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Since the publication of the Framingham Heart Study, which suggested that uric acid should no longer be associated with coronary heart disease after additional adjustment for cardiovascular disease risk factors, the number of publications challenging this statement has dramatically increased. The aim of this paper was to review and discuss the most recent studies addressing the possible relation between sustained elevated serum uric acid levels and the onset or worsening of cardiovascular and renal diseases. Original studies involving American teenagers clearly showed that serum uric acid levels were directly correlated with systolic and diastolic pressures, which has been confirmed in adult cohorts revealing a 2.21-fold increased risk of hypertension. Several studies involving patients with coronary artery disease support a role for serum uric acid level as a marker and/or predictor for future cardiovascular mortality and long-term adverse events in patients with coronary artery disease. Retrospective analyses have shown an inverse relationship between serum uric acid levels and renal function, and even a mild hyperuricemia has been shown to be associated with chronic kidney disease in patients with type 2 diabetes. Interventional studies, although of small size, showed that uric acid (UA)-lowering therapies induced a reduction of blood pressure in teenagers and a protective effect on renal function. Taken together, these studies support a role for high serum uric acid levels (>6 mg/dL or 60 mg/L) in hypertension-associated morbidities and should bring awareness to physicians with regards to patients with chronic hyperuricemia.

Background Cancer associated thrombosis is recognized. However, pulmonary embolism (PE) from testicular cancer is rarely reported. Right ventricular (RV) function and PE are closely related. The RV cannot cope with a sudden increase in afterload because of PE and this causes dysfunction, but isolated left ventricular dysfunction in this context is not reported in the literature. Case presentation We report an unusual association of pulmonary embolism and testicular germ cell tumor complicating severe left heart failure and full recovery at three months follow up in a 33-year-old patient with no prior medical history. The diagnosis was made after comprehensive history taking and physical examination with the help of different imaging modalities. Full recovery was achieved after optimal medical therapy. Conclusion This case raises our awareness of unusual clinical presentation as we report associated left-sided severe heart failure in cancer-related pulmonary embolism. Pulmonary embolism in healthy young adults warrant in-depth causative exploration.

A simple and accurate prognostic tool for Heart Failure (HF) patients is critical to improve follow-up. Different risk scores are accurate but with limited clinical applicability. The current study aims to derive and validate a simple predictive tool for HF prognosis. French outpatients with stable HF of two university hospitals were included in the derivation (N = 134) or in the validation (N = 274) sample and followed up for a median of 23 months. Potential predictors were variables with known association with mortality and easily available. The proSCANNED risk score was derived using a parametric survival model on complete case data; it includes 8 binary variables and its values are 0–8. In the validation sample, the ability of the score to discriminate the 1-year vital status was moderate (AUC = 0.71, IC95% = [0.64–0.71]). However, the stratification of the score in three groups showed a good calibration for patients in the low- and medium-risk risk group. The proSCANNED score is an easy-to-use tool in clinical practice with a good discrimination, stability, and calibration sufficient to improve the medical care of patients. Other follow up studies are necessary to assess score applicability in larger populations, and its impact.

The exact pathophysiology of Tako-Tsubo cardiomyopathy (TTC) remains unknown but a role for sympathetic hyperactivity has been suggested. Up to now, no direct evidence of sympathetic nerve hyperactivity has been established nor involvement of sympathetic baroreflex identified. The aim of our study was to determine, by direct sympathetic nerve activity (SNS) recording if sympathetic nervous system activity is increased and spontaneous baroreflex control of sympathetic activity reduced in patients with TTC. We included 13 patients who presented with TTC and compared their SNS activity and spontaneous baroreflex control of sympathetic activity with that of 13 control patients with acutely decompensated chronic heart failure. SNS activity was evaluated by microneurography, a technique assessing muscle sympathetic nerve activity (MSNA). Spontaneous baroreflex control of sympathetic activity was evaluated as the absolute value of the slope of the regression line representing the relationship between spontaneous diastolic blood pressure values and concomitant SNS activity. Control patients were matched for age, sex, left ventricular ejection fraction and creatinine clearance. The mean age of the patients with TTC was 80 years, all patients were women. There were no significant differences between the two groups of patients for blood pressure, heart rate or oxygen saturation level. TTC patients presented a significant increase in sympathetic nerve activity (MSNA median 63.3 bursts/min [interquartile range 61.3 to 66.0] vs median 55.7 bursts/min [interquartile range 51.0 to 61.7]; p = 0.0089) and a decrease in spontaneous baroreflex control of sympathetic activity compared to matched control patients (spontaneous baroreflex control of sympathetic activity median 0.7%burst/mmHg [interquartile range 0.4 to 1.9] vs median 2.4%burst/mmHg [interquartile range 1.8 to 2.9]; p = 0.005). We report for the first time, through direct measurement of sympathetic nerve activity, that patients with TTC exhibit elevated SNS activity associated with a decrease in spontaneous baroreflex control of sympathetic activity. These data may explain the pathophysiology and clinical presentation of patient with TTC.

