I read with great interest the editorial by JE Sanderson,[1] which
focuses on the current controversy about the term of "diastolic heart
failure".[2-5]
There is now evidence that in patients with symptoms and
signs of heart failure without overt evidence of impaired left ventricular
systolic function, delayed relaxation and/or abnormal stiffness are almost
constant regardless of the severity of s...
I read with great interest the editorial by JE Sanderson,[1] which
focuses on the current controversy about the term of "diastolic heart
failure".[2-5]
There is now evidence that in patients with symptoms and
signs of heart failure without overt evidence of impaired left ventricular
systolic function, delayed relaxation and/or abnormal stiffness are almost
constant regardless of the severity of symptoms.[6,7] Accordingly, the term
of "diastolic heart failure" has been simplistically proposed in this
setting by some authors.[6] However, besides the controversy that the term
of "diastolic heart failure" should be recognized or not as synonymous
with "heart failure with preserved systolic function", it appears on
interest to point out two major clinical features encountered in this
clinical syndrome in daily practice.
First, isolated symptoms such as
asthenia and breathless, that are well known to be non-specific for heart
failure, frequently result in the misdiagnosis of "diastolic heart
failure" when isolated diastolic abnormalities are found at Doppler
echocardiography.[8] Accordingly, the Brain Natriuretic Peptide assay may be
very helpful for an accurate diagnosis of heart failure when signs of
pulmonary congestion at the auscultation and on Xray, which respond
favourably to loop diuretics, are not present.
Second, the key-assumption
that signs and symptoms of heart failure with preserved systolic function
relate mainly to severe diastolic dysfunction, as it is generally observed
in hypertrophic and restrictive cardiomyopathies, is henceforth questioned
in the elderly.[7]
In this setting, associated factors, such as silent
myocardial ischemia, high systolic blood pressure, arrhythmia,
hypoalbuminemia and volume overload related to high sodium intake and
renal failure, are usually the straightforward events which precipitate
the critical decrease in the oncotic – hydrostatic pulmonary pressure
gradient and, therefore, lead to the transient exacerbation of heart
failure. Thus, these aggravating factors must be checked and treated
systematically.
(2) Banerjee P, Banerjee T, Khand A, et al. Diastolic heart failure :
neglected or misdiagnosed ? J Am Coll Cardiol 2002; 39: 138-41.
(3) Cohen Solal A. Diastolic heart failure : myth or reality ? Eur J
Heart Fail 2002; 4: 395-400.
(4) Burkhoff D, Maurer MS, Packer M. Heart failure with a normal
ejection fraction : is it really a disorder of diastolic function ?
Circulation 2003; 107: 656-8.
(5) Zile MR. Heart failure with preserved ejection fraction : is this
diastolic heart failure ? J Am Coll Cardiol 2003; 41: 1519-22.
(6) Zile MR, Gaasch WH, Carroll JD, et al. Heart failure with a normal
ejection fraction. Is measurement of diastolic function necessary to make
the diagnosis of heart failure? Circulation 2001; 104: 779-82.
(7) Arques S, Ambrosi P, Gelisse R, et al. Hypoalbuminemia in elderly
patients with acute diastolic heart failure. J Am Coll Cardiol 2003; 42:
712-6.
(8) Caruana L, Petrie M, Davie A, et al. Do patients with suspected
heart failure and normal systolic function suffer from `diastolic heart
failure' or from misdiagnosis? A prospective descriptive study. Br Med J
2000; 321: 215–9.
We read with interest the article by Nielsen et al.[1] One of the
interesting findings of that study is the rather low rates of ACE
inhibitor use (16% and 8% respectively for hospitalized and community
dwelling heart failure patients, and 1.7% for patients with heart disease
but no heart failure). The fact that the study was done conducted between
1993 and 1996 partly explains these low rates. H...
We read with interest the article by Nielsen et al.[1] One of the
interesting findings of that study is the rather low rates of ACE
inhibitor use (16% and 8% respectively for hospitalized and community
dwelling heart failure patients, and 1.7% for patients with heart disease
but no heart failure). The fact that the study was done conducted between
1993 and 1996 partly explains these low rates. However, survival benefit
of ACE inhibitors in heart failure patients with left ventricular systolic
dysfunction was well known by the early 1990’s.[2] In addition, the lack of
distinction between systolic and diastolic heart failure also likely have
diluted the rate of ACE inhibitor use. Assuming that about half of the
hospitalized and 20% of the community dwelling heart failure patients have
systolic heart failure, and all ACE inhibitors were used in these patients
(which was likely not the case), not all eligible heart failure patients
were receiving this life saving drug.
