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Aims Aortic valve calcification (AVC) of surgical valve bioprostheses (BPs) has been poorly explored. We aimed to evaluate in vivo and ex vivo BP AVCs and its prognosis value. Methods and results Between 2011 and 2019, AVC was assessed using in vivo computed tomography (CT) in 361 patients who had undergone surgical valve replacement 6.4 ± 4.3 years earlier. Ex vivo CT scans were performed for 37 explanted BPs. The in vivo CT scans were interpretable for 342 patients (19 patients [5.2%] were excluded). These patients were 77.2 ± 9.1 years old, and 64.3% were male. Mean in vivo AVC was 307 ± 500 Agatston units (AU). The AVC was 562 ± 570 AU for the 183 (53.5%) patients with structural valve degeneration (SVD) and 13 ± 43 AU for those without SVD (P < 0.0001). In vivo and ex vivo AVCs were strongly correlated (r = 0.88, P < 0.0001). An in vivo AVC > 100 AU (n = 147, 43%) had a specificity of 96% for diagnosing Stage 2–3 SVD (area under the curve = 0.92). Patients with AVC > 100 AU had a worse outcome compared with those with AVC ≤ 100 AU (n = 195). In multivariable analysis, AVC was a predictor of overall mortality (hazard ratio [HR] and 95% confidence interval = 1.16 [1.04–1.29]; P = 0.006), cardiovascular mortality (HR = 1.22 [1.04–1.43]; P = 0.013), cardiovascular events (HR = 1.28 [1.16–1.41]; P < 0.0001), and re-intervention (HR = 1.15 [1.06–1.25]; P < 0.0001). After adjustment for Stage 2–3 SVD diagnosis, AVC remained a predictor of overall mortality (HR = 1.20 [1.04–1.39]; P = 0.015) and cardiovascular events (HR = 1.25 [1.09–1.43]; P = 0.001). Conclusion CT scan is a reliable tool to assess BP leaflet calcification. An AVC > 100 AU is tightly associated with SVD and it is a strong predictor of overall mortality and cardiovascular events. [ABSTRACT FROM AUTHOR]

Checkpoint kinase inhibitors are increasingly used in oncology. The combination of atezolizumab and bevacizumab is currently the recommended first-line treatment for advanced hepatocellular carcinoma. Cardiac toxicities of immunotherapies are rare, but can lead to discontinuation of treatment. Transthyretin cardiac amyloidosis is a rare condition, but its incidence is probably underestimated. Its symptoms may suggest immunotherapy-induced myocarditis. When immune-mediated myocarditis is suspected, a thorough cardiac evaluation is necessary to confirm or refute the diagnosis of myocarditis and to avoid unnecessary interruption of immunotherapy. Cardiac magnetic resonance imaging may raise suspicion of transthyretin cardiac amyloidosis, the diagnosis being confirmed by technetium pyrophosphate bone scintigraphy. [ABSTRACT FROM AUTHOR]

