Recent eLetters
Displaying 1-10 letters out of 480 published
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Diagnosing an MI: don't trust the monitor - standardise it!
Submit responseWe read with interest Dr Tayler et al's piece entitled 'Diagnosing an MI: don't trust the monitor!'[1]. We have had a similar experience with ECG filter-related artefactual ST segment change, resulting in patient referral direct to the catheter lab for primary percutaneous coronary intervention. As a consequence, we have audited the variation in ECG filter settings utilised during the acute coronary syndrome 'patient journey'. We found that patients (n=50) had ECGs acquired using up-to 4 different (average 2.14 /-0.99) filter settings during their admission. Across the hospital trust, 15 different filter settings were in operation and only 10% of ECGs met the AHA standard of 0.05-100Hz[2]. Our audit findings have increased awareness of the importance of ECG filter settings in the fidelity of ECG recording and led to standardisation of all ECG equipment in the trust, hopefully limiting the inappropriate diagnosis of ST segment elevation. We congratulate the authors on raising awareness of this problem and encourage others to review the set-up of their ECG equipment
1. Tayler, D., J. Gunn, and D. Chamberlain, Diagnosing an MI: don't trust the monitor! Heart. 96(5): p. 408-408. 2. Bailey, J., et al., Recommendations for standardization and specifications in automated electrocardiography: bandwidth and digital signal processing. A report for health professionals by an ad hoc writing group of the Committee on Electrocardiography and Cardiac Electrophysiology of the Council on Clinical Cardiology, American Heart Association. Circulation, 1990. 81(2): p. 730-739.
Conflict of Interest:
None declared
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COURAGE RESULTS: QUALITY OF LIFE ALSO MATTERS
Submit responseWe have read with interest the article written by Curzen et all related with the results of the COURAGE study2. We agree with the author that different interests and points of view drive us to different interpretations. However, independently of which position we defend one fact should not be underestimated: in addition to the important limitations pointed out by the author such as that only 6 % of the 35539 screened were finally randomised, only 3 % of the stents were drug eluting designs and the lack of inclusion as an end-point the 32.6 % revascularizations needed in the group of medical treatment, patient´s quality of life deserves also an especial attention. As is mentioned by Curzen, percutaneous intervention can be accomplished to improve survival, to relief symptoms or both. Patients with stable coronary disease unfortunately present comorbid conditions that require additional treatments and it conducts to a long list of pills needed at the end of the day. Quality of life in ischemic heart disease may be measured as anginal class, but also as patient´s well being. Multiple drug treatment is associated with a limitation in patient´s perception of comfort and may contribute to depression disorders3. Percutaneous revascularization permits a significant reduction in the number of pills needed and thus, any intervention that may reduce this dependence will add quality of life and this reduction should be considered in the decission making of this cohort of patients. REFERENCES 1. Curzen NP. Is there evidence for prognostic benefit following PCI in stable patients? COURAGE and its implications: an interventionalist´s view. Heart 2010; 96: 103-5. 2. Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ et al. Optimal medical therapy with or without PCI for stable coronary disease. N.Engl.J Med. 2007;356:1503-16. 3. Lichtman JH, Bigger JT, Jr., Blumenthal JA, Frasure-Smith N, Kaufmann PG, Lesperance F et al. Depression and coronary heart disease: recommendations for screening, referral, and treatment: a science advisory from the American Heart Association Prevention Committee of the Council on Cardiovascular Nursing, Council on Clinical Cardiology, Council on Epidemiology and Prevention, and Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Psychiatric Association. Circulation 2008;118:1768-75. Conflict of Interest: None declared -
Trans-radial procedures -still two weights and two measures?
