Cardiogenic shock is an ominous complication of myocardial infarction
(MI), occurring in 4 to 7%of cases. The majority of patients have
an ST elevation (Q wave) MI, but cardiogenic shock can occur, although
less frequently after a non-ST elevation (non-Q wave) MI.[1,4]
The
clinical definition of cardiogenic shock is decreased cardiac output and
evidence of tissue hypoxia in the presence of adequ...
Cardiogenic shock is an ominous complication of myocardial infarction
(MI), occurring in 4 to 7%of cases. The majority of patients have
an ST elevation (Q wave) MI, but cardiogenic shock can occur, although
less frequently after a non-ST elevation (non-Q wave) MI.[1,4]
The
clinical definition of cardiogenic shock is decreased cardiac output and
evidence of tissue hypoxia in the presence of adequate intravascular
volume. Hemodynamic criteria for cardiogenic shock are hypotension
(systolic blood pressure <90 mm Hg) and a reduced cardiac index
(CI<2.2 L/min/m2) in the presence of elevated pulmonary capillary
wedge pressure (PCWP > 15 mm Hg). Cardiogenic shock, like other types
of shock, is characterized by systemic hypoperfusion, with consequent
tissue hypoxia and vital organ dysfunction. It must be emphasized that
hypotension is not synonymous with shock. Patients with low blood pressure
may have normal tissue perfusion if systemic vascular resistance (SVR) is
also decreased.
On the other hand, tissue perfusion may be impaired
despite normal blood pressure in the presence of severe sympathetically –
mediated peripheral vasoconstriction. Most patients with acute MI and
cardiogenic shock have severe and extensive coronary artery disease, often
involving all the three major coronary arteries. Fixed coronary stenoses
limit coronary blood flow despite maximal coronary arteriolar dilatation.
Coronary perfusion pressure then becomes the major determinant of coronary
blood flow.
Accordingly, any mild drop in blood pressure can significantly
reduce coronary perfusion pressure and hence coronary blood flow. The
combination of severe diffuse coronary artery disease and prolonged
hypotension are particularly detrimental to patients with cardiogenic
shock. The apparently limited efficacy of thrombolysis in patients with
acute MI complicated by cardiogenic shock may be due to failure to improve
coronary perfusion pressure during administration of thrombolytic agents.
The rate of coronary thrombolysis can be restored to normal levels if the
blood pressure is raised by aggressive use of vasopressors or insertion of
intra-aortic balloon pump.[28,29]
Historically, mortality rate of
cardiogenic shock complicating acute MI is 80 to 90 percent.[5] However,
lower values for in-hospital mortality have been noted in more recent
studies ranging from 56 to 74%.[1,4] This significant reduction
in mortality of cardiogenic shock may be attributed to the increased use
of intra-aortic balloon pump (IABP) and coronary reperfusion strategies
which, by restoring patency of the infarct-related artery, can limit the
infarct size.[2,3] There are promising data on the use of percutaneous
coronary intervention (PCI) for cardiogenic shock complicating acute MI.
The long-term outcome of patients with cardiogenic shock appears to be
improved with early revascularization using either PCI or CABG as
illustrated by the 1-year survival rate from the SHOCK trial.[2] Until
coronary revascularization can be performed, the circulation must be
supported either pharmacologically -by inotropics and vasopressors- or
mechanically by intra-aortic balloon pump. Sympathomimetic inotropic and
vasopressor agents remain the first-line therapy to reverse hypotension
and maintain vital organ perfusion. A second goal of therapy is to
maintain coronary perfusion pressure as high as possible during the
administration of thrombolytic agents to facilitate coronary reperfusion.
Dopamine is often used in cardiogenic shock as it increases myocardial
contractility and supports the blood pressure. Norepinephrine is a potent
vasopressor and is often used when dopamine is inadequate.
