The recent study by Ha et al (1) illustrates the potential benefit of
using exercise stress for detection of early myocardial disease in
diabetic patients. With modern advances in cardiac imaging the detection
and management sub-clinical disease in patients at high cardiovascular
risk is likely to become increasingly relevant. The use of exercise stress
and its application outside the conventional app...
The recent study by Ha et al (1) illustrates the potential benefit of
using exercise stress for detection of early myocardial disease in
diabetic patients. With modern advances in cardiac imaging the detection
and management sub-clinical disease in patients at high cardiovascular
risk is likely to become increasingly relevant. The use of exercise stress
and its application outside the conventional application of coronary
disease highlights an area of underutilisation in echocardiographic
practice.
The concept of applying a stress modality to assess cardiac status
has long been one of the basic principles of our assessment of patients
with known or suspected coronary disease and forms a large part of what we
do in routine clinical practice. It allows us to better understand the
nature of symptoms that develop during physical exertion and can detect
asymptomatic disease in at risk individuals. Stress testing also has a lot
to offer in other patient groups. As with coronary problems many patients
with significant disease have abnormal findings exclusively during stress,
resting abnormalities only being manifested in the advanced stages of the
process. For example, echocardiography is often performed in the resting
state in patients with exertional breathlessness. It frequently reveals
normal appearances or only subtle pathology such as early diastolic
relaxation abnormalities of uncertain significance. In these circumstances
it is plausible that supplementary haemodynamic information could be added
by a stress assessment.
In mobile patients exercise echocardiography is a highly feasible and
well-validated technique. It may be preferable to pharmacological stress
testing. In the setting of coronary disease incorporation of functional
treadmill variables into clinical decision-making adds useful information
to echocardiographic data (2). Previous studies have demonstrated the
value of exercise echocardiography in populations with valvular (3) and
myocardial (4) disease as well as pulmonary hypertension (5). Other
applications are developing with implications for diagnosis, therapy and
possibly prognosis.
Stress echocardiography is not just about using a pharmacological
agent to look for ischaemia and viability. An exercise protocol can be
used in a large proportion of patients and has applicability across a
range of clinical problems in cardiology where it supplements information
gained at rest.
REFERENCES
1. Ha JW, Lee HC, Kang ES et al. Abnormal left ventricular
longitudinal functional reserve in patients with diabetes mellitus: implication for detecting subclinical myocardial dysfunction using exercise tissue Doppler echocardiography. Heart. 2007;93:1571-6.
2. Marwick T, Case C, Vasey C, Allen S, Short L, Thomas J. Prediction of mortality by exercise echocardiography: a strategy for combination with the Duke treadmill score. Circulation 2001;103:2566–71.
3. Lee R, Haluska B, Leung DY, Case C, Mundy J, Marwick TH. Functional and prognostic implications of left ventricular contractile reserve in patients with asymptomatic severe mitral regurgitation. Heart 2005; 91: 1383-4.
4. Burgess MI, Jenkins C, Sharman JE, Marwick TH. Diastolic stress echocardiography: hemodynamic validation and clinical significance of estimation of ventricular filling pressure with exercise. J Am Coll Cardiol. 2006 May 2;47:1891-900.
5. Collins, N, Bastian B, Quiqueree L, Jones C, Morgan R, Reeves G. Abnormal pulmonary vascular responses in patients registered with a systemic autoimmunity database: Pulmonary Hypertension Assessment and Screening Evaluation using stress echocardiography (PHASE-I). Eur J Echocardiogr 2006; 7: 439-46.
Recently, Yacoub et al,[1] reviewed for the section Education in
Heart of the journal Heart, different clinical but also epidemiological,
diagnostic, therapeutic and other aspects of Chagas disease, “a neglected
tropical cardiomyopathy”. Although it should be acknowledge the importance
of such reviews, particularly in a topic that has been neglected in many
aspects, including research as well intern...
Recently, Yacoub et al,[1] reviewed for the section Education in
Heart of the journal Heart, different clinical but also epidemiological,
diagnostic, therapeutic and other aspects of Chagas disease, “a neglected
tropical cardiomyopathy”. Although it should be acknowledge the importance
of such reviews, particularly in a topic that has been neglected in many
aspects, including research as well international education, some aspects
needs further comments and discussion.
As Yacoub et al stated Chagas disease is caused by the protozoan
parasite Trypanosoma cruzi, its transmission (more than the spread) is due
to different species of hematophagous reduviidae bugs, that include
Triatoma infestans, but also Rhodnius prolixus, Triatoma dimidiata, and
Panstrongylus megistus, among others.[2] About the geographical
distribution is important to state that currently Chagas disease is
endemic in Latin America, ranging from Argentina to Mexico, but in North
America is present in also southern states of USA, including Texas,[3]
Oklahoma,[4] Alabama,[5] and more recently in Louisiana due to Triatoma
sanguisuga,[6] but also in western states such as Arizona,[7] New
Mexico,[8] California.[9]
Secondly, although the latin American immigration of patients with
Chagas disease to north America is one of the most important, recently
this phenomena has been increasingly relevant in other countries in
Europe, particularly to Spain,[10] but also France,[11] Germany,[12]
Switzerland,[13] among others. Even in the United Kingdom a patient from
this country returned from Argentina with Chagas disease.[14] In
Australia, Chagas disease in immigrants has been also reported.[10] In the
case of USA, although up to year 2000 just five cases were reported, the
diagnose of these cases included PCR,[15] and in 2007, when the
autochthonous transmission of T. cruzi occurred in Louisiana, the patient
had positive test results from 2 serologic tests and hemoculture at the
Centers for Disease Control, Atlanta, Georgia, and the Triatoma sanguisuga
(18) collected were positive for T. cruzi by PCR in 56%.[6] Then, Chagas
disease could be an emergent disease in the United States.
