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.
It is indeed very gratifying to read the report by Hsi et al.[1] that
sublingual nitroglycerin (NTG) administration causes significantly more
frequent headaches in patients with normal or minimally diseased coronary
arteries than in patients with significant coronary artery disease (CAD).
Over the years I have always felt that patients with chest pain who
complained of significant headaches following s...
It is indeed very gratifying to read the report by Hsi et al.[1] that
sublingual nitroglycerin (NTG) administration causes significantly more
frequent headaches in patients with normal or minimally diseased coronary
arteries than in patients with significant coronary artery disease (CAD).
Over the years I have always felt that patients with chest pain who
complained of significant headaches following sublingual NTG administration
usually do not have CAD of any significance. Now my clinical impression
receives scientific confirmation by the elegant study of Hsi et al.[1]
Their “headache test” had a sensitivity of 77% for predicting underlying
CAD if no headache followed NTG and a specificity of 73% in predicting no
or minimal CAD if headache developed following NTG administration.[1]
Of course, one must always be sure that the sublingual NTG tablets
are fresh. NTG tablets tend to lose their strength over a period of time,
especially if they are not kept in a dark-coloured vial or not stored in a
relatively cool environment. Oftentimes, my patients will tell me that
they no longer experience headaches from their sublingual NTG only to find
out that the medicines they kept in their pockets have lost their potency.
I always advised my patients to carry just a few pills of sublingual NTG
in a small pillbox to be put in their pocket, while keeping the rest in a
dark-coloured bottle placed in the medicine cabinet. If they still do not
experience headaches following the sublingual administration of NTG, I
would ask them to get a fresh bottle of the medicine from their
pharmacies. Sublingual NTG is so cheap that every patient can afford to
get a fresh supply every once in a while. This habit is particularly
relevant when patients are reluctant to take their sublingual NTG because
of the resultant headaches and thus let the medicine lose the potency.
Tsung O. Cheng, M.D.
Professor of Medicine
George Washington University
Washington, D.C.
Reference
1. Hsi DH, Roshandel A, Singh N, Szombathy T, Meszaros ZS: Headache
response to glyceryl trinitrate in patients with and without obstructive
coronary artery disease. Heart 2005;91:1164-1166.
I have read the letter from Professor Walley and colleagues with
interest. I have no desire to restate my editorial but would have the
following comments.
Comments such as “data is virtually complete”, “only two patients
underwent a second revascularisation in another north-west NHS hospital”
and the low diabetes rates “are probably due to ethnicity differences”
reflect all the problems of a...
I have read the letter from Professor Walley and colleagues with
interest. I have no desire to restate my editorial but would have the
following comments.
Comments such as “data is virtually complete”, “only two patients
underwent a second revascularisation in another north-west NHS hospital”
and the low diabetes rates “are probably due to ethnicity differences”
reflect all the problems of a single centre registry with locally recorded
data. National policy, which the authors aspire to be involved in via
their role in the National Institute of Clinical Excellence (NICE), should
be decided on the basis of well performed and scientifically sound
prospective multicentre randomised clinical trials.
To state that with regard to diabetes “Thomas misses our point
completely” is somewhat unnecessary and incorrect. I am fully aware that
in this analysis diabetes is not an independent risk factor for restenosis
when vessel architecture is taken into account. The problem is that this
is different to everywhere else in the world and, once again, this makes
me concerned about the quality of the data.
The statement that “Thomas fails to understand the distinction
between efficacy……effectiveness and cost effectiveness” is once more
unnecessary and (clearly!) I would argue incorrect. On a daily basis the
clinicians amongst us deal with patients, not numbers in a statistical
equation. I am not sure most of the authors in the current paper have any
experience of this. I have every desire to deliver the most efficacious,
effective and “NICE-accepted” cost effective treatment to my patients
undergoing percutaneous coronary intervention. I believe that this will
lead to a 70% drug eluting stent (DES) use in my patients. A re-assessment
of DES usage is currently being assessed by NICE. I am confident that
NICE will assess the need for this major advance in coronary intervention
on the basis of randomised clinical trials rather than single centre,
retrospective registries and I will be happy to stand by their
recommendations.