In spite of its
potent inotropic effect, dobutamine is less often used in cardiogenic
shock because it produces mild vasodilatation that may increase
hypotension. On the other hand, dopamine and Norepinephrine have several
deleterious effects in the setting of acute MI complicated by cardiogenic
shock. Excessive vasoconstriction in response to vasopressors increase
afterload and may further depress LV function and decrease cardiac output.
Systemic hypoperfusion may occur as a result of decreased cardiac output
and high SVR in spite of the relatively preserved blood pressure.
Furthermore, cardiac work and myocardial oxygen demand are increased
because of vasopressor – induced increase in afterload and heart rate that
may worsen myocardial ischemia. Hence, the potential beneficial effect of
vasopressors on coronary perfusion pressure and myocardial oxygen supply
may be offset by increased demand.
Finally, dopamine may increase whole-
body oxygen uptake - because of its calorigenic effect -and exacerbate
tissue hypoxia. Dobutamine may be particularly useful in cardiogenic shock
if improved tissue oxygenation rather than hemodynamic stability will be
the goal of therapy. In contrast to dopamine and norepinephrine,
dobutamine increases cardiac output, lowers afterload and SVR and improves
tissue perfusion with only minimal increase in myocardial oxygen demand
and whole-body oxygen uptake. We can hypothesize that maintaining adequate
perfusion and oxygenation to the heart, brain and other vital organs may
be more important than simply increasing the blood pressure - by excessive
vasoconstriction - even at the expense of cardiac output, myocardial
oxygen demand and tissue oxygenation. Tissue oxygenation can be monitored
directly by measuring whole-body oxygen uptake (by calorimetery) or
indirectly by calculating oxygen extraction ratio (O2 ER = SaO2 –SvO2/
SaO2) where SaO2 is arterial O2 saturation and SvO2 is mixed venous O2
saturation – of blood taken from pulmonary artery with Swan-Ganz catheter.
Other parameters of tissue oxygenation include arterial blood lactate and
gastric mucosal pH. Similarly, cerebral perfusion and oxygenation can be
evaluated by calculating cerebral O2 extraction ratio (cerebral O2 ER =
SaO2 – SvjO2/ SaO2) where SvjO2 is O2 saturation of blood taken from
internal jugular vein. Maintaining adequate coronary perfusion - while
preventing significant increase in myocardial O2 demand - is of critical
importance during pharmacologic and mechanical therapy of cardiogenic
shock. Myocardial oxygenation (reflecting the balance between O2 supply
and demand) can be evaluated directly by measuring myocardial blood
lactate, oxygen extraction ratio, regional pH, PCO2 and base deficit
during transvenous catheterization of the coronary sinus (that drains most
of the cardiac veins and opens into the right atrium). Adequacy of
coronary blood flow can be assessed indirectly by repeated
echocardiography to demonstrate any significant changes in ejection
fraction and regional wall-motion abnormalities. Serial ECGs can also be
used to detect early ST segment -T wave changes suggestive of increased
size of infarct or ischemic area. Mechanical ventilation may be
particularly important in cardiogenic shock - regardless of the blood
gases – as it significantly reduces oxygen uptake (VO2) - by allowing
adequate sedation, analgesia and muscle paralysis – in a clinical setting
of decreased oxygen delivery to the tissues (DO2). Furthermore, mechanical
ventilation can improve arterial oxygenation and increase myocardial O2
supply.
In conclusion, it may be more appropriate to titrate the
pharmacologic therapy of cardiogenic shock according to the parameters of
myocardial and tissue oxygenation rather than to the hemodynamic
parameters alone, while waiting for coronary revascularization.
References
1. Hochman, js, Boland, j, Sleeper, et al .and the SHOCK Registry
Investigators. Current spectrum of cardiogenic shock and effect of early
revascularization on mortality: Results of an international registry.
Circulation 1995; 91: 873.
2. Holmes, DR Jr, Bates, ER, Kleinman, NS, et al. Contemporary
reperfusion therapy for cardiogenic shock: The GUSTO-1 trial experience.
Global Utilization of Streptokinase and Tissue Plasminogen Activator for
Occluded Coronary Arteries.J Am Coll Cardiol 1995; 26:668.
