Search

Objectives Consent forms that are difficult to understand may jeopardize informed consent. The aim of this study was to determine whether consent documents for cardiology-related procedures could be easily read and understood by patients with low health literacy. Methods All 37 cardiology-related consent forms with patient information material were retrieved from a publicly available suite of documents from one state in Australia. Two raters independently assessed documents and resolved discrepancies through discussion. Understandability was assessed using the Patient Education Materials Assessment Tool for Printed materials (PEMAT-P). Readability was assessed using the Gunning Fog Index, SMOG and Flesch Reading Ease formulas. Images were assessed using the 5C Image checklist. Results were analyzed descriptively. Results Only 1 of 37 forms met the general PEMAT-P threshold (70%) for being ‘understandable’. The average readability score was high, requiring a grade 10–12 level of education to understand. Most images lacked useful captions, had low visual clarity, and were not purpose-designed for the material. Conclusions The current format for cardiology consent forms does not meet recommended standards for understandability and readability. Practice implications Development of consent forms would benefit from taking health literacy principles into account with patient input, and purpose-designed images should be included in all forms to reinforce text.

Background The linkage of primary care, hospital and other health registry data is a global goal, and a consent-based approach is often used. Understanding the attitudes of why participants take part is important, yet little is known about reasons for non-participation. The ATHENA COVID-19 feasibility study investigated: 1) health outcomes of people diagnosed with COVID-19 in Queensland, Australia through primary care health data linkage using consent, and 2) created a cohort of patients willing to be re-contacted in future to participate in clinical trials. This report describes the characteristics of participants declining to participate and reasons for non-consent. Methods Patients diagnosed with COVID-19 from January 1st, 2020, to December 31st, 2020, were invited to consent to having their primary healthcare data extracted from their GP into a Queensland Health database and linked to other data sets for ethically approved research. Patients were also asked to consent to future recontact for participation in clinical trials. Outcome measures were proportions of patients consenting to data extraction, permission to recontact, and reason for consent decline. Results 996 participants were approached and 853(86%) reached a consent decision. 581(69%), 623(73%) and 567(67%) consented to data extraction, recontact, or both, respectively. Mean (range) age of consenters and non-consenters were 50.6(range) and 46.1(range) years, respectively. Adjusting for age, gender and remoteness, older participants were more likely to consent than younger (aOR 1.02, 95%CI 1.01 to 1.03). The least socio-economically disadvantaged were more likely to consent than the most disadvantaged (aOR 2.20, 95% 1.33 to 3.64). There was no difference in consent proportions regarding gender or living in more remote regions. The main reasons for non-consent were ‘not interested in research’ (37%), ‘concerns about privacy’ (15%), ‘not registered with a GP’ (8%) and ‘too busy/no time’ (7%). ‘No reason’ was given in 20%. Conclusion Younger participants and the more socio-economically deprived are more likely to non-consent to primary care data linkage. Lack of patient interest in research, time required to participate and privacy concerns, were the most common reasons cited for non-consent. Future health care data linkage studies addressing these issues may prove helpful. Trial registration details: not applicable

Objective/background: Elevated arterial stiffness is a characteristic of abdominal aortic aneurysm (AAA), and is associated with AAA growth and cardiovascular mortality. A bout of exercise transiently reduces aortic and systemic arterial stiffness in healthy adults. Whether the same response occurs in patients with AAA is unknown. The effect of moderate- and higher intensity exercise on arterial stiffness was assessed in patients with AAA and healthy adults. Methods: Twenty-two men with small diameter AAAs (36 ± 5 mm; mean age 74 ± 6 years) and 22 healthy adults (mean age 72 ± 5 years) were included. Aortic stiffness was measured using carotid to femoral pulse wave velocity (PWV), and systemic arterial stiffness was estimated from the wave reflection magnitude (RM) and augmentation index (Alx75). Measurements were performed at rest and during 90 min of recovery following three separate test sessions in a randomised order: (i) moderate intensity continuous exercise; (ii) higher intensity interval exercise; or (iii) seated rest. Results: At rest, PWV was higher in patients with AAA than in healthy adults (p < .001), while AIx75 and RM were similar between groups. No differences were observed between AAA patients and healthy adults in post-exercise aortic and systemic arterial stiffness after either exercise protocol. When assessed as the change from baseline (delta, Δ), post-exercise ΔAIx75 was not different to the seated rest protocol. Conversely, post-exercise ΔPWV and ΔRM were both lower at all time points than seated rest (p < .001). ΔPWV was lower immediately after higher intensity than after moderate intensity exercise (p = .015). Conclusion: High resting aortic stiffness in patients with AAA is not exacerbated after exercise. There was a similar post-exercise attenuation in arterial stiffness between patients with AAA and healthy adults compared with seated rest. This effect was most pronounced following higher intensity interval exercise, suggesting that this form of exercise may be a safe and effective adjunctive therapy for patients with small AAAs.

Background: To date, there are limited Australian data on characteristics of people diagnosed with COVID-19 and on how these characteristics relate to outcomes. The ATHENA COVID-19 Study was established to describe health outcomes and investigate predictors of outcomes for all people diagnosed with COVID-19 in Queensland by linking COVID-19 notification, hospital, general practice and death registry data. This paper reports on the establishment and first findings for the ATHENA COVID-19 Study. Methods: Part 1 of the ATHENA COVID-19 Study used Notifiable Conditions System data from 1 January 2020 to 31 December 2020, linked to: Emergency Department Collection data for the same period; Queensland Health Admitted Patient Data Collections (from 1 January 2010 to 30 January 2021); and Deaths Registrations data (from 1 January 2020 to 17 January 2021). Results: To 31 December 2020, a total of 1,254 people had been diagnosed with SARS-CoV-2 infection in Queensland: half were female (49.8%); two-thirds (67.7%) were aged 20–59 years; and there was an over-representation of people living in less-disadvantaged areas. More than half of people diagnosed (57.6%) presented to an ED; 21.2% were admitted to hospital as an inpatient (median length of stay 11 days); 1.4% were admitted to an intensive care unit (82.4% of these required ventilation); and there were six deaths. Analysis of factors associated with these outcomes was limited due to small case numbers: people living in less-disadvantaged areas had a lower risk of being admitted to hospital (test for trend, p < 0.001), while those living in more remote areas were less likely than people living in major cities to present to an ED (test for trend: p=0.007), which may reflect differential health care access rather than health outcomes per se. Increasing age (test for trend, p < 0.001) and being a current/recent smoker (age-sex-adjusted relative risk: 1.61; 95% confidence interval: 1.00, 2.61) were associated with a higher risk of being admitted to hospital. Conclusion: Despite uncertainty in our estimates due to small numbers, our findings are consistent with what is known about COVID-19. Our findings reinforce the value of linking multiple data sources to enhance reporting of outcomes for people diagnosed with COVID-19 and provide a platform for longer term follow-up.

Stress echocardiography is an established cardiac imaging modality for the detection and quantification of severity of coronary artery disease. In recent years, there has also been an increasing use of stress echocardiography in the assessment of non-ischaemic cardiac disease given its ability to assess functional capacity and haemodynamic changes with exercise which can help guide therapy and inform prognosis. The emerging use of strain, myocardial contrast and three-dimensional (3D) echocardiography further assists in improving diagnostic accuracy particularly in patients with coronary artery disease. This paper summarises the protocols, indications and clinical applications of stress echocardiography in both ischaemic and non-ischaemic cardiac disease.