Submit responseTrans-radial procedures â₉€œ still two weights and two measures? (letter regarding article from SL Hetherington, Heart 2009;95:1612-1618)Bernardo Cortese, MD ª Cardiologia Interventistica, Fondazione IRCCS Caâ₉„¢ Granda Ospedale Maggiore Policlinico, Milano, Italy
We read with great interest the article from SL Hetherington et al. regarding the impact of trans-radial primary PCI on clinical outcome in a single-center experience.[1] Authors discovered lower (although not statistically significant) in-hospital mortality rates and lower major cardiac or cerebrovascular adverse events with this technique, compared to the standard trans-femoral route. Previous studies regarding this topic were small, single-centre experiences, therefore not powered enough to demonstrate a significant clinical impact of the trans-radial technique during urgent PCI. Today, this study covers a vacuum in the literature, and being us â₁“radialistsâ€� since our very first PCI, we appreciate that.
Anyhow, despite the well-known lower hospital stay and costs, and now with the help of such clinical evidence, Authors and the community of interventional cardiologists should now investigate why this technique is still so underused in western countries. We wonder why if a single centre uncontrolled clinical trial is able to change the overall acute myocardial infarction management in the cath lab,[2] multi-centre, multi-national, old and recent [1, and Schäufele TG, in http://directnews.americanheart.org/extras/sessions2009/slides/41_pslides.pdf, accessed 29 Nov 2009] clinical evidence-based and economical evidence-based medicine should not change current practice.
The extent of the problem of â₁“radial resistanceâ€� may be easily understood given the following numbers. Until a few years ago, only 30% of European centres adopted a routine trans-radial approach for PCIs.[3] And has been recently disclosed that in only 1.32% of overall procedures performed in the US such approach is used.[4]
We believe that the interventional community should stop seeing at radialists as weird colleagues and start to change their mind. Now it is not time to call for a randomized trial. This is time to call for awareness.
[1] Hetherington SL, Adam Z, Morley R, et al. Acute coronary syndromes: Primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction: changing patterns of vascular access, radial versus femoral artery. Heart 2009;95:1612-1618. [2] Vlaar PJ, Svilaas T, van der Horst IC, et al. Cardiac death and reinfarction after 1 year in the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS): a 1-year follow-up study. Lancet. 2008 Jun 7;371(9628):1915-20. [3] Lefevre T and Louvard Y. Description and management of difficult anatomy encountered during transradial intervention. In: M. Hamon and E. McFadden, Editors, Transradial approach for cardiovascular interventions, Europa Stethoscope Media, Carpiquet (2003),241-254.
[4] Rao SV, Ou FS, Wang TY, et al. Trends in the prevalence and outcomes of radial and femoral approaches to percutaneous coronary intervention: a report from the National Cardiovascular Data Registry. JACC Cardiovasc Interv. 2008 Aug;1(4):379-86.
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Heart Disease and South Asians 50 years later: a time for change
Submit responseChen and Whitlock mention differences in risk for heart disease among South Asians, Chinese and others, in seeking to unveil the causes of heart disease in China, regionally and globally (1). Continuing disparities and high rates of diabetes and premature heart disease continue among the 25 million South Asians abroad and the 1.3 billion in South Asia, with initial low rates in China and the Chinese diaspora now increasing.
The first research submitted showing differences in heart disease between South Asians and Chinese was to this journal (then the British Heart Journal) in February 1959 by Muir, published January 1960, exactly fifty years ago (2). This necropsy study showed disproportionate early mortality in South Asians in a study of seven racial groups in Singapore from 1948 to 1957 (2). The first research published was by Danaraj and co- authors, submitted April 1959 and published October 1959 in the American Heart Journal, from similar necropsy studies in Singapore from 1950 to 1954, showing similar results, and reprinted January 2010 with an accompanying editorial (3,4).
Credit for first publication and citations have gone to Danaraj, who became an esteemed physician and leader in Malaya. Muir, with scant reference to his publication in the extensive literature on this subject, became an acclaimed leader in cancer research in Scotland and globally.
Time to publication was longer for Muir, likely since the British Heart Journal was a quarterly then and the American Heart Journal, monthly, explaining earlier submission and later publication. The lack of credit and citations likely stems from the inadvertent omission of Muir's publication from the 131 references in the 1989 definitive review, and a typo in the text mentioning the first publication by Danaraj as 1957 rather than October 1959, making Muir's in January 1960, seem much later.