About the life cycle of the parasite, this involves many
morphologically distinct stages – more than described for any other genus
in the Family Trypanosomatidae. In the mammalian host, intracellularly
multiplying amastigotes develop via epi- and promastigote intermediate
stages to nonreplicative blood trypomastigotes. These trypomastigotes are
ingested by the insect vectors and transform in the lumen of the digestive
tract into dividing and nonreplicative amastigotes and spheromastigotes
and dividing epimastigotes. Later, nonreplicative infective
trypomastigotes develop. If the main intermediate stages are also
considered, more than 18 different forms can be classified in the
vector.[16]
Clinically, an area of inflammation at the site of inoculation,
called chagoma, when involves conjunctival inoculation could lead to the
triad of conjunctivitis, periorbital edema, and preauricular satellite
lymphadenopathy; and this is what is known as the Romaña sign.[17]
Regard to the pathology we consider that those developments recently
achieved in demonstrating that T. cruzi could be found in the myocardium
during the chronic phase of Chagas disease, should be acknowledged citing
some of them.[18, 19]
Finally, in the XXI century when HIV/AIDS pandemics is affecting the
human being worldwide, the interaction between T. cruzi and this
retrovirus, should be also considered, because produce a different
clinical spectrum. Chagas disease has been well recognized as an
opportunistic infection associated with AIDS.[20, 21] To date, the cases
reported largely represent reactivation of chronic infection, which is
expected because of the differing patterns of epidemiological risk for
these infections; T. cruzi infection occurs primarily in rural regions,
and HIV infection occurs primarily in urban regions, but this pattern is
changing and less rural and more urban pattern is now observed in
different countries allowing the geographical overlapping between both
entities.[22, 23] Clinical reactivation generally occurs in persons with
CD4+ T cell counts <200 cells/mm3 and most commonly involves the CNS.
Lesions are often multiple, with preferential involvement of the white
matter. Hemorrhagic foci can produce mass effects simulating brain tumors.
Histologically, brain lesions exhibit necrosis, hemorrhage, and
inflammatory infiltrates. Amastigote forms of the parasite are abundant in
glial cells and macrophages. Myocarditis is a common autopsy finding in
persons who have died of meningoencephalitis. Such myocarditis is often
clinically silent. When present, clinical manifestations include
arrhythmias and congestive heart failure.[20]
Cardiac manifestations previously seen only in resource-constrained
countries, including certain parasitic infections such as Chagas disease,
can be currently diagnosed anywhere in the globe. These epidemiologic
transitions have been favored by multiple factors: growing travel and
immigration, worldwide spread of HIV/AIDS epidemic, and growing number of
organ transplantation, increased use of immunosuppressive agents, and
blood transfusions.[23] Clinicians anywhere in the globe need to be aware
of the potential cardiac manifestations of parasitic diseases, such as the
American Trypanosomiasis, but also those related to other neglected
diseases.
2. Moncayo A. Chagas disease: current epidemiological trends after the
interruption of vectorial and transfusional transmission in the Southern Cone countries. Memorias do Instituto Oswaldo Cruz 2003;98:577-91.
3. Hanford EJ, Zhan FB, Lu Y, et al. Chagas disease in Texas: recognizing the significance and implications of evidence in the literature. Social science and medicine (1982) 2007;65:60-79.
4. Bradley KK. American trypanosomiasis: Chagas disease an emerging
zoonotic threat in Oklahoma? The Journal of the Oklahoma State Medical Association 1997;90:253-5.
5. Olsen PF, Shoemaker JP, Turner HF, et al. Incidence of Trypanosoma cruzi (Chagas) in Wild Vectors and Reservoirs in East-Central Alabama. The Journal of parasitology 1964;50:599-603.
6. Dorn PL, Perniciaro L, Yabsley MJ, et al. Autochthonous transmission of Trypanosoma cruzi, Louisiana. Emerging infectious diseases 2007;13:605-7.
7. Pfeiler E, Bitler BG, Ramsey JM, et al. Genetic variation, population structure, and phylogenetic relationships of Triatoma rubida and T. recurva (Hemiptera: Reduviidae: Triatominae) from the Sonoran Desert, insect vectors of the Chagas' disease parasite Trypanosoma cruzi. Molecular phylogenetics and evolution 2006;41:209-21.