Purpose: Leg muscle microvascular blood flow (perfusion) is impaired in response to maximal exercise in patients with peripheral artery disease (PAD); however, during submaximal exercise, microvascular perfusion is maintained due to a greater increase in microvascular blood volume compared with that seen in healthy adults. It is unclear whether this submaximal exercise response reflects a microvascular impairment, or whether it is a compensatory response for the limited conduit artery flow in PAD. Therefore, to clarify the role of conduit artery blood flow, we compared whole-limb blood flow and skeletal muscle microvascular perfusion responses with exercise in patients with PAD (n=9; 60±7 years) prior to, and following, lower-limb endovascular revascularization. Materials and Methods: Microvascular perfusion (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after a 5 minute bout of submaximal intermittent isometric plantar-flexion exercise using contrast-enhanced ultrasound imaging. Exercise contraction-by-contraction whole-leg blood flow and vascular conductance were measured using strain-gauge plethysmography. Results: With revascularization there was a significant increase in whole-leg blood flow and conductance during exercise (p−1; p=0.38). However, the parameters that determine microvascular perfusion changed, with a reduction in the microvascular volume response to exercise (pre-revascularization: 6.76±3.56; post-revascularization: 2.42±0.69 aU; p−1; p=0.02). Conclusion: These findings suggest that patients with PAD compensate for the conduit artery blood flow impairment with an increase in microvascular blood volume to maintain muscle perfusion during submaximal exercise. Clinical Impact The findings from this study support the notion that the impairment in conduit artery blood flow in patients with PAD leads to compensatory changes in microvascular blood volume and flow velocity to maintain muscle microvascular perfusion during submaximal leg exercise. Moreover, this study demonstrates that these microvascular changes are reversed and become normalized with successful lower-limb endovascular revascularization.

Peripheral arterial disease (PAD) is characterized by stenosis and occlusion of the lower limb arteries. Although leg blood flow is limited in PAD, it remains unclear whether skeletal muscle microvascular perfusion is affected. We compared whole leg blood flow and calf muscle microvascular perfusion after cuff occlusion and submaximal leg exercise between patients with PAD ( n = 12, 69 ± 9 yr) and healthy age-matched control participants ( n = 12, 68 ± 7 yr). Microvascular blood flow (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after the following: 1) 5 min of thigh-cuff occlusion, and 2) a 5-min bout of intermittent isometric plantar-flexion exercise (400 N) using real-time contrast-enhanced ultrasound. Whole leg blood flow was measured after thigh-cuff occlusion and during submaximal plantar-flexion exercise using strain-gauge plethysmography. Postocclusion whole leg blood flow and calf muscle microvascular perfusion were lower in patients with PAD than control participants, and these parameters were strongly correlated ( r = 0.84, P < 0.01). During submaximal exercise, total whole leg blood flow and vascular conductance were not different between groups. There were also no group differences in postexercise calf muscle microvascular perfusion, although microvascular blood volume was higher in patients with PAD than control participants (12.41 ± 6.98 vs. 6.34 ± 4.98 arbitrary units, P = 0.03). This study demonstrates that the impaired muscle perfusion of patients with PAD during postocclusion hyperemia is strongly correlated with disease severity and is likely mainly determined by the limited conduit artery flow. In response to submaximal leg exercise, microvascular flow volume was elevated in patients with PAD, which may reflect a compensatory mechanism to maintain muscle perfusion and oxygen delivery during recovery from exercise. NEW & NOTEWORTHY This study suggests that peripheral arterial disease (PAD) has different effects on the microvascular perfusion responses to cuff occlusion and submaximal leg exercise. Patients with PAD have impaired microvascular perfusion after cuff occlusion, similar to that previously reported after maximal exercise. In response to submaximal exercise, however, the microvascular flow volume response was elevated in patients with PAD compared with control. This finding may reflect a compensatory mechanism to maintain perfusion and oxygen delivery during recovery from exercise.

Background and Aim: Contrast-enhanced ultrasound (CEUS) measures of post-occlusion skeletal muscle microvascular responsiveness demonstrate the microvascular dysfunction associated with ageing and age-related disease. However, the accessibility of CEUS is limited by the need for intravenous administration of ultrasound contrast agents and sophisticated imaging analysis. Alternative methods are required for the broader assessment of microvascular dysfunction in research and clinical settings. Therefore, we aimed to evaluate the level of association and agreement between CEUS and near-infrared spectroscopy (NIRS)-derived measures of post-occlusion skeletal muscle microvascular responsiveness in older adults. Methods: During supine rest, participants (n=15, 67±11 years) underwent 5 minutes of thigh cuff-occlusion (200 mmHg). Post-occlusion CEUS measures of calf muscle microvascular responsiveness were made, including time to 95% peak acoustic intensity (TTP95 AI) and the rate of rise (slope AI). Simultaneous measures, including time to 95% peak oxygenated haemoglobin (TTP95 O2Hb) and slope O2Hb, were made using continuous-wave NIRS in the same muscle region. Results: There were strong correlations between TTP95 measures derived from CEUS and NIRS (r=0.834, p=

ObjectivesTo describe (1) absolute cardiovascular disease risk (ACVDR) scores in patients presenting to hospital with acute coronary syndrome (ACS) and (2) proportions of these patients on guideline-recommended pharmacotherapy according to their ACVDR score.DesignCross-sectional study.SettingSingle-site tertiary centre hospital, Queensland, Australia over a 12-month period.ParticipantsPatients >18 years of age presenting to hospital with ACS due to coronary artery disease (CAD) confirmed by angiography.Primary and secondary outcome measuresProportion of patients without prior history of CVD with a high ACVDR score, and of patients with a prior history of CVD, who are on guideline-recommended pharmacotherapy.Results527 ACS patients were included of whom the mean age was 63 years and 75% were male. Overall, 66% (350) had no prior CVD and 34% (177) patients had prior CVD.In patients with no prior CVD, the proportions of patients with low, intermediate and high CVD risk scores were 41%, 24% and 36%. In the no prior CVD, high-risk patient group, 48% were on no preventative pharmacotherapy, 32% on single pharmacotherapy and 20% patients on complete guideline-recommended pharmacotherapy. In the prior CVD group, 7% patients were on no pharmacotherapy, 40% on incomplete pharmacotherapy and 53% were on complete guideline-recommended pharmacotherapy.ConclusionThis study adds to the evidence on implementation gaps in guideline-recommended management of ACVDR, showing that a large proportion of patients presenting with ACS due to CAD were at high risk of developing CVD prior to the event and most were not on guideline-recommended treatment. A significant proportion of these events are likely to have been preventable, and therefore, increased assessment and appropriate treatment of ACVDR in primary care is needed to reduce the incidence of CVD events in the population.

Impairments in skeletal muscle microvascular function are frequently reported in patients with various cardiometabolic conditions for which older age is a risk factor. Whether aging per se predisposes the skeletal muscle to microvascular dysfunction is unclear. We used contrast‐enhanced ultrasound (CEU) to compare skeletal muscle microvascular perfusion responses to cuff occlusion and leg exercise between healthy young (n = 12, 26 ± 3 years) and older (n = 12, 68 ± 7 years) adults. Test–retest reliability of CEU perfusion parameters was also assessed. Microvascular perfusion (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after: (a) 5‐min of thigh‐cuff occlusion, and (b) 5‐min of submaximal intermittent isometric plantar‐flexion exercise (400 N) using CEU. Whole‐leg blood flow was measured using strain‐gauge plethysmography. Repeated measures were obtained with a 15‐min interval, and averaged responses were used for comparisons between age groups. There were no differences in post‐occlusion whole‐leg blood flow and muscle microvascular perfusion between young and older participants (p > .05). Similarly, total whole‐leg blood flow during exercise and post‐exercise peak muscle microvascular perfusion did not differ between groups (p > .05). The overall level of agreement between the test–retest measures of calf muscle perfusion was excellent for measurements taken at rest (intraclass correlation coefficient [ICC] 0.85), and in response to cuff occlusion (ICC 0.89) and exercise (ICC 0.95). Our findings suggest that healthy aging does not affect muscle perfusion responses to cuff‐occlusion and submaximal leg exercise. CEU muscle perfusion parameters measured in response to these provocation tests are highly reproducible in both young and older adults., We used contrast‐enhanced ultrasound (CEU) to compare skeletal muscle microvascular perfusion responses to cuff occlusion and leg exercise between healthy young (n = 12, 26 ± 3 years) and older (n = 12, 68 ± 7 years) adults. There were no differences in post‐occlusion whole‐leg blood flow and muscle microvascular perfusion between young and older participants (p > .05). Similarly, total whole‐leg blood flow during exercise and post‐exercise peak muscle microvascular perfusion did not differ between groups (p > .05).

