I enjoyed reading the recent article on the worldwide perspective of valve disease by Soler-Soler and Galve from Barcelona, Spain.[1] But I was surprised that no mention was made of mitral valve prolapse (MVP) anywhere in their article.
MVP is the commonest valve disorder in the United States as well as in many parts of the world.[2] It also has a prevalence of 4.3% in Spain (see table).
I enjoyed reading the recent article on the worldwide perspective of valve disease by Soler-Soler and Galve from Barcelona, Spain.[1] But I was surprised that no mention was made of mitral valve prolapse (MVP) anywhere in their article.
MVP is the commonest valve disorder in the United States as well as in many parts of the world.[2] It also has a prevalence of 4.3% in Spain (see table).
Prevalence (%) of mitral valve prolapse
Male
Female
Overall
Australia*
4
4
4
Brazil
-
-
4
Britain*
-
2
-
Britain
-
-
5
Britain**
3.9
5.2
4.5
Canada*
-
-
22
China (Hans in Sichuan)*
2.2
6.3
4.3
China (Kazaks in Xinjiang)
2.8
7.7
5.3
China (schoolchildren in Guangdong)
-
-
1.9
Denmark*
-
-
7
Ethiopia*
15.4
9.1
13.3
France
-
-
6
Germany*
6.89
13.84
9.8
Hong Kong (Chinese)
7.2*
8
7.7*
5.4**
6.4**
5.8**
India (outpatient)
-
2.7
-
India*
-
16
-
Israel
-
-
5
Italy
0.7
3.3
1.8
Italy (Blacks)
-
-
1.4
Italy (athletes)
-
-
10
Japan (schoolchildren)
0.78
1.26
1
Japan**
1x***
4X***
7.5
Japan*
11
8
11
Korea
3.3
10
6.7
Libya*
-
-
16.9
Poland
-
-
4
Russia*
-
-
2.64
Russia (high altitude)*
-
-
1.7-10.9
Saudi Arabia*
7.4
12
-
Spain
1x***
2x***
4.3
South Africa
-
-
14.3
South Africa (Blacks)
-
-
17.9
Sweden*
7
8
7.4
Turkey*
-
-
7.6
USA
3
6.2-17
-
USA (Blacks)
9
24
17
USA (health survey)
-
15.4
-
USA (non-careseeking adolescents)
2.25
6.16
4.18
USA (children)*
31
38
35
Yugoslavia (schoolchildren)
1.9*
12.8*
7.8*
-
-
18.1
Modified from reference 2.
*Echocardiographic study; **Necropsy study; ***Expressed as a ratio.
MVP is the commonest cause of mitral regurgitation in the United States and other developed countries[3] [4] as well as in the developing countries such as China.[5] [6] One of the serious complications of mitral regurgitation is atrial fibrillation which usually persists even after successful corrective surgery of the mitral valve and often recurs after pharmacologic or electric cardioversion.[7] Although postoperative atrial fibrillation can be successfully managed by antiarrhythmic drugs and long-term anticoagulant therapy to prevent thromboembolism, these therapeutic modalities are not without side-effects, torsades de pointes and bleeding, respectively. However, it was gratifying that the adjunctive use of the Cox maze procedure reported recently from the Mayo clinic increased the restoration of sinus rhythm to 82% of their patients.[8]
MVP is also the commonest cause of infective endocarditis.[9][10][11] The microbial agents causing infective endocarditis on prolapsing mitral valve are similar to those that infect valves deformed by congenital or rheumatic processes.[12] Although streptococci viridans are the most common organisms, coagulase-negative staphylococcal endocarditis is not an infrequent occurrence in patients with MVP. Recognition of the occurrence of endocarditis due to coagulase-negative staphylococci in patients with MVP is important for several reasons. First, blood cultures positive for these organisms are frequently disregarded in patients without prosthetic heart valves or intravascular catheters. Second, the indolent course of some coagulase-negative staphylococcal endocarditis may delay consideration of the correct diagnosis, particularly in patients without congenital or rheumatic heart disease. Finally, even with effective antimicrobial therapy on the basis of in vitro studies, the clinical course may be prolonged and characterized by multiple responses to and relapses following drug withdrawal.
Thus it was most unfortunate that such an important valve disease as MVP was inadvertently omitted from discussion in this otherwise comprehensive review of the subject.[1]
Tsung O. Cheng, M.D.
Professor of Medicine Division of Cardiology
The George Washington University Medical Center 2150 Pennsylvania Avenue, N.W. Washington, DC 20037, USA
2. Cheng TO, Barlow JB: Mitral leaflet billowing and prolapse. Its prevalence around the world. Angiology 1989;40:77-87.
3. Cheng TO: Mitral valve prolapse: an overview. J Cardiol 1989;19 (Suppl 21):3-20.
4. Danielsen R, Nordrehaug JE, Vik-Mo H: High occurrence of mitral valve prolapse in cardiac catheterization patients with pure isolated mitral regurgitation. Acta Med Scand 1987;221:33-38.
