The authors should be congratulated for providing timely guidance about the use of propofol for nurse-led sedation in modern cardiological practice.[1] The broad scope of the article surely prevented presentation of a comprehensive set of recommendations. However, a particularly important issue for the nursing staff who would be involved, which was not addressed in this article, deserves focused attention. A recent study reported...
The authors should be congratulated for providing timely guidance about the use of propofol for nurse-led sedation in modern cardiological practice.[1] The broad scope of the article surely prevented presentation of a comprehensive set of recommendations. However, a particularly important issue for the nursing staff who would be involved, which was not addressed in this article, deserves focused attention. A recent study reported that anaesthetists' radiation exposure is higher when sedation is used in comparison to general anaesthesia during cardiological procedures.[2] The reason radiation exposure was higher during sedation was the increased time spent in closer contact with the patient without additional shielding in circumstances where patients required manual ventilation or airway support.[2] Although radiation exposure was not specifically addressed in the previous reports of nurse-led propofol sedation for cardiological procedures that were cited by Furniss and Sneyd in their article1, nurses were required to support obstructed airways by applying jaw support and it was also reported that a small proportion of participants required manual ventilation in all of the studies. Therefore, there is the potential that nursing staff might be exposed to higher doses of radiation if nurse-led sedation with propofol is used during cardiological procedures in the place of general anaesthesia. For this reason, it would seem prudent to put systems in place to minimise radiation exposure as much as possible for nursing staff involved in nurse-led propofol sedation during cardiological procedures. It was recently reported that real-time radiation dosimeters reduced radiation exposure for anaesthetists during interventional radiology procedures.[3] Although further research would be required for confirmation, such technology may also be of use when propofol is used for nurse-led sedation in cardiological practice.
1. Furniss SS and Sneyd JR. Safe sedation in modern cardiological practice. Heart. 2015. doi:10.1136/heartjnl-2015-307656
2. Andreoli S, Moretti R, Lorini FL and Lagrotta M. RADIATION EXPOSURE OF AN ANAESTHESIOLOGIST IN CATHETERISATION AND ELECTROPHYSIOLOGICAL CARDIAC PROCEDURES. Radiation protection dosimetry. 2015. doi: 10.1093/rpd/ncv009
3. Baumann F, Katzen BT, Carelsen B, Diehm N, Benenati JF and Pe?a CS. The Effect of Realtime Monitoring on Dose Exposure to Staff Within an Interventional Radiology Setting. Cardiovascular and interventional radiology. 2015: 1-7. DOI: 10.1007/s00270-015-1075-6
We thank Iliodromitis and colleagues for their interest in our review
article1. Providing a comprehensive account of the extensive literature in
this field has been a very challenging task. We are aware of their
previous work2 3 on the feasibility of ischaemic postconditioning (IPost)
in acute coronary syndrome. Of note, this was a small study of 37 patients
and only included a total of 6 patients with non-ST elevation myoc...
We thank Iliodromitis and colleagues for their interest in our review
article1. Providing a comprehensive account of the extensive literature in
this field has been a very challenging task. We are aware of their
previous work2 3 on the feasibility of ischaemic postconditioning (IPost)
in acute coronary syndrome. Of note, this was a small study of 37 patients
and only included a total of 6 patients with non-ST elevation myocardial
infarction (NSTEMI)2 3. To our knowledge no other study has since
investigated the role of IPost in a larger cohort of NSTEMI. Therefore,
IPost was not included under NSTEMI in Figure 2 of our review article1 as
it has not been investigated in adequately powered studies for us to draw
any meaningful conclusions. With regards to the second point raised, we
acknowledge that the first study was by the authors' group4 investigating
the role of remote ischaemic preconditioning (RIPC) in 40 patients,
measuring serum cardiac enzymes as a marker for peri-procedural myocardial
injury and they actually demonstrated RIPC-induced myocardial injury. As
their study was probably underpowered, the findings should be interpreted
with caution. In retrospect, we should have made this clearer in the table
of "major" clinical studies in the review article1. The translation of
ischaemic conditioning has been challenging and we entirely support the
authors' view that all pieces of evidence in this field need to be taken
into consideration and critically appraised in order to pave the
transition of this intervention from bench to bedside in suitable clinical
setting.