3. Goldberg, RJ, Samad, NA, Yarzebski, J, et al. Temporal trends in
cardiogenic shock complicating acute myocardial infarction. N Engl j
Med1999; 340:1162.
4. Holmes, DR Jr, Berger, PB, Hochman, Js, et al. cardiogenic shock
in patients with acute ischemic syndromes with and without ST- segment
elevation. Circulation 1999; 100:2067.
5. Goldberg, RJ, Gore, JM, Alpert, JS, et al. Cardiogenic shock after
acute myocardial infarction.Incidence and mortality from a community wide
perspective, 1975 -1988. N Engl J Med 1991; 325: 1117.
The article by Professor Ferrières on the French Paradox,[1] suggests that “under certification of CHD deaths in France is a possible bias, but after correction, it remains a low bias”. However, MONICA data from Glasgow and Belfast show an underestimate of only 9.9% and -0.4% respectively, whereas those from Lille , Strasbourg and Toulouse underestimate CHD deaths by 93.3, 76.3 and 71.7% respectively. In ad...
The article by Professor Ferrières on the French Paradox,[1] suggests that “under certification of CHD deaths in France is a possible bias, but after correction, it remains a low bias”. However, MONICA data from Glasgow and Belfast show an underestimate of only 9.9% and -0.4% respectively, whereas those from Lille , Strasbourg and Toulouse underestimate CHD deaths by 93.3, 76.3 and 71.7% respectively. In addition, our statistics database 1 shows that whereas total mortality in France is similar to that in England and Wales , doctors in France have a much higher rate of reporting deaths from “all other causes” than doctors in England and Wales (see table 1). In our view, these data are inconsistent with a “low bias” in death certification and in part explain the so called French Paradox.
Table 1 Annual deaths by country, gender and “other causes”
England and Wales
France
Total deaths
Men
264
865
275
106
Women
294
416
256
512
Deaths from other causes
Men
32
263 (12.2%)
59
638 (21.7%)
Women
48
053 (16.5%)
68
719 (26.8%)
Reference
1. British Heart Foundation. European Cardiovascular Disease Statistics. London. 2000.
Steve Yentis raises relevant discussion points.[1] A detailed discussion
of anaesthetic methods was beyond the scope of the article and Steve's
comments regarding the safety of low-dose epidural are welcome.
I agree that assisted vaginal delivery is the safest mode of delivery
for most women with heart disease. His comments about instrumental vaginal
delivery for women with Marfan syndrome underl...
Steve Yentis raises relevant discussion points.[1] A detailed discussion
of anaesthetic methods was beyond the scope of the article and Steve's
comments regarding the safety of low-dose epidural are welcome.
I agree that assisted vaginal delivery is the safest mode of delivery
for most women with heart disease. His comments about instrumental vaginal
delivery for women with Marfan syndrome underlines the importance of
specialist obstetric units for women with heart disease. However aortic
disease in Marfan syndrome does carry a significant risk and elective
Caesarean section may still be a safer option outside units with
particular expertise in this condition.
Reference
1. S A Thorne. Pregnancy in heart disease. Heart 2004; 90: 450-456.
Schwerzmann et al.[1] report a
comparison
of 2 PFO closure devices, the Amplatzer and the PFO Star, and concluded
that
the Amplatzer device was superior. Even if the data are of some interest,
I
see some major limitations of this trial, making the conclusions of little
value
in the daily practice.
First, it is a non-randomized trial. In addition
the PFO
star device used in this comp...
Schwerzmann et al.[1] report a
comparison
of 2 PFO closure devices, the Amplatzer and the PFO Star, and concluded
that
the Amplatzer device was superior. Even if the data are of some interest,
I
see some major limitations of this trial, making the conclusions of little
value
in the daily practice.