Fox et al. raise the important issue of non-response to CRT and
suggest the rate of non-response to CRT is 25%, a figure which is widely
quoted. However a careful examination of the published data suggests that
this is a substantial underestimate of the problem.
The non-responder
rates in the studies using subjective or (relatively) objective functional
capacity as the main definition of respon...
Fox et al. raise the important issue of non-response to CRT and
suggest the rate of non-response to CRT is 25%, a figure which is widely
quoted. However a careful examination of the published data suggests that
this is a substantial underestimate of the problem.
The non-responder
rates in the studies using subjective or (relatively) objective functional
capacity as the main definition of response are generally lower (10.8-26%
non-responders)[1-3] than in the studies which used the wholly objective
LV remodelling (> 15% reduction in LVESV) as the definition (40-46% non-
responders).[4-7] This difference is likely related to the significant
placebo response to device implantation as shown by estimation of the
"placebo-subtracted" efficacy (intervention group minus control group
benefits).
Placebo-subtracted efficacy was not quoted in any of the
original CRT trial publications and it is only possible to secondarily
calculate these rates in a few instances from the available data. In the
MIRACLE trial[8] 28% of patients in the control group (inactive CRT) had a
placebo response as assessed by improvement by at least one NYHA class. In
the active CRT arm 63% of patients had an improvement by at least one NYHA
class and hence the placebo subtracted efficacy of CRT was only 35%
implying a 65% non-responder rate. In the Miracle ICD trial[9] 42.9% of
patients in the inactive CRT group reported feeling better after device
implant and 52.4% of in the active group felt better indicating a placebo
subtracted efficacy of only 9.5%.
A final point is that the studies mentioned above investigated
patients after technically successful CRT. About 10% of patients have
unsuccessful LV lead implants and these patients should also be added to
the group of non-responders. Thus in conclusion a critical analysis of the
data would suggest the true CRT non-responder rate can be estimated as
>50%.
References
1. Reuter S, Garrigue S, Barold SS et al. Comparison of
characteristics in responders versus nonresponders with biventricular
pacing for drug-resistant congestive heart failure. Am J Cardiol
2002;89:346-50.
2. Molhoek SG, Bax JJ, van Erven L et al. Comparison of benefits
from cardiac resynchronization therapy in patients with ischemic
cardiomyopathy versus idiopathic dilated cardiomyopathy. Am J Cardiol
2004;93:860-3.
3. Alonso C, Leclercq C, Victor F et al. Electrocardiographic
predictive factors of long-term clinical improvement with multisite
biventricular pacing in advanced heart failure. Am J Cardiol 1999;84:1417-
21.
4. Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. Predictors
of left ventricular reverse remodeling after cardiac resynchronization
therapy for heart failure secondary to idiopathic dilated or ischemic
cardiomyopathy. Am J Cardiol 2003;91:684-8.
5. Yu CM, Fung JW, Zhang Q et al. Tissue Doppler imaging is superior
to strain rate imaging and postsystolic shortening on the prediction of
reverse remodeling in both ischemic and nonischemic heart failure after
cardiac resynchronization therapy. Circulation 2004;110:66-73.
6. Penicka M, Bartunek J, De Bruyne B et al. Improvement of Left
Ventricular Function After Cardiac Resynchronization Therapy Is Predicted
by Tissue Doppler Imaging Echocardiography. Circulation 2004.
7. Notabartolo D, Merlino JD, Smith AL et al. Usefulness of the peak
velocity difference by tissue Doppler imaging technique as an effective
predictor of response to cardiac resynchronization therapy. Am J Cardiol
2004;94:817-20.
8. Abraham WT, Fisher WG, Smith AL et al. Cardiac resynchronization
in chronic heart failure. N Engl J Med 2002;346:1845-53.
