Gender Differences and Cardiometabolic Risk: The Importance of the Risk Factors.

Metabolic syndrome (Mets) is a clinical condition characterized by a cluster of major risk factors for cardiovascular disease (CVD) and type 2 diabetes: proatherogenic dyslipidemia, elevated blood pressure, dysglycemia, and abdominal obesity. Each risk factor has an independent effect, but, when aggregated, they become synergistic, doubling the risk of developing cardiovascular diseases and causing a 1.5-fold increase in all-cause mortality. We will highlight gender differences in the epidemiology, etiology, pathophysiology, and clinical expression of the aforementioned Mets components. Moreover, we will discuss gender differences in new biochemical markers of metabolic syndrome and cardiovascular risk.

Gender differences in the development of cardiac complications: a multicentre study in a large cohort of thalassaemia major patients to optimize the timing of cardiac follow-up.

We assessed whether male gender was associated with a higher risk of cardiac iron accumulation and fibrosis, heart dysfunction and complications in a large, multicentre cohort of thalassaemia major (TM) patients, in order to optimize the timing in cardiac follow-up. We considered 1711 TM patients (899 females, 31·09 ± 9·08 years), enrolled in the Myocardial Iron Overload in Thalassaemia Network. Clinical/instrumental data are recorded from birth to the first Cardiovascular Magnetic Resonance Imaging scan. Although having a similar risk of accumulating iron, males showed a significantly higher risk of developing cardiac dysfunction, heart failure, arrhythmias and cardiac complications overall, when compared to females (P < 0·0001). Up to 20-30 years of follow-up, the Kaplan-Meier curves for the outcomes for which the male sex was a significant prognosticator almost overlapped, whereas they clearly diverged after this period. In patients with follow-up longer than 20 years, males exhibited a significantly higher risk of ventricular dysfunction, heart failure, arrhythmias, and cardiac complications. Female patients may have an intrinsically better tolerance for iron toxicity. International guidelines suggest annual cardiac evaluation for thalassaemia patients. It is possible that female patients can be evaluated at longer intervals, thus reducing health costs.

Current views on anthracycline cardiotoxicity.

Anthracyclines are well established and effective anticancer agents used to treat a variety of adult and pediatric cancers. Unfortunately, these drugs are also among the commonest chemotherapeutic agents that have been recognized to cause cardiotoxicity. In the last years, several experimental and clinical investigations provided new information and perspectives on anthracycline-related cardiotoxicity. In particular, molecular mechanisms of cardiotoxicity have been better elucidated, early diagnosis has improved through the use of advanced noninvasive cardiac imaging techniques, and emerging data indicate a genetic predisposition to develop anthracycline-related cardiotoxicity. In this article, we review established and new knowledge about anthracycline cardiotoxicity, with special focus on recent advances in cardiotoxicity diagnosis and genetic profiling.

Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardiotoxicity and Cardioprotection.

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal models of chemotherapy-induced cardiomyopathy. This Position Paper of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology aims to: (1) define the distinctive etiopatogenetic features of cardiac toxicity induced by cancer therapy in humans, which include new aspects of mitochondrial function and oxidative stress, neuregulin-1 modulation through the ErbB receptor family, angiogenesis inhibition, and cardiac stem cell depletion and/or dysfunction; (2) review the new, more promising therapeutic strategies for cardioprotection, aimed to increase the survival of patients with severe antineoplastic-induced cardiotoxicity; (3) recommend the distinctive pathological features of cardiotoxicity induced by cancer therapy in humans that should be present in animal models used to identify or to test new cardioprotective therapies.

The different role of sex hormones on female cardiovascular physiology and function: not only oestrogens.

Human response to different physiologic stimuli and cardiovascular (CV) adaptation to various pathologies seem to be gender specific. Sex-steroid hormones have been postulated as the major contributors towards these sex-related differences. This review will discuss current evidence on gender differences in CV function and remodelling, and will present the different role of the principal sex-steroid hormones on female heart. Starting from a review of sex hormones synthesis, receptors and CV signalling, we will summarize the current knowledge concerning the role of sex hormones on the regulation of our daily activities throughout the life, via the modulation of autonomic nervous system, excitation-contraction coupling pathway and ion channels activity. Many unresolved questions remain even if oestrogen effects on myocardial remodelling and function have been extensively studied. So this work will focus attention also on the controversial and complex relationship existing between androgens, progesterone and female heart.

