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Cardiovascular (CV) disease is a condition with high levels of morbidity and mortality. Canakinumab is a novel monoclonal antibody therapy that has been shown to reduce CV events but is associated with side effects and high cost. The main objective for this analysis is to determine whether canakinumab use is cost-effective for the prevention of recurrent CV events.A decision model was developed to estimate the direct costs and outcomes among patients who have suffered a myocardial infarction and are treated with canakinumab. A lifetime study horizon was used to analyze the base-case costs and utilities from the perspective of the Canadian publicly funded healthcare system. Markov modeling was used in combination with Monte Carlo simulation to derive expected values for costs and quality-adjusted life years (QALYs), permitting the calculation of incremental cost-effectiveness ratios.Canakinumab was associated with higher average lifetime costs per patient ($457,982 vs $82,565) and higher average QALYs per patient (14.90 vs 14.20), compared with standard of care. Thus, the incremental cost per QALY gained for canakinumab treatment vs standard-of-care therapy was $535,365. The probability that canakinumab treatment is cost-effective was 0%. Results were consistent over a range of scenario analyses.Treatment of patients post-myocardial infarction with canakinumab is not cost-effective, compared with standard-of-care therapy at the current price. Based on currently accepted willingness-to-pay thresholds in Canada, a reduction in price of 91% is required to yield a cost per patient that would be considered appropriate.La maladie cardiovasculaire (CV) est une affection à forts taux de morbidité et de mortalité. Le canakinumab est un nouveau traitement par anticorps monoclonaux qui s’est avéré diminuer les événements CV, mais qui est associé à des effets secondaires et des coûts élevés. Le principal objectif de la présente analyse est de déterminer si l’utilisation du canakinumab est rentable dans la prévention des événements CV récidivants.Nous avons élaboré un modèle de prise de décision pour estimer les coûts directs et les résultats chez les patients qui ont souffert d’un infarctus du myocarde et qui sont traités par canakinumab. Nous avons utilisé un horizon d’étude sur la vie entière pour l’analyse coût-utilité de référence selon la perspective du système de soins de santé du Canada financé par l’État. La modélisation de Markov qui a été utilisée en combinaison avec la simulation Monte Carlo pour obtenir les valeurs attendues des coûts et des années de vie ajustées en fonction de la qualité (AVAQ) a permis le calcul des ratios coûts-efficacité différentiels.Le canakinumab a été associé à des coûts moyens sur la vie entière plus élevés par patient (457 982 $Le traitement des patients après un infarctus du myocarde par canakinumab n’est pas rentable comparativement au traitement selon la norme de soins au prix actuel. Selon les seuils de propension à payer actuellement acceptés au Canada, une réduction du prix de 91 % est requise pour obtenir un coût par patient qui serait considéré comme approprié.

Aim The aim of the study was to evaluate the changes in central vascular inflammation measured by FDG PET and myocardial blood flow reserve (MFR) determined by 82Rb PET following therapy with biologic agents for 6 months in patients with psoriatic arthritis (PsA) and/or cutaneous psoriasis (PsO) (group 1) and compare with PsO subjects receiving non-biologic therapy (group 2) and controls (group 3). Methods and Results Target-to-background ratio (TBR) by FDG PET in the most diseased segment of the ascending aorta (TBRmax) was measured to assess vascular inflammation. 82Rb PET studies were used to assess changes in left ventricular MFR. A total of 34 participants were enrolled in the study (11 in group 1, 13 in group 2, and 10 controls). A significant drop in the thoracic aorta uptake was observed in the biologic-treated group (ΔTBRmax: − .46 ± .55) compared to the PsO group treated with non-biologic therapy (ΔTBRmax: .23 ± .67). Those showing response to biologic agents maintained MFR compared to who showed no response. Conclusion In a cohort of psoriasis patients treated with biologics, FDG uptake in the thoracic aorta decreased over the study period. Patients who demonstrated a significant anti-inflammatory response on FDG PET imaging maintained their MFR compared to non-responders.

