Norris[1] reports that most out of hospital cardiac arrest occurs in
the home, but that as patients usually have premonitory symptoms, there is
an opening for education about these symptoms and how to act to avoid
delay and subsequent mortality. Although there is clearly a need to
educate the public at large to call an ambulance if they witness what
could be a heart attack or cardiac arrest, less is k...
Norris[1] reports that most out of hospital cardiac arrest occurs in
the home, but that as patients usually have premonitory symptoms, there is
an opening for education about these symptoms and how to act to avoid
delay and subsequent mortality. Although there is clearly a need to
educate the public at large to call an ambulance if they witness what
could be a heart attack or cardiac arrest, less is known about what is
effective in reducing individual delay time.
Our systematic review of interventions to reduce delay in patients
with suspected heart attack[2] concluded that there was little evidence
that community-wide media campaigns or one to one educational
interventions reduced delay time.
Supporting evidence came mainly from before and after studies; no RCT
provided positive results, suggesting a need for caution in attributing
any reported effects to the actual intervention. The methodological
quality of studies was generally poor and few studies reported mortality
data. While most studies reported pre-intervention baselines, few had a
reasonable post intervention follow-up-period (which should be measured in
years not months). The best RCT[3] with a large sample in an 18 month
intervention which included both a media campaign and a one-to-one
intervention with people at higher risk was negative. Few studies reported
the intervention in sufficient detail to draw any conclusions about which
elements were effective.
We now know about many potential psycho-social, clinical and
environmental factors that are associated with extended delay.[4] Most of
the interventions that have been tested are educational and education
alone has repeatedly been shown not to be an effective method for changing
behaviour. It is seems likely that we need to spend more time designing
cognitive-behavioural supportive interventions for patients, and
importantly their family or carers, then assessing these in a well
controlled RCT and using qualitative techniques to elicit which part, if
any, of the intervention led to appropriate actions. Once validated an
intervention might best be delivered through rehabilitation programmes,
NSF clinics and discharge planning. As Norris et al have shown there is
huge potential for saving lives.
Jill F Pattenden Robert J Lewin BHF Care and Education Research Group, Dept of Health Sciences,
University of York
References
1. RM Norris on behalf of the UK Heart Attack Study (UKHAS)
Collaborative Group. Heart 2005; 91 1537-1540.
2. Kainth A, Hewitt A, Pattenden J, Sowden A, Duffy S, Watt I, Thompson D,
Lewin R. A systematic review of interventions to reduce delay in patients
with suspected heart attack. Emergency Medicine Journal. 2004;21:506-508.
3. Luepker RV, Raczynski JM, Osganian s et al. Effect of a community
intervention on patient delay and emergency medical service use in acute
coronary heart disease: the rapid early action for coronary treatment
(REACT) trial. JAMA 2000; 284:60-67.
4. Pattenden J, Watt I, Lewin RJ et al. Decision making processes in people
with symptoms of acute myocardial infarction:qualitative study. BMJ
2002;324:1006-9.
We thank Dr Tom Quinn for his interest in this manuscript. His letter
addresses the realities of intra-country variation versus inter-country
variation in pre-hospital care. Dr Quinn appropriately points out in his
letter to the editor that the United Kingdom is made up of distinct
nations with distinct health systems. We have recognized this issue in the
manuscripts limitations section, “Because our stu...
We thank Dr Tom Quinn for his interest in this manuscript. His letter
addresses the realities of intra-country variation versus inter-country
variation in pre-hospital care. Dr Quinn appropriately points out in his
letter to the editor that the United Kingdom is made up of distinct
nations with distinct health systems. We have recognized this issue in the
manuscripts limitations section, “Because our study is based on a non-
randomized assessment of variation in process of care across international
boundaries in selected centres participating in ASSENT 3 PLUS, it may not
be generally representative of the standard of pre-hospital care in the
respective country and therefore has inherent limitations”. It is
encouraging that the past practice of contacting a primary care physician
prior to activate the emergency medical services is being modified,
specifically in England and Wales, with direct activation of the emergency
medical system and more expedited care.
Since myocardial infarction (MI) was redefined five years ago(1),
focus has been on troponins. However, with the consensus document the
presence of an abnormal Q wave has also been redefined, but this change
appears to have created only little controversy. Abnormal Q waves are
still considered a definite objective sign of an established MI, and in
this connection, the history of the patient is often in...
Since myocardial infarction (MI) was redefined five years ago(1),
focus has been on troponins. However, with the consensus document the
presence of an abnormal Q wave has also been redefined, but this change
appears to have created only little controversy. Abnormal Q waves are
still considered a definite objective sign of an established MI, and in
this connection, the history of the patient is often insufficient(2). For
decades the Minnesota criteria in different editions have been used
worldwide, but a set of generally accepted international
electrocardiographic criteria for an established MI have so far not been
available. Therefore, we welcome the joint European-American
initiative(1).