Heart rate variability shows different cardiovascular modulation in Parkinson's disease patients with tremor dominant subtype compared to those with akinetic rigid dominant subtype.

Parkinson's disease (PD) can present with different motor subtypes depending on the predominant symptoms (tremor or rigidity/bradykinesia). Slower disease progression and less cognitive decline are observed in tremor-dominant patients compared to those with akinetic-rigid subtype. Autonomic cardiovascular disorders have been described in parkinsonian patients, although the definite correlations with different subtypes of PD are not clear. In this context, heart rate variability (HRV) analysis represents a non-invasive and established tool in assessing cardiovascular autonomic modulation. We investigate cardiovascular autonomic modulation in PD patients with tremor dominant subtype in comparison to akinetic rigid dominant subtype subjects using HRV analysis. Twenty-eight PD patients (17 with tremor dominant subtype and 11 with akinetic rigid dominant subtype) were enrolled and compared to 17 age and sex-matched healthy controls. HRV was analyzed in time- and frequency-domains. Low-frequency (LF) values were significantly lower in the akinetic rigid dominant subtype than in the tremor dominant group [LF 41.4 ± 13.6 vs 55.5 ± 11.6 (p < 0.007)] indicating that the disease led to a more evident impairment of the baroreflex modulation of the autonomic outflow mediated by both sympathetic and parasympathetic systems in the first class of patients. These findings support the biological relevance of clinical subtypes supporting the idea of a different pathophysiological process between these subtypes. These differences also suggest that different subtypes may also result in different responses to therapy or in the possible development of cardiovascular side effects of dopaminergic drugs in these different populations.

Effects of metformin and exercise training, alone or in association, on cardio-pulmonary performance and quality of life in insulin resistance patients.

BACKGROUND: Metformin (MET) therapy exerts positive effects improving glucose tolerance and preventing the evolution toward diabetes in insulin resistant patients. It has been shown that adding MET to exercise training does not improve insulin sensitivity. The aim of this study was to determine the effect of MET and exercise training alone or in combination on maximal aerobic capacity and, as a secondary end-point on quality of life indexes in individuals with insulin resistance. METHODS: 75 insulin resistant patients were enrolled and subsequently assigned to MET (M), MET with exercise training (MEx), and exercise training alone (Ex). 12-weeks of supervised exercise-training program was carried out in both Ex and MEx groups. Cardiopulmonary exercise test and SF-36 to evaluate Health-Related Quality of Life (HRQoL) was performed at basal and after 12-weeks of treatment. RESULTS: Cardiopulmonary exercise test showed a significant increase of peak VO2 in Ex and MEx whereas M showed no improvement of peak VO2 (∆ VO2 [CI 95%] Ex +0.26 [0.47 to 0.05] l/min; ∆ VO2 MEx +0.19 [0.33 to 0.05] l/min; ∆ VO2 M -0.09 [-0.03 to -0.15] l/min; M vs E p < 0.01; M vs MEx p < 0.01; MEx vs Ex p = ns). SF-36 highlighted a significant increase in general QoL index in the MEx (58.3 ± 19 vs 77.3 ± 16; p < 0.01) and Ex (62.1 ± 17 vs 73.7 ± 12; p < 0.005) groups. CONCLUSIONS: We evidenced that cardiopulmonary negative effects showed by MET therapy may be counterbalanced with the combination of exercise training. Given that exercise training associated with MET produced similar effects to exercise training alone in terms of maximal aerobic capacity and HRQoL, programmed exercise training remains the first choice therapy in insulin resistant patients.

Cardiovascular Biomarkers in Cardio-Oncology: Antineoplastic Drug Cardiotoxicity and Beyond.