The 50th Anniversary of Muir's neglected landmark publication in this journal is an opportunity to correct this, to recognize Muir's and Danaraj's equally pioneering research on disparities in health, and an opportunity to review and reduce continuing disparities (4). With the causes of heart disease mostly unveiled, we now have a golden opportunity to change the course of heart disease for South Asians and for all communities globally (4).
1. Chen Z, Whitlock G. Unveiling the causes of heart disease in China. Ed. Heart 2009;95:1818-9.
2. Muir CS. Coronary Heart Disease in seven racial groups in Singapore. British Heart Journal 1960;22:45-53
3. Danaraj TJ, Acker MS, Danaraj W, et al. Ethnic Group Differences in Coronary Heart Disease in Singapore: An Analysis of Necropsy Records. American Heart Journal 1959;58:516-26.
4. Rambihar VS, Rambihar SP, Rambihar VS Jr. Race, Ethnicity and Heart Disease: a challenge for cardiology for the 21st century. Ed. Am Heart J 2010; 159:1-14.
Conflict of Interest:
None declared
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Frailty: the great confounder, the great forgotten
Submit responseCorresponding author information: Name: Roman Surname: Romero-Ortuno Email: romeror@tcd.ie Affiliation: Department of Medicine for the Elderly, St James's Hospital, James's Street, Dublin 8, IrelandFrailty: the great confounder, the great forgotten
To the editor: Ryan, Steen, Seifer, et al. [1] present the results of SAFE PACE-2, which are at odds with SAFE PACE-1 [2]. The authors discuss that this may be due to greater frailty in SAFE PACE-2 participants. This point is valid and merits further reflection in relation to recent frailty literature.
Frailty is a well recognised clinical syndrome, but remains difficult to define and measure. Central to the concept of frailty is the dysregulation of multiple systems (e.g. balance, muscle strength, cognition), all of which independently contribute to the high incidence of falls in frail older people [3].
If falls can be a hallmark of frailty, any research on interventions with falls as endpoint should be able to control for this confounder. Many frailty assessment tools have been (and are still being) proposed, but are rarely used to help interpret results of trials in geriatric medicine (e.g. by using frailty scales as covariates, or conducting subgroup analyses based on increasing frailty categories).
The above would help establish which types of patients are most likely to benefit from an intervention. Along these lines, Ryan, Steen, Seifer, et al. [1] argue that the main beneficiaries of pacing may be non-frail patients, who are at low risk of falls from other sources. It is reasonable to presume that frail patients will continue to fall, despite minimising the contributing effect of carotid sinus hypersensitivity.
The issue calls for a frailty-adjusted meta-analysis of all trials of pacing for carotid sinus hypersensitivity, before the intervention is regarded as lacking evidence. The point by Alboni, Dinelli, Gianfranchi L, et al. [4] remains valid, in that the treatment for recurrent vasovagal syncope âÃÆ’¢Ã‚‚¬ÃÆ’‹Ã‚Ã…“can be chosen by considering the clinical context, the risk of trauma and possible comorbidities, in addition to utilizing the little or controversial knowledge available, as well as common sense'.
Older people are very heterogeneous. We need frailty measures that serve as common language for comparing studies that, whilst asking the same questions and employing the same methodology, happened to recruit from different populations. This would contribute towards a better evidence base in Geriatric Medicine.
References:
1 Ryan D, Steen N, Seifer C, et al. Carotid Sinus Syndrome and falls, should we pace? A multi-centre, randomised control trial (Safepace 2). Heart 2009. 2 Kenny RA, Richardson DA, Steen N, et al. Carotid sinus syndrome: a modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol 2001;38:1491-6. 3 Nowak A, Hubbard RE. Falls and frailty: lessons from complex systems. J R Soc Med 2009;102:98-102. 4 Alboni P, Dinelli M, Gianfranchi L, et al. Current treatment of recurrent vasovagal syncope: between evidence-based therapy and common sense. J Cardiovasc Med (Hagerstown) 2007;8:835-9.
