'Unable to have a proper conversation over the phone about my concerns': a multimethods evaluation of the impact of COVID-19 on routine childhood vaccination services in London, UK.

OBJECTIVES: Investigating the completion rate of 12-month vaccinations and parental perspectives on vaccine services during COVID-19. STUDY-DESIGN: Service evaluation including parental questionnaire. METHODS: Uptake of 12-month vaccinations in three London general practices during three periods: pre-COVID (1/3/2018-28/2/2019, n = 826), during COVID (1/3/2019-28/2/2020, n = 775) and post-COVID first wave (1/8/2020-31/1/2021, n = 419). Questionnaire of parents whose children were registered at the practices (1/4/2019-1/22/2021, n = 1350). RESULTS: Comparing pre-COVID and both COVID cohorts, the completion rates of 12-month vaccines were lower. Haemophilus influenzae type B/meningococcal group C (Hib/MenC) vaccination uptake was 5.6% lower (89.0% vs 83.4%, P=<0.001), meningococcal group B (MenB) booster uptake was 4.4% lower (87.3% vs 82.9%, P = 0.006), pneumococcal conjugate vaccine (PCV) booster uptake was 6% lower (88.0% vs 82.0%, P < 0.001) and measles, mumps and rubella (MMR) vaccine uptake was 5.2% lower (89.1% vs 83.9%, P = 0.003). Black/Black-British ethnicity children had increased odds of missing their 12-month vaccinations compared to White ethnicity children (adjusted odds ratio 0.43 [95% confidence interval 0.24-0.79, P = 0.005; 0.36 [0.20-0.65], P < 0.001; 0.48 [0.27-0.87], P = 0.01; 0.40 [0.22-0.73], P = 0.002; for Hib/MenC, MenB booster, PCV booster and MMR. Comparing pre-COVID and COVID periods, vaccinations coded as not booked increased for MMR (10%), MenB (7%) and PCV booster (8%). Parents reported changes to vaccination services during COVID-19, including difficulties booking and attending appointments and lack of vaccination reminders. CONCLUSION: A sustained decrease in 12-month childhood vaccination uptake disproportionally affected Black/Black British ethnicity infants during the first wave of the pandemic. Vaccination reminders and availability of healthcare professionals to discuss parental vaccine queries are vital to maintaining uptake.

Making a move in exercise referral: co-development of a physical activity referral scheme.

Background: Translational research is required to ensure exercise referral schemes (ERSs) are evidence-based and reflect local needs. This article reports process data from the co-development phase of an ERS, providing an insight into (i) factors that must be considered when translating evidence to practice in an ERS setting, and (ii) challenges and facilitators of conducting participatory research involving multiple stakeholders. Methods: An ERS was iteratively co-developed by a multidisciplinary stakeholder group (commissioners, managers, practitioners, patients and academics) via five participatory meetings and an online survey. Audio data (e.g. group discussions) and visual data (e.g. whiteboard notes) were recorded and analysed using NVivo-10 electronic software. Results: Factors to consider when translating evidence to practice in an ERS setting included (i) current ERS culture; (ii) skills, safety and accountability; and (iii) resources and capacity. The co-development process was facilitated by needs-analysis, open questions, multidisciplinary debate and reflective practice. Challenges included contrasting views, irregular attendance and (mis)perceptions of evaluation. Conclusion: The multidisciplinary co-development process highlighted cultural and pragmatic issues related to exercise referral provision, resulting in an evidence-based intervention framework designed to be implemented within existing infrastructures. Further work is required to establish the feasibility and effectiveness of the co-developed intervention in practice.

Image-based closed-loop feedback for highly mono-dispersed microdroplet production.

Micron-scale droplets isolated by an immiscible liquid can provide miniaturised reaction vessels which can be manipulated in microfluidic networks, and has seen a rapid growth in development. In many experiments, the precise volume of these microdroplets is a critical parameter which can be influenced by many external factors. In this work, we demonstrate the combination of imaging-based feedback and pressure driven pumping to accurately control the size of microdroplets produced in a microfluidic device. The use of fast-response, pressure-driving pumps allows the microfluidic flow to be quickly and accurately changed, while directly measuring the droplet size allows the user to define the more meaningful parameters of droplet size and generation frequency rather than flow rates or pressures. The feedback loop enables the drift correction of pressure based pumps, and leads to a large increase in the mono-dispersity of the droplets produced over long periods. We also show how this can be extended to control multiple liquid flows, allowing the frequency of droplet formation or the average concentration of living cells per droplet to be controlled and kept constant.