Serum biomarkers represent a reproducible, sensitive, minimally invasive and inexpensive method to explore possible adverse cardiovascular effects of antineoplastic treatments. They are useful tools in risk stratification, the early detection of cardiotoxicity and the follow-up and prognostic assessment of cancer patients. In this literature review, we aim at describing the current state of knowledge on the meaning and the usefulness of cardiovascular biomarkers in patients with cancer; analyzing the intricate relationship between cancer and cardiovascular disease (especially HF) and how this affects cardiovascular and tumor biomarkers; exploring the role of cardiovascular biomarkers in the risk stratification and in the identification of chemotherapy-induced cardiotoxicity; and providing a summary of the novel potential biomarkers in this clinical setting.

Early impairment of contractility reserve in patients with insulin resistance in comparison with healthy subjects.

BACKGROUND: Insulin resistance (IR) is currently considered a crucial cardiovascular (CV) risk factor, which seems to play a dominant role in the evolution toward cardiac and vascular impairment. Early IR-induced cardiac dysfunction can be assessed by Doppler-derived myocardial systolic strain rate (SR) index, measured at baseline and after dobutamine stress echocardiography (DSE). METHODS: Thirty IR patients (HOMA-IR = 7 ± 5.2, age 52.6 ± 2.1 years), and 20 healthy, age and sex matched controls were studied. IR had been diagnosed in all patients in the 3 months preceding the study. Dobutamine echocardiography was performed in all subjects to exclude ischemic heart disease, and left ventricular contractile reserve (LVCR) was then assessed. LVCR was evaluated as an increase in the peak of an average longitudinal SR, measured in the basal and mid segments of 2 and 4 chamber ventricular walls. RESULTS: No significant differences between the 2 groups were revealed by baseline echocardiography. In contrast, after DSE a significant decrease of Delta SR was found in the IR group in comparison to the controls (0.54 ± 0.31 s⁻¹ vs 1.14 ± 0.45 s⁻¹; p < 0.0001). CONCLUSIONS: Our results show that IR, even if isolated and arising within a short time period, not only represents the initial phase of future diabetes, but may adversely affect heart function, as evidenced by the depressed LVCR. Our data strengthen the need for attention to be paid to IR state and for an early therapeutic approach.

Epicardial fat volume assessed with cardiac magnetic resonance imaging in patients with Takotsubo cardiomyopathy.

PURPOSE: The aims of our study were to investigate with cardiovascular magnetic resonance (CMR) the role of Epicardial Fat Volume (EFV) and distribution in patients with Takotsubo cardiomyopathy (TTC). Moreover, we explored EFV in patients with TTC and related this to comorbidities, cardiac biomarkers, and cardiac function. METHODS: This retrospective study performed CMR scans in 30 consecutive TTC patients and 20 healthy controls. The absolute amount of EFV was quantified in consecutive short-axis cine stacks through the modified Simpson's rule. In addition, the left atrio-ventricular groove (LV) and right ventricle (RV) Epicardial Fat Thickness (EFT) were measured as well. Besides epicardial fat, LV myocardial strain parameters and T2 mapping measurements were obtained. RESULTS: TTC patients and controls were of comparable age, sex, and body mass index. Compared to healthy controls, patients with TTC demonstrated a significantly increased EFV, epicardial fat mass, and EFV indexed for body 7surface area (p = 0.005; p = 0.003; p = 0.008; respectively). In a multiple regression model including age, sex, BMI, atrial fibrillation, and dyslipidemia, TTC remained an independent association with EFV (p = 0.008). Global T2 mapping and Global longitudinal strain in patients with TTC were correlated with EFV (r = 0.63, p = 0.001, and r = 0.44, p = 0.02, respectively). CONCLUSION: Patients with TTC have increased EFV compared to healthy controls, despite a similar body mass index. The amount of epicardial fat was associated with CMR markers of myocardial inflammation and subclinical contractile dysfunction.

Non-invasive coronary imaging in patients with COVID-19: A narrative review.

SARS-CoV-2 infection, responsible for COVID-19 outbreak, can cause cardiac complications, worsening outcome and prognosis. In particular, it can exacerbate any underlying cardiovascular condition, leading to atherosclerosis and increased plaque vulnerability, which may cause acute coronary syndrome. We review current knowledge on the mechanisms by which SARS-CoV-2 can trigger endothelial/myocardial damage and cause plaque formation, instability and deterioration. The aim of this review is to evaluate current non-invasive diagnostic techniques for coronary arteries evaluation in COVID-19 patients, such as coronary CT angiography and atherosclerotic plaque imaging, and their clinical implications. We also discuss the role of artificial intelligence, deep learning and radiomics in the context of coronary imaging in COVID-19 patients.