Presence of systolic dysfunction and lack of use of ACE inhibitors
are independently associated with increased mortality in heart failure
patients.[3] Once a clinical diagnosis of heart failure is made, the single
most important evaluation is the left ventricular systolic function
evaluation, preferably by an echocardiogram.[4] The authors’ conclusion that
echocardiography should be restricted to heart failure patients with
significant risk of death is in contradiction to the recommendation by
heart failure guidelines.[4,5] Once the diagnosis of systolic heart failure
is established, ACE inhibitors should be prescribed to all such patients
unless an absolute contraindication such as past history of allergy or
angioedema exists. Most general practitioners should also be able to
initiate a beta blocker. General practitioners unfamiliar or uncomfortable
with use of beta blockers in systolic heart failure should refer patients
to cardiologists. Systolic heart failure patients with angina or sudden
worsening of symptoms who are eligible and willing candidates for
revascularization should also be referred for cardiac catheterization and
coronary angiography.
Reference
(1) Wendelboe Nielsen O, Hilden J, McDonagh T, Fischer Hansen J.
Survival differences between heart failure in general practices and in
hospitals. Heart 2003; 89:1298-1302.
(2) Williams J, Bristow M, Fowler M, et al. Guidelines for the Evaluation
and Management of Heart Failure: Report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation 1995; 92:2764-84.
(3) Ahmed A, Roseman JM, Duxbury AS, Allman RM, DeLong JF. Correlates and
outcomes of preserved left ventricular systolic function among older
adults hospitalized with heart failure. Am Heart J 2002; 144:365-72.
(4) Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the
evaluation and management of chronic heart failure in the adult: executive
summary. A report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee to revise the
1995 Guidelines for the Evaluation and Management of Heart Failure). J Am
Coll Cardiol 2001; 38:2101-13.
(5) Remme WJ, Swedberg K. Guidelines for the diagnosis and treatment of
chronic heart failure. Eur Heart J 2001; 22:1527-60.
We sincerely appreciate the comments by Tetsuya Sato et al.
concerning our report of transient apical ballooning associated with
apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated,
using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients
have extensive myocardial stunning as the result of sympathetic
denervation. Reduction of MIBG accumulation, suggestive...
We sincerely appreciate the comments by Tetsuya Sato et al.
concerning our report of transient apical ballooning associated with
apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated,
using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients
have extensive myocardial stunning as the result of sympathetic
denervation. Reduction of MIBG accumulation, suggestive of sympathetic
denervation, normalized over time accompanied by the disappearance of
deeply negative T waves. A similar case, has recently been documented in
another patient with this syndrome.[3] Of interest, reduced myocardial
MIBG uptake has also been observed in patients with pheochromocytoma [4]
that also may exhibit left ventricular wall motion abnormalities and
striking electrocardiographic features. Likewise, Kurisu et al.[5] assessed myocardial perfusion and fatty acid metabolism (idodine-123-beta-
methyl-p-iodophenyl penta-decanoid acid), in a series of patients with
this condition. They demonstrated that the extent of fatty acid metabolism
derangement was greater than expected according to the size of the
myocardial perfusion defect, and that this abnormal metabolism gradually
improved over the time, suggesting again the presence of stunned
myocardium.
By definition, however, myocardial stunning consist of prolonged
“post-ischemia” ventricular dysfunction. A problem with the apical
ballooning syndrome is that the ultimate cause for ischemia -if any-,
remains elusive. Normal epicardial coronary arteries are required for the
diagnosis of this entity, that also includes extensive and reversible wall
motion abnormalities not necessarily following the distribution of a main
epicardic vessel. Enzyme release is typically disproportionate to the
striking "Tako-Tsubo" like left ventricular morphology described in
Japanese and, more recently in Western patients.[6-8] Our patient had a
clear-cut intense emotional stress (major family discussion) as the
potential trigger. Another condition that may be associated with deeply
negative T waves, even of acute onset, is hypertrophic cardiomyopathy.[9-11] In some of these patients ischemia and/or metabolic abnormalities at
the left ventricular apex have also been proposed. Of interest, dynamic
intraventricular gradients may also occur in patients with apical
ballooning, and sympathetic activation leading to basal hypercontractility
may be implicated in its genesis.[12,13] In fact, treatment with
adrenergic blockers has been suggested.[12]
Therefore the role of sympathetic denervation/activation in this
challenging novel syndrome remains yet to be fully established. The "unique" finding in our patient, however, was the associated huge left
ventricular thrombus that, to the best of our knowledge, has not been
previously described in this entity.
References
(1) Barrera Ramirez C, Jiménez Mazuecos J, Alfonso F. Apical thrombus
associated with left ventricular apical ballooning. Heart 2003;89:927.
(2) Sato T, Tani Y, Fujieda H, Murao S, Sato H. Extensive myocardial
stunning showing transient regression of prolonged T wave inversion and
prolonged sympathetic denervation. Internal Med 2001;40:312-319.