New Findings: What is the central question of the study? Cuff-occlusion duration may influence contrast-enhanced ultrasound (CEUS) assessments of skeletal muscle microvascular blood flow responsiveness: what are the effects of 1, 3 and 5 min cuff-occlusion on the magnitude and reliability of calf muscle microvascular blood flow responsiveness in older adults? What is the main finding and its importance? Calf muscle microvascular blood flow responsiveness was enhanced following 5 min cuff-occlusion compared with 1 min. The reliability of post-occlusion CEUS measurements was also improved following 5 min occlusion. The use of a standardized 5 min occlusion period should therefore be considered in future studies and clinical practice. Abstract: Contrast-enhanced ultrasound (CEUS) is increasingly used in assessments of skeletal muscle microvascular blood flow responsiveness. In response to limb cuff-occlusion, some studies have reported significant impairments in CEUS measurements of microvascular blood flow in older adults with cardiovascular or metabolic disease, whereas others have failed to detect significant between-group differences, which has brought the reliability of the technique into question. In the absence of a standardized CEUS protocol, there is variance in the duration of cuff-occlusion used, which is likely to influence post-occlusion measurements of muscle microvascular blood flow. We aimed to determine the effect of cuff-occlusion duration by comparing the magnitude and reliability of CEUS measurements of calf muscle microvascular blood flow responsiveness in older adults (n = 15, 67 ± 11 years) following 1, 3 and 5 min occlusion periods. Microvascular blood flow (= microvascular volume × microvascular velocity) within the calf muscle was measured using real-time destruction–replenishment CEUS. Measurements were made following thigh cuff-occlusion (200 mmHg) periods of 1, 3 and 5 min in a random order. Microvascular blood flow was higher following 3 min (3.71 ± 1.46 aU s−1) and 5 min (3.47 ± 1.48 aU s−1) compared with 1 min (2.42 ± 1.27 aU s−1, P = 0.002), which corresponded with higher microvascular volumes after 3 and 5 min compared with 1 min. Reliability was good following 5 min (intraclass correlation coefficient (ICC) 0.49) compared with poor following 1 min (ICC 0.34) and 3 min (ICC 0.35). This study demonstrates that the magnitude and reliability of calf muscle microvascular responsiveness is enhanced using a 5 min cuff-occlusion protocol compared with 1 min in older adults.

BackgroundIncomplete restoration of myocardial blood flow (MBF) is reported in up to 30% of ST-segment elevation myocardial infarction (STEMI) despite prompt mechanical revascularization. Experimental hyperinsulinemic euglycemia (HE) increases MBF reserve (MBFR). If fully exploited, this effect may also improve MBF to ischemic myocardium. Using insulin-dextrose infusions to induce HE, we conducted four experiments to determine (1) how insulin infusion duration, dose, and presence of insulin resistance affect MBFR response; and (2) the effect of an insulin-dextrose infusion given immediately following revascularization of STEMI on myocardial perfusion.MethodsThe MBFR was determined using myocardial contrast echocardiography. Experiment 1 (insulin duration): 12 participants received an insulin-dextrose or saline infusion for 120 minutes. MBFR was measured at four time intervals during infusion. Experiment 2 (insulin dose): 22 participants received one of three insulin doses (0.5, 1.5, 3.0 mU/kg/minute) for 60 minutes. Baseline and 60-minute MBFRs were determined. Experiment 3 (insulin resistance): five metabolic syndrome and six type 2 diabetes (T2DM) participants received 1.5 mU/kg/minute of insulin-dextrose for 60 minutes. Baseline and 60-minute MBFRs were determined. Experiment 4 (STEMI): following revascularization for STEMI, 20 patients were randomized to receive either 1.5 mU/kg/minute insulin-dextrose infusion for 120 minutes or standard care. Myocardial contrast echocardiography was performed at four time intervals to quantify percentage contrast defect length.ResultsExperiment 1: MBFR increased with time through to 120 minutes in the insulin-dextrose group and did not change in controls. Experiment 2: compared with baseline, MBFR increased in the 1.5 (2.42 ± 0.39 to 3.25 ± 0.77, P = .002), did not change in the 0.5, and decreased in the 3.0 (2.64 ± 0.25 to 2.16 ± 0.33, P = .02) mU/kg/minute groups. Experiment 3: compared with baseline, MBFR increase was only borderline significant in metabolic syndrome and T2DM participants (1.98 ± 0.33 to 2.59 ± 0.45, P = .04, and 1.67 ± 0.35 to 2.14 ± 0.21, P = .05). Experiment 4: baseline percentage contrast defect length was similar in both groups but with insulin decreased with time and was significantly lower than in controls at 60 minutes (2.8 ± 5.7 vs 13.7 ± 10.6, P = .02).ConclusionsPresence of T2DM, insulin infusion duration, and dose are important determinants of the MBFR response to HE. When given immediately following revascularization for STEMI, insulin-dextrose reduces perfusion defect size at one hour. Hyperinsulinemic euglycemia may improve MBF following ischemia, but further studies are needed to clarify this.

BACKGROUND: Although calcific aortic valve disease (CAVD) is associated with coronary atherosclerosis, it is not known whether early CAVD is associated with coronary microcirculatory dysfunction (CMD). We sought to investigate the relationship between myocardial blood flow reserve (MBFR) - a measure of CMD, and early CAVD in the absence of obstructive epicardial coronary artery disease. We also determined whether this relationship was independent of coronary artery disease (CAD) and hs-CRP, a marker of systemic inflammation. METHODS: 183 patients with chest pain and unobstructed coronary arteries were studied. Aortic valve calcification score (AVCS), coronary total plaque length (TPL), and coronary calcium score were quantified from multislice CT. MBFR was assessed using vasodilator myocardial contrast echocardiography. Hs-CRP was measured from venous blood using a particle-enhanced immunoassay. RESULTS: Mean (±SD) participant age was 59.8 (9.6) years. Mean AVCS was 68 (258) AU, TPL was 15.6 (22.2) mm, and median coronary calcification score was 43.5AU. Mean MBFR was 2.20 (0.52). Mean hs-CRP was 2.52 (3.86) mg/l. Multivariable linear regression modelling incorporating demographics, coronary plaque characteristics, MBFR, and inflammatory markers, demonstrated that age (β=0.05, 95% CI: 0.02, 0.08, P=0.007), hs-CRP (β=0.09, CI: 0.02, 0.16, P=0.010) and diabetes (β=1.03, CI: 0.08, 1.98, P=0.033), were positively associated with AVCS. MBFR (β=-0.87, CI: -1.44, -0.30, P=0.003), BMI (β=-0.11, CI: -0.21, -0.01, P=0.033), and LDL (β=-0.32, CI: -0.61, -0.03, P=0.029) were negatively associated with AVCS. TPL and coronary calcium score were not independently associated with AVCS when included in the regression model. CONCLUSION: Coronary microvascular function as determined by measurement of myocardial blood flow reserve is independently associated with early CAVD. This effect is independent of the presence of coronary artery disease and also systemic inflammation.

