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Displaying 1-10 letters out of 653 published

  1. Effect of incomplete revascularization

    In the above paper, there is no mention of the influence of incomplete revascularization on the results. This is an important variable that should be taken into account to show whether an independant effect of lesion calcification on outcomes exists.

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  2. Higher relative wall thickness in strength athletes using anabolic steroids

    In the study presented from Utomi et al (1), the Morganroth hypothesis concerning a different left ventricular (LV) adaptation between endurance and strength athletes has been tested. The authors demonstrated a normal LV geometry in male strength athletes and concluded that the hypothesis of a LV concentric hypertrophy should be revised. We would like to point out that we have questioned the disproportionate increase in LV wall thickness in strength athletes, resulting in a concentric hypertrophy, already in 1989 (2) and 1999 (3). We have demonstrated that pure resistance-trained athletes (weightlifters and bodybuilders) and combined resistance- and endurance-trained athletes (rowers) do not develop a LV concentric hypertrophy in the absence of pathological pressure loads or hypertrophic cardiomyopathy. Only strength athletes misusing anabolic steroids exhibited distinctly higher relative wall thicknesses compared to all other athletes (3). Unfortunately, in the publication of Utomi et al (1), the influence of anabolic steroids on the ratio between LV myocardial thickness and internal diameter is not discussed. Similarly, in most previous studies reporting on a concentric hypertrophy in strength athletes, a drug history, especially the misuse of anabolic steroids, is missing. Therefore, in apparently healthy athletes, exhibiting a disproportionate increase in wall thickness, misuse of anabolic steroids has to be considered. In addition, endurance exercise capacity, which is related to the athlete's heart size (4), should be tested (e.g. by VO2max) in such studies to validate the presumed fitness of the studied subjects.

    References 1. Utomi V, Oxborough D, Ashley E, et al. Predominance of normal left ventricular geometry in the male "athlete's heart". Heart Published Online First: June 10, 2014. doi: 10.1136/heartjnl-2014-305904. 2. Urhausen A, Holpes R, Kindermann W. One-and two-dimensional echocardiography in bodybuilders using anabolic steroids. Eur J Appl Physiol 1989; 58:633-40. 3. Urhausen A, Kindermann W. Sport-specific adaptations and differentiation of the athlete's heart. Sports Med 1999; 28:237-44. 4. Scharhag J, Schneider G, Urhausen A, Rochette V, Kramann B, Kindermann W. Athlete's heart: right and left ventricular mass and function in male endurance athletes and untrained individuals determined by magnetic resonance imaging. J Am Coll Cardiol 2002;40:1856-1863.

    Conflict of Interest:

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  3. Definition of peripheral arterial disease in South Asians

    Majority of the studies have defined peripheral arterial disease as ankle brachial index (which is a ratio of absolute systolic ankle blood pressures and absolute systolic brachial blood pressures) of <0.9. Peripheral arterial disease ought to be defined by both low ankle brachial index and high ankle brachial index as both low and high ankle brachial index are predictors of cardiovascular disease and mortality in Europeans. The prevalence of hypertension and its association with cardiovascular disease in South Asians do not significantly differ from that of Europeans. The prevalence of ankle brachial index <0.9 in South-Asians is less than in Europeans both in subjects with or without diabetes. However, absolute systolic ankle blood pressures increase with diabetes in young South Asians and these increases are greater in South-Asians compared to Europeans (Kain K, Heart 2013; 99:614-619). Therefore, in South Asians peripheral arterial disease ought to be defined by high ankle brachial index rather than low ankle brachial index and the paradox of lower prevalence of peripheral arterial disease even though South Asians have increased prevalence of ischemic heart disease and ischemic stroke will disappear.

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  4. A lot more work to do to improve Antipodean healthcare

    The researchers here used a specified two-week period and their outcome measures were not 'prospective' but effectively cross-sectional. The papers labels itself a 'prospective audit' which makes the fundamental error clinicians often make in confusing a 'de novo consecutive series' of patients with the epidemiologist's definition of a 'prospective' study which is of course a 'cohort study', one in which outcomes are collected later in time.

    Furthermore, secondary prevention and cardiac rehabilitation are not 'snapshot' care pathways. Much of the real work begins after discharge - the phone call to the patient at 48 hours, the invite to the post-ACS clinic a few weeks later, and then weeks to months of intensive input through a cardiac rehabilitation programme. This paper does not capture that.