High-throughput screening of antibiotic-resistant bacteria in picodroplets.

The prevalence of clinically-relevant bacterial strains resistant to current antibiotic therapies is increasing and has been recognized as a major health threat. For example, multidrug-resistant tuberculosis and methicillin-resistant Staphylococcus aureus are of global concern. Novel methodologies are needed to identify new targets or novel compounds unaffected by pre-existing resistance mechanisms. Recently, water-in-oil picodroplets have been used as an alternative to conventional high-throughput methods, especially for phenotypic screening. Here we demonstrate a novel microfluidic-based picodroplet platform which enables high-throughput assessment and isolation of antibiotic-resistant bacteria in a label-free manner. As a proof-of-concept, the system was used to isolate fusidic acid-resistant mutants and estimate the frequency of resistance among a population of Escherichia coli (strain HS151). This approach can be used for rapid screening of rare antibiotic-resistant mutants to help identify novel compound/target pairs.

The practical use of surface electromyography during running: does the evidence support the hype? A narrative review.

BACKGROUND/AIMS: Surface electromyography (sEMG) is a commonly used technique to investigate muscle activation and fatigue, which is non-invasive and can allow for continuous measurement. Systematic research on the use of sEMG in the sporting environment has been on-going for many years and predominantly based on cycling and rowing activities. To date there have been no reviews assessing the validity and reliability in sEMG exclusively in running activities specifically during on-field testing. The purpose of this review is to evaluate the use of sEMG in the practical context and whether this be translated to on-field testing. METHODS: Electronic literature searches were performed using the Cochrane Library, PUBMED, CINAHL and PeDro without restrictions on the study date to identify the relevant current English language literature. RESULTS: 10 studies were relevant after title and content review. All the studies identified were all level three evidence based. The general trends of the sEMG activity appear to correlate with running velocity and muscle fatigue seems almost always the consequence of prolonged, dynamic activity. However, these changes are not consistently measured or statistically significant throughout the studies raising the question of the accuracy and reliability when analysing sEMG measurements and making assumptions about the cause of fatigue. CONCLUSIONS: An agreed consensus when measuring and analysing sEMG data during running activities particularly in field testing with the most appropriate study design and reliable methodology is yet to be determined and further studies are required.

Impact of heating on passive and active biomechanics of suspended cells.

A cell is a complex material whose mechanical properties are essential for its normal functions. Heating can have a dramatic effect on these mechanical properties, similar to its impact on the dynamics of artificial polymer networks. We investigated such mechanical changes by the use of a microfluidic optical stretcher, which allowed us to probe cell mechanics when the cells were subjected to different heating conditions at different time scales. We find that HL60/S4 myeloid precursor cells become mechanically more compliant and fluid-like when subjected to either a sudden laser-induced temperature increase or prolonged exposure to higher ambient temperature. Above a critical temperature of 52 ± 1°C, we observed active cell contraction, which was strongly correlated with calcium influx through temperature-sensitive transient receptor potential vanilloid 2 (TRPV2) ion channels, followed by a subsequent expansion in cell volume. The change from passive to active cellular response can be effectively described by a mechanical model incorporating both active stress and viscoelastic components. Our work highlights the role of TRPV2 in regulating the thermomechanical response of cells. It also offers insights into how cortical tension and osmotic pressure govern cell mechanics and regulate cell-shape changes in response to heat and mechanical stress.

Prevalence of bronchoconstriction induced by eucapnic voluntary hyperpnoea in recreationally active individuals.