5. Zhou LY, Hu RD: Floppy valve syndrome: a clinicopathological analysis of 16 cases. Chin J Intern Med 1986;25:149-151.
6. Cheng TO: Mitral valve prolapse. A review. Chin J Intern Med 1988;27:56-60, 126-129.
7. Cheng TO: Combined mitral valve repair and the Cox maze procedure for mitral valve prolapse and regurgitation and associated atrial fibrillation. J Thorac Cardiovasc Surg 2000;119:634.
8. Handa N, Schaff HV, Morris JJ, Anderson BJ, Kopecky SL, Enriquez-Sarano M: Outcome of valve repair and the Cox maze procedure for mitral regurgitation and associated atrial fibrillation. J Thorac Cardiovasc Surg 1999;118:628-635.
9. McKinsey DS, Ratts TE, Bisno AL: Underlying cardiac lesions in adults with infective endocarditis. The changing spectrum. Am J Med 1987;82:681-688.
10. Atkinson JB, Virmani R: Infective endocarditis: changing trends and general approach for examination. Hum Pathol 1987;18:603-608.
12. Barlow JB, Cheng TO: Mitral valve billowing and prolapse. In: Cheng TO: The International Textbook of Cardiology. New York: Pergamon Press, 1987:497-524.
I read, with great interest the article by Alp et al comparing
intravenous and oral flecainide for the cardioversion of acute atrial
fibrillation.[1] However, the article concludes that if a patient
converts, there is no difference in the percentage of cardioversion by
either route (even though the numbers presented tend to favour the oral
route). But it fails to mention if there was any differences...
I read, with great interest the article by Alp et al comparing
intravenous and oral flecainide for the cardioversion of acute atrial
fibrillation.[1] However, the article concludes that if a patient
converts, there is no difference in the percentage of cardioversion by
either route (even though the numbers presented tend to favour the oral
route). But it fails to mention if there was any differences between those
who reverted to normal sinus rhythm compared to those who did not.
Particularly, since the reported span of time of the duration of AF is so
broad (1 to 40 hours) was there any relation between the length of the
arrhythmia and the propensity to cardiovert? This stems directly from the
postulate that the sooner therapy is started, the better the chances at
cardioversion are.
Another unclear point is whether the patients were known to be
paroxysmallly fibrillating or whether all of them were "completely" new
"fibrillators". If the former is correct, were they on any medications
(beta blockers, ACE inhibitors, etc) and were there any differences in the
rate they reverted to normal sinus rhythm?
Benjamin Mazouz MD
Psagot, D.N. Mizrach Binyamin
ISRAEL 90-624
The Heiden Department of Cardiology
3-5 Strauss Street
Jerusalem
ISRAEL 91-004
Reference
(1) Alp NJ, Bell JA, Shai M. Randomised double blind trial of oral
versus intravenous flecainide for the cardioversion of acute atrial
fibrillation. Heart 2000;84:37-40.
Cowie's editorial envisages a clinical role for measurement of brain
natriuretic peptide (BNP) in the near future.[1] However, while the
potential for risk stratification and monitoring of treatment in patients
with heart failure is encouraging, we would urge caution regarding the
diagnostic utility of plasma BNP concentration.
There is little doubt that the diagnosis of heart failure is
difficult -...
Cowie's editorial envisages a clinical role for measurement of brain
natriuretic peptide (BNP) in the near future.[1] However, while the
potential for risk stratification and monitoring of treatment in patients
with heart failure is encouraging, we would urge caution regarding the
diagnostic utility of plasma BNP concentration.
There is little doubt that the diagnosis of heart failure is
difficult - only about a third of patients referred for echocardiography
or to a cardiology clinic with suspected heart failure turn out to have
left ventricular systolic dysfunction.[2, 3] Nor is there any doubt that
a definitive diagnosis is important, as the institution of appropriate
treatments may have a significant impact on survival as well as symptoms,
while exclusion of left ventricular systolic dysfunction as a cause of
symptoms allows other investigations and treatment to be planned.
However, many echocardiography departments are becoming overwhelmed. Thus
a simple test that can "rule in" or "rule out" left ventricular
systolic dysfunction has considerable appeal.
