,
When I received the September issue of Heart, I was pleased to read
an article by Galasko and colleagues (Heart 2001; 86:271-276) on the
prospective comparison of echocardiographic wall motion score index and
radionuclide ejection fraction in predicting outcome following acute
myocardial infarction. In their introduction, they indicated that no
study has directly compared wall motion score index and l...
,
When I received the September issue of Heart, I was pleased to read
an article by Galasko and colleagues (Heart 2001; 86:271-276) on the
prospective comparison of echocardiographic wall motion score index and
radionuclide ejection fraction in predicting outcome following acute
myocardial infarction. In their introduction, they indicated that no
study has directly compared wall motion score index and left ventricular
ejection fraction in the assessment of prognosis.
I would like to call to the attention of these authors that an article
published in Clinical Cardiology (24, 191-195) (2001) by Smock, Larson,
Brown and Conti entitled 'Early prediction of 30 day mortality after Q wave
myocardial infarction by echocardiographic assessment of left ventricular
function - a pilot investigation.'
In this cohort of 201 consecutive patients with Q wave myocardial
infarction, echocardiographic assessment of left ventricular ejection
fraction within the first 24 hours after onset of myocardial infarction
was a powerful predictor of 30 day mortality. Wall motion score index was
also highly predictive of 30 day mortality. The relationship between wall
motion score index and left ventricular ejection fraction and 30 day
mortality was analyzed and there was no statistical advantage of one
method over the other or of combining left ventricular ejection fraction
and wall motion score index to determine prognosis. We believe that
focusing on left ventricular ejection fractions is a more practical of the
two approaches to assess 30 day mortality within 24 hours of admission to
hospital.
I congratulate these investigators on an excellent piece of work and
certainly concur that evaluating ventricular function is an excellent way
to assess prognosis in patients early after a myocardial infarction.
Sincerely,
C. Richard Conti, MD, MACC
Eminent Scholar, Cardiology
Professor of Medicine
A variety of potential causes have been proposed for HIV-associated cardiomyopathy, including myocardial infection with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection, drug-related cardiotoxicity, prolonged immunosuppression and
nutritional deficiencies [1]. Nutritional deficiencies are common in HIV infection [2,3]. Poor absorption and diarrhea can both lead to d...
A variety of potential causes have been proposed for HIV-associated cardiomyopathy, including myocardial infection with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection, drug-related cardiotoxicity, prolonged immunosuppression and
nutritional deficiencies [1]. Nutritional deficiencies are common in HIV infection [2,3]. Poor absorption and diarrhea can both lead to deficiencies of trace elements, which have been associated directly or indirectly with cardiomyopathy [2,3]. HIV disease may also be associated with altered levels of vitamin B12, carnitine, and growth and thyroid
hormone, all of which have been associated with left ventricular dysfunction [3]. The role of selenium deficiency in the development of HIV-associated dilated cardiomyopathy is still controversial[4].The relation between selenium deficiency and cardiomyopathy has also been studied in
selenium-deficient mice, with contrasting results[5]. Case reports have shown an improvement of cardiac function after selenium supplementations, especially in pediatric AIDS patients[4]. I agree with Dr.Yusuf and Vooletich that nutritional deficiency may have a role in favouring
opportunistic infection in HIV-infected patients by enhancement of the state of immunodeficiency. However,the selenium-deficiency hypothesis is still speculative and HIV-associated cardiomyopathy cannot be compared to
Keshan disease because of its multifactorial pathogenesis[1].
Giuseppe Barbaro,MD
Department of Emergency Medicine
University “La Sapienza”
Rome,Italy
(2) Miller TL. Cardiac complications of nutritional disorders. In Lipshultz SE(ed) .Cardiology in AIDS.New York:Chapman & Hall;307-16.
(3) Hoffman M, Lipshultz SE, Miller TL. Malnutrition and cardiac abnormalities in the HIV-infected patients. InMiller TL, Gorbach S(eds). Nutritional aspects of HIV infection.London:Arnold;33-9.
(4) Rerkpattanapipat P, Wongpraparut N, Jacobs L E et al. Cardiac manifestations of acquired immunodeficiency syndrome.Arch Intern Med 2000;160:602-8.