First, it is a non-randomized trial. In addition
the PFO
star device used in this comparison is of the first generation and has
nothing
to do with the current generation device which is hexagonally shaped with
6
arms and an articulating centerpost. The current generation was
designed
by the manufacturer based on data from previous generations. We, and other
authors using this later device, have reported much better results with a
low
incidence of complications, recurrence of stroke or persistent
permeability at
1 year.[2,3]
A residual shunt at 1 year was present in 8 to 13 % of the
patients,
far less than the 33 % reported by Shwerzmann.[1] The use of the old device
by Shwerzmann et al, certainly explains these differences. No
complications
are reported with the use of the Amplatzer in their comparison. This is a
little
bit surprising, since the same group 4 reported, in a previous paper,
their
results of PFO closure in 80 patients using several different devices.
Among
the 14 patients treated with the Amplatzer, 6 had complications and one
patient experienced an embolisation of the device. The recurrence of
stroke
was lower with the PFO Star compared to the Amplatzer. The period of
comparison of the devices overlaps the period of the inclusion in the
registry
of these 80 patients. This raises the question of how the selection was
done
for the comparison. A selection bias may be present. Embolisation is
usually
related to a technical problem during implantation or to the selection of
too
small of a device for a given defect.
In other reports, using the new PFO
Star
the incidence of acute complications is close to zero. Moreover, in 5
patients,
more than 1 placement attempt was required; this suggests an erroneous
choice of the device size rather than a problem related to the device
itself,
once again it is what is seen in the learning curve. In fact one
prospective
registry has recently been published and did not show any differences
between 3 devices 5 including the PFO star and the Amplatzer.
Finally, the
paper of Schwermann et al. does not help in the comparison of devices; the
conclusions are questionable, especially for those who have experience in
PFO closure.
References
1.Schwermann M, Windecker S, Wahl A, Nedeltchev K, Mattle H, Seiler C,
Meier
B. Percutaneous closure of patent foramen ovale: impact of device design
on
safety and efficacy. Heart 2004;90:186-190.
2. Stauffer JC, Serra M, Juillard JM, Seydoux C, Perret F, Owlya R, Savcic
M,
Beuret P, Goy J. Fermeture Archives des maladies du Coeur et des vaisseaux
2004;97:37-41. .
3. Schräder R. Indications and techniques of transcatheter closure of
patent
foramen ovale. J of Interv Cardiol 2003;6:543-551.
4. Windecker S, Wahl A, Chatterjee T, Garachemani A, Eberli F, Seiler C,
Meier
B. Percutaneous closure of patent foramen ovale in patients with
paradoxical
embolism. Long-term risk of recurrent thromboembolic events. Circulation
2000;101:893-898.
5. Braun M, Gliech V, Boscheri A, Schoen S, Gahn G, Reichmann H,
Haass M,
Schraeder R, Strasser RH. Transcatheter closure of patent foramen ovale
(PFO)
in patients with paradoxical embolism; Periprocedural safety and mid-term
follow-up results of three different device occluder systems. Eur Heart J
2004;
25:424-30.
We read Rizvi et al's article on the status of rheumatic heart
disease (RHD) in rural Pakistan with considerable interest.[1]
Rizvi and
colleagues highlight an extremely important problem facing cardiologists
in Pakistan. However, it is possible that the true prevalence of RHD in
this population may have been underestimated as echocardiography was only
performed in those with an audible...
We read Rizvi et al's article on the status of rheumatic heart
disease (RHD) in rural Pakistan with considerable interest.[1]
Rizvi and
colleagues highlight an extremely important problem facing cardiologists
in Pakistan. However, it is possible that the true prevalence of RHD in
this population may have been underestimated as echocardiography was only
performed in those with an audible murmur. Although the concordance
between auscultation by experienced cardiologists (such as the authors)
and echocardiography is fairly robust, auscultation is an operator-
dependent skill which is difficult to quantify. Furthermore, very early
RHD, particularly mitral valve disease, may be missed even by highly
experienced auscultators. The economics of performing an echocardiogram
in over 9000 subjects is clearly prohibitive; however, a random
echocardiographic verification of a prespecified number of patients deemed
to have "no RHD" by auscultation would have enhanced the robustness of
this estimate.
