Left ventricular systolic dysfunction in obesity: a meta-analysis of speckle tracking echocardiographic studies.

BACKGROUND: Obesity is a risk factor for left ventricular hypertrophy (LVH) and diastolic dysfunction. Available evidence on impaired myocardial deformation in obese patients without apparent systolic dysfunction assessed by LV ejection fraction (LVEF) is based on single studies. The aim of the present meta-analysis was to provide a comprehensive and updated information on this issue. METHODS: The PubMed, OVID-MEDLINE, and Cochrane library databases were analysed to search English-language articles published from the inception up to 31 December 2023. Studies were identified by using MeSH terms and crossing the following search items: 'myocardial strain', 'left ventricular mechanics', 'longitudinal global strain', 'speckle tracking echocardiography', 'systolic dysfunction', 'left ventricular ejection fraction', and 'obesity'. RESULTS: Twenty-four studies including 5792 obese and 5518 nonobese individuals from different clinical settings were considered for the analysis. LV global longitudinal strain (GLS) was significantly impaired in the obese group [standard means difference (SMD): -0.86 ±â€Š0.08; confidence interval (CI) -1.02 to -0.69, P < 0.0001] and this was paralleled by a significant difference in pooled LVEF between obese and controls (SMD -0.27 ±â€Š0.06; CI -0.40 to -0.15, P < 0.0001). Unlike GLS, however, the majority of the selected studies failed to show statistically significant differences in LVEF. Furthermore, in patients with advanced obesity (BMI > 35 kg/m2, data from six studies), LV systolic dysfunction was more significantly detected by GLS (SMD -1.24 ±â€Š0.19, CI -1.61/-0.87, P < 0.0001) than by LVEF (SMD -0.54 ±â€Š0.27, CI -1.07 to -0.01, P = 0.046). CONCLUSION: The present meta-analysis suggests that GLS may unmask systolic dysfunction often undetected by conventional LVEF in the obese setting; thus, this parameter should be incorporated into routine work-up aimed to identify obesity-mediated subclinical cardiac damage.

Targeting left atrial dysfunction: A new way to prevent cardiovascular disease?

Clinical and biochemical factorsassociated with worsening of left atrial function, as assessed by speckle tracking echocardiography (i.e. left atrial reservoir strain = LARS) in a population-based cohortover a five-year period of follow-up.

Targeting Hypertensive Response to Exercise and the Association of Masked Hypertension With Subclinical Organ Damage: A Mini-Review and Meta-Analysis.

BACKGROUND: Emerging evidence suggests that a hypertensive response to exercise (HRE) during dynamic or isometric stress tests assessing cardiac function is predictive of hypertension and cardiovascular events such coronary artery disease, heart failure and stroke. Whether HRE represents a marker of masked hypertension (MH) in individuals with no prior history of hypertension is still unclear. This is also the case for the association between MH and hypertension-mediated organ damage (HMOD) in the HRE setting. METHODS: We addressed this issue through a review and a meta-analysis of studies providing data on this topic in normotensive individuals undergone both to dynamic or static exercise and to 24-h blood pressure monitoring (ABPM). A systematic search was performed using Pub-Med, OVID, EMBASE and Cochrane library databases from inception up to February 28th 2023. RESULTS: Six studies including a total of 1,155 untreated clinically normotensive individuals were considered for the review. Data provided by the selected studies can be summarized as follows: (i) HRE is a BP phenotype linked to a high prevalence of MH (27.3% in the pooled population); (ii) MH is, in turn, associated with a greater, consistent likelihood of echocardiographic left ventricular hypertrophy (OR: 4.93, CI: 2.16-12.2, P < 0.0001) and vascular organ damage, as assessed by pulse wave velocity, (SMD: 0.34 ±â€…0.11, CI: 0.12-0.56, P = 0002). CONCLUSIONS: On the basis of this, albeit limited, evidence, the diagnostic work-up in individuals with HRE should primarily be addressed to look for MH as well as for markers of HMOD, a highly prevalent alteration in MH.

Methotrexate & rheumatoid arthritis associated atherosclerosis: A narrative review of multidisciplinary approach for risk modification by the international board of experts.