(3) Kawabata M, Suzuki K, Terai T, et al. Tako-Tsubo cardiomyopathy
associated with syndrome malign reversible left ventricular dysfunction.
Circ J 2003; 67:721-724.
(4) Suga K, Tsukamoto K, Nishigauchi K et al. Iodine-123-MIBG imaging in
pheochromocytoma with cardiomyopathy and pulmonary edema. J Nucl Med
1996;37:1361-4.
(5) Kurisu S, Inoue I, Kawagoe T et al. Myocardial perfusion and fatty
acid metabolism in patients with Tako-Tsubo-Like left ventricular
dysfunction. J Am Coll Cardiol 2003;41:743-8
(6) Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular
apical ballooning without coronary artery stenosis: a novel heart syndrome
mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-8.
(7) Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular
dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking
acute myocardial infarction. Am Heart J 2002;143:448-455.
(8) Desmet WJR, Adriaenssens BFM, Dens JAY. Apical ballooning of the left
ventricle first series in white patients. Heart 2003;89:1027-1031.
(9) Alfonso F, Nihoyannopoulos P, Stewart J, Dickie S, Lemery M, McKenna
WJ. Clinical significance of giant T waves in hypertrophic cardiomyopathy.
J Am Coll Cardiol 1990;15:965-971.
(10) Alfonso F, Balaguer J, Grande A, Palomo J, Macaya C, Zarco P. Sudden
appearance of "giant" negative T waves in patients with hypertrophic
cardimyopathy. Am Heart J 1992;123:1392-1394.
(11) Alfonso F, Frenaux P, McKenna WJ. Clinical sustained monomor-phic
ventricular tachycardia in hypertrophic cardiomyopathy: Association with
left ventricular apical aneurysm. Br Heart J 1989;61:178-181.
(12) Villareal RP, Achari A, Wilansky S, et al. Anteroapical stunning and
left ventricular outflow obstruction. Mayo Clin Proc 2001;76:79-83.
(13) Penas-LLado M,Barriales R, Goicolea J. Transient left ventricular
apical ballooning and outflow tract obstruction. J Am Coll Cardiol
2003;42:1143.
Like all medals, also flecainide has two faces. One is that of a fast
and efficient antiarrhythmic drug, the other one being that of a drug with
a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of
ventricular fibrillation in a neonate suffering from supraventricular
tachycardia (SVT), likely due to the pro...
Like all medals, also flecainide has two faces. One is that of a fast
and efficient antiarrhythmic drug, the other one being that of a drug with
a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of
ventricular fibrillation in a neonate suffering from supraventricular
tachycardia (SVT), likely due to the proarrhytmic effect of flecainide.
However, in their presentation several issues might be misleading or
neglected.
First of all, it is unclear what kind of rhythm disturbance the
neonate suffered from and if a specific pharmacological therapy had been
used during pregnancy, since an urgent caesarean section was necessary for
child delivery. Then, if the arrhythmia was not tolerated, it is unclear
why they chased an oral administration protocol of flecainide over an
intravenous one or why external electric cardioversion was not preferred
over drug therapy. The authors describe that after flecainide
administration, heart rate decreased from 240 beats/min to 170 beats/min
and then QRS complex duration increased. This behaviour is rather typical
of flecainide effect, relying on its own pharmacodynamics. Flecainide acts
blocking Na+ channels in myocardial cells membrane, thus prolonging the
duration of the action potential, possibly prolonging QRS duration. Thus,
the broad complex tachycardia seen after flecainide may well be the same
SVT with an aberrant conduction. Indeed, heart rate was the same for both
arrhythmias (170 beats/min). Flecainide administration in children has
been reported to be associated to a significant risk for arrhythmias and
fatal events,[3] as amiodarone.[4] Potential advantages of flecainide
over amiodarone are a faster effect, due to its high early uptake from the
heart, a shortest elimination (half-life of about 6 hours), and as
reported by Dr Ackland,[2] the plasmatic dosability, which may help to
avoid toxicity.