Rizvi et al. very appropriately point out the lack of initiative at
the government level to take measures to both, reduce the prevalence of
this disease as well as improve health care delivery to those afflicted
with RHD.
Reference
1. S F Rizvi, M A Khan, A Kundi, D R Marsh, A Samad, and O Pasha
Status of rheumatic heart disease in rural Pakistan
Heart 2004; 90: 394-399.
I read with great interest the recently published study by Eren et al. [1]
They reported that increased aortic stiffness in patients with
hypertension, diabetes mellitus, and both caused to impaired left
ventricular (LV) diastolic functions. Furthermore, they also found that
there was a relation between the diastolic function and aortic stiffness
in the patients. It is known that the ao...
I read with great interest the recently published study by Eren et al. [1]
They reported that increased aortic stiffness in patients with
hypertension, diabetes mellitus, and both caused to impaired left
ventricular (LV) diastolic functions. Furthermore, they also found that
there was a relation between the diastolic function and aortic stiffness
in the patients. It is known that the aorta is not a simple conduit for
the distribution of blood but rather has a fundamental role in the
function of the cardiovascular system. By virtue of its elastic
properties, aorta influences LV function and coronary blood flow. [2]
Although they excluded of coronary artery disease, it is convinced that
changes of myocardial tissue properties (intrinsic factors) affect LV
diastolic functions especially in patients with diabetes. On the other
hand, it is strikes me that decreased aortic distensibility and increased
aortic stiffness in pathologic conditions may facilitate to be upset the
diastolic functions like as a promoter factor.
What is more, with reference to our study, according to different
aspect aortic elastic properties are changed as a result of regular
exercise. [3-5] While aortic stiffness is decreased in endurance-trained
athletes [3], on the contrary, it is decreased in strength-trained
athletes [4]. However, in athletes who train both types of exercise,
diastolic functions of LV are better than those of sedentary subjects. In
the same way, we also found that multivariate analyses showed a strong
correlation between aortic distensibility and LV diastolic functions
(measured by standard and tissue Doppler echocardiography). [5]
Taking all studies into consideration, although the exact association
between aortic mechanical function parameters and LV diastolic properties
is not known, we conclude that aortic stiffness is one of the afterload
factors which may affect LV diastolic performance in disease, damaged of
physiological situation.
References
1. Eren M, Gorgulu S, Uslu N, Celik S, Dagdeviren B, Tezel T.
Relation between aortic stiffness and left ventricular diastolic function
in patients with hypertension, diabetes, or both. Heart 2004;90:37-43.
2. Stefanadis C, Stratos C, Vlachopoulos C, et al. Pressure-diameter
relation of the human aorta: a new method of determination by the
application of a special ultrasonic dimension catheter. Circulation
1995;92:2210-2219.
3. Kasikcioglu E, Oflaz H, Akhan H, et al. Aortic distensibility in
endurance athletes. Acta Cardiologica 2003;58:243-4.
4. Kasikcioglu E, Oflaz H, Akhan H, et al. Left ventricular remodeling and
aortic distensibility in elite power athletes. Heart Vessels 2004;(in
press).
5. Kasikcioglu E, Kayserilioglu A, Oflaz H, Akhan H. Aortic distensibility
and left ventricular diastolic functions in endurance athletes. Int J
Sports Med 2004; (in press).
As a response to the case report by Bilkhu et al,[1]we wish to report
our experience with a 66 year old lady with hypertension and
hypercholesteremia.
Our patient had had bypass graft surgery for triple
vessel disease - Left Internal mammary artery (LIMA) to Left anterior
descending (LAD), Radial A via LIMA to Obtuse Marginals (OM1 and OM2). She
presented with angina 6 months post CABG, and...
As a response to the case report by Bilkhu et al,[1]we wish to report
our experience with a 66 year old lady with hypertension and
hypercholesteremia.
