Herlitz and colleagues [1] paint a rather gloomy
picture of the impact of 20 years of effort in managing out of hospital
cardiac arrest. Their large population observations are very valuable and
will have a familiar feel to many practising cardiologists. The study
showing survival rates over the last 20 years have not improved is
comparable to previous studies.[2,3] If survival rates for victims of out-...
Herlitz and colleagues [1] paint a rather gloomy
picture of the impact of 20 years of effort in managing out of hospital
cardiac arrest. Their large population observations are very valuable and
will have a familiar feel to many practising cardiologists. The study
showing survival rates over the last 20 years have not improved is
comparable to previous studies.[2,3] If survival rates for victims of out-
of-hospital cardiac arrest are to improve, then one possible avenue is to
explore in greater detail the events leading up to the arrest. One aspect
we feel should be highlighted more clearly is the critical impact of
patient contact prior to any event.
Patients with known illness may contact support services early or may
defer contact such that arrest occurs in an unmonitored setting clearly
putting resuscitation attempts and survival at a disadvantage. This is
poorly defined in what is otherwise an extensively researched area.
Second, those patients with no prior medical contacts may react
differently again either presenting with undiagnosed or ‘atypical’
symptoms to one or other health professional. They may be treated for a
non-cardiac diagnosis that proves incorrect only in retrospect. Whilst
data on previous medical history (acute myocardial infarction, angina
pectoris, congestive heart failure and smoking status) were included in
Herlitz database there was typically no data on victims with no documented
previous medical history, and in particular whether these victims have any
contact with medical services in the hours or days prior to the event.
While information from relatives may be difficult to collect and perhaps
painful for the individual families, they might provide useful details on
circumstances prior to an individual arrest.
What we need to define by such work is whether there is a window of
opportunity for early intervention in these events, which could be
critical in defining individual outcome. It is not known what proportion
of victims of out-of-hospital cardiac arrest have occult cardiac or non-
cardiac disease whose first presentation is the cardiac arrest. This would
be an important finding as it would mean that appropriate diagnostic
effort could potentially abort these events. Unfortunately there was
minimal data in the current report on a final pathological diagnosis on
discharge from hospital.
The second useful point to emerge from Herlitz’s work involves the
poorer survival associated with diuretic use. The authors understandably
suggested the common association with cases of ‘congestive heart failure’.
This is a common presumption but in many studies a significant proportion
of people who are on diuretic therapy do not have any evidence of left
ventricular dysfunction even with a presumed ‘heart failure’ diagnosis in
the community.[4] That impaired systolic function is strongly associated
with sudden cardiac death is not at issue. Thiazide diuretic treatment is
far more often a marker of hypertension and this would be more likely to
be associated with occlusive coronary events than primary or secondary
arrhythmia in systolic dysfunction. Clearly this is important in terms of
the best therapeutic strategies that for coronary occlusive disease would
be accelerated revascularisation rather than for example device management
of arrhythmia in an already impaired left ventricle. Unfortunately the
population data presented by Herlitz or indeed from any comparable
database do not allow this to be defined.
In summary Herlitz large epidemiological survey serves to underline
the pressing need for new approaches to out of hospital arrest over and
above the fine tuning of resuscitation algorithms which are basically
showing little real progress despite the huge efforts of those concerned.
The published data look bleak on first reading but the outcome may be
improved by more detailed individual case recognition and should start
with more research on the perception of illness by patients in these
critical cases. Are all sudden arrests truly sudden/instantaneous or could
there be an early pattern of atypical symptoms in some prior to the
arrest? Surely Herlitz summary data shows well enough that continuing with
the current patterns is just not good enough?
References
(1) Herlitz J, Bång A, Gunnarsson J, Engdahl J, Karlson BW, Lindqvist J, Waagstein L. Factors associated with survival to hospital discharge among patients hospitalised alive after out of hospital cardiac arrest: change in
outcome over 20 years in the community of Göteborg, Sweden.
