I read with great interest the review by Wojakowski et
al about the mobilization of bone marrow-derived stem/progenitor cells
during acute coronary syndromes.1 The contribution of such cells,
including hematopoietic stem cells, mesenchymal stem cells (MSCs),
endothelial progenitor cells and other poorly defined progenitors, is well
in coronary heart diseases. I agree this review discusses and summa...
I read with great interest the review by Wojakowski et
al about the mobilization of bone marrow-derived stem/progenitor cells
during acute coronary syndromes.1 The contribution of such cells,
including hematopoietic stem cells, mesenchymal stem cells (MSCs),
endothelial progenitor cells and other poorly defined progenitors, is well
in coronary heart diseases. I agree this review discusses and summarizes
information regarding mechanisms of mobilization, homing and engraftment
of stem/progenitor cells that may take part in cardiac repair after
ischaemic injury.
Among all factors that can modulate the number of circulating
stem/progenitor cells, authors stated that “hypoxia induced a decrease of
(circulating) bone marrow-derived MSCs” (table 3)1; however, the quoted
references, authored by Rochefort et al, clearly demonstrated the
opposite.2 In fact, Rochefort et al evidenced that firstly MSCs were
regularly observed in the rat circulating blood and that secondly MSCs
were consistently and dramatically mobilized into the bloodstream after
chronic hypoxia.2 Although, mechanisms inducing such a mobilization
during chronic hypoxia remain unclear, this hypoxia-induced mobilization
model represents a great tool to study the in vivo effect of factors in
the MSC mobilization process.
To conclude, even if this specific point about the hypoxia-induced
mobilization was incorrect, data reported in the review by Wojakowski et
al were not affected and this excellent review is to be applauded.
References
1. Wojakowski W, Kucia M, Kazmierski M, et al. Circulating progenitor
cells in stable coronary heart disease and acute coronary syndromes:
relevant reparatory mechanism?
Heart 2008 94: 27-33
2. Rochefort G, Delorme B, Lopez A, et al. Multipotential mesenchymal
stem cells are mobilized into peripheral blood by hypoxia.
Stem Cells 2006; 24: 2202–8.
Adamson and Nelson-Piercy give a thorough overview of arrhythmias in
pregnancy1. However they mention that the presence of an automated
implantable cardio-defibrillator (AICD) poses no risk to the fetus as,
even after device therapy, ‘the electrical field to which the fetus is
exposed is minimal’.
We recently cared for a 23 year old patient with hypertrophic
cardiomyopathy who had an AICD...
Adamson and Nelson-Piercy give a thorough overview of arrhythmias in
pregnancy1. However they mention that the presence of an automated
implantable cardio-defibrillator (AICD) poses no risk to the fetus as,
even after device therapy, ‘the electrical field to which the fetus is
exposed is minimal’.
We recently cared for a 23 year old patient with hypertrophic
cardiomyopathy who had an AICD implanted at the age of 14 with a single
coil lead and abdominal box. The box was therefore acting as an active can
and any device therapy would involve a shock between the box and the
single coil on the lead. During pregnancy the box came to lie directly
over the uterus and any therapy would have resulted in a significant shock
to the fetus. The AICD was disabled throughout pregnancy and the patient
successfully delivered a healthy infant vaginally with no complications.
It is not uncommon for patients to have had single coil defibrillator
leads with abdominal generators implanted in childhood. The risks of
device therapy to the fetus should be considered when these patients are
assessed at cardiac pregnancy clinics.
References
1. Adamson DL, Nelson-Piercy C. Managing palpitations and arrhythmias
during pregnancy.
Heart 2007;93:1630-1636.
We thank Drs Mclaren et al. for their interest in our study.
Firstly, we
chose Vancomycin as we wished to use an antistaphylococcal drug that
had
been studied in cardiac surgical patients. Additional rifampicin was
used
in an attempt to prevent resistance developing. Clearly the strategy
was
successful as we did not see any increase in resistant organisms
during, or
for the 2 years after,...
We thank Drs Mclaren et al. for their interest in our study.
Firstly, we
chose Vancomycin as we wished to use an antistaphylococcal drug that
had
been studied in cardiac surgical patients. Additional rifampicin was
used
in an attempt to prevent resistance developing. Clearly the strategy
was
successful as we did not see any increase in resistant organisms
during, or
for the 2 years after, the study. We are interested in their statement
of a
change in their antibiotic prophylaxis with no difference. This
statement
was unpublished and is not publicly available. They have chosen
to retain a unique combination of cephazolin and rifampicin as their
prophylaxis. They continue to use an additional antistaphylococcal
agent and
their choice of rifampicin as a sole agent is unusual, with very little
prior experience. Even so, we would suggest that a randomised
controlled
prospective study is more relevant than the observational data that is
quoted.