Our patient had had bypass graft surgery for triple
vessel disease - Left Internal mammary artery (LIMA) to Left anterior
descending (LAD), Radial A via LIMA to Obtuse Marginals (OM1 and OM2). She
presented with angina 6 months post CABG, and on coronary angiography was
found to have severe native vessel disease but patent grafts and proximal
stenosis of the left subclavian artery (LSA).
In this case, due to the surgical technique both OM grafts also arose from
the internal mammary artery and therefore, all her grafts were rendered
“ischaemic” by the LSA stenosis. She underwent balloon dilatation of the
stenosis with good result and was discharged home.
This case has changed our pre-operative screening process and we
suggest that bilateral arm blood pressure (BP) measurements should be done
as routine practice. A recent study2 suggested that an upper extremity BP
difference of >or = 15 mmHg, identified most patients with >or = 50%
subclavian artery narrowing and recommended Brachiocephalic- subclavian
arteriography only in patients with abnormal non-invasive screening for
subclavian stenosis.
References
1. K. S. Bilkhu RS, Been M Subclavian artery stenosis as a cause for
recurrent angina after LIMA graft stenting Heart 89:1429(2003).
2. R. B. Osborn, L A.Vernon SM Screening for subclavian artery stenosis in
patients who are candidates for coronary bypass surgery. Catherisation
& Cardiovascular Intervention. 56:2;162-5(2002).
Sara Thorne give a comprehensive account of heart disease in
pregnancy [1] which, as she says, represents an increasing challenge to
high-risk obstetric teams. I wish to raise three points.
First, in most cases the "good analgesia" in labour mentioned by Dr
Thorne should be provided (anticoagulation allowing) by epidural analgesia
using modern low-dose solutions of local anaesthetic/opioid,...
Sara Thorne give a comprehensive account of heart disease in
pregnancy [1] which, as she says, represents an increasing challenge to
high-risk obstetric teams. I wish to raise three points.
First, in most cases the "good analgesia" in labour mentioned by Dr
Thorne should be provided (anticoagulation allowing) by epidural analgesia
using modern low-dose solutions of local anaesthetic/opioid, since this
both preserves cardiovascular stability and allows extension of the
epidural block to anaesthesia for caesarean section if required.[2] This
is in contrast to the traditional and outdated view that cardiac disease
is an absolute contra-indication to all regional techniques -- though use
of strong local anaesthetics by rapid injection (for example, single-shot
spinal anaesthesia for caesarean section) may indeed be hazardous.
Second, although Dr Thorne recommends elective caesarean section for
patients with aortic lesions, at the Chelsea and Westminster Hospital we
have developed a team-based approach whereby patients with aortic lesions
such as Marfan's disease and coarctation do not necessarily undergo
elective caesarean section, the risks from regional or general anaesthesia
(cardiovascular instability) and surgery (deep vein thrombosis, bleeding,
infection and the need for uterotonic drugs with their potentially
dangerous cardiovascular side effects) often being considered greater than
those of epidural analgesia and elective instrumental delivery.[3]
Third, Heart's readers may not be aware that the International
Journal of Obstetric Anesthesia, though not yet listed in the National
Library of Medicine's database, has an extensive collection of reports of
cardiac disease in pregnancy including the Obstetric Anaesthetists'
Associations' UK Registry of High-risk Obstetric Anaesthesia.[4,5] The
latter includes over 300 cases of cardiorespiratory disease managed in the
UK since 1996.
References
1. Thorne SA. Pregnancy in heart disease. Heart 2004; 90: 450-456.
2. Suntharalingam G, Dob D, Yentis SM. Obstetric epidural analgesia
in aortic stenosis: a low-dose technique for labour and instrumental
delivery. International Journal of Obstetric Anesthesia 2001; 10: 129-34.
3. Yentis S, Gatzoulis MA, Steer P. Pregnancy and coarctation of the
aorta. Journal of the Royal Society of Medicine 2003;96: 471.