Heart 2003;89:25-30.
(2) Nichol G, Detsky AS, Steill IG, O’Rourke K, Wells G, Laupacis A.
Effectiveness of emergency medical services for victims of out-of-hospital
cardiac arrest: a metaanalysis. Ann Emerg Med 1996;27:700-710.
(3) Eisenberg MS, Horwood BT, Cummins RO, Reynolds-Haertle R, Haerne
TR. Cardiac arrest and resuscitation: a tale of 29 cities. Ann Emerg Med
1990;19:179-180.
(4) Davies MK, Hobbs FDR, Davis RC, Kenkre JE, Raolfe AK, Hare R,
Wosornu D, Lancashire RJ. Prevalence of left-ventricular systolic
dysfunction and heart failure in the Echocardiographic Heart of England
Screening Study: a population based study. Lancet 2001;358:439-44.
We read with extreme interest the timely scientific letter which
addresses "why …UK surgeons not perform their first choice operation [all
arterial revascularization] for coronary artery bypass graft(ing)".[1]
The results are intriguing and confirm a related study recently published
by our group following a survey of US surgeons called "Is hybrid coronary
revascularization favored by cardiologists...
We read with extreme interest the timely scientific letter which
addresses "why …UK surgeons not perform their first choice operation [all
arterial revascularization] for coronary artery bypass graft(ing)".[1]
The results are intriguing and confirm a related study recently published
by our group following a survey of US surgeons called "Is hybrid coronary
revascularization favored by cardiologists or cardiac surgeons".[2]
Hybrid revascularization, also called integrated coronary
revascularization is a combined revascularization strategy. Typically, the
left internal mammary artery (LIMA) to left anterior descending (LAD)
artery anastomosis is performed via a minimally invasive approach (MIDCAB,
minimally invasive direct coronary artery bypass, or its robotic
equivalent) and non-LAD targets are revascularized percutaneously using
stents.
In our survey, surgeons and cardiologists were asked what the
optimal revascularization strategy was for the non-LAD target. As
expected, 68% of cardiologists believed that their current stents had
better patency rates than saphenous vein grafts anastomosed to non-LAD
targets. 75% of surgeons, however, believe that vein
grafts are better than stents for non-LAD targets. Both surgeons and
cardiologists believe in the "all arterial revascularization" strategy,
unanimously agreeing that almost every patient receive a LIMA anastomosis
for LAD disease, 78% of cardiologists support arterial conduits over vein
grafts to non-LAD targets.
Our study is similar to the study published by
Mr Taggart and his colleagues, as US surgeons infrequently (25%) used an
"all arterial revascularization" strategy beyond the LIMA to LAD
anastomosis during CABG. In the UK study, a little more than 15% of
surgeons used more than one arterial graft during CABG. Although the
reasons are multifactorial, both reports highlight the importance of
arterial revascularization but cite an increased learning curve with
higher morbidity and mortality. The findings are intriguing, as the impact
of drug-eluting stents may drastically change the practice of cardiac
surgery. If indeed stents are believed to have better patency rates than
vein grafts to non-LAD targets, we predict that cardiologists will soon
extrapolate this to drug eluting stents. Cardiac surgeons must change
their practices and use "all arterial revascularization" in order to
provide a more durable and cost effective alternative to the deployment of
2-4 drug-eluting stents in patients with multivessel coronary artery
disease.[3] This may limit the "full metal jacket" syndrome representing
overstenting.
We salute Mr Taggart and his colleagues for reporting this
important study which has significant implications for the practice of
coronary artery surgery worldwide.
References
(1) Catarino PA, Black E, Taggart DP. Why do UK cardiac surgeons not
perform their first choice operation for coronary artery bypass graft?
Heart 2002; 88643-644.