    Finally, the findings here that only 46% of ACS (acute coronary syndrome) patients were referred to cardiac rehabilitation are also much worse than European figures from the recent British Association for Cardiovascular Prevention and Rehabilitation (BACPR) audit where referral rates were very near the CVD Outcomes Strategy for England ambition of 65% uptake, (1) whilst according to the last annual report from the Swedish national ACS registry, 79% of all patients aged 75 years or younger attended the secondary prevention first visit (6-8 weeks after the event) and 73% attended the second visit (12-14 months after the event).(2) They are thus wrong to suggest that their results are similar to other international studies - comparing to other ACS registries is not relevant, they need to compare their results to other audits of cardiac rehabilitation.

    International comparisons of care does inform new research and policy initiatives that improve the quality of health systems, and this paper merely suggests that Australia and New Zealand are a long way behind Europe.

    1. Doherty P, and Lewin, B. The National Audit of Cardiac Rehabilitation: Annual Statistical Report 2013.

    2. SWEDEHEART Annual report http://www.ucr.uu.se/swedeheart/index.php/arsrapporter 2012.

    Conflict of Interest:

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  5. INVASIVE VERSUS CONSERVATIVE STRATEGY FOR THE MANAGEMENT OF SPONTANEOUS CORONARY ARTERY DISSECTION: WHICH IS BETTER?

    INVASIVE VERSUS CONSERVATIVE STRATEGY FOR THE MANAGEMENT OF SPONTANEOUS CORONARY ARTERY DISSECTION: WHICH IS BETTER ?

    Kenan YALTA, MD

    Mustafa YILMAZTEPE, MD

    Flora OZKALAYCI, MD

    Nasir SIVRI, MD

    Bilal GEYIK, MD

    Trakya ?niversity, Cardiology Department, Edirne, Turkey

    Corresponding Author: Kenan Yalta , e-mail: kyalta@gmail.com

    To the Editor,

    In the recent years, spontaneous coronary artery dissection (SCAD) has been a point of debate with regard to its management strategies. In their recently published article (1), Taleyratne JD et al described a case of spontaneous coronary artery dissection (SCAD) in a middle-aged woman presenting with acute coronary syndrome (ACS) (1). As far as we understand, the case was exclusively managed with a conservative strategy (with aspirin, ticagrelor, glycoprotein IIb/IIIa inhibitors and heparin) after coronary angiography (CAG) and intravascular ultrasound (IVUS). If that was the case, we strongly oppose the exclusive use of a non-interventional approach in this patient due to reasons described below.

    Regarding the single- vessel SCAD, conservative strategy is only warranted in asymptomatic cases in which the degree of stenosis due to SCAD is < 50% along with a distal perfusion of TIMI 3 in the affected vessel (2). In other terms, where applicable, PCI is strongly recommended in the setting of a high-risk SCAD associated with a severe luminal narrowing (70-99%) and/or a poor distal vessel perfusion (TIMI 0- 1) and presenting with an unstable condition (2) (as in the case reported by Taleyratne JD (1)). Surgical management might also be performed in a more selected portion of cases including those with left main coronary artery (LMCA) or multivessel involvement in which there is no SCAD extension to the distal segments of the affected vessel (2).

    There exists a strong rationale behind these therapeutic recommendations : SCADs treated conservatively might not always demonstrate a resolution or spontaneous healing, and might even worsen in some situations in the short and long terms (2,3). On follow-up, unfavorable results might be encountered in as high as 60% of SCADs managed with a conservative strategy alone (2,4). Among these long-term complications , late recurrences (2, 5) and aneurysm formation (3) in the affected vessel might be quite troublesome, and might be regarded as major therapeutic challenges in the conservatively treated patients with a SCAD. More importantly, witholding an early invasive strategy in the acute phase might be associated with acute life-threatening consequences including refractory arrhythmic events, retrograde propagation of the dissection towards the LMCA, etc. Interestingly, propagation of SCAD is more likely to occur in normal vessels in comparison to atherosclerotic ones (2) . On the other hand, PCI was previously suggested as the primary therapeutic option in the setting of SCAD (6). However, when the final decision is PCI, it should be done by expert hands: the operator should avoid advancing guide-wire into the false lumen to prevent SCAD extension (2). Direct stenting without stent oversizing should be the preferred strategy (2). Unfortunately, despite meticulous care, additional stents might be required in a portion of cases due to the propagation of SCAD after initial stenting (2,5). Nevertheless, PCI when combined with endovascular imaging techniques (IVUS, etc) seems to be a more promising therapeutic approach in the setting of SCAD particularly with high-risk features.