8. Wood SF, Wood FD. Observations on vectors of Chagas' disease in the United States. III. New Mexico. The American journal of tropical medicine and hygiene 1961;10:155-65.
9. Navin TR, Roberto RR, Juranek DD, et al. Human and sylvatic Trypanosoma cruzi infection in California. American journal of public health 1985;75:366-9.
10. Schmunis GA. Epidemiology of Chagas disease in non endemic countries:
the role of international migration. Mem Inst Oswaldo Cruz 2007.
11. Brisseau JM, Cebron JP, Petit T, et al. Chagas' myocarditis imported into France. Lancet 1988;1:1046.
12. Frank M, Hegenscheid B, Janitschke K, et al. Prevalence and epidemiological significance of Trypanosoma cruzi infection among Latin American immigrants in Berlin, Germany. Infection 1997;25:355-8.
13. Sztajzel J, Cox J, Pache JC, et al. Chagas' disease may also be encountered in Europe. European heart journal 1996;17:1289.
14. Todd IP, Porter NH, Morson BC, et al. Chagas disease of the colon and rectum. Gut 1969;10:1009-14.
15. Herwaldt BL, Grijalva MJ, Newsome AL, et al. Use of polymerase chain reaction to diagnose the fifth reported US case of autochthonous transmission of Trypanosoma cruzi, in Tennessee, 1998. The Journal of infectious diseases 2000;181:395-9.
16. Kollien AH, Schaub GA. The development of Trypanosoma cruzi in triatominae. Parasitology today, Personal ed 2000;16:381-7.
17. Prata A. Clinical and epidemiological aspects of Chagas disease. The Lancet infectious diseases 2001;1:92-100.
18. Anez N, Carrasco H, Parada H, et al. Myocardial parasite persistence in chronic chagasic patients. The American journal of tropical medicine and hygiene 1999;60:726-32.
19. Schijman AG, Vigliano CA, Viotti RJ, et al. Trypanosoma cruzi DNA in cardiac lesions of Argentinean patients with end-stage chronic chagas heart disease. The American journal of tropical medicine and hygiene
2004;70:210-20.
20. Karp CL, Auwaerter PG. Coinfection with HIV and tropical infectious diseases. I. Protozoal pathogens. Clin Infect Dis 2007;45:1208-13.
22. Guzman-Tapia Y, Ramirez-Sierra MJ, Dumonteil E. Urban Infestation by Triatoma dimidiata in the City of Merida, Yucatan, Mexico. Vector borne and zoonotic diseases (Larchmont, NY 2007;7:597-606.
23. Franco-Paredes C, Rouphael N, Mendez J, et al. Cardiac manifestations of parasitic infections part 1: overview and immunopathogenesis. Clinical cardiology 2007;30:195-9.
I read with great interest the report by Robles et al (1), recently
published in the Journal, that describes the occurrence of left
ventricular thrombus formation (LVTF) in a patient with apical ballooning
(Takotsubo-like syndrome).
This study likely provides further contribution to the knowledge on
the various clinical aspects of this stress-related cardiac disease.
In spite of the acut...
I read with great interest the report by Robles et al (1), recently
published in the Journal, that describes the occurrence of left
ventricular thrombus formation (LVTF) in a patient with apical ballooning
(Takotsubo-like syndrome).
This study likely provides further contribution to the knowledge on
the various clinical aspects of this stress-related cardiac disease.
In spite of the acute and often severe LV functional impairment in the
majority of the patients, the complication described by Robles seems to be
rare. Under a pathophysiological point of view, there are several reasons
to theorize a common causal mechanism of TF between Takotsubo-like
syndrome and ischemic (necrotic) apical dilatation. Apical blood flow
stasis, together with the known abnormalities in the electrical charges of
blood cells and endothelial or endocardial surface, and/or hyper-
coagulation are time-honoured determinants of cardiovascular thrombosis.
Therefore, it is conceivable that the occurrence of LVTF is not rigorously
related to the hyper-adrenergic storm, which is typical of the apical
ballooning, but to other pre-existing cofactor(s), as S- or C-protein, C-
reactive protein, factor V Leiden, platelet aggregation, hormone levels,
genetic factors, leukocyte adhesion molecules, fibrinogen, viscosity,
etc., that may be accounted for such inter-individual differences as in
patients with myocardial infarction.
One of the most puzzling questions in the patients with ballooning
concerns the discrepancy between the coronary bed (where thrombosis has
never been described) and left ventricular cavity (where it has been).
Recent working hypotheses have been addressed on adrenaline-induced
switching from Gs-protein to Gi-protein signaling of the beta2-
adrenoceptor that may make the apical myocardium more susceptible to
(structural or functional) damage than other cardiac sites (2).
However, though rare, LVTF has been already reported by at least 10
studies, including that one published in 2003 by Barrera-Ramirez et al (3)
(from the same Institution of Robles et al ?). Thus, it is rather
surprising that the Authors affirmed that "...a LV thrombus associated
with Takotsubo-like ventricular dysfunction has not been demonstrated,
although there have been reports regarding the embolic complications of
this disorder", since the first description dates just back to that study
(3).