However, using the new definition of an abnormal Q wave we recently
demonstrated an increase in the proportion of patients categorized as
having an established MI(3). This observation may result in additional
patient examinations and a change in outcome measures of clinical and
epidemiological trials. Finally, the redefinition may have consequences of
psycho-social importance to the individual patient. Of interest, the new
definition of an abnormal Q wave has been interpreted differently in
recent Danish guidelines and in the series "Education in Heart"(4, 5).
This, of course, is not appropriate and may cause confusion. A definition
should be unambiguous.
There exist no generally accepted set of rules defining how small the
rate of false positive and false negative diagnoses should be in order to
be "acceptable". This decision should preferably be based on a careful
clinical judgement. In the present case, we propose that the false
positive rate should be equal to the false negative rate and be <10-
15%.
Finally, cardiologists and other physicians treating patients with
ischemic heart disease should be familiar with the new Q wave definition
(Table 1)1 in order to cope with the clinical dilemmas it may give rise
to.
Table 1 Electrocardiographic changes in established MI
1. Any QR wave in leads V1 through V3 ≥ 30 ms (0.03 s);
abnormal Q wave in lead I, II, aVL, aVF or V4 through
V6 in any two contiguous leads and at least 1 mm in depth.
References
1. Myocardial infarction redefined--a consensus document of the joint
european society of cardiology/american college of cardiology committee
for the redefinition of myocardial infarction. Eur Heart J. 2000;21:1502-
1513
2. Ammar KA, Kors JA, Yawn BP, Rodeheffer RJ. Defining unrecognized
myocardial infarction: A call for standardized electrocardiographic
diagnostic criteria. Am Heart J. 2004;148:277-284
3. Jensen JK, Ovrehus K, Moldrup M, Mickley H, Hoilund-Carlsen PF.
Redefinition of the Q wave - is there a clinical problem? Am J Cardiol.
2005:Accepted
4. Grande P, Holmvang L. Akut koronart syndrom. Dansk Cardiologisk
Selskab. 2004
5. French JK, White HD. Clinical implications of the new definition of
myocardial infarction. Heart. 2004;90:99-106
Hsi et al. propose absence or presence of gyceryl trinitrate (GTN)-
induced headache as a possibly useful clinical tool to assist in the
initial risk stratification of patients with chest pain [1]. Several
issues merit attention:
1. The mechanism of action of GTN in precipitation of headache in
patients – regardless of status of the coronary circulation – is unknown.
Hsi et al. propose absence or presence of gyceryl trinitrate (GTN)-
induced headache as a possibly useful clinical tool to assist in the
initial risk stratification of patients with chest pain [1]. Several
issues merit attention:
1. The mechanism of action of GTN in precipitation of headache in
patients – regardless of status of the coronary circulation – is unknown.
2. Excluding patients with a known history of chronic headache adds
little in terms of mechanistic clarity about headache-provocation by GTN.
3. It is difficult to understand why -- as suggested by Hsi et al. --
nitrates should selectively dilate coronary arteries more than cerebral
arteries in patients with obstructive coronary artery disease (CAD). With
established obstructive CAD, the only component that is significantly
reversible is spasm. Second, regional distribution of GTN does not depend
on distribution of atherosclerotic lesions. It is understandable that
within one anatomical region, critically obstructive atherosclerotic
lesions might overperfuse (luxury overperfusion or steal syndrome) lesion-
free arteries but to apply the same principle across different regions is
speculative.
4. To reciprocally link CAD with cerebral circulation is a unique [1]
albeit logically challenging research premise. It is a rare case in which
a patient with atypical anginal pain might manifest a typical reassuring
response to GTN; in any case since the response is but subjective, it is
hardly advisable to lower the index of suspicion. To modify the index of
suspicion on the basis of occurrence of headache following GTN
administration does not appear to be a scientifically sound approach.
5. It is currently not known why GTN might precipitate primary
headaches such as migraine or cluster headache or non-primary headaches
one hour after administration. A peculiar as yet undefined neuroantomic
susceptibility seems to underlie provocation of headache following GTN
administration; the headache response is neither uniform nor predictable
indicating the importance of idiosyncratic features. To understand the
biological basis of GTN-headache headache we have to reflect on the time
elapsed between its sublingual administration and onset of headache. In my
experience, some patients given GTN for suspected CAD (angina or
infarction) develop a headache variant (not migrainous or cluster
headache) within 10-15 minutes or earlier. It is a common practice to
accept occurrence of headache as indicative of sufficient generalized and
coronary vasodilatation and to ask the patient to expel the remaining part
of the tablet.