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Preoperative NTproBNP and Perioperative Major Cardiovascular Events in Noncardiac Surgery
Submit responseWe read the paper by Choi et al with great interest. [1] Clearly NTproBNP (and CRP) appeared to predict perioperative major cardiovascular events (PCME) better than the Revised Cardiac Risk Index (RCRI). The most traditional way to depict that one predictor is better than other is to use the c-statistic or the area under the ROC curve (AUC). Although the abstract states that NTproBNP and CRP performed better than RCRI by ROC analysis, the paper does not tell us the actual c-statistic or AUC for either NTproBNP alone or CRP alone. This information would be useful in order to be able to compare directly the c-statistic of NTproBNP (or CRP) alone and RCRI alone. The c-statistic for the NTproBNP alone will help us to judge whether NTproBNP alone is as good as adding NTproBNP to the RCRI which is what the authors advocate. There would need to be a major advantage for combining NTproBNP and the RCRI over using NTproBNP alone for this to become practical reality since combining two separate risk scores is more cumbersome for the practicing clinicians than using either one alone. Instead of discussing the possibility that NTproBNP could replace the RCRI, the authors present the c-statistic data only for adding NTproBNP (and CRP) to the RCRI. We would urge the authors to now report c-statistic for NTproBNP alone (and CRP alone) so that it can be judged whether we really need to add NTproBNP (or CRP) to the RCRI (as they suggest) or whether NTproBNP (or CRP) can somehow replace the RCRI itself. 1 Choi JH, Cho DK, Song YB, et al. Preoperative NT-proBNP and CRP Predict Perioperative Major Cardiovascular Events in Noncardiac Surgery. Heart 2009. -
To the Editor: Ryan et al.
Submit responseTo the Editor: Ryan et al. report on the efficacy of Dual Chamber pacemaker implantation in patients with cardio-inhibitory carotid sinus hypersensitivity (CICSH) and falls in SAFEPACE-2 (Syncope And Falls in the Elderly- Pacing And Carotid sinus Evaluation)[1]. This study had the potential to expand on the findings of SAFEPACE-1 [2] and address some of the weaknesses of the latter with a blinded, multicenter, and less select cohort [3]. However, despite improved external validity, SAFEPACE-2 reports findings at odds with the prior results of SAFEPACE-1 by demonstrating that the null hypothesis was correct (pacemaker implantation did not reduce falls in CICSH)[1].
The authors of SAFEPACE-2 are to be applauded for their efforts to increase the generalizability of their results and for their attention to detail with regards to data acquisition and analysis. This begs the question, why the marked difference in findings between the two SAFEPACE trials [1-2]? While it is true that the cohort in SAFEPACE-2 had more comorbidity, one wonders whether further review of the trial methodology will yield another explanation.
The ‘double-blind’ design of SAFEPACE-2 seems difficult to achieve given the nature of the intervention. Pacemaker insertion requires the patient to carry a specific pacemaker card and to follow-up at specialized pacemaker clinics. In contrast, a loop recorder requires specific education as the patient self-activates the recorder with a hand-held device. Failure to blind the patients could significantly affect the primary outcome of self-reported falls, increasing the potential for recall bias in favor of the intervention. Therefore, this methodological issue may actually strengthen the author’s findings in SAFEPACE 2 and does not explain the difference in results between the trials.
At first glance, the difference may be explained by the lack of statistical power in SAFEPACE-2. It is true that SAFEPACE 2 is underpowered to detect a difference of 20% in the number of patients who fell, however it is almost fully powered to detect a difference of 40%. This was the power criteria used in SAFEPACE 1 [2]. Therefore, lack of statistical power also does not fully explain the difference in results between the trials.
