Wilmshurst et al.,[1] link inheritance of atrial shunts to
inheritance of migraine with aura in some families. The link between
migraine with aura and patent foramen ovale (PFO) appears to be gathering
strength and the plea for randomized controlled trials of PFO-closure in
migraine patients are beginning to appear justified.[2-4] The conclusion
that closure of atrial shunts usually improves or cures...
Wilmshurst et al.,[1] link inheritance of atrial shunts to
inheritance of migraine with aura in some families. The link between
migraine with aura and patent foramen ovale (PFO) appears to be gathering
strength and the plea for randomized controlled trials of PFO-closure in
migraine patients are beginning to appear justified.[2-4] The conclusion
that closure of atrial shunts usually improves or cures migraine with aura[1] reflects the philosophic commitment and excitement of the therapists.
As the momentum for PFO closure for prevention of migraine builds up,
it becomes increasingly difficult to maintain scientific equipoise.[5-8]
One, closure of both PFO (right-to-left shunt) as well as closure of
atrial septal defect (left- to-right shunt) has been proposed to prevent
migraine attacks.[5,6]
Two, migraine is generally a disorder with a
predictable onset and recurrences, and, is a characteristically
lateralizing disorder, with the headache persistently occurring
unilaterally (right or left), bilaterally, or in a side-shifting manner.
The Valsalva manœuvre can aggravate existent migraine headache but is not
known to precipitate migraine headache. A MEDLINE search does not reveal
any report of a direct link between Valsalva manœuvre and precipitation of
migraine. Cerebrovascular dysfunction secondary to a congenital defect
such as PFO cannot explain the late appearance (in teens or twenties),
disappearance (second and third trimesters of pregnancy and in later
decades), or periodic recurrences (menstrual migraine) of headache or aura
or both. Moreover, with the concept of paradoxical embolization of gas,
thrombi or vasoactive neuromediators, these potential precipitants are
presumed to be streamed regularly over decades to the same brain
parenchymal site or circulatory segment in order to produce lateralizing
headache or aura – such a pathophysiological mechanism is highly unlikely.[7-9]
Three, cluster headache (CH) is a strictly lateralized headache
without implication of brain ischemia in its pathogenesis; a remarkably
high incidence of right-to-left shunt (42.5%) has been seen in CH patients.[10] To conclude a striking effect on prevention of migraine aura or
headache or both simply by PFO closure is premature as we need to know:
(ii) why the incidence of PFO is higher in migraine or CH patients (or
other hitherto unknown subsets) than in the general population; and (ii)
why PFO-associated right-to-left shunt does not cause aura-like brain
dysfunction in most patients.
Four, drugs that do not cross the blood-
brain barrier and cannot critically influence brain neuronal function, are
effective migraine prophylactic (atenolol, verapamil or nadolol) or aura
abortive (nifedipine or isoproterenol) agents.[9] Migraine prevention
does not appear convincingly related to crucial modulation of a particular
brain neuronal function; a peripheral extra-CNS origin for migraine
appears to be distinctly plausible.[9,11]
Five, headaches are less
frequent, less severe and shorter in migraine with aura patients; the
likelihood of a placebo effect of PFO closure is much more likely in this
subset[5,8]
Six, migraine is more than twice as common in women than in
men but the incidence of PFO does not show a similar pattern.[1]
Seven,
it is debatable whether aspirin can be stopped altogether in migraine
patients after PFO closure, as implantation of an occluder device with a
left-atrial disc would augment platelet aggregation and embolism.
Eight, a
large PFO or small atrial septal defect as seen in migraine patients[1,3] would tend to maintain a left-to-right shunt under most circumstances.
Access to the left heart at the level of the atria in PFO by air-bubbles
during Valsalva manœuvre is a laboratory artifact that does not reflect a
real-life situation; in paradoxical embolism, it is a platelet-thrombin
plug that embolizes – such an embolus has physical properties not at all
akin to air bubbles. The larger-sized PFO may permit air bubbles to easily
cross over to the left heart due to rheological factors that fundamentally
differ from those that affect platelet-thrombin complexes.
