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Background Despite being recommended in acute coronary syndrome (ACS) guidelines, the use of invasive management within specific risk groups continues to be debated. This study examines the change in the use of invasive management in ACS by patient risk and the associated change in mortality within Australia over the last 17 years. Methods Pooled cohorts derived from five ACS registries (ACACIA, CONCORDANCE, GRACE, Snapshot-ACS, and Predict) spanned from 1999 to 2015. After excluding patients without a final diagnosis of ACS (n = 4460), enrolled outside Australia (n = 1477) and without an enrolling year (n = 4), 15 912 patients were analysed. Data was stratified across three time periods (1999–2004, 2005–2009, and 2010–2015) using clinical risk characteristics (age, ACS diagnosis, biomarker elevation, and GRACE score) to monitor change in practice. Results Over the 17-year period, the use of invasive management increased (4073/6863 (59.3%) cases [1999–2009] vs. 6670/8706 (76.6%) cases [2010–2015]). Invasive management accounted for improvements in mortality in intermediate- and high-risk groups (intermediate risk: 14% (95% CI 1–66%) [1999–2009] vs. 49% (95% CI 2–59%) [2010–2015]; high risk: 24% (95% CI 6–42%) [1999–2009] vs. 48% (95% CI 19–76%) [2010–2015]). Patients receiving no angiography compared with interventional management had worse outcomes (1999–2004 1.55 HR [95% CI 1.36–1.80], P < 0.0001 vs. 2010–2015 1.90 HR [95% CI 1.45–2.51], P < 0.0001). Conclusions Clinical practice in ACS has changed over the last 17 years with positive outcomes seen with invasive management among high-risk patients. Unfortunately, a considerable burden of mortality remains in patients managed medically, highlighting a need for more focused strategies that improve care and outcomes in this group.

The index of microcirculatory resistance (IMR), an invasive measure of microvascular function, has been shown to correlate with clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). The aim of this study is to evaluate the predictive value of IMR on left ventricular recovery in patients undergoing a pharmacoinvasive strategy for STEMI.The index of microcirculatory resistance was assessed following percutaneous coronary intervention (PCI) in 31 patients with STEMI who were initially managed with thrombolysis. Other markers of microvascular function such as coronary flow reserve (CFR), TIMI flow grade, corrected TIMI frame count (cTFC), and ST-segment resolution were also recorded. All indices were evaluated against measures of left ventricular function and recovery 3 months postindex event.The IMR correlated with left ventricular function, as assessed by wall motion score and ejection fraction at 3-month follow-up (r = 0.652, P = 0.005; r = -0.452, P = 0.011, respectively). The traditional methods of assessing microvascular function, such as CFR, TIMI flow grade, cTFC, and ST-segment resolution did not correlate with wall motion score and ejection fraction at 3 months. Post-PCI IMR was significantly lower in those patients with left ventricular recovery at 3 months (18 U vs 39 U, P 0.001). The optimal cut-off value for post-PCI IMR and left ventricular recovery was 32 U. In patients in whom the IMR was greater than 32 U, the percent change in ejection fraction was significantly lower than in those patients in whom the IMR was less than 32 U (2 ± 11 vs 12 ± 8, P = 0.012).In patients presenting with STEMI initially managed with thrombolysis and subsequently undergoing PCI, IMR correlates with measures of left ventricular function and has the potential to predict left ventricular recovery at 3 months.

The burden of cardiovascular disease for Indigenous people in Australia and New Zealand is high and reflects the failings of our health care system to meet their needs. Improving the hospital care for Indigenous people is critical in improving health outcomes. This paper provides the results from a facilitated discussion on the disparities in acute hospital care and workforce issues. The workshop was held in Alice Springs, Australia at the second Cardiac Society of Australia and New Zealand (CSANZ) Indigenous Cardiovascular Health Conference. Critical issues to be addressed include: addressing systemic racism; reconfiguring models of care to address the needs of Indigenous people; cultural competence training for all health professionals; increasing participation of Indigenous people in the health workforce; improving information systems and facilitating communication across the health care sector and with Indigenous communities. © 2012 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ).