(2) D'Ancona G, Boyd DW, Donias HW, Vassiliades TA Jr, Stahl K,
Karamanoukian HL. Is hybrid revascularization favored by cardiologists or
cardiac surgeons? Heart Surgery Forum [serial online]. Available at
http://www.hsforum.com/vol5/issue4/2002-50132.html Accessed December 03, 2002.
(3) Karamanoukian HL, Aoukar PS. What will be the impact of drug-
eluting stents on hybrid coronary revascularization? Heart Surgery Forum
[serial online]. Available at http://www.hsforum.com/vol5/issue4/2002-01110.html
Accessed December 03, 2002.
Dr Weerasinghe and colleagues have reported on seasonal variation in deaths from coronary artery disease, as have many authors previously. They report a kind of proportional mortality taking as denominator monthly all cause deaths,[1,2] although numerator (ischaemic heart disease ICD 410-414 deaths) and denominator (all cause deaths) were drawn from different data sources: hospital statistics and national s...
Dr Weerasinghe and colleagues have reported on seasonal variation in deaths from coronary artery disease, as have many authors previously. They report a kind of proportional mortality taking as denominator monthly all cause deaths,[1,2] although numerator (ischaemic heart disease ICD 410-414 deaths) and denominator (all cause deaths) were drawn from different data sources: hospital statistics and national statistics, respectively
However, since total mortality varies seasonally (in most temperate climates) and in the same direction as does heart disease mortality, a proportional mortality underestimates the amplitude of the nearly sinusoidal variation of a disease-specific mortality. Thus principal figures (e.g. figure 1) show that heart disease mortality varies between summer and winter more than mortality as a whole. This is interesting from an aetiological standpoint and the authors refer to some of the explanations that have been proffered over the years. However when interpreting analysis of mortality statistics, it should be appreciated that seasonal and shorter term temporal variation inform on possible causation of a 'final common pathway' rather than on causation of disease, particularly of a chronic disease.[3,4]
The authors conclude that their findings will help hospitals make contingency plans for increased activity in winter months. For service delivery purposes a proportional mortality is not appropriate, since it does not represent the seasonal variation in absolute need. A direct measure of seasonal variation in hospital admissions for heart disease would be relevant [5] and perhaps hospital's own data on acute medical admissions (irrespective of discharge diagnosis) even more relevant.
References
(1) World Health Organisation. Manual of Mortality analysis, WHO Geneva 1977
(2) West, RR. Geographical variation in mortality from ischaemic heart disease in England and Wales. Brit J Prev Soc Med 1977;31:245-250
(3) West RR, and Lowe CR. Mortality from ischaemic heart disease intertown variation and its association with climate in England and Wales. Int J Epidemiol 1976;5:195-201
(4) West RR, Seasonal variation in CHD mortality. Int J Epidemiol 1989;18:463
(5) Wolff L, White PD. Boston Med Surg J 1926;195:13
The editorial accompanying our paper on age, sex, and sudden death
questions the high mortality in consecutive patients after an acute
myocardial infarction (MI). The mortality we describe is high compared to
the patients randomised in various studies, but it is comparable to the
mortality found in other surveys.
The Minnesota Heart Survey[1] describes
the mortality of unselected patients be...
The editorial accompanying our paper on age, sex, and sudden death
questions the high mortality in consecutive patients after an acute
myocardial infarction (MI). The mortality we describe is high compared to
the patients randomised in various studies, but it is comparable to the
mortality found in other surveys.
The Minnesota Heart Survey[1] describes
the mortality of unselected patients below 75 years of age – and the
mortality is identical to patients younger than 75 years from the cohort
that we studied. The comparison with the mortality in a number of
randomised studies is not relevant. It is well known that randomised
patients are not typical patients and we have demonstrated the dramatic
effect of the selection procedure for a trial on the mortality eventually
found [2] in the randomised patients.
To further emphasize that the mortality we describe is abnormal our data
are compared with the Framingham Heart Study [3] in which the age-adjusted
annual rate of sudden death for men with a previous myocardial infarction
is 1.75%. This comparison is also not relevant because the mortality we
describe is during the initial 2-4 years after the acute event, whereas
the Framingham study describes mean event rates during 38 years – and the
event rates after a myocardial infarction are far from constant.