To the Editor: We read with interest the study by Black and colleagues1 on the effectiveness of a pro-active risk factor management strategy based on absolute cardiovascular disease risk score compared with usual care, in a rapid access chest pain clinic setting. The study suggested that such a strategy significantly improved 5-year cardiovascular risk scores; however, we would consider some caution before reaching such a conclusion. Although the authors point out several potential sources for bias in their study, there is an additional one that has not been highlighted. In the results, the authors state that “the increase in use of guideline-based therapies was similar in the two groups,” yet do not go on to explain the differential effect as to why the blood pressure and lipid profiles decreased in the interventional group only. We suggest that the reason for this lies in a fundamental difference between the groups selected. The interventional group at baseline was receiving proportionately greater amounts of lipid-lowering and anti-hypertensive therapy: 56% and 30% higher, respectively, than in the control arm. These higher treatment rates may explain the lower blood pressure, the lipid profiles observed and, consequently, the improved final risk scores in the interventional arm. Also, as the authors pointed out, almost a third of eligible patients approached declined to participate and is therefore an important source of potential selection bias. We also note that the offer of referral to a public smoking cessation service was limited to those in the intervention group. National guidelines recommend this strategy as part of standard care,2 and hence we question whether this intervention should truly be considered to deviate from best practice or usual care.

Cardiovascular disease is associated with increased risk for cognitive decline and dementia, but it is unclear whether this risk varies across disease states or occurs in the absence of symptomatic stroke. To examine the evidence of increased risk for cognitive decline and dementia following non-stroke cardiovascular disease we conducted two independent meta-analyses in accordance with PRISMA guidelines. The first review examined cardiovascular diagnoses (atrial fibrillation, congestive heart failure, periphery artery disease and myocardial infarction) while the second review assessed the impact of atherosclerotic burden (as indicated by degree of stenosis, calcification score, plaque morphology or number of plaques). Studies eligible for review longitudinally assessed risk for clinically significant cognitive decline and/or dementia and excluded stroke and cognitive impairment at baseline. Summary statistics were computed via the inverse variance weighted method, utilising Cox Proportional Hazards data (Hazard Ratios, HR). Both atrial fibrillation (n = 5, HR = 1.26, 95% CI [1.12, 1.43]) and severe atherosclerosis (n = 4, HR = 1.59, 95% CI [1.12, 2.26]) emerged as significant risk factors for cognitive decline and/or dementia. A small set of studies reviewed, insufficient for meta-analysis, examining congestive heart failure, peripheral artery disease and myocardial infarction suggested that these conditions may also be associated with an increased risk of cognitive decline/dementia. In the absence of stroke, patients with atrial fibrillation or generalised atherosclerosis are at heightened risk for cognitive deterioration. Nonetheless, this paper highlights the need for methodologically rigorous and prospective investigation of the relationship between CVD and dementia.

Cardiac patients with psychological distress have a poorer prognosis than patients without distress; which may in part reflect differences in treatment. We quantified variation in coronary angiography and revascularisation procedures according to psychological distress among patients admitted with incident acute myocardial infarction (AMI) or angina.Questionnaire data (collected 2006-09) from 45 and Up Study participants were linked to hospitalisation and mortality data, to 30 June 2016. Among patients free from ischaemic heart disease at baseline and subsequently hospitalised with AMI or angina, Cox regression was used to model the association between distress (Kessler-10 scores: low [10-12], mild [12-16], moderate [16-22] and high [22-50]) - assessed on the questionnaire - and coronary angiography and revascularisation procedures (percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]) within 30 days of admission, adjusting for personal characteristics, including physical functioning.Proportions receiving angiography and PCI/CABG were 71.4% and 51.7% following AMI (n = 3749), and 61.3% and 31.3% for angina patients (n = 3772), respectively. Following AMI, age-sex-adjusted rates of PCI/CABG were lower with higher levels of distress (test for trend: p = .037), as were rates of angiography and PCI/CABG (p .01) following admission with angina. After additional adjustment for personal characteristics, associations between distress and procedure rates attenuated substantively and were no longer significant, except that PCI/CABG rates remained lower among angina patients with high versus low distress (HR = 0.76, 95%CI: 0.59-0.99).Distress-related variation in coronary procedures largely reflects differences in personal characteristics. Whether lower revascularisation rates among angina patients with high compared to low distress are clinically appropriate or represent under-treatment remains unclear.

We performed real-time myocardial contrast echocardiography on a patient with cardiac amyloidosis and previous normal coronary angiography presenting with atypical chest pain to assess myocardial blood flow reserve (MBFR). Myocardial contrast echocardiography was performed and flash microbubble destruction and replenishment analysis was used to calculate myocardial blood flow. Dipyridamole was used to achieve hyperemia. MBFR was derived from the ratio of peak myocardial blood flow at hyperemia and rest. The results show a marked reduction in MBFR in our patient. Previous reports of luminal obstruction of intramyocardial rather than epicardial vessels by amyloid deposition may be causing microvascular dysfunction.

Objectives The Manchester Acute Coronary Syndromes (MACS) decision rule has been shown to be a powerful diagnostic tool in emergency department (ED) patients with suspected acute coronary syndromes (ACS). It has the potential to improve system efficiency by identifying patients suitable for discharge after a single blood draw for high-sensitivity troponin and heart-type fatty acid–binding protein (h-FABP) analysis at presentation to the ED. The objective was to externally validate the MACS decision rule and establish its diagnostic accuracy as a discharge tool in a new set of prospectively recruited ED patients. Methods In this preplanned analysis of a prospectively recruited single-center cohort, consecutive ED patients ≥18 years with suspected ACS were included. Testing for h-FABP and high-sensitivity troponin T was undertaken on serum drawn on arrival, and any clinical features required to calculate the MACS rule were recorded. The primary outcome was major adverse cardiac events (MACE) within 30 days (acute myocardial infarction [AMI], death, or revascularization). The secondary outcome was AMI alone, adjudicated using 6-hour troponin results. Results Of the 782 participants included, 78 (10.0%) developed MACE and 61 (7.8%) had an AMI. Of participants, 133 (17.0%) were identified as “very low risk” and therefore suitable for immediate discharge with a 0% incidence of MACE or AMI. Of remaining patients, 314 (40.2%) were “low risk,” 320 (40.9%) were “moderate risk,” and 15 (1.9%) were “high risk,” with incidences of MACE of 2.2, 19.7, and 53.3%, respectively. The sensitivity was 100% (95% confidence interval [CI] = 95.4% to 100%) for MACE at 30 days and 100% (95% CI = 94.1% to 100%) for AMI. The area under the receiver operating characteristic curve was 0.87 (95% CI = 0.83 to 0.91) for the MACS rule in the prediction of MACE. Conclusions In this prospectively recruited cohort of ED patients with suspected ACS, the MACS decision rule identifies a significant proportion of patients who are suitable for immediate discharge after a single blood draw at presentation, with a very low risk of MACE at 30 days. This study externally validates previous findings that the MACS rule is a powerful diagnostic tool in this setting. A randomized controlled trial to establish the utility of the rule in an everyday clinical setting is justified.