BACKGROUND Variation in the provision of coronary angiography is associated with health care inefficiency and inequity. We explored geographic, socio-economic, health service and disease indicators associated with variation in angiography rates across Australia. METHODS Australian census and National Health Survey data were used to determine socio-economic, health workforce and service indicators. Hospital separations and coronary deaths during 2011 were identified in the National Hospital Morbidity and Mortality databases. All 61 Medicare Locals responsible for primary care were included, and age- and sex-standardised rates of acute coronary syndrome (ACS) incidence, coronary angiography, revascularisation and mortality were tested for correlations, and adjusted by Bayesian regression. RESULTS There were 3.7-fold and 2.3-fold differences between individual Medicare Locals in the lowest and highest ACS and coronary artery disease mortality rates respectively, whereas angiography rates varied 5.3-fold. ACS and death rates within Medicare Locals were correlated (partial correlation coefficient [CC], 0.52; P

Aims Endurance training may be associated with arrhythmogenic cardiac remodelling of the right ventricle (RV). We examined whether myocardial dysfunction following intense endurance exercise affects the RV more than the left ventricle (LV) and whether cumulative exposure to endurance competition influences cardiac remodelling (including fibrosis) in well-trained athletes. Methods and results Forty athletes were studied at baseline, immediately following an endurance race (3–11 h duration) and 1-week post-race. Evaluation included cardiac troponin (cTnI), B-type natriuretic peptide, and echocardiography [including three-dimensional volumes, ejection fraction (EF), and systolic strain rate]. Delayed gadolinium enhancement (DGE) on cardiac magnetic resonance imaging (CMR) was assessed as a marker of myocardial fibrosis. Relative to baseline, RV volumes increased and all functional measures decreased post-race, whereas LV volumes reduced and function was preserved. B-type natriuretic peptide (13.1 ± 14.0 vs. 25.4 ± 21.4 ng/L, P = 0.003) and cTnI (0.01 ± .03 vs. 0.14 ± .17 μg/L, P < 0.0001) increased post-race and correlated with reductions in RVEF ( r = 0.52, P = 0.001 and r = 0.49, P = 0.002, respectively), but not LVEF. Right ventricular ejection fraction decreased with increasing race duration ( r = −0.501, P < 0.0001) and VO2max ( r = −0.359, P = 0.011). Right ventricular function mostly recovered by 1 week. On CMR, DGE localized to the interventricular septum was identified in 5 of 39 athletes who had greater cumulative exercise exposure and lower RVEF (47.1 ± 5.9 vs. 51.1 ± 3.7%, P = 0.042) than those with normal CMR. Conclusion Intense endurance exercise causes acute dysfunction of the RV, but not the LV. Although short-term recovery appears complete, chronic structural changes and reduced RV function are evident in some of the most practiced athletes, the long-term clinical significance of which warrants further study.

Pre-participation screening of all competitive athletes is recommended in some countries and mandated in others to prevent sudden cardiac death in predisposed athletes. Whilst the prevalence of some conditions, which are screened for such as coronary artery anomalies and long QT syndromes, are stable across different populations, the prevalence of underlying conditions such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia shows considerable geographic variability. Evidence exists that screening reduces sudden death, but the potential negative impact of exclusion from sport has not been quantified. Australia has a high rate of participation in sport and needs to consider whether screening is feasible, effective and affordable. It is difficult to make this decision currently as there is little information about the scope of the problem in Australia and whether the prevalence of underlying conditions which predispose to sudden cardiac death is similar or different to that in other countries. We review the evidence for and against screening and propose that systematic collection of Australian data is required before routine pre-participation screening can be introduced in Australia.

Objective To measure cognition in patients before and after coronary angiography. Design Prospective observational cohort study. Setting University teaching hospital. Patients 56 patients presenting for elective coronary angiography. Main outcome measures Computerised cognitive test battery administered before coronary angiography, before discharge from hospital and 7 days after discharge. A matched healthy control group was used as a comparator. Results When analysed by group, coronary angiography patients performed worse than matched controls at each time point. When the cognitive change was examined for each individual, of the 48 patients tested at discharge, 19 (39.6%) were classified as having a new cognitive dysfunction, and of 49 patients tested at day 7, six (12.2%) were classified as having a new cognitive dysfunction. Conclusions The results confirm that cognitive function is decreased in patients who have cardiovascular disease. Furthermore, coronary angiography may exacerbate this impaired cognition in some patients.