(5) Beck MA, Kolbeck PC, Shi Q et al. Increased virulence of a human enterovirus (coxackievirus B3) in selenium-deficient mice.J Infect Dis 1994;170:351-7.
We thank Drs Plummer and McComb for their interest in our estimate of the implications of the recently published NICE guidelines for United Kingdom electrophysiology centres [1]. We agree that an assessment of the workload implications of these guidelines is important for resource planning.
Using data gathered in clinical trials designed for different ends will always require assumptions and can therefor...
We thank Drs Plummer and McComb for their interest in our estimate of the implications of the recently published NICE guidelines for United Kingdom electrophysiology centres [1]. We agree that an assessment of the workload implications of these guidelines is important for resource planning.
Using data gathered in clinical trials designed for different ends will always require assumptions and can therefore be open to criticism. Studies detailing the prevalence of heart failure in the UK population vary in their findings also [2]. Our data, however, are based on a study where stable patients were enrolled by cardiologists in their clinics. Clearly, only a proportion of the
total heart failure population will be seen in this setting. It is unsurprising, therefore, that our estimate is lower than that predicted for the entire UK population.
The actual increase in ICD implantation rates will only become clear through the BPEG database and will depend upon local decision-making processes as to the implementation of a screening process. If all parts of primary, secondary and tertiary care were to be involved, the implications would clearly be considerable. Whether this will be possible in the days of limited resources is uncertain.
NP Gall, MT Kearney, A Zaman, S O'Nunain, KAA Fox, A Flapan, J Nolan.
References
(1) Gall NP, Kearney MT, Zaman A, O'Nunain S, Fox KAA, Flapan A, Nolan J. Implementation of the NICE guidelines for the primary prevention of mortality from ventricular tachyarrhythmias. Implications for UK electrophysiology centres; activity modelling from the UK-HEART study. HEART 2001;86:219-220.
(2) Davies MK , Hobbs FDR , Davis RC , Kenkre JE, Roalfe 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
Barbaro G et al have nicely described the cardiological manifesations of
HIV infection[1].However no mention is made about the concomitant
nutritional deficiencies, which may contribute to cardiomyopathy in these
cases.Selenium deficiency,a well known cause of reversible
cardiomyopathy(Keshan disease)[2],has been linked to cardiomyopathy in HIV
disease[3].Selenium is an essential component of glutathione
p...
Barbaro G et al have nicely described the cardiological manifesations of
HIV infection[1].However no mention is made about the concomitant
nutritional deficiencies, which may contribute to cardiomyopathy in these
cases.Selenium deficiency,a well known cause of reversible
cardiomyopathy(Keshan disease)[2],has been linked to cardiomyopathy in HIV
disease[3].Selenium is an essential component of glutathione
peroxidase(GPX)[4],which provides a defense against pro-oxidant
molecules.In the absence of Selenium,GPX is inactive and low GPX is found
in HIV disease[4],with increase in GPX activity after Selenium
supplementation[4].Factors like stress or infection may lead to the
production of hydrogen peroxide,which cannot be metabolized by the GPX
deficient tissues,leading to irreparable cardiac damage.Decreased level of
Selenium and antioxidant vitamins are found in HIV disease[4,5].Impaired
nutritional state in HIV disease is significantly associated with
mortality[5].In these patients Selenium deficiency is the only independent
predictor of survival[5].
The pathogenesis of dilated cardiomyopathy in HIV remains unclear.It
may be related to either direct action of HIV or to an autoimmune
process,possibly in association with other cardiotropic virus,notably
coxsackie group[6].Nutritional deficiency may be a precipitating factor in
these patients,as Selenium deficiency increases cardiac damage in mice
infected with coxsackie B virus[7],altering the viral genotype with
conversion of a normally benign coxsackie virus to a virulent one[7].
