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.
Assessment of QT Interval and QT Dispersion for Prediction of All-Cause
and Cardiovascular Mortality in American Indians. The Strong Heart Study.
Circulation. 2000;101:61-6.
5. Hodges M. Rate Correction of the QT Interval. Card Electrophysiol Rev
1997; 1:360-3.
6. Batchvarov VN, Ghuran A, Smetana P, Hnatkova K, Harries M, Dilaveris P,
Camm AJ, Malik M. QT-RR relationship in healthy subjects exhibits
substantial intersubject variability and high intrasubject stability. Am J
Physiol Heart Circ Physiol 2002; 282: H2356–H2363.
7. Brendorp B, Elming H, Jun L, Køber L, Malik M, Jensen GB, Torp-Pedersen
C, for the DIAMOND Study Group. QTc Interval as a Guide to Select Those
Patients With Congestive Heart Failure and Reduced Left Ventricular
Systolic Function Who Will Benefit From Antiarrhythmic Treatment With
Dofetilide. Circulation. 2001; 103:1422-7.
8. Fauchier L, Maison-Blanche P, Forhan A, D’Hour A, Le´pinay P, Tichet J,
Vol S, Coumel P, Fauchier JP, Balkau, B, and the DESIR Study Group.
Association Between Heart Rate–Corrected QT Interval and Coronary Risk
Factors in 2,894 Healthy Subjects (The DESIR Study). Am J Cardiol 2000;
86:557-9.
9. Malik M. Problems of Heart Rate Correction in Assessment of Drug-
Induced QT Interval Prolongation. J Cardiovasc Electrophysiol 2001;12:411-
20.
Newman's article [1] underscores the link
between thoughts (cognitions), emotions and the behaviour that results
from the combination. This is the basis of psychology but this model of
human behaviour is not always understood by Cardiology colleagues.
It is
sometimes assumed that health threatening behaviour, for example
continuing to smoke after a cardiac event, is a form of willful self-
negle...
Newman's article [1] underscores the link
between thoughts (cognitions), emotions and the behaviour that results
from the combination. This is the basis of psychology but this model of
human behaviour is not always understood by Cardiology colleagues.
It is
sometimes assumed that health threatening behaviour, for example
continuing to smoke after a cardiac event, is a form of willful self-
neglect or the result of lack of knowledge about the harmful effects of
smoking.
As a result of this inappropriate model of behaviour, inappropriate
interventions are offered: more education by nurses or scare tactics by
the cardiologist. Although each may work for a small number of people,
neither is optimally effective as it does not target the belief system
that maintains the emotional distress and perpetuates the behaviour.
Cardiology care would be more effective if it adopted a model of behaviour
that is consistent with the evidence base. The time is right for cross-
fertilisation of evidence and Psychologists have a responsibility to make
this available to Cardiologists who, inturn, have a responsibility to use
it.
Reference
(1) Newman S. The psychological perspective: a professional view. Heart 2003; 89: 16ii-18ii
In their recent article,[1] Martin et al. describe an interesting
modelling exercise to estimate the need for coronary revascularisation
based on the incidence of indications. We have used this population
perspective model to help inform our current review of angiography
services in Northumberland by using local data and report here the
experience of using this model as a planning tool for a...
In their recent article,[1] Martin et al. describe an interesting
modelling exercise to estimate the need for coronary revascularisation
based on the incidence of indications. We have used this population
perspective model to help inform our current review of angiography
services in Northumberland by using local data and report here the
experience of using this model as a planning tool for angiography
commissioning.
Instead of comparing current practice to the model of need as in
Martin’s paper, we compared maximum and minimum values of parameters
available for all three indications up to Parameter 4 (number of those
referred to secondary care undergoing angiography).
