BackgroundHigh-sensitivity cardiac troponin assays enable the early risk stratification of patients with suspected acute coronary syndrome to identify those at low risk of myocardial infarction or cardiac death. We evaluated the performance of a novel high-sensitivity cardiac troponin I assay in early rule out pathways.MethodsIn 1920 patients with suspected acute coronary syndrome, cardiac troponin was measured using the Siemens Atellica high-sensitivity cardiac troponin I assay (99th centile: 34 ng/L women, 53 ng/L men). We evaluated three pathways which use either low risk-stratification thresholds of cardiac troponin (High-SensitivityTroponin in the Evaluation of patients with Acute Coronary Syndrome (High-STEACS) and the European Society of Cardiology (ESC) 1 hour pathway) or the 99th centile diagnostic threshold (ESC 3 hour pathway) to rule out myocardial infarction.ResultsThe primary outcome of myocardial infarction or cardiac death at 30 days occurred in 14.4% (277/1920). The High-STEACS pathway ruled out 63% of patients (1218/1920), with five missed events for a negative predictive value (NPV) of 99.5% (95% CI (CI) 99.1% to 99.8%). Similar performance was observed for the ESC 1 hour pathway with an NPV of 99.0% (97.6% to 99.8%). In contrast, the ESC 3 hour pathway ruled out 65% of patients (1248/1920), but missed 25 events for an NPV of 98.0% (97.1% to 98.7%).ConclusionsA novel high-sensitivity cardiac troponin I assay can safely identify patients at low risk of myocardial infarction or cardiac death. Diagnostic pathways that use low cardiac troponin concentrations for risk stratification miss fewer events than those that rely on the 99th centile to rule out myocardial infarction.Trial registrationNCT1852123.

Background: Mitral annular calcification (MAC) is associated with cardiovascular events and mitral valve dysfunction. However, the underlying pathophysiology remains incompletely understood. In this prospective longitudinal study, we used a multimodality approach including positron emission tomography, computed tomography, and echocardiography to investigate the pathophysiology of MAC and assess factors associated with disease activity and progression. Methods: A total of 104 patients (age 72±8 years, 30% women) with calcific aortic valve disease, therefore predisposed to MAC, underwent 18 F-sodium fluoride (calcification activity) and 18 F-Fluorodeoxyglucose (inflammation activity) positron emission tomography, computed tomography calcium scoring, and echocardiography. Sixty patients underwent repeat computed tomography and echocardiography after 2 years. Results: MAC (mitral annular calcium score >0) was present in 35 (33.7%) patients who had increased 18 F-fluoride (tissue-to-background ratio, 2.32 [95% CI, 1.81–3.27] versus 1.30 [1.22–1.49]; P <0.001) and 18 F-Fluorodeoxyglucose activity (tissue-to-background ratio, 1.44 [1.37–1.58] versus 1.17 [1.12–1.24]; P <0.001) compared with patients without MAC. MAC activity ( 18 F-fluoride uptake) was closely associated with the local calcium score and 18 F-Fluorodeoxyglucose uptake, as well as female sex and renal function. Similarly, MAC progression was closely associated with local factors, in particular, baseline MAC. Traditional cardiovascular risk factors and calcification activity in bone or remote atherosclerotic areas were not associated with disease activity nor progression. Conclusions: MAC is characterized by increased local calcification activity and inflammation. Baseline MAC burden was associated with disease activity and the rate of subsequent progression. This suggests a self-perpetuating cycle of calcification and inflammation that may be the target of future therapeutic interventions.

Aims Post-infarction ventricular septal defect (PIVSD) is a mechanical complication of acute myocardial infarction (AMI) with a poor prognosis. Surgical repair is the mainstay of treatment, although percutaneous closure is increasingly undertaken. Methods and resuts Patients treated with surgical or percutaneous repair of PIVSD (2010–2021) were identified at 16 UK centres. Case note review was undertaken. The primary outcome was long-term mortality. Patient groups were allocated based upon initial management (percutaneous or surgical). Three-hundred sixty-two patients received 416 procedures (131 percutaneous, 231 surgery). 16.1% of percutaneous patients subsequently had surgery. 7.8% of surgical patients subsequently had percutaneous treatment. Times from AMI to treatment were similar [percutaneous 9 (6–14) vs. surgical 9 (4–22) days, P = 0.18]. Surgical patients were more likely to have cardiogenic shock (62.8% vs. 51.9%, P = 0.044). Percutaneous patients were substantially older [72 (64–77) vs. 67 (61–73) years, P &lt; 0.001] and more likely to be discussed in a heart team setting. There was no difference in long-term mortality between patients (61.1% vs. 53.7%, P = 0.17). In-hospital mortality was lower in the surgical group (55.0% vs. 44.2%, P = 0.048) with no difference in mortality after hospital discharge (P = 0.65). Cardiogenic shock [adjusted hazard ratio (aHR) 1.97 (95% confidence interval 1.37–2.84), P &lt; 0.001), percutaneous approach [aHR 1.44 (1.01–2.05), P = 0.042], and number of vessels with coronary artery disease [aHR 1.22 (1.01–1.47), P = 0.043] were independently associated with long-term mortality. Conclusion Surgical and percutaneous repair are viable options for management of PIVSD. There was no difference in post-discharge long-term mortality between patients, although in-hospital mortality was lower for surgery.