    In summary; conservative management might pose a significant risk to patients with SCAD (2-4) particularly to those with high- risk features both in the short and long terms. On the other hand, invasive strategy including PCI, when performed by experienced operators and with the assistance of endovascular imaging techniques, seems to be a radical and efficient alternative in these patients (2,6). We wonder why Taleyratne JD et al (1) preferred a 'wait and see' approach rather than performing an IVUS-guided urgent PCI in their high-risk patient. Furthermore, as SCAD might be regarded as a continuum of evolving vascular pathology with an unpredictable course even after healing, their patient (1) needs to be monitored closely for potential late complications including recurrence , aneurysm formation, etc. Accordingly, the authors (1) may want to make clear their future strategies (follow-up, medication, repeat CAG or non-invasive imaging ?, etc.) regarding their patient in a more comprehensive manner. However, future studies are still warranted to establish furher risk prediction models that might help determine the initial therapeutic strategy, and more importantly, might allow timely diagnosis and management of acute and chronic complications in patients with SCAD.

    REFERENCES: 1- Taleyratne JD, Fernandez JP. Anterior ST elevation myocardial infarction in a 40-year-old woman. Heart. 2014 Jun 27. pii: heartjnl-2014- 305985. doi: 10.1136/heartjnl-2014-305985. [Epub ahead of print. 2- Giacoppo D, Capodanno D, Dangas G, Tamburino C. Spontaneous coronary artery dissection. Int J Cardiol. 2014; 175(1): 8-20. 3- Furuichi, S. , Montorfano, M., Godino, C., Murino, M., Sangiorgi, G.M., Colombo, A. How should I treat a long and huge coronary pseudoaneurysm after spontaneous coronary artery dissection? EuroIntervention. 2011; 6: 1131-1136. 4- Shamloo BK, Chintala RS, Nasur A, Ghazvini M, Shariat P, Diggs JA, Singh SN. Spontaneous coronary artery dissection: aggressive vs. conservative therapy. J Invasive Cardiol. 2010; 22(5): 222-8. 5- Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, Gersh BJ, Khambatta S, Best PJ, Rihal CS, Gulati R. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012; 126(5) :579-88. 6- Butler R, Webster MW, Davies G, Kerr A, Bass N, Armstrong G, Stewart JT, Ruygrok P, Ormiston J. Spontaneous dissection of native coronary arteries. Heart. 2005; 91(2) :223-4.

    Conflict of Interest:

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  6. PATIENT-PROSTHESIS MISMATCH IN PATIENTS UNDER 70 YEARS OF AGE: DOES IT HAVE AN IMPACT ON SURVIVAL BUT NOT ON VENTRICULAR MASS REGRESSION?

    Left ventricular (LV) hypertrophy caused by severe aortic stenosis is highly associated with sudden death, congestive heart failure and stroke. After aortic valve replacement (AVR) the pressure gradient between the left ventricle and ascending aorta decreases and reverse left ventricular modeling begins to appear. However, if a certain degree of residual aortic stenosis remains, reverse modeling may be compromised which can affect clinical outcomes. With great interest, we read the article by Price J and associates1 on the importance of age as a modifier of the relationship between patient-prosthesis mismatch (PPM) and outcomes. Although this article tries to clarify the controversy around this issue, the results are, in absence of an explanation, contradictory in themselves. These conclusions1 may be summarized in: 1. In patients older than 70 years of age, PPM reduced the LV mass index (LVMI) regression in patients with LV dysfunction but not in those with normal LV function. Conversely, PPM had no effect on death or congestive heart failure regardless of LV function. 2. In patients under 70 years of age, PPM did not reduce LVMI regression regardless of LV function. Conversely, PPM was associated with increased death or congestive heart failure in patients with LV dysfunction but not in those with normal LV function. Therefore, it seems that LVMI regression and clinical outcomes are two independent circumstances when intuitively one should cause the other. At this point, we would like to note that, although there are several ways to detect PPM, only two have been considered acceptable in the last years.2 One way is to perform an echocardiography for each patient several months after the intervention. This method has some limitations due to technical difficulties in measurements of echocardiography. Moreover, it is impossible to know if those patients who dye before the echocardiography have mismatch, being precisely these echocardiograms those that could provide more relevant information. Probably due to these limitations, Price J et al.1 opted for the use of tables derived from the literature. However, one must be aware that this method cannot detect all patients with PPM, and there are false-positive and false-negative categorizations.3 Bleiziffer et al.2 demonstrated that the sensitivity and specificity to detect PPM are 71% and 67% when using echocardiographically derived reference tables. Hence, estimations of PPM based on reference tables yield low sensitivity and specificity, leading to incorrect categorization of patients. This effect of false categorization might outweigh that of inaccurate echocardiographic measurements because the effective orifice area of the same prosthesis can vary widely among patients.3 Therefore, so far we have not found the perfect way to detect PPM. This circumstance can explain the contradictory results observed by Price J et al.1 and is probably the main reason why after almost 40 years of research4 we continue to discuss the clinical relevance of a residual aortic stenosis in our postoperative patients. REFERENCES 1. Price J, Toeg H, Lam BK et al. The impact of prosthesis-patient mismatch after aortic valve replacement varies according to age at operation. Heart. 2014;100:1099-106. 2. Bleiziffer S1, Eichinger WB, Hettich I et al. Prediction of valve prosthesis-patient mismatch prior to aortic valve replacement: which is the best method? Heart. 2007;93:615-20. 3. Bleiziffer S, Eichinger WB, Lange R. Letter by Bleiziffer et al regarding article, "Long-term outcomes after valve replacement for low-gradient aortic stenosis: impact of prosthesis-patient mismatch". Circulation. 2006;114:e627. 4. Rahimtoola SH. The problem of valve prosthesis-patient mismatch. Circulation. 1978;58:20-4

