Vascular conditioning prevents adverse left ventricular remodelling after acute myocardial infarction: a randomised remote conditioning study

Aims: Remote ischemic conditioning (RIC) alleviates ischemia–reperfusion injury via several pathways, including micro-RNAs (miRs) expression and oxidative stress modulation. We investigated the effects of RIC on endothelial glycocalyx, arterial stiffness, LV remodelling, and the underlying mediators within the vasculature as a target for protection. Methods and results: We block-randomised 270 patients within 48 h of STEMI post-PCI to either one or two cycles of bilateral brachial cuff inflation, and a control group without RIC. We measured: (a) the perfusion boundary region (PBR) of the sublingual arterial microvessels to assess glycocalyx integrity; (b) the carotid-femoral pulse wave velocity (PWV); (c) miR-144,-150,-21,-208, nitrate-nitrite (NOx) and malondialdehyde (MDA) plasma levels at baseline (T0) and 40 min after RIC onset (T3); and (d) LV volumes at baseline and after one year. Compared to baseline, there was a greater PBR and PWV decrease, miR-144 and NOx levels increase (p  15% (odds-ratio of 3.75, p = 0.029). MiR-144 and PWV changes post-RIC were interrelated and associated with LVESV reduction at follow-up (r = 0.40 and 0.37, p < 0.05), in the single-cycle RIC. Conclusion: RIC evokes “vascular conditioning” likely by upregulation of cardio-protective microRNAs, NOx production, and oxidative stress reduction, facilitating reverse LV remodelling

Imaging Risk in Multisystem Inflammatory Diseases

Rheumatic diseases are immune-mediated inflammatory multisystem diseases with frequent cardiovascular manifestations including perimyocarditis, valvular disease, coronary artery disease, heart failure with or without preserved ejection fraction, pulmonary hypertension, aneurysms, and thrombosis. Echocardiography, carotid ultrasonography, cardiac computed tomography, cardiac magnetic resonance imaging, and positron emission tomography are valid diagnostic tools for the detection of the cardiovascular complications of the multisystem diseases that frequently determine prognosis. Furthermore, the findings of these methods may offer additive risk stratification in asymptomatic patients over the conventional risk scores used to assess cardiovascular risk in the primary prevention setting. Finally, the imaging methods offer a unique opportunity to monitor the effects of treatment on atherosclerotic lesions, coronary microcirculatory dysfunction, myocardial inflammation and fibrosis. However, studies are needed to investigate whether improvement of imaging markers by treatment or selection of treatment according to its effects on surrogate imaging markers is linked to improved prognosis. © 2019 American College of Cardiology Foundatio

Multidimensional contractile reserve predicts adverse outcome in patients with severe systolic heart failure: a 4-year follow-up study

Aims: Left ventricular contractile reserve is a prognostic indicator for adverse outcome in patients with severe chronic heart failure with reduced ejection fraction (HFrEF). We investigated the dobutamine-induced changes of LV multidimensional deformation and their predictive value for cardiac mortality of patients with severe chronic HFrEF. Methods and results: In this prospective study, out of 130 patients with severe HFrEF who underwent a low-dose dobutamine stress echocardiography (LDSE) study using speckle tracking imaging, 100 patients were followed up for the occurrence of cardiac death over a period of 4 years. Compared with survivors, non-survivors (n = 32) had lower radial strain (RS) and strain rate (RSR) (10.7 ± 5.9 vs. 20.1 ± 8% and 0.5 ± 0.2 vs. 0.8 ± 0.3 L/s, P &lt; 0.001), a smaller increase of global longitudinal strain (GLS) and strain rate after LDSE (0.9 ± 1.5 vs. –3.3 ± 3.5% and −0.1 ± 0.1 vs. –0.3 ± 0.3 L/s, P &lt; 0.001), and a lack of change in the circumferential and radial deformation. The dobutamine-induced changes of all speckle tracking indices predicted cardiac mortality, while, among resting echocardiographic parameters, only RS and RSR predicted survival, after adjusting for age, sex, cardiomyopathy aetiology, NYHA class, AF, BNP levels, resting LVED, and LV outflow tract velocity–time integral, and their respective changes produced by dobutamine (P &lt; 0.05). The dobutamine-induced change of GLS and resting RS were the best additive predictors of mortality with a net reclassification improvement of 0.518 (P = 0.022). Conclusion: In severe chronic HFrEF, resting RS and the dobutamine-induced change of GLS are independent predictors of cardiac mortality. © 2017 The Authors. European Journal of Heart Failure © 2017 European Society of Cardiolog

Hypertrophic cardiomyopathy: an updated review on diagnosis, prognosis, and treatment

Hypertrophic cardiomyopathy (HCM) represents a phenotype of left ventricular hypertrophy unexplained by abnormal loading conditions. The definition is based on clinical criteria; however, there are numerous underlying etiologic factors. The MOGE(S) classification provides a standardized approach for multimodal characterization of HCM. HCM is associated with increased morbidity and mortality, and especially the assessment of the risk of sudden cardiac death is of paramount importance. In this review, we summarize essential knowledge and recently published data on clinical presentation, diagnosis, genetic analyses, differential diagnosis, prognosis, and treatment options that are necessary for understanding and management of HCM. © 2019, Springer Science+Business Media, LLC, part of Springer Nature

Deformation Analysis of Myocardial Layers Detects Early Cardiac Dysfunction after Chemotherapy in Bone Marrow Transplantation Patients: A Continuous and Additive Cardiotoxicity Process