ObjectivesTo describe general practitioners’ (GPs’) absolute cardiovascular disease risk (ACVDR) self-reported assessment practices and their relationship to knowledge, attitudes and beliefs about ACVDR.DesignCross-sectional survey with opportunistic sampling (October–December 2017).SettingSunshine Coast region, Queensland, Australia.Participants111 GPs responded to the survey.Primary and secondary outcome measuresProportion of GPs reporting a high (≥80%) versus moderate (60%–79%)/low (ResultsOf the 111 respondents, 78% reported using the Australian ACVDR calculator; 45% reported high, 25% moderate and 30% low ACVDR assessment rates; >85% reported knowing how to use ACVDR assessment tools, believed assessment valuable and were comfortable with providing guideline-recommended treatment. Around half believed patients understood the concept of high risk and were willing to adopt recommendations. High assessment rates (vs moderate/low) were less likely among older GPs (≥45 vs ≤34 years, age-adjusted and sex-adjusted OR (aOR) 0.36, 95% CI 0.12 to 0.97). Those who answered knowledge-based questions about the guidelines incorrectly had lower assessment rates, including those who answered questions on patient eligibility (aOR 0.13, 95% CI 0.02 to 1.11). A high assessment rate was more likely among GPs who believed there was sufficient time to do the assessment (aOR 3.79, 95% CI 1.23 to 11.61) and that their patients were willing to undertake lifestyle modification (aOR 2.29, 95% CI 1.02 to 5.15). Over 75% of GPs agreed better patient education, nurse-led assessment and computer-reminder prompts would enable higher assessment rates.ConclusionsAlthough the majority of GPs report using the ACVDR calculator when undertaking a CVD risk assessment, there is a need to increase the actual proportion of eligible patients undergoing ACVDR assessment. This may be achieved by improving GP assessment practices such as GP and patient knowledge of CVD risk, providing sufficient time and nurse-led assessment.

Objective Epicardial fat (EF) is metabolically active adipose tissue positioned between the epicardial surface of the heart and the pericardium. We investigated whether there is a relationship between EF and Coronary Microvascular Dysfunction (CMD) in patients presenting with chest pain and unobstructed coronary arteries. Materials and Methods This study recruited patients referred to cardiology clinics for assessment of chest pain who subsequently underwent assessment via CT coronary angiogram (CTA). Myocardial blood flow reserve (MBFR) was assessed using myocardial contrast echocardiography. Epicardial fat volume (EFV) was measured by tracing serial slices on CTA with corresponding Hounsfield units of −195 to −45. Results We recruited 134 participants with a mean age of 59.2 (9.8) years. CMD was present in 54 (40%) patients, and the measured mean EFV was 128 mm3 (96, 168). Fortythree patients (32%) had a coronary artery calcium score (CACS) of 0, 64 (48%) had a CACS of 1–100, 18 (13%) had a CACS of 101–400, and 9 (7%) had a CACS >400. Univariate regression analysis showed that EFV and MBFR had a correlation coefficient of R=−0.22, with a significant regression slope (β=−0.002, p=0.012). Multivariable linear regression analysis using MBFR as a continuous outcome variable revealed age (β=−0.012, p=0.011) and CACS (β=−0.003, p=0.023) to be associated with MBFR. EFV was not associated with MBFR (β=−0.0007, p=0.538). Model repetition with MBFR as a dichotomous variable (MBFR ≥2 or

Increased arterial stiffness is observed with ageing and in individuals with low cardiorespiratory fitness ( $$\dot {V}$$ O2peak), and associated with cardiovascular risk. Following an exercise bout, transient arterial stiffness reductions offer short-term benefit, but may depend on exercise intensity. This study assessed the effects of exercise intensity on post-exercise arterial stiffness in older adults with varying fitness levels. Fifty-one older adults (72 ± 5 years) were stratified into fitness tertiles ( $$\dot {V}$$ O2peak: low-, 22.3 ± 3.1; mid-, 27.5 ± 2.4 and high-fit 36.3 ± 6.5 mL kg−1 min−1). In a randomised order, participants underwent control (no-exercise), moderate-intensity continuous exercise (40% of peak power output; PPO), and higher-intensity interval exercise (70% of PPO) protocols. Pulse wave velocity (PWV), augmentation index (AIx75) and reflection magnitude (RM) were assessed at rest and during 90 min of recovery following each protocol. After control, delta PWV increased over time (P

A 69-year old man presented with a 2-week history of back discomfort and fevers, having had bioprosthetic aortic valve replacement (AVR) for prosthetic valve infective endocarditis (PVE) 4-months ago. Past medical history included coronary artery bypass grafting in 2008, bioprosthetic AVR with root replacement for ascending aortic dissection in 2010, diabetes mellitus, and chronic renal impairment. In June 2016, he was admitted with Streptococcus mitis bacteraemia treated with 6 weeks of ceftriaxone. Transoesophageal echocardiography was negative for endocarditis and root abscess. In November 2016, the patient was admitted with heart failure secondary to new severe aortic regurgitation. Transoesophageal echocardiography showed dehiscence of the anterior leaflet of aortic valve prosthesis. Blood cultures were negative. He was commenced on vancomycin prior to re-do AVR and discharged on lifelong amoxycillin.

The vasodilatory effects of insulin may mitigate myocardial ischaemia, thus we conducted a series of experiments under hyperinsulinaemic euglycaemic conditions to determine how insulin infusion duration, insulin dose administered and type 2 diabetes (T2DM) affect myocardial blood flow reserve (MBFR

Inflammation and extracellular matrix degeneration contribute to abdominal aortic aneurysm (AAA) development. We aimed to assess the effect of exercise intensity on circulating biomarkers of inflammation and extracellular matrix degeneration in patients with AAA and healthy older adults.Twenty patients with AAA (74 ± 6 yr) and 20 healthy males (72 ± 5 yr) completed moderate-intensity cycling at 40% peak power output, higher-intensity intervals at 70% peak power output, and control (rest) on separate days. Circulating matrix metalloproteinase-9 (MMP-9), transforming growth factor beta 1, interleukin-6 (IL-6), IL-10, and tumor necrosis factor alpha (TNF-α) were analyzed at rest and 0 to 90 min postexercise.Biomarkers at baseline were similar between groups. IL-6 responses to exercise were similar between groups, with a greater increase in ΔIL-6 after moderate-intensity compared with higher-intensity exercise (P0.001). Delta MMP-9 showed a 118-ng·mL (95% confidence interval = 23 to 214, P = 0.02) greater increase immediately after higher-intensity exercise compared with changes in control in both groups. Delta MMP-9 then decreased by 114 ng·mL (18 to 211, P = 0.02) 90 min after higher-intensity exercise compared with the changes in control. Delta TNF-α was not different between protocols in healthy adults. In patients with AAA, delta TNF-α showed a greater decrease after higher-intensity compared with moderate-intensity exercise (-6.1 pg·mL, -8.5 to -3.6, P0.001) and control (-4.9 pg·mL, -7.4 to -2.4, P0.001). IL-10 and transforming growth factor beta 1 did not change in either group.These findings suggest that a bout of higher-intensity exercise elicits a greater anti-inflammatory response compared with moderate-intensity exercise, which may be further augmented in patients with AAA. Exercise-induced reductions in biomarkers associated with AAA progression may represent a protective effect of exercise in patients with AAA.