6. Onset of migraine after GTN manifests a significantly longer
prodrome [2]. The physiological system(s) primarily affected in migraine
must necessarily be afforded a considerable (but limited and exhaustible)
degree of protection by homeostatic defense mechanisms, thereby allowing
the subject to continue to function despite the stressful stimulus or
situation; this protection is obviously unlimited or inexhaustible in the
majority of the general population who are not susceptible to migraine [3]
or GTN-induced non-migrainous headache. Opposing the headache-provoking
effects of GTN is the parallel activation of a composite adaptive system
comprised of vasopressin release coupled to hyperfunction of the
sympathetic (noradrenergic) and serotonergic systems [4]. Pain of angina
pectoris or acute myocardial infarction is commonly associated with a
pronounced hyperactivation of the sympathetic nervous system that might
underlie the fact that not all patients given GTN develop headache.
7. The assumption that a diffuse cerebral vasodilatation underlies
GTN-induced headache is open to debate. Propranolol and verapamil have
opposite actions on intracranial circulation, decreasing and increasing
it, respectively; yet both agents are used commonly for prevention of
migraine [5], the prototypic primary vascular headache. Atenolol, nadolol,
or verapamil do not cross the blood-brain-barrier and do not influence any
neuronal function, whether central (brain, peripheral neural or central-
peripheral neuronal connections). Migraine prevention does not involve
critical alteration of either any known brain neuronal function or of
cerebrovascular circulation [5, 6]. Finally, the vasodilator sildenafil
can induce migraine without initial dilatation of the middle cerebral
artery [7].
8. GTN-induced ocular choroidal venous congestion may underlie the
headache of migraine [8]; GTN associated rapid ophthalmic arterial
vasodilatation may underlie cluster headache [9]. Headaches that do not
fit into strictly defined definitive primary categories [10] may reflect
attenuated or incomplete forms of such headaches.
As the letter of Professor Cheng testifies, the index idea seems
attractive and even persuasive. Nevertheless, where one starts often
affects where one ends. Belief in any hypothesis is a powerful philosophic
commitment, one that can lead forward as well as to nowhere. Worse, the
need to believe can impede scientific progress by coming up with data that
challenge and defy logic and cannot be integrated into an intelligible
synthesis. That GTN might cause headache more frequently in patients with
normal coronary arteries [1] is a hypothesis that challenges rational
thinking. The best biological explanation for the statistically valid
results of this study may lie in the differences between the test and
control cohorts. CAD positive patients were over a decade older than CAD
negative patients; also, the sex ratio was markedly skewed between the two
cohorts, with the percentage of male patients being far higher in the CAD
positive group (Table 1). While CAD progresses with age particularly in
males, the migrainous tendency in adulthood primary affects females
(F:M=5:1).
References
1. Hsi DH, Roshandel A, Singh N, Szombathy T, Meszaros. Headache
response to gylceryl trinitrate in patients with and without obstructive
coronary artery disease. Heart 2005;91:1164-1166.
4. Gupta VK. A clinical review of the adaptive potential of
vasopressin in migraine.
Cephalalgia 1997;17:561-569.
5. Gupta V. Silent or non-clinical infarct-like lesions in the
posterior circulation territory in migraine: brain hypoperfusion or
hyperperfusion? Brain 2005 (In press).
6. Gupta VK. Migraine, cortical excitability and evoked potentials: a
clinico-pharmacological perspective. Brain 2005;128:E36.
7. Kruuse C, Thomsen LL, Birk S; Olesen J. Migraine can be induced by
sildenafil without changes in middle cerebral artery diameter. Brain 2003
;126:241-7.
8. 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
10. Headache Classification Subcommittee of the International
Headache Society. The Interrnational Classification of Headache Disorders.
2nd edition. Cephalalgia;2004;24 (Suppl 1):9--160.
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.
Dear Editor,
Norris[1] reports that most out of hospital cardiac arrest occurs in the home, but that as patients usually have premonitory symptoms, there is an opening for education about these symptoms and how to act to avoid delay and subsequent mortality. Although there is clearly a need to educate the public at large to call an ambulance if they witness what could be a heart attack or cardiac arrest, less is k...
Dear Editor,
We thank Dr Tom Quinn for his interest in this manuscript. His letter addresses the realities of intra-country variation versus inter-country variation in pre-hospital care. Dr Quinn appropriately points out in his letter to the editor that the United Kingdom is made up of distinct nations with distinct health systems. We have recognized this issue in the manuscripts limitations section, “Because our stu...
Dear Editor
Since myocardial infarction (MI) was redefined five years ago(1), focus has been on troponins. However, with the consensus document the presence of an abnormal Q wave has also been redefined, but this change appears to have created only little controversy. Abnormal Q waves are still considered a definite objective sign of an established MI, and in this connection, the history of the patient is often in...
Dear Ediutor
Hsi et al. propose absence or presence of gyceryl trinitrate (GTN)- induced headache as a possibly useful clinical tool to assist in the initial risk stratification of patients with chest pain [1]. Several issues merit attention:
1. The mechanism of action of GTN in precipitation of headache in patients – regardless of status of the coronary circulation – is unknown.
2. Exc...
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.
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