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Soft materials are usually defined as materials made of mesoscopic entities, often self-organised, sensitive to thermal fluctuations and to weak perturbations. Archetypal examples are colloids, polymers, amphiphiles, liquid crystals, foams. The importance of soft materials in everyday commodity products, as well as in technological applications, is enormous, and controlling or improving their properties is the focus of many efforts. From a fundamental perspective, the possibility of manipulating soft material properties, by tuning interactions between constituents and by applying external perturbations, gives rise to an almost unlimited variety in physical properties. Together with the relative ease to observe and characterise them, this renders soft matter systems powerful model systems to investigate statistical physics phenomena, many of them relevant as well to hard condensed matter systems. Understanding the emerging properties from mesoscale constituents still poses enormous challenges, which have stimulated a wealth of new experimental approaches, including the synthesis of new systems with, e.g. tailored self-assembling properties, or novel experimental techniques in imaging, scattering or rheology. Theoretical and numerical methods, and coarse-grained models, have become central to predict physical properties of soft materials, while computational approaches that also use machine learning tools are playing a progressively major role in many investigations. This Roadmap intends to give a broad overview of recent and possible future activities in the field of soft materials, with experts covering various developments and challenges in material synthesis and characterisation, instrumental, simulation and theoretical methods as well as general concepts.

Background: Advances in treatment for acute myocardial infarction (AMI) are likely to have had a beneficial impact on the incidence of and deaths attributable to heart failure (HF) complicating AMI, although limited data are available to support this contention.Methods and Results: Western Australian linked administrative health data were used to identify 20 812 consecutive patients, aged 40 to 84 years, without prior HF hospitalized with an index (first) AMI between 1996 and 2007. We assessed the temporal incidence of and adjusted odds ratio/hazard ratio for death associated with HF concurrent with AMI admission and within 1 year after discharge. Concurrent HF comprised 75% of incident HF cases. Between the periods 1996–1998 and 2005–2007, the prevalence of HF after AMI declined from 28.1% to 16.5%, with an adjusted odds ratio of 0.50 (95% CI, 0.44 to 0.55). The crude 28-day case-fatality rate for patients with concurrent HF declined marginally from 20.5% to 15.9% (P<0.05) compared with those without concurrent HF, in whom the case-fatality rate declined from 11.0% to 4.8% (P<0.001). Concurrent HF was associated with a multivariate-adjusted odds ratio of 2.2 for 28-day mortality and a hazard ratio of 2.2 for 1-year mortality in 28-day survivors. Occurrence of HF within 90 days of the index AMI was associated with an adjusted hazard ratio of 2.7 for 1-year mortality in 90-day survivors.Conclusions: Despite encouraging declines in the incidence of HF complicating AMI, it remains a common problem with high mortality. Increased attention to these high-risk patients is needed given the lack of improvement in their long-term prognosis.

Background: We investigated the relationship between Aboriginality and 2-year cardiovascular disease outcomes in non-fatal first-ever myocardial infarction during 2000–04, with progressive adjustment of covariates, including comorbidities. Design: Historical cohort study. Methods: Person-linked hospital and mortality records were used to identify 28-day survivors of first-ever myocardial infarction in Western Australia during 2000–04 with 15-year lookback. The outcome measures were: (1) cardiovascular disease death; (2) recurrent admission for myocardial infarction; and (3) the composite of (1) and (2). Results: Compared with non-Aboriginal patients, Aboriginals were younger and more likely to live remotely. The proportions having 5-year histories of diabetes and chronic kidney disease were double and triple those of non-Aboriginals. When adjusting for demographic variables alone, the Aboriginal to non-Aboriginal hazard ratios for cardiovascular death or recurrent myocardial infarction were 3.6 (95% CI 2.5–5.3) in men and 4.5 (95% CI 2.8–7.3) in women. After adjustment for comorbidities, including diabetes, chronic kidney disease and heart failure, the hazard ratios decreased 36% and 47% to 2.3 (1.6–3.0) and 2.4 (1.5–4.0) in males and females, respectively. Conclusions: The high prevalence of comorbidities in Aboriginal people, including diabetes, kidney disease, heart failure, and other risk factors contribute substantially to the disparity in post-myocardial infarction outcomes in Aboriginal people, reinforcing the importance of both primary prevention and comprehensive management of chronic conditions in this population. Aboriginality remains a significant independent risk factor for disease recurrence or mortality, even after adjusting for comorbidity, suggesting the need for society-level interventions addressing social disadvantage.