Rheumatoid arthritis (RA) is an idiopathic, autoimmune connective tissue disorder that primarily affects the synovial joints, causing symmetric, erosive-deforming polyarthritis. It is also associated with extra-articular manifestations, particularly cardiovascular (CV) diseases (CVD). CV risk modification in RA remains unsolved despite recent advances in the management of RA. RA is an independent risk factor for atherosclerosis. RA and atherosclerosis share similar pathophysiological features (such as the pro-inflammatory cascade activation including interleukin-6) and risk factors (such as microflora dysbacteriosis and smoking). Patients with RA experience an exacerbation of atherogenesis, with atheromas destabilization, endothelial dysfunction, vasculitis, and hypercytokinemia. Consequently, the inflammatory response associated with RA is the basis for CVD development. The treat-to-target strategy not only improved RA control but also had a favorable effect on the morpho-functional state of the CV system in patients living with RA. Thus, disease-modifying antirheumatic drugs (DMARDs) - in particular methotrexate - may have a beneficial effect on the prevention of CV events in RA. It must be mentioned that RA is a serious multi-system disease, not only because of a window period during which the course of RA can be reversed, but also due to early damage to the heart and blood vessels. For this reason, a thorough cardiological assessment must be performed for all patients with RA, regardless of sex, age, disease stage, and disease activity score.

Do We Need New Electrocardiographic Criteria for Left Ventricular Hypertrophy? The Case of the Peguero-Lo Presti Criterion. A Narrative Review.

The cardiovascular risk associated with left ventricular hypertrophy (LVH) in the community and, particularly, in the hypertensive fraction of the general population, represents the rationale for its timely and accurate identification in order to implement adequate preventive strategies. Although electrocardiography (ECG) is the first-line and most economical method of diagnosing LVH its accuracy is largely suboptimal. Over the last 70 years, dozens of different ECG criteria, mostly based on measurements of QRS voltages, have been proposed. In this long journey, a few years ago Peguero et al. developed a novel ECG voltage criterion, currently recognized as Peguero-Lo Presti (PLP) suggesting that it has greater sensitivity than traditional ECG-LVH criteria. Considering that in the last 5 years numerous studies have investigated the diagnostic value of this new index, this review aimed to summarize the data published so far on this topic focusing both on the accuracy in identifying the presence of LVH compared with imaging techniques such as echocardiography (ECHO) and magnetic resonance imaging (MRI) and the value in predicting hard outcomes. The evidence in favor of the greater diagnostic accuracy of the PLP criterion in detecting LVH, phenotyped by ECHO or MRI, and in the stratification of hard outcomes compared with traditional ECG criteria does not appear to be sufficiently proven. Given that the diagnosis of LVH by all ECG criteria (including the PLP) exclusively based on the QRS amplitude is largely imprecise, the development of new multiparametric ECG criteria based on artificial intelligence could represent a real improvement in the diagnostic capacity of the ECG.

Uric acid and left ventricular hypertrophy: a gender-based meta-analysis of echocardiographic studies.

AIM: Gender-based evidence on the association between serum uric acid (SUA) and left ventricular hypertrophy (LVH), as assessed by echocardiography, is still based on single studies. Thus, we performed a systematic meta-analysis of echocardiographic studies in order to provide an updated and comprehensive information on this issue. METHODS: The PubMed, OVID-MEDLINE, and Cochrane library databases were analyzed to search English-language articles published from the inception up to March 31, 2023. Studies were identified by using MeSH terms and crossing the following search items: 'uric acid', 'hyperuricemia', 'left ventricular mass', 'left ventricular hypertrophy', 'echocardiography', 'female', 'male'. RESULTS: Six studies including 2791 normotensive and hypertensive individuals were considered for the analysis. In women, increasing values of SUA were associated with progressively higher values of age, body mass index (BMI) and systolic blood pressure (SBP). This was not the case for men. In women, the meta-analysis comparing LV mass index (LVMI) in low versus high SUA group showed a greater pooled LVMI in the high SUA group [standard means difference (SMD): 0.81 ±â€Š0. 24, confidence interval (CI) 0.34-1.27, P  < 0.0001]. On the contrary, in men no statistical difference was found between the low group and high SUA group (SMD: 0.27 ±â€Š0.27, CI: -0.27/0.81, P  = 0.32). CONCLUSIONS: Our meta-analysis suggests that hyperuricemia portends the likely presence of increased LVMI in women but not in men. However, as hyperuricemia in the female pooled population, different from men, was associated with older age, higher BMI and SBP, the present findings do not support an independent role of the SUA in LV remodelling process in women.

Melatonin mitigates oxidative damage induced by anthracycline: a systematic-review and meta-analysis of murine models.