Background Chemotherapy-induced cardiotoxicity has not been extensively validated in bone marrow transplantation (BMT) patients. Speckle-tracking echocardiography is a sensitive method for the detection of subclinical cardiac dysfunction. Methods Cardiac function was prospectively assessed in 80 patients (44 men; mean age, 45 ± 11 years) after BMT for non-Hodgkin&apos;s lymphoma and acute or chronic myeloid leukemia by means of various echocardiographic techniques. Before chemotherapy for BMT, 89% of the patients had previously been treated with anthracyclines. Patients had normal left ventricular ejection fraction (LVEF). Left ventricular (LV) global longitudinal strain (GLS), subendocardial and subepicardial longitudinal strain, circumferential strain, LV twist, and right ventricular GLS were measured by speckle-tracking, and (2) three-dimensionally derived LVEF and right ventricular ejection fraction were also assessed. Abnormal LVEF was defined as &lt;53%. Studies were performed before (baseline) and 1, 3, 6, and 12 months after chemotherapy conditioning followed by BMT. Results Impaired LV GLS values were observed at 1 month after chemotherapy and at 3, 6, and 12 months compared with baseline (−20 ± 2.2% at baseline, −18.4 ± 2.1% at 1 month, −17.3 ± 2.2% at 3 months, −17.1 ± 2.1% at 6 months, and −17.1 ± 2.2% at 12 months; P =.001). Early LV GLS changes were driven mostly by changes in subendocardial longitudinal strain (−22.5 ± 2.4% at baseline, −20.5 ± 2.3% at 1 month, −19.2 ± 2.3% at 3 months, −19.2 ± 2.4% at 6 months, and −19.1 ± 2.4 at 12 months; P =.001), whereas significant subepicardial strain changes were observed at 3 months after BMT. Compared with baseline, right ventricular GLS was also impaired early after chemotherapy. Compared with baseline, LVEF was slightly reduced (P =.02) at the end of the follow-up. Among echocardiographic markers, LV GLS at 1 month had the strongest predictive value for abnormal LVEF (&lt;53%) at 12 months (area under the curve 0.86; 95% CI, 0.76–0.96). A cutoff LV GLS value of −18.4% had sensitivity of 84.6% and specificity of 71.9% for the identification of abnormal LVEF at the end of follow-up. Conclusions In BMT patients, myocardial deformation analysis detected early and progressive subclinical cardiac dysfunction. Impaired LV GLS had predictive value for the detection of abnormal LVEF at 12-month follow-up. Thus, myocardial deformation study should be applied early after BMT to prevent irreversible cardiac dysfunction by appropriate treatment. © 2017 American Society of Echocardiograph

Investigating the link between psoriasis and cardiovascular disease: Current evidence, therapeutic implications and perspectives

Psoriasis; a chronic inflammatory disease is characterized by symmetric hyperkeratotic plaques affecting any part of the body. Psoriasis is nowadays considered as a systemic inflammation linked with several comorbidities as metabolic syndrome, depression, anxiety and increased prevalence of cardiovascular (CV) disease. The hypothesis that psoriasis is an independent CV risk factor leading to atherosclerosis via inflammation is now widely accepted. Deciphering the underlying mechanisms inter-connecting psoriasis and CV disease may have significant implications in treatment decisions. Accumu-lating evidence suggests that systematic therapies and recently introduced biologic agents, that control psoriasis by suppressing the chronic and systemic inflammation, may alter the progression of CV dis-ease. We herein attempt a review of current evidence analysing the relationship between psoriasis and CV comorbidities, comment on the mechanisms underlying this association and investigate the consequences for the management of psoriasis. © 2020 Bentham Science Publishers

Chronic inflammatory diseases, myocardial function and cardioprotection

The association between chronic inflammatory diseases (CIDs) and increased cardiovascular (CV) risk is well documented and can be a most threatening complication in these patients. However, the pathogenetic mechanisms underlying increased CV risk remain elusive, especially in their cellular and biochemical pathways. Using animal models to understand mechanisms underlying cardiac involvement are limited. Additionally, treatments may influence cardiovascular events through different outcomes. Some drugs used to treat CIDs can negatively affect cardiac function by a direct toxicity, whereas others may protect the myocardium. In the present article, we focus on the cardiac manifestations and risk factors, the pathogenetic mechanisms, and the effect of treatments on myocardial function and cardioprotection for five common worldwide CIDs (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, psoriasis and inflammatory bowel disease). We also give recommendations in order to evaluate common targets between CID and CV disease (CVD) and to design therapies to alleviate CID-related CVD. LINKED ARTICLES: This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.23/issuetoc. © 2020 The British Pharmacological Societ

Chronic inflammatory diseases, myocardial function and cardioprotection

© 2020 The British Pharmacological Society The association between chronic inflammatory diseases (CIDs) and increased cardiovascular (CV) risk is well documented and can be a most threatening complication in these patients. However, the pathogenetic mechanisms underlying increased CV risk remain elusive, especially in their cellular and biochemical pathways. Using animal models to understand mechanisms underlying cardiac involvement are limited. Additionally, treatments may influence cardiovascular events through different outcomes. Some drugs used to treat CIDs can negatively affect cardiac function by a direct toxicity, whereas others may protect the myocardium. In the present article, we focus on the cardiac manifestations and risk factors, the pathogenetic mechanisms, and the effect of treatments on myocardial function and cardioprotection for five common worldwide CIDs (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, psoriasis and inflammatory bowel disease). We also give recommendations in order to evaluate common targets between CID and CV disease (CVD) and to design therapies to alleviate CID-related CVD. LINKED ARTICLES: This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.23/issuetoc