In the assessment of any diagnostic test, it is useful to consider
both the properties of the test (sensitivity and specificity) and the
baseline probability of the diagnosis (ie, the probability before the test
result is known). The use of decision analysis, based upon Bayesian
statistics is invaluable in this regard and is recommended in standard
textbooks of evidence-based medicine.[4]
Plasma natriuretic peptides are highly sensitive (over 90%) but only
moderately specific (approximately 60%) tests for left ventricular
systolic dysfunction.[5] As a consequence low plasma concentrations of
natriuretic peptides will be helpful in "ruling out" the diagnosis of
left ventricular systolic dysfunction but high concentrations will be of
little value as they may be associated with a number of other diagnoses.[1] Hence, while plasma BNP concentrations will be very helpful in
screening large numbers of patients where the overall prevalence of left
ventricular systolic dysfunction is low,[5] their use in the
investigation of patients with suspected heart failure will be much more
limited.
In a study of patients referred to outpatients with suspected
heart failure, we found that 15% of those with a normal plasma brain
natriuretic peptide concentration had left ventricular systolic
dysfunction.[3]
A further important question is whether BNP provides additional
information aborve and beyond that given by current investigations. In
our study, the use of plasma BNP concentration did not add significantly
to more simple "tests" - a history of previous myocardial infarction and
an electrocardiogram.[3] While history and an electrocardiogram are
mainstays of the investigation of the breathless patient, a false negative
rate for plasma BNP concentration of approximately 15% is too high to
obviate the need for echocardiography in such individuals.
We believe that in the setting of patients with "suspected heart failure", an echocardiogram rather than plasma brain natriuretic peptide
concentration remains the investigation of choice. Despite the exciting
potential for estimating prognosis and adjusting treatment, there is
currently no role for measurement of brain natriuretic peptide in routine
clinical practice.
References
(1) Cowie MR. BNP: soon to become a routine measure in the care of
patients with heart failure? Heart 2000:83:617-18.
(2) Francis CM, Caruana L, Kearney P, et al. Open access echocardiography
in management of heart failure in the community. BMJ 1995;310:634-6.
(3) Landray MJ, Lehman R, Arnold IR. Measuring brain natriuretic peptide
in suspected left ventricular systolic dysfunction in general practice:
cross-sectional study. BMJ 2000;320:985-6.
(4) Sackett DL, Richardson WS, Rosenberg W, Haynes RB. Evidence-based
medicine. How to practice and teach EBM. Churchill Livingstone 1998:118-28.
(5) McDonagh TA, Robb SD, Murdoch DR, et al. Biochemical detection of left-
ventricular systolic dysfunction. Lancet 1998;351:9-13.
Martin J Landray
Lecturer in Medicine
University of Birmingham
Birmingham B15 2TH, UK
Richard Lehman
General Practice Principal
Hightown Surgery
Banbury OX16 9DB, UK
Ian Arnold
Consultant Cardiologist
Horton Hospital
Oxford Radcliffe Hospitals NHS Trust
Banbury OX16 9AL, UK
In the case report by Sutaria et al (Heart 2000;83:97-98) an acute anterior MI complicated the routine administration of ergometrine after a
spontaneous vaginal delivery. A peak creatinine kinase (CK) of 9858 U/l
was reported (CK-MB fraction 8%) with the apparent implication that this
CK rise reflected solely myocardial damage. The myometrium, however, is a
source of CK and childbirth results in six fold...
In the case report by Sutaria et al (Heart 2000;83:97-98) an acute anterior MI complicated the routine administration of ergometrine after a
spontaneous vaginal delivery. A peak creatinine kinase (CK) of 9858 U/l
was reported (CK-MB fraction 8%) with the apparent implication that this
CK rise reflected solely myocardial damage. The myometrium, however, is a
source of CK and childbirth results in six fold rise in maternal CK
activity[1] and this rise starts to occur within thirty minutes of
delivery.[2] The increase in CK is higher in surgical compared to vaginal
deliveries.
References
1. Burtis CA, Ashwood ER, editors. Tietz textbook of clinical chemistry.
2nd ed. Philadelphia: WB Saunders; 1986.
2. Jouppila R, Jouppila P, Koivisto M, Virkkunen L, von Wendt L,
Pakarinen A. Maternal, foetal and neonatal blood creatinine-phosphokinase
activities and creatinine-phosphokinase co-enzymes after labour with and
without epidural analgesic and after caesarean section. Acta Anaesth Scand
1978;22:491-496
The recent article by Ghuran and Nolan is a valuable review about cardiovascular effects of recreational drugs.[1] We would like to provide additional information, not included in the review, about the induction of changes in the QT interval by some recreational substances.
The long QT syndrome has been associated with the occurrence of ventricular tachyarrhythmias (torsades de pointes). Considering the s...
The recent article by Ghuran and Nolan is a valuable review about cardiovascular effects of recreational drugs.[1] We would like to provide additional information, not included in the review, about the induction of changes in the QT interval by some recreational substances.