Secondly, they have criticised our use of vancomycin timed at
induction
of
anaesthesia. This is frequently how vancomycin for antibiotic
prophylaxis
is given in many surgical centres, is seen in the study they quote
(Vuorisalo) and in other studies that compare vancomycin with
cephalosporins, which we have referred to. Others1 have shown that
administration more than 60 mins before surgical incision surprisingly
may
reduce efficacy. Furthermore, our strategy was effective and a more
efficacious administration regime could only make this more effective
if it
had any further effect at all.
Thirdly, they advocate an even higher
dose of
cefuroxime but such a dose has not been published in any guideline or
used
by any other study. We are confident in our dosage and formulation of
cefuroxime, as the incidence of infection in the low risk patients (
where
cefuroxime was used) operated at the same time, as referred to in our
paper
and not part of our study, was extremely low.
Fourthly, Mclaren has questioned the security of blinding in our
study
with
the use of Rifampicin. We clearly acknowledge this limitation in our
paper,
but the very significant results in further infection surgical
procedures,
deep SSI and readmission to hospital is unlikely to be accounted for by
the
possibility of noticing orange colouration of the urine at the time of
surgery. Lastly, we used the term ‘longer’ , referring to our 48 hr
regime,
as increasingly guidelines on surgical prophylaxis are limiting
prophylaxis
to 24hrs, with little real evidence. The 2 articles quoted in support
of
their criticism (Habarth & Kato) use ‘48 hours ‘as their definition of
short/long term and therefore do not contradict our study.
To reiterate, in our cohort of patients at high risk of SSI, i.e.
obese,
diabetic or undergoing bilateral LITA, we showed that longer and
broader
antibiotic prophylaxis, reduced SSI with clinical, economic and
statistical
significance.
References
1. Kevin W. Garey, Thanh Dao, Hua Chen, et al. Timing of vancomycin
prophylaxis for cardiac surgery patients and the risk of surgical site
infections.
Journal of Antimicrobial Chemotherapy (2006) 58, 645*650
We thank Dr. Ballo and colleagues for their interesting comments on
our article.
In agreement with our study, Ballo et al show a nonlinear association
between circumferential midwall and longitudinal LV systolic function in
patients with hypertension [1]. It is particularly noteworthy that this
nonlinear association is apparent in two different study populations. The
patients in our study were suff...
We thank Dr. Ballo and colleagues for their interesting comments on
our article.
In agreement with our study, Ballo et al show a nonlinear association
between circumferential midwall and longitudinal LV systolic function in
patients with hypertension [1]. It is particularly noteworthy that this
nonlinear association is apparent in two different study populations. The
patients in our study were suffering from idiopathic heart failure (mean
LVEF 44±17% and AVPD 6.9±2.7 mm) whereas the patients in Ballo´s study had
a less severe diagnosis (arterial hypertension, mean LVEF 62 ±9.7% and
AVPD 12.5±2.5 mm). Longitudinal function is dependent on subendocardial
muscle fibres that are extremely sensitive to ischemia and increases in
wall stress, and consequently capable of detecting small ventricular
changes[2-4].
REFERENCES
[1] Ballo P, Quatrini I, Giacomin E, Motto A, Mondillo S. Circumferential versus longitudinal systolic function in patients with
hypertension: a nonlinear relation.
J Am Soc Echocardiogr. 2007;20:298-306.
[2] Nikitin NP, Loh PH, Silva R, et al. Prognostic value of systolic mitral annular velocity measured with Doppler
tissue imaging in patients with chronic heart failure caused by left
ventricular systolic dysfunction.
Heart. 2006;92:775-9.
[3] Gruner Svealv B, Fritzon G, Andersson B. Gender and age related differences in left ventricular function and
geometry with focus on the long axis.
Eur J Echocardiogr. 2006;7:298-307.
[4] Gruner Svealv B, Tang MS, Waagstein F, Andersson B. Pronounced improvement in systolic and diastolic ventricular long axis
function after treatment with metoprolol.
Eur J Heart Fail. 2007.
The recent study by Dhadwal et al. (1) has a number of weaknesses
which merit discussion. The study appears to have been initiated by a
“perceived increase in crude infection rates” but the organisms
responsible for this increase were not presented. Unless there was a high
incidence of infection with resistant organisms such as methicillin-
resistant Staphylococcus aureus (MRSA) prior to study comme...