1. Bulluck H, Hausenloy DJ. Ischaemic conditioning: are we there yet?
Heart 2015;101(13):1067-77.
2. Iliodromitis EK, Paraskevaidis IA, Fountoulaki K, et al. Staccato
reperfusion prevents reperfusion injury in patients undergoing coronary
angioplasty: a 1-year follow-up pilot study. Atherosclerosis
2009;204(2):497-502.
3. Ikonomidis I, Iliodromitis EK, Tzortzis S, et al. Staccato reperfusion
improves myocardial microcirculatory function and long-term left
ventricular remodelling: a randomised contrast echocardiography study.
Heart 2010;96(23):1898-903.
4. Iliodromitis EK, Kyrzopoulos S, Paraskevaidis IA, et al. Increased C
reactive protein and cardiac enzyme levels after coronary stent
implantation. Is there protection by remote ischaemic preconditioning?
Heart 2006;92(12):1821-6.
Nairooz and Naidu [1] claim that definitions of complete and non-
complete MV-PCI in our meta-analysis[2] (multivessel percutaneous coronary
intervention) might have been missed or misinterpreted in one included
study. As a matter of fact, CvLPRIT trial randomized STEMI (ST-elevation
myocardial infarction) patients to either complete revascularization
(including all N-IRAs [non-infarct related artery]) or IRA-only treatmen...
Nairooz and Naidu [1] claim that definitions of complete and non-
complete MV-PCI in our meta-analysis[2] (multivessel percutaneous coronary
intervention) might have been missed or misinterpreted in one included
study. As a matter of fact, CvLPRIT trial randomized STEMI (ST-elevation
myocardial infarction) patients to either complete revascularization
(including all N-IRAs [non-infarct related artery]) or IRA-only treatment.
Indeed, by study design, complete revascularization was recommended during
index procedure, truly reflecting the inclusion criteria of our meta-
analysis.
Nairooz and Naidu are once more wrong when they argue that different time
frames between index PCI and second procedure across the studies might
have influenced the outcomes. While small number of studies conducted so
far precludes detailed analyses, to assess the optimal timing of the
second procedure, was not indeed the objective of the current meta-
analysis. Nairooz and Naidu claim that staged PCI became anyhow bundled in
the same group with IRA-only revascularization. These patients are
similarly different to complete MV-PCI; indeed, the risk of MI in the IRA-
only treated patients accrues over time; a difference in time in this
group is pivotal also to demonstrate the impact of leaving a non culprit
plaque untreated; the approach in our analysis therefore reflects the true
clinical practice and indeed is based on coronary- and risk profile
evaluation of the patients with non culprit plaques. An arbitrary,fixed
time-frame second revascularisation for all patients with non culprit
lesions is not only infeasible in clinical setting but ,indeed, dangerous
treating in the same way patients with different coronary artery lesions;
as a sensitivity analysis, a stratified meta-analysis by intervention in
the control group was performed as well and results reported, showing
consistency of results. Our study was not designed to compare same setting
complete revascularization (CR) vs index hospitalization CR vs later date
CR vs IRA only revascularization; neither was any study conducted to date.
The criticism about methodology or clinical meaningfulness of a meta-
analysis should be based upon specific clinical knowledge of the topic,
and, above all, careful reading of the meta-analysis design.
References:
1. Nairooz R, Naidu SS. Complete revascularization in STEMI. Heart
2015 [Epub ahead of print]
2. Kowalewski M, Schulze V, Berti S, et al. Complete revascularisation in
ST-elevation myocardial infarction and multivessel disease: meta-analysis
of randomised controlled trials. Heart. 2015 Jun 2.