Worthwhile studies can be made from many sources of data, including data
from randomised studies. However, it should always be kept in mind that
patients in randomised studies are highly selected and not representative
of the main selection criteria. A genuine high risk in such populations
is extremely rare. Therefore, studies on unselected populations such as
the one we have performed are important to ensure that findings from more
selected populations can be extrapolated to the findings in society.
References
(1) McGovern PG, Pankow JS, Shahar E, Doliszny KM, Folsom AR,
Blackburn H et al. Recent trends in acute coronary heart disease--
mortality, morbidity, medical care, and risk factors. The Minnesota Heart
Survey Investigators. N Engl J Med 1996;334:884-90.
(2) Køber L, Torp-Pedersen C. Clinical characteristics and mortality of patients screened for entry into the Trandolapril Cardiac Evaluation
(TRACE) study. Am J Cardiol 1995;76:1-5.
(3) Kannel WB, Wilson PW, D'Agostino RB, Cobb J. Sudden coronary death in
women. Am Heart J 1998;136:205-12.
Fruhwald FM and their colleagues mentioned about ANP synthesis from
the atrium in their lecture.
Most of the ANP is synthesized in the myocites of atrium and the synthesis
is prominent in the right atrium than the left. Another location of the
ANP synthesis is the ventricles. The highest ANP expression is in the
intrauterine period, it declines after birth and reaches to the adult
levels of 1-2% of atriu...
Fruhwald FM and their colleagues mentioned about ANP synthesis from
the atrium in their lecture.
Most of the ANP is synthesized in the myocites of atrium and the synthesis
is prominent in the right atrium than the left. Another location of the
ANP synthesis is the ventricles. The highest ANP expression is in the
intrauterine period, it declines after birth and reaches to the adult
levels of 1-2% of atrium.[1] Ventricular expression increases with volume
overload,increased pressure or both.[2] Also, it has been shown that, ANP
can be released from the ventriculs in dilated cardiomyopathy as
well.[3] As the heart failure progresses, the atrial ANP synthesis and the
gene expression decreases, but the expression continous from the ventricle.[4]
BNP has been mentioned another good predictor of heart failure in the
literature. However, Wei et al, reported that, the plasma levels of BNP
remains the same in the early stages of heart failure.[6] Therefore, in
this study ANP has been decleared by early predictor of heart failure in
the asymptomatic stage.
(3) Yasue H, Obata K, Okumura K, Kurose M, Ogawa H, Matsuyama K, Jougasaki
M: Increased secretion of atrial natriuretic polypeptide from the left
ventricule in patients with dilated cardiomyopathy. J Clin Invest 1989;83:46-51.
(4) Satio Y, Nakao K, Nishimura K, Sugawara A, Okumura K, Obata K: Clinical
application of atrial natriuretic polypeptide in patients with congestive
heart failure: Beneficial effects on left ventricular function.
Circulation 1987;76:115-124.
(5) Yoshimura M, Yasue H, Okumura K, Ogawa H, Jougasaki M, Mukoyama M:
Different secretion patterns of atrial natriuretic peptide and brain
natriuretic peptide in patients with congestive heart failure. Circulation 1993;
87:464-469.
(6) Wei CM, Heublein DM, Perrella MA, Lerman A, Rodeheffer RJ, Mc Gregor
CGA, Edwards WD: Natriuretic peptide system in human heart failure.
Circulation 1993;88:1004-9.
We appreciated the comments of Dr Guntheroth et al. We specifically
chose to eliminate patent foramen ovale from our study, hence patients
with a defect...