4. Dob DP, Yentis SM. UK Registry of High-risk Obstetric Anaesthesia:
report on cardiorespiratory disease. International Journal of Obstetric
Anesthesia 2001; 10: 267-72.
5. Lewis N, Dob DP, Yentis SM. UK Registry of High-risk Obstetric
Anaesthesia: arrhythmias, cardiomyopathy, aortic stenosis, transposition
of the great arteries and Marfan’s syndrome. International Journal of
Obstetric Anesthesia 2003; 12: 28-34.
Conflicting interests
I am a member of the Editorial Board of the International Journal of
Obstetric Anesthesia and Hon. Secretary of the Obstetric Anaesthetists'
Association
We read with great interest the published study by Fagard.[1]
Cardiovascular adaptations in athletes are dependent multi-
factorial parameters (genetic, age, type of exercise, exercise duration).
However, it is accepted that type of exercise is key role for cardiac
remodelling to regularly and intensive exercise training. The review on
this topic confirmed how endurance- and strength-training may...
We read with great interest the published study by Fagard.[1]
Cardiovascular adaptations in athletes are dependent multi-
factorial parameters (genetic, age, type of exercise, exercise duration).
However, it is accepted that type of exercise is key role for cardiac
remodelling to regularly and intensive exercise training. The review on
this topic confirmed how endurance- and strength-training may determine
either extreme volume or pressure load, thus causing the ventricular
cavity diameters and wall thicknesses with different degree.[1]
Great vascular adaptation to habitual exercise also shows variability and
affects left ventricular remodelling in two different exercise types,
static or dynamic. According to our reports, aortic distensibility was
increased and associated with maximal oxygen consumption in endurance
athletes; however, it was decreased in strength-trained athletes.[2,3]
Our findings provide evidence about the close association of the aortic
stiffness and left ventricular hypertrophy.3 We speculated that aortic
stiffness might be an indirect effect of afterload factors which cause the
ventricular hypertrophy. However, developed concentric hypertrophy with
reduced ventricular radius is perfect adaptation mechanism in power
athletes. Then, wall stress is decreased while aortic stiffness increases
at rest period in power athletes.[3]
Recently, an easily measured tissue Doppler index was proposed as a
potentially useful method for differentiating physiological variants from
structural heart disease.[4] We found that tissue Doppler indices in power
athletes were higher than those of sedentary subjects.
In keeping with perfect diastolic function, these vascular changes may be
a physiologically cardiovascular adaptation to habitual isometric
exercise.
References
1. Fagard R. Athlete’s heart. Heart 2003;89:1455-61.
2. Kasikcioglu E, Oflaz H, Akhan H, et al. Aortic distensibility in
endurance athletes. Acta Cardiologica 2003;58:243-4.
3. Kasikcioglu E, Oflaz H, Akhan H, et al. Left ventricular remodeling and
aortic distensibility in elite power athletes. Heart Vessels (in press),
2004.
4. Kasikcioglu E, Akhan H. Echocardiographic limits of left ventricular
remodeling in athletes. J Am Coll Cardiol 2004; (in press).
One of the main concerns is that the incidence of atrial fibrillation
increase with age; almost doubling every decade in adult life.[1] Although,
there are various options available for the management of this very common
condition, the main hurdle that we have to overcome in clinical practice
is the age factor. Many of them develop side effects to the antiarrhytmic
drugs which has been well documented in...
One of the main concerns is that the incidence of atrial fibrillation
increase with age; almost doubling every decade in adult life.[1] Although,
there are various options available for the management of this very common
condition, the main hurdle that we have to overcome in clinical practice
is the age factor. Many of them develop side effects to the antiarrhytmic
drugs which has been well documented in the AFFIRM study.[2]
Warfarinisation is difficult because of risk of falls especially in people
with disability with stroke – in whom it is probably most useful.
Compliance is also an issue in these patients. New surgical methods like
radiofrequency pulmonary vein ablation and Maze procedures are coming into
practice.[1] Though these new and exiting treatment options are becoming
available, the concern is whether it be applicable to the older population
who are most affected
References
1. Medical Progress ; Atrial Fibrillation
Falk R. H.