BACKGROUND: Quantification of left ventricular torsion may provide new indices of systolic and diastolic function. We sought to characterize the effect of acute manipulation of load on cardiac torsion, plecotropy in human subjects. METHODS: Simultaneous Millar LV pressure, micromanometry, and echocardiograms were performed on 18 patients (10 male, mean age 66 years) with normal systolic function. Loading was altered sequentially by the administration of glyceryl trinitrate (GTN) and saline fluid loading. Echocardiographic speckle tracking imaging was used to quantify LV torsion and event timing was recorded relative to mitral valve opening (MVO). RESULTS: GTN administration decreased preload (LV end diastolic pressure: 15.7 vs 8.4 mmHg, P < 0.001), and afterload (wall stress: 140 vs 84 x10(3)dyn/cm(2), P < 0.02). Administration of fluid increased preload (LVEDP 11.3 vs 18.1 mmHg, P < 0.001) and increased wall stress, but to a lesser extent (102 vs 117 x10(3)dyn/cm(2), P < 0.003). GTN administration augmented peak torsion (8.4 vs 11.0 deg, P < 0.05), increased systolic torsion velocity (46.6 vs 65.3deg/sec, P < 0.01) and resulted in earlier onset of untwisting (-105 vs -127ms, P < 0.05). Fluid loading decreased the proportion of untwisting prior to MVO (39.0 vs 31.0%, P < 0.05), untwisting acceleration (-750 vs -592deg/sec/sec, P < 0.05) and delayed the timing of peak untwisting (-37.0 vs 9.1ms, P < 0.01), but did not affect systolic torsion parameters. CONCLUSIONS: Left ventricular torsion parameters are sensitive to acute changes in load and therefore need to be interpreted in the context of current loading conditions.

Recent data suggests hospitals fail to meet guideline specified time to PCI for a proportion of STEMI presentations. Implicit in achieving this time is the rapid assembly of crucial catheter laboratory staff. As proof of concept, we integrated traffic congestion data, distance to destination, and

We report two cases of late occurring drug-eluting stent thrombosis (ST) where coronary angiography failed to identify the cause but intravascular ultrasound (IVUS) revealed underlying mechanical problems with the initial stent deployment. Mechanical factors such as stent underexpansion and residual edge stenoses may be more important in the pathogenesis of late drug-eluting ST than previously recognized. Intravascular ultrasound is required to reliably detect these problems and optimize subsequent reintervention.

ObjectivesWe sought to establish the relationship between invasive measures of diastolic function and untwisting parameters measured with speckle tracking imaging.BackgroundLeft ventricular (LV) diastolic function is determined by early diastolic relaxation (which creates suction gradients for LV filling) and myocardial stiffness. Assessment of LV torsion has shown that untwisting begins before aortic valve closure and, in animals, might be an important component of normal diastolic filling. Studies in human subjects using indirect indexes derived from right heart catheterization have suggested a relationship between τ and measures of untwisting, but the relationship between directly measured diastolic function indexes with micromanometer catheters and untwisting parameters has not been established in human subjects.MethodsSimultaneous Millar micromanometer LV pressure and echocardiographic assessment was performed on 18 patients (10 male, mean age 66 years) with normal systolic function and a spectrum of diastolic function. Invasive rate of the rise of LV pressure, dp/dt minimum and τ were recorded as measures of active relaxation, and the LV minimum diastolic pressure was recorded as an index of diastolic suction. The LV stiffness constant and functional chamber stiffness were estimated from hybrid pressure-volume loops. Echocardiographic speckle tracking imaging was used to quantify torsion.ResultsAs relaxation was impaired, (prolonged τ) untwisting was delayed (r = 0.35, p < 0.01). There were nonsignificant associations between reduced untwisting and longer values of τ and lower dp/dt minimum. Reduction in the extent of untwisting before mitral valve opening was associated with increased LV minimum diastolic pressure (r = −0.30, p < 0.034). No relation was observed between the LV stiffness constant (β: r = 0.11, p = NS) or the functional LV chamber stiffness (b: r = 0.11, p = NS) and untwisting.ConclusionsUntwisting parameters are related to invasive indexes of LV relaxation and suction but not to LV stiffness. These data suggest that untwisting is an important component of early diastolic LV filling but not later diastolic events.