For Parameters 1 and 2, incidence and prevalence data was extracted
from local Hospital Episode Statistics (HES) and the Northumberland MEDICS
project[2] which is a primary care data collection system that regularly
feeds back comparative reports of morbidity and clinical care indicators
to practices. Where data was unavailable, four GP practices which record
high quality ischaemic heart disease computerised data supplied rates
which were extrapolated to the Northumberland population. Referral rates
for chronic stable angina quoted in Martin’s paper were used as upper and
lower limits. Parameter 1 was not computed for acute MI and unstable
angina as the sources of data fed into Parameter 2 only. We assumed 100%
survival for Parameter 3 in chronic stable angina. Local HES data
survival rates in the other indications groups was compared to that
supplied by Martin. Angiography referral rates in Parameter 4 for cardiac
origin chest pain from rapid access chest pain clinic reports were
utilised for chronic stable angina. The upper limit was kept at 51%
following a previous review of angiography rates in Newcastle upon Tyne
which showed a similar result. We had no local data for acute MI and
unstable angina referral rates so Martin’s figures were used.
Table
of incidence of indications in Northumberland approach to angiography
rates for revascularisation
Presentation
Chronic
Stable Angina
Acute
Myocardial Infarction
Unstable angina
Total
Parameter
Min
Max
Min
Max
Min
Max
Min
Max
1
Number
of total population of Northumberland (aged 45-84) developing new clinical
presentation*
1934
(1.5%)
2128
(1.6%)
2
Number
of incident cases referred to secondary care
638
(33%)
1532
(72%)
459
674
567
665
1664
2871
3
Number
surviving to angiography
638
(100%)
1532
(100%)
403
(88%)
607
(90%)
550
(97%)
660
(99.3%)
1591
2799
4
Number
of those referred to secondary care undergoing angiography
89
(13.9%)
781
(51%)
32
(8%)
182
(30%)
148
(27%)
330
(50%)
269
1294
*including
15% of prevalent cases for chronic stable angina
The range of angiography need was wide (269 to 1294). The highest
figure would be the maximum number of angiographies needed if best
practice is applied to all patients and is therefore aspirational. The
key step where more detailed data would make the tool more precise for
planning is the chronic stable angina referral rate to secondary care. If
the lower referral limit of 33% (current practice based on the general
Practice Research Database) and the maximum number of incident cases for
chronic stable angina are used, the total number of angiographies required
would be between 269 and 870. Our current projected angiography rate of
512 in the last financial year sits in the middle of this range. Better
local recording of angiography rates for acute MI and unstable angina
would also improve the model’s precision.
Using the model as a planning tool obviously has some limitations,
which Martin acknowledges will either over or under estimate the need. In
addition to these is the effect that the RITA 3[3] trial may have on
increasing intervention during acute coronary syndromes. The changing
diagnosis of Acute MI could also lead to the misclassification of
diagnoses. The generalisability of extrapolating incident data from a few
GP practices is questionable but the rates did agree with population data
except for unstable angina where the GP rates were grossly less than the
HES data and were therefore excluded. Because of the limitations of our
local data, non-standardised rates were used throughout our model.
We felt overall the model was useful as a guide and helped focus our
thoughts on angiography from a population perspective. It helped compare
current with aspirational practice. However, from a commissioner’s
perspective, the maximum rates are aspirational and major changes in the
referral patterns from primary care would have to take place to meet them.
We recommend further studies look at current and optimum referral rates
for chronic stable angina based on need.
References
(1) Martin RM, Hemingway H, Gunnell D, Karsch KR, Baumbach A, Frankel S.
Population need for coronary revascularisation: are national targets for
England credible? Heart 2002;88:627-633.
(2) Edwards R, Murphy P, Allan K, Gordon S, Singleton S. Comparative
morbidity data in primary care: the Northumberland MEDICS project. Primary
Health Care Research and Development 2002;3:217-227.
(3) Fox KA, Poole-Wilson PA, Henderson RA, Clayton TC, Chamberlain DA, Shaw
TR, Wheatley DJ, Pocock SJ, Randomized Intervention Trial of unstable
Angina I. Interventional versus conservative treatment for patients with
unstable angina or non-ST-elevation myocardial infarction: the British
Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of
unstable Angina. Lancet 2002;360:743-51.
We wish to thank Claudia Stöllberger and Josef Finsterer very much for their comments on our paper.
The primary aim of our study was to correlate clinical risk factors for
thromboembolism with transoesephageal markers of a thrombogenic milieu.
Actually, we could demonstrate that those parameters were related
closely. 58.8% of patients with clinical risk factors had a thrombogenic
milieu. An incre...
