We have read with great interest the article by Roudaut et al entitled
"Thrombosis of prosthetic heart valves: Diagnosis and therapeutic
considerations" published in the last issue of your journal.(1)
According to the authors, the first therapeutic consideration in
obstructive left-sided prosthetic valve thrombosis (PVT) should be surgery
and thrombolysis should be reserved for patients with contrain...
We have read with great interest the article by Roudaut et al entitled
"Thrombosis of prosthetic heart valves: Diagnosis and therapeutic
considerations" published in the last issue of your journal.(1)
According to the authors, the first therapeutic consideration in
obstructive left-sided prosthetic valve thrombosis (PVT) should be surgery
and thrombolysis should be reserved for patients with contraindications to
surgery. The Consensus Conference recommended surgical treatment for
critically unstable patients (NYHA class III-IV) and thrombolysis for
those with high surgical risk or clear contraindications to surgery. In
hemodynamically stable patients (NYHA class I-II) full anticoagulation
with heparin has been the recommended treatment. (2)
However, more recent data have shown that thrombolysis is superior to
surgery in the most critical patients (class III-IV) and to heparin when a
non obstructive thrombosis is present. (3)
This therapeutic decision was based fundamentally on the occurrence of
embolism. Roudaut himself (4) demonstrated that embolic events post-
thrombolysis were less frequent and more benign than previously thought.
Alpert recommended in an editorial that guidelines should be revised and
proposed thrombolysis for patients in NYHA classes III-IV as initial
therapy, reserving surgery for the patients who fail to respond to this
approach. (5)
In NYHA Class IV patients with PVT published results show a lower
mortality with thrombolysis (13%) than surgery (33%). (6)
Reviewing the published literature Lengyel cited post-thrombolysis
mortality of 5% vs 30% post-surgery. In 89 NYHA Class IV patients from
five different studies, late post-thrombolysis mortality was 7% compared
to 17 to 54% post-surgery. In NYHA Class I-III patients mortality was
approximately 5% with both therapeutic approaches. (7)
In 2005 Lengyel, published a letter in the Journal of the American College
of Cardiology with results of thrombolysis in 53 studies in different time
periods (1974-1995 vs 1996-2003). The number of treated episodes was
similar at 235 vs 234, success rate increased from 77% to 90%, embolic
events decreased from 13% to 4% and deaths from 7.5% to 2.5. The author
thus considers thrombolysis the first therapeutic choice in patients with
PVT, independent of the functional class and the thrombus size, if there
are no contraindications for it. (8)
Current data of surgical series have reported elevated rates of mortality.
Durrleman and coworkers presented a series of 39 patients with PVT over a
20 year-period who underwent thrombectomy or valve replacement with an
associated mortality of 25% and 41%, respectively.(9)
Oskokeli et al, in 30 patients with left-side PVT, reported a post-
operative early hospital mortality of 7.1% (NYHA classes II-III) and
31.3% (NYHA IV) (10) and Toker et al, in 63 cases a total mortality of 20,6%. (11)
In our experience of a series of 68 patients with a diagnosis of PVT
treated with thrombolysis, therapeutic success was achieved in 62 patients
(91,2%) and failure in 6 patients (8,8%). In NYHA IV patients the success
rate was 88.9% (32/36 patients). Systemic embolism occurred in five
patients (three cerebral and two peripheral). We used recombinant
streptokinase (250 000 UI / 30 min and continuous infusion 100 000 UI / h,
up to 72 hours). This also appears to be the most widely used and
recommended protocol according to the literature. (12)
Despite advances in surgery; anesthesia and peri-operative care, the
evidence is in favour of thrombolytic treatment for PVT due to its high
effectiveness, easy applicability, low complication rate and cost.
In agreement with other authors, we use and recommend thrombolysis as the
first therapeutic choice for patients with PVT, provided there are no
contraindications, regardless of the degree of valve obstruction, NYHA
functional class or thrombus size. Surgery should be reserved for those
patients with major contraindications or failure of thrombolysis.
REFERENCES
1. Roudaut R, Serri K, Lafitte S. Thrombosis of prosthetic heart valves: Diagnosis and therapeutic considerations. Heart 2007;93:137-42.
2. Lengyel M, Fuster V, Keltai M, Roudaut R, Schulte HD, Seward JB, et al. Guidelines for management of left-side prosthetic valve thrombosis: a role for thrombolytic therapy. Consensus Conference on prosthetic valve thrombosis. J Am Coll Cardiol 1997;30:1521-6.
3. Lengyel M, Horstkotte D, Völler H, Mistiaen WP. Recommendations for the Management of Prosthetic Valve Thrombosis. J Heart Valve Dis 2005;14:567-75.
4. Rodaut R, Lafitte S, Rodaut MF, Courtault C, Perron JM, Jais C, et al. Fibrinolysis of mechanical prosthetic valve thrombosis: a single center study of 127 cases. J Am Coll Cardiol 2003;41:653-8.
5. Alpert J. The thrombosed prosthetic valve. Current recommendations
based on evidence from the literature. J Am Coll Cardiol 2003;41:659-60.
6. Lengyel M, Vandor L. The role of thrombolysis in the management of left-sided prosthetic valve thrombosis: a study of 85 cases diagnosed transesophageal echocardiography. J Heart Valve Dis 2001;10:636-49.