One methodological issue which may account for the different trial results is the ‘randomization to implantation’ time. The overall relative risk (RR) for falls with pacemaker implantation in SAFEPACE-2 was 0.79 (95% Confidence Interval [CI], 0.4-1.5), but was 0.23 (95% CI, 0.15-0.32) when comparing patients before and after device implantation [1]. The latter RR suggests that device implantation made a difference to fall rates and raises the possibility that the overall result was obscured by a prolonged ‘randomization to implantation’ time. Given the multicenter nature of this trial it seems likely that this time was longer in SAFEPACE -2 than the single centre SAFEPACE-1. Therefore, it seems possible that inclusion of fall data prior to device implantation (the intervention) obscured the result of SAFEPACE-2 and may partially explain the difference in results between the two SAFEPACE trials.
Reporting the mean and median time from ‘randomization to implantation’, and exclusion of the pre-implantation fall data from the analysis may help shed more light on this important issue.
John W. McEvoy M.B., M.R.C.P.I. The Johns Hopkins Hospital 600 N. Wolfe Street Baltimore, Maryland 21287 Jmcevoy1@jhmi.edu
1. Ryan D, Steen N, Seifer C, Kenny RA. Carotid Sinus Syndrome and falls, should we pace? A multi-centre, randomised control trial (Safepace 2). Heart 2009. 2. Kenny RA, Richardson DA, Steen N, Bexton RS, Shaw FE, Bond J. Carotid sinus syndrome: a modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol 2001;38(5):1491-6. 3. McAnulty JH. Carotid sinus massage in patients who fall: will it define the role of pacing? J Am Coll Cardiol 2001;38(5):1497.
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Understanding myocardial deformation, ‘global systolic function’ and abnormal geometry.
Submit responseTo the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1 The study showed the presence of abnormal longitudinal left ventricular strain in patients with aortic stenosis and concentric left ventricular hypertrophy. Similar observations of reduced (less negative) peak longitudinal strain have been made in hypertensive-hypertrophic heart disease,2 heart failure with a normal ejection fraction (HFNEF),3, 4 and other causes of pathological left ventricular hypertrophy5, 6, 7
Further, abnormalities of midwall circumferential shortening have been shown in hypertensive-hypertrophic left ventricular disease2 and in HFNEF.8 Wang also showed a trend to reduced circumferential strain from -20% to -15% in HFNEF.3 The effect of myocardial disease on circumferential strain appears to be slightly less marked than that on longitudinal strain.3 In addition, there is significantly reduced radial strain in HFNEF despite the apparent normal radial ‘function’ and ejection fraction.3, 4
An increase in end-diastolic wall thickness may explain the combination of reduced myocardial shortening and yet a normal ejection fraction. This can be understood by considering a cube of myocardium 9 x 9 x 9 mm as a non-compressible elastomer. If circumferential and longitudinal strain are both normal (-20%) then radial strain (i.e. relative wall thickening) is +56% and absolute wall thickening is 5.1 mm (see Table). When there is left ventricular hypertrophy with an end-diastolic wall thickness of 13 mm and circumferential and longitudinal strain are reduced (-15%), radial strain is also significantly reduced (38%) but absolute wall thickening remains almost identical at 5.0 mm (see Table). Therefore, it is important to differentiate between absolute and relative radial thickening.
Three dimensional modelling demonstrates that ejection fraction is principally determined by both myocardial shortening (strain) and end-diastolic wall thickness independently of loading conditions.9 The normal absolute wall thickening in presence of reduced strain results in the normal ejection fraction.9, 10 End-diastolic wall thickness and strain are the determinants of absolute wall thickening; absolute wall thickening is the main determinant of left ventricular ejection fraction in a curvilinear manner.10
An individual’s resting metabolic requirements demand a reasonably normal stroke volume (SV) in stable heart failure regardless of ejection fraction.10 Ejection fraction is merely the ratio of gross SV and end-diastolic volume (where, gross SV = net SV + valvular regurgitant volume). If the numerator is relatively fixed the denominator must change; accordingly the relationship between ejection fraction and end-diastolic volume is reciprocal even in heart failure.11 Three-dimensional modelling suggests thatthe end-diastolic volume may be physiologically regulated by the need to have an appropriate net stroke volume to satisfy the physiological needs of peripheral tissues in health (e.g. growth, pregnancy) and in heart disease.10
An increase in end-diastolic wall thickness with normal shortening must lead to an increased absolute thickening; in order for the absolute wall thickening to remain normal, myocardial shortening must be reduced. Myocardial strain has to be reduced proportionally to the degree of concentric hypertrophy otherwise the ejection fraction and stroke volume will be inappropriately increased.