We thank Drs. MacIver and Clark for their comments regarding the role
of the right ventricle in the development of acute pulmonary edema. We
agree that a relative mismatch in stroke volume from the right and left
sides of the heart can contribute to alveolar congestion [1]. Although
we did mention preload as an important contributor to development of
hypertensive acute heart failure (AHF), we chose to simplify the
dis...
We thank Drs. MacIver and Clark for their comments regarding the role
of the right ventricle in the development of acute pulmonary edema. We
agree that a relative mismatch in stroke volume from the right and left
sides of the heart can contribute to alveolar congestion [1]. Although
we did mention preload as an important contributor to development of
hypertensive acute heart failure (AHF), we chose to simplify the
discussion of right heart circulation, treating it as more of a passive
conduit rather than an active precipitant for the purposes of our short,
specific review. We believe this is appropriate for the intent of our
discussion as it is the specific acute insult of systemic hypertension on
the left ventricle that causes an imbalance in stroke volume, not an
isolated increase right heart function relative to left. Stated another
way, it is uncoupling of the left ventricular-vascular relationship in the
setting of acute hypertension and a chronically remodeled heart that leads
to an imbalance in right and left stroke volume rather than an
amplification of right ventricular contractile force induced by
catecholamine effects, in and of itself. Evidence for the importance of
this can be seen in optimal therapeutic management of hypertensive AHF, in
which rapid reduction in afterload via vasodilation produces dramatic
improvement of dyspnea and resolution of acute pulmonary edema [2, 3, 4].
While the net effect most certainly reflects a re-alignment of stroke
volume mismatch, the same degree of benefit is not seen with treatments
that predominantly target preload reduction. Such insight suggests that,
while right ventricle function can indeed be an important player in the
pathogenesis of congestion, its clinical relevance for patients with
hypertensive AHF may be largely academic but this mechanism should be
included in any comprehensive review of all potential contributors to the
complex issue of pulmonary congestion in heart failure..
1 MacIver DH, Clark AL. The vital role of the right ventricle in the
pathogenesis of acute pulmonary edema. Am J Cardiol 2015;115:992-1000.
2 Peacock WF, Chandra A, Char D, et al. Clevidipine in acute heart
failure: Results of the A Study of Blood Pressure Control in Acute Heart
Failure-A Pilot Study (PRONTO). Am Heart J 2014;167:529-36.
3 Levy P, Compton S, Welch R, et al. Treatment of severe decompensated
heart failure with high-dose intravenous nitroglycerin: a feasibility and
outcome analysis. Ann Emerg Med 2007;50:144-52.
4 Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose
isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide
plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet
1998;351:389-93.
As a part of a low-fat diet regular consumption of chocolate
(containing plant sterols [PS] and cocoa flavanols [CF] ) improve
cardiovascular health by lowering cholesterol and improving blood pressure
[1]. Exact mechanism remains uncertain. Chocolates are a rich source of
catechins, a protective molecule against heart diseases, cancer, and other
medical conditions. Catechin content highest in dark, bitter chocolate and
l...
As a part of a low-fat diet regular consumption of chocolate
(containing plant sterols [PS] and cocoa flavanols [CF] ) improve
cardiovascular health by lowering cholesterol and improving blood pressure
[1]. Exact mechanism remains uncertain. Chocolates are a rich source of
catechins, a protective molecule against heart diseases, cancer, and other
medical conditions. Catechin content highest in dark, bitter chocolate and
lowest in light or milk chocolate. Chocolates & cocoa products also
contain addictive compounds such as n-acylethanolamines (cannabis),
phenylethylamine (stimulants), also provides copper, which inhibits the
action of Hesperidin (an essential flavanone). High copper activity
increases the risk for vascular degeneration such as varicose veins,
hemorrhoids, aneurysms, bruising, heart disease, and stroke. Copper level
highest in dark, bitter chocolate and lowest in light or milk
chocolate[2].There is a inverse relationship between chocolate consumption
and CVD risk through reducing BP. The inverse relation appeared stronger
for stroke than for MI. For consistent results randomized clinical trials
(RCT) are required [3].