Cardiovascular Risk Perception and Knowledge among Italian Women: Lessons from IGENDA Protocol.

A multicenter, cross-sectional observational study (Italian GENder Differences in Awareness of Cardiovascular risk, IGENDA study) was carried out to evaluate the perception and knowledge of cardiovascular risk among Italian women. An anonymous questionnaire was completed by 4454 women (44.3 ± 14.1 years). The 70% of respondents correctly identified cardiovascular disease (CVD) as the leading cause of death. More than half of respondents quoted cancer as the greatest current and future health problem of women of same age. Sixty percent of interviewed women considered CVD as an almost exclusively male condition. Although respondents showed a good knowledge of the major cardiovascular risk factors, the presence of cardiovascular risk factors was not associated with higher odds of identifying CVD as the biggest cause of death. Less than 10% of respondents perceived themselves as being at high CVD risk, and the increased CVD risk perception was associated with ageing, higher frequency of cardiovascular risk factors and disease, and a poorer self-rated health status. The findings of this study highlight the low perception of cardiovascular risk in Italian women and suggest an urgent need to enhance knowledge and perception of CVD risk in women as a real health problem and not just as a as a life-threatening threat.

Non-invasive estimation of stroke volume during exercise from oxygen in heart failure patients.

AIMS: In heart failure, oxygen uptake and cardiac output measurements at peak and during exercise are important in defining heart failure severity and prognosis. Several cardiopulmonary exercise test-derived parameters have been proposed to estimate stroke volume during exercise, including the oxygen pulse (oxygen uptake/heart rate). Data comparing measured stroke volume and the oxygen pulse or stroke volume estimates from the oxygen pulse at different stages of exercise in a sizeable population of healthy individuals and heart failure patients are lacking. METHODS: We analysed 1007 subjects, including 500 healthy and 507 heart failure patients, who underwent cardiopulmonary exercise testing with stroke volume determination by the inert gas rebreathing technique. Stroke volume measurements were made at rest, submaximal (∼50% of exercise) and peak exercise. At each stage of exercise, stroke volume estimates were obtained considering measured haemoglobin at rest, predicted exercise-induced haemoconcentration and peripheral oxygen extraction according to heart failure severity. RESULTS: A strong relationship between oxygen pulse and measured stroke volume was observed in healthy and heart failure subjects at submaximal (R2 = 0.6437 and R2 = 0.6723, respectively), and peak exercise (R2 = 0.6614 and R2 = 0.5662) but not at rest. In healthy and heart failure subjects, agreement between estimated and measured stroke volume was observed at submaximal (-3 ± 37 and -11 ± 72 ml, respectively) and peak exercise (1 ± 31 and 6 ± 29 ml, respectively) but not at rest. CONCLUSION: In heart failure patients, stroke volume estimation and oxygen pulse during exercise represent stroke volume, albeit with a relevant individual data dispersion so that both can be used for population studies but cannot be reliably applied to a single subject. Accordingly, whenever needed stroke volume must be measured directly.

Protective effects of the angiotensin II receptor blocker telmisartan on epirubicin-induced inflammation, oxidative stress, and early ventricular impairment.