Résumé: L'amylose cardiaque dite sénile, également dénommée « sauvage », était considérée comme une maladie rare. Actuellement, grâce à des moyens diagnostiques non invasifs et à partir d'études autopsiques, nous estimons la prévalence à environ 10 à 20 % des sujets de plus de 80 ans. De même, l'amylose était un diagnostic sans conséquence thérapeutique, mis à part le traitement de l'insuffisance cardiaque et des troubles de conduction. De nouveaux traitements permettent de stabiliser le tétramère de transthyrétine et de diminuer la production d'oligomères, sources des dépôts d'amylose, en cas de formes héréditaires et sauvage d'amylose à transthyrétine. Deux médicaments bloquant la production de transthyrétine (anti-sens et oligonucléotides) sont également en phase d'essais cliniques dans les amyloses cardiaques. Ainsi, le diagnostic et la prise en charge de l'amylose cardiaque deviennent des démarches diagnostiques de pratique clinique et doivent être connus des cardiologues, mais également des gériatres qui permettront une prise en charge précoce et donc plus efficace. So-called senile cardiac amyloidosis was considered rare. Nowadays, thanks to non-invasive diagnostic means and autopsy studies, we estimate the prevalence to be about 20% of subjects over 75 years of age. Similarly, amyloidosis was a diagnosis with no therapeutic consequences, apart from the treatment of heart failure and conduction disorders. New treatments make it possible to stabilise the transthyretin tetramer and to reduce the production of oligomers that are the source of amyloid deposits, by acting in a non-genetic way and therefore adapted to the "wild" transthyretin forms of so-called senile cardiac amyloidosis. Thus, the diagnosis and management of cardiac amyloidosis are becoming diagnostic procedures in clinical practice and must be known by cardiologists, but also by geriatricians, who will allow early and therefore more effective management. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed at determining the diagnostic implications of indirect signs of infection at FDG-PET—i.e., hypermetabolisms of the spleen and/or bone marrow (HSBM)—when documented in patients with known or suspected infective endocarditis (IE). Methods: HSBM were defined by higher mean standardized uptake values comparatively to that of the liver on FDG-PET images from patients with a high likelihood of IE and prospectively included in a multicenter study. Results: Among the 129 included patients, IE was ultimately deemed as definite in 88 cases. HSBM was a predictor of definite IE (P = 0.014; odds ratio (OR) 3.2), independently of the criterion of an abnormal cardiac FDG uptake (P = 0.0007; OR 9.68), and a definite IE was documented in 97% (29/30) of patients showing both HSBM and abnormal cardiac uptake, 78% (7/9) of patients with only abnormal cardiac uptake, 67% (42/63) of patients with only HSBM, and 37% (10/27) of patients with neither one. Conclusion: In this cohort with a high likelihood of IE, HSBM is an additional albeit indirect sign of IE, independently of the criterion of an abnormal cardiac uptake, and could reinforce the suspicion of IE in the absence of any other infectious, inflammatory, or malignant disease. [ABSTRACT FROM AUTHOR]

Background Diagnostic and patients' management modifications induced by whole-body 18F-FDG-PET/CT had not been evaluated so far in prosthetic valve (PV) or native valve (NV) infective endocarditis (IE)-suspected patients. Methods In sum, 140 consecutive patients in 8 tertiary care hospitals underwent 18F-FDG-PET/CT. ESC-2015-modified Duke criteria and patients' management plan were established jointly by 2 experts before 18F-FDG-PET/CT. The same experts reestablished Duke classification and patients' management plan immediately after qualitative interpretation of 18F-FDG-PET/CT. A 6-month final Duke classification was established. Results Among the 70 PV and 70 NV patients, 34 and 46 were classified as definite IE before 18F-FDG-PET/CT. Abnormal perivalvular 18F-FDG uptake was recorded in 67.2% PV and 24.3% NV patients respectively (P <.001) and extracardiac uptake in 44.3% PV and 51.4% NV patients. IE classification was modified in 24.3% and 5.7% patients (P =.005) (net reclassification index 20% and 4.3%). Patients' managements were modified in 21.4% PV and 31.4% NV patients (P =.25). It was mainly due to perivalvular uptake in PV patients and to extra-cardiac uptake in NV patients and consisted in surgery plan modifications in 7 patients, antibiotic plan modifications in 22 patients and both in 5 patients. Altogether, 18F-FDG-PET/CT modified classification and/or care in 40% of the patients (95% confidence interval: 32–48), which was most likely to occur in those with a noncontributing echocardiography (P <.001) or IE classified as possible at baseline (P =.04), while there was no difference between NV and PV. Conclusions Systematic 18F-FDG-PET/CT did significantly and appropriately impact diagnostic classification and/or IE management in PV and NV-IE suspected patients. Clinical Trials Registration NCT02287792. [ABSTRACT FROM AUTHOR]