We identified the prevalence of elevated high-sensitivity C-reactive protein and interleukin-6 in patients with recent cardiovascular (CV) events with or without prediabetes/diabetes, and in a control group of patients with remote CV events. Interleukin-6 was elevated in patients with prediabetes/diabetes and recent CV events (median, 4.84 pg/mL; interquartile range, 3.27-7.45) compared with patients with remote events (2.36 pg/mL; interquartile range, 1.09-4.00). There was a trend for elevated high-sensitivity C-reactive protein in patients with acute events and prediabetes/diabetes (P = 0.147). This supports the notion that patients with prediabetes/diabetes and recent CV events have higher inflammatory burdens than patients without recent CV events or dysglycemia. Résumé: Nous avons défini la prévalence de l’augmentation du taux de protéine C réactive à haute sensibilité et d’interleukine-6 chez des patients ayant récemment subi des événements cardiovasculaires (CV), atteints ou non de prédiabète ou de diabète, et dans un groupe témoin de patients ayant subi des événements CV antérieurement. Le taux d’interleukine-6 était élevé chez les patients atteints de prédiabète ou de diabète ayant récemment subi des événements CV (médiane de 4,84 pg/ml; écart interquartile de 3,27 à 7,45) par rapport aux patients ayant subi des événements antérieurement (2,36 pg/ml; écart interquartile de 1,09 à 4,00). Le taux de protéine C réactive à haute sensibilité avait tendance à être élevé chez les patients atteints de prédiabète ou de diabète ayant subi des événements aigus (p = 0,147). Ces données appuient la notion selon laquelle les patients atteints de prédiabète ou de diabète qui ont récemment subi des événements CV présentent des fardeaux inflammatoires supérieurs à ceux des patients qui n’ont pas récemment subi d’événements CV ou présenté de dysglycémie.

Molecular imaging with positron emission tomography (PET) and single-photon emission computed tomography (SPECT) serves numerous applications in clinical cardiology and research. Similar to other medical imaging technologies, this area has undergone and continues to experience rapid changes resulting from technological and medical advances. These have immediate impacts on diagnosis, treatment planning, and patient care, as well as supplying innovative tools for fundamental and translational research. A broad shift toward hybrid PET systems and incorporation of advanced computational tools has been accompanied by mechanism-specific, targeted radiopharmaceuticals that seek to address long-standing limitations in cardiac imaging. While this review addresses some of the still-emerging clinical uses of established radiopharmaceuticals, it too highlights newer imaging probes, applications, and imaging techniques and instrumentation on the horizon. We highlight molecular imaging advances in inflammatory and infiltrative myocardial conditions, heart metabolism, vascular and valvular diseases, neurohormonal dysregulation, and transformational technical advances such as the rise of artificial intelligence and theranostic approaches to cardiovascular disease.

Thoracic aortic aneurysm (TAA) is associated with high morbidity and mortality, and there is a critical need for improved tools for risk assessment and prognostication. We have previously shown that aortic stiffness, measured from arterial tonometry (carotid-femoral pulse wave velocity [cfPWV]), is independently associated with TAA expansion. To increase clinical applicability, we sought to determine the association of mathematically estimated aortic pulse wave velocity (e-PWV) with TAA expansion.One-hundred and five consecutive unoperated subjects with TAA were recruited. We used arterial tonometry to measure cfPWV and used mean arterial pressure and age to calculate e-PWV according to validated equations. Multivariable linear regression assessed associations of baseline e-PWV with future aneurysm growth. Given sex differences in TAA outcomes, sex-stratified analyses were performed.Seventy-eight percent of subjects were men. Mean ± standard deviation (SD) age, baseline aneurysm size, and follow-up time were 62.6 ± 11.4 years, 46.2 ± 3.8 mm, and 2.9 ± 1.0 years, respectively. Aneurysm growth was 0.43 ± 0.37 mm per year; e-PWV was independently associated with future aneurysm expansion (β ± SE: 0.240 ± 0.085, P = 0.006). In sex-specific analyses, e-PWV was associated with aneurysm growth in both men (β ± standard error (SE) : 0.076 ± 0.022, P = 0.001) and women (β ± SE : 0.145 ± 0.050, P = 0.012), but the strength of association nearly twice as strong in women as in men.Greater aortic stiffness reflects worse aortic health and provides novel insights into disease activity; e-PWV is independently associated with TAA growth. This finding increases clinical applicability, as e-PWV can be estimated simply, quickly, and free of cost without the need for specialized equipment.