In a recently published paper [5] we reported our very
good results with the use of intravenous flecainide for the treatment of
postoperative junctional ectopic tachycardia in neonates, which is often a
lifethreatening arrhythmia. About 35 children followed-up at our centre
(with an age range at administration from 2 days to 13 years) currently
receive daily flecainide for their arrhythmias and only one adverse event
occurred in a 5-years-old girl who presented with a sinus rhythm at 65
beats/min and a QRS duration of about 200 milliseconds. Parent’s interview
revealed an over-administration of the drug. Blood sample revealed a
plasmatic drug concentration of 720 mcg/l at about 12 hours after the last
administration. Owing a flecainide elimination half life of 6 hours, we
presumed peak plasmatic values exceeding 1000 mcg/l (which is the upper
limit to avoid toxicity). Further caution should be taken with flecainide
administration in critically ill infants, since drug metabolism may be
impaired, thus accumulating in the blood. Therefore, in the setting of
resistant SVT, we endorse the use of intravenous flecainide at the loading
dose of 0.5-2 mg/kg with continuous infusion of 0.4 mg/Kg/h when the
arrhythmia is tolerated, using a smaller bolus (0.5-1 mg/kg) when the
clinical condition suggests an impaired metabolism, like in low cardiac
output patients. Immediate external electric cardioversion represents the
treatment of choice when collapse is pending. In conclusion, we do not
think that the case report by Ackland [2] should discourage the use of
flecainide in neonates with SVT, but it rather draws the attention to the
fact that all care providers should be aware of drug toxicity and of
possible proarrhythmic effects related to the administration of this
powerful drug.
References
(1) The Cardiac Arrhythmia Suppression Trial (CAST) Investigators:
Preliminary report: effect of encainide and flecainide on mortality in a
randomized trial of arrhythmia suppression after myocardial infarction. N
Engl J Med 1989;321:406-412.
(2) Ackland F, Singh R, Thayyil S. Flecainide induced ventricular
fibrillation in a neonate.Heart 2003;89:1261
(3) Fish FA, Gillette PC, Benson DW Jr. Proarrhythmia, cardiac arrest and
death in young patients receiving encainide and flecainide. The Pediatric
Electrophysiology Group. J Am Coll Cardiol 1991;18:356-365.
(4) Figa FH, Gow RM, Hamilton RM, Freedom RM. Clinical efficacy and safety
of intravenous Amiodarone in infants and children. Am J Cardiol
1994;74:573-577.
(5) Bronzetti G, Formigari R, Giardini A, et al. Intravenous Flecainide for
the Treatment of Junctional Ectopic Tachycardia after Surgery for
Congenital Heart Disease. Ann Thorac Surg 2003:76:148-151.
We greatly appreciate Dr Nobrega’s interest in our recent
publication on
the acute effects of pyridostigmine on post-exercise heart rate recovery
in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic
threshold, our more complete analysis of submaximal exercise
demonstrated no differences between the effects of pyridostigmine 30
mg and pl...
We greatly appreciate Dr Nobrega’s interest in our recent
publication on
the acute effects of pyridostigmine on post-exercise heart rate recovery
in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic
threshold, our more complete analysis of submaximal exercise
demonstrated no differences between the effects of pyridostigmine 30
mg and placebo on heart rate, oxygen consumption, or oxygen pulse at
work rates corresponding to 25-50% of maximal oxygen uptake.
Contrary findings during submaximal exercise or mental stress cited by
Dr Nobrega may be attributable to differences in the study populations,
confounding effects of background medications, or dose of
pyridostigmine.[2,3] Indeed, in two of the studies cited by Dr Nobrega, 30mg of pyridostigmine did not change heart rate during submaximal
exercise or mental stress in normal subjects.[4,5] We chose to
administer 30 mg of pyridostigmine to our heart failure subjects as
higher doses have been associated with mild cholinergic side effects in
normal subjects.[5,6]
A recent publication on the effects of pyridostigmine on heart rate
variability in chronic heart failure patients was not available at the
time
of our manuscript submission.[7] We agree that our study and the recent
publication by Dr Nobrega and colleagues together provide preliminary
evidence to suggest that cholinesterase inhibition with pyridostigmine
may be a promising new therapeutic modality in patients with chronic
heart failure.[1,7] Additional work is needed to determine the optimal
dose, formulation, and longer-term safety profile of cholinesterase
inhibition in chronic heart failure.
References
(1) Androne AS, Hryniewicz K, Goldsmith R, Arwady A, Katz SD.
Acetylcholinesterase inhibition with pyridostigmine improves heart rate
recovery after maximal exercise in patients with chronic heart failure.
Heart 2003;89(8):854-8.
(2) Kawada T, Sugimachi M, Shishido T, Miyano H, Sato T, Yoshimura R, et al. Simultaneous identification of static and dynamic vagosympathetic
interactions in regulating heart rate. Am J Physiol 1999;276(3 Pt
2):R782-9.
(3) Nakahara T, Kawada T, Sugimachi M, Miyano H, Sato T, Shishido T, et al. Cholinesterase affects dynamic transduction properties from vagal
stimulation to heart rate. Am J Physiol 1998;275(2 Pt 2):R541-7.
(4) Nobrega AC, Carvalho AC, Santos KB, Soares PP. Cholinergic
stimulation with pyridostigmine blunts the cardiac responses to mental
stress. Clin Auton Res 1999;9(1):11-6.
