A single bout of cardiovascular exercise can enhance plasticity in human cortex; however, the intensity required for optimal enhancement is debated. We investigated the effect of exercise intensity on motor cortex synaptic plasticity, using transcranial magnetic stimulation. Twenty healthy adults (Mage = 35.10 ± 13.25 years) completed three sessions. Measures of cortico-motor excitability (CME) and inhibition were obtained before and after a 20-min bout of either high-intensity interval exercise, moderate-intensity continuous exercise, or rest, and again after intermittent theta burst stimulation (iTBS). Results showed that high-intensity interval exercise enhanced iTBS plasticity more than rest, evidenced by increased CME and intracortical facilitation, and reduced intracortical inhibition. In comparison, the effect of moderate-intensity exercise was intermediate between high-intensity exercise and rest. Importantly, analysis of each participant's plasticity response profile indicated that high-intensity exercise increased the likelihood of a facilitatory response to iTBS. We also established that the brain-derived neurotrophic factor Val66Met polymorphism attenuated plasticity responses following high-intensity exercise. These findings suggest that high-intensity interval exercise should be considered not only when planning exercise interventions designed to enhance neuroplasticity, but also to maximize the therapeutic potential of non-invasive brain stimulation. Additionally, genetic profiling may enhance efficacy of exercise interventions for brain health.

Despite numerous advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains a leading cause of morbidity and mortality. Novel and inexpensive interventions that can contribute to the primary and secondary prevention of cardiovascular disease are of interest. Numerous studies have reported on the benefits of meditation. Meditation instruction and practice is widely accessible and inexpensive and may thus be a potential attractive cost-effective adjunct to more traditional medical therapies. Accordingly, this American Heart Association scientific statement systematically reviewed the data on the potential benefits of meditation on cardiovascular risk. Neurophysiological and neuroanatomical studies demonstrate that meditation can have long-standing effects on the brain, which provide some biological plausibility for beneficial consequences on the physiological basal state and on cardiovascular risk. Studies of the effects of meditation on cardiovascular risk have included those investigating physiological response to stress, smoking cessation, blood pressure reduction, insulin resistance and metabolic syndrome, endothelial function, inducible myocardial ischemia, and primary and secondary prevention of cardiovascular disease. Overall, studies of meditation suggest a possible benefit on cardiovascular risk, although the overall quality and, in some cases, quantity of study data are modest. Given the low costs and low risks of this intervention, meditation may be considered as an adjunct to guideline-directed cardiovascular risk reduction by those interested in this lifestyle modification, with the understanding that the benefits of such intervention remain to be better established. Further research on meditation and cardiovascular risk is warranted. Such studies, to the degree possible, should utilize randomized study design, be adequately powered to meet the primary study outcome, strive to achieve low drop-out rates, include long-term follow-up, and be performed by those without inherent bias in outcome.

Coronary heart disease is the major cause of global cardiovascular mortality and morbidity. Lifestyle behaviour contributes as a risk factor: unhealthy diet, sedentary lifestyle, tobacco, alcohol, hypertension, diabetes, dyslipidemia and psychosocial stress. Atherosclerosis pathologic mechanisms involving oxidative stress, dyslipidemia, inflammation and senescence are associated with arterial wall damage and plaque formation. Stress reduction was observed in several types of meditation. After meditation, hormonal orchestration modulates effects in the central nervous system and in the body. All types of meditation are associated with blood pressure control, enhancement in insulin resistance, reduction of lipid peroxidation and cellular senescence, independent of type of meditation. This review presents scientific evidence to explain how meditation can produce beneficial effects on the cardiovascular system, and particularly regarding vascular aspects.

OBJECTIVES:To our knowledge, no study has addressed the relationship between adherence to a Mediterranean diet style and severity of heart failure. The aim of this retrospective study was to evaluate the relationship between adherence to the Mediterranean diet assessed using the calculation of Mediterranean diet score and congestive heart failure (CHF), its severity, and pathogenesis.

METHODS:We analyzed charts and collected data of all consecutive patients with a diagnosis of CHF at admission to our Internal Medicine Ward from 2008 to 2014.

RESULTS:We analyzed 209 patients with CHF and 200 controls. Patients with CHF showed a significantly lower mean MeDi score than controls. At receiver operating characteristic curve analysis, we found a good sensitivity and specificity of mean MeDi score to predict CHF. We also observed a significant positive correlation between MeDi score and ischemic pathogenesis of CHF, a positive relationship between New York Heart Association (NYHA) class and ischemic heart disease, and a significant negative relationship between NYHA class and MeDi score.