Hypertrophic left ventricular disease occurs in numerous conditions including hypertension, aortic stenosis, hypertrophic cardiomyopathy, HFNEF, Fabry disease and amyloid. Each condition can be explained by the combination of abnormal myocardial shortening and increased end-diastolic wall thickness determining the absolute myocardial thickening and ejection fraction. The end-diastolic volume being adjusted to normalise net stroke volume for the given ejection fraction.10
These proposals explain the geometric findings in hypertrophic heart disease regardless of the cause. A normal ejection fraction does not equate to normal deformation or even normal systolic function. The term ‘global systolic function’ is meaningless, misleading and should be abandoned.
Table
Normal peak strain
-20%
Abnormal peak strain
-15%
Abnormal strain
-10%
End-diastolic thickness (mm)
9
13
17
21
9
13
17
21
9
13
17
21
End-systolic thickness (mm)
14
20
27
33
13
19
25
31
13
18
24
29
Radial strain (%)
56
56
56
56
38
38
38
38
23
23
23
23
Absolute wall thickening (mm)
5.1
7.3
9.6
11.8
3.5
5.0
6.5
8.1
2.1
3.1
4.0
4.9
DH MacIver
Taunton & Somerset Hospital, Taunton, UK.
Correspondence to: Dr DH MacIver
Conflict of interest: None.
1 Cramariuc D, Gerdts E, Davidsen ES, et al. Myocardial deformation in aortic valve stenosis - relation to left ventricular geometry. Heart 2009:hrt.2009.172569.
2 Shimizu G, Hirota Y, Kita Y, et al. Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy. Circulation 1991;83:1676-84.
3 Wang J, Khoury DS, Yue Y, et al. Preserved left ventricular twist and circumferential deformation, but depressed longitudinal and radial deformation in patients with diastolic heart failure. Eur Heart J 2008;29:1283-9.
4 Tan YT, Wenzelburger F, Lee E, et al. The pathophysiology of heart failure with normal ejection fraction: exercise echocardiography reveals complex abnormalities of both systolic and diastolic ventricular function involving torsion, untwist, and longitudinal motion. J Am Coll Cardiol 2009;54:36.
5 Nagueh SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy. Circulation 2001;104:128-30.
6 Weidemann F, Breunig F, Beer M, et al. Improvement of cardiac function during enzyme replacement therapy in patients with Fabry disease. A prospective strain rate imaging study. Circulation 2003;108:1299-301.
7 Koyama J, Ray-Sequin PA, Falk RH. Longitudinal myocardial function assessed by tissue velocity, strain, and strain rate tissue Doppler echocardiography in patients with AL (primary) cardiac amyloidosis. Circulation 2003;107:2446-52.
8 Vinch C, Aurigemma G, Simon H, et al. Analysis of left ventricular systolic function using midwall mechanics in patients > 60 years of age with hypertensive heart disease and heart failure. Am J Cardiol 2005;96:1299-303.
9 MacIver DH, Townsend M. A novel mechanism of heart failure with normal ejection fraction. Heart 2008;94:446-9.
10 MacIver DH. Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction? Basic Res Cardiol 2009:Online first DOI: 10.1007/s00395-009-0063-x.