The recent study by Dhadwal et al. (1) has a number of weaknesses
which merit discussion. The study appears to have been initiated by a
“perceived increase in crude infection rates” but the organisms
responsible for this increase were not presented. Unless there was a high
incidence of infection with resistant organisms such as methicillin-
resistant Staphylococcus aureus (MRSA) prior to study commencement, the
routine use of vancomycin in a multi-drug regimen is hard to justify (2,
3). The authors stated that their antibiotic regimen was based, at least
in part, on Spelman et al. (4). However, it is worth noting that the
prevalence of MRSA at this author’s institution fell significantly
following an intensive infection control programme, prompting a return to
cephazolin and rifampicin as prophylaxis against cardiac surgical-site
infection (SSI). No significant increase in the incidence of SSI has been
observed since the change (unpublished data).
Dhadwal et al. (1) administered vancomycin after induction of
anaesthesia. This approach is not recommended by the Centres for Disease
Control and Prevention, as it does not provide adequate tissue levels of
antibiotic at the time of surgical incision (2). Nonetheless, the authors
documented a decrease in SSI. One explanation for this that appears not to
have been considered was that the cefuroxime regimen used in the control
arm was suboptimal. Other studies of cefuroxime in cardiac surgery have
used considerably higher doses and a 1.5g load may be inadequate (5, 6).
Moreover, a recent report highlighted significant problems with some
formulations of cefuroxime (7). Dhadwal et al. (1) did not state which
formulation they used.
Blinding in the study was suboptimal both due to the orange
discolouration of urine seen in patients given rifampicin and because the
study required antibiotics to be given at different times and for
different durations, potentially unmasking patient assignment.
The authors concluded that longer duration of antibiotic prophylaxis
reduces the incidence of SSI. However, this was not a study comparing two
identical antibiotic regimens with different durations. We believe that
this conclusion is both misleading and unjustified. There is substantial
evidence that prolonged duration of prophylactic antibiotic therapy is
detrimental to patients (8-10).
References:
1. Dhadwal K., Al-Ruzzeh S., Athanasiou T., et al. Comparison of
clinical and economic outcomes of two antibiotic prophylaxis regimens for
sternal wound infection in high-risk patients following coronary artery
bypass grafting surgery: a prospective randomised double-blind trial.
Heart 2007:93:1126-1133
2. Mangram AJ., Horan TC., Pearson ML., Silver LC., Jarvis WR. Guideline for prevention of surgical site infection, 1999. Hospital
Infection Control Practices Advisory Committee
Infect Control Hosp
Epidemiol 1999:20:250-278
3. Vuorisalo S., Pokela R., Syrjala H. Comparison of vancomycin and
cefuroxime for infection prophylaxis in coronary artery bypass surgery.
Infect Control Hosp Epidemiol 1998:19:234-239
4. Spelman D., Harrington G., Russo P., Wesselingh S. Clinical,
microbiological, and economic benefit of a change in antibiotic
prophylaxis for cardiac surgery.
Infect Control Hosp Epidemiol 2002:23:402
-404
5. Mandak J., Pojar M., Malakova J., et al. Tissue and plasma
concentrations of cephuroxime during cardiac surgery in cardiopulmonary
bypass- a microdialysis study.
Perfusion 2007:22:129-136
6. Nascimento JW., Carmona MJ., Strabelli TM., Auler JO Jr., Santos SR. Systemic availability of prophylactic cefuroxime in patients submitted
to coronary artery bypass grafting with cardiopulmonary bypass.
J Hosp
Infect 2005:59:299-303
7. Mastoraki E., Michalopoulos A., Kriaras I., et al. Incidence of
postoperative infections in patients undergoing coronary artery bypass
grafting surgery receiving antimicrobial prophylaxis with original and
generic cefuroxime.
J Infect 2007: Epub ahead of print.
8. Harbarth S., Samore MH., Lichtenberg D., Carmeli Y. Prolonged
antibiotic prophylaxis after cardiovascular surgery and its effect on
surgical site infections and antimicrobial resistance.
Circulation
2000:101:2916-2921
9. Kato Y., Shime N., Hashimoto S., et al. Effects of controlled
perioperative antimicrobial prophylaxis on infectious outcomes in
pediatric cardiac surgery.
Crit Care Med 2007:35:1763-1768
10. Edwards FH., Engelman RM., Houck P., Shahian DM., Bridges CR. The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic
Prophylaxis in Cardiac Surgery, Part I: Duration.