Background: Oxidative stress induced by the excessive production of reactive oxygen species is one of the primary mechanisms implicated in anthracycline (ANT)-induced cardiotoxicity. There is a strong clinical need for a molecule capable of effectively preventing and reducing the oxidative damage caused by ANT. In vitro and in vivo studies conducted in mice have shown that melatonin stimulates the expression of antioxidative agents and reduces lipid peroxidation induced by ANT. Methods: We investigated this issue through a meta-analysis of murine model studies. The outcome of the meta-analysis was to compare oxidative damage, estimated by products of lipid peroxidation (MDA = Malondialdehyde) and markers of oxidative stress (SOD = Superoxide Dismutase, GSH = Glutathione), along with a marker of cardiac damage (CK-MB = creatine kinase-myocardial band), assessed by measurements in heart and/or blood samples in mice undergoing ANT chemotherapy and assuming melatonin vs. controls. The PubMed, OVID-MEDLINE and Cochrane library databases were analysed to search English-language review papers published from the inception up to August 1st, 2023. Studies were identified by using Me-SH terms and crossing the following terms: "melatonin", "oxidative stress", "lipid peroxidation", "anthracycline", "cardiotoxicity". Results: The metanalysis included 153 mice administered melatonin before, during or immediately after ANT and 153 controls from 13 studies. Compared with controls, the levels of all oxidative stress markers were significantly better in the pooled melatonin group, with standardized mean differences (SMD) for MDA, GSH and SOD being -8.03 ± 1.2 (CI: -10.43/-5.64, p < 0.001), 7.95 ± 1.8 (CI: 4.41/11.5, p < 0.001) and 3.94 ± 1.6 (CI: 0.77/7.12, p = 0.015) respectively. Similarly, compared with controls, CK-MB levels reflecting myocardial damage were significantly lower in the pooled melatonin group, with an SMD of -4.90 ± 0.5 (CI: -5.82/-3.98, p < 0.001). Conclusion: Melatonin mitigates the oxidative damage induced by ANT in mouse model. High-quality human clinical studies are needed to further evaluate the use of melatonin as a preventative/treatment strategy for ANT-induced cardiotoxicity.

Echocardiographic Phenotypes of Subclinical Organ Damage: Clinical and Prognostic Value in the General Population. Findings from the Pamela Study.

Subclinical alterations in cardiac structure and function include a variety of abnormal phenotypes of established adverse prognostic significance such as left ventricular hypertrophy (LVH), alterations of LV geometry, left atrial (LA) enlargement, and aortic root (AR) dilatation. The excess cardiovascular (CV) risk associated with these phenotypes has been consistently demonstrated in different clinical settings such in patients with systemic hypertension, coronary heart disease, diabetes mellitus, chronic kidney disease, heart failure and in geneal population samples. The Pressioni Monitorate e Loro Associazioni (PAMELA), a longitudinal population-based study originally designed to assess the normality values, prognostic significance of office, home and 24-hour blood pressure, including among the many clinical and laboratory variables the collection of echocardiographic data, allowed to gather important information on the clinical prognostic significance of subclinical cardiac damage during a long follow-up period. This article summarizes the original findings provided by the PAMELA study on the clinical correlates and prognostic significance of echocardiographic markers of subclinical organa damage namely LVH, left atrial enlargement (LA) and AR dilatation at the community level.

Aortic Valve Stenosis and Cancer: Problems of Management.

Aortic valve stenosis and malignancy frequently coexist and share the same risk factors as atherosclerotic disease. Data reporting the prognosis of patients with severe aortic stenosis and cancer are limited. Tailoring the correct and optimal care for cancer patients with severe aortic stenosis is complex. Cancer patients may be further disadvantaged by aortic stenosis if it interferes with their treatment by increasing the risk associated with oncologic surgery and compounding the risks associated with cardiotoxicity and heart failure (HF). Surgical valve replacement, transcatheter valve implantation, balloon valvuloplasty, and medical therapy are possible treatments for aortic valve stenosis, but when malignancy is present, the choice between these options must take into account the stage of cancer and associated treatment, expected outcome, and comorbidities. Physical examination and Doppler echocardiography are critical in the diagnosis and evaluation of aortic stenosis. The current review considers the available data on the association between aortic stenosis and cancer and the therapeutic options.

Case report: Sodium-glucose cotransporter 2 inhibitors induce left ventricular reverse remodeling in anthracycline-related cardiac dysfunction-a case series.