This observational study is similar to data dredging ; Data dredging,
bias, or confounding [4].
This observational study has several limitations; self-reported data is
the major limitation, and the results cannot provide evidence of
causality, also correlation does not equal causation. The study
highlights, how reporting observational study facts can be dangerous and
why critical analysis of evidence is required .
Because of wide coverage of this report in media, chocolate manufacturers
have been taking advantage of these findings to target conscious consumers
for health benefits, but the main agenda of the chocolate manufacturers is
business i.e to earn money by selling chocolate.
References:
1.Robin R. Allen, LeaAnn Carson, Catherine Kwik-Uribe, Ellen M.
Evans, John W. Erdman, Jr, Daily Consumption of a Dark Chocolate
Containing Flavanols and AddedSterol Esters Affects Cardiovascular Risk
Factors in a NormotensivePopulation with Elevated Cholesterol J. Nutr.
April 2008 138: 725-731
2.Chocolate Science and Technology, Emmanuel Ohene Afoakwa. WILEY-
BLACKWELL, ISBN 978-1-4051-9906-3.
3.Brian Buijsse; Cornelia Weikert; Dagmar Drogan; Manuela
Bergmann;Heiner Boeing, Chocolate Consumption in Relation to Blood
Pressure and Risk of Cardiovascular Disease in German Adults. Eur Heart J.
2010;21(13):1554-1556.
4.Smith GD, Ebrahim S. Data dredging, bias, or confounding. BMJ
2002;325(7378):1437-8
We have read over and agree with the insightful comments of Lazaros
at al. Our clinical vignette mainly focused on the hemodynamic
abnormalities and post-pericardiocentesis diagnosis. Therefore, some of
the clinical details had to be omitted for purposes of brevity. A
pericardial rub was present during our patient's initial evaluation, and
she later developed chest pain consistent with pericardi...
We have read over and agree with the insightful comments of Lazaros
at al. Our clinical vignette mainly focused on the hemodynamic
abnormalities and post-pericardiocentesis diagnosis. Therefore, some of
the clinical details had to be omitted for purposes of brevity. A
pericardial rub was present during our patient's initial evaluation, and
she later developed chest pain consistent with pericardial irritation,
confirming the diagnosis of "pericarditis". However, we do agree with the
authors that the diagnosis is one that requires at least 2 out of 4 main
criteria. With respect to treatment, nonsteroidal anti-inflammatory agents
were not prescribed by the outside institution due a reported bleeding
diathesis (which was later ruled out after hematologic evaluation at our
institution), but we totally agree that colchicine should not be
prescribed as monotherapy for acute pericarditis. The C-reactive protein
was normal post-pericardiocentesis which, in the past, was thought to rule
out an active inflammatory process. However, we have seen a number of
patients with signs of pericardial inflammation on MRI scanning, despite
normal serum inflammatory makers who have either responded to anti-
inflammatory treatment or have been found to have an inflamed pericardium
at the time of surgery. This indicates to us that MRI imaging may be more
sensitive than serum markers in diagnosing pericardial inflammation.
Finally, we agree that this was a case of "transient constriction" [1]
which was unmasked after removal of a hemodynamically significant
pericardial effusion. We do thank Lazaros et al for their comments.
References:
1 Feng D, Glockner J, Kim K, et al. Cardiac magnetic resonance
imaging pericardial late gadolinium enhancement and elevated inflammatory
markers can predict the reversibility of constrictive pericarditis after
antiinflammatory medical therapy: a pilot study. Circulation 2011;124:1830
-7.
I read with great interest the report by Kang et al., (1) who
conducted one-year prospective study in 1670 patients with heart failure
(HF). The authors measured plasma N-terminal-pro-brain natriuretic peptide
(NT-proBNP), and left ventricular ejection fraction (LVEF) was used for
binary classification of HF. Although patients with keeping LVEF showed
significantly lower NT-proBNP level than those with reduced LVEF, all-...