Ann Thorac Surg
2006:81:397-404
Grüner Sveälv et al.(1) recently found that left ventricular (LV)
long-axis atrioventricular plane displacement (AVPD) in heart failure (HF)
patients was linearly correlated with short-axis fractional shortening
(LVFS) in the lower range of AVPD, but not in the higher range of AVPD.
They also observed that decreasing AVPD quartiles showed a stepwise
association with worsening prognosis. Notably, a sim...
Grüner Sveälv et al.(1) recently found that left ventricular (LV)
long-axis atrioventricular plane displacement (AVPD) in heart failure (HF)
patients was linearly correlated with short-axis fractional shortening
(LVFS) in the lower range of AVPD, but not in the higher range of AVPD.
They also observed that decreasing AVPD quartiles showed a stepwise
association with worsening prognosis. Notably, a similar gradual
association with outcome was less evident for LVFS, as no differences in
outcome were found between the third and fourth LVFS quartiles.
These interesting results agree with our recent finding that the
relation between longitudinal and circumferential systolic performance is
nonlinear, as a depression in longitudinal indices such as AVPD and mitral
annulus peak systolic velocity precedes that in endocardial or midwall
circumferential function(2). Therefore, when plotting a long-axis versus a
short-axis index (e.g., AVPD on the X-axis and LVFS on the Y-axis), the
resulting relation tends to be horizontal in the higher range of indices,
reflecting isolated long-axis impairment in the early stages of systolic
dysfunction. Conversely, the slope of the relation rapidly increases in
the lower range of indices, reflecting simultaneous deterioration in
longitudinal and circumferential function in more advanced stages of HF.
This explains the presence of linear correlation between AVPD and LVFS
only in the lower range of AVPD.
Intriguingly, the more gradual association with prognosis observed
for AVPD than LVFS may represent the clinical correlate of their nonlinear
relation. Based on currently recommended cut-offs for normal LVFS (>25%
in males and >27% in women)(3), most patients in the two highest LVFS
quartiles (23-31% and >31%, respectively; overall, 72% males) had
preserved short-axis function. These subjects fall in the horizontal
portion of the AVPD-LVFS curve, where circumferential indices cannot
identify patients at heightened risk due to subtle systolic dysfunction.
In contrast, because longitudinal systolic impairment is an early and
progressive event in the natural history of HF, and considering that it
represents a powerful prognostic predictor in HF patients(4), decreasing
AVPD values may be expected to reflect the effective stage of LV
dysfunction and to parallel the corresponding increase in cardiovascular
risk better than circumferential indices.
References
1. Grüner Sveälv N, Olofsson EL, Andersson B. Ventricular long axis
function is of major importance for long-term survival in heart failure
patients.
Heart 2007 Jun 17; [Epub ahead of print].
2. Ballo P, Quatrini I, Giacomin E, Motto A, Mondillo S. Circumferential versus longitudinal systolic function in subjects with
hypertension: a nonlinear relation.
J Am Soc Echocardiogr 2007;20:298-306.
3. Recommendations for chamber quantification: a report from the
American Society of Echocardiography's Guidelines and Standards Committee
and the Chamber Quantification Writing Group, developed in conjunction
with the European Association of Echocardiography, a branch of the
European Society of Cardiology.
J Am Soc Echocardiogr 2005;18:1440-1463.
4. Nikitin NP, Loh PH, Silva R, Ghosh J, Khaleva OY, Goode K, Rigby
AS, Alamgir F, Clark AL, Cleland JG. Prognostic value of systolic mitral
annular velocity measured with Doppler tissue imaging in patients with
chronic heart failure caused by left ventricular systolic dysfunction.
Heart 2006;92:775-9.
McMahon et al reported in a recent article a reduction of TD velocities in children with noncompaction of the left ventricle, compared with normal controls. The authors concluded their work saying that the reduction of lateral mitral Ea velocity helps to predict children with LVNC who are at risk of adverse clinical outcomes including death and need for cardiac transplantation. In a precedent report our group re...
McMahon et al reported in a recent article a reduction of TD velocities in children with noncompaction of the left ventricle, compared with normal controls. The authors concluded their work saying that the reduction of lateral mitral Ea velocity helps to predict children with LVNC who are at risk of adverse clinical outcomes including death and need for cardiac transplantation. In a precedent report our group reported a strong correlation between pathological tissue Doppler and reduction of ejection fraction. In our report the tissue Doppler analysis was performed segment by segment, and a correlation had been ob served only in patients with a low EF.