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  7. Promising for prognostic evaluation but cost-effectiveness and frequency of monitoring require consideration

    Firstly, looking at the study design the selected age range of HCM subjects (mean age of 56 years) may at least in part account for the high percentage of myocardial fibrosis at baseline (66 %) as in addition to the fibrosis likely being a pathological consequence of HCM itself, this age group of participants may harbour occult or sub-clinical coronary artery disease and a prior association between cardiac ischemia and myocardial fibrosis has been reported in the literature (1).

    While these findings theoretically justify the use of routine cardiac MRI at the time of HCM diagnosis in conjunction with echocardiography (enabling the detection of two predictive variables of sudden cardiac death, fibrosis and left ventricular ejection fraction, respectively) as a comprehensive diagnostic work-up, this consideration needs to be carefully balanced against the economic burden of widely implementing such sophisticated imaging and the realisation that such techniques do not exist widely in all centres for effective risk stratification to take place on a national level (2).

    Finally, the question remains as to what represents an appropriate time interval for monitoring the progression of myocardial fibrosis once already detected and how this will be determined? This may be of particular importance as you have established that the extent of myocardial fibrosis (if we place this irreversible process along a continuum) was a statistically significant predictor of sudden cardiac death. Thus, if the fibrotic process wasn't monitored linearly over time in these patients, and the myocardial fibrosis was detected once already 'extensive', the risk of sudden cardiac death in this subset of HCM subjects may remain high despite any prevailing medical or surgical intervention.

    References:-

    1) Wilson JM, Villareal RP, Hariharan R, Massumi A, Muthupillai R, Flamm SD. Magnetic Resonance Imaging of Myocardial Fibrosis in Hypertrophic Cardiomyopathy (2002). Tex Heart Inst J.29:176-180.

    2) To ACY, Dhillon A, Desai MY. Cardiac Magnetic Resonance in Hypertrophic Cardiomyopathy (2011). J Am Coll Cardiol Img. 4(10):1123- 1137.

    Conflict of Interest:

    None declared

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  8. Cardiac Troponin T assay is not cardiac specific.

    The authors have compared clinical outcomes between the use of a conventional cardiac Troponin I ( cTnI) assay and a high sensitivity cardiac Troponin T (hs-cTnT)assay. They conclude that the introduction of the hs-cTnT assay did not influence outcomes at 6 months. Their conclusions might have been different if they had compared a conventional cTnI assay with a hs-cTnI assay. We now know that there are major differences between cTnI and cTnT assays (1). The cTnT protein , unlike its cTnI counterpart, is found in both myocardium and diseased skeletal muscle. The Roche cTnT assay cannot distinguish between cTnT from myocardium and re-expressed cTnT found in diseased skeletal muscle (2). Elevated cTnT in the circulation can have dual significance, myocardial or skeletal muscle injury. Patients with several different types of acquired or inherited skeletal muscle diseases have persistent elevation of cTnT without clinical or cTnI evidence of myocardial injury. It has also been shown that elevation of cTnT in these patients has no adverse impact on cardiovascular outcomes. The use of hs-cTnT has made the problem of cardiac specificity worse as it identifies low levels of elevated cTnT in additional patients with skeletal muscle diseases, which would not have been detected by standard cTnT assay. It should also be noted that many of these patients have subclinical skeletal myopathies. It is currently unknown what proportion of patients attending the emergency department with chest pain have elevated cTnT due to skeletal muscle diseases, not myocardial injury. It would be interesting if the authors were able to re-analyse any stored samples they may have with hs- cTnI.