(5) Serra SM, Costa RV, Bastos BG, Santos KB, Ramalho SH, da Nobrega
AC. Exercise stress testing in healthy subjects during cholinergic
stimulation after a single dose of pyridostigmine. Arq Bras Cardiol
2001;76(4):279-84.
(6) Sant'anna ID, de Sousa EB, de Moraes AV, Loures DL, Mesquita ET, da
Nobrega AC. Cardiac function during mental stress: cholinergic
modulation with pyridostigmine in healthy subjects. Clin Sci
(Lond) 2003;105(2):161-5.
(7) Behling A, Moraes RS, Rohde LE, Ferlin EL, Nobrega AC, Ribeiro JP.
Cholinergic stimulation with pyridostigmine reduces ventricular
arrhythmia and enhances heart rate variability in heart failure. Am Heart
J 2003;146(3):494-500.
I was very pleased to see Professor Vano's editorial[1] and the
reference to our Publication,[2] on this topic. He
makes the important point that interventional cardiologists are at greater
risk from radiation exposure than most other medical specialists. Of
course, interventional procedures are also a potential source of quite
serious radiation detriment to patients, so it is important to apply thes...
I was very pleased to see Professor Vano's editorial[1] and the
reference to our Publication,[2] on this topic. He
makes the important point that interventional cardiologists are at greater
risk from radiation exposure than most other medical specialists. Of
course, interventional procedures are also a potential source of quite
serious radiation detriment to patients, so it is important to apply these
very valuable procedures in a proper manner.
ICRP Publication 85 discusses these topics in some detail. Your
readers may be interested in knowing that a set of PowerPoint slides
supporting and summarising the main features of the report is available
for downloading at no cost and no registration from our website, at http://www.icrp.org/educational_area.htm.
References
(1) Vano E. Radiation exposure to cardiologists: how it could be reduced. Heart 2003;89:1123-1124 .
(2) International Commission on Radiological Protection. ICRP Publication 85. Avoidance of radiation injuries from medical interventional procedures. Annals ICRP 2000;30(2). Oxford: Pergamon, Elsevier Science Ltd.
I read the recent paper by Pascual et al.[1] with interest and have
some comments.
They found that subclinical left ventricular diastolic dysfunction occurs
in all grades of “isolated” obesity and is associated with an increased
systolic function only in the early stages of obesity.
These findings are substantially consistent with previous reports.[2-
5] Appreciating their accuracy...
I read the recent paper by Pascual et al.[1] with interest and have
some comments.
They found that subclinical left ventricular diastolic dysfunction occurs
in all grades of “isolated” obesity and is associated with an increased
systolic function only in the early stages of obesity.
These findings are substantially consistent with previous reports.[2-
5] Appreciating their accuracy in describing diastolic function I would
like to discuss some issues on systolic function evaluation and results
interpretation. In addition, some limitations on the study design should
be enhanced. The authors include subjects with BMI between 25–29.9 kg/m2,
really classified as overweight and not obese subjects. They correctly
enrolled in this study subjects with “isolated” obesity, meaning
uncomplicated obesity, in order to avoid confounding factors on cardiac
parameters evaluation. Nevertheless, the presence of impaired glucose
tolerance was not estimated and no data on the duration of obesity and
body fat distribution were provided. Finally, they calculated left
ventricular diameters and relative wall thickness, but no data on left
ventricular mass and geometry were reported. In spite of the lacking of
these crucial parameters, they concluded that obesity is associated with
eccentric hypertrophy, structural changes and that a specific
cardiomyopathy occurs in all obese individuals.
I have performed an investigation on the influence of only excess fat
on cardiac morphology and function.[2] That study showed the obesity per
se, although a long duration of disease, in absence of glucose
intolerance, diabetes, hypertension and dyslipidemia, is associated only
with an impairment of diastolic function and hyperkinetic systole and not
with left ventricular hypertrophy. Uncomplicated obese subjects present
left atrium and aortic root enlargement as consequences of impaired
diastole and hyperdinamic systole. Hyperkinetic systole, estimated by both
endocardial and midwall parameters, seems to be due to the increased
cardiac work necessary to supply a high oxygen consumption for the large
body surface of obese subjects. My preliminary data on extreme obesity
show that systolic function, at the rest, remains hyperdinamic and
effective also in obese subjects with BMI >50 kg/m2. I agree with
Pascual that an increase of preload, probably partially due also to
hyperinsulinemia and its sodium retentive action, could lead to the
development of left ventricle eccentricity. Nevertheless, no left
ventricular hypertrophy occurs in uncomplicated obese subjects. However,
insulin resistance seems to be a determinant of left ventricular mass
stronger than BMI.[6] Finally, to better address the relationship between
central obesity and cardiac parameters, I suggest to use echocardiographic
epicardial adipose tissue, as easy and reliable index of visceral fat
deposition. [7-8]
References
(1) M Pascual, DA Pascual, F Soria, T Vicente, AM Hernández, FJ Tébar, M Valdés. Effects of isolated obesity on systolic and diastolic
left ventricular function Heart 2003;89:1152–1156.