BACKGROUND: Oxidative stress and RAAS play an important role in the occurrence of anthracyclines-induced cardiotoxicity. Telmisartan, an angiotensin II type 1 receptor blocker, inhibits activation of superoxide sources and induces anti-inflammatory effects. METHODS: The possible role of telmisartan in preventing myocardial damage induced by epirubicin (EPI) was investigated. Forty-nine patients free from cardiovascular diseases affected by a variety of solid cancers were examined. Eligible patients were randomized to receive telmisartan (40 mg/d; TEL, n = 25) or placebo (PLA, n = 24) starting 1 week before chemotherapy. Patients were studied by means of echocardiography, tissue Doppler, and strain and strain rate (SR) imaging. We also measured plasma levels of inflammatory and oxidative stress markers. All parameters were assessed at baseline and 7 days after every new EPI dose of 100 mg/m(2). RESULTS: An impairment of the SR peak was observed at the EPI dose of 200 mg/m(2), with no significant differences between TEL and PLA (1.41 +/- 0.31 vs 1.59 +/- 0.36/s). At growing cumulative doses of EPI, SR normalized only in TEL, showing a significant difference in comparison to PLA at EPI doses of 300 mg/m(2) (1.69 +/- 0.42 vs 1.34 +/- 0.18/s, P < .001) and 400 mg/m(2) (1.74 +/- 0.27 vs 1.38 +/- 0.24/s, P < .001). Moreover, a significant increase in reactive oxygen species and interleukin-6 was found in PLA; but these remained unchanged in TEL. CONCLUSIONS: We confirmed that EPI-induced cardiotoxicity is primarily related to the inactivation of the cardiac antioxidant defenses. In addition, we showed that telmisartan can reduce EPI-induced radical species, antagonize the inflammation, and reverse the early myocardial impairment.

Echocardiographic accidental finding of asymptomatic cardiac and pulmonary embolism caused by cement leakage after percutaneous vertebroplasty.

Percutaneous vertebroplasty (PVP) is a therapeutic, interventional radiological procedure involving bone cement injection into a vertebral body. Although PVP is considered a minimally invasive procedure, cement leakage into the perivertebral venous system can occur with its migration towards the right heart and the pulmonary circulation. We report a case of accidental finding of asymptomatic cardiac and pulmonary embolism caused by cement leakage after PVP.

Multimodality Imaging Diagnosis of Multiple Ventricular Thrombosis and Massive Stroke after Gemcitabine and Cisplatin Chemotherapy for Urothelial Cancer.

Cancer and chemotherapy are known to be risk factors for developing coagulative disorders, venous thrombosis, adverse cardiovascular events, and cardiotoxicity. Combined modality gemcitabine-cisplatin chemotherapy is often administered to treat a few solid tumors. We report the unusual case of a man suffering from urothelial cancer and admitted for chemotherapy, who developed an ischemic stroke after the last chemotherapeutical cycle. During his hospital stay, at echocardiographic examination, left ventricular transient hypokinesia and two intraventricular thrombi were detected, without evidence of acute coronary syndrome. Multimodality imaging approach (i.e., transthoracic echo, transoesophageal echo, computed tomography, and cardiac magnetic resonance imaging) played a pivotal role for a clear diagnosis and prompt decision-making. This is the first report of an intraventricular-related arterial thromboembolic event in a patient treated with the combination gemcitabine-cisplatin.

Women-specific predictors of cardiovascular disease risk - new paradigms.

Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality in women in spite of the overall reduction in age-adjusted CVD mortality in the past few years. Although traditional risk factors for CVD are predictors of increased risk in both men and women, risk factors that are unique to women and related to their reproductive history have recently been considered to be important. The development of CVD in women may correlate with specific events taking place throughout a woman's obstetric and gynaecological history. Gynaecological conditions such as polycystic ovary syndrome, premature ovarian failure, surgical and spontaneous menopause, and conditions related to pregnancy, i.e. gestational diabetes, preeclampsia, intrauterine growth restriction, miscarriages, and preterm birth, may affect the onset, clinical features, and prognosis of CVD later in women's lives. These pathological conditions that develop during the fertile period of life or peri-menopause have been suggested to be early markers of future CVD; their presence presents a unique opportunity for the early identification of women who may be at an increased risk of CVD. The assessment of CV risk in women should not just focus on conventional risk factors but also on different aspects of the gynaecological history to allow specific preventive and therapeutic strategies to be established. This paper reviews the various pathological conditions occurring in women during their fertile period of life and peri-menopause, which have been identified to potentially increase CVD risk.

From Molecular Mechanisms to Clinical Management of Antineoplastic Drug-Induced Cardiovascular Toxicity: A Translational Overview.