Based on the published reports, fortunately, embolic complications
are not so frequent. About 20% of cadioembolic stroke, as the main
clinical presentation, and another case of late renal infarct, but no
fatal outcomes, have been reported in the patients with patent LVTF (4-6).
On the other hand, we should also consider that over the last decade
the diagnosis of Takotsubo-like disease was performed only by angiography,
so that some LVTF might have been overlooked in the past. Contemporary
techniques, such as high-resolution echocardiography or cardiac magnetic
resonance, together with a rising clinical awareness about the syndrome,
surely contribute to a better knowledge of its various aspects, even if
lots of pathophysiological questions are still open.
REFERENCES
1. Robles P, Jimenez JJ, Alonso M. Left ventricular thrombus associated with left ventricular apical ballooning. Heart 2007;93:861.
3. Barrera-Ramirez CF, Jimenez-Mazuecos JM, Alfonso F. Apical thrombus associated with left ventricular apical ballooning. Heart 2003;89:927.
4. Grabowski A, Kilian J, Strank C, Cieslinski G, Meyding-Lamad¨¦ U. Takotsubo cardiomyopathy. A rare cause of cardioembolic stroke. Cerebrovasc Dis 2007;24:146¨C8.
5. Nerella N, Lodha A, T¨ªu CT, Chandra PA, Rose M. Thromboembolism in Takotsubo syndrome: A case report. Int J Cardiol 2007;doi:10.1016/j.ijcard.2006.11.186.
6. de Gregorio C, Cento D, Di Bella G, Coglitore S. Minor stroke in a Takotsubo-like syndrome: a rare clinical presentation due to transient left ventricular thrombi. Int J Cardiol (in press).
With great interest we read the article of Balint and coworkers (1),
in which they report the results of catheter-closure of an atrial septal
defect (ASD) in 54 patients with associated pulmonary arterial
hypertension (PAH). The authors describe successful closure and a decrease
in pulmonary artery pressure and NYHA functional class at one year follow
up in the majority of patients. On the other han...
With great interest we read the article of Balint and coworkers (1),
in which they report the results of catheter-closure of an atrial septal
defect (ASD) in 54 patients with associated pulmonary arterial
hypertension (PAH). The authors describe successful closure and a decrease
in pulmonary artery pressure and NYHA functional class at one year follow
up in the majority of patients. On the other hand, more than half of the
patients had persistent PAH (moderate or severe) after closure and two
patients died during follow up. The interpretation of the authors of these
data is that catheter-closure of ASD in patients with PAH is successful
and has a good outcome. In our opinion, however, this conclusion is not
justified and we feel that it is important to add some considerations on
PAH associated with congenital pulmonary-to-systemic shunts, in order to
put the interpretation of the data, as presented by the authors, in a
broader perspective.
PAH in congenital heart defects associated with a systemic-to-
pulmonary shunt, including atrial septal defect, is a progressive
pulmonary vascular disease. Its progressive course is characterized by a
reversible phase early in the disease versus a progressive, irreversible
phase in the advanced stage of the disease (2). When the heart defect is
adequately corrected in the early, reversible phase of the pulmonary
vascular disease (either surgically or by catheter intervention), the PAH
will disappear and remodeled pulmonary arteries will normalize (1,2).
However, when the heart defect is corrected late, in the advanced stage of
the pulmonary vascular disease, and characteristic vascular lesions have
developed, including concentric laminar intimal fibrosis and plexiform
lesions, the pulmonary vascular disease will be not only irreversible, but
will progress in time despite closure of the shunt (2,3). In this latter
scenario, closure of the heart defect will eventually lead to
deterioration of the clinical condition and a decreased survival in these
patients. This is because the defect is no longer able to serve, in case
of right ventricular failure, as an escape to maintain cardiac output at
the cost of cyanosis as is the case in Eisenmenger’s syndrome.(3,4)
The considerations above lead to two important comments with respect
to the data presented by Balint and coworkers and to the interpretation of
these data by the authors.
The first question that should be asked in a patient with ASD and PAH,
before attempting to close the defect is: How far is the progression of
the pulmonary vascular disease in this individual patient? The authors
provide no data regarding assessment of the progression of the pulmonary
vascular disease in the patients studied. Determination of the acute
response to pulmonary vasodilator testing, with nitric oxide, oxygen or
other agents, has been generally used to assess this progression in
patients with CHD and to assess the possibility to close the defect. (3)
Although it is recognized that there is a grey area in which it may be
difficult to distinguish between reversible and irreversible disease, most
patients with advanced pulmonary vascular disease can be identified, in
whom closure of the defect will have a detrimental effect in time (3).
The second comment addresses the suggestion by the paper that a decrease
in pulmonary artery pressure early after closure of the ASD is reassuring
and can be regarded as a successful outcome of the procedure for the
patient. In our opinion this is absolutely not the case. If an increased
pulmonary blood flow is diminished by closure of a heart defect, the
pulmonary artery pressure will always decrease, independent from pulmonary
vascular resistance. This will also occur in patients with advanced,
progressive, pulmonary vascular disease. In these latter patients,
however, PAP will gradually increase again parallel with the progression
of the vascular disease, and eventually outcome will be worse than that
with an unclosed defect (4).