OBJECTIVE: Exercise-induced bronchoconstriction (EIB) is more prevalent in elite athletes than in the general population. Many of these athletes provide a positive eucapnic voluntary hyperpnoea (EVH) challenge without previous diagnosis of EIB. It is unknown whether this is specific to elite athletes or whether the same risk applies to recreationally active individuals. The purpose of this study was to investigate the prevalence of a positive EVH challenge in a population of recreationally active individuals. METHODS: 136 recreationally active individuals (Age: 21.9 ± 3.7 years; Height: 175 ± 9 cm; Weight: 70.9 ± 10.0 kg) without previous history of asthma or EIB, volunteered to take part in the study. All participants completed an EVH challenge, which was deemed positive if FEV1 fell ≥10% from baseline at two consecutive time points, and was reversible following inhalation of a short acting ß2-agonist. RESULTS: 18 of 136 (13.2%) participants had a positive EVH challenge. Of the 18 individuals, the fall in FEV1 from baseline ranged from -12% to -50%. At baseline, percentage predicted FEV1 (97.5 ± 12.5% versus 104.9 ± 10%; p < 0.01), FEV1/FVC ratio (79.5 ± 6.9% versus 87.8 ± 5.5%; p < 0.01), FEF25-75 (3.73 ± 1.00 versus 4.73 ± 1.00 l/s; p < 0.01) and predicted PEF (89.4 ± 8.8% versus 97.5 ± 13.6%; p < 0.05) values for EVH positive participants were significantly lower than EVH negative participants respectively. CONCLUSIONS: Overall, 13.2% of recreationally active individuals with no previous history of asthma presented with a positive EVH challenge. Individuals who are recreationally active may benefit from an objective bronchial provocation challenge, given that self-reported symptoms alone only provide a supportive role towards a valid EIB diagnosis.

Cardiac electromechanical delay is increased during recovery from 40 km cycling but is not mediated by exercise intensity.

Cardiac electrical-mechanical delay (cEMD), left ventricular (LV) function, and cardiac troponin I (cTnI) were assessed after 40 km cycle time trials completed at high (HIGH) and moderate (MOD) intensities in 12 cyclists. Echocardiograms and blood samples were collected before, 10, and 60 min after cycling. cEMD as assessed by time from QRS onset to peak systolic (S') tissue velocity was lengthened after both bouts of cycling but was not mediated by cycling intensity (HIGH: 174 ± 52 vs 198 ± 26 ms; MOD: 151 ± 40 vs 178 ± 52 ms, P < 0.05). Global LV systolic function was unaltered by exercise. cEMD from QRS to peak early (E') diastolic tissue velocity was also increased post-exercise (HIGH: 524 ± 95 vs 664 ± 68 ms; MOD: 495 ± 62 vs 604 ± 91 ms, P < 0.05). Indices of LV diastolic function was reduced after cycling but were not mediated by exercise intensity. cTnI was elevated in two participants after HIGH trial (0.06 ug/L; 0.04 ug/L) and one participant after MOD trial (0.02 ug/L). While cEMD is lengthened and LV diastolic function was reduced post-cycling, altering time-trial intensity had little impact upon cEMD, LV function, and cTnI release.

Do the effects of high intensity 40 km cycling upon left ventricular function and cardiac biomarker during recovery vary with time of day?

Twelve healthy participants performed two identical high-intensity 40 km cycling trials (morning and evening) under controlled laboratory conditions. Echocardiograms and venous blood samples were collected before and after each exercise bout. Cardiac electro-mechanical-delay (cEMD) was measured as QRS-complex onset to peak systolic (S') and early diastolic (E') tissue velocities. Myocardial strain and strain rates were assessed in longitudinal, circumferential and radial planes at the left ventricular apex and base. Cardiac troponin I (cTnI) and N-terminal Pro-Brain Natriuretic Peptide (NT-proBNP) were assessed as biomarkers of cardiomyocyte damage and wall stress. cEMD was lengthened after both morning (S': 160 ± 30 vs. 193 ± 27; E': 478 ± 60 vs. 620 ± 87, P < 0.05) and evening (S': 155 ± 29 vs. 195 ± 31; E': 488 ± 42 vs. 614 ± 61, P < 0.05) trials. A reduction in peak S' (morning: 6.96 ± 1.12 vs. 6.66 ± 0.89; evening: 7.09 ± 0.94 vs. 7.02 ± 0.76) was correlated with cEMD (r = -0.335, P < 0.05). Peak longitudinal strain was reduced, atrial strain rates were sporadically increased in both trials post-cycling. cTnI was elevated in only two participants (0.04 µg · L(-1), 0.03 µg · L(-1)), whilst NT-proBNP was below the clinical cut-off point in all participants. Prolonged-cycling resulted in a lengthening of cEMD, small changes in aspects of left ventricular deformation and sporadic increases in cardiac biomarkers. None of these effects were moderated by time-of-day.