We wish to thank Claudia Stöllberger and Josef Finsterer very much for their comments on our paper.
The primary aim of our study was to correlate clinical risk factors for
thromboembolism with transoesephageal markers of a thrombogenic milieu.
Actually, we could demonstrate that those parameters were related
closely. 58.8% of patients with clinical risk factors had a thrombogenic
milieu. An increasing number of clinical risk factors was correlated with
a higher incidence of a thrombogenic milieu. Stöllberger et al. is correct
that we also observed the absence of a thrombogenic milieu on
transoesophageal echocardiography (TOE) despite the presence of clinical
risk factors in a small number of patients (17.4%). Since a number of
studies demonstrated that patients with atrial fibrillation and a TOE
finding of a thrombogenic milieu have an increased thromboembolic risk we
suggested that patients without clinical risk factors and a thrombogenic
milieu may have an increased thromboembolic risk.[1,2] In contrast to
the latter studies, Stöllberger and coworkers did not analyze peak
emptying velocities in their study and did not account for different
degrees of spontaneous echo contrast.[3] This may explain, why
Stöllberger et al. did not identify a thrombogenic milieu as an
independent risk factor for thromboembolism in their study. The technical
aspects of analyzing left atrial appendage function was published in a
number of studies by our study group and others.[4-9] We agree that the
value of systematic TOE screening in all patients with atrial fibrillation
has to be assessed in future prospective studies as already stated in our
paper. Nevertheless, it would be useful for planning large scale
prospective studies to know the incidence of a thrombogenic milieu in
patients with and without clinical risk factors.
References
(1) Leung DY, Black IW, Cranney GB, Hopkins AP, Walsh WF. Prognostic
implications of left atrial spontaneous echo contrast in nonvalvular
atrial fibrillation.
J Am Coll Cardiol 1994;24:755-762
(2) The Stroke Prevention in Atrial Fibrillation Committee on Echocardiography. Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med 1998;128:639-647
(3) Stöllberger C, Chnupa P, Kronik G, Brainin M, Finsterer J,
Schneider B, Slany J.
Transesophageal echocardiography to assess embolic risk in patients with
atrial fibrillation.
Ann Intern Med 1998;128:630-638
(4) Chan SK, Kannam JP, Douglas PS, Manning WJ. Multiplane
transesophageal assessment of left atrial appendage anatomy and function.
Am J Cardiol 1995;76(7):528-530
(5) Agmon Y, Khandheria BK, Gentile F, Seward JB. Echocardiographic
assessment of the left atrial appendage.
J Am Coll Cardiol 1999;34(7):1867-1877
(6) Omran H, Jung W, Rabahieh R, Schimpf R, Wolpert C, Hagendorff A, Fehske W, Lüderitz B. Left atrial chamber and appendage function after
internal atrial defibrillation: a prospective and serial transesophageal
echocardiographic study.
J Am Coll Cardiol 1997;29(1):131-8.
(7) Omran H, Jung W, Rabahieh R, Wirtz P, Becher H, Illien S, Schimpf
R, Lüderitz B. Imaging of thrombi and assessment of left atrial appendage
function: a prospective study comparing transthoracic and transoesophageal
echocardiography.
Heart 1999;81(2):192-8.
(8) Omran H, Rang B, Schmidt H, Illien S, Schimpf R, MacCarter D,
Kubini R, von der Recke G, Tiemann K, Becher H, Lüderitz B. Incidence of
left atrial thrombi in patients in sinus rhythm and with a recent
neurologic deficit.
Am Heart J 2000 Oct;140(4):658-62.
(9) Schmidt H, von der Recke G, Illien S, Lewalter T, Schimpf R,
Wolpert C, Becher H, Lüderitz B, Omran H. Prevalence of left atrial
chamber and appendage thrombi in patients with atrial flutter and its
clinical significance.
J Am Coll Cardiol 2001;38(3):778-84.
We are grateful to Dr Francis for his response to our analysis [1] of
the real implications, both clinical and financial, of implementing a
policy of implanting drug-eluting stents. He has stated the case rather
more starkly than we did, but we would agree that the main problem is
pricing. If these new stents were only slightly more expensive than the
current (rather satisfactory) generation of con...