We appreciated the comments of Dr Guntheroth et al. We specifically
chose to eliminate patent foramen ovale from our study, hence patients
with a defect <_3mm were="were" excluded="excluded" from="from" inclusion.="inclusion." dr="dr" gunteroth="gunteroth" raises="raises" an="an" interesting="interesting" point="point" that="that" some="some" of="of" the="the" small="small" asds="asds" which="which" we="we" described="described" as="as" undergoing="undergoing" spontaneous="spontaneous" closure="closure" particularly="particularly" those="those" measuring="measuring" approximately="approximately" _3-4mm="_3-4mm" may="may" have="have" in="in" fact="fact" represented="represented" stretched="stretched" patent="patent" foramen="foramen" ovale="ovale" if="if" infant="infant" was="was" young="young" and="and" had="had" a="a" recent="recent" arterial="arterial" duct="duct" with="with" left="left" atrial="atrial" enlargement.="enlargement." cases="cases" underwent="underwent" diagnosed="diagnosed" all="all" children="children" greater="greater" than="than" _1="_1" year="year" age="age" no="no" case="case" there="there" prominent="prominent" septal="septal" flap="flap" to="to" raise="raise" suspicion="suspicion" pfo.="pfo." p="p"/>
Likewise, all these children had a left-to-right shunt
via the defect which given such considerations resulted in our calling
them small ASDs. Whether some of these represented stretched PFO is
however quite difficult to refute emphatically. The question does however
raise the interesting point of where the cut-off point is between a
stretched PFO and a small ASD when solely using echocardiography to make
this judgement? Irrespective of this point however our study set out to
determine how many ASDs outgrew the potential for transcatheter closure
using the specific device we had available at our institution at the time.
In the March issue of Heart, McMahon and colleagues
presented an excellent review of this subject.[1] I have one question for the
authors. You describe four patients with small ASDs that had spontaneous
closure of the defect. Since the method for spontaneous closure for
ventricular septal defects, by consensus, is roughening of the endocardium
of the rim of the defect by the high velocity of the jet,...
In the March issue of Heart, McMahon and colleagues
presented an excellent review of this subject.[1] I have one question for the
authors. You describe four patients with small ASDs that had spontaneous
closure of the defect. Since the method for spontaneous closure for
ventricular septal defects, by consensus, is roughening of the endocardium
of the rim of the defect by the high velocity of the jet, but the velocity
across most ASDs is less than 1 m/s, it is difficult to think that an ASD
would ever close from that means. Isn't it likely that these were simply
foramen ovale that were stretched by enlargement of the left atrium due to
ductal flow as an infant that has closed, leaving the incompetent foramen
ovale to gradually regress as the enlargement disappeared. We found that
this was a frequent occurrence in the premature infant population (Zhou and Guntheroth).[2]
References
(1) C J McMahon, T F Feltes, J K Fraley, J T Bricker, R G Grifka, T A Tortoriello, R Blake, and L I Bezold. Natural history of growth of secundum atrial septal defects and implications for transcatheter closure. Heart 2002; 87:256-259.
(2) Zhou TF, Guntheroth WG. Valve-incompetent foramen ovale in premature infants
with ductus arteriosus. JACC 1987;10:193-9
In writing our editorial,[1] we were well aware of the HOPE
substudy,[2] reported in the journal ‘Hypertension’, which described the
results of ambulatory blood pressure monitoring in 38 patients with
peripheral vascular disease. The substudy found that, compared with
placebo, ramipril treatment produced a significant reduction in ambulatory
blood pressure (10/4 mm Hg, p = 0.03) and a non-significant...
In writing our editorial,[1] we were well aware of the HOPE
substudy,[2] reported in the journal ‘Hypertension’, which described the
results of ambulatory blood pressure monitoring in 38 patients with
peripheral vascular disease. The substudy found that, compared with
placebo, ramipril treatment produced a significant reduction in ambulatory
blood pressure (10/4 mm Hg, p = 0.03) and a non-significant reduction in
office blood pressure (8/2 mm Hg, p = NS).