Importance: High-sensitivity cardiac troponin I testing is widely used to evaluate patients with suspected acute coronary syndrome. A cardiac troponin concentration of less than 5 ng/L identifies patients at presentation as low risk, but the optimal threshold is uncertain.Objective: To evaluate the performance of a cardiac troponin I threshold of 5 ng/L at presentation as a risk stratification tool in patients with suspected acute coronary syndrome.Data Sources: Systematic search of MEDLINE, EMBASE, Cochrane, and Web of Science databases from January 1, 2006, to March 18, 2017.Study Selection: Prospective studies measuring high-sensitivity cardiac troponin I concentrations in patients with suspected acute coronary syndrome in which the diagnosis was adjudicated according to the universal definition of myocardial infarction.Data Extraction and Synthesis: The systematic review identified 19 cohorts. Individual patient-level data were obtained from the corresponding authors of 17 cohorts, with aggregate data from 2 cohorts. Meta-estimates for primary and secondary outcomes were derived using a binomial-normal random-effects model.Main Outcomes and Measures: The primary outcome was myocardial infarction or cardiac death at 30 days. Performance was evaluated in subgroups and across a range of troponin concentrations (2-16 ng/L) using individual patient data.Results: Of 11 845 articles identified, 104 underwent full-text review, and 19 cohorts from 9 countries were included. Among 22 457 patients included in the meta-analysis (mean age, 62 [SD, 15.5] years; n = 9329 women [41.5%]), the primary outcome occurred in 2786 (12.4%). Cardiac troponin I concentrations were less than 5 ng/L at presentation in 11 012 patients (49%), in whom there were 60 missed index or 30-day events (59 index myocardial infarctions, 1 myocardial infarction at 30 days, and no cardiac deaths at 30 days). This resulted in a negative predictive value of 99.5% (95% CI, 99.3%-99.6%) for the primary outcome. There were no cardiac deaths at 30 days and 7 (0.1%) at 1 year, with a negative predictive value of 99.9% (95% CI, 99.7%-99.9%) for cardiac death.Conclusions and Relevance: Among patients with suspected acute coronary syndrome, a high-sensitivity cardiac troponin I concentration of less than 5 ng/L identified those at low risk of myocardial infarction or cardiac death within 30 days. Further research is needed to understand the clinical utility and cost-effectiveness of this approach to risk stratification.

This review will provide an overview of supraventricular tachycardias (SVTs), their classification, diagnostic features, and management in the perioperative period of adult non-cardiac surgery. The term ‘SVT’ refers to paroxysmal tachyarrythmias that require atrial or atrioventricular (AV) nodal tissue, or both, for their initiation and maintenance. The incidence of persistent SVT is 2% before operation and 6% in the postoperative period. In non-cardiac surgery, perioperative arrhythmias are more likely to be supraventricular than ventricular in origin. Atrial arrhythmias occur most frequently 2–3 days post-surgery similar to perioperative acute coronary syndromes and are likely related to sympathetic stimulation associated with an inflammatory response. Other precipitants of SVT often associated with high sympathetic tone are summarized in Table 1. Such arrhythmias are important for the anaesthetist; in particular, atrial fibrillation (AF) is associated with haemodynamic derangement, postoperative stroke, perioperative myocardial infarction, ventricular arrhythmia, heart failure, and longer hospital stay.

Hypoglycaemia is associated with increased cardiovascular and all-cause mortality in both subjects with and without coronary artery disease (CAD) [1]. Our group recently demonstrated that insulin-induced hypoglycaemia (IIH) is associated with a 14% reduction of myocardial blood flow reserve (MBFR) compared to baseline, in both healthy subjects and those with type 1 diabetes mellitus (T1DM) [2]. Cardiac troponin is a sensitive marker of myocardial injury and higher levels have been linked to adverse outcomes in patients with ACS [3]. A new ultrasensitive cardiac troponin I (us-cTnI) has been developed which has a limit of detection of at least one order of magnitude lower below that of current commercial assays. In comparison with current generation troponin assays, us-cTnI has been shown to be more sensitive in the detection of myocardial ischaemia. Furthermore, low but elevated levels of us-cTnI in patients presenting with suspected ACS, have been linked to adverse cardiovascular outcomes and death [4]. This study investigated whether 60 min duration of symptomatic IIH and reduction in MBFR, was associated with myocardial injury as determined by a change in serum levels of us-cTnI measured immediately following hypoglycaemia, in healthy and diabetic subjects without obstructive CAD.

Summary A papillary fibroelastoma is a rare, avascular, cardiac tumour that is often found incidentally using transthoracic echocardiography (TTE). Peripheral i.v. injection of a microbubble contrast agent is often used to characterize abnormal masses within the heart allowing further delineation of physical features, the area of attachment, and vascularity of the mass in order to differentiate the growth from a tumour or a thrombus. This case highlights a potential pitfall when assessing a cardiac tumour's vascularity using contrast TTE. A cardiac mass was identified on a TTE of a 53-year-old man and was further investigated with microbubble contrast-enhanced TTE. Contrast TTE imaging suggested a vascularized structure in the left ventricle. However, after histological examination the tumour was found to be entirely avascular. Learning points Differentiation of cardiac tumour is usually best performed with contrast echocardiography. Contrast echocardiography may not be best tool to determine if cardiac mass is vascularized. A papillary fibroelastoma can appear vascularized with contrast echocardiography due to it's frond-like structures. Physicians should be aware of this potential confusion when assessing a cardiac tumour in patients.

Endothelial dysfunction is observed in patients with abdominal aortic aneurysm (AAA), who have increased risk of cardiovascular events and mortality. This study aimed to assess the acute effects of moderate- and higher-intensity exercise on endothelial function, as assessed by flow-mediated dilation (FMD), in AAA patients (74 ± 6 yr old, n = 22) and healthy adults (72 ± 5 yr old, n = 22). Participants undertook three randomized visits, including moderate-intensity continuous exercise [40% peak power output (PPO)], higher-intensity interval exercise (70% PPO), and a no-exercise control. Brachial artery FMD was assessed at baseline and at 10 and 60 min after each condition. Baseline FMD was lower [by 1.10% (95% confidence interval: 0.72−.81), P = 0.044] in AAA patients than in healthy adults. There were no group differences in FMD responses after each condition ( P = 0.397). FMD did not change after no-exercise control but increased by 1.21% (95% confidence interval: 0.69−1.73, P < 0.001) 10 min after moderate-intensity continuous exercise in both groups and returned to baseline after 60 min. Conversely, FMD decreased by 0.93% (95% confidence interval: 0.41−1.44, P < 0.001) 10 min after higher-intensity interval exercise in both groups and remained decreased after 60 min. We found that the acute response of endothelial function to exercise is intensity-dependent and similar between AAA patients and healthy adults. Our findings provide evidence that regular exercise may improve vascular function in AAA patients, as it does in healthy adults. Improved FMD after moderate-intensity exercise may provide short-term benefit. Whether the decrease in FMD after higher-intensity exercise represents an additional risk and/or a greater stimulus for vascular adaptation remains to be elucidated. NEW & NOTEWORTHY Abdominal aortic aneurysm patients have vascular dysfunction. We observed a short-term increase in vascular function after moderate-intensity exercise. Conversely, higher-intensity exercise induced a prolonged reduction in vascular function, which may be associated with both short-term increases in cardiovascular risk and signaling for longer-term vascular adaptation in abdominal aortic aneurysm patients.