Purpose: To describe the efficacy and safety of sodium-glucose cotransporter 2 inhibitors as a specific treatment for anthracycline-related cardiac dysfunction in a small real-world population. Methods: Seven patients with anthracycline-related cardiac dysfunction were clinically and echocardiographically evaluated before and after the introduction of sodium-glucose cotransporter 2 inhibitors. Results: After a median period of 24 weeks with uninterrupted sodium-glucose cotransporter 2 inhibitors treatment, a significant clinical improvement was observed with at least one New York Heart Association Functional Class (NHYA FC) improvement in all patients (median NYHA FC: I vs. III, p < 0.010). A noteworthy left ventricular reserve remodeling (median left ventricular end diastolic volume indexed: 53 vs. 82.5 ml/m2, p = 0.018; median left ventricular ejection fraction: 50% vs. 40%, p = 0.17) was also observed. Sodium-glucose cotransporter 2 inhibitors therapy was well tolerated by every patients; no cases of discontinuation or relevant side effects were observed. Conclusion: Sodium-glucose cotransporter 2 inhibitors induce a significant clinical improvement and left ventricular reserve remodeling in patients affected by anthracycline-related cardiac dysfunction.

Induced myocardial ischemia in candidates to liver transplantation without evidence of heart disease.

BACKGROUND: Coronary artery disease (CAD) is associated with perioperative liver transplantation (LT) mortality. In absence of a defined risk algorithm, we aimed to test whether stress echocardiography and coronary computed tomography angiography (CCTA) could detect CAD in end-stage liver disease (ESLD) patients without previous evidence of heart disease. METHODS: LT candidates ≥30 years underwent a cardiovascular (CV) assessment through stress echocardiography. CCTA was performed in patients ≥50 years with two or more CV risk factors (e.g. diabetes, CAD family history, dyslipidaemia). Coronary angiography (CAG) was scheduled when stress echocardiography and/or CCTA were positive. Sensibility, specificity, positive and negative predictive values of stress echocardiography and CCTA were assessed by numbers of coronary revascularization (true positives) and lack of acute coronary events over a mean follow-up of 3 years (true negatives). RESULTS: Stress echocardiography was performed in 273 patients, CCTA in 34 and CAG in 41. Eight patients had critical coronary lesions, and 19 not-critical lesions. Sensitivity, specificity, positive and negative predictive values were 50.0%, 90.2%, 13.3% and 98.4% for stress echocardiography and 100%, 76.7%, 36.4% and 100% for CCTA. Among 163 patients who underwent LT (57.6%), 16 died and 5 had major adverse CV events over a mean follow-up of 3 years. CONCLUSIONS: A very low prevalence of CAD in a selected population of ESLD at intermediate to high CV risk was found. A screening based on stress echocardiography and CCTA resulted in low incidence of post-LT acute coronary events in ELSD patients. CAD has no impact on mid-term survival.

Long-Term Effects of Sacubitril-Valsartan on Cardiac Remodeling: A Parallel Echocardiographic Study of Left and Right Heart Adaptive Response.

Sacubitril/Valsartan (S/V) carries potential anti-remodeling properties, however long-term effects and biventricular adaptive response are poorly described. 76 HFrEF patients who underwent progressive uptitration of S/V, completed the annual scheduled follow-up. After a median follow-up of 11 (8-13) months, left ventricular (LV) reverse remodeling (RR) is defined as (1) absolute increase in LV ejection fraction (EF) ≥ 10% or LVEF ≥ 50% at follow-up and (2) decrease in indexed LV end-diastolic diameter (LVEDDi) of at least 10% or indexed LVEDDi ≤ 33 mm/m2, occurred in 27.6%. Non-ischemic etiology, shorter duration of HF, and absence of a history of AF were independently associated with LVRR (p < 0.05). TAPSE and TAPSE/PASP, a non-invasive index of right ventricular (RV) coupling to the pulmonary circulation, significantly improved at follow-up (0.45 vs. 0.56, p = 0.02). 41% of patients with baseline RV dysfunction obtained favorable RV remodeling despite only a moderate correlation between RV and LV function was observed (r = 0.478, p = 0.002). Our data point to a potential long-term reverse global remodeling effect by S/V, especially in patients who start S/V at an early stage of the disease, and focus our attention on a possible direct effect of the drug in synergistic hemodynamics between RV and pulmonary circulation.

SGLT2-i prevent left ventricular dysfunction induced by anthracycline in mouse model: A systematic-review and meta-analysis.

CLINICAL QUESTION: Could SGLT2-i be helpful for the prevention of left ventricular dysfunction induced by anthracycline? WHAT IS THE MAIN FINDING?: SGLT2-i appear effective for the prevention of left ventricular dysfunction induced by anthracycline in mouse model.