Nine, reduced
frequency of migraine in patients started on oral anticoagulation[2] does
not directly support a pathogenetic role for PFO in migraine. Besides the
placebo effect of warfarin which is quite significant in a highly variable
condition such as migraine, by impairing blood coagulability warfarin may
increase vasopressin bioavailability; sub-clinical rises in vasopressin
might, in turn, prevent recurrences of migraine.[11,12]
Prevention of migraine following PFO-closure is the pursuit of possible
benefit involving a remote circulatory effect on the brain circulation.
While the practice of PFO-closure for migraine itself cannot be currently
recommended, serious conceptual groundwork is still missing from the
research endeavour. Neither the aura nor the headache represents the true
onset of the migraine attack; brain circulatory changes or cortical
spreading depression must not be construed as the part of the early
physiological changes in migraine.[11] The primary pathogenetic
aberrations in migraine lie buried in the largely clinically inaccessible
but variably extended prodromal and “pre-prodromal” phases.[11] Larger
studies with optimal designs will not eliminate these basic scientific
issues.[5-9] Since almost 50% of migraine with aura patients do not have
a PFO,[3] pathogenetic mechanisms other than PFO-related are clearly
operative.[1] The emphasis on relatively larger atrial shunts in migraine
with aura patients[1] does not diminish the strength of the arguments
against such a pathogenetic mechanism.
To suspend clinical disbelief at this stage of evolution of migraine
mechanisms does not appear justifiable. From beta-blockers to magnesium[14] to botulinum toxin,[15] serendipity has (mis)guided migraine
research. Migraine therapeutics, particularly preventive or prophylactic
therapy, remains purely empirical. PFO has simply been detected in a
fraction of migraine patients; any conclusion that it might be involved in
the pathogenesis of migraine is premature. Whether the presence of a PFO
in primary headache patients confers a teleological or physiological
advantage is an intriguing question. Precipitation of migraine following
closure of atrial septal defect[16] suggests that a higher stoke volume /
cardiac output might worsen or unmask a migrainous diathesis.[6]
No theory should be allowed to exist in a vacuum; all theories must
be generalizable and should gather strength by an increasing number of
logically defensible clinical associations and links with basic science
tenets that, in turn, lead towards the evolution of an intelligible
synthesis. The occurrence of migraine in any one individual is probably
based on a polygenic trait superimposed on a highly variable state. The
link between PFO and primary headaches, both migraine and cluster
headache, may lie in the expression of a connective tissue disorder that
affects both inter-atrial septal closure as well as visco-elastic
properties and pressure-volume relationship of the corneo-scleral envelope.[17,18]
References:
1. Wilmshurst PT, Pearson MJ, Nightingale S, Walsh KP, Morrison WL.
Inheritance of persistent foramen ovale and atrial septal defects and the
relation to familial migraine with aura. Heart 2004;90:1315-20.
2. Zanchetta M, Rigatelli G, Ho SY. A mystery featuring right-to-left
shunting despite normal intracardiac pressure. Chest 2005;128:998-1002.
3. Schwerzmann M, Nedeltchev K, Lagger F, Mattle HP, Windecker S,
Meier B, Seiler C. Prevalence and size of directly detected patent foramen
ovale in migraine with aura. Neurology 2005 (Published online before print
September 7, 2005).
4. Morandi E, Anzola GP, Casilli F, Onorato E. Migraine: traditional
or “innovative” treatment? A preliminary case-control study. Pediatr
Cardiol 2005;25:1-3.
5. Gupta VK. Percutaneous closure of patent foramen ovale reduces the
frequency of migraine attacks. Neurology 2004;63:1760-1761.
6. Gupta VK. Closure of atrial septal defect and migraine. Headache
2004;44:291-292.
7. Gupta VK. ASD closure for migraine: is there a scientific basis?
Eur Heart J 2005; 2005;14:1446.
8. Gupta VK. Patent foramen ovale / atrial septal defect closure and
migraine: searching the rationale for the procedure. J Am Coll Cardiol
2005;46:737-8.
9. Gupta VK. Non-lateralizing brain PET changes in migraine:
phenomenology versus pharmacology? Brain 2004 127:E12.