(2) Iacobellis G, Ribaudo MC, Leto G, Zappaterreno A, Di Mario U, Leonetti
F. Influence of excess fat on cardiac morphology and function: study in
uncomplicated obesity. Obes Res 2002;10:767-773.
(3) Stoddard MF, Tseuda K, Thomas M, Dillon S, Kupersmith J. The influence
of obesity on left ventricular filling and systolic function. Am Heart J 1992;124:694-699.
(4) Alpert MA, Lambert CR, Terry BE, Cohen MV, Mukerji V, Massey CV,
Hashimi MW, Panayiotou H. Influence of left ventricular mass on left
ventricular diastolic filling in normotensive morbid obesity. Am Heart J
1995;130:1068-73.
(5) Alpert MA, Lambert CR, Terry BE, Cohen MV, Mukerji V, Massey CV,
Hashimi MW, Panayiotou H. Interrelationship of left ventricular mass,
systolic function and diastolic filling in normotensive morbidly obese
patients. Int J Obes Relat Metab Disord 1995;19:550-7.
(6) Iacobellis G, Ribaudo MC, Zappaterreno A, Vecci E, Tiberti C, Di
Mario U, Leonetti F. Relationship of insulin sensitivity and left
ventricular mass in uncomplicated obesity. Obes Res 2003;11:518-524.
(7) Iacobellis G, Assael F, Ribaudo MC, Zappaterreno A, Alessi G, Di Mario
U, Leonetti F. Epicardial fat from echocardiography: a new method for
visceral adipose tissue prediction. Obes Res 2003; 11:304-310.
(8) Iacobellis G, Assael F, Ribaudo MC, Zappaterreno A, Vecci E, Tiberti C
Di Mario U, Leonetti F. Echocardiographic epicardial adipose tissue is
related to anthropometric and clinical parameters of metabolic syndrome. A
new indicator of cardiovascular risk. J Clin Endocrinol Metab 2003;88:11 November; in press.
In a response letter Cope et al. stated that smoking or the amount of
tobacco consumed did not influence the biochemical risk factors for
coronary artery disease such as cholesterol and HDL, but increased many of
the cellular factors which we have reported in the recent review article
as contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]...
In a response letter Cope et al. stated that smoking or the amount of
tobacco consumed did not influence the biochemical risk factors for
coronary artery disease such as cholesterol and HDL, but increased many of
the cellular factors which we have reported in the recent review article
as contributors to the inflammatory response and to the formation and
instability of the atheromatous plaque.[1]
We agree with Dr Cope regarding the possible relationship of smoking with
inflammatory process associated with the development of coronary
atherosclerosis and acute coronary thrombosis. However, the underlining
mechanisms remain obscure.
Therefore, we have examined whether chronic smoking is associated
with increased thrombosis and inflammatory process. We also investigated
the role of oxidative stress and the impact of antioxidant vitamins in
chronic smokers. We found that smoking is related with abnormalities in
thombosis/fibrinolysis system, such as increased levels of von Willebrand
factor (vWF), plasminogen activator inhibitor 1 (PAI-1) and increased PAI-
1/tPA ratio. These changes are partly reversible by high-dose antioxidant
treatment with vitamins C (2g/day) plus E (800IU/day) for a short period
of 4 weeks administration.[2] Furthermore, we have also shown that this
combination of antioxidants also decrease the expression of several
inflammatory markers such as interleukins 1b and 6, vascular cell adhesion
molecule and intercellular adhesion molecule.[3]
This beneficial effect of antioxidants reflects the possible role of
oxidative stress as a connective link between smoking, inflammatory
process and thrombosis/fibrinolysis system. It is widely believed, that
oxygen free radicals produced as a result of smoking, lead to both,
oxidative inactivation of endothelium-derived nitric oxide and direct
oxidative damage of endothelial cells. This phenomenon may increase the
release of endothelium-derived components of thrombosis/fibrinolysis
system and trigger a generalized vascular inflammatory process, associated
with increased risk for atherothrombosis.
The findings of Cope et al. and our observations indicate that smoking may
indirectly lead to increased risk for coronary atherosclerosis and acute
coronary syndromes, by affecting the inflammatory process and
thrombosis/fibrinolysis system.
References
(1) Tousoulis D, Davies GJ, Stefanadis C, Toutouzas P, Ambrose JA.
Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart
2003;89:993-997.