Significance of deep T-wave inversions in asymptomatic athletes with normal cardiovascular examinations: practical solutions for managing the diagnostic conundrum.

Preparticipation screening programmes for underlying cardiac pathologies are now commonplace for many international sporting organisations. However, providing medical clearance for an asymptomatic athlete without a family history of sudden cardiac death (SCD) is especially challenging when the athlete demonstrates particularly abnormal repolarisation patterns, highly suggestive of an inherited cardiomyopathy or channelopathy. Deep T-wave inversions of ≥ 2 contiguous anterior or lateral leads (but not aVR, and III) are of major concern for sports cardiologists who advise referring team physicians, as these ECG alterations are a recognised manifestation of hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC). Subsequently, inverted T-waves may represent the first and only sign of an inherited heart muscle disease, in the absence of any other features and before structural changes in the heart can be detected. However, to date, there remains little evidence that deep T-wave inversions are always pathognomonic of either a cardiomyopathy or an ion channel disorder in an asymptomatic athlete following long-term follow-up. This paper aims to provide a systematic review of the prevalence of T-wave inversion in athletes and examine T-wave inversion and its relationship to structural heart disease, notably HCM and ARVC with a view to identify young athletes at risk of SCD during sport. Finally, the review proposes clinical management pathways (including genetic testing) for asymptomatic athletes demonstrating significant T-wave inversion with structurally normal hearts.

Quantification of hypercoagulable state after blunt trauma: microparticle and thrombin generation are increased relative to injury severity, while standard markers are not.

BACKGROUND: Major trauma is an independent risk factor for developing venous thromboembolism. While increases in thrombin generation and/or procoagulant microparticles have been detected in other patient groups at greater risk for venous thromboembolism, such as cancer or coronary artery disease, this association has yet to be documented in trauma patients. This pilot study was designed to characterize and quantify thrombin generation and plasma microparticles in individuals early after traumatic injury. METHODS: Blood was collected in the trauma bay from 52 blunt injured patients (cases) and 19 uninjured outpatients (controls) and processed to platelet poor plasma to allow for (1) isolation of microparticles for identification and quantification by flow cytometry, and (2) in vitro thrombin generation as measured by calibrated automatic thrombography. Data collected are expressed as either mean ± standard deviation or median with interquartile range. RESULTS: Among the cases, which included 39 men and 13 women (age, 40 ± 17 years), the injury severity score was 13 ± 11, the international normalized ratio was 1.0 ± 0.1, the thromboplastin time was 25 ± 3 seconds, and platelet count was 238 ± 62 (thousands). The numbers of total (cell type not specified) procoagulant microparticles, as measured by Annexin V staining, were increased compared to nontrauma controls (541 ± 139/µL and 155 ± 148/µL, respectively; P < .001). There was no significant difference in the amount of thrombin generated in trauma patients compared to controls; however, peak thrombin was correlated to injury severity (Spearman correlation coefficient R, 0.35; P = .02). CONCLUSION: Patients with blunt trauma have greater numbers of circulating procoagulant microparticles and increased in vitro thrombin generation. Future studies to characterize the cell-specific profiles of microparticles and changes in thrombin generation kinetics after traumatic injury will determine whether microparticles contribute to the hypercoagulable state observed after injury.

Measurement of shear-activated platelet aggregate formation in non-anticoagulated blood: utility in detection of clopidogrel-aspirin-induced platelet dysfunction.

We studied the ability of a new instrument, the PlaCor PRT that measures shear-induced platelet aggregation in fingerstick, non-anticoagulated blood without added agonists, to detect platelet dysfunction ex vivo. Platelet reactivity time (PRT) and whole blood aggregation (WBA) were measured in 160 healthy volunteers, before and after aspirin and in 170 participants with established vascular disease or risk factors thereof treated with aspirin ± clopidogrel. Pretreatment PRT and WBA were significantly correlated (collagen r = -.63; arachidonate r = -.65; P < .0001). Following aspirin, the mean PRT increased from 82 to 142 seconds (P < .0001), and in participants treated with clopidogrel-aspirin, the mean PRT (286 seconds, n = 65) was significantly longer than with aspirin alone (166 seconds, n = 105; P < .001). Only 13% of PRTs of participants treated with clopidogrel and aspirin were within the normal range. We conclude that the PlaCor PRT is a simple, rapid, point-of-care instrument that compares favorably with published descriptions of other platelet function instruments.