10. Finocchi C, Del Sette M, Angeli S, Rizzi D, Gandolfo C. Cluster
headache and right-to-left shunt on contrast transcranial Doppler. A case-
control study. Neurology 2004;63:1309-1310.
11. Gupta V. Migraine, cortical excitability and evoked potentials: a
clinico-pharmacological perspective. Brain 2005;128:E36.
12. Gupta VK. Does vasopressin mediate the migraine-remitting
influence of warfarin? Headache 1999;39:140-141.
13. Gupta VK. A clinical review of the adaptive role of vasopressin
in migraine. Cephalalgia 1997;17:561-569.
14. Gupta VK. Magnesium therapy for migraine: do we need more trials
or more reflection? Headache 2004; 44: 445-446.
15. Gupta VK. Botulinum toxin type A therapy for chronic tension-type
headache: fact versus fiction. Pain 2005; 116: 166-167.
16. Yankovsky AE, Kuritzky A. Transformation into daily migraine with
aura following transcutaneous atrial septal defect closure. Headache
2003;43:496-498.
17. Gupta V. Does the eye modulate the clinical expression of cluster
headache? BMC Neurology 2005;5:6 (Published online 17 May 2005). Available
at: http://www.biomedcentral.com/1471-2377/5/6/comments#201461
18. Gupta VK. Glyceryl trinitrate and migraine: nitric oxide donor
precipitating and aborting migrainous aura. J Neurol Neurosurg Psychiatry.
Published online 24 October 2005. Available at:
http://jnnp.bmjjournals.com/cgi/eletters/76/8/1158
In patients with hypertrophic cardiomyopathy (HC) followed in our
institution[1], the annual mortality rate was 1%, unexpectedly low for a
selected cohort of patients with HC. Now, in view of the excellent recent
article of Elliot et al.[2], in which they presented and discussed survival
rates in HC, we are happy with the confirmation that even selected
patients with HC may survive at high rates when...
In patients with hypertrophic cardiomyopathy (HC) followed in our
institution[1], the annual mortality rate was 1%, unexpectedly low for a
selected cohort of patients with HC. Now, in view of the excellent recent
article of Elliot et al.[2], in which they presented and discussed survival
rates in HC, we are happy with the confirmation that even selected
patients with HC may survive at high rates when followed in institutions
dedicated to HC.
This good news should be increasingly reported to the
patients and their families, to the public health agents, and to the
general cardiologists who believe that CH is a particularly ominous
disease. In the era of implantable defibrillators and of the evolving
myocardial reparatory therapeutic strategies[3,4], every effort should be
taken to identify undiagnosed patients with HC in the general population.
No matter the costs, such actions would surely save a considerable number
of lives.
References:
1. Arteaga E, Ianni BM, Fernandes F, et al. Benign outcome in a long-
term follow-up of patients with hypertrophic cardiomyopathy in Brazil. Am
Heart J 2005;149:1099-105.
2. Elliott PM, Gimeno JR, Thaman R, Historical trends in reported
survival rates in patients with hypertrophic cardiomyopathy. Heart
2005;Oct 10:Epub.
3. Lim DS, Lutucuta S, Bachireddy P, et al. Angiotensin II blockade
reverses myocardial fibrosis in a transgenic mouse model of human
hypertrophic cardiomyopathy. Circulation 2001;103:789-91.
4. Araujo AQ, Arteaga E, Ianni BM, et al. Effect of losartan on left
ventricular diastolic function in patients with nonobstructive
hypertrophic cardiomyopathy. Am J Cardiol: In Press.
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that
caused the person to seek medical attention in the first instance.
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that
caused the person to seek medical attention in the first instance.
While many experience 'typical text book chest pain ', I have found a
larger number do not. These people experience various intensity of
discomfort and many have described their symptoms as in one arm or both
with no chest symptoms, or an aching in the jaw or throat or shoulders and
more than half the clients with chest symptoms describe a 'tightness'
rather than a pain.