7. Lengyel M. Management of prosthetic valve thrombosis. J Heart Valve Dis 2004;13:329-334.
8. Lengyel M. Thrombolysis should be regarded as first-line therapy for prosthetic valve thrombosis in the absence of contraindications. J Am Coll Cardiol 2005;45:325.
9. Durrleman N. Pellerin M, Bouchard D, Hebert Y, Cartier R, Perraul LP, et al. Prosthetic valve thrombosis: twenty-year experience at the Montreal Heart Institute. J Thorac Cardiovasc Surg 2004;127:1388-92.
10. Ozkokeli M, Sensoz Y, Ates M, Ekinci A, Akcar M, Yekeler I. Surgical treatment of left-sided prosthetic valve thrombosis: short and long-term results. Int Heart J 2005;46:105-11.
11. Toker ME, Eren E, Balkanay M, Kirali K, Yarartas M, Caliskan A, et al. Multivariate analysis for operative mortality in obstructive prosthetic valve dysfunction due to pannus and thrombus formation. Int Heart J 2006;47:237-45.
12. Cáceres-Lóriga FM, Pérez-López H, Morlans-Hernández K, Facundo-Sánchez H, Santos-Gracia J, Valiente-Mustelier J, et al. Thrombolysis as first choice therapy in prosthetic heart valve thrombosis. A study of 68 patients. J Thromb Thrombolysis 2006;21:185-90.
The debate on the role of antimicrobial prophylaxis to prevent
infective endocarditis (IE) has intensified as a consequence of the
recently published guidelines from the Working Party of the British
Society for Antimicrobial Chemotherapy (BSAC). In the review by Ashrafian
and Bogle, reference is made to the dental community’s satisfaction with
these new guidelines, highlighting a “victory for scien...
The debate on the role of antimicrobial prophylaxis to prevent
infective endocarditis (IE) has intensified as a consequence of the
recently published guidelines from the Working Party of the British
Society for Antimicrobial Chemotherapy (BSAC). In the review by Ashrafian
and Bogle, reference is made to the dental community’s satisfaction with
these new guidelines, highlighting a “victory for science and common
sense”. Cardiologists are likely to question the validity of such a
statement. The decision by BSAC to exclude patients deemed at
“intermediate risk” of developing endocarditis from bacteraemia, induced
by dental or surgical procedures is raising alarm bells in the cardiology
community. Cardiologists are the people most able to risk stratify
patients with acquired or congenital heart disease in relation to IE
prophylaxis. For example, Ashrafian and Bogle quote mitral valve prolapse
(MVP) in relation to the need for prophylaxis. MVP associated with a
turbulent jet of mitral regurgitation is more likely to produce
endocardial disruption than ‘slight prolapse of the posterior mitral
leaflet’, yet both are regarded equal under the BSAC guidelines.
A change in clinical practice will occur with the BSAC guidelines
which is certain to cause confusion both to the patient and the dentist
(or any other surgical practitioner) involved in patient care. Over the
years, patients, cardiologists and dental practitioners have communicated
well. Dental practitioners will often write to cardiologists seeking
advice on specific antibiotic dosage or timing etc. and this may have
positively contributed to the present low annual case load of IE. No
cardiologist would argue against the statement that many cases of IE are
of non-dental origin but many are likely to question the decision to
withhold prophylaxis for general surgical or genito-urinary procedures in
patients with haemodynamically significant murmurs.
Ashrafian and Bogle highlight the risk of anaphylaxis associated with
severe penicillin allergy. Most allergies to antibiotics are not life-
threatening however and will often have declared themselves previously by
taking a careful medical history. Several alternative antibiotics are
also now available to substitute for a penicillin preparation when
concerns over potential allergy are raised.
Cardiologists are at the ‘front line’ in the treatment of patients
with IE and recognise the high morbidity and mortality associated with the
condition. It is unlikely therefore that the British Cardiovascular
Society will support the new guidelines. It is extremely unlikely
organisations such as the American Heart Association will do so also for
fear of litigation issues. The benefits of antibiotic prophylaxis for IE
outweigh the risk for more patients than is presently recommended by the
BSAC. The debate must continue.
As cardiac surgeons we read and reread the editorial by Ashrafian
and
Bogle initially with interest and subsequently bemusement looking for a
definitive message. The title was clear enough; the editorial was not.
The conclusion that good practice will be served if “patients are
adequately counselled on the benefits of good dental hygiene and a
discussion is undertaken and documented on the ri...
As cardiac surgeons we read and reread the editorial by Ashrafian
and
Bogle initially with interest and subsequently bemusement looking for a
definitive message. The title was clear enough; the editorial was not.
The conclusion that good practice will be served if “patients are
adequately counselled on the benefits of good dental hygiene and a
discussion is undertaken and documented on the risks/benefits of
antibiotic prophylaxis” is superficially attractive if one ignores the
practicalities of who is making the decision and on what basis. Is this
the responsibility of cardiologist or dentist? Does this mean the
patient
agreeing to bad advice is acceptable? I agree that dental practitioners
are independent practitioners and carry legal responsibility for their
commission (antibiotic administration) – but omission is equally
legally
liable. Whose advice should they follow and on what basis?
The representative cardiological bodies in UK, USA and Europe have
all published guidelines on the prevention of infective endocarditis.
Their guidance is clear. The guidance from BSAC on the other hand
carries
with it a feeling of selfrighteousness but its position is not
rational.