The long QT syndrome has been associated with the occurrence of ventricular tachyarrhythmias (torsades de pointes). Considering the substances of abuse, to our knowledge, at least cocaine, 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) and alcohol[2] can induce changes in the QT/QTc interval. There are published clinical case reports describing this kind of change for MDMA,[3, 4] and for cocaine it has also been described the presence of torsades de pointes in a patient with idiopathic long QT syndrome.[5]
In addition we would like to present results of the ECG-recording obtained during a clinical trial where MDMA was administered. Eight healthy male recreational users of MDMA participated in a randomized, double blind, cross-over and placebo controlled study. All subjects received, in different experimental sessions, a single oral dose of placebo, MDMA 125 mg; MDMA 75 mg and d,l-amphetamine 40 mg. A 12 lead-electrocardiogram (50 mm/sec) was performed prior treatment (baseline measure) and 1, 2, 4, 8 and 24 hours after drug administration. Cycle length (RR) and QT interval were measured manually by the same blinded investigator. Both measures were performed in all 12 leads of each ECG recording. Corrected QT was calculated with Bazett's formula. Interlead QTc dispersion was determined as the longest minus the shortest QTc on the 12-lead ECG. Changes in the T wave and appearance of U waves were also considered. Individual changes after each treatment conditions were evaluated according to criteria suggested by the Committee for Proprietary Medicinal Products (CPMP).[6] Other details of the trial have been previously published.[7] The table shows the number of subjects (maximal 8) who fulfil any criteria for prolonged cardiac repolarisation:
Mean QTc values (ms; n = 8) for each administered substance
Criteria
Placebo
MDMA 125 mg
MDMA 75 mg
Amphetamine
QTc between 431-450 ms*
0
1 (446 ms)
0
0
QTc change from baseline*
Between 30-60 ms
0
2
3
1
> 60 ms
0
1
0
0
QTc dispersion > 100 ms*
0
3
1
0
T wave changes
0
2
2
2
U wave appearance
0
2
1
1
*Following CPMP criteria
The maximal effects were observed two hours after MDMA administration and returned to normal values at 4-8 hours. For amphetamine the maximal effects were observed lately, 8 to 24 hours after drug administration. Although the magnitude of mean QTc increase was not clinically relevant, individual data of some subjects might be interpreted as important "warning" signs of possible malignant arrhythmia in accordance to the CPMP recommendation. The mean QTc increase observed for MDMA is similar to that described after the administration of therapeutic doses of prescription drugs as terfenadine or cisapride in clinical trials.
The administration of a single oral dose of MDMA, in the range of those consumed recreationally, produce a slight increase of QTc. Although these changes are mild in magnitude, MDMA could enhance the risk of ventricular arrhytmia in subjects with genetic predisposition to present an acquired long QT syndrome, and/or when used in combination with other well known arrhythmogenic drugs.
Supported by grants FIS 97/1198, CIRIT 1997SGR00077, ISC-III-97/4344 and Plan Nacional sobre Drogas (Madrid).
Magí Farré
Marta Mas
Lluis Molina
Jordi Camí
Units of Pharmacology and Cardiology
IMIM-Hospital del Mar, UAB - UPF
Barcelona, Spain
References
(1) Ghuran A, Nolan J. Recreational drug misuse: issues for the cardiologist. Heart 2000;83:627-33.
(2) Rossinen J, Sinisalo J, Partanen J, et al. Efects of acute alcohol infusion on duration and dispersion of QT interval in male patients with coronary artery disease and in healthy controls. Clin Cardiol 1999;22:591-4.
(3) Maxwell DL, Polkey MI, Henry JA. Hyponatremia and catatonic stupor after taking "ecstasy". BMJ 1993;307:1399.
(4) Drake WM, Broadhurst PA. QT-interval prolongation with ecstasy. S Afr Med J 1996;86:180-1.
(5) Schrem SS, Belsky P, Schwartzman D, et al. Cocaine-induced torsades de pointes in a patient with the idiopathic long QT syndrome. Am Heart J 1990;120:980-4.
(6) Committee for Proprietary Medicinal Products (CPMP). The assessment of the potential for QT interval prolongation by non-cardiovascular medicinal products. London: Commission of the European Communities, 1997 (Available from URL: http://www.eudra.org/en_home.htm).
(7) Mas M, Farré M, de la Torre R, et al. Cardiovascular and neuroendocrine effects, and pharmacokinetics of MDMA in humans. J Pharmacol Exp Ther 1999;290:136-45.
I read with interest Kübler’s review[1] and Willenheimer and colleagues’ viewpoint[2] on a similar theme about the application of drug trial results in
clinical practice, an area that remains controversial.
Florey’s penicillin trial in the 1940s only involved 8 mice. The mice were
inoculated with streptococci and only the four that were treated survived.
