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BACKGROUND: While left ventricular ejection fraction (LVEF) is the primary variable utilized for prognosis following myocardial infarction (MI), it is relatively indiscriminate for survival in patients with mildly reduced (> 40%) or preserved LVEF (> 50%). Improving risk stratification in patients with mildly reduced or preserved LVEF remains an unmet need, and could be achieved by using a combination approach using prognostically validated measures of left-ventricular (LV) size, geometry, and function. AIMS: The aim of this study was to compare the prognostic utility of a Combined Echo-Score for predicting all-cause (ACM) and cardiac mortality (CM) following MI to LVEF alone, including the sub-groups with LVEF > 40% and LVEF > 50%. METHODS: Retrospective data on 3094 consecutive patients with MI from 2013 to 2021 who had inpatient echocardiography were included, including both patients with ST-elevation MI (n = 869 [28.1%]) and non-ST-elevation MI (n = 2225 [71.9%]). Echo-Score consisted of LVEF < 40% (2 points) or LVEF < 50% (1 point), and 1 point each for left atrial volume index > 34 mL/m2, septal E/e' > 15, abnormal LV mass-index, tricuspid regurgitation velocity > 2.8 m/s, and abnormal LV end-systolic volume-index. Simple addition was used to derive a score out of 7. RESULTS: At a median follow-up of 4.5 years there were 445 deaths (130 cardiac deaths). On Cox proportional-hazards multivariable analysis incorporating significant clinical and echocardiographic predictors, Echo-Score was an independent predictor of both ACM (HR 1.34, p < .001) and CM (HR 1.59, p < .001). Inter-model comparisons of model 𝛘2, Harrel's C and Somer's D, and Receiver operating curves confirmed the superior prognostic value of Echo-Score for both endpoints compared to LVEF. In the subgroups with LVEF > 40% and LVEF > 50%, Echo-Score was similarly superior to LVEF for predicting ACM and CM. CONCLUSIONS: An Echo-Score composed of prognostically validated LV parameters is superior to LVEF alone for predicting survival in patients with MI, including the subgroups with mildly reduced and preserved LVEF. This could lead to improved patient risk stratification, better-targeted therapies, and potentially more efficient use of device therapies. Further studies should be considered to define the benefit of further investigation and treatment in high-risk subgroups.

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BACKGROUND: Historically, differences in timely reperfusion and outcomes have been described in females who suffer ST-segment elevation myocardial infarction (STEMI). However, there have been improvements in the treatment of STEMI patients with contemporary Percutaneous Coronary Intervention (PCI) strategies. METHODS: Comparisons between sexes were performed on STEMI patients treated with primary PCI over a 4-year period (January 1, 2017-December 31, 2020) from the Queensland Cardiac Outcomes Registry. Primary outcomes were 30-day and 1-year cardiovascular mortality. Secondary outcomes were STEMI performance measures. The total and direct effects of gender on mortality outcomes were estimated using logistic and multinomial logistic regression models. RESULTS: Overall, 2747 (76% male) were included. Females were on average older (65.9 vs. 61.9 years; p < 0.001), had longer total ischemic time (69 min vs. 52 min; p < 0.001) and less achievement of STEMI performance targets (<90 min) (50% vs. 58%; p < 0.001). There was no evidence for a total (odds ratio [OR] 1.3 (95% confidence interval [CI]: 0.8-2.2; p = 0.35) or direct (adjusted OR 1.2 (95% CI: 0.7-2.1; p = 0.58) effect of female sex on 30-day mortality. One-year mortality was higher in females (6.9% vs. 4.4%; p = 0.014) with total effect estimates consistent with increased risk of cardiovascular mortality (Incidence rate ratio [IRR]: 1.5; 95% CI: 1.0-2.3; p = 0.059) and noncardiovascular mortality (IRR: 2.1; 95% CI: 0.9-4.7; p = 0.077) in females. However, direct (adjusted) effect estimates of cardiovascular mortality (IRR: 1.0; 95% CI: 0.6-1.6; p = 0.94) indicated sex differences were explained by confounders and mediators. CONCLUSION: Small sex differences in STEMI performance measures still exist; however, with contemporary primary PCI strategies, sex is not associated with cardiovascular mortality at 30 days or 1 year.