We are grateful to Dr Francis for his response to our analysis [1] of
the real implications, both clinical and financial, of implementing a
policy of implanting drug-eluting stents. He has stated the case rather
more starkly than we did, but we would agree that the main problem is
pricing. If these new stents were only slightly more expensive than the
current (rather satisfactory) generation of conventional stents, they
would be implanted universally. At the price at which they have been
pitched, the manufacturers are forcing us to analyse which patients and
lesions we should target with a policy of limited implantation. This
requires a detailed knowledge of the risks and benefits inherent in
tackling the problem of restenosis – a problem which we demonstrated, in
our analysis, to be one which obeys a law of diminishing returns. For
sure, limited extra expenditure will reduce the restenosis rate, but only
marginally; stent expenditure would have to triple or quadruple to
eliminate the last few patients with restenosis. Is this justified, when
many more cases could be treated with conventional technology with the
same budget?
We would not want to give the impression that current drug-elution
costs are ‘never financially justifiable’; rather, they make us sit up and
think about what we are actually achieving with this huge increase in
expenditure. We are not sure NICE will help selectivity. NICE may well
endorse the use of this product in the lesion types included in RAVEL [2]
and SIRIUS [3] trials. We will then have a clinical mandate to use them
in a large proportion of our patients, but this will not solve the
financial dilemma. Competition with other devices is the most likely long-term solution to this conundrum.
References
(1) Gunn J, Morton A, Wales C, Newman C, Crossman D, Cumberland D. Drug-eluting stents: maximising benefit and minimising cost. Heart 2003;89:127-31.
(2) Morice MC, Serruys PW, Sousa JE,et al. A randomised comparison of
a sirolimus-eluting stent with a standard stent for coronary
revascularization. N Engl J Med 2002;346:1773-80.
(3) Moses J, Leon M, et al. The SIRIUS trial. Results presented at
Transcatheter Cardiovascular Therapeutics meeting, Washington DC,
September 24, 2002.
I have read the fifth report on services for patients with coronary
heart disease and while primary care, district, tertiary services, cardiac
nursing etc. all duely given emphasis, nowwhere is there a mention of
cardiac pathology services. Under the chapter on audit, clinical
governence and CPD, I eagerly expected some token reference especially
under Bristol enquiry where autopsy reports formed part...
I have read the fifth report on services for patients with coronary
heart disease and while primary care, district, tertiary services, cardiac
nursing etc. all duely given emphasis, nowwhere is there a mention of
cardiac pathology services. Under the chapter on audit, clinical
governence and CPD, I eagerly expected some token reference especially
under Bristol enquiry where autopsy reports formed part of the enquiry,
but alas not a word!
I believe the provision of an expert pathological
opinion is essential especially in the area of operative deaths and audit
of surgical procedures. Cardiac pathologists are a rare breed and becoming
rarer, with no specific training programme within UK or Europe. Tertiary
centres in particular need their expertise in order to maintain the
highest standard of care and pathologists are an essential part of the
audit process with an emphasis on mortality audit, quality of care and
also education. I consider myself to be an essential member of the
multidisciplinary team, looking after patients during life and monitoring
the outcome after death of both established and innovinative procedures.
In the provision of any service for patients with heart disease, pathology
must be given its due place and not be ignored.
In their interesting study, Illien et al.[1] recently reported that
among 302 consecutive patients with nonrheumatic atrial fibrillation(AF),
8 were detected who had no clinical risk factors for stroke/embolism
(age>65, previous stroke/embolism, arterial hypertension, diabetes
mellitus, heart failure) but a transesophageal echocardiographic(TEE)
finding of a “thrombogenic milieu”, either sponta...