Noncompaction of the ventricular myocardium (LVNC) is a rare congenital cardiomyopathy resulting from an arrest in normal endomyocardial embryogenesis; it is characterized by a thin compacted epicardial and an extremely thickened endocardial layer with prominent trabeculations and deep intertrabecular recesses (1-6). In this rare cardiomyopathy clinical presentation and outcome is variable, but heart failure, arrhythmias and sudden cardiac death are described like common clinical findings (1-6). Unfortunately the pathophysiological mechanisms are unknown. In 2002 Jenni et al. (7) reported a microvascular dysfunction in 12 patients affected by non compaction: areas of restricted myocardial perfusion have been documented by scintigraphy, suggesting a reduction of Coronary flow reserve (CFR). The decreased of CFR is not confined to noncompacted segments, but extends to most segments with wall motion abnormalities, thus global coronary microcirculatory dysfunction could be associated with IVNC (7-12). McMahon et al (1) reported in a recent article a reduction of TD velocities in children with noncompaction of the left ventricle, compared with normal controls. In a precedent report our group reported a strong correlation between pathological tissue Doppler and reduction of ejection fraction. In this study we performed a Tissue Doppler analysis, segment by segment, in a series of 15 children affected by non-compaction. The bidimensional echocardiogram showed a strong correlation between systolic function and diastolic dysfunction (2). Alterations of the diastolic function compared in 7 (49%) patients: in 2 cases, a reduction of the Ea wave was present in all segments. In 3 patients the diastolic dysfunction was limited to apical and lateral segments. In the last 2 children a reduction of the Ea wave interested only the apical segments. Every patient with diastolic dysfunction also presented a severe reduction of the systolic function (less then 40%). In our opinion the late enhancement can be depend on a CFR, and is the determinant of the tissue Doppler alterations. So the TD alteration is associated with EF, and is an indirect index of poor clinical outcome, like EF (1-12). McMahon et al (1) concluded their work saying that the reduction of lateral mitral Ea velocity helps to predict children with LVNC who are at risk of adverse clinical outcomes including death and need for cardiac transplantation. In our opinion, more then the Em, the EF at the admission can help to predict the mortality in these patients.
References
1)McMahon CJ, Pignatelli RH, Nagueh SF, Lee VV, Vaughn W, Valdes SO, Kovalchin JP, Jefferies JL, Dreyer WJ, Denfield SW, Clunie S, Towbin JA, Eidem BW Left ventricular non-compaction cardiomyopathy in children: characterisation of clinical status using tissue Doppler-derived indices of left ventricular diastolic relaxation
Heart. 2007; 93:676-81.
2)Fazio G, Pipitone S, Iacona MA, Marchì S, Mongiovì M, Zito R, Sutera L, Novo G, Novo S Evaluation of diastolic function by the Tissue doppler in children affected by non-compaction
Int J Cardiol. 2007;116:e60-2.
3)Fazio G, Sutera L, Corrado G, Novo S The chronic heart failure is not so frequent in non-compaction
Eur Heart J. 2007; 28:1269.
4) Fazio G, Corrado G, Pizzuto C, Zachara E, Rapezzi C, Sulafa AK, Sutera L, Stollberger C, Sormani L, Finsterer J, Benatar A, Di Gesaro G, Novo G, Cavusoglu Y, Baumhakel M, Drago F, Carerj S, Pipitone S, Novo S. Supraventricular arrhythmias in noncompaction of left ventricle: Is this a frequent complication?
Int J Cardiol. 2007; [Epub ahead of print]
5)Fazio G, Corrado G, Zachara E, Rapezzi C, Sulafa AK, Sutera L, Pizzuto C, Stollberger C, Sormani L, Finsterer J, Benatar A, Di Gesaro G, Cascio C, Cangemi D, Cavusoglu Y, Baumhakel M, Drago F, Carerj S, Pipitone S, Novo S. Ventricular tachycardia in non-compaction of left ventricle: is this a frequent complication?
Pacing Clin Electrophysiol. 2007; 30:544-6
6) Fazio G, Sutera L, Vernuccio F, Fazio M, Vernuccio D, Pizzuto C, Di Gesaro G, Cascio C, Novo S Heart failure and cardiomyopathies: a case report
G Ital Cardiol. 2007; 8:129-32
7) Jenni R, Wyss CA, Oechslin EN, Kaufmann PA Isolated ventricular noncompaction is associated with coronary microcirculatory dysfunction.
J Am Coll Cardiol. 2002; 39:450-4
8) Hamamichi Y, Ichida F, Hashimoto I, Uese KH, Miyawaki T, Tsukano S, Ono Y, Echigo S, Kamiya T Isolated noncompaction of the ventricular myocardium: ultrafast computed tomography and magnetic resonance imaging.