References
(1) Barbaro G,Fisher SD,Pellicelli AM,Liphultz SE. The expanding role of
cardiologist in the care of HIV patients. Heart2001;86:365-67
(2) Keshan Disease Research Group of Chinese Medical Academy of Medical
Sciences, Beijing. Epidemiological studies on the etiliogic relationship of
selenium and Keshan disease.Chinese Med J 1979;92:477-76
(3) Dworkin BM, Antonecchia PP,Smith F,Weiss L et al. Reduced selenium
content in the acquired imunodefeciency syndrome. JPEN 1989;13(6):644-47
(4) Delmas-Beauneux MC,Peuchant E,Conchouran A,Constans J et al. The
enzymatic antioxidant system in blood and glutathione status in human HIV
infected patients;effect of suplementation with selenium and beta
carotene. Am J Clin Nutr 1996;64:101-107
(5) Baum MK,Shor-Posner G.Mictonutrient status in relationship to mortality
in HIV disease. Nutr Rev 1998;56(1):S135-S139
(6) Barbaro G,DiLorenzo G,Grisorio B,Barbarini G. Incidence of dilated
cardiomyopathy and detection of HIV in myocardial cells of HIV positive
patients. N Engl J Med 1998;39:1093-99
(7) Beck MA. The influence of anti-oxidant nutrients on viral infection. Nutr
Rev 1998;56(1):S140-S146
We read with great interest the recent article by Dorsch and Lawrance.[1] Using data from the EMMACE (Evaluation of Methods and Management of Acute Coronary Events) study they derived a simple model for prediction of 30-day mortality in patients with acute myocardial infarction. Their model included age, heart rate, and systolic blood pressure and had very good predictive accuracy with areas under the receiver o...
We read with great interest the recent article by Dorsch and Lawrance.[1] Using data from the EMMACE (Evaluation of Methods and Management of Acute Coronary Events) study they derived a simple model for prediction of 30-day mortality in patients with acute myocardial infarction. Their model included age, heart rate, and systolic blood pressure and had very good predictive accuracy with areas under the receiver operating characteristic curves of 0.79 and 0.76 for the reference and test cohort, respectively.
Risk stratification in acute myocardial infarction and acute coronary syndromes in general is an area of active investigation. Several models [2-5] have been developed for mortality prediction: all of them include age and most include systolic blood pressure and heart rate, the 3 components of the EMMACE model. A significant limitation of those models is that they were derived from trial populations, which are selected and typically have lower mortality compared to non-trial populations. The EMMACE model addresses this concern since all patients with myocardial infarction from 20 adjacent hospitals in the former Yorkshire region were included.
Community populations in different areas of the world may differ and these differences may not be accounted for entirely by the proposed models. That is why we attempted to examine the performance of the EMMACE model in a US patient population of 875 consecutive Olmsted County, MN patients with acute myocardial infarction admitted to the coronary care unit of our institution between 1988 and 1998.[6] Myocardial infarction was defined by the WHO criteria as in the EMMACE study. Compared to the EMMACE population, our patient population was more likely to have hypertension (29.1% vs 44.7%, p<_0.001 and="and" diabetes="diabetes" mellitus="mellitus" _13.0="_13.0" vs="vs" _15.8="_15.8" p0.05="p0.05" less="less" likely="likely" to="to" be="be" currently="currently" smoking="smoking" _33.6="_33.6" _28.3="_28.3" p0.01.="p0.01." women="women" were="were" equally="equally" represented="represented" in="in" both="both" populations="populations" _39.4="_39.4" _38.6="_38.6" p="non-significant).<p"/>
The predicted and the observed 30-day mortality were compared by use of the chi-square test for each decile of the predicted mortality. Thirty-day mortality was 10.3% in our patients compared with 24.4% in the EMMACE population (p<_0.001. the="the" observed="observed" mortality="mortality" was="was" similar="similar" to="to" predicted="predicted" in="in" patients="patients" lower="lower" _5="_5" deciles="deciles" but="but" significantly="significantly" last="last" figure.="figure." predictive="predictive" accuracy="accuracy" of="of" emmace="emmace" model="model" good="good" c-statistic="0.76).<p"/>
Therefore, the EMMACE model overestimated mortality in higher risk patients of our population. Whether this difference resulted from different baseline characteristics or therapy administered is unknown. However, it highlights the difficulty in comparing quality of care between hospitals in different areas of the world; caution should be undertaken when applying a model for mortality prediction in a new patient population. A potential approach would be to repeat the excellent study by Dorsch and Lawrance when different populations are being evaluated to derive a population-specific model.