Ideally the working party felt a prospective double blind trial should
be
carried out and that withholding antibiotic prophylaxis for dental
procedures was radical but logical. That being the case why compromise?
If
there are 1.35 million dental procedures performed on “at risk”
patients
each year (and how reliable is that figure?) there is certainly a
substantial pool available for randomisation – why not push hard for
what
is believed to be right?
The science of endocarditis is clear enough – valves become
infected
secondary to bacteraemia. The argument that rabbit models do not
replicate
strictly the pathogenesis of endocarditis in humans and as such the
evidence is questionable confines much of 20th century progress to the
intellectual dustbin. The incidence of endocarditis will depend on the
organism type, the immune status of the patient and the bacteriological
load. The argument that the patients with cardiac abnormalities are at
risk all year round and therefore should not be covered at recognizable
points when bacteraemia is predictable and can be adequately covered
beggars belief. People die in cars despite or because of seatbelts –
this
does not render ‘belting up’ impractical or inappropriate nor reduce
its
effectiveness in saving lives. The risk of antibiotic related death
from
penicillin anaphylaxis (quoted in the editorial) as five times higher
that
the risk of IE is unreferenced (and in our experience unbelievable) and
gives no indication of IE risk without antibiotics. Patients undergoing
dental procedures develop bacteraemias with a higher bacteriological
load
than the background risk from chewing or brushing. Doctors and dentists
cannot cover patient risk at all times. However they have a duty to
reasonably cover risks that are recognizable and potentially treatable.
No
treatment is 100% effective: antibiotic prophylaxis should not be
expected
to be so. Failure to stop all events does not indicate ineffectiveness
in
the majority. If the philosophy followed is that the risk of dental
treatment is tiny why cover any patients at all – the argument of
covering
patients at particularly high risk if they become infected applies to
all
patients not just those with prostheses or shunts. Endocarditis as a
whole
carries a mortality of at least 20% despite best available management.
Likewise, if the background risk is so small, why should a patient who
has
suffered endocarditis represent a higher risk of infection than one,
with
equivalent pathology, who has not? This does not appear a rational
stance
(from a group who require hard evidence). Isn’t this emotion rather
than
science?
The BSAC guidelines go on to outline indications for non-dental
procedures which by their own admission are “inferred by two equally
unsatisfactory sources” – the chance of a procedure causing bacteraemia
and whether such procedures have been anecdotally linked to
endocarditis –
exactly the evidence they find uncompelling in relation to dental
prophylaxis. It does not appear reasonable to adopt two differing
levels
of proof for the same type of evidence.
Bacterial endocarditis is a severe life threatening infection with
significant mortality and morbidity which despite best efforts and
prophylactic therapy continues to present on a regular basis in a
typical
cardiological and cardiac surgical practice. Most clinicians can
anecdotally confirm the association of infection following dental
intervention. Appendix 1 in the BSAC guidelines states “patients should
concentrate on achieving and keeping a high standard of oral and dental
hygiene, as this does reduce the risk of endocarditis.” The presumption
is
minimisation of the level of bacteraemia associated with chewing and
brushing will reduce the background risk of endocarditis. The same
rational should therefore be applied to recognizable periods of
increased
bacteraemia.
The advice from BSAC has produced a situation where confusion
reigns.
Although dentists may not use the defence of the “the cardiologist made
me
do it” likewise “BSAC told me so” is unlikely to be more effective.
Recommendations of this nature adopted unilaterally against the
best
advice of representative cardiological bodies put dentists in an
invidious
position. They will be liable for omissions in cover and are unlikely
to
be supported if the treatment given runs contrary to the
recommendations
of the patient’s cardiologist. I would doubt clinicians outside the UK
are
likely to find the reasoning of BSAC compelling or defensible.
Patients deserve clear and consistent advice from their
clinicians.
Unfortunately the advice inherent in the guidelines and your editorial
will not have helped to foster either.
Mr John AC Chalmers FRCS
Consultant Cardiac Surgeon
The Cardiothoracic Centre
Thomas Drive
Liverpool
L14 3PE
Mr D M Pullan FRCS
Consultant Cardiac Surgeon and Clinical Director
The Cardiothoracic Centre
References
1. Ashrafian H, Bogle R. Antimicrobial prophylaxis for endocarditis: Emotion or science Heart 2007; 93:5-6
2. Gould FK, Elliott TSJ, Foweraker J et al. Guidelines for the prevention of endocarditis: report of the Working Party of the British Society for Antimicrobial Therapy J Antimicrob Chemother 2006; 57: 1035-42
In the report by Ashrafian1 and Bogle, the authors highlight new
recommendations by the British Society for Antimicrobial Chemotherapy to
limit prophylaxis to high-risk patients with previously documented
endocarditis or surgical shunt/valve procedures (1). Although dental
prophylaxis have an impact on systemic disease, they do not eliminate
bacteremia altogether. Thus, in addition to antibiotic the...
In the report by Ashrafian1 and Bogle, the authors highlight new
recommendations by the British Society for Antimicrobial Chemotherapy to
limit prophylaxis to high-risk patients with previously documented
endocarditis or surgical shunt/valve procedures (1). Although dental
prophylaxis have an impact on systemic disease, they do not eliminate
bacteremia altogether. Thus, in addition to antibiotic therapy, education
and additional treatment modalities should also be available to prevent
systemic conditions following dental procedures (2-3).