Background: There is a paucity of data on outcomes in patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) caused by left main stem (LMS) thrombosis. Objectives: We sought to determine (i) the clinical features, (ii) correlates of early mortality, and (iii) long-term outcomes in contemporary patients undergoing primary PCI for unprotected LMS thrombosis. Methods: From 1,115 consecutive primary PCI cases at two tertiary referral centers between January 2004 and September 2007, 28 cases (2.5%) with unprotected LMS culprit lesions were identified. Data were obtained from review of institutional databases, folder audit, telephone survey of patients, and independent review of angiograms. Results: The mean age of patients was 68 ± 14 years. Males comprised 76%, and 21% had diabetes. Significant morbidity was noted at presentation: shock in 18 (62%), pulmonary oedema in 15 (52%), and cardiac arrest in 10 (35%) patients, respectively. Lesion location was ostial in 7 (25%), body in 8 (29%), and distal in 13 (46%) patients, respectively. Angiographic success was achieved in 24 patients (83%). Stents were deployed in 27 patients (96%); drug-eluting stents in 11 patients (39%). No patient required in-hospital CABG. Cumulative in-hospital mortality was 36%. Univariate predictors of in-hospital mortality included shock, preceding cardiac arrest, and angiographic failure (all P < 0.05). At a mean follow-up of 26 ± 12 months in hospital survivors, there were two TVR (elective CABGs), one death, and no reinfarctions. Conclusion: We report a lower than previously reported in-hospital mortality of 36% in contemporary patients undergoing primary PCI for unprotected LMS thrombosis. Long-term outcomes in hospital survivors appear favorable. © 2009 Wiley-Liss, Inc.

There is evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death.To quantify the extent and duration of post-exercise cardiac injury with particular attention to right ventricular (RV) dysfunction.27 athletes (20 male, 7 female) were tested 1 week before, immediately after and 1 week after an ultra-endurance triathlon. Tests included cardiac troponin I (cTnI), B-type natriuretic peptide (BNP) and comprehensive echocardiographic assessment.26 athletes completed the race and testing procedures. Post-race, cTnI was raised in 15 athletes (58%) and the mean value for the entire cohort increased (0.17 vs 0.49 microg/l, p0.01). BNP rose in every athlete and the mean increased significantly (12.2 vs 42.5 ng/l, p0.001). Left ventricular ejection fraction (LVEF) was unchanged (60.4% vs 57.5%, p = 0.09), but integrated systolic strain decreased (16.9% vs 15.1%, p0.01). New regional wall motion abnormalities developed in seven athletes (27%) and LVEF was reduced in this subgroup (57.8% vs 45.9%, p0.001). RV function was reduced in the entire cohort with decreases in fractional area change (0.47 vs 0.39, p0.01) and tricuspid annular plane systolic excursion (21.8 vs 19.1 mm, p0.01). At follow-up, all variables returned to baseline except in one athlete where RV dysfunction persisted.Myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. Almost all abnormalities resolve within 1 week.

Left ventricular torsion, resulting from the rotation of the base and apex of the ventricle in opposite directions, may be an important component of normal cardiac function both at rest and with exercise. The effect of exercise on torsion in the general population and the influence of aging on changes in torsion with exercise are not known.Analysis of torsion, positive and negative torsion velocities, and negative torsion acceleration was performed using speckle tracking imaging on 33 stress echocardiograms using supine bicycle stress.Resting and postexercise torsion could be assessed in 14 patients (42%). A total of 19 patients who were significantly older and larger (mean age 57 years, mean body mass index 28.2, both P.03) were excluded as a result of inadequate frame rate and image quality after exercise. After exercise, significant increases in peak torsion (10.3 +/- 0.8 vs 13.3 +/- 1.3 degrees, P.04), peak positive torsion (54.2 +/- 5.6 vs 113.6 +/- 12.3 degrees/s, P.0001), and peak negative torsion (-56.3 +/- 7.9 vs -100.8 +/- 14.8 degrees/s, P.03) velocities were observed. Ejection fraction correlated with torsion both at rest and after exercise (r = 0.63, P.0004). At rest, torsion was greater in older individuals (8.9 +/- 0.6 vs 11.6 +/- 1.2 degrees, P.04). With increasing age, exercise resulted in less augmentation of torsion (r = 0.59, P.02) and positive torsion velocity (r = -0.79, P.003), and decreased negative torsional acceleration (r = 0.60, P.035).Exercise results in increased cardiac plecotropy (the augmentation of torsion parameters in response to load or stimulus) but this effect is attenuated with aging. Further investigation is required to determine whether impairment of plecotropy contributes to the reduced exercise capacity associated with aging.