Methodology for isolation, identification and characterization of microvesicles in peripheral blood.

RATIONALE: Analyses of circulating cell membrane-derived microvesicles (MV) have come under scrutiny as potential diagnostic and prognostic biomarkers of disease. However, methods to isolate, label and quantify MV have been neither systematized nor validated. OBJECTIVE: To determine how pre-analytical, analytical and post-analytical factors affect plasma MV counts, markers for cell of origin and expression of procoagulant surface phosphatidylserine. METHODS AND RESULTS: Peripheral venous blood samples were collected from healthy volunteers and patients with cardiovascular disease and/or diabetes. Effects of blood sample collection, anticoagulant and sample processing to platelet free plasma (PFP), and MV isolation, staining and storage (freeze-thaw) and cytometer design were evaluated with replicate samples from these populations. The key finding is that use of citrate or EDTA anticoagulants decreases or eliminates microvesicles from plasma by inducing adhesion of the microvesicles to platelets or other formed elements. Protease inhibitor anticoagulants, including heparin, preserve MV counts. A centrifugation protocol was developed in which recovery of isolated MV was high with resolution down to the equivalent light scatter of 0.2 µm latex beads. Each procedure was systematically evaluated for its impact on the MV counts and characteristics. CONCLUSION: This study provides a systematic methodology for MV isolation, identification and quantification, essential for development of MV as diagnostic and prognostic biomarkers of disease.

Prevalence of electrocardiographic abnormalities in West-Asian and African male athletes.

OBJECTIVES: To evaluate the electrocardiographic (ECG) characteristics of West-Asian, black and Caucasian male athletes competing in Qatar using the 2010 recommendations for 12-lead ECG interpretation by the European Society of Cardiology (ESC). DESIGN: Cardiovascular screening with resting 12-lead ECG analysis of 1220 national level athletes (800 West-Asian, 300 black and 120 Caucasian) and 135 West-Asian controls was performed. RESULTS: Ten per cent of athletes presented with 'uncommon' ECG findings. Black African descent was an independent predictor of 'uncommon' ECG changes when compared with West-Asian and Caucasian athletes (p<0.001). Black athletes also demonstrated a significantly greater prevalence of lateral T-wave inversions than both West-Asian and Caucasian athletes (6.1% vs 1.6% and 0%, p<0.05). The rate of 'uncommon' ECG changes between West-Asian and Caucasian athletes was comparable (7.9% vs 5.8%, p>0.05). Seven athletes (0.6%) were identified with a disease associated with sudden death; this prevalence was two times higher in black athletes than in West-Asian athletes (1% vs 0.5%), and no cases were reported in Caucasian athletes and West-Asian controls. Eighteen West-Asian and black athletes were identified with repolarisation abnormalities suggestive of a cardiomyopathy, but ultimately, none were diagnosed with a cardiac disease. CONCLUSION: West-Asian and Caucasian athletes demonstrate comparable rates of ECG findings. Black African ethnicity is positively associated with increased frequencies of 'uncommon' ECG traits. Future work should examine the genetic mechanisms behind ECG and myocardial adaptations in athletes of diverse ethnicity, aiding in the clinical differentiation between physiological remodelling and potential cardiomyopathy or ion channel disorders.

A unique case series of novel biomarkers of cardiac damage in cyclists completing the 4800 km Race Across America (RAAM).