I read with great interest the report by Kang et al., (1) who
conducted one-year prospective study in 1670 patients with heart failure
(HF). The authors measured plasma N-terminal-pro-brain natriuretic peptide
(NT-proBNP), and left ventricular ejection fraction (LVEF) was used for
binary classification of HF. Although patients with keeping LVEF showed
significantly lower NT-proBNP level than those with reduced LVEF, all-
cause death did not differ between two groups. In addition, plasma NT-
proBNP and obesity were significant predictors of all-cause death
regardless of the levels of LVEF. I have some concerns on their study.
First, the authors selected the Cox proportional hazard model using
forward selection method (Wald statistic) with 20 independent variables
for predicting all-cause mortality. As LVEF was not selected as a
significant variable, and Kaplan-Meier survival curves, stratified by
LVEF, have small meaning in their study. Instead, the effect of obesity on
all-cause death should be speculated. I suspected that obesity at baseline
was partly caused by edema, although there was a decreasing trend of body
mass index as plasma NT-proBNP increased. It seems appropriate that the
authors selected body mass index instead of body fat mass as the indicator
of obesity. On this point, further consideration is needed.
Second, the authors conducted receiver operating characteristic curve
analysis for predicting all-cause of death by using four models. I
understand the disadvantage of model 1 with LVEF3, and model 2 with plasma
NT-proBNP seems satisfactory for predicting all-cause of death. But model
3 with 5 clinical factors is also useful for the prediction. I suppose
that body mass index would contribute for the statistical result.
Their study presented that only use of LVEF for predicting all-cause
death in patients with HF has a risk in clinical procedure. Although the
authors explained one reference as presenting a tendency towards potential
harm for survival by NT-proBNP guided therapy, (2) I think that the study
design differs between two studies. Anyway, I recommend the authors
additional survival analysis by excluding data of death in early period of
time from the baseline to avoid unsuspected reason of death.
References
1. Kang SH, Park JJ, Choi DJ, et al. Prognostic value of NT-proBNP in
heart failure with preserved versus reduced EF. Heart 2015 Aug 28. doi:
10.1136/heartjnl-2015-307782
2. Maeder MT, Rickenbacher P, Rickli H, et al. N-terminal pro brain
natriuretic peptide-guided management in patients with heart failure and
preserved ejection fraction: findings from the Trial of Intensified versus
standard medical therapy in elderly patients with congestive heart failure
(TIME-CHF). Eur J Heart Fail 2013;15:1148-56.
Last year, in response to Priest and Ashley's paper on genomics in
cardiology1, we urged close collaboration of congenital cardiologist and
geneticist for some adults with congenital heart conditions, who had not
been tested in childhood2. The converse is also pertinent. A recent case
(23year old female) with chromosome 1p36 deletion* (previous PDA and VSD
closure in childhood) presented at another hospital with TIA's;...
Last year, in response to Priest and Ashley's paper on genomics in
cardiology1, we urged close collaboration of congenital cardiologist and
geneticist for some adults with congenital heart conditions, who had not
been tested in childhood2. The converse is also pertinent. A recent case
(23year old female) with chromosome 1p36 deletion* (previous PDA and VSD
closure in childhood) presented at another hospital with TIA's;
echocardiography demonstrated impaired left ventricular function (40%) the
cause of which was not clear. There were no residual septal defects and no
arrhythmias were documented on extended ambulatory monitoring. Cardiac
involvement in 1p36 deletion is well described, predominantly ASD (28%),
VSD (23%), valvar anomalies (20.5%) and PDA (12.8%)3. 1p36 is one of the
most common distal terminal deletion syndromes. It is a contiguous gene
deletion syndrome involving haploinsufficiency of several genes, which is
associated with a multisystem disorder including developmental delay and
mental retardation. Yet it was only in 2008 that an association with left
ventricular non-compaction (LVNC) was observed in a cohort of 60 patients
(23%)3. LVNC is a distinct cardiomyopathy characterised by abnormal
persistence of left ventricular trabeculations; it may be associated with
left ventricular hypertrophy or dilatation, or both. Important sequelae
do occur - heart failure, ventricular arrhythmias, complete heart block,
and thromboembolic disease arising from the recesses between trabeculae.