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BACKGROUND: Adverse outcomes from moderate aortic stenosis (AS) may be caused by progression to severe AS or by the effects of comorbidities. In the absence of randomized trial evidence favoring aortic valve replacement (AVR) in patients with moderate AS, phenotyping patients according to risk may assist decision making. OBJECTIVES: This study sought to identify and validate clusters of moderate AS that may be used to guide patient management. METHODS: Unsupervised clustering algorithms were applied to demographics, comorbidities, and echocardiographic parameters in a training data set in patients with moderate AS (n = 2,469). External validation was obtained by assigning the defined clusters to an independent group with moderate AS (n = 1,358). The primary outcome, a composite of cardiac death, heart failure hospitalization, or aortic valve (AV) intervention after 5 years, was assessed between clusters in both data sets. RESULTS: Four distinct clusters-cardiovascular (CV)-comorbid, low-flow, calcified AV, and low-risk-with significant outcomes (log-rank P < 0.0001 in both data sets) were identified and replicated. The highest risk was in the CV-comorbid cluster (validation HR: 2.00 [95% CI: 1.54-2.59]; P < 0.001). The effect of AVR on cardiac death differed among the clusters. There was a significantly lower rate of outcomes after AVR in the calcified AV cluster (validation HR: 0.21 [95% CI: 0.08-0.57]; P = 0.002), but no significant effect on outcomes in the other 3 clusters. These analyses were limited by the low rate of AVR. CONCLUSIONS: Moderate AS has several phenotypes, and multiple comorbidities are the key drivers of adverse outcomes in patients with moderate AS. Outcomes of patients with noncalcified moderate AS were not altered by AVR in these groups. Careful attention to subgroups of moderate AS may be important to define treatable risk.

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Background Prehospital activation of the cardiac catheter laboratory is associated with significant improvements in ST-segment-elevation myocardial infarction (STEMI) performance measures. However, there are equivocal data, particularly within Australia, regarding its influence on mortality. We assessed the association of prehospital activation on performance measures and mortality in patients with STEMI treated with primary percutaneous coronary intervention from the Queensland Cardiac Outcomes Registry (QCOR). Methods and Results Consecutive ambulance-transported patients with STEMI treated with primary percutaneous coronary intervention were analyzed from January 1, 2017 to December 31, 2020 from the QCOR. The total and direct effects of prehospital activation on the primary outcomes (30-day and 1-year cardiovascular mortality) were estimated using logistic regression analyses. Secondary outcomes were STEMI performance measures. Among 2498 patients (mean age: 62.2±12.4 years; 79.2% male), 73% underwent prehospital activation. Median door-to-balloon time (34 minutes [26-46] versus 86 minutes [68-113]; P<0.001), first-electrocardiograph-to-balloon time (83.5 minutes [72-98] versus 109 minutes [81-139]; P<0.001), and proportion of patients meeting STEMI targets (door-to-balloon <60 minutes 90% versus 16%; P<0.001), electrocardiograph-to-balloon time <90 minutes (62% versus 33%; P<0.001) were significantly improved with prehospital activation. Prehospital activation was associated with significantly lower 30-day (1.6% versus 6.6%; P<0.001) and 1-year cardiovascular mortality (2.9% versus 9.5%; P<0.001). After adjustment, no prehospital activation was strongly associated with increased 30-day (odds ratio [OR], 3.6 [95% CI, 2.2-6.0], P<0.001) and 1-year cardiovascular mortality (OR, 3.0 [95% CI, 2.0-4.6]; P<0.001). Conclusions Prehospital activation of cardiac catheterization laboratory for primary percutaneous coronary intervention was associated with significantly shorter time to reperfusion, achievement of STEMI performance measures, and lower 30-day and 1-year cardiovascular mortality.