Emmanouil S. Brilakis
Stephen L. Kopecky
R. Scott Wright
Guy S. Reeder
Brent A. Williams
Ian P. Clements
References
(1) Dorsch MF, Lawrance RA, Sapsford RJ, et al. A simple benchmark for evaluating quality of care of patients following acute myocardial infarction. Heart 2001; 86:150-4.
(2) Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. Jama 2000; 284:835-42.
(3) Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation 2000; 101:2557-67.
(4) Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation 2000; 102:2031-7.
(5) Lee KL, Woodlief LH, Topol EJ, et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation 1995; 91:1659-68.
(6) Brilakis ES, Wright RS, Kopecky SL, Reeder GS, Williams BA, Miller WL. Bundle branch block as a predictor of long-term survival after acute myocardial infarction. Am J Cardiol 2001; 88:205-9.
We read with great interest the article by Rallidis et
al. [1] that elevated concentrations of macrophage colony
stimulating factor (MCSF) predict a worse short term
prognosis in patients with unstable angina. Recent studies
have clarified the significance of monocyte-related
cytokines such as MCSF in the development of
atherosclerosis, atheromatous plaque rupture and restenosis
after coronary angioplas...
We read with great interest the article by Rallidis et
al. [1] that elevated concentrations of macrophage colony
stimulating factor (MCSF) predict a worse short term
prognosis in patients with unstable angina. Recent studies
have clarified the significance of monocyte-related
cytokines such as MCSF in the development of
atherosclerosis, atheromatous plaque rupture and restenosis
after coronary angioplasty.
We previously investigated changes in MCSF in the
coronary circulation induced by percutaneous transluminal
coronary angioplasty (PTCA) and their clinical significance
[2]. A 5F Amplatz catheter was placed in the coronary
sinus of 40 patients with angina pectoris, and blood
samples were obtained through the catheter before,
immediately after, and 4 and 24 hours after angioplasty.
MCSF levels in the coronary sinus blood showed a
significant increase 4 and 24 hours after PTCA (from
[mean�}SD] 671�}51 to 942�}63 and to 1,220�}79 pg/mL,
respectively). We performed follow-up coronary angiography
after 6 months; MCSF levels in the coronary sinus blood 24
hours after PTCA in patients with restenosis were
significantly higher than those in patients without
restenosis (1,470�}133 vs. 1,061�}110 pg/mL, P<_0.05. a="a" significant="significant" positive="positive" correlation="correlation" was="was" observed="observed" between="between" mcsf="mcsf" levels="levels" and="and" loss="loss" index="index" r="0.59," p0.01.="p0.01." p="p"/> We also investigated the clinical significance of MCSF
expression in 20 patients with unstable angina [3]. Plasma
levels of MCSF on admission in patients with unstable
angina (736�}74 pg/mL) were significantly higher than those
in patients with stable angina (544�}35 pg/mL) or control
subjects (405�}44 pg/mL). Patients with unstable angina
were further divided into sub-groups according to their
clinical classification [4]; Levels of MCSF in patients who
had anginal attacks at rest within the 48 hours prior to
admission (Braunwald class IIIB) were significantly higher
than those in patients who did not have attacks at rest
(class IB, IIB). Five of the 20 unstable patients who were
refractory to medical therapy and were referred for
emergency coronary revascularization showed marked
elevation of plasma MCSF levels than the other 15 patients
(1,072�}135 vs. 624�}67 pg/mL, p<_0.01. p="p"/> These observations suggest that activation of monocytes/
macrophages by MCSF is involved in vulnerability of
atheromatous plaque as well as neointima formation after
angioplasty, and they support the conclusions of Rallidis
et al.
References
(1) Rallidis LS, Thomaidis KP, Zolindaki MG, Velissaridou
AH, Papasteriadis EG. Elevated concentrations of macrophage
colony stimulating factor predict worse in-hospital
prognosis in unstable angina. Heart 2001;86:92.