In their interesting study, Illien et al.[1] recently reported that
among 302 consecutive patients with nonrheumatic atrial fibrillation(AF),
8 were detected who had no clinical risk factors for stroke/embolism
(age>65, previous stroke/embolism, arterial hypertension, diabetes
mellitus, heart failure) but a transesophageal echocardiographic(TEE)
finding of a “thrombogenic milieu”, either spontaneous echo contrast(SEC)
or decreased left atrial appendage(LAA) flow velocities. From these
findings, the authors conclude that AF patients without clinical risk
factors and a thrombogenic milieu constitute a subgroup of patients with
increased risk for stroke/embolism. Patients of this subgroup will be
missed at clinical risk stratification. Thus, the practical consequences
of these assumptions would be to perform TEE in all AF patients without
clinical risk factors for stroke/embolism in order to look for a
thrombogenic milieu. There are several objections that have to be raised
against these hypotheses: 1. The authors did not demonstrate that in any of these 8 patients
stroke/embolism had occurred, neither in their previous history nor at
follow-up investigations, which were not carried out. Based on this lack
of information, it is not justified to conclude that these patients have
an increased thromboembolic risk.
2. We have previously shown in a prospective study including 409 AF
patients that SEC and LAA thrombi were no independent risk factors for
stroke/embolism during a follow-up period of 5[2] and 10[3] years.
3. According to the retrospective design of Illien’s study, thromboembolic
risk was only assessed by presence or absence of clinical risk factors. It
has been repeatedly confirmed that there is an association between the
prevalence of spontaneous echo contrast, LAA thrombi, decreased LAA
velocities and clinical risk factors for stroke/embolism. However, no
prospective study demonstrated so far, that spontaneous echo contrast and
decreased LAA flow velocities are risk factors for stroke/embolism
independent from the clinical risk factors.
4. Additionally, no clinical information is provided about the 8 patients
with thrombogenic milieu in the absence of clinical risk factors for
stroke/embolism. Particularly, it is not mentioned, whether they were
treated with betablockers, a condition reported to induce SEC, decrease
LAA flow velocity and promote thrombus formation.[4]
5. Furthermore, measurements of LAA flow velocities in AF are flawed by
influences like heart rate and especially the duration of diastole [5]. It
is not mentioned, how many heart cycles were taken for calculation of the
mean LAA flow velocity, which is of particular importance when
investigating AF patients. Blood pressure values, which also influence LAA
flow velocity, are not given [4,5].
From these objections we conclude that it is still reasonable to assess
the risk for stroke/embolism of AF patients on well established clinical
criteria and not on TEE findings. It would be useful, however, to assess
the risk for stroke/embolism in patients without clinical risk factors for
stroke/embolism, but with spontaneous echo contrast or decreased LAA flow,
by means of a prospective long-term follow-up study.
References
(1) Illien S, Maroto-Järvinen S, von der Recke G, Hammerstingl C, Schmidt
H, Kuntz-Hehner S, Lüderitz B, Omran H. Atrial fibrillation: relation
between clinical risk factors and transesophageal echocardiographic risk
factors for thromboembolism. Heart 2003;89:165-8.
(2) Stöllberger C, Chnupa P, Kronik G, Brainin M, Finsterer J, Schneider B,
Slany J, for the ELAT Study Group. Transesophageal echocardiography to
assess embolic risk in patients with atrial fibrillation. Ann Intern Med
1998:128;630-8.
(3) Stöllberger C, Chnupa P, Abzieher C, Länger T, Finsterer J, Klem I,
Hartl E, Wehinger C, Schneider B. Mortality and rate of stroke or embolism
in atrial fibrillation during long-term follow-up in the ELAT (Embolism in
Left Atrial Thrombi) study. Clin Cardiol 2003 (in press).
(4) Bilge M, Güler N, Eryonucu B, Erkoc M. Does acute-phase beta blockade
reduce left atrial appendage function in patients with chronic nonvalvular
atrial fibrillation? J Am Soc Echocardiogr 2001;14:194-9.
(5) Noda T, Arakawa M, Miwa H, Ito Y, Kagawa K, Nishigaki K, Hirakawa S,
Fujiwara H. Effects of heart rate on flow velocity of the left atrial
appendage in patients with nonvalvular atrial fibrillation. Clin Cardiol
1996;19:295-300.
The authors superbly and convincingly
demonstrate the difference between clear advantage for the patient
(reduced risk of restenosis) and unclear benefit to the healthcare
system (increased cost per lesion managed, or reduced number of
patients manageable per year). Ultimately, mathematical analysis is
likely to reveal that the breakeven point is when the scale factor of
the price of the drug eluting stent e...