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Background: ST-segment elevation myocardial infarction (STEMI) is a common cause of out-of-hospital cardiac arrest (OHCA). For these patients, urgent angiography and revascularization is an important treatment goal. There is a lack of data on the prognosis of STEMI patients after OHCA, who are diagnosed and treated by paramedics prior to hospital transport for primary percutaneous coronary intervention (PCI). Methods: Included were adult STEMI patients identified and treated by paramedics in Queensland (Australia) from January 2016 to December 2019, transported to a hospital for primary PCI, and receiving primary PCI. Patients were grouped into those with resuscitated OHCA and those without OHCA. Clinically-important time intervals, angiographic and clinical profiles, and survival were described. Results: Patients with OHCA had longer time intervals from prehospital STEMI identification to reperfusion than those without OHCA (median 97 versus 87 mins, p = 0.001). The former had higher rates of cardiac arrhythmia history (50.5 versus 12.4%, p < 0.001), classified low left ventricular ejection fraction on admission (64.9 versus 50.1%, p = 0.006), and cardiogenic shock (5.2 versus 1.2%, p = 0.011) than the latter. A significantly higher proportion of patients with OHCA had multiple diseased vessels (16.9 versus 8.3%, p = 0.005). In-hospital, 30-day, and one-year mortality was low, being 4.1%, 4.1% and 5.2%, respectively, for STEMI patients with OHCA. The corresponding figures for those without OHCA were 1.6%, 1.8% and 3.3%, respectively. Conclusions: Survival in paramedic-identified STEMI patients treated with primary PCI following OHCA resuscitation was high. Rapid angiography and reperfusion are critical in these patients.

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BACKGROUND: Field identification and treatment of ST-segment elevation myocardial infarction (STEMI) by paramedics is an important component of care for these patients. There is a paucity of studies in the setting of paramedic-identified STEMI. This study investigated mortality and factors associated with mortality in a large state-wide prehospital STEMI sample. Methods: Included were adult STEMI patients identified and treated with reperfusion therapy by paramedics in the field between January 2016 and December 2018 in Queensland, Australia. 30-day and one-year all-cause mortality was compared between two prehospital reperfusion pathways: prehospital fibrinolysis versus direct referral to a hospital for primary percutaneous coronary intervention (direct percutaneous coronary intervention [PCI] referral). For prehospital fibrinolysis patients, factors associated with failed fibrinolysis were investigated. For direct PCI referral patients, factors associated with mortality were examined. Results: The 30-day mortality was 2.2% for prehospital fibrinolysis group and 1.8% for direct PCI referral group (p = 0.661). One-year mortality for the two groups was 2.7% and 3.2%, respectively (p = 0.732). Failed prehospital fibrinolysis was observed in 20.1% of patients receiving this therapy, with male gender and history of heart failure being predictors. For direct PCI referral group, low left ventricular ejection fraction (LVEF) on admission and cardiogenic shock prior to PCI were predictors of both 30-day and one-year mortality. Aboriginal and Torres Strait Islander status, and impaired kidney function on admission, were associated with one-year but not 30-day mortality. Being overweight was associated with lower 30-day mortality. Conclusions: Mortality in STEMI patients identified and treated by paramedics was low, and the prehospital fibrinolysis treatment pathway was effective with a mortality rate comparable to that of patients undergoing primary PCI. Key words: prehospital; Queensland; cardiac reperfusion; STEMI.

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Background: Field identification and treatment of ST-segment elevation myocardial infarction (STEMI) by paramedics is an important component of the continuum of care for these patients. This study described real-world clinical practice in prehospital management of STEMI patients in Queensland, Australia. Methods: Retrospective analysis of data sourced from the STEMI database of the Queensland Ambulance Service, Australia. Adult STEMI patients identified by paramedics between February 2008 and December 2018 in Queensland were included. Key aspects of prehospital STEMI care were described. Clinically-important time intervals from symptom onset to reperfusion were reported. Results: A total of 8,388 patients were included. The proportion of patients receiving prehospital reperfusion treatment has improved markedly, increasing from 34% in 2008 to 65% in 2018 (p < 0.001). Direct referral of patients to a hospital for primary percutaneous coronary intervention (pPCI), and administration of preparatory antiplatelet and anticoagulant medications, was the main reperfusion treatment pathway, accounting for 75% of patients receiving reperfusion treatment. Time from paramedic arrival at scene to first 12-lead electrocardiogram has significantly reduced, from 11 minutes in 2008 to 6 minutes from 2012 onwards (p < 0.001). Median (interquartile range, IQR) time from prehospital STEMI identification to reperfusion was 88 (74-103) minutes for patients referred by paramedics to a hospital for pPCI. Fifty-five percent of patients who underwent pPCI achieved time from STEMI identification to reperfusion within 90 minutes. For patients receiving prehospital fibrinolysis, median (IQR) time from STEMI identification to administration of a fibrinolytic agent was 21 (12-33) minutes. Conclusion: The implementation of a statewide prehospital reperfusion strategy has markedly improved the rate of prehospital reperfusion treatment and key time metrics. Ongoing quality improvement efforts are required to further reduce delays in reperfusion.

