distinguish between the clinical entities (su...
While the debate goes on as to whether elevated office readings with white-coat hypertension are diagnostic inaccuracies, or such patients
are at increased risk of development of vascular disease events such as-
stroke, acute coronary syndromes, congestive heart failure, and
hypertensive renal disease; it becomes all the more vital to be attentive
to detect and distinguish between the clinical entities (such as
pseudohypertension and cuff-inflation hypertension) associated with
apparently uncertain therapeutic significance that may even have
confounding effect on the accuracy of the blood pressure recordings in our
routine practice of clinical medicine.
White-coat hypertension is defined as an elevated systolic blood
pressure between 140 and 180 mm Hg in clinic that is associated with a 24-
hour ambulatory systolic BP of less than 140 mm Hg and a diastolic BP less
than 90 mm Hg.[1] Even though such individuals do not really report
nervousness during clinic visits or while performing regular routine
activities; such conditional increases in blood pressure are generally
considered to point to typical anxiety responses. White-coat hypertension
occurs in about 20-40% of individuals. It can be minimized by having a
nurse take the blood pressure rather than the physician himself and can be
confirmed by 24 hours ambulatory blood pressure monitoring.[2]
Nonetheless, physicians still remain unsure of the actual mechanism and
the significance of white-coat hypertension. Although, previously
believed to be a benign medical condition with no evidence of end organ
damage (e.g. left ventricular hypertrophy on echocardiogram); the current
data suggests that the subjects with white-coat hypertension have cardiac
morphological indices in-between those of normotensive people and those
with persistent hypertension.[3] The findings of subclinical carotid
artery atherosclerosis and the presence of endothelial dysfunction in
healthy men with white-coat hypertension indicates that it is relatively
premature to consider this entity as benign.[4-7]
Many elderly people have thickened (atherosclerotic) and /or
calcified arteries; as a result compression of the brachial artery with a
sphygmanometer requires a cuff pressure greater than the one present
within the artery and the thickened vessel will also cease to pulsate more
quickly during diastole leading to more rapid deterioration of Korotkoff
sounds and a higher estimated diastolic blood pressure. So, the net effect
called pseudohypertension is that the systolic and diastolic pressures
estimated from the sphygmanometer may be considerably higher than those
directly measured intra-arterial pressure giving the impression of
hypertension though it is not in true sense.
Pseudohypertension should be suspected in an elderly patient with
marked hypertension (on occasions even labelled as “resistant”) in the
absence of end organ damage and induction of symptoms compatible with
hypoperfusion (e.g. dizziness, weakness, confusion) upon instituting
antihypertensive drug treatment. In addition, these patients may reveal
locomotor brachial on clinical examination of the partly flexed elbow and
the “pipestem calcification” on brachial artery radiograph. The diagnosis
of pseudohypertension can only be confirmed by direct measurement of the
intraarterial pressure but Osler’s maneuver might allow the diagnosis to
be made inflating a sphygmanometer to a level above systolic pressure,
thereby collapsing the radial artery.[8] In this condition, the radial artery
would only be palpable if vascular wall is markedly thickened.
Cuff inflation hypertension needs to be specially mentioned as it may
be confused with the white-coat hypertension or pseudohypertension and may
even be considered in the differential diagnosis of resistant hypertension
if physician is not aware of this entity. Cuff inflation hypertension in
induced by the excess and rapid inflation of cuff to a level far above the
systolic blood pressure and by the muscular activity associated with the
inflating cuff, while blood pressure is measured.[9] A neurogenic theory
has also been postulated. It can be diagnosed by comparing the directly
measured intraarterial diastolic pressure both before and after cuff
inflation, and at the Korotkoff phase V.
References
(1) Khattar RS, Senior R, Lahiri A. Cardiovascular outcome in white-
coat versus sustained mild hypertension: a 10-year follow-up study.
Circulation 1998; 98:1892-97.
(2)The National High Blood Pressure Education Program Coordinating
Committee. The National High Blood Pressure Education Program Working
Party Report on ambulatory blood pressure monitoring. Arch Intern Med 1990;
150:2270-77
(3) Julius S, Mejia A, Jones K, et al. "White coat" versus "sustained"
borderline hypertension in Tecumseh, Michigan. Hypertension 1990; 16:617-
23
(4) Egan BM, Mejia AD, Schork. Artifacts in measurement of blood
pressure 1and lack of target organ involvement in assessment of the
patients with resistant hypertension. Ann Intern Med 1990; 112:270-275
(5) Verdecchia P, Porcellati C, Schillaci G, et al. Ambulatory blood
pressure: an independent predictor of prognosis in essential hypertension.
Hypertension 1994; 24:793-801
(6) Muldoon M. F, Nazzaro P, Sutton-Tyrrell K, Manuck S B. White-Coat
Hypertension and Carotid Artery Atherosclerosis: A Matching Study. Arch Int Med 2000; 160: 1507 -12.