We undertook a CT heart (MRI intolerant) in the patient referred to our
GUCH service. She had dominant apical non compaction poorly characterised
on 2D or 3D echo, fulfilling the criteria for a diagnosis of LVNC.
Anticoagulation has been recommended.
Deletion of 1p36 was first described in the early 1980's. Further advances
have identified mutations in the PRDM16 gene within the 1p36 region,
encoding a transcription factor. It is suggested that a gene deletion
within the 1p36 region may be one cause of LVNC and dilated
cardiomyopathy4. Cardiologists and Geneticists working together, sharing
new knowledge in their particular specialities, is beneficial for them and
their patients. We have striven (unfunded) to create that service. This
case is an example of that practice. Commissioners please take note.
*She also has a terminal 5p15.3 trisomy which has not been associated with
LVNC.
References:
1. Priest J.R., Ashley E.A., Genomics in clinical practice. Heart
Published Online First: July 25th 2014 doi:10.1136/heartjnl-2014-306111
2. Rafiq I., Freeman L. Clinical genomics and the adult with congenital
heart disease: new opportunities. Heart published online October 6, 2014.
doi: 10.1136/heartjnl-2014-306802
3. Battaglia, A., Hoyme, H. E., Dallapiccola, B., et al. Further
delineation of deletion 1p36 syndrome in 60 patients: a recognizable
phenotype and common cause of developmental delay and mental retardation.
Pediatrics 121: 404-410, 2008.
4. Arndt A.K., Schafer S., Drenckhahn J.D., et al. Fine mapping of the
1p36 deletion syndrome identifies mutation of PRDM16 as a cause of
cardiomyopathy. Am J Hum Genet. 2013 Jul 11;93(1):67-77
I read with great interest the above guidelines published for this
rare inherited heart disorder. Over the past few years, much work has gone
into elucidating possible risk factors and markers which can help predict
sudden cardiac death in such patients. Namely, we have already established
that myocardial fibrosis, age and certain mutations in cardiac genes are
markers indicative of a higher risk of sudden cardiac death for t...
I read with great interest the above guidelines published for this
rare inherited heart disorder. Over the past few years, much work has gone
into elucidating possible risk factors and markers which can help predict
sudden cardiac death in such patients. Namely, we have already established
that myocardial fibrosis, age and certain mutations in cardiac genes are
markers indicative of a higher risk of sudden cardiac death for these
individuals (1).
Whilst biochemically, we have a clear understanding of the mutations
and the pathological mechanisms which appear to lead to asymmetrical
septal hyertrophy and consequent left ventricular outflow obstruction, the
current difficulties instead lie with early identification, and ways in
which this can be enhanced through modern imaging techniques (2). Indeed,
since the disease is inherited in an autosomal dominant pattern, one
pertinent question that should be carefully considered is whether those
who already with affected family members should undergo early gene
mutation analysis and trans-thoracic echocardiography to enhance the
possibility of early detection. Moreover, once already detected, how
frequently would echocardiography surveillance be indicated (to monitor
for progression of hyertrophy) and justifiable from an economical point of
view ? One could rationalise that such imaging may not be entirely
yielding as the largest cause of death in HOCM patients remains
potentially fatal ventricular arrhythmias, and thus may vindicate that
primary interventions such as ICD implantation and symptom monitoring are
the most prudent steps initially to mimimising cardiac death in this
population.
The fact that in the past few years, several athletes have nearly
succumbed to this potentially catastrophic condition, including a high-
profile Tottenham footballer, raises many issues regarding the validity of
echocardiography alone in helping to diagnose and risk stratify HCM
patients. Indeed, because professional athletes undergo 'compensatory'
left ventricular hypertrophy in response to high-intensity aerobic
training, it may practically difficult to distinguish the hyertrophy that
is attributable to pathology (HCM) or instead a physiological change (3).