Reports indicate that regular postgraduate courses may be an
effective avenue to educate practioners on appropriate antibiotic usage in
patients with endocarditis. (4). As well, treatment options like stannous
fluoride (5) and preventative care (6) may provide additional systemic
protection to patients. Finally, a review of individual dental practices
may also curb inappropriate antibiotic usuage (7).
References
1. Ashrafian H, Bogle RG. Antimicrobial prophylaxis for endocarditis: emotion or science? Heart 2007; 93: 5-6.
2. Ito HO. Infective endocarditis and dental procedures: evidence,
pathogenesis, and prevention. J Med Invest. 2006; 53(3-4):189-98
3. Brincat M, Savarrio L, Saunders W. Endodontics and infective endocarditis--is antimicrobial chemoprophylaxis required? Int Endod J. 2006; 39(9):671-82.
5. Ramji N, Baig A, He T, Lawless MA, Saletta L, Suszcynsky-Meister E, Coggan J. Sustained antibacterial actions of a new stabilized stannous fluoride dentifrice containing sodium hexametaphosphate. Compend Contin Educ Dent. 2005; 26(9 Suppl 1):19-28.
6. Gottehrer NR, Berglund SE. Antimicrobial host response therapy in periodontics: a modern way to manage disease. Dent Today. 2006 Sep;25(9):84-7.
7. Chate RA, White S, Hale LR, Howat AP, Bottomley J, Barnet-Lamb J, Lindsay J, Davies TI, Heath JM. The impact of clinical audit on antibiotic prescribing in general dental practice. Br Dent J. 2006; 201(10):635-41.
The editorial by Ashrafian and Bogle[1] suggests that the authors
have little clinical experience in the management of patients with
infective endocarditis (IE). The body of cardiologists and cardiac
surgeons in Europe, North America and the UK would disagree that the BSAC
guidelines are important or “a step in the right direction” and almost
certainly the guidelines will be disregarded by the rest o...
The editorial by Ashrafian and Bogle[1] suggests that the authors
have little clinical experience in the management of patients with
infective endocarditis (IE). The body of cardiologists and cardiac
surgeons in Europe, North America and the UK would disagree that the BSAC
guidelines are important or “a step in the right direction” and almost
certainly the guidelines will be disregarded by the rest of the world as
an eccentricity not based on any evidence whatsoever. Without doubt, they
are out of line with the views of physicians who have cared for patients
with IE over the last 50 years and of those who continue to have this
responsibility. The Joint Formulary Committee of the British National
Formulary and our dental colleagues would do well to take note of the
advice from specialist cardiologists from Europe and the USA regarding
antibiotic prophylaxis (ABP) for those at risk of IE and remember the
devastating consequences that often occur in those patients who are
unfortunately affected. Sadly, within our own Centre we have recently seen
two patients who developed IE after dental treatment who despite
requesting ABP from their dentist, were told that based on the new BSAC
guidelines ABP was not necessary and hence not administered.
Although a very large randomised controlled clinical trial of ABP
prior to dental treatment in those patients considered to be at
high/moderate risk of IE because of their cardiac structural abnormality
might help quantify the benefit/risks of ABP, we think it would prove
difficult to obtain ethical approval and even the patients’ consent for
such a study. With regards to the cost-effectiveness and safety of oral
amoxicillin, we believe it is very cost-effective at ₤1.50 per 3G
sachet, set against the high cost of a prolonged in-patient stay for
parenterally administered antibiotics, the high morbidity and mortality
and the need for surgery in those individuals with the serious destructive
cardiac and extracardiac complications of IE. Although anaphylaxis may
occur as an allergic response to penicillin, this is extremely rare and
not a reason for the omission of ABP.
Patients who place their trust in health professionals to do
everything in their power to protect them deserve a sensible cautious
approach from their physician to diminish the risk of developing a life-
threatening illness with high morbidity and mortality. Dentists look to
cardiologists and not microbiologists for advice about the need for ABP
for patients with cardiac abnormalities that place them at increased risk
of IE. Not to offer ABP to those patients who cardiologists consider to be
at risk of IE is a disservice and in most countries in the Western World
would be considered medico-legally negligent. Dentists will find it
difficult to obtain the support of the patient’s cardiologist when
disaster strikes their patient as a result of omitting ABP when this has
been recommended.
Dr David R Ramsdale MD FRCP, Consultant Cardiologist and Dr Nick D
Palmer MD MRCP, Consultant Cardiologist,
The Cardiothoracic Centre,
Thomas Drive,
Liverpool.
Reference
1. Ashrafian H and Bogle RG. Antimicrobial prophylaxis for endocarditis:emotion or science? Heart 2007;93:5-6.
with respect to the article on hepatic changes in the failing Fontan
circulation by Kiesewetter et al (1), we would like to respectfully point
out that large hypervascular regenerative nodules arising in the setting
of vascular hepatic disorders (especially Budd-Chiari syndrome) should be
considered as a different entity in comparison to regenerative nodules
found in cirrhotic liver. At our referra...
with respect to the article on hepatic changes in the failing Fontan
circulation by Kiesewetter et al (1), we would like to respectfully point
out that large hypervascular regenerative nodules arising in the setting
of vascular hepatic disorders (especially Budd-Chiari syndrome) should be
considered as a different entity in comparison to regenerative nodules
found in cirrhotic liver. At our referral centers we have had the
opportunity to study more than 100 cases of patients with vascular
disorders of the liver and large hypervascular regenerative nodules (2-5),
and we have never observed development of hepatocellular carcinoma in any
of these cases, nor we are aware of any report in the literature
demonstrating evolution of large hypervascular regenerative nodules into
hepatocellular carcinoma. On the other side, high grade dysplastic nodules
(and not regenerative nodules) commonly found in cirrhotic liver should be
considered a premalignant condition and are at risk of evolving into
hepatocellular carcinoma (6).