Objectives The aim of the present study was to explore Aboriginal patients’ lived experiences of cardiac care at a major metropolitan hospital in Melbourne. Methods The study was a qualitative study involving in-depth interviews with a purposive sample of 10 Aboriginal patients who had been treated in the cardiology unit at the study hospital during 2012–13. A phenomenological approach was used to analyse the data. Results Eight themes emerged from the data, each concerning various aspects of participants’ experiences: ‘dislike of hospitals’, ‘system failures’, ‘engagement with hospital staff’, ‘experiences of racism’, ‘health literacy and information needs’, ‘self-identifying as Aboriginal’, ‘family involvement in care’ and ‘going home and difficulties adapting’. Most participants had positive experiences of the cardiac care, but hospitalisation was often challenging because of a sense of dislocation and disorientation. The stress of hospitalisation was greatly mediated by positive engagements with staff, but at times exacerbated by system failures or negative experiences. Conclusion Cardiac crises are stressful and hospital stays were particularly disorienting for Aboriginal people dislocated from their home land and community. What is known about the topic? Aboriginal people have higher mortality rates due to cardiovascular diseases compared with other Australians. Along with different factors contributing to the life expectancy gap, Aboriginal people also face significant barriers in the use of the healthcare system. What does this paper add? Aboriginal patients’ lived experience of cardiac care at a major metropolitan hospital in Melbourne is explored in this paper. Different issues were revealed during their interaction with the hospital staff and the hospital system in conjunction with their cultural aspect of patient care. What are the implications for practitioners? Positive interactions with staff, ongoing support from family and community, culturally appropriate cardiac rehabilitation programs can improve the cardiac care experiences of Aboriginal patients.

Methamphetamines are increasingly popular drugs of abuse in Australia, and are rising in purity. The rising popularity and purity of methamphetamines has notably increased demands upon Australian medical services. Methamphetamines are sympathomimetic amines with a range of adverse effects upon multiple organ systems. Cardiovascular complications are the second leading cause of death in methamphetamine abusers, and there appears to be a high prevalence of cardiac pathology. Cardiovascular pathology frequently seen in methamphetamine abusers includes hypertension, aortic dissection, acute coronary syndromes, pulmonary arterial hypertension and methamphetamine-associated cardiomyopathy. The rising prevalence of methamphetamine abuse is likely to increase the burden of cardiovascular pathology in Australians. A National Parliamentary Enquiry was opened in March 2015 to address concerns regarding the medical and social impacts of methamphetamine abuse. From April 2015, a National 'Ice Taskforce' was also created in parallel. Reversal of cardiac pathology appears to be achievable with abstinence from methamphetamines and initiation of appropriate treatment. It is key to appreciate that the pathogenesis of methamphetamine-induced cardiac complications arises as a result of the specific toxic effects of methamphetamines. Clinical management is hence individualised; suggested management approaches for methamphetamine-induced cardiac complications are detailed within this article.

Left ventricular diastolic dysfunction is a well-described complication of systemic hypertension. However, less is known regarding the effect of chronic pressure overload on right ventricular (RV) diastolic function. We hypothesized that pulmonary hypertension (PHT) is associated with abnormal RV early relaxation and that this would be best shown by invasive pressure measurement. Twenty-five patients undergoing right heart catheterization for investigation of breathlessness and/or suspected PHT were studied. In addition to standard measurements, RV pressure was sampled with a high-fidelity micromanometer, and RV pressure/time curves were analyzed. Patients were divided into a PHT group and a non-PHT group on the basis of a derived mean pulmonary artery systolic pressure of 25 mmHg. Eleven patients were classified to the PHT group. This group had significantly higher RV minimum diastolic pressure ([Formula: see text] vs. [Formula: see text] mmHg, [Formula: see text]) and RV end-diastolic pressure (RVEDP; [Formula: see text] vs. [Formula: see text] mmHg, [Formula: see text]), and RV τ was significantly prolonged ([Formula: see text] vs. [Formula: see text] ms, [Formula: see text]). There were strong correlations between RV τ and RV minimum diastolic pressure ([Formula: see text], [Formula: see text]) and between RV τ and RVEDP ([Formula: see text], [Formula: see text]). There was a trend toward increased RV contractility (end-systolic elastance) in the PHT group ([Formula: see text] vs. [Formula: see text] mmHg/mL, [Formula: see text]) and a correlation between RV systolic pressure and first derivative of maximum pressure change ([Formula: see text], [Formula: see text]). Stroke volumes were similar. Invasive measures of RV early relaxation are abnormal in patients with PHT, whereas measured contractility is static or increasing, which suggests that diastolic dysfunction may precede systolic dysfunction. Furthermore, there is a strong association between measures of RV relaxation and RV filling pressures.