In the current paper, Balint and co-workers report that PAH was still
present after one year in more than half of their patients. In the lights
of the conceptual considerations as described above, one could argue if
the conclusion of the authors, “Transcatheter closure in patients with
secundum ASD and PAH …is associated with good outcomes…” is justified. We
think it is not: concerns are in place regarding the outcome of these
patients at long term follow up (which is more than one year) compared to
similar patients in whom the ASD is not closed. We absolutely do agree
with the authors that follow up studies in this respect are needed.
References
1) Balint OH, Samman A, Haberer K, Tobe L, Mc Laughlin P, Siu SC, Horlick E, Granton J, Silversides CK. Outcomes in Patients with Significant Pulmonary Hypertension Undergoing Percutaneous Atrial Septal Defect
Closure. Heart. 2007; doi:10.1136/hrt.2006.114660
2) Wagenvoort CA. Morphological substrate for the reversibility and irreversibility of pulmonary hypertension. Eur Heart J. 1988; Suppl J:7-12.
3) Berger RMF. Possibilities and impossibilities in the evaluation of
pulmonary vascular disease in congenital heart defects. Eur Heart J. 2000;1:17-27
4) Law MA, Grifka RG, Mullins CE, Nihill MR. Atrial septostomy improves survival in select patients with pulmonary hypertension. Am Heart J. 2007;153:779-84.
An accurate selection and optimal timing in addressing patients to
CRT is important in order to optimize the treatment. Consequently the
identification of outcome predictors is critical.
For these reasons we greatly appreciated the paper by Gradaus et al.
entitled and stating that “diastolic filling pattern and left ventricular
diameter predict response and prognosis after cardiac resynch...
An accurate selection and optimal timing in addressing patients to
CRT is important in order to optimize the treatment. Consequently the
identification of outcome predictors is critical.
For these reasons we greatly appreciated the paper by Gradaus et al.
entitled and stating that “diastolic filling pattern and left ventricular
diameter predict response and prognosis after cardiac resynchronization
therapy” that adds, on a larger scale, further evidence to the recently
“in extenso” reported RESYNC results (Gimelli et al, 2007) about the
relevance of the pre-CRT left ventricular dimensions (both systolic and
diastolic) on functional response after CRT in patients with chronic heart
failure (CHF) and left bundle branch block (LBBB).
Particularly, an indexed left ventricular end-diastolic volume
(iLVEDV), i.e. LVEDV/body surface area, upper than 142 ml/square meter at
myocardial gated single photon emission computed tomography has been found
(Valle et al, 2005) and has been emphasised (Cuocolo et al, 2006) to be a
reliable predictor of functional recovery after CRT.
RESYNC study survival branch is still ongoing, however the data
already collected agree with those by Gradaus et al. about the critical
role of left ventricular dimensions not only on functional outcome but
also on the frequency of heart-related fatalities after CRT.
In our opinion, according to Gradaus et al., left ventricular
dimensions are critical prognostic parameters and should be carefully
taken into account in view of a CRT. Moreover all these data probably
justify an earlier recourse to CRT in managing patients with CHF and LBBB.
REFERENCES
1. Cuocolo A. et al. Eur. J. Nucl. Med. Mol. Imaging 2006; 33: 360-381
2. Gimelli A. et al. J. Cardiovasc. Med. 2007; 8: 575-581
3. Valle G. et al. Eur. J. Nucl. Med. Mol. Imaging 2005; 32 (Suppl.1):S165
We read with interest the study by Norhammar et al (1) describing the
treatment and myocardial infarction survival rates according to the
presence of diabetes. In this study, one-year mortality rates decreased
from 1995 to 2002 from 16.6 to 12.1% in patients without diabetes and from
29.7 to 19.7%, respectively, in those with diabetes. Despite improved pre-admission and in-hospital treatment, diabetic...
We read with interest the study by Norhammar et al (1) describing the
treatment and myocardial infarction survival rates according to the
presence of diabetes. In this study, one-year mortality rates decreased
from 1995 to 2002 from 16.6 to 12.1% in patients without diabetes and from
29.7 to 19.7%, respectively, in those with diabetes. Despite improved pre-admission and in-hospital treatment, diabetic patients were less often
offered acute reperfusion therapy, acute revascularisation or
revascularisation within 14 days, aspirin and lipid-lowering treatment at
discharge.
Although it is important the acute management in the treatment of patients
with myocardial infarction, it is also crucial the secondary prevention of
this population, especially of those at higher risk such as diabetics. In
a study recently performed in Spanish clinical practice setting, in 2,024
hypertensive patients with chronic ischemic heart disease, the influence
of diabetes on the diagnosis and therapeutic approach was analysed (2,3).