Dr. Giuseppe Brancatelli
Sezione di Scienze Radiologiche, Università di Palermo, Palermo, Italy
Dr. Michael P. Federle
University of Pittsburgh, Department of Radiology, Pittsburgh, PA
Dr. Valérie Vilgrain
Hopital Beaujon, Department of Radiology, Clichy, France
References
1. Kiesewetter C, Sheron N, Vettukattill J. e. Hepatic changes in the
failing Fontan circulation. Heart. 2006 Sep 27.
doi:10.1136/hrt.2006.094516
2.
Brancatelli G, Federle MP, Grazioli L, Golfieri R, Lencioni R. Benign regenerative nodules in Budd-Chiari syndrome and other vascular
disorders of the liver: radiologic-pathologic and clinical correlation. Radiographics 2002;22:847-862
3.
Brancatelli G, Federle MP, Grazioli L, Golfieri R, Lencioni R. Large regenerative nodules in Budd-Chiari syndrome and other vascular
disorders of the liver: CT and MR imaging findings with clinicopathologic
correlation. AJR 2002;178:877-883
4. Vilgrain V, Lewin M, Vons C, et al. Hepatic nodules in Budd-Chiari
syndrome: imaging features. Radiology 1999;210:443-450
5. Cazals-Hatem D, Vilgrain V, Genin P, et al. Arterial and portal
circulation and parenchymal changes in Budd-Chiari syndrome: a study in 17
explanted livers. Hepatology 2003;37:510-519
6. International Working Party. Terminology of nodular hepatocellular
lesions. Hepatology 1995;22:983-989.
We read with great interest the very important article by Dilaveris
et al about the climate impacts on myocardial infarction deaths in Athens,
Greece [1].
Several reports have already proved that the number of deaths related to
acute myocardial infarction (AMI) shows a seasonal variation, with a peak
in winter, and a lowest number of mortality rates during the months of
summer [2,3,4]. The effects o...
We read with great interest the very important article by Dilaveris
et al about the climate impacts on myocardial infarction deaths in Athens,
Greece [1].
Several reports have already proved that the number of deaths related to
acute myocardial infarction (AMI) shows a seasonal variation, with a peak
in winter, and a lowest number of mortality rates during the months of
summer [2,3,4]. The effects of meteorological variables on the human
organism have been studied for more than fifty years, and changes in the
number of AMI events have been related to both cold or warm temperatures
[5,6,7]. Some authors have found that the incidence of a hear attack may
also be influenced by changes of atmospheric pressure and front movements
[8,9].
Hungary is a small country in the middle of Europe, laying in the
Carpathian basin. Based on our results it may be stated that the number of
cardiac mortality (N=16.160) in Hungary shows a steadily decreasing
tendency between 2000 and 2005, with a seasonal variation regardless of
age or sex. Studying year 2001 in more detail, the peak period of AMI
mortality was during the months of spring, with a lowest value during the
summer. There was a significant difference between seasons (F=3.027;
p<0.05; N=2850). The daily average of cardiovascular mortality during
each season was the following: 8.48 during spring, 7.23 during the summer,
7.79 during autumn, and 7.76 during winter. The low rate of AMI mortality
during the months of summer may be related to summer holidays in addition
to favourable meteorological conditions. In addition to these findings, it
seems that the changes of weather conditions also influence the mortality
of other cardiovascular events. In Hungary the highest average daily
temperature in year 2001 was 28.83 Celsius grade in the month of July,
while the lowest average daily temperature was -10.93 Celsius grade in
December.
With consideration to meteorological conditions, our results show, that
the sharp temperature increase during spring, and the similarly
significant decrease of temperatures during autumn, both have an
increasing effect on heart attack related mortality. Studying the moving-
average of AMI mortality (k=7), and the relation with the daily average
temperature of the preceding 7 days, we have found a medium value negative
correlation (r = -0.466, p<0.01).
Categorizing our data according to age groups, the strongest correlation
was found in the age group of above 70 (r = -0.41, p<0.01), with a
weaker relation in the age group between 50 and 70 (r = -0.315,
p<0.01), while in the age group below 50 years of age, no correlation
was found. Considering the moving average of deaths (k=7) and the average
daily temperature of the preceding seven days above and below 20 Celsius
grade, we have found a significant difference. When the average daily
temperature of the preceding 7 days was above 20 Celsius grade, the
average of daily mortality was 7.23, while below 20 Celsius grade the
average of deaths was 7.93.
In the year 2001 in Hungary, the average daily atmospheric pressure showed
its lowest seasonal average during spring (with a value of 1013.14 hPa),
and the highest during autumn (1022.30 hPa). The moving average of deaths
during spring (k=7) shows a weak negative correlation with average daily
atmospheric pressure (r = -0.343, p<0.01).
This finding suggests, that the mortality of acute myocardial infarction
may be related to the internal biological rhythm of the organism, and also
to such external conditions as weather. From a biometeorological point of
view, the combined effect of certain meteorological factors, such as a
sudden temperature or atmospheric pressure change, or the number of front
movements, may be considered as a risk factor in the mortality of a heart
attack. The more risk factors one bares, the higher the chance of
developing a cardiovascular disease.