9. Young JB, Abraham WT, Smith AL et al. Combined cardiac
resynchronization and implantable cardioversion defibrillation in advanced
chronic heart failure: the MIRACLE ICD Trial. JAMA 2003;289:2685-94.
In the recent issue of Heart, Egred et al.[1] reported an
important example of pseudo-myocardial infarction in a patient with
diabetic ketoacidosis. This was presumably related to hyperkalaemic
effects on the ECG.
However, in the current case report it is not mentioned
why the patient developed ketoacidosis and in the context of a sepsis
syndrome other factors may be at play to orchestrate the...
In the recent issue of Heart, Egred et al.[1] reported an
important example of pseudo-myocardial infarction in a patient with
diabetic ketoacidosis. This was presumably related to hyperkalaemic
effects on the ECG.
However, in the current case report it is not mentioned
why the patient developed ketoacidosis and in the context of a sepsis
syndrome other factors may be at play to orchestrate these changes. Indeed
whilst hyperkalaemia has been previously shown to cause ST elevation, this
has been often in the context of other pathology.[1-6]
It has also been
suggested that IV potassium replacement in hypokalaemic patients may also
cause a pseudo-infarct ECG pattern.[5] In addition, we have recently seen a
case of a 30 year old female IV drug user who presented with sepsis and
pulmonary embolism. On admission to the high dependency unit her ECG
showed similar ECG changes to that reported by Egred et al. of tall peaked
T waves (Panel A) but conversely the potassium was 3.1 mmol/l, corrected
calcium 2.01 mmol/l, phosphate 0.6 mmol/l and magnesium 0.9 mmol/l. She
was therefore given gradual IV potassium replacement.
On day 2 of her stay
she developed again remarkably similar ECG changes as that reported by
Egred et al. (Panel B) and whilst fibrinolytic therapy was considerd; this
was rejected on the lack of ischaemic symptoms and the bizarre nature to
these ECG changes. Of particular note was normal serial troponin levels
and lack of wall motion abnormalities on echocardiography. Also serial
ECGs revealed a gradual improvement in these changes as the patient’s
electrolyte abnormalities and sepsis improved.
We feel, therefore, that there are other possible alternative
explanations to these ECG changes including sepsis with intracellular
shifts in potassium, pulmonary embolism and even adrenergic
hyperstimulation which could all lead to a picture of ‘sick’
cardiomyocytes with alteration in their action potential mimicking an
injury current seen in myocardial necrosis.
Yours faithfully,
Robert J Huggett*
Gillian E Payne†
SpR Cardiology*
Consultant Cardiologist†
Competing interests: None declared.
1. M Egred, W L Morrison. Diabetic keto-acidosis and hyperkalaemia
induced pseudo-myocardial infarction Heart 2005;91;1180.
2. Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in
potassium intoxication resembling acute myocardial infarction or
pericarditis. Circulation 1956;13:29-36.
3. Boulmier D, Bazin P. Myocardial pseudo-infarction: "stress"-
associated catecholamine-induced acute cardiomyopathy or coronary spasm?
Ann Cardiol Angeiol 2000;49:449-54.
4. Lim YH, Anantharaman V. Pseudo myocardial infarct--
electrocardiographic pattern in a patient with diabetic ketoacidosis.
Singapore Med J. 1998;39:504-6.
5. Madias JE, Madias NE. Hyperkalemia-like ECG changes simulating
acute myocardial infarction in a patient with hypokalemia undergoing
potassium replacement. J Electrocardiol. 1989;22:93-7.
Notable by its absence from the list of predictors of severe
rheumatic valvar disease[1] was the mention of the role of gender,
especially when one considers the fact that rheumatic mitral stenosis is
reportedly twice as common in females as in males.[2-4] This was also
a missed opportunity to test the hypothesis that there is a role for
oestrogen in the expression of rheumatic mitral stenosis. If tha...