(2) Hojo Y, Ikeda U, Katsuki T, Mizuno O, Fukazawa H,
Fujikawa H, Shimada K. Chemokine expression in coronary
circulation after coronary angioplasty as a prognostic
factor for restenosis. Atherosclerosis 2001;156:165-170.
(3) Hojo Y, Ikeda U, Takahashi M, Shimada K. Increased
levels of monocyte-related cytokines in patients with
unstable angina. Atherosclerosis (in press).
(4) Braunwald E. Unstable angina: A classification.
Circulation 1989;80:410-414.
The activity monitoring analysis of the UK-HEART study published by
Gall et al. [1] is very welcome. They calculate that screening of 551
ambulant patients with stable heart failure according to NICE guidance [2]
would result in 142 electrophysiology studies (EPS) and the implantation
of 50 implantable cardioverter defibrillators (ICDs). Thus 9% of their
population were found to have a primary preve...
The activity monitoring analysis of the UK-HEART study published by
Gall et al. [1] is very welcome. They calculate that screening of 551
ambulant patients with stable heart failure according to NICE guidance [2]
would result in 142 electrophysiology studies (EPS) and the implantation
of 50 implantable cardioverter defibrillators (ICDs). Thus 9% of their
population were found to have a primary prevention indication for ICD
implantation. They conclude that “Overall, these data provide evidence
that implementation of the NICE guidelines for the use of ICDs in primary
prevention is unlikely to lead to an unmanageable increase in EPS or ICD
implantation in UK electrophysiology centres.” We are concerned that this
analysis under estimates the true number of patients who fulfil NICE
primary prevention criteria, and that this conclusion is therefore
unrealistic.
European estimates put the prevalence of heart failure due to LV
dysfunction at 9,000 [3] to 10,000 [4] per million. Screening this
population as envisaged by Gall et al. would require 18,000 to
20,000/million Holter recordings, 2,300 to 2,600/million EPSs and would
identify 800 to 900/million patients requiring ICD implantation. The UK
Heart Study recruited patients between 18 and 80 years with NYHA class I-
III heart failure. 21% of the new incident heart failure patients in UK
are over 80 [5], and 16% have class IV heart failure [5], and would have
been excluded from UK Heart. Excluding these patients from the European
prevalence gives an estimate of 535/million requiring ICD implantation.
Clearly, these figures do not exclude patients with other
contraindications to ICD therapy such as terminal illness, but,
conservatively, this would suggest that over 500/million of the general
population (approximately 30,000 patients in the UK) have a primary
prevention indication for ICD implantation.
Other estimates put the prevalence a little lower; published data
suggest that approximately 3% of the UK population have a history of MI
[3]. Of these, 16% have an EF <_35 _6="_6" _16="_16" of="of" those="those" have="have" non-sustained="non-sustained" vt="vt" on="on" holter="holter" monitoring="monitoring" and="and" _35="_35" sustained="sustained" monomorphic="monomorphic" inducible="inducible" at="at" eps="eps" _7.="_7." this="this" implies="implies" a="a" prevalence="prevalence" primary="primary" prevention="prevention" icd="icd" indications="indications" in="in" the="the" population="population" around="around" _270="_270" million.="million." new="new" incidence="incidence" these="these" can="can" be="be" estimated="estimated" from="from" number="number" mi="mi" survivors="survivors" each="each" year="year" _="_" approximately="approximately" _200000="_200000" uk="uk" giving="giving" figure="figure" for="for" icds="icds" _30="_30" million="million" per="per" year.="year." p="p"/> Both our and Gall et al.’s calculations are hypothetical and have
been based on a variety of estimates and assumptions derived from the
literature. However the number of patients fulfilling NICE criteria is
calculated, it exceeds that suggested by NICE (a total of 50 per million,
which is equivalent to 33 new implants per million per year)[2] by a
factor of more than 10, when both prevalence and new incidence are taken
into account.
All these estimates far exceed the total number of new ICD implants
performed in England (12/million)[8], Europe (31/million)[9] Denmark
(47/million)[10] and even the USA (154/million)[9]. Indications for ICD
implantation in Europe do not in practice include primary prevention, (for
example, 96% of implants in Denmark [10] are for secondary prevention
indications) so these patients, whatever their real number, are currently
not being considered for ICDs at all.