Such simplistic demonstration of a positive...
I read with interest Kübler’s review[1] and Willenheimer and colleagues’ viewpoint[2] on a similar theme about the application of drug trial results in
clinical practice, an area that remains controversial.
Florey’s penicillin trial in the 1940s only involved 8 mice. The mice were
inoculated with streptococci and only the four that were treated survived.
Such simplistic demonstration of a positive drug effect is unfortunately
not possible in preventative cardiovascular medicine where multiple
factors are at work. The advent of modern drug trials however has allowed
the efficacy of many cardiac drugs to be proved, but only with an
assumption of homogeneity in large numbers of study patients. The call for
more “overly” inclusive trials by Willenheimer and colleagues such as the
HOPE study could potentially be problematic. This empirical approach
“treats the many to benefit the few”. This invariably removes the need for
any understanding of the individual pathophysiologic process resulting in
unnecessary multiple drug therapy in many patients. Also, this encourages
an unhealthy “pill-pushing” culture and not enough on the need for
lifestyle modification. For example, the benefit of cholesterol lowering
with a statin is completely negated by smoking.[3]
For a given drug trial, theoretically there will be 4 outcome groups:
(a) those who survive because of a positive drug effect
(b) the vast
majority whose survivals are not dependent on treatment
(c) those whose
deaths are contributed by adverse drug reactions
(d) those whose
deaths are inevitable; either due to inadequate drug effect or alternate
pathophysiology.
If (a) > (c) then (a) divided by (a) + (c) + (d) gives
the relative risk reduction, in many positive cardiovascular trials, this
being greater than 25%. The problem is, it is necessary to treat a large
number of patients to uncover a drug effect.
As pointed out by
Willenheimer and colleagues, the survival of “32” out of 696 heart failure
patients treated in the US carvedilol trial established the statistical
efficacy of the drug. In other words, 19 out of every 20 patients treated
did not benefit from the drug as a whole (the inverse of number needed to
treat). Unfortunately, it is not possible to distinguish (a) from
(b) patients. There is therefore room to find reliable markers of drug
efficacy (or the lack of) to monitor the progress of drug treatment. The
lack of drug efficacy in (c) and (d) patients should perhaps be more
carefully explored clinically, and post-mortems should be carried out if
feasible. Some would argue that the (b) patient population would also
benefit from drug-induced alteration of the disease process. This however
has not yet been borne out in population mortality curves which appear to
have flattened out.[4]
Pitt O Lim
Department of Clinical Pharmacology and Therapeutics
Ninewells Hospital
Dundee, DD1 9SY UK
References
(1) Kubler W. Treatment of cardiac diseases: evidence based or
experience based medicine? Heart 2000;84:134-6.
(2) Willenheimer R, Dahlof B, Gordon A. Clinical trials in cardiovascular
medicine: are we looking for statistical significance or clinical
relevance? Heart 2000;84:129-33.
(3) Isles CG, Norrie J. Lipid lowering drugs for patients who continue to
smoke? Heart 2000;83:619-20.
(4) Fuster V. Epidemic of cardiovascular disease and stroke: the three main
challenges: presented at the 71st scientific sessions of the American
Heart Association - Dallas, Texas. Circulation 1999;99:1132-7.
The article by Viskin et al[1] adds some confusion to the definition of "the typical" electrocardiographic pattern associated with the syndrome of sudden death and right bundle branch delay described by Nava and Martini in 1988-1989,[2, 3] by Aihara in 1990, and by Brugada in 1992. As clearly documented,[3] three (and not one as discussed by Viskin et al) of six patients with aborted sudden death showed differe...
The article by Viskin et al[1] adds some confusion to the definition of "the typical" electrocardiographic pattern associated with the syndrome of sudden death and right bundle branch delay described by Nava and Martini in 1988-1989,[2, 3] by Aihara in 1990, and by Brugada in 1992. As clearly documented,[3] three (and not one as discussed by Viskin et al) of six patients with aborted sudden death showed different degrees of right bundle branch block, left axis deviation, prolonged PR interval and ST segment elevation. Two more patients had mild isolated ST elevation with T inversion. The same polymorphic patterns were lately documented either with standard electrocardiography or after class 1C drugs (in subjects with normal ECG or minor ST-T abnormalities), either in Brugada's or other series.[4] Thus a typical sign of the syndrome is a fascinating but not confirmed statement.
Viskin probably wants to emphasise the first and the most popular electrocardiogram of the syndrome, which is the one published in 1988[1] and 1989 (patient 3 of figure 1 in reference 2), and reprocessed by Brugada on his web site.
This electrocardiogram shows an R' wave in V1 (incorrectly called J wave), very similar to an incomplete right bundle branch block, followed by a coved ST elevation.