Background There are limited data on the effects of prolonged acute hypoxia on individual and global measures of biventricular function. Aims The aim of this study was to assess its effects on conventional and novel measures of biventricular function, including the recently defined E′/(A′×S′) (EAS) index, obtained using pulsed-wave tissue Doppler Imaging (PWTDI) and associated blood brain natriuretic peptide (BNP) levels. Methods In this study, 14 healthy subjects aged 30.5 years were assessed at baseline and at >150 minutes following hypobaric hypoxia (HH) to the equivalent altitude of 4800 m for a total of 180 minutes. The combined EAS index (E′/(A′ × S′)) was calculated at the mitral and tricuspid annulus using data from the peak systolic (S′) early (E′) and late (A′) diastolic filling. Results It was seen that HH increased resting heart rate (63.4 ± 8.4 vs. 85.2 ± 10.2/min; P

The role of insulin in the treatment of acute coronary syndrome (ACS) has been widely studied over the past 100 years. The current indication for its use in this context is the treatment of hyperglycemia, irrespective of diabetes, which is associated with adverse outcome. Initial theories proposed that glucose was beneficial in the context of myocardial ischemia and insulin was required to enable glucose cell uptake. However, studies testing this hypothesis with routine insulin administration during ACS have produced disappointing results and research interest has therefore declined. We propose that the less well known but important vasodilator effect of insulin has been overlooked by some of these studies and warrants further consideration. Previous reports have shown that hyperinsulinemic euglycaemia improves myocardial blood flow reserve. With this in mind, this review considers the role of insulin in the context of ACS from the perspective of a vasodilator rather than a metabolic modulator. We discuss the importance of time to treatment, dosage of insulin administered, problems with hypoglycaemia and insulin resistance, and how they may have affected the outcomes of the major trials. Finally, we propose new study designs that allow determination of the optimal vasodilator conditions for the use of insulin as adjunctive pharmacotherapy during myocardial ischaemia.

An 82-year-old man with previous bioprosthetic aortic valve replacement for aortic stenosis had a routine ECG (figure 1). This was thought to represent an atrial tachycardia with cycle length 280 ms and 3:1 atrioventricular response. A diagnosis of atrial flutter was made based on tachycardia cycle length, p-wave morphology and previous cardiac surgery. He had a mild left-sided tremor in keeping with known Parkinson's disease. The patient was anticoagulated and admitted electively for an electrophysiology (EP) study. In the EP laboratory, the patient had …

Objective To evaluate the incidence of major adverse cardiac events (MACE) at 1 year in emergency department (ED) patients with possible acute coronary syndromes, stratified by high sensitivity troponin (hs-cTnI) concentrations using sex-specific cut points compared with overall cut points. Methods In a multicentre observational study of 2841 patients, presentation hs-cTnI concentrations were categorised using sex-specific (women 16 ng/L; men 34 ng/L) and overall (26 ng/L) cut points. The primary outcome was MACE occurring within 1 year of presentation. Patients with hs-cTnI values concentrations within these categories were reported by sex and 1-year MACE. Net reclassification improvement (NRI) was computed to measure the change in prediction after altering the hs-cTnI cut points, and was calculated separately for events and non-events. Results Application of sex-specific 99th percentile cut points rather than the overall cut point of 26 ng/L, reclassified 25 females from having a non-elevated troponin to having an elevated troponin, and 29 males from having an elevated troponin value to having a non-elevated troponin value on presentation. Of these, 7 (28.0%) females and 12 (41.4%) males had a 1-year MACE. There was no reclassification improvement for those with or without 1-year MACE (NRI events =−1.5%, 95% CI −4.0% to 1.1%; NRI non-events −0.04%, 95% CI −0.5% to 0.4%). Conclusions Sex-specific cut points improve the identification of women but not men at risk for 1-year MACE. The net-effect across the whole ED population with possible cardiac chest pain is minimal. Lowering the clinical cut point for both sexes may be appropriate for prognostic purposes. Trial registration number ISRCTN No. 21109279, ACTRN12609000283279.

To the Editor: Several issues around rule-out strategies utilizing low concentrations of high-sensitivity cardiac troponin assays taken at presentation to the Emergency Department (ED)1 remain unexplored. First, large-scale analyses investigating cutoff concentrations for high-sensitivity cardiac troponin I (hs-cTnI; Abbott Architect)

Cardiorenal syndrome (CRS) is the umbrella term used to describe clinical conditions in which cardiac and renal dysfunctions coexist. Much has been written on this subject, but underlying pathophysiological mechanisms continue to be unravelled and implications for management continue to be debated. A classification system—incorporating five subtypes—has recently been proposed though it has yet to permeate into day-to-day clinical practice. CRS has garnered much attention from both the cardiological and nephrological communities since the condition is associated with significant morbidity and mortality. Renal dysfunction is highly prevalent amongst patients with heart failure and has been shown to be as powerful and independent a marker of adverse prognosis as ejection fraction. Similarly, patients with renal failure are considerably more likely to suffer cardiovascular disease than matched subjects from the general population. This paper begins by reviewing the epidemiology and classification of CRS before going on to consider the different pathological mechanisms underlying cardiorenal dysfunction. We then focus on management strategies and conclude by discussing future directions in the diagnosis and management of patients suffering with CRS.

A 79 year-old female presented after a syncopal episode on a background of 12 hours of lethargy, dry cough and severe left shoulder pain. A liver transplant was performed 20 years ago for primary biliary cirrhosis with a daily immunosuppressive regimen of Prednisolone, Cyclosporine and Azathioprine. Further history included hypertension and osteoarthritis. On physical examination the patient was hypotensive and required high flow oxygen to maintain oxygen saturations above 95%. General clinical examination was unremarkable except for a delayed response to verbal commands. Laboratory investigations revealed an elevated white cell count of 16.5×10 9/L and reduced glomerular filtration rate of 57 ml/min/1.73m 2, otherwise all other values were within normal limits. Contrast enhanced computed tomography (CT) of the chest and abdomen revealed three penetrating aortic ulcers of varying size along the ascending and descending aorta ( Figure 1, Figure 2, Figure 3) complicated by type A dissection and haemopericardium along the central bronchovascular structures with no evidence of dissection into the pleural space. Transthoracic echocardiography showed a dissection flap as well as a large pericardial effusion and right ventricular tamponade. The left ventricle was compressed with normal systolic function. Due to the patient's chronic immunosuppression and general frailty surgical intervention was not deemed suitable thus supportive therapy and comfort measures were instituted. The patient died six days later.

Impaired left ventricular systolic function secondary to sepsis can occur in up to 20% of patients with septic shock. The electrocardiogram (ECG) and echocardiographic changes it produces can be very similar to those occurring during acute coronary syndromes (ACS). Myocardial contrast echocardiography (MCE) allows assessment of myocardial perfusion. This technique can be performed at the bedside of the critically unwell patient. We describe a patient presenting with septic shock secondary to pneumonia. While sedated and ventilated in the intensive care unit, the patient developed marked ECG changes, a troponin rise and widespread left ventricular wall motion abnormality. The clinical picture suggested ACS or stress cardiomyopathy was unlikely and was more in keeping with a diagnosis of sepsis-induced left ventricular systolic dysfunction. To support this, resting and flash impulse MCE was performed which revealed normal perfusion in areas of both normal and abnormal wall motion. This suggested that the cardiac presentation was more likely to be due to left ventricular impairment secondary to sepsis and ACS therapy was discontinued. Pre-discharge ECG and transthoracic echocardiogram were normal. Percutaneous coronary angiography 6 weeks later was also normal. This is the first described case of MCE being used to aid in the decision-making process in distinguishing between ACS, stress cardiomyopathy, and left ventricular systolic impairment secondary to sepsis.