Background Cardiogenic shock (CS) is associated with significant morbidity and mortality. The impact of beta-blocker (BB) use on patients who develop CS remains unknown. We sought to evaluate the clinical outcomes and hemodynamic response profiles in patients treated with BB in the 24 h prior to the development of CS. Methods Patients with CS enrolled in the DObutamine compaREd to MIlrinone trial were analyzed. The primary outcome was a composite of all-cause mortality, resuscitated cardiac arrest, need for cardiac transplant or mechanical circulatory support, non-fatal myocardial infarction, transient ischemic attack or stroke, or initiation of renal replacement therapy. Secondary outcomes included the individual components of the primary composite and hemodynamic response profiles derived from pulmonary artery catheters. Results Among 192 participants, 93 patients (48%) had received BB therapy. The primary outcome occurred in 47 patients (51%) in the BB group and in 52 (53%) in the no BB group (RR 0.96; 95% CI 0.73–1.27; P = 0.78) throughout the in-hospital period. There were fewer early deaths in the BB group (RR 0.41; 95% CI 0.18–0.95; P = 0.03). There were no differences in other individual components of the primary outcome or in hemodynamic response between the two groups throughout the remainder of the hospitalization. Conclusions BB therapy in the 24 h preceding the development of CS did not negatively influence clinical outcomes or hemodynamic parameters. On the contrary, BB use was associated with fewer deaths in the early resuscitation period, suggesting a paradoxically protective effect in patients with CS. Trial registration ClinicalTrials.gov Identifier: NCT03207165

This study aimed to evaluate markers of systemic as well as imaging markers of inflammation in the ascending aorta, bone marrow, and spleen measured by 18F-FDG PET/CT, in HIV+ patients at baseline and following therapy with rosuvastatin. Of the 35 HIV+ patients enrolled, 17 were randomized to treatment with 10 mg/day rosuvastatin and 18 to usual care for 6 months. An HIV− control cohort was selected for baseline comparison of serum inflammatory markers and monocyte markers of inflammation. 18F-FDG-PET/CT imaging of bone marrow, spleen, and thoracic aorta was performed in the HIV+ cohort at baseline and 6 months. While CD14++CD16− and CCR2 expressions were reduced, serum levels of IL-7, IL-8, and MCP-1 were elevated in the HIV+ population compared to the controls. There was a significant drop in FDG uptake in the bone marrow (TBRmax), spleen (SUVmax) and thoracic aortic (TBRmax) in the statin-treated group compared to the control group (bone marrow: − 10.3 ± 16.9% versus 5.0 ± 18.9%, p = .0262; spleen: − 9.8 ± 20.3% versus 11.3 ± 28.8%, p = .0497; thoracic aorta: − 19.1 ± 24.2% versus 4.3 ± 15.4%, p = .003). HIV+ patients had significantly markers of systemic inflammation including monocyte activation. Treatment with low-dose rosuvastatin in the HIV+ cohort significantly reduced bone marrow, spleen and thoracic aortic FDG uptake.

Background Acute Heart Failure (AHF) is a potentially lethal pathology and is often encountered in the prehospital setting. Although an association between prehospital arterial hypercapnia in AHF patients and admission in high-dependency and intensive care units has been previously described, there is little data to support an association between prehospital arterial hypercapnia and mortality in this population. Methods This was a retrospective study based on electronically recorded prehospital medical files. All adult patients with AHF were included. Records lacking arterial blood gas data were excluded. Other exclusion criteria included the presence of a potentially confounding diagnosis, prehospital cardiac arrest, and inter-hospital transfers. Hypercapnia was defined as a PaCO2 higher than 6.0 kPa. The primary outcome was in-hospital mortality, and secondary outcomes were 7-day mortality and emergency room length of stay (ER LOS). Univariable and multivariable logistic regression models were used. Results We included 225 patients in the analysis. Prehospital hypercapnia was found in 132 (58.7%) patients. In-hospital mortality was higher in patients with hypercapnia (17.4% [23/132] versus 6.5% [6/93], p = 0.016), with a crude odds-ratio of 3.06 (95%CI 1.19–7.85). After adjustment for pre-specified covariates, the adjusted OR was 3.18 (95%CI 1.22–8.26). The overall 7-day mortality was also higher in hypercapnic patients (13.6% versus 5.5%, p = 0.044), and ER LOS was shorter in this population (5.6 h versus 7.1 h, p = 0.018). Conclusion Prehospital hypercapnia is associated with an increase in in-hospital and 7-day mortality in patient with AHF.