The authors superbly and convincingly
demonstrate the difference between clear advantage for the patient
(reduced risk of restenosis) and unclear benefit to the healthcare
system (increased cost per lesion managed, or reduced number of
patients manageable per year). Ultimately, mathematical analysis is
likely to reveal that the breakeven point is when the scale factor of
the price of the drug eluting stent equals the reciprocal of the
scale factor of the total number of procedures required per lesion
(assuming all procedures will be stents, and the drug-eluting
strategy uses exclusively drug-eluting stents).
Thus, in a lesion and patient with a
restenosis risk of 10% for bare stenting (expected number of
procedures = 1.1111...) and 5% for drug-eluting stenting (expected
number of procedures = 1.0525...), the ratio is 1.06. The
drug-eluting strategy is therefore more cost-effective only if the
drug-eluting stent is priced at less than a 6% premium above bare
metal. Not likely!
Considering drug elution to roughly
halve restenosis, we can make the following table of the premium that
can justified for a bare-metal stent for any particular baseline
estimate of restenosis rate.
Baseline restenosis rate (%)
Price premium justifiable for drug coating (%)
0
0
5
3
10
6
20
12
30
21
40
33
50
50
60
75
70
117
80
200
90
450
Therefore, I would go beyond the
conclusions of the paper to say that in a cash-limited health care
system, only when the baseline risk of restenosis is around 90% is it
possibly cost-effective to reach for a drug-eluting stent. Such
lesions are unusual...
Perhaps the government will come to our
rescue with funding? Or NICE give us backing to spend the money
despite these cost-effectiveness facts-of-life? Or maybe price
competition will resolve the problem.
In the meantime, irrespective of
all the above, if I should come in with an acute coronary syndrome,
and any of you should be intervening, please can I have a
drug-eluting stent. Thanks
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...
Dear Editor
Newman's article [1] underscores the link between thoughts (cognitions), emotions and the behaviour that results from the combination. This is the basis of psychology but this model of human behaviour is not always understood by Cardiology colleagues.
It is sometimes assumed that health threatening behaviour, for example continuing to smoke after a cardiac event, is a form of willful self- negle...
Dear Editor
In their recent article,[1] Martin et al. describe an interesting modelling exercise to estimate the need for coronary revascularisation based on the incidence of indications. We have used this population perspective model to help inform our current review of angiography services in Northumberland by using local data and report here the experience of using this model as a planning tool for a...
Dear Editor
We wish to thank Claudia Stöllberger and Josef Finsterer very much for their comments on our paper.
The primary aim of our study was to correlate clinical risk factors for thromboembolism with transoesephageal markers of a thrombogenic milieu. Actually, we could demonstrate that those parameters were related closely. 58.8% of patients with clinical risk factors had a thrombogenic milieu. An incre...
Dear Editor
We are grateful to Dr Francis for his response to our analysis [1] of the real implications, both clinical and financial, of implementing a policy of implanting drug-eluting stents. He has stated the case rather more starkly than we did, but we would agree that the main problem is pricing. If these new stents were only slightly more expensive than the current (rather satisfactory) generation of con...
Dear Editor
I have read the fifth report on services for patients with coronary heart disease and while primary care, district, tertiary services, cardiac nursing etc. all duely given emphasis, nowwhere is there a mention of cardiac pathology services. Under the chapter on audit, clinical governence and CPD, I eagerly expected some token reference especially under Bristol enquiry where autopsy reports formed part...
Dear Editor
In their interesting study, Illien et al.[1] recently reported that among 302 consecutive patients with nonrheumatic atrial fibrillation(AF), 8 were detected who had no clinical risk factors for stroke/embolism (age>65, previous stroke/embolism, arterial hypertension, diabetes mellitus, heart failure) but a transesophageal echocardiographic(TEE) finding of a “thrombogenic milieu”, either sponta...
Dear Editor
The authors superbly and convincingly demonstrate the difference between clear advantage for the patient (reduced risk of restenosis) and unclear benefit to the healthcare system (increased cost per lesion managed, or reduced number of patients manageable per year). Ultimately, mathematical analysis is likely to reveal that the breakeven point is when the scale factor of the price of the drug eluting stent e...
Pages