Following ST elevation acute myocardial infarction (STEMI) and reperfusion therapy, there are often persistent wall thickening (WT) abnormalities and perfusion defects due to variable degree of myocardial stunning and necrosis. We hypothesised that following STEMI and reperfusion therapy, the extent of residual perfusion assessed by myocardial contrast echocardiography (MCE) and not the extent of WT abnormalities would predict subsequent global recovery of left ventricular (LV) function.Accordingly, 112 patients with STEMI underwent simultaneous assessment of WT abnormality and perfusion using MCE 7+/-2 days after AMI and reperfusion therapy. Both WT and perfusion were scored on a 16 segment LV model. Contrast perfusion index (CPI), and global LV function were calculated. Echocardiography was repeated 12 weeks after reperfusion to assess recovery of LV function.Of the 112 patients recruited, follow up echocardiography 12 weeks after reperfusion was available in 98 patients. CPI was significantly higher (p0.0001) in the 66 patients, who showed late recovery of LV function (1.67+/-0.27) compared to those who did not show recovery of function (1.25+/-0.04). No significant difference was noted in the indices of baseline LV function in patients with (1.67+/-0.32) and without (1.80+/-0.36) recovery of LV function. The multivariable predictors of late recovery of function were MCE (p=0.02), absence of diabetes (p=0.02) and lower peak creatine kinase (p=0.01).The extent of residual contrast perfusion and not WT abnormalities predicts late recovery of global LV function after acute myocardial infarction and reperfusion therapy.

Objective: Total cardiovascular disease risk scoring assessment (CVDRSA) in the general population is low. This study aimed to better understand the use of CVDRSA among general practitioners (GPs), and the barriers and enablers to them undertaking CVDRSA. Design and participants: A cross-sectional survey using an online and paper-based questionnaire of 80 GPs in the Sunshine Coast region during June to December 2017. Outcomes: The outcomes were the proportion of: GPs being aware of CVDRSA, eligible patients in whom CVDRSA is undertaken, and GPs agreeing to suggested barriers and enablers to completing CVDRSA. Results: Ninety-six percent of GPs were aware of the concept of CVDRSA, 75% agreed it was a valuable tool. A total of 14% undertook CVDRSA in all eligible patients, 64% in at least six out of ten patients, and 20% in less than four out of ten patients. A total of 68% used the Australian Absolute Cardiovascular Disease Risk Score system; 6% used their own clinical judgement. Barriers to performing CVDRSA included a lack of incentives (25% agreed), and ineffective (24%) and inadequately funded (43%) lifestyle modification services. Of the GPs, 47% agreed that there was sufficient time during a routine appointment to undertake CVDRSA. Highest-rated enablers to increasing CVDRSA uptake included: patient education about CVDRSA (44% agreed), computer-prompted reminders to GPs (58%), prescreening by practice nurses (59%), and recall of eligible patients (43%). Conclusions: The majority of GPs were aware and believed that CVDRSA is a valuable prevention tool, but a significant proportion of eligible patients were not assessed. There is significant scope to increase CVDRSA within general practice through IT systems, prescreening, and education interventions.

Although repair of Tetralogy of Fallot (TOF) and transposition of the great arteries (TGA) has facilitated survival into adulthood, many survivors have residual haemodynamic abnormalities, including exercise intolerance and late right ventricular (RV) failure.We studied 40 asymptomatic adult subjects (31.3+/-1.5 years) after congenital heart disease (CHD) surgery during childhood, using tissue Doppler echocardiography (TDE). We compared systolic (S') and diastolic (E' for early filling) RV and LV velocities, with 40 age matched controls (29.5+/-1.0 years).Both RV S' and E' velocities were significantly slower in the CHD group compared to controls (6.3+/-0.4 cm/s vs. 9.3+/-0.3 cm/s; 8.5+/-0.5 cm/s vs. 10.9+/-0.4 cm/s, respectively, p0.001 for both). By contrast, LV S' and E' velocities were similar in both groups. Interestingly, in 50% of CHD subjects where RV function was reported as 'normal', both RV S' and E' velocities were significantly slower compared with controls (6.5+/-0.6 cm/s vs. 9.3+/-0.3 cm/s, p0.0001 and 9.4+/-0.7 cm/s vs. 10.9+/-0.4 cm/s, p0.05 respectively).RV S' and E' velocities are frequently abnormal in asymptomatic survivors of TOF and TGA repair, even where RV function appears 'normal'. Hence TDE during follow up may be a sensitive means of detecting pre-clinical abnormalities in RV performance.

We hypothesized that myocardial contrast echocardiography (MCE) could be used to stratify risk in patients with suspected acute coronary syndrome but a nondiagnostic electrocardiogram and negative troponin. Pretest Thrombolysis In Myocardial Infarction (TIMI) scores were determined. Exercise electrocardiographic data in those patients undergoing treadmill stress echocardiography as part of risk evaluation were analyzed independently of echocardiographic data. On a separate day, low-power MCE at rest and during vasodilator stress was performed. All patients were followed for cardiac events (cardiac death, myocardial infarction, and revascularization). Of 148 patients, 27 demonstrated abnormal myocardial contrast echocardiographic results and had higher cardiac event rates compared with those with normal myocardial contrast echocardiographic findings (59% vs 7%, p0.0001) at follow-up (8 +/- 5 months). Hard cardiac event rates (death and nonfatal myocardial infarction) were low (3%) in patients with normal myocardial contrast echocardiographic findings. Cardiac events in patients with abnormal myocardial contrast echocardiographic findings (59%) were significantly higher than those predicted by a high-risk TIMI score (33%, p = 0.0023) and compared with those predicted by high-risk exercise electrocardiography (80% vs 57%, p = 0.0003). In conclusion, stress MCE was superior to TIMI risk score and exercise electrocardiography in the assessment of risk in patients with suspected acute coronary syndrome, nondiagnostic electrocardiogram, and negative troponin.

Background Physicians rely upon chest pain history to make management decisions in patients with suspected acute coronary syndromes, particularly where the diagnosis is not immediately apparent through electrocardiography and troponin testing. The objective of this study was to establish the discriminatory value of "typicality of chest pain" and the effect of clinician experience, for the prediction of acute myocardial infarction and presence of significant coronary artery disease. Methods This prospective single-center observational study was undertaken in a UK General Hospital emergency department. We recruited consecutive adults with chest pain and a nondiagnostic electrocardiogram, for whom the treating physician determined that delayed troponin testing was necessary. Using their own clinical judgment, physicians recorded whether the chest pain described was typical or atypical for acute coronary syndrome. Physicians were defined as "experienced" or "novice" according to postgraduate experience. Acute myocardial infarction was adjudicated using a high-sensitivity troponin (hs-cTn) assay, whereas coronary artery disease was adjudicated angiographically. Results Overall, 912 patients had typicality of chest pain assessed, of whom 114/912 (12.5%) had an acute myocardial infarction and 157/912 (17.2%) underwent angiography. In patients undergoing angiography, 90/157 (57.3%) had hs-cTn elevation, of whom 60 (66.7%) had significant coronary artery disease. Sixty-seven of 157 (42.7%) patients had angiography without hs-cTn elevation; of these, 31 (46.2%) had significant coronary artery disease. For the diagnosis of acute myocardial infarction, chest pain typicality had an area under the curve (AUC) of 0.54 (95% confidence interval [CI], 0.49-0.60). For the prediction of significant coronary artery disease with hs-cTn elevation AUC: 0.54 (95% CI, 0.40-0.67), and without hs-cTn elevation AUC: 0.45 (95% CI, 0.31-0.59). When assessed by experienced physicians, specificity for the diagnosis of acute myocardial infarction was higher at 65.8% (95% CI, 63.1%-68.7%) vs 55.4% (95% CI, 53.9%-56.8%) for novices. Conclusions Subjective interpretation of "typicality of chest pain" is of limited discriminatory value in the assessment of suspected acute coronary syndromes, in the context of a nondiagnostic electrocardiogram. Greater clinical experience improves accuracy as a rule-in tool but does not improve overall discriminatory ability.