Thoracic aortic aneurysm is a disease associated with high morbidity and mortality. Clinically useful strategies for medical management of thoracic aortic aneurysm are critically needed. To address this need, we sought to determine the role of aortic stiffness and pulsatile arterial load on future aneurysm expansion. One hundred five consecutive, unoperated subjects with thoracic aortic aneurysm were recruited and prospectively followed. By combining arterial tonometry with echocardiography, we estimated measures of aortic stiffness, central blood pressure, steady, and pulsatile arterial load at baseline. Aneurysm size was measured at baseline and follow-up with imaging; growth was calculated in mm/y. Stepwise multivariable linear regression assessed associations of arterial stiffness and load measures with aneurysm growth after adjusting for potential confounders. Mean±SD age, baseline aneurysm size, and follow-up time were 62.6±11.4 years, 46.24±3.84 mm, and 2.92±1.01 years, respectively. Aneurysm growth rate was 0.43±0.37 mm/y. After correcting for multiple comparisons, higher central systolic (β±SE: 0.026±0.009, P =0.007), and pulse pressures (β±SE: 0.032±0.009, P =0.0002), carotid-femoral pulse wave velocity (β±SE: 0.032±0.011, P =0.005), amplitudes of the forward (β±SE: 0.044±0.012, P =0.0003) and reflected (β±SE: 0.060±0.020, P =0.003) pressure waves, and lower total arterial compliance (β±SE: −0.086±0.032, P =0.009) were independently associated with future aneurysm growth. Measures of aortic stiffness and pulsatile hemodynamics are independently associated with future thoracic aortic aneurysm growth and provide novel insights into disease activity. Our findings highlight the role of central hemodynamic assessment to tailor novel risk assessment and therapeutic strategies to patients with thoracic aortic aneurysm.

Introduction: Cardiovascular disease (CVD) is a major source of morbidity and mortality in HIV+ patients, which is thought to be in part due to a state of persistent systemic inflammation that results in accelerated atherosclerosis. Hypothesis: We hypothesized that inflammation, as measured by 18F-fluorodeoxyglucose (18F-FDG) uptake measured by 18F-FDG positron emission tomography/computed tomography (18F-FDG-PET/CT) in the bone marrow, spleen and thoracic aorta would improve in HIV+ patients following therapy with rosuvastatin compared to HIV+ patients not receiving a statin. Methods: HIV+ patients with a moderate Framingham risk score were enrolled in the study and randomized to treatment with rosuvastatin or usual treatment for 6 months. Patients were matched for age, sex, smoking status, Framingham risk score, duration of anti-retroviral therapy (ART) and type of ART. Fasting blood was collected and 18F-FDG-PET/CT imaging of bone marrow, spleen, and thoracic aorta was performed at baseline and 6 months. Results: Thirty-five HIV+ patients were enrolled in the study; 17 were randomized to treatment with rosuvastatin and 18 were randomized to the control group. There was a significant drop in the 18F-FDG bone marrow, spleen and thoracic aortic uptake in the statin-treated group compared to the control group (bone marrow: -10.3±16.9% versus 5.0±18.9%, p=0.0262; spleen: -9.8±20.3% versus 11.3±28.8%, p=0.0497; thoracic aorta: -8.6±24.5% versus 12.6±29.5%, p=0.0343). 18F-FDG changes over the study period are shown in Figure 1. Conclusions: The present study observed a significant decrease in 18F-FDG-PET uptake in the bone marrow, spleen, and thoracic aorta following treatment with rosuvastatin for 6 months in HIV+ patients. These data suggest a wide-range anti-inflammatory effect of rosuvastatin in HIV+ individuals with well-controlled infection on ART, ultimately resulting in decreased inflammatory activity in the arterial walls of these patients.