Delay in seeking medical attention is reported to me often as 'not
relating their symptoms to being cardiac in origin' rather than any
denial. There is often a comment such as: " I didn’t really think it was my heart because I guess I expected the symptoms would be worse if it was my heart." It raises the question weather health professionals in the ambulance service and ED, GP practice and cardiac wards should change their
questioning of people about their acute symptoms from "how much chest pain
do you have?" to "do you have any discomfort or pain between the ear lobe
or belly button, front or back?”.
As part of our cardiac rehab education sessions on symptom recognition and
when to seek medical attention in both the cardiac and community groups,
we now use the patient experience as examples . This has improved
confidence and communication.
For the sake of completeness, the thesis that the renin-angiotensin-
aldosterone system (RAAS) might have a role in the pathogenesis of aortic
stenosis[1], also requires a recognition that angiotensin converting
enzyme(ACE)inhibitor therapy[2] might, on its own, be insufficient to
retard progression of this disorder, and that a cardioprotective component
specifically targeting aldosterone blockade by co...
For the sake of completeness, the thesis that the renin-angiotensin-
aldosterone system (RAAS) might have a role in the pathogenesis of aortic
stenosis[1], also requires a recognition that angiotensin converting
enzyme(ACE)inhibitor therapy[2] might, on its own, be insufficient to
retard progression of this disorder, and that a cardioprotective component
specifically targeting aldosterone blockade by co-prescribing the ACE
inhibitor with eplerenone as in the two EPHESUS studies[3,4] might be
crucial in retarding disease progression in patients who are not eligible
for aortic valve replacement because they belong to the two categories
identified by Shavelle, namely, the asymptomatic phase or prohibitive
operative risk in spite of significant symptomatology.[2]The proposed
rationale is that left ventricular hypertrophy in aortic stenosis might be
maladaptive and potentially promotive of systolic dysfunction[5], and that
if myocardial fibrosis were an intermediate stage in this progression this
might be prevented through the use of aldosterone blockade.
Yours sincerely,
OMP Jolobe (retired geriatrician)
References
1. O'Brien KD., Shavelle DM., Caulfield MT., et al
Association of angiotensin-converting enzyme with low density lipoprotein
in aortic valve lesions and in human plasma
Circulation 2002:106:2224-30.
2. Shavelle DM
Are angiotensin converting enzyme inhibitors beneficial in patients with
aortic stenosis?
HEART 2005:91:1257-59.
3. Pitt B.,Remme W., Zannad F., et al
Eplerenone, a selective aldosterone blocker, in patients with ventricular
dysfunction after myocardial infarction
New England Journal of Medicine 2003:348:1309-24.
4. Pitt B., White H., Nicolau J et al
Eplerenone redices mortality 30 days after randomisation following acute
myocardial infarction in patients with left ventricular systolic
dysfunction and heart failure
Journal of th American College of Cardiology 2005:46:425-31.
5. Kupari M., Turto H., Lommi J
Left ventricular hypertrophy in aortic valve stenosis:preventive or
promotive of systolic dysfunction and heart failure?
European Heart Journal 2005:26:1790-6.
The Rosengren’s et al. work is interesting by the great number of
cases and by the accuracy of analysis.[1] However, we must mention that this
study is reffering only to so-called “traditional” cardiovascular risk
factors such as smoking, dyslipidaemia, diabetes, arterial hypertension,
obesity. In actual phase of knowledge in the field of cardiovascular risk
factors we need to analyze the other risk f...
The Rosengren’s et al. work is interesting by the great number of
cases and by the accuracy of analysis.[1] However, we must mention that this
study is reffering only to so-called “traditional” cardiovascular risk
factors such as smoking, dyslipidaemia, diabetes, arterial hypertension,
obesity. In actual phase of knowledge in the field of cardiovascular risk
factors we need to analyze the other risk factors too, so-called “new”
cardiovascular risk factors, such as low level of not specific
inflammation markers (fibrinogen, C reactive protein-CRP, 6-interleukine)
and dental state. These “new” risk factors may significantly intervene in
atherogenesis.[2,3,4]
For example, in a personal analysis on a smaller number of patients
with coronary and cerebrovascular atherosclerosis (216 subjects, including
patients with acute coronary syndrome) we detected that 12% (27 subjects)
had no traditional atherosclerosis risk factors; this percentage being
very close to Rosengren and all. results.[5]
Nevertheless, in this group we have detected high level serum
fibrinogen in 14 patients (52%), high CRP serum level in 12 (44%), and a
mean value of missing teeth of 12.6+/-7.9, very different of the mean
value found in the rest of the patients.