Prolonged strenuous exercise is associated with the appearance of biomarkers of cardiac cell damage and a decline in cardiac function during recovery. Few studies have assessed repeated bouts of prolonged exercise and whether this results in further biomarker accumulation and greater dysfunction. Further, it may be useful to describe the changes in a range of biomarkers that may provide additional insight into the clinical significance of cardiac biomarker release. Four highly trained cyclists completed the 4800 km Race Across America (RAAM) in 7 days. Venous blood samples and echocardiograms were taken prior to, every 24 hours during and immediately after the RAAM. Venous blood was analysed for cardiac troponin I (cTnI), creatine kinase MB (CK-MB), fatty acid binding protein (HFABP), glycogen phosphorylase BB (GPBB) and N-Terminal Brain Natriuretic Peptide (NTproBNP). Echocardiograms allowed analysis of septal, left ventricular free wall and right ventricular free wall tissue velocities during systole and diastole. Before the RAAM cTnI levels were below the assay detection level (0.02 ng.ml⁻¹). In three riders cTnI peaked on day one (0.03 ng.ml⁻¹) and returned below detection levels post race. In the 4th rider cTnI peaked on day 5 (0.08 ng.ml⁻¹) and was still elevated post-race. Both CK-MB and H-FABP were increased during the RAAM in all 4 cyclists. In three riders H-FABP peaked on day one (3.49 to 5.09 ng.ml⁻¹) and declined over the rest of the RAAM. In the final rider H-FABP peaked on day two (5.90 ng.ml⁻¹) and then dropped back to baseline by the post-RAAM assessment. Interestingly, changes in H-FABP mirrored, temporally, changes in CK-MB in places and this may reflect an association with skeletal muscle damage. Data for GPBB value to (2.9 - 149.6 ng.ml⁻¹) and NTproBNP value to (27.3 - 310.0 ng.L⁻¹) were variable but again was elevated in all riders during the course of the RAAM. Changes in ventricular wall tissue velocities were minor and not cumulative. Peak atrial diastolic tissue velocity in the left ventricular free wall increased (P < 0.05) from 11 to 18 cm.s⁻¹ over the last two race days but this did not significantly impact the ratio of early to late diastolic wall motion. Cardiac biomarkers were elevated during the completion of the RAAM in all 4 cyclist but changes were not cumulative which suggest that the hearts of the cyclists coped well with the extreme cardiac work demanded by this ultra-endurance exercise challenge.

Alterations in platelet function and cell-derived microvesicles in recently menopausal women: relationship to metabolic syndrome and atherogenic risk.

A woman's risk for metabolic syndrome (MS) increases at menopause, with an associated increase in risk for cardiovascular disease. We hypothesized that early menopause-related changes in platelet activity and concentrations of microvesicles derived from activated blood and vascular cells provide a mechanistic link to the early atherothrombotic process. Thus, platelet functions and cellular origin of blood-borne microvesicles in recently menopausal women (n = 118) enrolled in the Kronos Early Estrogen Prevention Study were correlated with components of MS and noninvasive measures of cardiovascular disease [carotid artery intima medial thickness (CIMT), coronary artery calcium (CAC) score, and endothelial reactive hyperemic index (RHI)]. Specific to individual components of the MS pentad, platelet number increased with increasing waist circumference, and platelet secretion of ATP and expression of P-selectin decreased with increasing blood glucose (p = 0.005) and blood pressure (p < 0.05), respectively. Waist circumference and systolic blood pressure were independently associated with monocyte- and endothelium-derived microvesicles (p < 0.05). Platelet-derived and total procoagulant phosphatidylserine-positive microvesicles, and systolic blood pressure correlated with CIMT (p < 0.05), but not with CAC or RHI. In summary, among recently menopausal women, specific platelet functions and concentrations of circulating activated cell membrane-derived procoagulant microvesicles change with individual components of MS. These cellular changes may explain in part how menopause contributes to MS and, eventually, to cardiovascular disease.

Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes.