(2) Antoniades C, Tousoulis D, Tentolouris C, et al. Effects of Antioxidant Vitamins C and E on Endothelial Function and
Thrombosis/Fibrinolysis System in Smokers. Thromb/Haemost 2003;85:190-6
(3) Tousoulis D, Antoniades C, Tentolouris C, et al. Antioxidant
Vitamins C and E Administration in Smokers: Effects on Endothelial
Function and Adhesion Molecules. Atherosclerosis 2003; in press.
I would like to point out that Maisch and Ristic's recomendations [1]
on the duration of treatment and the use of adjuvant steroids in
tuberculous pericarditis are not consistent with the best available
evidence. They advise treatment for '9-12 months' with anti-tuberculous
drugs. In a recent systematic review of clinical trials of antituberculous
chemotherapy in patients with tuberculous pericarditis,...
I would like to point out that Maisch and Ristic's recomendations [1]
on the duration of treatment and the use of adjuvant steroids in
tuberculous pericarditis are not consistent with the best available
evidence. They advise treatment for '9-12 months' with anti-tuberculous
drugs. In a recent systematic review of clinical trials of antituberculous
chemotherapy in patients with tuberculous pericarditis, we found no
evidence that treatment for 9 months or more was any better than treatment
for the standard duration of 6 months.[2] Thus, the current
recommendation is that these patients should be treated with stanrd
antituberculous chemotherapy for 6 months.[3]
Furthermore, a meta-analysis of trials of the the effectiveness of
adjuvant steroids in tuberculous pericarditis showed promising but
inconclusive results.[4] These trials included very small numbers of
patients with HIV infection, and the potentially harmful side effects of
steroid use in immunocompromised patients has not been examined adequately.[5] Therefore, the routine use of adjuvant steroids in all patients with
tuberculous pericarditis (as recommended by Maisch and Rustic) is not
supported by current best evidence. The effectiveness and safety of
adjuvant corticosteroids in tuberculous pericarditis remains to be
established in large, well-designed placebo-controlled trials that involve
adequate numbers of HIV postive patients.[2,3,4].
References
(1) Maisch B, Ristic AD. Practical aspects of the management of pericardial
disease. Heart 2003;89:1096-1103.
(2) Mayosi BM, Ntsekhe M, Volmink JA, Commerford PJ. Tuberculous
pericarditis treatment (Cochrane Review). In The Cochrane Library, Issue
4, 2001. Oxford: Update Software.
(3) Mayosi BM, Volmink JA, Commerford PJ. Pericardial disease: an evidence
based approach to diagnosis and treatment. In Evidence Based Cardiology, 2nd edition, Yusuf S, Cairns JA, Camm
AJ, Fallen EL, Gersh BJ, (Eds). London:
BMJ Books, 2002:735-48.
(4) Ntsekhe M, Wiysonge C, Volmink J, Commerford PJ, Mayosi BM. Adjuvant
corticosteroids for tuberculous pericarditis: promising, but not proven.
QJM 2003;96:593-599.
(5) Elliott AM, Halwaiindi B, Bagshawe A, et al. Use of prednisolone in the
treatment of HIV-positive tuberculosis patients. QJM 1992;85:855-60.
We read with great interest the report discussing the management
strategies of low pressure giant pulmonary artery aneurysms.[1] As these
cases are uncommon, the natural history ill defined, and management
controversial, we wish to further contribute to the literature, discussing
two adult cases of giant low pressure pulmonary artery aneurysms, one
presenting with and the other without symptoms.
We read with great interest the report discussing the management
strategies of low pressure giant pulmonary artery aneurysms.[1] As these
cases are uncommon, the natural history ill defined, and management
controversial, we wish to further contribute to the literature, discussing
two adult cases of giant low pressure pulmonary artery aneurysms, one
presenting with and the other without symptoms.
Case 1 is a 38-year-old man with no prior cardiac history including
heart murmurs, which presented with a chronic cough, chest pains, and
exertional dyspnea. He had an unremarkable physical examination, but chest
radiograph suggested enlargement of the pulmonary artery. Transthoracic
echocardiography revealed a normal appearing pulmonary valve with trivial
regurgitation, and aneurysmal dilatation of the proximal pulmonary artery.
Computed tomography confirmed a 9 cm pulmonary artery aneurysm of the main
pulmonary artery. Because of his symptoms, he underwent surgical repair
with a 28 mm intervascular graft. The pulmonary valve was found to be
trileaflet, and the pulmonary artery was free of intimal tear or
calcification. At 6 months’ follow up, his symptoms have completely
resolved.