It must be remembered that the typical J wave is those recorded in leads II, III, aVF, V5-V6 in vagotonia, and other pathological conditions.[5] Thus R' in V1 is an atypical J wave, or something else.
Different from a right bundle branch delay, the atypical J wave seen in V1 shows neither a late and slurred S wave in V6, or the typical vectorcardiographic terminal loop.[1] Late potentials often characterise this pattern, but are absent in pure incomplete right bundle branch block. Thus the trace proposed by Viskin et al in figure 2 as the typical sign of the syndrome is, in reality, a typical incomplete right bundle branch block, while the trace presented in figure 3A closely resembles a true atypical J wave with coved ST elevation, and not a questionable sign.
This does not means that Viskin et al's patients do not have the syndrome, because this is not characterised by a single electrocardiographic pattern, but by polymorphic right bundle branch delays with ST elevation.[2] The latter can be the only basal abnormality, with the atypical J wave appearing spontaneously, or being induced after class 1C drugs.
The significance of all the electrocardiographic patterns of the syndrome, particularly of the atypical J wave and coved ST elevation, is strongly debated. Brugada favours a functional repolarisation abnormality, while we think, according to electrical and anatomic demonstration, that it represents an organic depolarisation abnormality.[4]
This can be easily demonstrated by recording late potentials. As mentioned before, in patients with the discussed "typical" electrocardiogram late potentials are almost always present, clearly demonstrating that the atypical J wave and coved ST elevation is due to a delayed QRS activity, probably of the outflow tract of the right ventricle.[4]
Please contact Dr Martini for a copy of the figure described below (unfortunately we cannot support illustrations in Rapid Responses)
The atypical J wave with coved ST elevation in V1, is identical in these two subjects with the syndrome. The trace on the left is the patient of Brugada described in Heart[6] after ajmaline; this pattern was ascribed to a functional repolarisation abnormality. The trace on the right is that of an apparently normal patient, belonging to a family affected by a minor form of right ventricular cardiomyopathy. This patient has a very positive late potentials study, indicating that the atypical J wave and ST elevation, both spontaneous and drug inducible, represents a late depolarisation abnormality of the cardiac activity, probably at the right ventricular outflow tract level. A repolarisation abnormality can never induce late potentials.
Bortolo Martini MD* Andrea Nava MD+ Sergio Cannas MD*
*Department of Cardiology, Ospedale Civile di Thiene
+Department of Cardiology, University of Padua
Correspondence to:
Bortolo Martini MD
Via Gioberti 9
36016 Thiene (VI), Italy
Fax +39 445 368537
References
(1) Viskin S, Fish R, Eldar M, et al. Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls. Heart 2000;84:31-6.
(2) Nava A, Canciani B, Schiavinato ML, Martini B, Buja GF, La repolarisation precoce dans le precordiales droites: trouble de la conduction intraventriculaire droite? Correlations de l'electrocardiographie- vectorcardiographie avec l'electro- physiologie. Mises a Jour Cardiologiques 1988;17:157-9.
(3) Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989;11:1203-9.
(4) Martini B, Corrado D, Nava A, Thiene G. Syndrome of right bundle branch block, ST segment elevation and sudden death: evidence of an organic substrate. In: Nava A, Thiene G, eds. Arrhythmogenic right ventricular cardiomyopathy. Elsevier 1997:438-53.
(5) Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372-9.
(6) Brugada P. Brugada syndrome: an electrocardiographic
diagnosis not to be missed. Heart 2000;84:1-3.
Nava and coworkers[1] and Martini and coworkers[2] described a
single patient with the diagnois of right ventricular dysplasia who,
retrospectively analyzed by the same authors, may have suffered from the
syndrome of right bundle branch block, ST segment elevation and sudden
death, now known as Brugada disease.
As they have no genetic analysis
on that patient (to exclude among others Naxos syndrome) t...
Nava and coworkers[1] and Martini and coworkers[2] described a
single patient with the diagnois of right ventricular dysplasia who,
retrospectively analyzed by the same authors, may have suffered from the
syndrome of right bundle branch block, ST segment elevation and sudden
death, now known as Brugada disease.
As they have no genetic analysis
on that patient (to exclude among others Naxos syndrome) their recent
letter to Heart[3] ads only confusion to an excellent study by Viskin and
coworkers.[4] Their speculations on the mechanisms of right ventricular
dysplasia and Brugada disease are no more than speculations and devoid of
any scientific basis.
Prof Dr Pedro Brugada
Cardiovascular Research and Teaching Institute Aalst Belgium
References
(1) Nava A, Canciani B, Schiavinato ML, Martini B, Buja GF, La repolarisation precoce
dans le precordiales droites: trouble de la conduction intraventriculaire droite? Correlations
de l'electrocardiographie- vectorcardiographie avec l'electro- physiologie. Mises a Jour
Cardiologiques 1988;17:157-9.