The Cardiac Society of Australia and New Zealand (CSANZ) Position Statement describes evidence-based standards of training, pre-procedural assessment, procedural conduct and post-procedure care with respect to sedation for cardiovascular procedures. It also describes the environment in which sedation for electrophysiological and other cardiac procedures may be performed. This Statement was developed by a Working Group of the Cardiac Society of Australia and New Zealand. It was reviewed by the Continuing Education and Recertification Committee and ratified at the CSANZ Board meeting held on Friday 7 March 2014.

This issue of the Journal contains a Discussion Paper and two Commentaries arising from attempts to develop an Australian and New Zealand Position Statement on Myocardial Revascularisation [1–3]. Myocardial revascularisation is undoubtedly an important topic which has been the subject of a large amount of clinical and research data. In December 2014, a simple PubMed search for the phrases ‘‘myocardial revascularisation’’ and ‘‘clinical trial’’ returned 17494 publications. It is a difficult task to synthesise such a broad range of data from a vast variety of sources, especially where this involves applying group data to individual patients. The interpretation of the literature often varies between commentators who place a different emphasis on various clinical trials and the relative importance of their endpoints, even when data has been categorised by a standard level of evidence criteria such as those promulgated by the NH&MRC [4]. The interpretation of a scene is often dependent on the vantage point of the observer. When it comes to the publication of research, guidelines and policies, they are often presented with a conflict of interest statement, aimed at exposing the bias or prejudice of those reporting and interpreting the data. However, we all have our own innate biases and prejudices beyond those revealed by a financial or academic conflict of interest statement. As you read this editorial, it would be remiss of me not to inform you that I am a practicing Interventional Cardiologist and have devoted a considerable amount of my medical training and practice to percutaneous myocardial revascularisation. It would be reasonable to conclude that I would not have done so if I had not developed a belief that percutaneous interventions are of considerable benefit to the patients I treat. Similarly, it is reasonable to assume that a cardiac surgeon would not operate if he/she did not hold similar beliefs about the value

Abnormal motion of the interventricular septum (ASM), seen post cardiac operation, with left bundle branch block or right ventricular pacing, may affect septal mitral annular motion and correlation of the ratio between the velocity of early diastolic mitral inflow and the early diastolic mitral annular velocity (E/Ea) with pulmonary capillary wedge pressure (PCWP). We examined the effect of ASM on the relationship between E/Ea and E/Vp (propagation velocity of mitral inflow) ratios and PCWP in adult patients in the intensive care unit (14 with normal septal motion [NSM], 36 with ASM) undergoing echocardiography and pulmonary artery catheterization. E/Ea correlated well with PCWP during NSM ( r = 0.86 lateral annulus, r = 0.75 septal annulus), but poorly during ASM ( r = 0.36 lateral annulus, r = 0.39 septal annulus). E/Vp correlated poorly with PCWP ( r = 0.05 NSM, r = 0.17 ASM). For patients who are critically ill, E/Vp ratios poorly estimate PCWP. During NSM, E/Ea ratios measured at the lateral or septal annulus correlate well with PCWP. ASM affects E/Ea ratios at both the septal and lateral annulus, making E/Ea ratios unreliable for estimating PCWP in this group.

We present a case of takotsubo cardiomyopathy and demonstrate an initial elevation of microcirculatory resistance (IMR) that reduced on follow-up evaluation. This corresponded with improvements in left ventricular function. We postulate that the changes in microvascular resistance reflect favourable left ventricular microvascular remodelling. The measurement of IMR, a novel marker of microcirculatory dysfunction, provides novel insights into the pathophysiology of this condition.

Background Non-ST-segment elevation acute coronary syndromes include unstable angina and non-ST-segment elevation myocardial infarction. Most randomized controlled trials of routine versus selective invasive coronary angiography have high rates of crossover from control to intervention groups and do not include subgroup analysis for unstable angina. Consequently, no clear, specific recommendations exist regarding the use of angiography in unstable angina. Objective To assess the effect of angiography on mortality in unstable angina, incorporating the results of additional cardiac procedures and events. Design Longitudinal study using hospital discharge data, discrete-time survival analysis with propensity score adjustment, and sensitivity analysis. Setting Victoria, Australia, 2001 to 2011. Participants All residents, all ages. Intervention Routine invasive coronary angiography. Measurements 12-month all-cause mortality. Results Emergently admitted patients with unstable angina (n = 33 901) who did or did not receive angiography during their first hospitalization were balanced on 44 covariates of propensity score. Routine angiography was associated with a 52% decrease in 12-month mortality (hazard ratio, 0.48 [95% CI, 0.38 to 0.61]); revascularization offered no additional statistical mortality benefit compared with diagnostic angiography alone. The predicted cumulative probability of death at 12 months was 0.024 (CI, 0.021 to 0.027) for patients receiving angiography within 2 months of their index unstable angina versus 0.097 (CI, 0.090 to 0.105) for those not receiving it. Sensitivity analysis demonstrated that to negate the observed effect size, an unmeasured confounder must independently decrease mortality by 90% and have a prevalence gap of 15% or greater between the angiographic groups. Limitation Nonrandom allocation of angiography. Conclusion Patients with unstable angina benefit from an invasive management pathway initiated by invasive coronary angiography during their hospitalization and up to 2 months after discharge. Primary funding sources National Health and Medical Research Council, Australia and BUPA Health Foundation.