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BACKGROUND: Right ventricular (RV) function assumes prognostic significance in various disease states, but RV geometry is not amenable to volumetric assessment by two-dimensional echocardiography. Intra-ventricular pressure rate of rise (dP/dt) predicts myocardial contractility and adjusting for the maximal regurgitant velocity (Vmax) corrects for preload. We examined the relationship of noninvasive tricuspid dP/dt and dP/dt/Vmax with RV ejection fraction (RVEF) by cardiac magnetic resonance imaging (CMR) as a measure of RV function. METHODS: Fifty CMRs and echocardiograms performed within 30 days were included. Tricuspid regurgitation (TR) spectral Doppler trace was analyzed offline. TR dP/dt was calculated using simplified Bernoulli equation (dP/dt between 1 and 2 m/sec). dP/dt/Vmax was calculated as a ratio of dP/dt and TR Vmax . RV end-diastolic (EDV) and end-systolic volumes (ESV) were obtained from contouring of steady-state-free precession axial stack CMR images; RVEF was calculated as [(RVEDV - RVESV)/RVEDV] × 100. RVEF >42% was considered normal. RESULTS: Majority of studies were suitable for analysis. Median age was 48 years (IQR = 36-63); 56.4% were female (n = 22/39). There was correlation between dP/dt and RVEF (r(2) = 0.51, P < 0.01) which improved with dP/dt/Vmax (r(2) = 0.59, P < 0.01). dP/dt >400 mmHg/sec had a positive predictive value of 91%, sensitivity and specificity of 74% and 84% respectively for normal RVEF. Inter-observer agreement and repeatability analysis showed no significant difference. CONCLUSION: Tricuspid dP/dt correlates well with CMR RVEF. A dP/dt of more than 400 mmHg/sec strongly predicts normal RVEF. Adjusting for preload (dP/dt/Vmax) further improves this correlation.

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OBJECTIVE: To optimise an echocardiographic estimation of pulmonary vascular resistance (PVR(e)) for diagnosis and follow-up of pulmonary hypertension (PHT). DESIGN: Cross-sectional study. SETTING: Tertiary referral centre. PATIENTS: Patients undergoing right heart catheterisation and echocardiography for assessment of suspected PHT. METHODS: PVR(e) ([tricuspid regurgitation velocity ×10/(right ventricular outflow tract velocity-time integral+0.16) and invasive PVR(i) ((mean pulmonary artery systolic pressure-wedge pressure)/cardiac output) were compared in 72 patients. Other echo data included right ventricular systolic pressure (RVSP), estimated right atrial pressure, and E/e' ratio. Difference between PVR(e) and PVR(i) at various levels of PVR was sought using Bland-Altman analysis. Corrected PVR(c) ((RVSP-E/e')/RVOT(VTI)) (RVOT, RV outflow time; VTI, velocity time integral) was developed in the training group and tested in a separate validation group of 42 patients with established PHT. RESULTS: PVR(e)>2.0 had high sensitivity (93%) and specificity (91%) for recognition of PVR(i)>2.0, and PVR(c) provided similar sensitivities and specificities. PVR(e) and PVR(i) correlated well (r=0.77, p<0.01), but PVR(e) underestimated marked elevation of PVR(i)-a trend avoided by PVR(c). PVR(c) and PVR(e) were tested against PVR(i) in a separate validation group (n=42). The mean difference between PVR(e) and PVR(i) exceeded that between PVR(c) and PVR(i) (2.8±2.7 vs 0.8±3.0 Wood units; p<0.001). A drop in PVR(i) by at least one SD occurred in 10 patients over 6 months; this was detected in one patient by PVR(e) and eight patients by PVR(c) (p=0.002). CONCLUSION: PVR(e) distinguishes normal from abnormal PVR(i) but underestimates high PVR(i). PVR(c) identifies the severity of PHT and may be used to assess treatment response.

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