Notable by its absence from the list of predictors of severe
rheumatic valvar disease[1] was the mention of the role of gender,
especially when one considers the fact that rheumatic mitral stenosis is
reportedly twice as common in females as in males.[2-4] This was also
a missed opportunity to test the hypothesis that there is a role for
oestrogen in the expression of rheumatic mitral stenosis. If that
hypothesis were validated the insights obtained thereby might lead to
therapeutic interventions which might favourably modify the natural
history of rheumatic heart disease so as to reduce the devastating impact
of mitral stenosis on women's health during the child bearing years.
Yours sincerely,
OMP Jolobe
MRCP (UK) (retired geriatrician)
References
1. Meira ZMA., Goulart EMA., Colosime EA., Mota CCC
Long term follow up of rheumatic fever and predictors of severe rheumatic
valvar disease in Brazilian children and adolescents
Heart 2005:91:1019-22.
2. Wood P. An appreciation of mitral stenosis:Part 1
British Medical Journal 1954:1:1051-63.
3. Rowe JC., Bland EF., Sprague HB. The course of mitral stenosis without surgery: Ten and twenty years perspectives. Annals of Internal Medicine 1960:52:741-9.
4. Olsen K. The natural history of 271 patients with mitral stenosis under medical
treatment. British Heart Journal 1962:24:349-57.
To estimate children’s intake of fish from total household dietary
intake is a daring enterprise. Most children hate fish because of the
bones. Here is a likely scenario:
Father or mother: “There is no dessert before you have eaten up that
fish!”
Therefore, if the figures aren’t a result of chance, they may rather
reflect the effect of childhood stress rather than the result of a hi...
To estimate children’s intake of fish from total household dietary
intake is a daring enterprise. Most children hate fish because of the
bones. Here is a likely scenario:
Father or mother: “There is no dessert before you have eaten up that
fish!”
Therefore, if the figures aren’t a result of chance, they may rather
reflect the effect of childhood stress rather than the result of a high
intake of fish.
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...
Dear Editor,
It is indeed very gratifying to read the report by Hsi et al.[1] that sublingual nitroglycerin (NTG) administration causes significantly more frequent headaches in patients with normal or minimally diseased coronary arteries than in patients with significant coronary artery disease (CAD). Over the years I have always felt that patients with chest pain who complained of significant headaches following s...
Dear Editor,
I have read the letter from Professor Walley and colleagues with interest. I have no desire to restate my editorial but would have the following comments.
Comments such as “data is virtually complete”, “only two patients underwent a second revascularisation in another north-west NHS hospital” and the low diabetes rates “are probably due to ethnicity differences” reflect all the problems of a...
Dear Editor,
Fox et al. raise the important issue of non-response to CRT and suggest the rate of non-response to CRT is 25%, a figure which is widely quoted. However a careful examination of the published data suggests that this is a substantial underestimate of the problem.
The non-responder rates in the studies using subjective or (relatively) objective functional capacity as the main definition of respon...
Dear Editor,
In the recent issue of Heart, Egred et al.[1] reported an important example of pseudo-myocardial infarction in a patient with diabetic ketoacidosis. This was presumably related to hyperkalaemic effects on the ECG.
However, in the current case report it is not mentioned why the patient developed ketoacidosis and in the context of a sepsis syndrome other factors may be at play to orchestrate the...
Dear Editor,
Notable by its absence from the list of predictors of severe rheumatic valvar disease[1] was the mention of the role of gender, especially when one considers the fact that rheumatic mitral stenosis is reportedly twice as common in females as in males.[2-4] This was also a missed opportunity to test the hypothesis that there is a role for oestrogen in the expression of rheumatic mitral stenosis. If tha...
Dear Editor,
To estimate children’s intake of fish from total household dietary intake is a daring enterprise. Most children hate fish because of the bones. Here is a likely scenario:
Father or mother: “There is no dessert before you have eaten up that fish!”
Therefore, if the figures aren’t a result of chance, they may rather reflect the effect of childhood stress rather than the result of a hi...
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