Accordingly to the paper of Norhammar et al, the presence of other risk
factors and cardiovascular comorbidities was also more frequent in
diabetics. Overall, diabetic patients were taking more medication (96.9%
of diabetics vs 85.4% of no-diabetics were treated with ≥4 drugs,
p<0.001). With regard to antihypertensive agents, calcium channel
blockers (49.1 vs 42.2%), diuretics (45.1 vs 30.4%) and renin-angiotensin
system inhibitors (83.6 vs 72.9%) were more commonly prescribed in
diabetics (all of them p <0.01), while beta blockers were used more
frequently in no diabetics (63.8 vs 68.7% p=0.01). BP control rates
(<130/80 mmHg) were higher in no diabetics (19.7% vs 26.4% p=0.001).
Concerning lipid lowering drugs, they were more frequently prescribed in
diabetics (77.8 vs 73.9%, p=0.036), nevertheless there were no differences
in LDL-cholesterol control rates in both groups. Notably, patients with
diabetes were surprisingly taking less antiplatelet agents than no
diabetics (85.2 vs 89.7%, p=0.003). Finally, with regard to diagnostic
procedures, no differences were found in the performance of stress test
(84.5 vs 86.9%) or coronary angiography (60.9 vs 58.1%).
In agreement with Norhammar et al, although in the last years the
management of diabetics with coronary heart disease is improving, our data
also confirm there is still a lack of application of evidence-based
treatment.
References
1. Norhammar A, Lindbäck J, Rydén L, Wallentin L, Stenestrand U. Improved but still high short- and long-term mortality rates after myocardial infarction in patients with diabetes mellitus: a time-trend report from the Swedish Register of Information and Knowledge about Swedish Heart Intensive Care Admission.
Heart 2007;93:1577-83.
2. Escobar C, Barrios V, de Pablo C, Bertomeu V, Murga N, Calderon A, et al. Associated cardiovascular risk factors control in the hypertensive population with chronic ischemic heart disease attended by cardiologists in Spain. Data from the CINHTIA study.
Eur Heart J 2007;28(Abst Suppl):684-85.
3. Barrios V, Escobar C, Bertomeu V, de Pablo C, Murga N, Calderon A, et al. Blood pressure control in the hypertensive population with chronic ischemic heart disease attended by cardiologists in Spain.
Eur Heart J 2007;28(Abst Suppl):867.
The recent study by Grotenhuis and colleagues demonstrated the
increased
peak flow velocity across the pulmonary trunk, right ventricular
hypertrophy
and right ventricular relaxation abnormalities in patients after the
arterial
switch operation (1). The authors argued that one of the possible causes
of
the increased peak flow velocity was local scar tissue with loss of
pulmonary
artery diste...
The recent study by Grotenhuis and colleagues demonstrated the
increased
peak flow velocity across the pulmonary trunk, right ventricular
hypertrophy
and right ventricular relaxation abnormalities in patients after the
arterial
switch operation (1). The authors argued that one of the possible causes
of
the increased peak flow velocity was local scar tissue with loss of
pulmonary
artery distensibility.
I recognize the soundness of the report.
We previously analyzed an input impedance spectrum of pulmonary artery in
patients after the arterial switch procedure, and reported the increased
pulmonary artery stiffness of them (2). Concerning systemic circulation,
many
reports have demonstrated that the augmented aortic stiffness, which
increases left ventricular pulsatile work, induces left ventricular
hypertrophy
(3). As for pulmonary circulation, it has reported that the increased
pulmonary artery stiffness enhances right ventricular load (4). Therefore,
the
increased stiffness of pulmonary artery in arterial switch patients would
cause right ventricular hypertrophy. I agree with Grotenhuis and
colleagues in
thinking that careful observation about right ventricular function (and
arrhythmia) is needed in follow-up of the patients after the arterial
switch
procedure.
References
1. Grotenhuis HB, Kroft LM, van Elderen SGC, et al. Right ventricular hypertrophy and diastolic dysfunction in arterial switch patients without pulmonary artery stenosis. Heart. 2007;93:1604-1608
2. Murakami T, Nakanishi T, Nakazawa M, et al. The spectrum of pulmonary input impedance in children with complete transposition after the arterial switch procedure. Cardiol Young. 1998;8:180-186
3. Ou P, Celermajer DS, Jolivet O, et al. Increased central aortic stiffness and left ventricular mass in normotensive young subjects after successful
coarctation repair.
Am Heart J. 2008;155:187-193
4. Hunter KS, Lee P, Lanning CJ, et al. Pulmonary vascular input impedance is a combined measure of pulmonary vascular resistance and stiffness and predicts clinical outcomes better than pulmonary vascular resistance alone in pediatric patients with pulmonary hypertension.
Am Heart J. 2008;155:166-174
We congratulate Dr A Steptoe and associates on their extensive epidemiological research concerning the cardiovascular risk and its association with the pathogen burden depending on the socio-economic status (1). Since the middle of the 20th century, the cardiovascular risk in the populations of Europe and the United States has shown a reverse dependence on the economic and professional status. Many rese...