As a conclusion, in an important number of patients without
traditional cardiovascular risk factors there is necessary to investigate
all known new cardiovascular risk factors. We think that the intervention
of these new cardiovascular risk factors should not be neglected, mainly
due to a classical conception. So, identification of these new factors may
be the first step to a complete prophylactic cure of all detectable
atherosclerosis risk factors.
References
1. Rosengren A, Wallentin L, Simmoons M, and all: Cardiovascular risk
factors and clinical presentation in acute coronary syndromes. Heart
2005;01;1141-1147.
2. Hansson GK: Mechanisms of Disease: Inflammation, Atherosclerosis, and
Coronary Artery Disease. N Engl J Med 2005; 352:1685-1695.
3. Janket SJ, Qvarnstroem M, Meurman JK, et all: Asymptotic Dental Score
and Prevalent Coronary Heart Disease. Circulation 2004;109:1095-1109.
4. Desvariuex M, Demmer RT, Rundek T, et all: Relationship Between
Periodontal Disease, Tooth Loss, and Carotid Artery Plaque. The Oral
Infections and Vascular Disease Epidemiology Study (INVEST). Stroke
2003;34:2120-2125.
5. Gutiu IA, Gutiu LI: Association of atherosclerosis risk factors in
patients with cardiovascular and cerebrovascular disease, role of
inflammation and dental state. Cerebrovascular Dis. 2005;19/S2:142.
Abstract to 14th European Stroke Conference, Bologna, Italy, May 25-28,
2005.
In the methods section, the formula for the Bazett correction should
be indicated as QTc = QT/(RR ^ 0.5) with RR in seconds and the Fridericia
correction formula should be indicated as QTc = QT/(RR ^ 0.333) with the
RR in seconds. This would more clearly indicate the square root and cube
root calculations used and also the relationship between the 2
corrections.
The mechanisms underlying chronic cerebral damage in cardiological
patients, as well as the risks of interventional procedures on older
subjects is still debated.
Gribbin work presents interesting data regarding the possible influence of
cardiac pacing on cognitive impairment in older patients. The study,
conducted using a single well designed prospective neuropsychological
protocol, demonstrated a trend...
The mechanisms underlying chronic cerebral damage in cardiological
patients, as well as the risks of interventional procedures on older
subjects is still debated.
Gribbin work presents interesting data regarding the possible influence of
cardiac pacing on cognitive impairment in older patients. The study,
conducted using a single well designed prospective neuropsychological
protocol, demonstrated a trend over VVI(R) patients to develop cognitive
disturbances.
According to the observations of Tse and co-workers, published on Heart
2005 Mar;91(3):362-4, nearly a half of patients with pacemakers (PM) are
likely to have diagnosed episodes of AF during long term follow up.
The reading of Gribbin’ study aroused two questions:
i) There is any
possibility that a current or previous use of any antithrombotic could be
protective against neurological impairment due to cerebrovascular events
after PM implantation?
This is consistent with the hypothesis that also
chronic patterns of brain damage may be incisively influenced by
appropriate medical preventive strategies. Taking into account the
subgroup of patients under cumarins and antiplatelet agents we can
speculate a higher protective effect of the first regimen over the second
in AF subjects;
ii) Is not clearly stated the real embolic potential of
paroxysmal AF respect to the chronic subtype, and thereby the risk of
cognitive impairment in paced patients with previous history of embolic
arrhythmias. Did the studied patients have history of AF? Many
observational data suggest how the embolic potential of paroxysmal AF
should be lower than in the chronic permanent subtype. In smaller series
Petersen reported a not increased risk of ischemic damage in paroxysmal AF
compared with matched sinus rhythm controls. Feinberg reported a higher
prevalence of ischemic brain lesions on AF patients but markedly on
chronic AF subjects respect to the paroxysmal subtype.