Case 2 is a 60-year-old female with isolated congenital pulmonary
stenosis who underwent a Brock valvotomy at age 16 for severe valvar
stenosis. She has been followed over the last 3 years for severe pulmonary
regurgitation and a pulmonary artery aneurysm. She is asymptomatic with a
preserved functional capacity on stress testing. Transthoracic
echocardiography shows severe pulmonary regurgitation, and severe right
ventricular enlargement with normal systolic function. Computed tomography
confirmed a 6.1 cm pulmonary artery aneurysm involving the main pulmonary
artery and proximal branches. Because of her lack of symptoms, preserved
right ventricular function and exercise capacity, she continues to be
conservatively managed with regular follow up.
The series by Veldtman [1] reports survival of four patients with low
pressure giant pulmonary artery aneurysms to a median age of 52 years,
with the oldest being 64 years. Our second case provides further
confirmation of the potential for late survival with a conservative
management strategy. None of the reported patients in the series [1] had
pulmonary hypertension, intracardiac shunts, systemic vasculitides, or
connective tissue disorders, similar to our two patients. Should this
patient profile be present in the setting of an asymptomatic giant
pulmonary artery aneurysm, we agree that a conservative approach can be
adopted. Careful clinical and echocardiographic follow up is indicated to
detect evidence of right ventricular dysfunction from chronic volume
overload, which seems to be the most common indication prompting surgical
intervention.
Reference
(1) Veldtman GR, Dearani JA, Warnes CA. Low pressure giant pulmonary artery
aneurysms in the adult: natural history and management strategies. Heart
2003;89:1067-1070.
Dear Editor
I read with great interest the editorial by JE Sanderson,[1] which focuses on the current controversy about the term of "diastolic heart failure".[2-5]
There is now evidence that in patients with symptoms and signs of heart failure without overt evidence of impaired left ventricular systolic function, delayed relaxation and/or abnormal stiffness are almost constant regardless of the severity of s...
Dear Editor
We read with interest the article by Nielsen et al.[1] One of the interesting findings of that study is the rather low rates of ACE inhibitor use (16% and 8% respectively for hospitalized and community dwelling heart failure patients, and 1.7% for patients with heart disease but no heart failure). The fact that the study was done conducted between 1993 and 1996 partly explains these low rates. H...
Dear Editor
We sincerely appreciate the comments by Tetsuya Sato et al. concerning our report of transient apical ballooning associated with apical thrombus.[1]
In a prior study,[2] they elegantly demonstrated, using 123I-Metaiodobenzylguanidine (MIBG), that some of these patients have extensive myocardial stunning as the result of sympathetic denervation. Reduction of MIBG accumulation, suggestive...
Dear Editor
Like all medals, also flecainide has two faces. One is that of a fast and efficient antiarrhythmic drug, the other one being that of a drug with a very bad reputation.[1]
In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of ventricular fibrillation in a neonate suffering from supraventricular tachycardia (SVT), likely due to the pro...
Dear Editor
We greatly appreciate Dr Nobrega’s interest in our recent publication on the acute effects of pyridostigmine on post-exercise heart rate recovery in patients with chronic heart failure.[1]
In accord with our published submaximal exercise data at anaerobic threshold, our more complete analysis of submaximal exercise demonstrated no differences between the effects of pyridostigmine 30 mg and pl...
Dear Editor
I was very pleased to see Professor Vano's editorial[1] and the reference to our Publication,[2] on this topic. He makes the important point that interventional cardiologists are at greater risk from radiation exposure than most other medical specialists. Of course, interventional procedures are also a potential source of quite serious radiation detriment to patients, so it is important to apply thes...
Dear Editor
I read the recent paper by Pascual et al.[1] with interest and have some comments. They found that subclinical left ventricular diastolic dysfunction occurs in all grades of “isolated” obesity and is associated with an increased systolic function only in the early stages of obesity.
These findings are substantially consistent with previous reports.[2- 5] Appreciating their accuracy...
Dear Editor
In a response letter Cope et al. stated that smoking or the amount of tobacco consumed did not influence the biochemical risk factors for coronary artery disease such as cholesterol and HDL, but increased many of the cellular factors which we have reported in the recent review article as contributors to the inflammatory response and to the formation and instability of the atheromatous plaque.[1]...
Dear Editor
I would like to point out that Maisch and Ristic's recomendations [1] on the duration of treatment and the use of adjuvant steroids in tuberculous pericarditis are not consistent with the best available evidence. They advise treatment for '9-12 months' with anti-tuberculous drugs. In a recent systematic review of clinical trials of antituberculous chemotherapy in patients with tuberculous pericarditis,...
Dear Editor
We read with great interest the report discussing the management strategies of low pressure giant pulmonary artery aneurysms.[1] As these cases are uncommon, the natural history ill defined, and management controversial, we wish to further contribute to the literature, discussing two adult cases of giant low pressure pulmonary artery aneurysms, one presenting with and the other without symptoms.
...
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