We congratulate Dr A Steptoe and associates on their extensive epidemiological research concerning the cardiovascular risk and its association with the pathogen burden depending on the socio-economic status (1). Since the middle of the 20th century, the cardiovascular risk in the populations of Europe and the United States has shown a reverse dependence on the economic and professional status. Many researchers including the authors of this study have attempted to find the causes of this tendency (2). The study referred to provides a lot of epidemiological information about the role played in vasculitis and the pathogenesis of atherosclerosis by the universally appearing infectious factors. The idea of associating the infectious factors initiating inflammatory changes in vessels influencing the development of atheroclerosis with the socio-economic status is inventive and interesting.
Examinations were conducted on 1201 patients aged 40-60 selected from the population of Lublin (Poland), (3). Obesity and overweight were the most frequent cardiovascular risk factors. The most frequent occurrence of this disease was noted among patients with primary education, the fewest among those with higher education. Similarly, it was proved that the lower the patients' level of education, the greater and more severe the cigarette smoking habit. Hence the cardiovascular risk factors regarded as the indicators of social stress (obesity, smoking) occurred more frequently among the least educated patients. Moreover, the social stress is believed to belong to the obesity and smoking causes in the final phase.
Having assessed the total cardiovascular risk, we observed the existence of higher level coronary artery disease risk in patients with vocational education as compared to people with higher education.
Our findings accord with those recorded and currently observed in many European countries, where researchers have noticed a reverse dependence of the coronary artery disease on high standard of living. Consequently, there are more cases of the disease among lower social classes. Identifying the causes of this tendency will allow for designing better therapy and prevention strategies. My presentation and discussion of dr A Steptoe's research aims at finding the underlying cause of this tendency.
References
1. Steptoe A, Shamaei-Tousi A, Gylfe A et. al. Socioeconomic status, pathogen burden and cardiovascular disease risk.
Heart. 2007; 93:1567-70.
2. Bunde J Suls J. A quantitative analysis of the relationship between the Cook-Medley Hostility Scale and traditional coronary artery disease risk factors.
Health Psychol Psychoz 2006;25:493-500.
3. Mieczkowska J, Baraniak J, Kozak-Szkopek E. The influence of education on the cardiovascular risk.
Annales Universitatis Mariae Curie-Sk³odowska Sectio D-Medicina 2006; 61(1): 290-295,
Though the mandate of Karthikeyan et al’s article is the management
of manifest coronary disease, primary prevention at the population level
should not be ignored. India is rapidly urbanising, and urban India shows
marked increases in both coronary heart disease prevalence and risk
factors when compared with rural settings. (1)Though coronary risk factors
tend to be concentrated in those of higher s...
Though the mandate of Karthikeyan et al’s article is the management
of manifest coronary disease, primary prevention at the population level
should not be ignored. India is rapidly urbanising, and urban India shows
marked increases in both coronary heart disease prevalence and risk
factors when compared with rural settings. (1)Though coronary risk factors
tend to be concentrated in those of higher social classes, (2) the poor in
India are also increasingly affected whilst continuing to suffer from
diseases of the age of pestilence and famine. Prevalence of cardiovascular
risk factors such as smoking, high blood pressure and overweight are also
higher than might have been expected in rural settings. (3) More than 70%
of India still lives outside cities, and these data provide an early
indication of the burden of heart disease that will occur in rural India
in the coming years.
Geoffrey Rose presented two approaches to prevention of disease—one
based on the individual and the other on populations. In the individual
strategy, high-risk individuals are sought and offered individual
protection. In contrast, the ‘population strategy’ seeks to control the
determinants of incidence in the population as a whole. (4) Rose argued
that though the ‘high-risk’ strategy was the traditional medical approach
to prevention and though this approach allowed the doctor to identify
appropriate interventions for their patient in clinic, it was palliative
and temporary in that it did not seek to alter the underlying causes of
the disease but to identify individuals who were particularly susceptible
to those causes.
The population approach to primary prevention seeks to achieve
leftward shift in the normal distribution of cardiovascular risk. The
decline in coronary heart disease deaths in the developed world has been
mostly attributed to primary prevention. (5)
The Seven Countries Study initially led to the concept that
cardiovascular disease prevention should be implemented at the population
level. Though both individual and population approaches to disease
prevention are needed, implementation and evaluation of the population
approach is difficult whereas proof of efficacy is easier in the high-risk
approach. (6)
The policies for the primary prevention of cardiovascular diseases in
most developed countries thus emphasise high-risk rather than population
strategies. (7) However, to create an environment in which individual
behavioural initiatives can succeed, major shifts in population behaviour
through public health policy are necessary. The wider environment impacts
on the health of an individual in addition to individual behavioural and
biological influences. In developing countries such as India, any
increase expenditure on 'healthcare' should not be used to imitate the
western model of high-risk and secondary prevention but focus more on
primary prevention at the population level. Without this approach,
inequities in care - especially in urban poor and rural communities - are
bound to worsen.