References
Corea F, Tambasco N. Cardiac pacing: atrial fibrillation may go
unrecognised. Lancet Neurol. 2005 May;4(5):265
Bornstein N, Corea F, Galllai V, Parnetti L. Heart-brain
relationship: atrial fibrillation and stroke. Clin Exp Hypertens. 2002 Oct
-Nov;24(7-8):493-9.
Silent brain infarction in nonrheumatic atrial fibrillation. EAFT
Study Group. European Atrial Fibrillation Trial. Neurology. 1996
Jan;46(1):159-65.
Feinberg WM, Seeger JF, Carmody RF, Anderson DC, Hart RG, Pearce LA.
Epidemiologic features of asymptomatic cerebral infarction in patients
with nonvalvular atrial fibrillation. Arch Inter Med 1990;150:2340-2344.
Ezekowitz MD, James KE, Nazarian SM, Davenport J, Broderick JP, Gupta
SR, Thadani V, Meyer ML, Bridgers SL. Silent cerebral infarction in
patients with nonrheumatic atrial fibrillation. The Veterans Affairs
Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.
Circulation 1995;92:2178-2182
Tse HF, Lau CP. Prevalence and clinical implications of atrial
fibrillation episodes detected by pacemaker in patients with sick sinus
syndrome. Heart 2005; 91: 362.
I read with great interest a paper by TomcsaáLnyi J and associates. [1] They presented a case of ischemic heart failure with unilateral
pulmonary edema and hypothesized that a large eccentric mitral
regurgitation jet reaching the left pulmonary veins caused the pulmonary
edema. The paper is informative and shows convincing images.
We have also have experienced a similarly unique case with unilate...
I read with great interest a paper by TomcsaáLnyi J and associates. [1] They presented a case of ischemic heart failure with unilateral
pulmonary edema and hypothesized that a large eccentric mitral
regurgitation jet reaching the left pulmonary veins caused the pulmonary
edema. The paper is informative and shows convincing images.
We have also have experienced a similarly unique case with unilateral
pulmonary edema associated with ischemic heart failure after anterolateral
myocardial infarction.[2] A 72-year-old woman was in severe respiratory
distress. Chest roentgenogram showed right side pulmonary edema with a
clear left lung field. Computed tomographic scan showed no abnormality of
the bilateral lung fields; however, pulmonary perfusion scan and pulmonary
angiography revealed reduced blood perfusion in the entire left lung
field.
Unfortunately, no histological examination was performed in this case. We
concluded that the unilateral pulmonary edema on the right side was caused
by the blood perfusion difference between the right and left lung fields,
exhibiting reduced perfusion to the left.
The mechanisms of unilateral pulmonary edema include an increase in
capillary blood flow, reduced surfactant, rapid re-expansion of a
collapsed
lung, disruption of a venular post-capillary sphincter after
sympathectomy,
and a specific cause such as Swyer-James syndrome. [3-8] The possibility of
a
large eccentric mitral regurgitation jet, as TomcsaáLnyi J and associates
postulated, might indeed cause unilateral pulmonary edema. The mechanism
is similar to the disruption of a venular post-capillary sphincter after
sympathetectomy. I pay my respects to their insight into such an
extraordinary clinical situation.
References
1. TomcsaáLnyi J, Arabadzisz H, BoóLzsik B. Left sided unilateral
pulmonary
edema. Heart 2005; 91:1157-7
2. Misawa Y, Konishi H, Hasegwa T, Fuse K, Shimada K. Unilateral pulmonary
edema in a patient with ischemic heart failure. Jpn Heart J 1997; 38:859-
63
I have reviewed the article carefully. As the author himself states an ACE inhibitor considered as a contraindication in aortic stenosis. There are certain limitations with the study, which I will like to point out:
1. The samle size of the study is too small.
2. Study is single blinded.
3. What other drug pateint is taking not specified.
4. Most of t...
I have reviewed the article carefully. As the author himself states an ACE inhibitor considered as a contraindication in aortic stenosis. There are certain limitations with the study, which I will like to point out:
1. The samle size of the study is too small.
2. Study is single blinded.
3. What other drug pateint is taking not specified.
4. Most of the patient were taking ACE inhibitor for long before in to the inclusion of study.
Considering the above, would the author not think it logical to recommend an ACE inhibitor as the drug of choice in aortic stenosis patients suffering from hypertension, to whom it otherwise is considered as unsuitable.