    1.Rittoo D, Jones A, Lecky B, Neithercut D . Elevation of cardiac troponin T, but not cardiac troponin I, in patients with neuromuscular diseases: implications for the diagnosis of myocardial infarction. J Am Coll Cardiol. 2014 Jun 10;63(22):2411-20.

    2.Jaffe AS, Vasile VC, Milone M, Saenger AK, Olson KN, Apple FS. Diseased skeletal muscle: a noncardiac source of increased circulating concentrations of cardiac troponin T. J Am Coll Cardiol. 2011 Oct 18;58(17):1819-24.

    Conflict of Interest:

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  9. Right ventricular stroke work in children with pulmonary arterial hypertension: a promising approach

    We read with great interest the article by Di Maria et al. [1], describing the importance of right ventricular (RV) performance, especially RV stroke work (RVSW) in children with pulmonary arterial hypertension (PAH). The authors investigated the relation between echocardiographic measurements of RV function and the "gold standard" of right heart catheterization in children and found that the RVSW strongly correlates with non-invasive data of RV function [1]. The authors concluded that RVSW correlates with outcome parameters, e.g. abnormal WHO class, and mortality, in children with PAH. We completely agree with the findings of Di Maria et al. [1] and want to emphasize the importance of echocardiographic evaluation, e.g. tricuspid annular peak systolic excursion (TAPSE) for longitudinal management of pediatric patients with PAH. Di Maria et al. compared data of patients with adverse outcomes to patients with WHO class I-III, of different age groups: median 16.9 versus 11.8 years (table 1) and found no statistically significant difference of TAPSE (mean values 1.3 versus 1.5 cm, respectively) between those groups [1]. In our opinion their data would have been more promising and statistically significant, if the authors would have compared their TAPSE data with already existing normative data of TAPSE [2] (comparing 1.5 to 2.14 cm for 12 years of age, and 1.3 cm to 2.45 cm for 17 years of age). This might highlight the importance of their data for future pediatric PAH follow ups. We want to encourage the prospective use of echocardiography for routine assessment of RV systolic function in pediatric PAH patients.

    References 1.) Di Maria MV, Younoszai AK, Mertens L, Landeck BF 2nd, Ivy DD, Hunter KS, Friedberg MK. RV stroke work in children with pulmonary arterial hypertension: estimation based on invasive haemodynamic assessment and correlation with outcomes. Heart 2014 Apr 29. doi: 10.1136/heartjnl-2013- 305298 [Epub ahead of print].

    2.) Koestenberger M, Nagel B, Ravekes W, Avian A, Heinzl B, Fandl A, et al. Tricuspid annular peak systolic velocity (S') in children and young adults with pulmonary artery hypertension secondary to congenital heart diseases, and in those with repaired tetralogy of Fallot: echocardiography and MRI data. J Am Soc Echocardiogr 2012; 25: 1041-9.

    Conflict of Interest:

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  10. Female sex as a determinant of prehospital 12-lead ECG in ST elevation and non-ST elevation myocardial infarction patients

    To the editor: We read the article by Quinn et al1on the effects of prehospital 12-lead ECG (PHECG) on processes of care and mortality with great interest. The authors conclude that when a PHECG was used, patients with ST-elevation myocardial infarction and non-ST elevation myocardial infarction had better survival compared to those without. Interestingly, among the determinants associated with PHECG use, the authors identify female patients to be less likely to have a PHECG than male patients.

    When the authors discuss possible explanations to the sex differences in PHECG use, they suggest that the predominately male emergency medical services workers might be reluctant to perform a PHECG on female patients because of the need for intimate exposure. Furthermore female patients might also be less willing to agree to a PHECG compared to men. We argue that a more plausible explanation is uncontrolled confounding of presenting symptoms and type of myocardial infarction.

    When we analysed a similar ST-elevation myocardial infarction and non -ST elevation myocardial infarction population in the Swedish comprehensive SWEDEHEART2 register we found an odds ratio for women vs. men to receive a PHECG comparable to that in the article by Quinn et al: (SWEDEHEART: OR=0.89; 95 % CI 0.87-0.92) vs. (Quinn et al: OR=0.87; 95% CI 0.86-0.89). In Sweden 64% of the ambulance specialist nurses were male (The National Board of Health and Welfare).