Background Thoracic aortic aneurysm (TAA) is a deadly disease in critical need of novel strategies for risk assessment and medical management. To address this need, we have previously shown that directly measured carotid-femoral pulse wave velocity (cfPWV), a marker of aortic stiffness and health, independently predicts future TAA expansion. Since aortic pulse wave velocity can be estimated from age and mean arterial pressure (MAP), in the present study we sought to determine whether estimated aortic pulse wave velocity (e-aPWV) also predicts TAA expansion. Methods One hundred and five consecutive, unoperated subjects with TAA were recruited. e-aPWV was estimated from validated equations based on age and MAP. cfPWV was measured with arterial tonometry according to guidelines. TAA size was measured at baseline and at the latest follow-up using available imaging modalities according to guidelines. Stepwise multivariable linear regression (P≤0.25 to enter, P≤0.10 to stay in the model) assessed independent associations of e-aPWV and cfPWV with future TAA growth. Variables considered in the models were: age, sex, BSA, MAP, TAA etiology and location, baseline TAA size, follow-up time, imaging modality, history of hypertension, diabetes and smoking. Results Seventy eight percent of subjects were men. Mean±SD age, baseline aneurysm size and follow-up time were 62.6±11.4 years, 46.2±3.8 mm and 3.0±1.0 years, respectively. e-aPWV and cfPWV were moderately correlated (Pearson's correlation coefficient = 0.61). Results of the linear regression analyses showed that both measured (cfPWV) and estimated (e-aPWV) independently predicted future TAA expansion (β±SE: 0.032±0.011, P=0.048 and 0.240±0.085, P=0.006, respectively). The base model's R-squared value of 0.39 was increased to 0.44 with addition of either cfPWV or e-aPWV to the model, confirming that each parameter of aortic stiffness enhances prediction of TAA growth. Conclusion Aortic stiffness is relevant for assessment of TAA disease activity. Similar to cfPWV, e-aPWV is also independently associated with future TAA expansion. Thus, e-aPWV represents a tool to improve TAA risk stratification that is simple, free of cost, and obviates the need for specialized equipment or dedicating training, which leads to excellent potential for widespread incorporation into clinical practice. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Canadian Institutes of Health Research

BACKGROUND There are discrepancies in the quantitative echocardiographic criteria for the right ventricle (RV) between the revised task force criteria (TFC) for Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) and the guidelines for RV assessment endorsed by American Society of Echocardiography (ASE). Importantly, these criteria do not take into account potential adaptation of the RV to exercise. The goal of this study was to compare the revised TFC quantitative echocardiographic parameters in patients with ARVC/D, athletes and matched controls. METHODS Echocardiographic parameters of the RV were retrospectively collected in patients who fulfilled the TFC for ARVC/D, an age- matched, sex-matched, and body surface area-matched control population, and athletes (defined as individuals who exercised for more than 7 hours per week). Patients with structural heart disease were excluded in the control and athlete groups. RESULTS Twenty patients with ARVC/D, 11 athletes and 20 matched controls were included. There was no significant difference between ARVC/D patients and athletes with the exception of the parasternal long axis right ventricular outflow tract diameter. All parameters were significantly different between ARVC/D patients and the control group. Furthermore, when subjects were categorized into meeting 1 major revised TFC/abnormal ASE criteria or not, only ASE criteria were able to differentiate ARVC/D from control population. Both were unable to differentiate ARVC/D from athletes. CONCLUSIONS Right ventricle quantitative echocardiographic criteria in the revised TFC are not specific for ARVC/D. Care should be taken in applying these criteria in athletes.

Aneurysm formation is a complex multifactorial process with both genetic and environmental influences. Over recent years, there has been increasing recognition of sex-specific differences regarding the prevalence and natural history of cardiovascular diseases in the population. In particular, there is a growing body of evidence showing that aneurysm behaviour differs based on sex. Although most types of aneurysms are more common in men, their growth rates and outcomes are worse in women. This fact raises attention about potential underlying differences in the arteries of men and women that may contribute to differences in aneurysm prevalence and outcomes. There are complex biochemical and mechanical mechanisms at play that contribute to vascular health. Furthermore, many studies have suggested potential differences in the hormonal milieu and underlying arterial anatomy between men and women. Based on the data reviewed in this article, assessment of the underlying pathophysiology of aneurysms in women might prove clinically useful regarding prevention, early detection, and management of aneurysms in women. Sex-specific research, screening, and treatment guidelines for aneurysm disease should be introduced to reflect the differing natural history of these diseases in men and women.