Int J Cardiovasc Imaging. 2001;17:305-14
9) Sato Y, Matsumoto N, Matsuo S, Kunimasa T, Yoda S, Tani S, Kasamaki Y, Kunimoto S, Saito S. Myocardial perfusion abnormality and necrosis in a patient with isolated noncompaction of the ventricular myocardium: Evaluation by myocardial perfusion SPECT and magnetic resonance imaging.
Int J Cardiol. 2007; [Epub ahead of print]
10) Jassal DS, Nomura CH, Neilan TG, Holmvang G, Fatima U, Januzzi J, Brady TJ, Cury RC. Delayed enhancement cardiac MR imaging in noncompaction of left ventricular myocardium.
J Cardiovasc Magn Reson. 2006;8:489-91
11) Korcyk D, Edwards CC, Armstrong G, Christiansen JP, Howitt L, Sinclair T, Bargeois M, Hart H, Patel H, Scott T Contrast-enhanced cardiac magnetic resonance in a patient with familial isolated ventricular non-compaction.
J Cardiovasc Magn Reson. 2004;6:569-76
12) Soler R, Rodríguez E, Monserrat L, Alvarez N MRI of subendocardial perfusion deficits in isolated left ventricular noncompaction.
J Comput Assist Tomogr. 2002; 26:373-5
In the context of involvement of the right pulmonary artery by aortic
dissection, instead of being caused by extrinsic compression attributable
to a haematoma(1)(2)(3), obstruction of the right pulmonary artery might
be attributable to thrombosis, with associated extrinsic compression by a
massively dilated aorta, as shown in the instance of a 69 year old man who
initially presented with stigmata of...
In the context of involvement of the right pulmonary artery by aortic
dissection, instead of being caused by extrinsic compression attributable
to a haematoma(1)(2)(3), obstruction of the right pulmonary artery might
be attributable to thrombosis, with associated extrinsic compression by a
massively dilated aorta, as shown in the instance of a 69 year old man who
initially presented with stigmata of pulmonary embolism including chest
pain, dyspnoea, severe hypotension, and raised levels of D-dimer. In
addition, through the medium of pulmonary artery digital subtration
angiography, there was documentation of right pulmonary artery thrombosis
with total peripheral avascularity. In view of his poor haemodynamic
status thoracotomy was undertaken with a view to performing surgical
thrombectomy. At operation, however, he was found to have, not only a
large thrombus in the right pulmonary artery, but also an acute dissection
of the ascending aorta. Extrinsic compression of the right pulmonary
artery had also occured, immediately distal to its origin, but this was
attributable to the massively dilated ascending aorta. Evidence of
associated pulmonary embolism(PE) was obtained post-operatively when a
ventilation/perfusion scan showed multiple mismatched
ventilation/perfusion defects in the right lung, compatible with residual
obstruction of distal branches of the right pulmonary artery(4). The
occasional co-existence of PE and aortic dissection is also exemplified by
a 74 year old man who presented with dyspnoea, and in whom spiral computed
tomography demonstrated PE involving the right pulmonary artery, as well
as thrombosed dissection of the abdominal aorta.
Comment:-
The irony of the overlap between stigmata of PE and those of aortic
dissection, and the occasional co-existence of the two disorders is that,
with the exception of exploratory thoracotomy(4), their therapeutic
stategies are mutually incompatible. No wonder it was the considered
opinion of Sir William Osler that "There is no disease more conducive to
clinical humility than aneurysms of the aorta"(4)
References
1) Stougiannos PN., Mytas DZ., Pyrgakis VN The changing faces of aortic dissection: an unusual presentation mimicking
pulmonary embolism Heart 2007:93:1324
2) Nasrallah A., Goussous Y., El-Said G., Garcia E., Hall RJ Pulmonary artery compression due to acute dissecting aortic aneurysm: a
clinical and angiographic diagnosis Chest 1975:67:228-230
3) Charnsangavej C Occlusion of the right pulmonary artery by acute dissecting aortic
aneurysm American Journal of Roentgenology 1979:132:274-6
4) Neri E., Toscano T., Civelli L et al Acute dissecting aneurysm of the ascending thoracic aorta causing
obstruction and thrombosis of the right pulmonary artery Texas Heart Institute Journal 2001:28:149-151
5) Gupta R., Uhrbrock D., Burnbaum Y Images in cardiology: Coexisting pulmonary embolism and abdominal aortic
dissection Clinical Cardiology 2003:26:395
I would like to draw your attention to the statement"As far as we
know, this is the first reported case of all three coronaries originating
from a single ostium from the aorta." in the above article.