This study examined the cardiac structure and function of a unique cohort of documented lifelong, competitive endurance veteran athletes (>50 yr). Twelve lifelong veteran male endurance athletes [mean ± SD (range) age: 56 ± 6 yr (50-67)], 20 age-matched veteran controls [60 ± 5 yr; (52-69)], and 17 younger male endurance athletes [31 ± 5 yr (26-40)] without significant comorbidities underwent cardiac magnetic resonance (CMR) imaging to assess cardiac morphology and function, as well as CMR imaging with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Lifelong veteran athletes had smaller left (LV) and right ventricular (RV) end-diastolic and end-systolic volumes (P < 0.05), but maintained LV and RV systolic function compared with young athletes. However, veteran athletes had a significantly larger absolute and indexed LV and RV end-diastolic and systolic volumes, intraventricular septum thickness during diastole, posterior wall thickness during diastole, and LV and RV stroke volumes (P < 0.05), together with significantly reduced LV and RV ejection fractions (P < 0.05), compared with veteran controls. In six (50%) of the veteran athletes, LGE of CMR indicated the presence of myocardial fibrosis (4 veteran athletes with LGE of nonspecific cause, 1 probable previous myocarditis, and 1 probable previous silent myocardial infarction). There was no LGE in the age-matched veteran controls or young athletes. The prevalence of LGE in veteran athletes was not associated with age, height, weight, or body surface area (P > 0.05), but was significantly associated with the number of years spent training (P < 0.001), number of competitive marathons (P < 0.001), and ultraendurance (>50 miles) marathons (P < 0.007) completed. An unexpectedly high prevalence of myocardial fibrosis (50%) was observed in healthy, asymptomatic, lifelong veteran male athletes, compared with zero cases in age-matched veteran controls and young athletes. These data suggest a link between lifelong endurance exercise and myocardial fibrosis that requires further investigation.

Underlying cause discovered for a prior idiopathic AMI.

The authors previously reported on an active, young male with normal coronaries who sustained an acute myocardial infarction (AMI). The acute cause was a coronary thrombus; however, the cause of this thrombus and a definitive diagnosis remained elusive for 18 months until a new series of events, including symptoms of breathlessness, dizziness and collapse led to acute hospital admission. CT scan revealed numerous deep venous thromboses in the right leg and bilateral pulmonary emboli (PE). Acute pharmacological thrombolysis eliminated breathlessness and significantly reduced the risk of mortality. Clinical consensus suggests a coagulopathy, requiring indefinite treatment with Warfarin. In young individuals presenting with AMI, lifestyle, personal, family and clinical history should be considered and coronary artery disease should not be assumed until further tests have eliminated coagulopathy. In those presenting with breathlessness and a history which includes AMI, a CT scan is indicated to eliminate concerns of venous thromboembolism generally and PE specifically where untreated survival times are short.

Biological markers of cardiac damage are not related to measures of cardiac systolic and diastolic function using cardiovascular magnetic resonance and echocardiography after an acute bout of prolonged endurance exercise.

OBJECTIVES: Seventeen male participants (mean (SD) (range): age 33.5 (6.5) years (46-26 years), body mass 80 (9.2) kg (100-63 kg), height 1.81 (0.06) m (1.93- 1.70 m)) ran a marathon to investigate the relationship between systolic function (using cardiac magnetic resonance (CMR)) and diastolic function (using echocardiography) against biomarkers of cardiac damage. METHODS: Echocardiographic and cardiac troponin I (cTnI)/N-terminal pro-B-type natriuretic peptide (NTproBNP) data were collected 24 h premarathon, immediately postmarathon and 6 h postmarathon. CMR data were collected 24 h premarathon and at 6 h postmarathon. RESULTS: Body mass was significantly reduced postmarathon (80 (9.2) vs 78.8 (8.6) kg; p<0.001). There was a significant E/A reduction postmarathon (1.11 (0.34) vs 1.72 (0.44); p<0.05) that remained depressed 6 h postmarathon (1.49 (0.43); p<0.05). CMR demonstrated left ventricular end-diastolic and end-systolic volumes were reduced postmarathon, with a preserved stroke volume. Left ventricular ejection fraction 6 h postmarathon significantly increased (64.4% (4.2%) vs 67.4% (5%); p<0.05). There were significant elevations in cTnI (0.00 vs 0.04 (0.03) µg/l; p<0.05) and NTproBNP (37.4 (24.15) ng/l vs 59.34 (43.3) ng/l; p<0.05) immediately postmarathon. Eight runners had cTnI elevations immediately postmarathon above acute myocardial infarction cutoff levels (≥0.03 µg/l). No correlations between cTnI/NTproBNP and measures of diastolic function (E, A, E/A, isovolumic relaxation time, E deceleration time and E/E') or measures of systolic function (stroke volume or ejection fraction) were observed immediately postmarathon or 6 h postmarathon. CONCLUSIONS: Biomarkers of cardiac damage after prolonged exercise are not associated with either systolic or diastolic functional measures.