(2) Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart
disease: description of six cases. Am Heart J 1989;11:1203-9.
(3)Martini B, Nava A, Cannas S. There is not a single typical ECG pattern for the syndrome of sudden
death, RBBB, and ST elevation [Rapid response]. Heart 15 August 2000.
(4) Viskin S, Fish R, Eldar M, et al. Prevalence of the Brugada sign in idiopathic ventricular
fibrillation and healthy controls. Heart 2000;84:31-6.
We thank Lawrance et al for their letter that raises several
important points about the implementation of the national audit of
myocardial infarction.[1] Until the numerator and denominator can be
confidently stated there is little point in producing case fatality data
either nationally or locally. The data that they quote in their letter
strongly support this view. There is an urgent need to address thi...
We thank Lawrance et al for their letter that raises several
important points about the implementation of the national audit of
myocardial infarction.[1] Until the numerator and denominator can be
confidently stated there is little point in producing case fatality data
either nationally or locally. The data that they quote in their letter
strongly support this view. There is an urgent need to address this
problem.
The definition of myocardial infarction which can be used in
hospital, and which we propose to use for the national audit relies
primarily on the demonstration of an elevation of a cardiac specific
enzyme such as creatine kinase to a level greater than twice the upper
limit of normal for the local laboratory, or the elevation of serial non-specific enzymes to a level greater than twice the upper limit of normal
with an appropriate pattern of release in relation to the relevant
symptoms. This elevation must be accompanied by a history of symptoms
consistent with a myocardial infarction and/or cardiographic changes
consistent with infarction. Rarely it is necessary for a clinician to
need to make a judgment about a patient dying in hospital before
significant enzyme release has occurred.
As we point out in the Acute Myocardial Infarction - A Core data
Set,[2] the recognition of all patients admitted with myocardial
infarction may be difficult for some hospitals. Norris, in an unpublished
study from four South Coast Hospitals demonstrated that between 68% and
98% of patients admitted with myocardial infarction to those hospitals
were admitted to the Cardiac Care Unit (CCU). How patients having
infarction not going to CCU should be identified is a problem which
requires a local solution. However this is achieved, accurate coding
remains of paramount importance.
Adjustment for case mix in myocardial infarction is a unresolved
problem. The work outlined by Lawrance and his colleagues may be a
solution. We did not include clinical variables in the initial data set
because there were no compelling data to show they would add to the
analysis. However, the dataset is not static, and the addition of
further fields was always anticipated. It may be that the simple and
objective measures proposed by the EMMACE study group will be the first to
be added. We will be shortly start collecting data on large numbers of
patients with myocardial infarction in the National Audit, together with
planned mortality flagging. The introduction of a robust case mix model
will be potentially of great value to the National Audit.
J S Birkhead
Clinical Lead National Audit of Myocardial Infarction
Clinical Effectiveness and Evaluation Unit
Royal College of Physicians
London NW1 4LE, UK
References
(1) Lawrance RA. National Service Framework – core data set [Rapid response] Heart 18 August 2000.
(2) Birkhead JS, Norris RM, Quinn T, Pearson M, on behalf of the
Coronary Heart Disease National Service Framework for coronary disease:
Acute Myocardial Infarction - a core data set for monitoring standards of
care. Royal College of Physicians, London. December 1999.
We read with interest the editorial by Birkhead,[1]
concerning the implementation of the National Service Framework core data
set for myocardial infarction, and would like to comment on several of the
points raised.
Birkhead emphasises a need for confidence in data collection and its
subsequent analysis. The EMMACE study identified 2153 consecutive cases
of AMI admitted to 20 adjacent hospita...
We read with interest the editorial by Birkhead,[1]
concerning the implementation of the National Service Framework core data
set for myocardial infarction, and would like to comment on several of the
points raised.
Birkhead emphasises a need for confidence in data collection and its
subsequent analysis. The EMMACE study identified 2153 consecutive cases
of AMI admitted to 20 adjacent hospitals during a 3 month period (1st
September to 30th November 1995) from biochemistry, coding and CCU
records, with 1,391 fulfilling World Health Organisation (WHO) criteria.
Of those flagged by coding, 33.5% did not fulfill the WHO criteria. In
fact 21.3% of individuals fulfilling these criteria were not coded as AMI.
In addition, we found a 2.5-fold increase in 30-day mortality between
those patients labelled as AMI on the basis of the physician’s final
diagnosis (39.4%) and those fulfilling strict criteria (15.8%).
This leads
us to pose two questions: (1) What definition of AMI should be used when
collecting the NSF data set? (2) In view of numbers of AMI patients not
admitted to coronary care units, how should such patients be identified?