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated with irreversible cardiac cell injury, and it is typically caused by anthracyclines and traditional chemotherapeutics. Type II CTX is generally caused by novel biologics and more targeted drugs, and it is associated with reversible myocardial dysfunction. Therefore, patients undergoing anti-cancer treatments should be closely monitored, and patients at risk of CTX should be identified before beginning treatment to reduce CTX-related morbidity. Future Directions: Genetic profiling of clinical risk factors and an integrated approach using molecular, imaging, and clinical data may allow the recognition of patients who are at a high risk of developing chemotherapy-related CTX, and it may suggest methodologies to limit damage in a wider range of patients. The involvement of redox mechanisms in cancer biology and anticancer treatments is a very active field of research. Further investigations will be necessary to uncover the hallmarks of cancer from a redox perspective and to develop more efficacious antineoplastic therapies that also spare the cardiovascular system.

Persistence, up to 18 months of follow-up, of epirubicin-induced myocardial dysfunction detected early by serial tissue Doppler echocardiography: correlation with inflammatory and oxidative stress markers.

A phase II, open, nonrandomized trial was carried out in a group of epirubicin-treated cancer patients with the aim of detecting early preclinical changes that are predictive of the risk for heart failure. Thirty-one patients (male/female ratio, 8/23; mean age +/- standard deviation, 59 +/- 14 years) with tumors at different sites and scheduled to be treated with an epirubicin-based chemotherapy regimen, were enrolled. We prospectively evaluated the acute (1 week after) and late (3, 6, 12, and 18 months of follow-up) effects of epirubicin administration. A significant impairment in systolic left ventricular (LV) function was observed at a cumulative epirubicin dose of 200 mg/m(2). This was shown by a reduction in the strain rate (SR) peak in comparison with baseline and persisted throughout the treatment and follow-up, up to 18 months; strain (Sigma) remained unchanged. The Sm wave showed a progressive reduction that became significant only at the 18-month follow-up. On TDI the E(m)/A(m) ratio declined at the 200-mg/m(2) cumulative epirubicin dose versus baseline and persisted throughout the treatment and up to the 18-month follow-up. On conventional echocardiography the E/A ratio declined significantly only at the 300-mg/m(2) cumulative epirubicin dose. Interleukin (IL)-6, soluble IL-6 receptor, and reactive oxygen species (ROS) increased significantly at the 200-mg/m(2) dose, and IL-6 was persistently high at the 300- and 400-mg/m(2) doses, returning to within baseline values during follow-up. ROS, after the peak reached at the 200-mg/m(2) dose, returned to within baseline values. A significant inverse correlation between DeltaSR and the increase in both IL-6 and ROS was observed. A multiple regression analysis showed that both the IL-6 and ROS variables were independent and strongly predictive of DeltaSR. The clinical meaningfulness of our findings warrants further investigations on a larger number of patients for a longer period of follow-up.

Effects of a mini-trampoline rebounding exercise program on functional parameters, body composition and quality of life in overweight women.

BACKGROUND: Mini-trampoline rebounding exercise (MRE) is becoming a very popular form of fitness training. Despite awareness of this activity worldwide, a limited number of studies have systematically investigated the health effects correlated with MRE training. The aim of our study was to evaluate manifold health outcomes after 12 weeks of an MRE program in a group of overweight Italian women. METHODS: Eighteen overweight women (age 38.05±10.5 years, BMI: 27.6±2.1 kg/m2) were enrolled in this study. Functional profile, strength, body composition, quality of life and pain intensity were assessed at baseline and after 12 weeks of MRE. RESULTS: Significant improvements were observed in the measurements of anthropometric profile and body composition (circumferences, fat mass, lean and muscular mass). Both a significant decrease in systolic and diastolic blood pressure values (from 128/80.5 to 123/71 mmHg, P<0.05) and an improvement in lipid and glucose profiles were observed. At maximal exercise testing, an increase in work capacity (from 104 to 123 watts, P=0.003) and VO2max (from 15.4 to 16.9 mL/kg/min, P=0.04) was found. SF-36 showed positive changes in four of the eight items as well as in the Mental Component Summary. With regard to the Brief Pain Inventory-SF, a decrease in both pain severity and the pain interference score was detected. CONCLUSIONS: MRE appears feasible to ensure positive effects on overall health and can be proposed to populations that could greatly benefit from training programs, such as overweight women.