There were important differences between this small substudy cohort
and the overall HOPE study population, including a higher incidence of
peripheral vascular disease (100% versus 19%), higher office blood
pressure at baseline (151/81 mm Hg versus 139/79 mm Hg) and older age (71
years versus 66 years).
Whether the benefit of ramipril in the HOPE study was due largely to
blood pressure lowering or to other effects was not the focus of our
editorial. This issue has been discussed recently by the authors of the
HOPE study in ‘The Lancet’.[3] Instead, our editorial highlighted the
importance of assiduous blood pressure control after acute coronary events
and the rationale for the use of an ACE inhibitor.
We agree that clinicians need to consider all relevant information
when attempting to integrate findings from trials into clinical practice.
References
(1) Wong CK, White HD. Relation between blood pressure after an acute
coronary event and subsequent cardiovascular risk [editorial]. Heart
2002;88:555-8.
(2) Svensson P, de Faire U, Sleight P, Yusuf S, Ostergren J.
Comparative effects of ramipril on ambulatory and office blood pressures:
a HOPE substudy. Hypertension 2001;38:e28-e32.
(3) Sleight P, Pogue J, Yusuf S. Blood pressure and cardiovascular
risk in the HOPE study [letter]. Lancet 2002;359:2117-8.
Wong and White are responsible for perpetuating inaccuracies in their
article. Unfortunately, the ambulatory BP data on the HOPE trial was not
published in the NEJM, but in a more obscure hypertension journal, but
even the authors conceded that blood pressure reduction in the HOPE trial
played a major role that was not "initially appreciated". The BP
differences between the two groups were staggering, exp...
Wong and White are responsible for perpetuating inaccuracies in their
article. Unfortunately, the ambulatory BP data on the HOPE trial was not
published in the NEJM, but in a more obscure hypertension journal, but
even the authors conceded that blood pressure reduction in the HOPE trial
played a major role that was not "initially appreciated". The BP
differences between the two groups were staggering, explained in part by the
giving of ramipril at night in the trial. Wong and White nearly got it
right when they noticed the blood pressure differences between the QUIET
and the HOPE trials, but did not conclude that it is reduction in blood
pressure that counts.
The HOPE trial was the first hypertension trial that analysed blood
pressure lowering in a high risk group of "so-called" normotensives. To
imply anything else about the trial is pure conjecture and unfortunately
exposes the pharmaceutical industry's desire to niche a drug.
People writing reviews should analyse each paper quoted independently,
before sprouting the "common wisdom".
Dr Otterstad makes some incisive points about the reproducibility of
left ventricular volumes and ejection fractions. In general, it is
remarkable how silly we are from a quantitative point of view, when we
plan research. We make extensive arrangements to design a study, consent
subjects, transport them to hospital, arrange them on an echo table, set
up our machinery, measure our variable of interest jus...
Dr Otterstad makes some incisive points about the reproducibility of
left ventricular volumes and ejection fractions. In general, it is
remarkable how silly we are from a quantitative point of view, when we
plan research. We make extensive arrangements to design a study, consent
subjects, transport them to hospital, arrange them on an echo table, set
up our machinery, measure our variable of interest just once, and then do
all the previous steps in reverse. The only scientifically valuable step
is the measurement of the variable with as little random error as
possible, yet (usually) we spend no time on minimising this error.
The consequences are not only the problem that Dr Otterstad points
out, but also failure of the measured variable to show its true
correlation with any other variable.[1]
There are many strategies we can take to minimise random error, but
the only universally effective technique is to measure the variable more
than once and take the average. As a (remarkable) consequence of the
central limits theorem of statistics, regardless of the distribution of
the measurements we make (i.e. even if they are skewed), the mean of
several measurements takes on a normal distribution whose standard
deviation falls with the square root of the number of measurements we have
meaned.