Previous studies have demonstrated that left atrial (LA) volume has incremental prognostic value in predicting major adverse cardiac events (MACE). However, the predictive ability of LA volume in mid diastasis has not been investigated. We determined the incremental predictive value of LA volume indexed to body surface area (LAVi) measured in mid ventricular diastasis.A total of 96 patients with MACE (all-cause mortality and nonfatal myocardial infarction) were matched to 96 controls without adverse events on follow-up. Coronary computed tomographic angiography images were reconstructed at the 75% phase (mid ventricular diastasis). LA volumes were measured and indexed to the body surface area. The predictive value of LAVi was assessed using Cox proportional hazard models for the MACE.LAVi was significantly larger (P0.001) in the cases with adverse clinical outcomes (63.8±2.1 mL/m) versus the controls (50.3±1.2 mL/m). In a multivariate analysis, both significant coronary artery disease (defined as70% stenosis in at least 1 coronary artery) and LAVi emerged as significant predictors of MACE with P-values of 0.0022 and 0.0001, respectively.A significantly larger LAVi was associated with MACE. LAVi was an incremental predictor to traditional clinical variables for MACE. The assessment of LAVi may be considered during coronary computed tomographic angiography and could potentially be incorporated into risk stratification and decision-making strategies.

Background: Cardiotoxicity from anthracycline-based chemotherapy is an important cause of early and late morbidity and mortality in breast cancer patients. Left ventricular (LV) function is assessed for patients receiving anthracycline-based chemotherapy to identify cardiotoxicity. However, animal studies suggest that right ventricular (RV) function may be a more sensitive measure to detect LV dysfunction. The purpose of this pilot study was to determine if breast cancer patients undergoing anthracycline-based chemotherapy experience RV dysfunction. Methods: Forty-nine breast cancer patients undergoing anthracycline-based chemotherapy at the Ottawa Hospital between November 2007 and March 2013 and who had 2 echocardiograms performed at least 3 months apart were retrospectively identified. Right atrial area (RAA), right ventricular fractional area change (RV FAC) and RV longitudinal strain of the free wall (RV LSFW) were evaluated according to the American Society of Echocardiography guidelines. Results: The majority (48/49) of patients were females with an average age of 53.4 (95% CI: 50.1-56.7 years). From baseline to follow-up study, average LV ejection fraction (LVEF) decreased from 62.22 (95% CI: 59.1-65.4) to 57.4% (95% CI: 54.0-60.9) (P = 0.04). During the same time period, the mean RAA increased from 12.1 cm2 (95% CI: 11.1-13.0 cm2) to 13.8 cm2 (95% CI: 12.7-14.9 cm2) (P = 0.02), mean RV FAC decreased (P = 0.01) from 48.3% (95% CI: 44.8-51.74) to 42.1% (95% CI: 38.5-45.6%), and mean RV LSFW worsened from -16.2% (95% CI: -18.1 to -14.4%) to -13.81% (95% CI: -15.1 to -12.5%) (P = 0.04). Conclusion: This study demonstrates that breast cancer patients receiving anthracycline-based chemotherapy experience adverse effects on both right atrial size and RV function. Further studies are required to determine the impact of these adverse effects on right heart function and whether this represents an earlier marker of cardiotoxicity.

Women with thoracic aortic aneurysms (TAAs) have higher risk of acute aortic syndromes and death than men. We have shown that TAA growth is accelerated in women, helping explain the sex differences in TAA outcomes. Since aortic stiffness reflects the health of the aorta, we sought to determine the sex-specific role of aortic stiffness on TAA growth. One hundred thirty unoperated people with TAA were recruited. Maximal aneurysm size at the oldest and latest imaging studies was measured to calculate TAA growth rate. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) using applanation tonometry. Multivariable linear regression adjusted for confounders assessed the association of cfPWV with TAA growth. Seventy-three percent of subjects were men. Mean±SD age, baseline aneurysm size, follow-up time, and cfPWV were 62.5±11.5 years, 45.3±4.0 mm, 3.3±3.0 years and 9.6±3.5 m/s, and not different based on sex. TAA growth rate was 0.96±1.00 mm/y in women and 0.45±0.58 mm/y in men ( P=0.006). In the whole group, cfPWV was independently associated with TAA growth (β±SE: 0.06±0.02, P=0.02). However, in sex-specific analyses cfPWV was independently associated with faster aneurysm growth in women (β±SE: 0.21±0.09, P=0.03), but not in men (β±SE: -0.002±0.02, P=0.94), with a significant sex×cfPWV interaction ( P0.0001). In patients with TAA, aneurysm growth is more than twice as fast in women than men, and aortic stiffness is associated with greater TAA growth in women, but not in men. Our findings highlight greater aortic stiffness as an important correlate of TAA expansion in women.