Therefore, further work is needed to establish the best imaging modality
for these patients. While recent work is being faceted towards gadolinum-
enhancement MRI and the benefits this could have in detecting myocardial
fibrosis and hypertrophy, we are in the present moment unfortunately
limited by its availability and cost-effectiveness.
Ultimately, whilst further work is targeted at risk stratification
and studying the biochemical changes which lead to HCM, a low threshold
for suspecting HCM must be maintained amongst healthcare professionals,
including primary care and secondary care physicians. In particular, young
patients presenting with chest pain, syncopal episodes and shortness of
breath unexplained by alternative pathology, should undergo detailed
evaluation and referred to specialist cardiology services in secondary
care promptly.
References:-
1) Christiaans I, van Engelen K, van Langen IM, Birnie E, Bonsel GJ,
Elliott PM, Wilde AA. Risk stratification for sudden cardiac death
in hypertrophic cardiomyopathy: systematic review of clinical risk
markers. Europace Journal 2010. 4 (12): 667-76.
2) Frey N1, Luedde M, Katus HA. Mechanisms of disease:
hypertrophic cardiomyopathy. Nature Review Cardiology 2011. 9(2):91-100
3) S Basavarajaiah, M Wilson, S Junagde, G Jackson, G Whyte, and S
Sharma. Physiological left ventricular hypertrophy or hypertrophic
cardiomyopathy in an elite adolescent athlete: role of detraining in
resolving the clinical dilemma. British Journal of Sports Medicine 2006
(8): 727-729.
Tanu Pramanik Senior Lecturer (Psychology)
Effect of sleep deprivation on cardiac patients is an well documented clinical entity which the authors of the current article established with experimental data and therefore deserve sincere applause(1).
WHO guideline:
The World Health Organization guidelines say that for a good sleep, sound level should not exceed 30 dB(A) for continuous background noise, and 45 dB(A) for individual no...
Tanu Pramanik Senior Lecturer (Psychology)
Effect of sleep deprivation on cardiac patients is an well documented clinical entity which the authors of the current article established with experimental data and therefore deserve sincere applause(1).
WHO guideline:
The World Health Organization guidelines say that for a good sleep, sound level should not exceed 30 dB(A) for continuous background noise, and 45 dB(A) for individual noise events.(2)
Clinical Psychologists point of view:
Many clinical psychologists and sleep medicine experts consider that normal sleep should be regarded as one of the basic human rights, because chronic sleep disturbance due to any kind of noise pollution is a well-documented cause of several psychosomatic disorders(3).
Cardiologists point of view:
Major part of effective treatment result depends on restful sleep for the patients suffering from cardiac arrhythmia , myocardial infarction and related cardiac ailments.These autonomic responses to noise during sleep can be obtained for much lower peak noise intensities as during wake states. These effects, mainly involving increased heart rate and vaso-constriction, have been found to habituate over successive noise-exposed nights as opposed to long exposure times. This could indicate an effect on cardiovascular response over the long term exposure (4). During sleep, heart rate is related to changes in the parasympathetic-sympathetic balance with an increase in sympathetic tone associated with activation and with electroencephalogram (EEG) arousal. Catecholamine levels and sympathetic activity decrease during sleep.This association has been observed not only with sleep deprivation but also with regard to sleep disruption.(5) Brief awakenings from sleep for only a few seconds are associated with temporary elevation in blood pressure and heart rate that results from an autonomic reflex.(6) Currently, we proposed a well organized case control study to explore effect of sleep fragmentation on cardiac arrhythmia patients due to noise generated from cell phone and cardiac monitors in intensive coronary units.We are concerned that otherwise negligible noise pollution may cause delayed recovery of vulnerable cardiac patients.
References:
1. e0265 Analysis of 24 h sleep deprivation on arrhythmia and heart rate variability:Wei-Ren Chen, and Xiang-Min Shi:Heart 2010 96:A83; doi:10.1136/hrt.2010.208967.265
2. Berglund B, Lindvall T, Schwela DH. Guidelines for Community Noise. World Health Organization 1999. Available from: http://www.who.int/docstore/peh/noise/guidelines2.html . [Accessed on 2010 March 28].