Background: Troponins (highly sensitive biomarkers of myocardial damage) increase counts of myocardial infarction (MI) in clinical practice, but their impact on trends in admission rates for MI in National statistics is uncertain. Methods: Cases coded as MI or other cardiac diagnoses in the Hospital Morbidity Data Collection (MI-HMDC) in Western Australia in 1998 and 2003 were classified using revised criteria for MI developed by an International panel convened by the American Heart Association (AHA criteria) using information on symptoms, ECGs and cardiac biomarkers abstracted from samples of medical notes. Age-sex standardized rates of MI-HMDC were compared with rates of MI based on AHA criteria including troponins (MI-AHA) or traditional biomarkers only (MI-AHAck). Results: Between 1998 and 2003, rates of MI-HMDC decreased by 3.5% whereas rates of MI-AHA increased by 17%, a difference largely due to increased false-negative cases in the HMDC associated with marked increased use of troponin tests in cardiac admissions generally, and progressively lower test thresholds. In contrast, rates of MIAHAck declined by 18%. Conclusions: Increasing misclassification of MI-AHA by the HMDC may be due to reluctance by clinicians to diagnose MI based on relatively small increases in troponin levels. These influences are likely to continue. Monitoring MI using AHA criteria will require calibration of commercially available troponin tests and agreement on lower diagnostic thresholds for epidemiological studies. Declining rates of MI-AHAck are consistent with longstanding trends in MI in Western Australia, suggesting that neither MI-HMDC nor MI-AHA reflect the true underlying population trends in MI.

Background. Measuring the real burden of cardiovascular disease in Australian Aboriginals is complicated by under-identification of Aboriginality in administrative health data collections. Accurate data is essential to measure Australia's progress in its efforts to intervene to improve health outcomes of Australian Aboriginals. We estimated the under-ascertainment of Aboriginal status in linked morbidity and mortality databases in patients hospitalised with cardiovascular disease. Methods. Persons with public hospital admissions for cardiovascular disease in Western Australia during 2000-2005 (and their 20-year admission history) or who subsequently died were identified from linkage data. The Aboriginal status flag in all records for a given individual was variously used to determine their ethnicity (index positive, and in all records both majority positive or ever positive) and stratified by region, age and gender. The index admission was the baseline comparator.Results. Index cases comprised 62,692 individuals who shared a total of 778,714 hospital admissions over 20 years, of which 19,809 subsequently died. There were 3,060 (4.9%) persons identified as Aboriginal on index admission. An additional 83 (2.7%) Aboriginal cases were identified through death records, increasing to 3.7% when cases with a positive Aboriginal identifier in the majority (≥50%) of previous hospital admissions over twenty years were added and by 20.8% when those with a positive flag in any record over 20 years were incorporated. These results equated to underestimating Aboriginal status in unlinked index admission by 2.6%, 3.5% and 17.2%, respectively. Deaths classified as Aboriginal in official records would underestimate total Aboriginal deaths by 26.8% (95% Confidence Interval 24.1 to 29.6%). Conclusions. Combining Aboriginal determinations in morbidity and official death records increases ascertainment of unlinked cardiovascular morbidity in Western Australian Aboriginals. Under-identifi

Background. Despite Coronary Heart Disease exacting a heavy toll among Aboriginal Australians, accurate estimates of its epidemiology are limited. This study compared the incidence of acute myocardial infarction (AMI) and 28-day case fatality (CF) among Aboriginal and non-Aboriginal Western Australians aged 25–74 years from 2000–2004. Methods. Incident (AMI hospital admission-free for 15 years) AMI events and 28-day CF were estimated using person-based linked hospital and mortality data. Age-standardised incidence rates and case fatality percentages were calculated by Aboriginality and sex.Results. Of 740 Aboriginal and 6933 non-Aboriginal incident events, 208 and 2352 died within 28 days, respectively. The Aboriginal age-specific incidence rates were 27 (males) and 35 (females) times higher than non-Aboriginal rates in the 25–29 year age group, decreasing to 2–3 at 70–74 years. The male:female age-standardised incidence rate ratio was 2.2 in Aboriginal people 25–54 years compared with 4.5 in non-Aboriginal people. Aboriginal age-standardised CF percentages were 1.4 (males) and 1.1 (females) times higher at age 25–54 years and 1.5 times higher at age 55–74 years. Conclusion. These data suggest higher CF and, more importantly, AMI incidence contribute to the excess ischaemic heart disease mortality in Aboriginal Western Australians. The poorer cardiovascular health in Aboriginal women, particularly in younger age groups, should be investigated.

Objectives. To investigate the impact of prevalence correction of population denominators on myocardial infarction (MI) incidence rates, rate ratios, and rate differences in Aboriginal vs. non-Aboriginal Western Australians aged 25–74 years during the study period 2000–2004.Study Design and Setting. Person-based linked hospital and mortality data sets were used to estimate the number of prevalent and first-ever MI cases each year from 2000 to 2004 using a 15-year look-back period. Age-specific and -standardized MI incidence rates were calculated using both prevalence-corrected and -uncorrected population denominators, by sex and Aboriginality.Results. The impact of prevalence correction on rates increased with age, was higher for men than women, and substantially greater for Aboriginal than non-Aboriginal people. Despite the systematic underestimation of incidence, prevalence correction had little impact on the Aboriginal to non-Aboriginal age-standardized rate ratios (6% and 4% underestimate in men and women, respectively), although the impact on rate differences was more marked (12% and 6%, respectively). The percentage underestimate of differentials was greater at older ages. Conclusion. Prevalence correction of denominators, while more accurate, is difficult to apply and may add modestly to the quantification of relative disparities in MI incidence between populations. Absolute incidence disparities using uncorrected denominators may have an error >10%.