References
1. Ganesan Karthikeyan, Denis Xavier, Doriaraj Prabhakaran, and Prem Pais Perspectives on the management of coronary artery disease in India
Heart 2007; 93: 1334-1338
2. Gupta R, Gupta VP Meta-analysis of coronary heart disease prevalence in India
Indian Heart J, vol. 48, no. 3, pp. 241-245.
3. Singh RB, Beegom R, Mehta AS, Niaz MA, De AK,
Mitra RK, Haque M, Verma SP, Dube GK, Siddiqui HM Social class, coronary risk factors and undernutrition, a double
burden of diseases, in women during transition, in five Indian cities
International Journal of Cardiology, vol. 69, no. 2, pp. 139-147.
4. Chow C, Cardona M, Raju PK, Iyengar S, Sukumar A,
Raju R, Colman S, Madhav P, Raju R, Srinath RK, Celermajer
D, Neal B Cardiovascular disease and risk factors among 345 adults in rural India-the Andhra Pradesh Rural Health Initiative
Int.J.Cardiol
5. ROSE GEOF. Sick Individuals and Sick Populations
International Journal of Epidemiology, vol. 14, no. 1, pp. 32-38
6. Unal B, Critchley JA, Capewell S Modelling the decline in coronary heart disease deaths in England and Wales, 1981-2000: comparing contributions from primary prevention and secondary
prevention
BMJ, vol. 331, no. 7517, p. 614
7. Emberson J, Whincup P, Morris R, Walker M, Ebrahim
S Evaluating the impact of population and high-risk strategies for the primary prevention of cardiovascular disease
European Heart Journal, vol. 25, no. 6, pp. 484-491
8. Department of Health National Service Framework for coronary heart disease: modern standards and service models
Thank you for forwarding us the leter of Dr Rochefort and his kind
comments on the paper. He has made a good point, and of course he is right
about the increased mobilization of the MSC in experimental hypoxia, which
he confirmed in an elegant experiment. Table 3 contains an typing error,
which we are sorry to have missed during proofreading.
The correct meaning of the sentence is "Increase of bone ma...
Thank you for forwarding us the leter of Dr Rochefort and his kind
comments on the paper. He has made a good point, and of course he is right
about the increased mobilization of the MSC in experimental hypoxia, which
he confirmed in an elegant experiment. Table 3 contains an typing error,
which we are sorry to have missed during proofreading.
The correct meaning of the sentence is "Increase of bone marrow-dependent
mesenchymal stem cells (rats)".
Again I apologize for the mistake.
Sincerely,
Wojciech Wojakowski MD on behalf of the authors
Dear Editor,
The recent study by Ha et al (1) illustrates the potential benefit of using exercise stress for detection of early myocardial disease in diabetic patients. With modern advances in cardiac imaging the detection and management sub-clinical disease in patients at high cardiovascular risk is likely to become increasingly relevant. The use of exercise stress and its application outside the conventional app...
Dear Editor,
Recently, Yacoub et al,[1] reviewed for the section Education in Heart of the journal Heart, different clinical but also epidemiological, diagnostic, therapeutic and other aspects of Chagas disease, “a neglected tropical cardiomyopathy”. Although it should be acknowledge the importance of such reviews, particularly in a topic that has been neglected in many aspects, including research as well intern...
Dear Editor,
I read with great interest the report by Robles et al (1), recently published in the Journal, that describes the occurrence of left ventricular thrombus formation (LVTF) in a patient with apical ballooning (Takotsubo-like syndrome).
This study likely provides further contribution to the knowledge on the various clinical aspects of this stress-related cardiac disease. In spite of the acut...
Dear Editor,
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Dear Editor,
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For these reasons we greatly appreciated the paper by Gradaus et al. entitled and stating that “diastolic filling pattern and left ventricular diameter predict response and prognosis after cardiac resynch...
Dear Editor,
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Dear Editor,
The recent study by Grotenhuis and colleagues demonstrated the increased peak flow velocity across the pulmonary trunk, right ventricular hypertrophy and right ventricular relaxation abnormalities in patients after the arterial switch operation (1). The authors argued that one of the possible causes of the increased peak flow velocity was local scar tissue with loss of pulmonary artery diste...
Dear Editor,
We congratulate Dr A Steptoe and associates on their extensive epidemiological research concerning the cardiovascular risk and its association with the pathogen burden depending on the socio-economic status (1). Since the middle of the 20th century, the cardiovascular risk in the populations of Europe and the United States has shown a reverse dependence on the economic and professional status. Many rese...
Dear Editor,
Though the mandate of Karthikeyan et al’s article is the management of manifest coronary disease, primary prevention at the population level should not be ignored. India is rapidly urbanising, and urban India shows marked increases in both coronary heart disease prevalence and risk factors when compared with rural settings. (1)Though coronary risk factors tend to be concentrated in those of higher s...
Dear Editor,
Thank you for forwarding us the leter of Dr Rochefort and his kind comments on the paper. He has made a good point, and of course he is right about the increased mobilization of the MSC in experimental hypoxia, which he confirmed in an elegant experiment. Table 3 contains an typing error, which we are sorry to have missed during proofreading. The correct meaning of the sentence is "Increase of bone ma...
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