Thus measuring left ventricular volumes 4 times (i.e. from 4 separate
echo recordings), rather than once, and then taking the mean, may be
expected to halve the reproducibility range. Our instincts may be to laugh
at the prospect of repeating the study so many times, but actually it is
probably the most effective use of the time of staff and patients. It only
seems time-wasting if one ignores the consequences of a study whose
reproducibility is twice as wide -- four times as many patients are
needed!
Which is more wasteful - quadrupling the scanning time or quadrupling
the study size overall?
Darrel Francis
Specialist Registrar in Cardiology
St Mary's Hospital
Reference
(1) Francis DP, Gibson DG, Coats AJS. How high can a correlation
coefficient be? Effects of limited reproducibility of common cardiological
measures. Int J Cardiol 1999, 65:185-189.
Dear Editor
Herlitz and colleagues [1] paint a rather gloomy picture of the impact of 20 years of effort in managing out of hospital cardiac arrest. Their large population observations are very valuable and will have a familiar feel to many practising cardiologists. The study showing survival rates over the last 20 years have not improved is comparable to previous studies.[2,3] If survival rates for victims of out-...
Dear Editor
We read with extreme interest the timely scientific letter which addresses "why …UK surgeons not perform their first choice operation [all arterial revascularization] for coronary artery bypass graft(ing)".[1]
The results are intriguing and confirm a related study recently published by our group following a survey of US surgeons called "Is hybrid coronary revascularization favored by cardiologists...
Dear Editor
Dr Weerasinghe and colleagues have reported on seasonal variation in deaths from coronary artery disease, as have many authors previously. They report a kind of proportional mortality taking as denominator monthly all cause deaths,[1,2] although numerator (ischaemic heart disease ICD 410-414 deaths) and denominator (all cause deaths) were drawn from different data sources: hospital statistics and national s...
Dear Editor
The editorial accompanying our paper on age, sex, and sudden death questions the high mortality in consecutive patients after an acute myocardial infarction (MI). The mortality we describe is high compared to the patients randomised in various studies, but it is comparable to the mortality found in other surveys.
The Minnesota Heart Survey[1] describes the mortality of unselected patients be...
Dear Editor
Fruhwald FM and their colleagues mentioned about ANP synthesis from the atrium in their lecture. Most of the ANP is synthesized in the myocites of atrium and the synthesis is prominent in the right atrium than the left. Another location of the ANP synthesis is the ventricles. The highest ANP expression is in the intrauterine period, it declines after birth and reaches to the adult levels of 1-2% of atriu...
Dear Editor
We appreciated the comments of Dr Guntheroth et al. We specifically chose to eliminate patent foramen ovale from our study, hence patients with a defect...
Dear Editor
In the March issue of Heart, McMahon and colleagues presented an excellent review of this subject.[1] I have one question for the authors. You describe four patients with small ASDs that had spontaneous closure of the defect. Since the method for spontaneous closure for ventricular septal defects, by consensus, is roughening of the endocardium of the rim of the defect by the high velocity of the jet,...
Dear Editor
In writing our editorial,[1] we were well aware of the HOPE substudy,[2] reported in the journal ‘Hypertension’, which described the results of ambulatory blood pressure monitoring in 38 patients with peripheral vascular disease. The substudy found that, compared with placebo, ramipril treatment produced a significant reduction in ambulatory blood pressure (10/4 mm Hg, p = 0.03) and a non-significant...
Dear Editor
Wong and White are responsible for perpetuating inaccuracies in their article. Unfortunately, the ambulatory BP data on the HOPE trial was not published in the NEJM, but in a more obscure hypertension journal, but even the authors conceded that blood pressure reduction in the HOPE trial played a major role that was not "initially appreciated". The BP differences between the two groups were staggering, exp...
Dear Editor
Dr Otterstad makes some incisive points about the reproducibility of left ventricular volumes and ejection fractions. In general, it is remarkable how silly we are from a quantitative point of view, when we plan research. We make extensive arrangements to design a study, consent subjects, transport them to hospital, arrange them on an echo table, set up our machinery, measure our variable of interest jus...
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