References
1. Dilaveris P, Synetos A, Giannopoulos G. et al. Climate Impacts on
Myocardial infarction deaths in the Athens Territory: the CLIMATE study. Heart 2006;92:1747-51.
2. Gerber Y, Jacobsen SJ, Killian JM. et al. Seasonality and daily weather
conditions in relation to myocardial infarction and sudden cardiac death
in Olmsted County, Minnesota, 1979 to 2002. J Am Coll Cardiol 2006;48:287-
92.
3. Sayer JW, Wilkinson P, Ranjadayalan K, et al. Attenuation or absence of
circadian and seasonal rhythms of acute myocardial infarction. Heart
1997;77:325-9.
4. Spencer FA, Goldberg RJ, Becker RC. et al. Seasonal distribution of
acute myocardial infarction in the second National Registry of Myocardial
Infarction. J Am Coll Cardiol 1998;3:1226-33.
5. Mestan JF, Kral V, Horni J. Meteorological effects on myocardial
infarct. Cas Lek Cesk 1956;95:581-5.
6. Ku CS, Yang CY, Lee WJ. et al. Absence of a seasonal variation in
myocardial infarction onset in a region without temperature extremes. Cardiology 1998;89:277-82.
7. Panagiotakos DB, Chrysohoou C, Pitsavos C. et al. Climatological
variations in daily hospital admissions for acute coronary syndromes. Int
J Cardiol 2004;94:229-33.
8. Houck PD, Lethen JE, Riggs MW. et al. Relation of atmospheric pressure
changes and the occurrences of acute myocardial infarction and stroke. Am
J Cardiol 2005;96:45-51.
9. Kveton V. Weather fronts and acute myocardial infarction. Int J
Biometeorol 1991;35:10-7.
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-...
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations. The methods and interpretation of the results, however, raise several concerns:
In this study, the left ventricular diastolic function parameters, for example, E, A, and E-wave deceleration time, E/A ratio, the maximal velocity during early diastole, the maximal velocity during atrial contraction and the ratio of them of mitral annulus etc., however, were not included in baseline parameters. It is well known that the marked diastolic dysfunction which could be promoted by PAH inducing increased RV pressure typically displace the pressure-volume relationship in an upward direction, resulting in increased left ventricular end-diastolic, left atrial, and rising pulmonary capillary wedge pressures, even aggravating right ventricular dysfunction. And then, is there a significant difference of left ventricular diastolic function condition at baseline, 12 months bosentan and 12 months bosentan + 3 months combination of the study groups? Is there a relation of left ventricular diastolic function condition to therapeutic advantages offered by bosentan and combination therapy? Similarly, the difference of RV diastolic function at baseline, 12 months bosentan and 12 months bosentan + 3 months combination are not described. Is there a relation of the difference of RV diastolic function at baseline, 12 months bosentan and 12 months bosentan + 3 months combination to therapeutic advantages offered by bosentan and combination therapy? They needs to be further evaluated.
An echocardiography study of Lopez-Candales et al2 certify that a very strong correlation between RV mechanical delay and RV fractional area change was noted in patients with PAH, suggesting RV mechanical delay could be a mechanism of RV dysfunction induced by PAH. In this study, however, RV mechanical delay at baseline, 12 months bosentan and 12 months bosentan + 3 months combination were not described. It is very important because several new and effective treatment options for RV dysfunction induced by PAH which could significantly improve the prognosis of the PAH patients would be proposed, if there was a relation of the therapeutic advantages offered by bosentan and combination therapy to improvement of RV mechanical delay. Therefore, the mechanism of RV dysfunction induced by PAH and the therapeutic advantages offered by bosentan and combination therapy needs to be further evaluated.
References
1. Wolferen SAV, Boonstra A, Marcus JT, et al. Right ventricular reverse remodelling after sildenafil in pulmonary arterial hypertension. Heart 2006; 92: 1860-1861.
2. Lopez-Candales A, Dohi K, Bazaz R, et al. Relation of right ventricular free wall mechanical delay to right ventricular dysfunction as determined by tissue Doppler imaging. Am J Cardiol 2005; 96: 602-606.
I read with great interest the recent report from Schmid and
coworkers regarding the hemodynamic changes induced in water, which is of
special interest among patients with deteriorated cardiac function. The
hypothesis is interesting, however the methods used for cardiac output
determination in a swimming pool have to be discussed. Schmid used an
inert gas rebreathing method using an infrared photoa...
I read with great interest the recent report from Schmid and
coworkers regarding the hemodynamic changes induced in water, which is of
special interest among patients with deteriorated cardiac function. The
hypothesis is interesting, however the methods used for cardiac output
determination in a swimming pool have to be discussed. Schmid used an
inert gas rebreathing method using an infrared photoacustic gas analyser,
which has been validated in land situations only by the references given
by the authors. Gabrielsen (1) and coworkers studied 11 patients with
dilated cardiomyopathy or primary pulmonary hypertension regarding the
rebreathing technique vs. direct Fick measurement using a catheter in the
cath lab up to cardiac outputs of from 2 to 6.5l/min only. Agostoni (2)
and coworkers studied 20 patients with chronic heart failure (Vo2
16.6±2.9ml/min/kg) on a cycle ergometer vs. thermodilution and vs. Fick
method with good correlation from cardiac output of 4.5l/min to 12l/min.