It remains unknown whether β‐blockers are useful and safe in acute myocardial infarction (MI). Owing to its pharmacological profile and vasodilating action, nebivolol (N) is useful in MI. The aim of the present study was to assess in rat whether early nebivolol treatment could be beneficial in MI. It remains unknown whether β‐blockers are useful and safe in acute MI. On day (D) 0, male Sprague‐Dawley rats underwent left coronary artery ligation (MI) or simple thoracotomy (SHAM). On D1 and D2, the rats were treated with either nebivolol (5 mg.kg−1.day−1, MI‐N and Sham‐N) or vehicle (V, MI‐V and Sham‐V). On D3, heart rate, left ventricle (LV) intrinsic contractility (PESmid) and arterial elastance were measured. Cardiac and aortic β‐Adrenoceptor (AR) subtype mRNA were quantified using real time quantitative RT‐qPCR. Catecholamine response was assessed on isolated heart and aortic rings with isoproterenol. PESmid was decreased in MI without worsening the decrease nebivolol. In LV, β1‐ and β3‐AR mRNA were respectively decreased and increased in all MI. β3‐AR mRNA increase was partly limited by nebivolol. Ex vivo, basal contractility was less decreased in MI‐N than in MI‐V. Isoproterenol response was only altered in MI‐V. In MI aorta, Nebi prevented β2‐ and β3‐AR mRNA increases. In addition, Acetylcholine‐induced relaxation was lowered in MI‐V but preserved with nebivolol. We demonstrated an early modulation of cardiovascular β3‐AR transcription early MI. Despite its putative negative inotropic properties, nebivolol did not worsen cardiac function in basal conditions and preserved LV catecholamine response. [ABSTRACT FROM AUTHOR]

Aims: Diastolic dysfunction is common in cardiovascular diseases, particularly in the case of heart failure with preserved ejection fraction. The challenge is to develop adequate animal models to envision human therapies in the future. It has been hypothesized that this diastolic dysfunction is linked to alterations in the nitric oxide (•NO) pathway. To investigate this issue further, we investigated the cardiac functions of a transgenic rat model (Tgβ3) that overexpresses the human β3‐adrenoceptor (hβ3‐AR) in the endothelium with the underlying rationale that the •NO pathway should be stimulated in the endothelium. Methods and results: Transgenic rats (Tgβ3) that express hβ3‐AR under the control of intercellular adhesion molecule 2 promoter were developed for a specific expression in endothelial cells. Transcriptomic analyses were performed on left ventricular tissue from 45‐week‐old rats. Among all altered genes, we focus on •NO synthase expression and endothelial function with arterial reactivity and evaluation of •NO and O2•− production. Cardiac function was characterized by echocardiography, invasive haemodynamic studies, and working heart studies. Transcriptome analyses illustrate that several key genes are regulated by the hβ3‐AR overexpression. Overexpression of hβ3‐AR leads to a reduction of Nos3 mRNA expression (−72%; P < 0.05) associated with a decrease in protein expression (−19%; P < 0.05). Concentration‐dependent vasodilation to isoproterenol was significantly reduced in Tgβ3 aorta (−10%; P < 0.05), while •NO and O2•− production was increased. In the same time, Tgβ3 rats display progressively increasing diastolic dysfunction with age, as shown by an increase in the E/A filing ratio [1.15 ± 0.01 (wild type, WT) vs. 1.33 ± 0.04 (Tgβ3); P < 0.05] and in left ventricular end‐diastolic pressure [5.57 ± 1.23 mmHg (WT) vs. 11.68 ± 1.11 mmHg (Tgβ3); P < 0.05]. In isolated working hearts, diastolic stress using increasing preload levels led to a 20% decrease in aortic flow [55.4 ± 1.9 mL/min (WT) vs. 45.8 ± 2.5 mL/min (Tgβ3); P < 0.05]. Conclusions: The Tgβ3 rat model displays the expected increase in •NO production upon ageing and develops diastolic dysfunction. These findings provide a further link between endothelial and cardiac dysfunction. This rat model should be valuable for future preclinical evaluation of candidate drugs aimed at correcting diastolic dysfunction. [ABSTRACT FROM AUTHOR]