(7) Gómez-Cerezo J, Blanco J R, Garcia IS et al. Noninvasive Study of
Endothelial Function in White Coat Hypertension. Hypertension 2002;
40:304.
(8) Tsapatsaris NP, Napolitana GT, Rotchild J. Osler’s maneuver in an
out-patients clinic setting. Arch Intern Med 1991; 151: 2209-12
(9) Veerman DP, Van Montfrans GA, Weiling W. Effects of cuff inflation
on self-recorded blood pressure. Lancet 1990; 335:451.
Yu et al.[1] presented the association between self-
reported leisure-time physical activity (LTPA) and 10-year cardiovascular
(CVD) mortality among 1975 men who were 49-64 years and free of CVD at
baseline. Based on 111 CVD deaths from 20,703 man-years of exposure, and
after adjustment for selected confounding effects, the investigators
concluded that higher levels of daily energy expenditure in v...
Yu et al.[1] presented the association between self-
reported leisure-time physical activity (LTPA) and 10-year cardiovascular
(CVD) mortality among 1975 men who were 49-64 years and free of CVD at
baseline. Based on 111 CVD deaths from 20,703 man-years of exposure, and
after adjustment for selected confounding effects, the investigators
concluded that higher levels of daily energy expenditure in vigorous
intensity LTPA were significantly related with reduced risk of CVD death.
However, energy expenditure combined from light and moderate intensity
activities was not significantly related to CVD mortality.
The study findings are important as they provide further
documentation of the cardioprotective effects of an active lifestyle. However, we
are concerned about the conflict between the current study’s
conclusion that vigorous physical activity is required to lower
cardiovascular risk and the large evidence base supporting cardiovascular
risk reduction from regular moderate intensity activity.[2-5]
Conclusive evidence for a specific dose-response relationship between
physical activity volume or intensity and CVD mortality remains elusive.[6] A major limitation to assessing, interpreting, and comparing dose-
response characteristics between physical activity and CVD mortality is
considerable inter-study variability in quantifying physical activity as
an exposure variable.[6,7]
We believe measurement issues may underlie the
lack of association between moderate intensity activity and CVD mortality
reported by Yu et al. First, the authors indicate that a physical activity
questionnaire previously validated among middle-aged American men was
modified to survey physical activity among the study’s cohort of British
men. It is known that responses to physical activity questionnaires vary
by age, sex, race-ethnicity, and sociocultural factors.[7] Therefore, it
would be useful to know how the questionnaire’s original format was
modified and whether these changes altered the validity and reliability
characteristics of the physical activity measure, particularly with
respect to moderate intensity activities which are more difficult to
recall than vigorous intensity activities.[7] Second, the observed
association between energy expended in vigorous intensity activity and CVD
mortality is based on a relatively small proportion of the sample’s total
energy expenditure (see Yu et al, Table 1), which should be taken into
account when interpreting the practical implications of these findings.
Third, the authors collapsed energy expended in light activity with energy
expended in moderate activity without providing a rationale for this
aspect of their analysis. The more appropriate examination of the effect
of energy expended in different intensities of leisure physical activity
on CVD mortality would come from separate models of the association
between intensity-specific energy expenditure and CVD mortality.[8]
Furthermore, current public health recommendations indicate the
cardioprotective effects of physical activity are derived mostly from
energy expended in moderate-to-vigorous intensity activities with an
absence of evidence supporting such benefits from light intensity
activities.[2-5] It, therefore, seems the author’s analytic model
combining light and moderate intensity activity is contrary to existing
evidence and should be justified in their text. We believe this approach
would suppress the true effect of moderate intensity energy expenditure on
CVD mortality, and bias the strength of association for the model of
“light-moderate intensity” activity and CVD mortality towards the null. We
are concerned that misinterpretation of this finding will result in
confusion among practitioners as to the appropriate type of activity to
recommend to sedentary or irregularly active individuals. More
importantly, this might dissuade such individuals from adopting a more
active lifestyle of moderate intensity activities through which
substantial health benefits and cardiovascular risk reduction can be
obtained.[2,6]
References
(1) Yu S, Yarnell JWG, Sweetnam PM, and Murray L. What level of
physical activity protects against premature cardiovascular death? The
Caerphilly study. Heart 2003;89:502-506.
(2) Fletcher GF, Blair SN, Blumenthal J. et al. Statement on exercise:
benefits and recommendations for physical activity programs for all
Americans. Circulation 1992;86:340-344.
(3) US Department of Health and Human Services. Physical Activity
and Health: A Report of the Surgeon General. Atlanta, GA: USDHHS, Centers
for Disease Control and Prevention, National Center for Chronic Disease
Prevention and Health Promotion, 1996.