A further point highlighted in this editorial, refers to the need to
take case-mix variables and age into account, in order to allow meaningful
comparisons of data. The majority of case-mix-adjusted models suffer from
(a) over-complexity (b) excluding significant proportions of patients with
higher risk profiles (c) using administrative data without clinical
detail sor (d) being applicable to selected subgroups only.
The NSF core
data set aims to collect around 50 treatment and investigation parameters
with the only presenting clinical data being age and sex.[2] Using a risk
model based on three clearly objective admission clinical characteristics;
age, heart rate and systolic blood pressure, we propose that a greater
correction for case-mix can be applied to audit data collected as part of
the NSF requirements. This model has been validated both internally within
our UK population and externally using the MITI AMI population, and
appears to accurately reflect patient outcome in both UK and USA practice,
achieving an area under the receiver operating characheristic (ROC) curve
of 0.78. Interestingly, gender adds nothing either to this model or to one
based on age alone.
We feel that the incorporation of this routine, non-manipulable
clinical information to the NSF core data set would allow a simple
adjustment for case-mix that most clinicians would be happy to accept.
The subsequent analyses, therefore, are more likely be viewed as a fair
reflection of the quality of care offered to their AMI patients.
R A LAWRANCE
M F DORSCH
R J SAPSFORD
A S HALL
FOR THE EMMACE (EVALUATION OF METHODS AND MANAGEMENT OF ACUTE CORONARY
EVENTS) STUDY GROUP
Institute for Cardiovascular Research
The BHF Heart Research Centre at Leeds
Leeds General Infirmary
Great George Street
Leeds LS1 3EX, UK
Email: medral@leeds.ac.uk
References
(1) Birkhead JS. Responding to the requirements of the National
Service Framework for coronary disease: a core data set for myocardial
infarction. Heart 2000;84:116-117.
(2) Birkhead JS, Norris RM, Quinn T, et al, on behalf of the Coronary heart
Disease National Service framework Steering group. Acute myocardial
infarction: a core data set for monitoring standards of care. London:
Royal College of Physicians, December 1999.
I enjoyed reading the recent article on the worldwide perspective of valve disease by Soler-Soler and Galve from Barcelona, Spain.[1] But I was surprised that no mention was made of mitral valve prolapse (MVP) anywhere in their article.
MVP is the commonest valve disorder in the United States as well as in many parts of the world.[2] It also has a prevalence of 4.3% in Spain (see table).
Prevalence (%...
Dear Editor
I read, with great interest the article by Alp et al comparing intravenous and oral flecainide for the cardioversion of acute atrial fibrillation.[1] However, the article concludes that if a patient converts, there is no difference in the percentage of cardioversion by either route (even though the numbers presented tend to favour the oral route). But it fails to mention if there was any differences...
Cowie's editorial envisages a clinical role for measurement of brain natriuretic peptide (BNP) in the near future.[1] However, while the potential for risk stratification and monitoring of treatment in patients with heart failure is encouraging, we would urge caution regarding the diagnostic utility of plasma BNP concentration.
There is little doubt that the diagnosis of heart failure is difficult -...
In the case report by Sutaria et al (Heart 2000;83:97-98) an acute anterior MI complicated the routine administration of ergometrine after a spontaneous vaginal delivery. A peak creatinine kinase (CK) of 9858 U/l was reported (CK-MB fraction 8%) with the apparent implication that this CK rise reflected solely myocardial damage. The myometrium, however, is a source of CK and childbirth results in six fold...
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Dear Editor:
I read with interest Kübler’s review[1] and Willenheimer and colleagues’ viewpoint[2] on a similar theme about the application of drug trial results in clinical practice, an area that remains controversial.
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Nava and coworkers[1] and Martini and coworkers[2] described a single patient with the diagnois of right ventricular dysplasia who, retrospectively analyzed by the same authors, may have suffered from the syndrome of right bundle branch block, ST segment elevation and sudden death, now known as Brugada disease.
As they have no genetic analysis on that patient (to exclude among others Naxos syndrome) t...
We thank Lawrance et al for their letter that raises several important points about the implementation of the national audit of myocardial infarction.[1] Until the numerator and denominator can be confidently stated there is little point in producing case fatality data either nationally or locally. The data that they quote in their letter strongly support this view. There is an urgent need to address thi...
Dear Editor:
We read with interest the editorial by Birkhead,[1] concerning the implementation of the National Service Framework core data set for myocardial infarction, and would like to comment on several of the points raised.
Birkhead emphasises a need for confidence in data collection and its subsequent analysis. The EMMACE study identified 2153 consecutive cases of AMI admitted to 20 adjacent hospita...
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