11 MacIver DH. Surgical ventricular reconstruction: an oversimplified hypothesis? N Engl J Med 2009;361:529-32.
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ozone protective effect
Submit responseNovember 11, 2009 Editor, Heart British Medical Journal Dear Sir: I am writing to comment on the excellent article by Bhaskaran et al in Heart[1], and especially on the editorial by David Newby [2] that commented on this paper. In my opinion, Dr. Newby has missed the most important conclusion of the Bhaskaran paper. Dr. Newby’s editorial was focused mainly on the cardiac effects of fine particulate pollution, and included a graph of data from Beijing, China. However, it seems to me that a far more important contribution of the Bhaskaran paper was the observation of an “ozone protective effect” in several parts of the world. The authors pointed out that this effect is probably due to some pollutant that is negatively correlated with ozone, and cites my previous paper[3] suggesting that the effect could be due to unsuspected methyl nitrite (MN) in the air. This hypothesis has a high degree of plausibility because it is known that MN, unlike ozone, is rapidly destroyed by sunlight and so would be negatively correlated with ozone. To the best of my knowledge, this ozone protective effect is totally inexplicable unless an unknown pollutant, such as MN, is present. If Dr. Newby’s point of view is to be accepted, then presumably he must argue that fine particulate pollution is also the cause of the ozone protective effect. However, that hypothesis has been thoroughly discredited in another paper [4]. In that paper I showed that fine particulate matter can not explain the negative ozone associations in any parts of the world in which there is published evidence for the negative effects. I particularly showed that explanation is extremely unlikely in Hong Kong, China. Hence, I feel that the most important contribution of the Bhaskaran paper is to alert the world to the possible existence of a very important toxic pollutant whose presence has escaped attention. Most desperately needed is funding for research to identify MN in engine exhaust. To date, such funding has not been available in the United States. Sincerely, Professor Peter M. Joseph, Ph.D. School of Medicine University of Pennsylvania Philadelphia, PA, USA email = joseph@rad.upenn.edu REFERENCES 1. Bhaskaran K, Hajat S, Haines A, Herrett E, Wilkinson P, Smeeth L. Effects of air pollution on the incidence of myocardial infarction. Heart 2009;95:1746-1759. 2. Langrish JP, Mills NL, Newby DE. Heat and haze: a forecast for myocardial infarction? Heart 2009;95:1721-1722. 3. Joseph PM. Paradoxical ozone associations could be due to methyl nitrite from combustion of methyl ethers or esters in engine fuels. Environ Int 2007;33:1090-106. 4. Joseph PM. Can fine particulate matter explain the paradoxical ozone associations? Environ Int 2008;34:1185-91. -
Inflamatory Biomarkers
Submit responseDear Sir, We enjoyed the recent paper in Heart by Rana et 1, but were concerned that the sample was composed of approximately 80% of individuals with intermediate or high-risk of having an event, which impaired the diagnostic and prognostic accuracy of the assessed test. The markers used reflect the biological state of elevated risk of an adverse outcome in the studied subjects that is secondary to the interaction of risk-factors such as smoking, diabetes mellitus and dyslipidemia that can affect the endothelium 2,3,4.1. Rana JS, Cote M, Despres JP, Sandhu MS, Talmud PJ, Ninio E, et al. Inflammatory biomarkers and the prediction of coronary events among people at intermediate risk: the EPIC-Norfolk prospective population study. Heart 2009;95(20):1682-7.
2. Koskinen J, Kahonen M, Viikari JS, Taittonen L, Laitinen T, Ronnemaa T, et al. Conventional cardiovascular risk factors and metabolic syndrome in predicting carotid intima-media thickness progression in young adults: the cardiovascular risk in young Finns study. Circulation 2009;120(3):229-36.
3. Kalra L, Iveson E, Rambaran C, Sherwood R, Chowienczyk P, Ritter J, et al. Homocysteine, migration and early vascular impairment in people of African descent. Heart 2008;94(9):1171-4.
4. De Michele M, Iannuzzi A, Salvato A, Pauciullo P, Gentile M, Iannuzzo G, et al. Impaired endothelium-dependent vascular reactivity in patients with familial combined hyperlipidaemia. Heart 2007;93(1):78-81.
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