As stated by the authors repetitive calibration is mandatory even in the
lab setting and we do not have any data from the authors regarding the
intra- and interobserver reliability of the rebreathing method used in the
swimming pool.
Schmid reported significant stroke volume changes from 60ml to more
than 100ml among healthy subjects with consecutive increase of cardiac
index from 2.3l/min/m2 to 5l/min/m2 in the healthy subjects. Systemic
vascular resistance decreased significantly in immersion using the
rebreathing method.
We tested thirteen cardiac healthy swimming athletes with real-time
continuous wave (CW) Doppler based hemodynamic monitoring using the USCOM
device (3) at rest at land, at immersion and following a swimming
endurance protocol. In contrast to rest at land whole body immersion
increased heart rate from 94±17/min to 100±14/min, stroke volume from
42±18ml to 81±18/ml, and cardiac output from 4.0±0.9l/min to 8±1.6l/min
(cardiac index 2.17±0.6l/min/m2 vs. 4.3±0.9l/min/m2), which is somehow in
line with the data presented by Schmid using the rebreathing method.
Systemic vascular resistance declined from 2053±469 to 986±249dyne*s*cm-5
significantly in our small study which also is in line with the reported
data from Schmid. The endurance swimming test lead to significant
upregulation of heart rate from baseline to 160±12/min, stroke volume
(95±9ml), cardiac output (15.4±1.6l/min), and cardiac index
(8.3±1.0l/min/m2).
Therefore, based on the results of Schmid using the rebreathing
method and our direct ultrasound cardiac monitoring using the USCOM in
healthy swimming athletes, significant changes of hemodynamics are
encountered in immersion at rest especially regarding the upregulation of
the stroke volume rather than an increased heart rate. Further studies are
mandatory to elucidate the immediate hemodynamic response among patients
with heart failure in physical exercise in the water, such as aqua
jogging, moderate swimming or even diving.
References
(1) Gabrielsen A, Videbaek R, Schou M, Damgaard M, Kastrup J, Norsk P. Non-invasive measurment of cardiac output in heart failure patients using a new foreign gas rebreathing technique. Clin Sci (Lond) 2002;102:247-52.
(2) Agostoni P, Cattadori G, Apostolo A, Contini M, Palermo P, Marenzi G, Wasserman K. Noninvasive measurment of cardiac output during exercise by inert gas rebreating technique: a new tool for heart failure evaluation. J Am Coll Cardiol 2005;46:1779-81.
(3) Knobloch K, Lichtenberg A, Winterhalter M, Rossner D, Pichlmaier M, Phillips R. Non-invasive cardiac output determination by twodimensional independent Doppler during and after cardiac surgery. Ann Thorac Surg 2005;80:1479-83.
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and
environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with...
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and
environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with a large increase in cardiovascular risk,present even in absence of hypertension and
prehypertension itself.The prevalence of obesity varies between 5-7%, in the Asian urban population.The paradox is that despite low rates of obesity, the prevalence of central obesity (40-60%),prediabetes(10-15%),overswinging of BP(10-15%),type 2 diabetes(6-15%),and ACS(9-14%) are
higher, in urban areas, which are much higher among Asian immigrants to developed countries(2).The prevalence of metabolic syndrome is 5% in rural and 15%in urban south India whereas in north and western India,the prevalences appear to be slightly lower. In a cross-sectional survey, in five Indian cities,among 6940 subjects aged 25years and above, the prevalence of obesity was approximately 7% but more than half of the subjects had central obesity and one third had prehypertension,one quarter hypertension and one fifth prediabetes.About three quarters of hypertensives had central obesity in both sexes. In a subsample,(n=1633), the prevalence of metabolic syndrome comprising of central obesity, hypertension and hypertriglyceridemia and low HDL was approximately 13% and premetabolic syndrome comprising of prehypertension, prediabetes and
central obesity in 19.5%. The emerging typical South Asian, urban or immigrant has phenotype of higher percentage of body fat at a lower value of BMI,high WHR at a relatively low waist circumference and less lean body
mass compared to other ethnic groups. A similar genotype is present among Chinese and other Asians.However,in case control studies,the mean age in south Asia varies between 48 to 51 years,which is againt the finding of 61 years mean age among Asians,(3) in the study by Teo and co-workers(1,3).
In one study among 54 patients with acute coronary syndromes(ACS), 41 patients had acute myocardial infarction(AMI),5 possible MI, 4 cases unstable angina and rest 4 angina pectoris.The control subjects(n=85) were randomly selected from the population from the city of Moradabad, drawn from a similar age and sex of the subjects.Serum level of nitrite(a indicator of nitric oxide,NO) was significantly lower in patients with AMI compared to controls(mean+SD:0.36+1.42 vs 0.96+1.48uM,CI difference
0.60,0.34-1.02,P<0.03).After 4 weeks of follow up,serum nitrite level recovered showing significant increase without such changes in the control group.(0.88 vs 1.09uM;CI 0.21,0.67-1.12,P<0.05) The incidence of
lipoprotein(a) excess(>30mg/dl) and mean levels of
lipoprotein(a)(difference 6.4mg/dl,95% confidence interval 2.8-10.5,P<0.05) was significantly greater in the acute CAD group compared to control subjects.Serum levels of vitamins E,C and beta-carotine,coenzyme Q10,magnesium and potassium were significantly lower and insulin, glucose, triglycerides, and lipoprotein(a) were significantly higher
in ACS compared to their levels after 4 weeks of follow up.There was a significantly greater occurrence of acute ACS events in the second quarter of the day compared to other quarters.A circadian rhythm was also noted
for serum level of NO showing significantly lower nitrite in 6.00-12.00 AM period compared to afternoon,12.00-18.00hours period(0.27+1.12 vs 0.42+1.44 uM,P<0.04).