I have read the article by T Nageh et al. They concluded that in patients with chronic ischemiuc heart disease who subjected to the PCI, developed the periprocedural increase in the cTROP-I in 30%, among these 18% required reintervention.
It is not clear in the study whether patients presenting with periprocedural increase in enzyme were considered for aggressive antiplatelet therapy, they might required...
I have read the article by T Nageh et al. They concluded that in patients with chronic ischemiuc heart disease who subjected to the PCI, developed the periprocedural increase in the cTROP-I in 30%, among these 18% required reintervention.
It is not clear in the study whether patients presenting with periprocedural increase in enzyme were considered for aggressive antiplatelet therapy, they might required less reintervention if they would have been received aggressive antiplatelet and antithrombin therapy.
Dear Editor,
Wilmshurst et al.,[1] link inheritance of atrial shunts to inheritance of migraine with aura in some families. The link between migraine with aura and patent foramen ovale (PFO) appears to be gathering strength and the plea for randomized controlled trials of PFO-closure in migraine patients are beginning to appear justified.[2-4] The conclusion that closure of atrial shunts usually improves or cures...
Dear Editor,
In patients with hypertrophic cardiomyopathy (HC) followed in our institution[1], the annual mortality rate was 1%, unexpectedly low for a selected cohort of patients with HC. Now, in view of the excellent recent article of Elliot et al.[2], in which they presented and discussed survival rates in HC, we are happy with the confirmation that even selected patients with HC may survive at high rates when...
Dear Editor,
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that caused the person to seek medical attention in the first instance.
While many experience 'typical text book...
Dear Editor,
For the sake of completeness, the thesis that the renin-angiotensin- aldosterone system (RAAS) might have a role in the pathogenesis of aortic stenosis[1], also requires a recognition that angiotensin converting enzyme(ACE)inhibitor therapy[2] might, on its own, be insufficient to retard progression of this disorder, and that a cardioprotective component specifically targeting aldosterone blockade by co...
Dear Editor,
The Rosengren’s et al. work is interesting by the great number of cases and by the accuracy of analysis.[1] However, we must mention that this study is reffering only to so-called “traditional” cardiovascular risk factors such as smoking, dyslipidaemia, diabetes, arterial hypertension, obesity. In actual phase of knowledge in the field of cardiovascular risk factors we need to analyze the other risk f...
Dear Editor,
In the methods section, the formula for the Bazett correction should be indicated as QTc = QT/(RR ^ 0.5) with RR in seconds and the Fridericia correction formula should be indicated as QTc = QT/(RR ^ 0.333) with the RR in seconds. This would more clearly indicate the square root and cube root calculations used and also the relationship between the 2 corrections.
Dear Editor
The mechanisms underlying chronic cerebral damage in cardiological patients, as well as the risks of interventional procedures on older subjects is still debated. Gribbin work presents interesting data regarding the possible influence of cardiac pacing on cognitive impairment in older patients. The study, conducted using a single well designed prospective neuropsychological protocol, demonstrated a trend...
Dear Editor
I read with great interest a paper by TomcsaáLnyi J and associates. [1] They presented a case of ischemic heart failure with unilateral pulmonary edema and hypothesized that a large eccentric mitral regurgitation jet reaching the left pulmonary veins caused the pulmonary edema. The paper is informative and shows convincing images.
We have also have experienced a similarly unique case with unilate...
I have reviewed the article carefully. As the author himself states an ACE inhibitor considered as a contraindication in aortic stenosis. There are certain limitations with the study, which I will like to point out:
1. The samle size of the study is too small.
2. Study is single blinded.
3. What other drug pateint is taking not specified.
4. Most of t...
I have read the article by T Nageh et al. They concluded that in patients with chronic ischemiuc heart disease who subjected to the PCI, developed the periprocedural increase in the cTROP-I in 30%, among these 18% required reintervention.
It is not clear in the study whether patients presenting with periprocedural increase in enzyme were considered for aggressive antiplatelet therapy, they might required...
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