Aims Cardiovascular thrombosis is responsible a quarter of deaths annually worldwide. Current imaging methods for cardiovascular thrombosis focus on anatomical identification of thrombus but cannot determine thrombus age or activity. Molecular imaging techniques hold promise for identification and quantification of thrombosis in vivo. Our objective was to assess a novel optical and positron-emitting probe targeting Factor XIIIa (ENC2015) as biomarker of active thrombus formation. Methods and results Optical and positron-emitting ENC2015 probes were assessed ex vivo using blood drawn from human volunteers and passed through perfusion chambers containing denuded porcine aorta as a model of arterial injury. Specificity of ENC2015 was established with co-infusion of a factor XIIIa inhibitor. In vivo18F-ENC2015 biodistribution, kinetics, radiometabolism, and thrombus binding were characterized in rats. Both Cy5 and fluorine-18 labelled ENC2015 rapidly and specifically bound to thrombi. Thrombus uptake was inhibited by a factor XIIIa inhibitor. 18F-ENC2015 remained unmetabolized over 8 h when incubated in ex vivo human blood. In vivo, 42% of parent radiotracer remained in blood 60 min post-administration. Biodistribution studies demonstrated rapid clearance from tissues with elimination via the urinary system. In vivo,18F-ENC2015 uptake was markedly increased in the thrombosed carotid artery compared to the contralateral patent artery (mean standard uptake value ratio of 2.40 vs. 0.74, P &lt; 0.0001). Conclusion  ENC2015 rapidly and selectively binds to acute thrombus in both an ex vivo human translational model and an in vivo rodent model of arterial thrombosis. This probe holds promise for the non-invasive identification of thrombus formation in cardiovascular disease.

Background. 18 F-Fluoride uptake denotes calcification activity in aortic stenosis and atherosclerosis. While PET/MR has several advantages over PET/CT, attenuation correction of PET/MR data is challenging, limiting cardiovascular application. We compared PET/MR and PET/CT assessments of 18 F-fluoride uptake in the aortic valve and coronary arteries. Methods and results. 18 patients with aortic stenosis or recent myocardial infarction underwent 18 F-fluoride PET/CT followed immediately by PET/MR. Valve and coronary 18 Ffluoride uptake were evaluated independently. Both standard (Dixon) and novel radial GRE) MR attenuation correction (AC) maps were validated against PET/CT with results expressed as tissue-to-background ratios (TBRs). Visually, aortic valve 18 F-fluoride uptake was similar on PET/CT and PET/MR. TBR MAX values were comparable with radial GRE AC (PET/CT 1.55±0.33 vs. PET/MR 1.58 ± 0.34, P 5 0.66; 95% limits of agreement 2 27% to 1 25%) but performed less well with Dixon AC (1.38 ± 0.44, P 5 0.06; bias (2)14%; 95% limits of agreement 2 25% to 1 53%). In native coronaries, 18 F-fluoride uptake was similar on PET/ MR to PET/CT regardless of AC approach. PET/MR identified 28/29 plaques identified on PET/CT; however, stents caused artifact on PET/MR making assessment of 18 F-fluoride uptake challenging.

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ObjectiveCT quantification of aortic valve calcification (CT-AVC) is useful in the assessment of aortic stenosis severity. Our objective was to assess its ability to track aortic stenosis progression compared with echocardiography.MethodsSubjects were recruited in two cohorts: (1) a reproducibility cohort where patients underwent repeat CT-AVC or echocardiography within 4 weeks and (2) a disease progression cohort where patients underwent annual CT-AVC and/or echocardiography. Cohen’s d-statistic (d) was computed from the ratio of annualised progression and measurement repeatability and used to estimate group sizes required to detect annualised changes in CT-AVC and echocardiography.ResultsA total of 33 (age 71±8) and 81 participants (age 72±8) were recruited to the reproducibility and progression cohorts, respectively. Ten CT scans (16%) were excluded from the progression cohort due to non-diagnostic image quality. Scan-rescan reproducibility was excellent for CT-AVC (limits of agreement −12% to 10 %, intraclass correlation (ICC) 0.99), peak velocity (−7% to +17%; ICC 0.92) mean gradient (−25% to 27%, ICC 0.96) and dimensionless index (−11% to +15%; ICC 0.98). Repeat measurements of aortic valve area (AVA) were less reliable (−44% to +28%, ICC 0.85).CT-AVC progressed by 152 (65–375) AU/year. For echocardiography, the median annual change in peak velocity was 0.1 (0.0–0.3) m/s/year, mean gradient 2 (0–4) mm Hg/year and AVA −0.1 (−0.2–0.0) cm2/year. Cohen’s d-statistic was more than double for CT-AVC (d=3.12) than each echocardiographic measure (peak velocity d=0.71 ; mean gradient d=0.66; AVA d=0.59, dimensionless index d=1.41).ConclusionCT-AVC is reproducible and demonstrates larger increases over time normalised to measurement repeatability compared with echocardiographic measures.

In the current era of transcatheter device therapy, the prevalence of prosthetic aortic valves and their associated complications is increasing. Echocardiography remains the first-line imaging investigation for the assessment of prosthetic valve complications, however, this often fails to identify the underlying mechanism of prosthesis failure. Recently, cardiac CT has emerged as an imaging technique capable of providing high isotropic spatial resolution of the prosthetic valve and its utility can provide important complementary diagnostic information. In this pictorial review, we present a series of common prosthetic aortic valve complications imaged with cardiac CT and demonstrate how use of this modality can enhance diagnostic accuracy.