    In accordance with previous findings3 we found women to report chest pain as their presenting symptom in a lesser degree than men, 77.5% vs. 84.8%. Patients with atypical MI symptoms (e.g. no chest pain) are less likely to receive a PHECG compared to patients with chest pain, in SWEDEHEART 12.6% vs. 35.1%. When stratifying according to presenting symptoms, the sex differences almost disappeared, table 1. In addition non -ST elevation myocardial infarction patients are less likely to receive a PHECG compared to ST-elevation myocardial infarction patients, in SWEDEHEART 23.4% vs. 46.4%. Non-ST elevation myocardial infarction occurs more frequently than ST-elevation myocardial infarction in female patients, in SWEDEHEART 38.0% vs. 33.6%. Similarly in the Myocardial Ischaemia National Audit Project (MINARP) cohort4 which Quinn et al analysed. After stratification of presenting symptom and myocardial infarction type, the sex differences completely disappeared.

    We believe that if Quinn et al controls for presenting symptom and myocardial infarction type, the difference in PHECG use among men and women will disappear.

    Kristina Klerdal1 Christoph Varenhorst2 Stefan James2 Lars Alfredsson1 Hans Blomberg3 Tahereh Moradi1,4

    1Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Sweden

    2Department of Medical Sciences, Cardiology and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden

    3Department of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University, Uppsala, Sweden

    4Centre for Epidemiology and Social Medicine, Health Care Services, Stockholm County Council, Sweden

    Contributors TM acquisition of data. KK conceived the letter, analysed the data and wrote the first draft. CV, SJ, LA, HB and TM contributed with editing of the content and specifics of the letter. All authors reviewed and approved the final product.

    Correspondence to MSc Kristina Klerdal, Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-171 77 Stockholm, Sweden; Kristina.Klerdal@ki.se

    Competing interest None

    REFERENCES 1 Quinn T, Johnsen S, Gale CP, et al. Effects of prehospital 12-lead ECG on processes of care and mortality in acute coronary syndrome: a linked cohort study from the Myocardial Ischaemia National Audit Project. Heart 2014;100:944-50. 2 Jernberg T, Attebring MF, Hambraeus K, et al. The Swedish Web-system for enhancement and development of evidence-based care in heart disease evaluated according to recommended therapies (SWEDEHEART). Heart 2010;96:1617-21. 3 Coventry LL, Finn J, Bremner AP. Sex differences in symptom presentation in acute myocardial infarction: a systematic review and meta- analysis. Heart Lung 2011;40:477-91. 4 Gale CP, Cattle BA, Woolston A, et al. Resolving inequalities in care? Reduced mortality in the elderly after acute coronary syndromes. The Myocardial Ischaemia National Audit Project 2003-2010. Eur Heart J. 2012;33:630-9.

    ? Table 1 Prehospital 12-lead electrocardiogram (PHECG) use and sex in patients who came via emergency medical services

    Overall PHECG No PHECG OR estimate 95% CI

    women vs. men All patients (n)

    81,190 25,210 55,980

    Female

    36.5% 34.8% 37.3% 0.89 0.87 to 0.92

    Patients chest pain* (n)

    66,695 23,389 43,306

    Female

    34.5% 34.0% 34.7% 0.97 0.94 to 1.00

    STEMI

    24,450 12,062 12,388

    Female

    32.4% 32.3% 32.4% 0.99 0.94 to 1.05

    NSTEMI

    42,245 11,327 30,918

    Female

    35.7% 35.8% 35.7% 1.01 0.96 to 1.05

    Patients atypical symptoms* (n)

    11,799 1,487 10,312

    Female

    45.9% 45.1% 46.0% 0.96 0.86 to 1.08

    STEMI

    2,030 363 1,667

    Female

    46.3% 43.0% 47.0% 0.85 0.68 to 1.07

    NSTEMI

    9,769 1,124 8,645

    Female

    45.9% 45.8% 45.9% 1.00 0.88 to 1.13

    STEMI, ST-elevation myocardial infarction; NSTEMI, non ST-elevation myocardial infarction Crude odds ratios (OR) with 95% confidence intervals (CI) were calculated by logistic regression analysis. *Patients with missing information on presenting symptoms were deleted.

    Conflict of Interest:

    None declared

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