Aims: Several data suggest that acute myocarditis could be related to genetic variants involved in familial cardiomyopathies, particularly arrhythmogenic cardiomyopathy, but the management of patients with acute myocarditis and their families regarding their risk for having an associated inherited cardiomyopathy is unclear. Methods and results: Families with at least one individual with a documented episode of acute myocarditis and at least one individual with a cardiomyopathy or a history of sudden death were included in the study. Comprehensive pedigree, including genetic testing, and history of these families were analysed. Six families were included. Genetic analysis revealed a variant in desmosomal proteins genes in all the probands [five in desmoplakin (DSP) gene and one in desmoglein 2 gene]. In the five families identified with a DSP variant, genetic testing was triggered by the association of an acute myocarditis with a single case of apparently isolated dilated cardiomyopathy or sudden death. Familial screening identified 28 DSP variant carriers; 39% had an arrhythmogenic left ventricular (LV) cardiomyopathy phenotype. Familial histories of sudden death were frequent, and a remarkable phenotype of isolated LV late gadolinium enhancement on contrast‐enhanced cardiac magnetic resonance without any other structural abnormality was found in 38% of asymptomatic mutation carriers. None of the DSP variant carriers had imaging characteristics of right ventricle involvement meeting current Task Force criteria for arrhythmogenic right ventricular cardiomyopathy. Conclusions: Comprehensive familial screening including genetic testing in case of acute myocarditis associated with a family history of cardiomyopathy or sudden death revealed unknown or misdiagnosed arrhythmogenic variant carriers with left‐dominant phenotypes that frequently evade arrhythmogenic right ventricular cardiomyopathy Task Force criteria. In view of our results, acute myocarditis should be considered as an additional criterion for arrhythmogenic cardiomyopathy, and genetic testing should be advised in patients who experience acute myocarditis and have a family history of cardiomyopathy or sudden death. [ABSTRACT FROM AUTHOR]

Aims: The MITRA-FR trial showed that among symptomatic patients with severe secondary mitral regurgitation, percutaneous repair did not reduce the risk of death or hospitalization for heart failure at 12 months compared with guideline-directed medical treatment alone. We report the 24-month outcome from this trial.Methods and Results: At 37 centres, we randomly assigned 304 symptomatic heart failure patients with severe secondary mitral regurgitation (effective regurgitant orifice area >20 mm2 or regurgitant volume >30 mL), and left ventricular ejection fraction between 15% and 40% to undergo percutaneous valve repair plus medical treatment (intervention group, n = 152) or medical treatment alone (control group, n = 152). The primary efficacy outcome was the composite of all-cause death and unplanned hospitalization for heart failure at 12 months. At 24 months, all-cause death and unplanned hospitalization for heart failure occurred in 63.8% of patients (97/152) in the intervention group and 67.1% (102/152) in the control group [hazard ratio (HR) 1.01, 95% confidence interval (CI) 0.77-1.34]. All-cause mortality occurred in 34.9% of patients (53/152) in the intervention group and 34.2% (52/152) in the control group (HR 1.02, 95% CI 0.70-1.50). Unplanned hospitalization for heart failure occurred in 55.9% of patients (85/152) in the intervention group and 61.8% (94/152) in the control group (HR 0.97, 95% CI 0.72-1.30).Conclusions: In patients with severe secondary mitral regurgitation, percutaneous repair added to medical treatment did not significantly reduce the risk of death or hospitalization for heart failure at 2 years compared with medical treatment alone. [ABSTRACT FROM AUTHOR]