We have recently completed a local audit of cardiac patients
presenting to Freeman Hospital [11], and have found that complying with
NICE guidance for both primary and secondary prevention would require an
extra 2-3 EPS and 2-3 ICDs per week, compared with Gall et al.’s estimate
of one extra ICD per implanting centre per month.
We therefore have concerns about the manageability of the expected
increase in ICD implantation if NICE guidance is to be implemented. We
agree with Gall et al. [1] that implementation of the NICE guidance on the
use of ICDs is a desirable goal but we do not think that this can be
achieved with current resources, at least in the North East. It is
important that we do not underestimate the additional resources required
if we are to plan for the successful implementation of the NICE guidance.
C. J. Plummer, J. M. McComb, Freeman Hospital, Newcastle upon Tyne.
NE7 7DN. UK.
References
(1) Gall NP, Kearney MT, Zaman A, O'Nunain S, Fox KAA, Flapan A, Nolan
J. Implementation of the NICE guidelines for the primary prevention of
mortality from ventricular tachyarrhythmias: implications for UK
electrophysiology centres; activity modelling from the UK-HEART study.
Heart 2001;86:219-220
(4) Cleland JGF, Clark A, Caplin JL. Taking heart failure seriously.
Diagnosis and initiation of treatment are the aspects to concentrate on.
BMJ 2000;321:1095-1096
(5) Johansson S, Wallander M-A, Ruigómez A, Alberto L, Rodríguez G.
Incidence of newly diagnosed heart failure in UK general practice. Eur J
Heart Failure 2001;3:225-231
(6) Hohnloser SH, Klingenheben T, Zabel M, Schöpperal M, Mauß O.
Prevalence, characteristics and prognostic value during long-term follow-
up of nonsustained ventricular tachycardia after myocardial infarction in
the thrombolytic era. J Am Coll Cardiol 1999;33:1895-902
(7) Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley
G. A randomized study of the prevention of sudden death in patients with
coronary artery disease. The Multicenter Unsustained Tachycardia Trial
(MUSTT). N Engl J Med 1999;341:1882-90
(8) Cunningham D. Rickards A. Cunningham M. National Pacemaker and ICD
database, United Kingdom and Republic of Ireland, Annual Report 1998 and
1999. Available from URL http://ccad3.biomed.gla.uk/bpeg
(9) Camm AJ, Nisam S. The utilization of the implantable defibrillator
– a European enigma. Eur Heart J 2000;21:1998-2004
(10) Møller M, Arnsbo P. Danish Pacemaker and ICD Register. 2000.
Available from URL http://www.pacemaker.dk
(11) Plummer CJ, McComb JM. Audit of potential implantable
cardioverter defibrillator (ICD) patients. Europace 2001 Ed. Bloch Thomsen
PE. Monduzzi Editore International Proceedings Division, Bologna, Italy.
2001.
We have read with interest the article by Takeda et al.[1]. Our group has previously observed that patients with aortic stenosis often have selective decreases in ventricular longitudinal shortening and wall thickening concomitant with normal fractional shortening and ejection
fraction [2-4]. In the same studies, we also postulated that since subendocardial fibres are oriented longitudinally, this selective dec...
We have read with interest the article by Takeda et al.[1]. Our group has previously observed that patients with aortic stenosis often have selective decreases in ventricular longitudinal shortening and wall thickening concomitant with normal fractional shortening and ejection
fraction [2-4]. In the same studies, we also postulated that since subendocardial fibres are oriented longitudinally, this selective decrease in longitudinal shortening may be the result of an increase in subendocardial wall stress and the associated subendocardial abnormalities that are often observed in patients with aortic stenosis. Moreover, the potential interest of longitudinal shortening in patients with aortic
stenosis is also confirmed by our recent observation [5] that the main change in left ventricular function occurring after aortic valve replacement is a selective improvement of the left ventricular longitudinal shortening. These previously reported data are thus highly consistent with the data of Takeda et al and we fully agree with their interpretation that these observations are likely due to changes in subendocardial myocardial function. In this context, the relation they found between long axis excursion and symptoms is particularly interesting and coherent.