There are mulitiple papers on single coronary artery, there are
classifications for single coronary artery (e.g Smiths'), people have done
treadmill testing in patients with single coronary ar...
I would like to draw your attention to the statement"As far as we
know, this is the first reported case of all three coronaries originating
from a single ostium from the aorta." in the above article.
There are mulitiple papers on single coronary artery, there are
classifications for single coronary artery (e.g Smiths'), people have done
treadmill testing in patients with single coronary artery.
There are so many case reports on angioplasty and bypass surgery in
single coronary artery.
in order to highlight this issue, I am attaching articles from HEART
itself on this issue.
E. S. J. King
A SINGLE CORONARY ARTERY Heart, Apr 1940; 2: 79 – 84
Peter Swann and Margaret Fitzpatrick
SINGLE CORONARY ARTERY Heart, Oct 1954; 16: 457 - 459.
S J Leslie and I R Starkey
Embolism of thrombus in the right coronary artery to the left anterior
descending artery in a woman with a single coronary artery Heart, May 2004; 90: 562
P O Lim
Single coronary artery: circumflex/right coronary circle Heart, Nov 2007; 93: 1472.
D A H Neil, R S Bonser, and J N Townend
Coronary arteries from a single coronary ostium in the right coronary
sinus: a previously unreported anatomy Heart, May 2000; 83: e9.
Marc Hartmann, Patrick M J Verhorst, and Clemens von Birgelen
Isolated "superdominant" single coronary artery: a particularly rare
coronary anomaly Heart, Jun 2007; 93: 687.
P G Horan, G Murtagh, and P P McKeown
Single coronary artery: a familial clustering Heart, Dec 2003; 89: e27.
H Guven, J Billadello, and M Beardslee
An isolated single coronary artery supplying the entire myocardium in a
patient with congenitally corrected transposition of the great vessels Heart, Dec 2004; 90: 1410.
S MIKETIC, J CARLSSON, and U TEBBE
An isolated single coronary artery Heart, May 1998; 79: 515.
P. J. D. Snow
A CASE OF SINGLE CORONARY ARTERY WITH STEREOGRAPHIC DEMONSTRATION OF THE
ARTERIAL DISTRIBUTION Heart, Apr 1953; 15: 261 - 263.
I Porto and A P Banning
Unstable angina in a patient with single coronary artery Heart, Aug 2004; 90: 858.
Yu-Kang Tu brilliant work investigated the complex emerging field of
microbial risk factors and cardiovascular disease. The paper concluded
that tooth loss (used as an index for poor oral health) is related to CVD
mortality. However, a clear link between both conditions is missing in the
study. This publication raised in our group many reflections. The related
editorial published in the same issue of...
Yu-Kang Tu brilliant work investigated the complex emerging field of
microbial risk factors and cardiovascular disease. The paper concluded
that tooth loss (used as an index for poor oral health) is related to CVD
mortality. However, a clear link between both conditions is missing in the
study. This publication raised in our group many reflections. The related
editorial published in the same issue of Heart only partially cover our
questions.
A crucial point to reduce potential confounders in similar experiences
deals with the socioeconomic status of the enrolled population.
Race/ethnicity, education, and socioeconomic environment are important for
periodontal health. Poverty and residence in a disadvantaged environment
are associated with higher risk of periodontitis as well. Moreover low
socioeconomic status seems associated with progression of atherosclerosis.
Consistent data demonstrated also the association between adverse
socioeconomic circumstances in childhood and both adult dental diseases
and atherosclerosis. Children who grew up in low socioeconomic status
families have poorer dental health including dental caries, plaque scores,
gingival bleeding and periodontal diseases compared with those from high
socioeconomic backgrounds.
This study offers a unique, at our knowledge, chance to understand the
relationship between social aspects and oral disease leading to higher
vascular risk.
We can’t forget how the birth time interval of the Glasgow Alumni study
started right when the Great War came to an end until the United Nations
headquarters officially open in New York City. This is a timeline of great
changes in the western societies, where also UK specific socioeconomical
features may have played a big role in the study.
British economic growth between 1950 and 1955, as measured by an average
annual increase in gross national product of 2.9 per cent , has been the
slowest: less than one-third that of Germany (9.8), half of Austria (6.9),
and Italy (5.9), lower than France (4.2), Belgium (3.1), the Netherlands
(4.9) or Norway (3.5). And this trend was similar according to the United
Nation reports in the following years.