Purpose: Stress cardiomyopathy is a common life-threatening complication after aneurysmal subarachnoid hemorrhage (SAH). We hypothesized that left ventricular (LV) longitudinal strain alterations assessed with speckle tracking could identify early systolic function impairment.Methods: This was an observational single-center prospective pilot controlled study conducted in a neuro-intensive care unit. Forty-six patients with severe SAH with a World Federation of Neurological Surgeons grade (WFNS) ≥ III were included. Transthoracic echocardiography (TTE) was performed on day 1, day 3, and day 7 after the patient's admission. A cardiologist blinded to the patient's management analyzed the LV global longitudinal strain (GLS). The control group comprised normal subjects matched according to gender and age.Results: On day 1 median (25th-75th percentile) GLS was clearly impaired in SAH patients compared to controls [-16.7 (-18.7/-13.7) % versus -20 (-22/-19) %, p < 0.0001], whereas LVEF was preserved [65 (59-70) %]. GLS was severely impaired in patients with a WFNS score of V versus III-IV [-15.6 (-16.9/-12.3) % versus -17.8 (-20.6/-15.8) %, p = 0.008]. Seventeen (37 %) patients had a severe GLS alteration (>- 16 %). In these patients, GLS improved from day 1 [-12.4 (-14.8/-10.9) %] to last evaluation [-16.2 (-19/-14.6) %, p = 0.0007] in agreement with the natural evolution of stress cardiomyopathy.Conclusions: On the basis of LV GLS assessment, we demonstrated for the first time that myocardial alteration compatible with a stress cardiomyopathy is detectable in up to 37 % of patients with severe SAH while LVEF is preserved. GLS could be used for sensitive detection of stress cardiomyopathy. This is critical because cardiac impairment remains a major cause of morbidity and mortality after SAH. [ABSTRACT FROM AUTHOR]

Background: The toxicity of doxorubicin, leading to an irreversible heart failure, limits its use as chemotherapeutic agent. The beneficial effects of early administration of β-blocker were reported in patients with heart failure due to doxorubicin, suggesting an important role of β-adrenoceptors (β-ARs). This study aimed to identify a putative target (β-AR and/or its effectors) at the early phase of a chronic doxorubicin-induced cardiomyopathy (Dox-CM) in a rat model. Methodology: Dox-CM was induced by six doxorubicin injections (cumulative dose: 15 mg.kg−1) and validated by echocardiography and left ventricle (LV) catheterization. The β-AR protein expressions in LV were evaluated by western-blot at days 35 (d35) and 70 (d70) after the first doxorubicin injection. Ex vivo cardiac contractility (dP/dtmax, dP/dtmin) was evaluated on isolated heart in response to specific β-AR stimulations at d35. Results: At d35, Dox-CM hearts were characterized by mild LV systolic and diastolic dysfunctions, which were exacerbated at d70. In Dox-CM hearts, β3-AR expression was only decreased at d70 (-37±8%). At d35, β1-AR expression was decreased by 68±6%, but ex vivo β1-AR function was preserved due to, at least in part, an increased adenylyl cyclase response assessed by forskolin. β2-AR expression was increased both at d35 (+58±22%) and d70 (+174±35%), with an increase of ex vivo β2-AR response at d35. Inhibition of Gi protein with pertussis toxin did not affect β2-AR response in Dox-CM hearts, suggesting a decoupling of β2-AR to Gi protein. Conclusion: This study highlights the β1/β2-AR imbalance in early Dox-CM and reveals the important role that β2-AR/Gi coupling could play in this pathology. Our results suggest that β2-AR could be an interesting target at early stage of Dox-CM. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 41 year old woman where cardiac magnetic resonance (CMR) imaging was started for an acute coronary syndrome, normal coronary angiography, high-sensitive Tc troponin increase and impaired left ventricle ejection fraction (LVEF). It states that CMR showed a drop of LVEF with continuous Late gadolinium enhancement (LGE) in anterior and inferior walls. It mentions that cardiac positron emission tomography (PET) with 18-fluorodeoxyglucose (FDG) was started.