On the other hand, Takeda et al measured the absolute change in longitudinal shortening using M-mode echocardiography whereas we have evaluated relative longitudinal shortening using M-mode echocardiography
and a validated mathematical model of the dynamic geometry of the left ventricle. We would like to submit that relative shortening is probably more sensitive to intrinsic changes in function since absolute shortening is also influenced by the size of the ventricle, irrespective of function. For the same reason, it could also better correlate with the appearance of symptoms but this remains to be demonstrated. From a practical standpoint, it should also be emphasized that newer methods such as analysis of strain using Doppler tissue imaging [6] will probably render the evaluation of relative left ventricular longitudinal shortening much easier compared to the M-mode method. The use of the latter in the context of aortic stenosis however needs to be validated.
References
(1). Takeda S, Rimington H, Smeeton N, Chambers J. Long axis excursion in aortic stenosis. Heart 2001;86(1):52-6
(2). Dumesnil J G, Shoucri R M, Laurenceau J L, Turcot J. A mathematical model of the dynamic geometry of the intact left ventricle and its application to clinical data. Circulation 1979;59(5):1024-34.
(3). Dumesnil J G, Shoucri R M. Effect of the geometry of the left ventricle on the calculation of ejection fraction. Circulation 1982;65(1):91-8.
(4). Dumesnil J G, Shoucri R M. Quantitative relationships between left ventricular ejection and wall thickening and geometry. J Appl Physiol 1991;70(1):48-54.
(5). Pibarot P, Dumesnil J G, LeBlanc M H, Cartier P, Métras J. Changes in left ventricular mass and function after aortic valve replacement: A comparison between stentless and stented bioprosthetic valves.
J Am Soc Echocardiogr 1999;12(11):981-7.
(6). Voigt J-U, Arnold M F, Karlsson M, Hübbert L, Kukulski T, Hatle L, Sutherland G R. Assessment of regional longitudinal myocardial stain rate derived from Doppler myocardial imaging indexes in normal and infarcted
myocardium. J Am Soc Echocardiogr 2000;13:588-98.
Saliba and colleagues are to be congratulated on their study to establish the quality of life in the setting of complex congenital cardiac malformations. My comments are in no way intended as a criticism of their excellent and much-needed investigation. It is depressing, however, to
note that anatomical description lags so far behind the sophisticated evaluation of status of health. It is very likely that none of the patien...
Saliba and colleagues are to be congratulated on their study to establish the quality of life in the setting of complex congenital cardiac malformations. My comments are in no way intended as a criticism of their excellent and much-needed investigation. It is depressing, however, to
note that anatomical description lags so far behind the sophisticated evaluation of status of health. It is very likely that none of the patients studied possessed an anatomically univentricular heart. Indeed, the criterion for inclusion was "complex congenital heart disease in which
a biventricular repair can never be achieved". These patients have a functionally univentricular circulation, but the anatomic features unifying the group is presence of one big and one small ventricle. Can we not aspire to describe such patients in terms which even they themselves
might understand?
The occurrence of drug-related prerenal uraemia and, hence,
hyperkalemia [1,2] is an entirely predictable outcome if the precaution
is not taken to reduce the dose of loop diuretics when sprironolactone is
added to existing angiotensin converting enzyme (ACE) inhibitor therapy.
This given the fact that the coprescription of all three modalities (ie
spironolactone, loop diuretics, and ACE inhibitors) can...
The occurrence of drug-related prerenal uraemia and, hence,
hyperkalemia [1,2] is an entirely predictable outcome if the precaution
is not taken to reduce the dose of loop diuretics when sprironolactone is
added to existing angiotensin converting enzyme (ACE) inhibitor therapy.
This given the fact that the coprescription of all three modalities (ie
spironolactone, loop diuretics, and ACE inhibitors) can powerfully augment
diuresis even to the extent of precipitating prerenal uraemia [3,4] as a
consequence of the enhancement of natriuresis arising from the synergism
between spironolactone and ACE inhibitors [5].