The differences in the nitrite levels in the two groups indicate that low levels of nitrite appears to be a risk factor of ACS.Lower levels of nitrite during acute stage of AMI and its recovery after 4 weeks of follow up indicate that transient hyperglycemia and hyperinsulinemia may also be responsible for its increase, (apart from low arginine intake and sedentary behaviour,) by inhibiting the expression of NO receptors caused by metabolic reactions evoked by ACS. Reduction in antioxidants vitamins may be due to increased oxidative stress which is common in AMI due to enhanced free radical generation which may also influence NO levels and cause endothelial dysfunction.More studies would be necessary to
demonstrate that NO deficiency is a risk factor of ACS.There is a need to compare association of protective factors; physical activity, fruit and begetable intake,n-6/n-3 ratio in the diet, moderate alcohol intakes and
stress to find out their roles in the pathogenesis of ACS among Asians and Caucasians(1-5).
In rural population of India and China,there is low plasma insulin, low glucose, triglycerides and angiotensin. There is low prevalence of central obesity and obesity is uncommon in rural areas of Asia.When these
populations migrate to urban slums or to industrialized countries, they substitute cereal based diet from ready prepared fast foods containing more linoleic acid, saturated fat, trans fatty acids, sugar, and flesh
foods and dairy products in conjunction with sedentary behaviour and increased mental stress.It seems that rapid changes in diet and lifestyle due to modest but unsustainable, economic development, without learning of
methods of prevention, result into maladaptations, that are important in the pathogenesis of acute coronary syndromes among Asians.
icn2008@mickyonline.com
REFERENCES
1.Teo M, Lalondrel S, Roughton M, Mason RG, Dubrey SW Acute coronary syndromes and their presentation in Asian and Caucasian patients in Britain Heart 2007, 93: 183-188
2.Singh RB, Suh IL, Singh VP et al. Hypertension and stroke in Asia;prevalence, control, and strategies in developing countries for prevention J Human Hyper 2000 ,14:740-763
3.Singh RB,Rastogi SS, Verma R et al. An Indian experiment with nutritional modulation in acute myocardial infarction Am J Cardiol 1992, 69: 879-885
4.Singh RB, Pella D, De Meester F What to eat and chew in acute myocardial infarction Eur Heart J 2006,27: 1628-29
5.Janus ED, Postiglion E, Singh RB, Lewis B. Coronary heart disease in Asia Circulation 1996,94: 2671-73
Dear Editor,
We have read with great interest the article by Roudaut et al entitled "Thrombosis of prosthetic heart valves: Diagnosis and therapeutic considerations" published in the last issue of your journal.(1) According to the authors, the first therapeutic consideration in obstructive left-sided prosthetic valve thrombosis (PVT) should be surgery and thrombolysis should be reserved for patients with contrain...
Dear Editor,
The debate on the role of antimicrobial prophylaxis to prevent infective endocarditis (IE) has intensified as a consequence of the recently published guidelines from the Working Party of the British Society for Antimicrobial Chemotherapy (BSAC). In the review by Ashrafian and Bogle, reference is made to the dental community’s satisfaction with these new guidelines, highlighting a “victory for scien...
Dear Editor,
As cardiac surgeons we read and reread the editorial by Ashrafian and Bogle initially with interest and subsequently bemusement looking for a definitive message. The title was clear enough; the editorial was not.
The conclusion that good practice will be served if “patients are adequately counselled on the benefits of good dental hygiene and a discussion is undertaken and documented on the ri...
Dear Editor,
In the report by Ashrafian1 and Bogle, the authors highlight new recommendations by the British Society for Antimicrobial Chemotherapy to limit prophylaxis to high-risk patients with previously documented endocarditis or surgical shunt/valve procedures (1). Although dental prophylaxis have an impact on systemic disease, they do not eliminate bacteremia altogether. Thus, in addition to antibiotic the...
Dear Editor,
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Dear Editor,
with respect to the article on hepatic changes in the failing Fontan circulation by Kiesewetter et al (1), we would like to respectfully point out that large hypervascular regenerative nodules arising in the setting of vascular hepatic disorders (especially Budd-Chiari syndrome) should be considered as a different entity in comparison to regenerative nodules found in cirrhotic liver. At our referra...
Dear Editor,
We read with great interest the very important article by Dilaveris et al about the climate impacts on myocardial infarction deaths in Athens, Greece [1]. Several reports have already proved that the number of deaths related to acute myocardial infarction (AMI) shows a seasonal variation, with a peak in winter, and a lowest number of mortality rates during the months of summer [2,3,4]. The effects o...
Dear Editor,
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-...
Dear Editor,
I read with great interest the recent report from Schmid and coworkers regarding the hemodynamic changes induced in water, which is of special interest among patients with deteriorated cardiac function. The hypothesis is interesting, however the methods used for cardiac output determination in a swimming pool have to be discussed. Schmid used an inert gas rebreathing method using an infrared photoa...
Dear Editor,
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with...
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