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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.

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 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.

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

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.

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