3. Tanu Pramanik.Re: wind turbine noise: Response to:-
Editorials:Wind turbine noise.BMJ 2012; 344 doi: http://dx.doi.org/10.1136/bmj.e1527 (Published 08 March 2012) Cite this as: BMJ 2012;344:e1527.
4. Muzet A, Ehrhart J, Eschenlauer R, Lienhard JP. Habituation and age differences of cardiovascular responses to noise during sleep. In Sleep 1980;212-5.
5. Sforza E, Chapotot F, Lavoie S, Roche F, Pigeau R, Buguet A. Heart rate activation during spontaneous arousals from sleep: Effect of sleep deprivation. Clin Neurophysiol 2004;115:2442-51.
6. Bonnet MH, Arand DL. Clinical effects of sleep fragmentation versus sleep deprivation. Sleep Med Rev 2003;7:297-310.
We thank Iliodromitis and colleagues for their interest in our review article1. Providing a comprehensive account of the extensive literature in this field has been a very challenging task. We are aware of their previous work2 3 on the feasibility of ischaemic postconditioning (IPost) in acute coronary syndrome. Of note, this was a small study of 37 patients and only included a total of 6 patients with non-ST elevation myoc...
Nairooz and Naidu [1] claim that definitions of complete and non- complete MV-PCI in our meta-analysis[2] (multivessel percutaneous coronary intervention) might have been missed or misinterpreted in one included study. As a matter of fact, CvLPRIT trial randomized STEMI (ST-elevation myocardial infarction) patients to either complete revascularization (including all N-IRAs [non-infarct related artery]) or IRA-only treatmen...
We thank Drs. MacIver and Clark for their comments regarding the role of the right ventricle in the development of acute pulmonary edema. We agree that a relative mismatch in stroke volume from the right and left sides of the heart can contribute to alveolar congestion [1]. Although we did mention preload as an important contributor to development of hypertensive acute heart failure (AHF), we chose to simplify the dis...
As a part of a low-fat diet regular consumption of chocolate (containing plant sterols [PS] and cocoa flavanols [CF] ) improve cardiovascular health by lowering cholesterol and improving blood pressure [1]. Exact mechanism remains uncertain. Chocolates are a rich source of catechins, a protective molecule against heart diseases, cancer, and other medical conditions. Catechin content highest in dark, bitter chocolate and l...
To the Editor:
We have read over and agree with the insightful comments of Lazaros at al. Our clinical vignette mainly focused on the hemodynamic abnormalities and post-pericardiocentesis diagnosis. Therefore, some of the clinical details had to be omitted for purposes of brevity. A pericardial rub was present during our patient's initial evaluation, and she later developed chest pain consistent with pericardi...
I read with great interest the report by Kang et al., (1) who conducted one-year prospective study in 1670 patients with heart failure (HF). The authors measured plasma N-terminal-pro-brain natriuretic peptide (NT-proBNP), and left ventricular ejection fraction (LVEF) was used for binary classification of HF. Although patients with keeping LVEF showed significantly lower NT-proBNP level than those with reduced LVEF, all-...
Last year, in response to Priest and Ashley's paper on genomics in cardiology1, we urged close collaboration of congenital cardiologist and geneticist for some adults with congenital heart conditions, who had not been tested in childhood2. The converse is also pertinent. A recent case (23year old female) with chromosome 1p36 deletion* (previous PDA and VSD closure in childhood) presented at another hospital with TIA's;...
I read with great interest the above guidelines published for this rare inherited heart disorder. Over the past few years, much work has gone into elucidating possible risk factors and markers which can help predict sudden cardiac death in such patients. Namely, we have already established that myocardial fibrosis, age and certain mutations in cardiac genes are markers indicative of a higher risk of sudden cardiac death for t...
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