Background New-onset or worsening heart failure is the most common extra-pulmonary complication of community-acquired pneumonia (CAP) during the first 30 days after diagnosis. Methods We evaluated the changes in the right ventricular function amongst adult CAP survivors from the time of acute infection to its resolution. We performed comprehensive transthoracic echocardiographic examinations to assess right heart function during the acute illness and the convalescent period (four to six weeks after hospital discharge). Results Twenty-six patients underwent acute measurements, of which convalescent measurements were completed in 19 subjects. There was no significant change in any of the right heart function parameters from the acute to convalescent stage of CAP. Conclusions Our results suggest that right ventricular function does not meaningfully change in the transition from the acute to convalescent stage of CAP in non-critically ill adult CAP survivors.

Introduction Aortic valve calcification (AVC) has been associated with major adverse cardiovascular events and all-cause mortality. We sought to develop and validate a method to quantify AVC using coronary CT angiography (CTA). Methods Of 59 patients who underwent both non-contrast and contrast enhanced coronary CTA, 25 patients served as the derivation cohort and 34 patients served as the validation cohort. For non-contrast enhanced CT, quantification of AVC was performed using the Agatston method for coronary artery calcification (CAC). For contrast enhanced coronary CTA, a region of interest (ROI) was placed in the ascending aorta and the mean aortic attenuation value (HU Aorta ) and standard deviation (SD) were measured. Using a calcium threshold of mean HU Aorta + 2SD, the AVC CTA was calculated. All other Agatston score parameters (weighting factors and area calculations) remained unchanged. Results In the derivation cohort, the correlation between AVC CAC and AVC CTA was excellent (r = 0.982). Using the line of best fit, a correction factor was calculated enabling the conversion of AVC CTA results to a AVC CAC equivalent (AVC Corrected = 1.868 × AVC CTA ). Using this correction in the validation cohort, the correlation and agreement between AVC CAC and AVC Corrected were good (ICC = 0.939; 95% CI: 0.881–0.969; kappa = 0.700; 95% CI: 0.469–0.931). Conclusion The quantification of AVC Corrected using contrast enhanced CTA is feasible using a systematic approach with very good reliability and good agreement with AVC CAC . Larger-scale validation studies are needed to determine whether the use of AVC CAC can be eliminated in favour of AVC Corrected .

Women with thoracic aortic aneurysms (TAAs) have higher risk of acute aortic syndromes and death than men. We have shown that TAA growth is accelerated in women, helping explain the sex differences in TAA outcomes. Since aortic stiffness reflects the health of the aorta, we sought to determine the sex-specific role of aortic stiffness on TAA growth. One hundred thirty unoperated people with TAA were recruited. Maximal aneurysm size at the oldest and latest imaging studies was measured to calculate TAA growth rate. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) using applanation tonometry. Multivariable linear regression adjusted for confounders assessed the association of cfPWV with TAA growth. Seventy-three percent of subjects were men. Mean±SD age, baseline aneurysm size, follow-up time, and cfPWV were 62.5±11.5 years, 45.3±4.0 mm, 3.3±3.0 years and 9.6±3.5 m/s, and not different based on sex. TAA growth rate was 0.96±1.00 mm/y in women and 0.45±0.58 mm/y in men ( P =0.006). In the whole group, cfPWV was independently associated with TAA growth (β±SE: 0.06±0.02, P =0.02). However, in sex-specific analyses cfPWV was independently associated with faster aneurysm growth in women (β±SE: 0.21±0.09, P =0.03), but not in men (β±SE: −0.002±0.02, P =0.94), with a significant sex×cfPWV interaction ( P