The relationship between arteriovenous access flow (Qa) and cardiovascular changes is complex. Several studies have shown cardiac remodeling and symptoms of heart failure for high-flow arteriovenous fistulas (AVF). To evaluate the early cardiovascular impact of AVF. Forty-seven patients with an AVF, hospitalized for the evaluation of high-flow AVF or a pre-kidney transplant assessment were included. We collected clinical and biological data. We also collected data of the assessment by transthoracic echocardiography, functional evaluation by 6-min-walk test and peak oxygen consumption, and measurement of coronary flow reserve by dynamic myocardial perfusion imaging. The measurement of Qa was performed by color Doppler ultrasound and then indexed to the body surface area (Qai) and to the cardiac output (CO) (Qa/CO). Patients were poorly symptomatic (18 and 1 patients NYHA stage 2 and 3, respectively). There was no correlation between Qa, Qai, or Qa/CO and functional status, assessed by peak oxygen consumption ( P  = 0.891; P  = 0.803; P  = 0.939, respectively). Symptomatic patients did not have higher Qa, Qai or Qa/CO than asymptomatic (2260 vs 2197 mL/min, P  = 0.402; 1257 vs 1256 mL/min/m 2 , P  = 0.835; and 34% vs 37%, P  = 0.701, respectively). There was no correlation between Qa, Qai or Qa/CO and left ventricular end-diastolic volume or left ventricular ejection fraction. There was no correlation between coronary flow reserve and these 3 parameters of vascular access flow. However, the global longitudinal strain (GLS) was correlated with Qa and Qa/CO ( R  = 0.331, P  = 0.023 and R  = 0.380, P  = 0.008, respectively). Increase of Qa or Qa/CO was associated with an alteration of the GLS. A cut-off value of 2250 mL/min for Qa allowed 83% sensitivity and 63% specificity for detecting an alteration of the GLS > − 18%. A cut-off value of 33% for Qa/CO allowed 92% sensitivity and 65% specificity. Impact of AVF on cardiac parameters is weak. However, GLS is the first parameter to be impacted by the flow of the fistula. Systematic transthoracic echocardiography evaluation with measurement of GLS should be proposed for all patients with Qa > 2250 mL/min or Qa/CO > 33%, to detect those at higher risk of cardiac impact of the AVF.

Transplantation of mesenchymal stem cells (MSCs) in the setting of cardiovascular disease, such as heart failure, cardiomyopathy and ischemic heart disease, has been associated with good clinical outcomes in several trials. A reduction in left ventricular remodeling, myocardial fibrosis and scar size, an improvement in endothelial dysfunction and prolonged cardiomyocytes survival were reported. The regenerative capacity, in addition to the pro-angiogenic, anti-apoptotic and anti-inflammatory effects represent the main target properties of these cells. Herein, we review the different preconditioning methods of MSCs (hypoxia, chemical and pharmacological agents) and the novel approaches (genetically modified MSCs, MSC-derived exosomes and engineered cardiac patches) suggested to optimize the efficacy of MSC therapy.

Diabetic cardiomyopathy is a secondary complication of diabetes with an unclear etiology. Based on a functional genomic evaluation of obesity-associated cardiac gene expression, we previously identified and cloned the gene encoding apolipoprotein O (APOO), which is overexpressed in hearts from diabetic patients. Here, we generated APOO-Tg mice, transgenic mouse lines that expresses physiological levels of human APOO in heart tissue. APOO-Tg mice fed a high-fat diet exhibited depressed ventricular function with reduced fractional shortening and ejection fraction, and myocardial sections from APOO-Tg mice revealed mitochondrial degenerative changes. In vivo fluorescent labeling and subcellular fractionation revealed that APOO localizes with mitochondria. Furthermore, APOO enhanced mitochondrial uncoupling and respiration, both of which were reduced by deletion of the N-terminus and by targeted knockdown of APOO. Consequently, fatty acid metabolism and ROS production were enhanced, leading to increased AMPK phosphorylation and Ppara and Pgc1a expression. Finally, we demonstrated that the APOO-induced cascade of events generates a mitochondrial metabolic sink whereby accumulation of lipotoxic byproducts leads to lipoapoptosis, loss of cardiac cells, and cardiomyopathy, mimicking the diabetic heart-associated metabolic phenotypes. Our data suggest that APOO represents a link between impaired mitochondrial function and cardiomyopathy onset, and targeting APOO-dependent metabolic remodeling has potential as a strategy to adjust heart metabolism and protect the myocardium from impaired contractility.