(4) Pate RR, Pratt M, Blair SN, et al. Physical activity and public
health: a recommendation from the Centers for Disease Control and
Prevention and the American College of Sports Medicine. JAMA 1995;273:402-407.
(5) NIH Consensus Development Panel on Physical Activity and
Cardiovascular Health. Physical activity and cardiovascular health. JAMA 1996;276:241-246.
(6) Kohl HW. Physical activity and cardiovascular disease: evidence
for a dose-response. Medicine and Science in Sports and Exercise 2001;33(6 Suppl):S472-S483.
(7) LaMonte MJ, and Ainsworth BE. Quantifying energy expenditure and
physical activity in the context of dose response. Medicine and Science in
Sports and Exercise 2001;33(6 Suppl):S370-S378.
(8) Lee IM and Paffenbarger RS. Associations of light, moderate and
vigorous intensity physical activity with longevity. The Harvard Alumni
Health Study. American Journal of Epidemiology 2000;151:293-299.
We read with interest the report by Wong et al [1], one of the very
few [2,3] to demonstrate prognostic value of prolonged heart rate-
corrected QT (QTc) interval in patients with stroke. In clinical practice,
repolarisation abnormalities occurring during cerebrovascular incidents
such as “cerebral T-waves” are still regarded merely as a
electrocardiographical (ECG) peculiarity with no other significa...
We read with interest the report by Wong et al [1], one of the very
few [2,3] to demonstrate prognostic value of prolonged heart rate-
corrected QT (QTc) interval in patients with stroke. In clinical practice,
repolarisation abnormalities occurring during cerebrovascular incidents
such as “cerebral T-waves” are still regarded merely as a
electrocardiographical (ECG) peculiarity with no other significance but
the potential of confounding the ECG interpretation. The report by Wong et
al [1] will help to change this attitude.
However, similar to some other reports about the prognostic value of
the QTc interval [4], Wong et al have provided no data about the heart
rate, which is likely to have been higher in victims of cardiac and total
mortality compared to survivors. It is well known that Bazett formula
generally renders QTc intervals that are positively correlated with heart
rate, and thus artificially prolonged and artificially shortened at higher
and lower heart rates, respectively [5]. The degree of this artefact of
Bazett’s correction is impossible to predict because the relation between
QT interval and heart rate differs between different individuals [6] and,
hence also between different populations. Bazett’s formula can be applied
safely (i.e. producing QTc intervals not significantly correlated with
heart rate) only within a very narrow range of resting heart rates around
60 beats per minute.
In studies testing the association between QTc interval and outcome
it seems therefore imperative not only to report the heart rate, but also
to include it as a separate variable in addition to the QTc (Bazett)
interval in multivariate regression models [7]. A superior strategy is to
apply linear and non-linear regression analysis to the pooled QT and RR
interval data of all patients and to derive the optimum heart rate
correction for the particular dataset of the given study (i.e. a
correction that provides QTc intervals uncorrelated with the RR intervals)
[8,9].
References:
1. Wong KYK, Mac Walter RS, Douglas D, Fraser HW, Ogston SA, Struthers AD.
Long QTc predicts future cardiac death in stroke survivors. Heart 2003;
89:377–81.
2. Singla SL, Jagdish, Garg P, Mehta RK. Electrocardiographic changes in
craniocerebral trauma -could they serve as prognostic indicators? J Indian
Med Assoc 2002; 100:188-90.
3. Villa A, Bacchetta A, Milani O, Omboni E, QT interval prolongation as
predictor of early mortality in acute ischemic stroke patients. Am J Emerg
Med 2001; 19: 332-3.
4. Okin PM, Devereux RB, Howard BV, Fabsitz RR, Lee ET, Welty TK.
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20.
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...
Dear Editor
While the debate goes on as to whether elevated office readings with white-coat hypertension are diagnostic inaccuracies, or such patients are at increased risk of development of vascular disease events such as- stroke, acute coronary syndromes, congestive heart failure, and hypertensive renal disease; it becomes all the more vital to be attentive to detect and distinguish between the clinical entities (su...
Dear Editor
Yu et al.[1] presented the association between self- reported leisure-time physical activity (LTPA) and 10-year cardiovascular (CVD) mortality among 1975 men who were 49-64 years and free of CVD at baseline. Based on 111 CVD deaths from 20,703 man-years of exposure, and after adjustment for selected confounding effects, the investigators concluded that higher levels of daily energy expenditure in v...
Dear Editor,
We read with interest the report by Wong et al [1], one of the very few [2,3] to demonstrate prognostic value of prolonged heart rate- corrected QT (QTc) interval in patients with stroke. In clinical practice, repolarisation abnormalities occurring during cerebrovascular incidents such as “cerebral T-waves” are still regarded merely as a electrocardiographical (ECG) peculiarity with no other significa...
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