Objective The aim of the present study was to explore the association of health insurance status on the provision of guideline-advocated acute coronary syndrome (ACS) care in Australia. Methods Consecutive hospitalisations of suspected ACS from 14 to 27 May 2012 enrolled in the Snapshot study of Australian and New Zealand patients were evaluated. Descriptive and logistic regression analysis was performed to evaluate the association of patient risk and insurance status with the receipt of care. Results In all, 3391 patients with suspected ACS from 247 hospitals (23 private) were enrolled in the present study. One-third of patients declared private insurance coverage; of these, 27.9% (304/1088) presented to private facilities. Compared with public patients, privately insured patients were more likely to undergo in-patient echocardiography and receive early angiography; furthermore, in those with a discharge diagnosis of ACS, there was a higher rate of revascularisation (P

63-year-old woman has had 2 hospital admissions for central chest pain occurring in the setting of emotional stress over the last 11 years. Her other medical history included anxiety, hypertension, and dyslipidemia. At 52 years of age, she presented to the hospital with central chest pain after a major argument with her mother. An ECG demonstrated sinus rhythm with 1-mm ST-segment elevation in leads I and aVL. Her serum troponin I was mildly elevated at 0.63 μg/L (normal

Department of Cardiology, St. Vincent’s Hospital Melbourne, Victoria Parade, Fitzroy, Victoria, Australia 3065 Consultant Cardiologist, Department of Cardiology, St. Vincent’s Hospital Melbourne, Victoria Parade, Fitzroy, Victoria, Australia 3065 Consultant Cardiothoracic Surgeon, Department of Cardiothoracic Surgery, St. Vincent’s Hospital Melbourne, Victoria Parade, Fitzroy, Victoria, Australia 3065 Associate Professor, Director of Cardiology, St. Vincent’s Hospital Melbourne, Victoria Parade, Fitzroy, Victoria, Australia 3065

Acute coronary syndrome (ACS) contributes to the disparity in life expectancy between Aboriginal and non-Aboriginal Australians. Improving hospital care for Aboriginal patients has been identified as a means of addressing this disparity. This project developed and implemented a working together model of care, comprising an Aboriginal Hospital Liaison Officer and a specialist cardiac nurse, providing care coordination specifically directed at improving attendance at cardiac rehabilitation services for Aboriginal Australians in a large metropolitan hospital in Melbourne. A quality improvement framework using a retrospective case notes audit evaluated Aboriginal patients’ admissions to hospital and identified low attendance rates at cardiac rehabilitation services. A working together model of care coordination by an Aboriginal Hospital Liaison Officer and a specialist cardiac nurse was implemented to improve cardiac rehabilitation attendance in Aboriginal patients admitted with ACS to the cardiac wards of the hospital. A retrospective medical records audit showed that there were 68 Aboriginal patients admitted to the cardiac wards with ACS from 1 July 2008 to 30 June 2011. A referral to cardiac rehabilitation was recorded for 42% of these. During the implementation of the model of care, 13 of 15 patients (86%) received a referral to cardiac rehabilitation and eight of the 13 (62%) attended. Implementation of the working together model demonstrated improved referral to and attendance at cardiac rehabilitation services, thereby, has potential to prevent complications and mortality. What is known about the topic? Aboriginal Australians experience disparities in access to recommended care for acute coronary syndrome. This may contribute to the life expectancy gap between Aboriginal and non-Aboriginal Australians. What does this paper add? This paper describes a model of care involving an Aboriginal Hospital Liaisons Officer and a specialist cardiac nurse working together to improve hospital care and attendance at cardiac rehabilitation services for Aboriginal Australians with acute coronary syndrome. What are the implications for practitioners? The working together model of care could be implemented across mainstream health services where Aboriginal people attend for specialist care.