Postwar British society grew slowly until 1973 placed in comparison with
international context. According to the British Nutrition Foundation the
weekly intake of sugar in England and Wales in the decade 1942-1952 was
below 300g, raising above 500g per week in 1962. Food rationing in UK
ended around 1954. We can easily speculate on the large effect of sugar
rationing measures, taken by British authorities, may have on the oral
pathology of the study population. No comparable measures were taken in
other western countries during postwar period.
Adverse socioeconomic circumstances in childhood confer a greater risk for
adult-life vascular diseases. We should also take into account how the
1918-19 influenza epidemic killed at least 40 million people worldwide and
675,000 people in the United States, exceeding the US combat deaths in the
two World Wars combined.
The first cases of the influenza epidemic in Britain appeared right in
Glasgow in May, 1918. It soon spread to other towns and cities and during
the next few months the virus killed 228,000 people in Britain. This was
the highest mortality rate for any epidemic since the outbreak of cholera
in 1849.
In UK desperate methods were used to prevent the spread of the disease.
However, despite attempts, all treatments devised to cope with this new
strain of influenza were completely ineffectual.
Besides its extraordinary virulence, the 1918-19 epidemic was also unique
in that enormous number of its victims were men and women aged 15 and 44,
giving the age profile of mortality a distinct ‘W’ shape rather than the
customary ‘U’ shape, and leading to extremely high death rates in the
working ages.
Infants and young children are traditionally a more vulnerable group, both
to influenza and other forms of infectious disease, and their relative
mortality was also increased dramatically. The dependence of the very
young on their parents, particularly their mothers, however, suggests that
high adult illness and mortality is likely to have an impact on infants
and children, and this makes discussion on the effects of a similar
infants selection on the Glasgow Alumni study population. Another possible
confounder is connected to the possible variation in attributes of
coronary heart disease cases suggesting a change in the primary source-
subpopulation of cases over time. It was proposed that an early 20th-
century expansion of a coronary heart disease–prone subpopulation,
characterized by high serum-cholesterol phenotype and high case-fatality
which contributed to most of the coronary heart disease cases and deaths
during the 1960s may be a late result of the 1918 pandemia. The same
abnormal immune response to infection that in 1918 killed mostly men,
whites, and born from 1880 to 1900 (20–40 years old) may have “primed”
survivors of those birth cohorts to late vascular mortality. The
extinction of such birth cohorts would result in a relative increase in
cases coming from a 2nd subpopulation, which was characterized by insulin
resistance and chronic expression of low-grade inflammation markers and
was comparatively less vulnerable to die acutely from coronary heart
disease.
In conclusion the Glasgow Alumni experience may be biased by some global
and local confounder that include:
(i) a birth cohort selection bias: influenza survivors less vulnerable to
vascular diseases;
(ii) the study took place in a time span when UK may not represent the
general socioeconomic trends in western countries and continental Europe:
resulting in lower caloric and nutritional standards leading to peculiar
patterns of dental status;
(iii) no clear data regarding the familial income, and hygienic standards
in the study population are available.
References
1. Tu YK, Galobardes B, Smith GD, McCarron P, Jeffreys M, Gilthorpe MS. Associations between tooth loss and mortality patterns in the Glasgow
Alumni Cohort. Heart. 2007 Sep;93(9):1098-103. Epub 2006 Dec 12.
2. Samuel P. Perry, Jr Economic Survey of Europe in 1956 by United
Nations Economic Commission for Europe Annals of the American Academy of
Political and Social Science Vol. 313, (Sep., 1957), pp. 190-191
3. Abbas MA, Galantucci S, Parnetti L, Corea F. Atherosclerosis
assessment confounders in the Rancho Bernardo study. Am J Cardiol. 2007
Mar 15;99(6):876.
4. Corea F, Kwan J, Abbas MA. Predisposition to carotid
atherosclerosis in ICARAS dental substudy. Stroke. 2007 Jan;38(1):12;
author reply 13. Epub 2006 Nov 16.
5. Abbas M, Sessa M, Corea F. Asymptomatic carotid lesions:
traditional vs. emerging risk factors. Arch Med Res. 2006 Jul;37(5):687-8.
6. Abbas M, Bignamini V, Corea F. Effects of chronic microbial
infection on atherosclerosis. Atherosclerosis. 2006 Aug;187(2):439-40.
7. Data downloaded from www.nutrition.org.uk on 30 August 2007
8. Madjid M, Naghavi M, Litovsky S, Casscells SW Influenza and
cardiovascular disease: a new opportunity for prevention and the need for
further studies. Circulation. 2003 Dec 2;108(22):2730-6. Epub 2003 Nov 10
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