The prevalence of non‐alcoholic fatty liver disease (NAFLD) in heart failure (HF) preserved left ventricular ejection fraction (HFpEF) patients could reach 50%. Therefore, NAFLD is considered an emerging risk factor. In 20% of NAFLD patients, the condition progresses to non‐alcoholic steatohepatitis (NASH), the aggressive form of NAFLD characterized by the development of fibrosis in the liver, leading to cirrhosis. The purpose of this review is to provide an overview of the relationships between NAFLD and HFpEF and to discuss its impact in clinical setting. Based on international reports published during the past decade, there is growing evidence that NAFLD is associated with an increased incidence of cardiovascular diseases, including impaired cardiac structure and function, arterial hypertension, endothelial dysfunction, and early carotid atherosclerosis. NAFLD and HFpEF share common risk factors, co‐morbidities, and cardiac outcomes, in favour of a pathophysiological continuum. Currently, NAFLD and NASH are principally managed with non‐specific therapies targeting insulin resistance like sodium‐glucose co‐transporter‐2 inhibitors and liraglutide, which can effectively treat hepatic and cardiac issues. Studies including HFpEF patients are ongoing. Several specific NAFLD‐oriented therapies are currently being developed either alone or as combinations. NAFLD diagnosis is based on a chronic elevation of liver enzymes in a context of metabolic syndrome and insulin resistance, with fibrosis scores being available for clinical practice. In conclusion, identifying HF patients at risk of NAFLD is a critically important issue. As soon as NAFLD is confirmed and its severity determined, patients should be proposed a management focused on symptoms and co‐morbidities.

To evaluate the contribution and performance of multimodal imaging in the diagnostic and therapeutic management of cardiac masses. We carried out a monocentric retrospective study on patients referred for cardiac mass assessment between 2006 and 2019, and analyzed the respective contribution of transesophageal echocardiography (TEE), cardiac computed tomography (CT), cardiac magnetic resonance (CMR) and 18F-fluorodeoxyglucose positron emission tomography coupled with CT (18F-FDG PET-CT). For each test, we determined strategy before and after its completion (need for another imaging or decision-making) as well as result on benign, malignant or indeterminate nature. For the 119 patients included, all imaging modalities increased decision-making rates, which rose from 2 to 54%, 23 to 62%, 31 to 85% and 49 to 100% before and after TEE, CT, CMR and 18F-FDG PET-CT, respectively (P < 0.001 before vs. after). TEE was particularly efficient for atrial masses, especially for the left atrium, with a decision rate rising from 0 to 74% (P < 0.001). 18F-FDG PET-CT was the most efficient to differentiate benign and malignant etiologies (area under the curve 0.89 ± 0.06 and 0.94 ± 0.05 for benign and malignant, respectively, P < 0.001). A benign or undetermined result on each modality was associated with a good prognosis, compared to malignant. All modalities studied are useful for cardiac mass decision-making. First-line TEE is particularly efficient for atrial masses, whereas CT and CMR are useful for ventricular masses or suspicion of malignancy. A benign or malignant result for each modality is correlated to survival and 18F-FDG PET-CT is the most effective to define it.

Ultra-high-density mapping allows very accurate characterization of circuits/mechanisms in atrial tachycardia (AT). Whether these advantages will translate into a better procedural or long-term clinical outcome is unknown. Sixty consecutive AT ablation procedures using ultra-high-density mapping (Rhythmia™, group 1) were retrospectively compared to 60 consecutive procedures using standard high-density mapping (Carto/NavX™, group 2) (total 209 AT, 79% left AT). A higher number of maps were performed in group 1 (4.8 ± 2.5 vs 3.2 ± 1.7, p  = 0.0001) with similar acquisition duration (12 ± 5 vs 13 ± 6 min per map, p  = ns), although with a greater number of activation points (10,543 ± 5854 vs 689 ± 1827 per map, p  < 0.0001). AT location remained undetermined in 5 AT in group 1 vs 10 ( p  = 0.1). Mechanism remained undetermined in 5 AT from group 1 vs 11 ( p  = 0.06). Acute complete success was achieved in 77%, in both groups. At 1-year follow-up, AT recurred in 37% in group 1 vs 50% in group 2 ( p  = 0.046). There are less long-term recurrences after AT ablation using ultra-high-density mapping system compared to standard high-density 3D mapping, possibly because of a better comprehensive approach of AT mechanisms.