Myocardial infarction has a high rate of morbidity and mortality. There are major social, psychological and legal implications associated with the diagnosis of myocardial infarction (MI).We present three case studies of different chest pain syndromes presenting with serum troponin elevation, and use these cases to form the basis of a review of the updated definition of MI. A practical approach to the diagnosis of myocardial infarction is also discussed.The measurement of serum troponin levels was a great diagnostic advance and provided powerful prognostic information. Although elevated serum troponin levels were originally considered pathognomonic of MI, it has become clear that highly sensitive troponin assays detected the presence of elevated troponin levels in the absence of MI. This has led to the recent 'Third universal definition of myocardial infarction' consensus document.

Background— The use of fractional flow reserve in patients with non–ST-segment–elevation myocardial infarction (NSTEMI) is a controversial issue. We undertook a study to assess the vasodilatory capacity of the coronary microcirculation in patients with NSTEMI when compared with a model of preserved microcirculation (stable angina [SA] cohort: culprit and nonculprit vessel) and acute microcirculatory dysfunction (ST-segment–elevation myocardial infarction [STEMI] cohort). We hypothesized that the vasodilatory response of the microcirculation would be preserved in NSTEMI. Methods and Results— A total of 140 patients undergoing single vessel percutaneous coronary intervention were included: 50 stable angina, 50 NSTEMI, and 40 STEMI. The index of microvascular resistance (IMR), fractional flow reserve, and coronary flow reserve were measured before stenting in the culprit vessel and in an angiographically normal nonculprit vessel in patients with SA. The resistive reserve ratio, a measure of the vasodilatory capacity of the microcirculation and calculated using the equation: baseline resistance index ( Tmn Base × Pa Base [ Pd Base – Pw / Pa Base – Pw ])–IMR/IMR, where Tmn Base referred to nonhyperemic transit time; Pa Base and Pd Base , the nonhyperemic aortic and distal coronary pressures, respectively; and Pw referred to the coronary wedge pressure, was also measured. Troponin was also measured ≤24 hours after percutaneous coronary intervention. The resistive reserve ratio was significantly lower in the STEMI patients compared with the stable angina patients both culprit and nonculprit vessel (STEMI, 1.7 versus SA culprit, 2.8; P ≤0.001 and SA nonculprit, 2.9; P P ≤0.001). The resistive reserve ratio was similar in stable angina and NSTEMI patients ( P =0.6). IMR was significantly higher pre-PCI in STEMI compared with SA and NSTEMI (IMR STEMI, 36.51 versus IMR NSTEMI, 22.73 [ P =0.01] versus IMR SA, 18.26 [ P P =0.1]). Conclusions— The vasodilatory capacity of the microcirculation is preserved in selected patients with NSTEMI. The clinical use of fractional flow reserve in the culprit vessel may be preserved in selected patents with NSTEMI.

Background Basic fibroblast growth factor (bFGF) has been shown to reduce infarct size in canine acute myocardial infarction; however, the mechanism of tissue salvage remains uncertain. We evaluated the effect of bFGF on infarct size in a model of acute infarction in which coronary occlusion was followed by prolonged reperfusion and sought to determine whether reperfusion attenuates the stimulus for myocardial neovascularization. Methods and Results Anesthetized dogs undergoing 4-hour balloon occlusion of the left anterior descending coronary artery were treated with intracoronary bFGF (n=8) or vehicle (n=6). Ten-microgram doses of bFGF were administered 10 minutes after occlusion and again immediately before reperfusion. Left ventriculograms were obtained before occlusion, after reperfusion, and preceding euthanasia on day 7. Infarct size, expressed as a percentage of the area at risk, was reduced in bFGF-treated dogs (13.7±2.1% versus 28±3.4%; P =.002). Changes in left ventricular ejection fraction, capillary density, and cellular proliferation—assessed immunohistochemically with factor VIII and proliferating cell nuclear antigen antibodies—were similar in both groups. To assess coronary vasomotor responses to bFGF, a separate hemodynamic study was performed in five anesthetized nonischemic dogs in which incremental bFGF doses up to 100 μg induced no vasodilator response. Conclusions Treatment with bFGF was associated with a reduction in infarct size without hemodynamic effects or evidence of neovascularization. These data suggest that bFGF mediates myocardial salvage independently of angiogenesis and that reperfusion after infarction may attenuate the stimulus for neovascularization.