N Engl J Med 2001; 344:1067-1078, Apr 5, 2001.
2. The Atrial Fibrillation Follow-up Investigation of Rhythm
Management (AFFIRM) Investigators. A comparison of rate control and rhythm
control in patients with atrial fibrillation. N Engl J Med
2002;347:1825–33
Dear Editor
Cardiogenic shock is an ominous complication of myocardial infarction (MI), occurring in 4 to 7%of cases. The majority of patients have an ST elevation (Q wave) MI, but cardiogenic shock can occur, although less frequently after a non-ST elevation (non-Q wave) MI.[1,4]
The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequ...
Dear Editor
The article by Professor Ferrières on the French Paradox,[1] suggests that “under certification of CHD deaths in France is a possible bias, but after correction, it remains a low bias”. However, MONICA data from Glasgow and Belfast show an underestimate of only 9.9% and -0.4% respectively, whereas those from Lille , Strasbourg and Toulouse underestimate CHD deaths by 93.3, 76.3 and 71.7% respectively. In ad...
Dear Editor
Steve Yentis raises relevant discussion points.[1] A detailed discussion of anaesthetic methods was beyond the scope of the article and Steve's comments regarding the safety of low-dose epidural are welcome.
I agree that assisted vaginal delivery is the safest mode of delivery for most women with heart disease. His comments about instrumental vaginal delivery for women with Marfan syndrome underl...
Dear Editor
Schwerzmann et al.[1] report a comparison of 2 PFO closure devices, the Amplatzer and the PFO Star, and concluded that the Amplatzer device was superior. Even if the data are of some interest, I see some major limitations of this trial, making the conclusions of little value in the daily practice.
First, it is a non-randomized trial. In addition the PFO star device used in this comp...
Dear Editor
We read Rizvi et al's article on the status of rheumatic heart disease (RHD) in rural Pakistan with considerable interest.[1]
Rizvi and colleagues highlight an extremely important problem facing cardiologists in Pakistan. However, it is possible that the true prevalence of RHD in this population may have been underestimated as echocardiography was only performed in those with an audible...
Dear editor
I read with great interest the recently published study by Eren et al. [1]
They reported that increased aortic stiffness in patients with hypertension, diabetes mellitus, and both caused to impaired left ventricular (LV) diastolic functions. Furthermore, they also found that there was a relation between the diastolic function and aortic stiffness in the patients. It is known that the ao...
Dear Editor
As a response to the case report by Bilkhu et al,[1]we wish to report our experience with a 66 year old lady with hypertension and hypercholesteremia.
Our patient had had bypass graft surgery for triple vessel disease - Left Internal mammary artery (LIMA) to Left anterior descending (LAD), Radial A via LIMA to Obtuse Marginals (OM1 and OM2). She presented with angina 6 months post CABG, and...
Dear Editor
Sara Thorne give a comprehensive account of heart disease in pregnancy [1] which, as she says, represents an increasing challenge to high-risk obstetric teams. I wish to raise three points.
First, in most cases the "good analgesia" in labour mentioned by Dr Thorne should be provided (anticoagulation allowing) by epidural analgesia using modern low-dose solutions of local anaesthetic/opioid,...
Dear Editor
We read with great interest the published study by Fagard.[1]
Cardiovascular adaptations in athletes are dependent multi- factorial parameters (genetic, age, type of exercise, exercise duration). However, it is accepted that type of exercise is key role for cardiac remodelling to regularly and intensive exercise training. The review on this topic confirmed how endurance- and strength-training may...
Dear Editor
One of the main concerns is that the incidence of atrial fibrillation increase with age; almost doubling every decade in adult life.[1] Although, there are various options available for the management of this very common condition, the main hurdle that we have to overcome in clinical practice is the age factor. Many of them develop side effects to the antiarrhytmic drugs which has been well documented in...
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