O M P Jolobe
References
(1) Berry C, McMurray JJV. Serious adverse events experienced by patients
with chronic heart failure taking spironolactone. Heart 2001;85:e8(April).
(2) Schepkens H, Vanholder R, Billouw J-M, Lamiere N. Life-threatening
hyperkalaemia during combined therapy with angiotensin-converting enzyme
inhibitors and spironolactone. An analysis of 25 cases. American Journal
of Medicine 2001;110:438-441.
(3) Ikram H, Lewis GRJ, Webster MWI, Richards AM, Nicholls MG, Crozier IG.
Combined spironolactone and converting enzyme inhibitor therapy for
refractory heart failure. Australian and New Zealand Journal of Medicine
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Dear Editor
, When I received the September issue of Heart, I was pleased to read an article by Galasko and colleagues (Heart 2001; 86:271-276) on the prospective comparison of echocardiographic wall motion score index and radionuclide ejection fraction in predicting outcome following acute myocardial infarction. In their introduction, they indicated that no study has directly compared wall motion score index and l...
A variety of potential causes have been proposed for HIV-associated cardiomyopathy, including myocardial infection with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection, drug-related cardiotoxicity, prolonged immunosuppression and nutritional deficiencies [1]. Nutritional deficiencies are common in HIV infection [2,3]. Poor absorption and diarrhea can both lead to d...
We thank Drs Plummer and McComb for their interest in our estimate of the implications of the recently published NICE guidelines for United Kingdom electrophysiology centres [1]. We agree that an assessment of the workload implications of these guidelines is important for resource planning.
Using data gathered in clinical trials designed for different ends will always require assumptions and can therefor...
Barbaro G et al have nicely described the cardiological manifesations of HIV infection[1].However no mention is made about the concomitant nutritional deficiencies, which may contribute to cardiomyopathy in these cases.Selenium deficiency,a well known cause of reversible cardiomyopathy(Keshan disease)[2],has been linked to cardiomyopathy in HIV disease[3].Selenium is an essential component of glutathione p...
We read with great interest the recent article by Dorsch and Lawrance.[1] Using data from the EMMACE (Evaluation of Methods and Management of Acute Coronary Events) study they derived a simple model for prediction of 30-day mortality in patients with acute myocardial infarction. Their model included age, heart rate, and systolic blood pressure and had very good predictive accuracy with areas under the receiver o...
We read with great interest the article by Rallidis et al. [1] that elevated concentrations of macrophage colony stimulating factor (MCSF) predict a worse short term prognosis in patients with unstable angina. Recent studies have clarified the significance of monocyte-related cytokines such as MCSF in the development of atherosclerosis, atheromatous plaque rupture and restenosis after coronary angioplas...
Dear Editor,
The activity monitoring analysis of the UK-HEART study published by Gall et al. [1] is very welcome. They calculate that screening of 551 ambulant patients with stable heart failure according to NICE guidance [2] would result in 142 electrophysiology studies (EPS) and the implantation of 50 implantable cardioverter defibrillators (ICDs). Thus 9% of their population were found to have a primary preve...
We have read with interest the article by Takeda et al.[1]. Our group has previously observed that patients with aortic stenosis often have selective decreases in ventricular longitudinal shortening and wall thickening concomitant with normal fractional shortening and ejection fraction [2-4]. In the same studies, we also postulated that since subendocardial fibres are oriented longitudinally, this selective dec...
Saliba and colleagues are to be congratulated on their study to establish the quality of life in the setting of complex congenital cardiac malformations. My comments are in no way intended as a criticism of their excellent and much-needed investigation. It is depressing, however, to note that anatomical description lags so far behind the sophisticated evaluation of status of health. It is very likely that none of the patien...
The occurrence of drug-related prerenal uraemia and, hence, hyperkalemia [1,2] is an entirely predictable outcome if the precaution is not taken to reduce the dose of loop diuretics when sprironolactone is added to existing angiotensin converting enzyme (ACE) inhibitor therapy. This given the fact that the coprescription of all three modalities (ie spironolactone, loop diuretics, and ACE inhibitors) can...
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