CONCLUSION:The beneficial effects of adherence to the Mediterranean diet suggest a possible answer to the question of the biochemical bases of our data, which should be seen as the direct consequence of the anti-inflammatory, antioxidant, and anti-remodeling effects linked to the diet.

To update the clinical practice guidelines for nutrition therapy of the European Association for the Study of Diabetes, we conducted a systematic review and meta-analysis of prospective cohort studies and randomized clinical trials (RCTs) to evaluate the effect of the Mediterranean diet (MedDiet) on the prevention of cardiovascular disease (CVD) incidence and mortality. We searched Medline, EMBASE (through April 20, 2018) and Cochrane (through May 7, 2018) databases. Pooled relative risks (RRs) and 95% confidence interval (CI) were calculated by the generic inverse variance method. A total of 41 reports (3 RCTs and 38 cohorts) were included. Meta-analyses of RCTs revealed a beneficial effect of the MedDiet on total CVD incidence (RR: 0.62; 95% CI: 0.50, 0.78) and total myocardial infarction (MI) incidence (RR: 0.65; 95% CI: 0.49, 0.88). Meta-analyses of prospective cohort studies, which compared the highest versus lowest categories of MedDiet adherence, revealed an inverse association with total CVD mortality (RR: 0.79; 95% CI: 0.77, 0.82), coronary heart disease (CHD) incidence (RR: 0.73; 95% CI: 0.62, 0.86), CHD mortality (RR: 0.83; 95% CI: 0.75, 0.92), stroke incidence (RR: 0.80; 95% CI: 0.71, 0.90), stroke mortality (RR: 0.87; 95% CI: 0.80, 0.96) and MI incidence (RR: 0.73; 95% CI: 0.61, 0.88). The present study suggests that MedDiet has a beneficial role on CVD prevention in populations inclusive of individuals with diabetes.

MicroRNAs (miRNAs, miRs), a group of small non-coding RNAs, repress gene expressions at posttranscriptional level in most cases and are involved in cardiovascular physiology and disease pathogenesis. Increasing evidence has proved that miRNAs are potential regulators of exercise induced cardiac growth and mediate the benefits of exercise in a variety of cardiovascular diseases. In this chapter, we will review the regulatory effects of miRNAs in cardiac adaptations to exercise, and summarize their cardioprotective effects against myocardial infarction, ischemia/reperfusion injury, heart failure, diabetic cardiomyopathy, atherosclerosis, hypertension, and pulmonary hypertension. Also, we will introduce circulating miRNAs in response to acute and chronic exercise. Therefore, miRNAs may serve as novel therapeutic targets and potential biomarkers for cardiovascular diseases.

Regular physical activity with aerobic and muscle-strengthening training protects against the occurrence and progression of cardiovascular disease and can improve cardiac function in heart failure patients. In the past decade significant advances have been made in identifying mechanisms of cardiomyocyte re-programming and renewal including an enhanced exercise-induced proliferational capacity of cardiomyocytes and its progenitor cells. Various intracellular mechanisms mediating these positive effects on cardiac function have been found in animal models of exercise and will be highlighted in this review. 1) activation of extracellular and intracellular signaling pathways including phosphatidylinositol 3 phosphate kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), EGFR/JNK/SP-1, nitric oxide (NO)-signaling, and extracellular vesicles; 2) gene expression modulation via microRNAs (miR), in particular via miR-17-3p and miR-222; and 3) modulation of cardiac cellular metabolism and mitochondrial adaption. Understanding the cellular mechanisms, which generate an exercise-induced cardioprotective cellular phenotype with physiological hypertrophy and enhanced proliferational capacity may give rise to novel therapeutic targets. These may open up innovative strategies to preserve cardiac function after myocardial injury as well as in aged cardiac tissue.

Ischemia-reperfusion injury (IRI) is a major cause of cardiac dysfunction during cardiovascular surgery, heart transplantation and cardiopulmonary bypass procedures. The purpose of the present study was to explore, firstly, whether ozone induces oxidative preconditioning by activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and, secondly, whether ozone oxidative preconditioning (OzoneOP) can protect the heart against IRI by attenuating mitochondrial damage. Rats were subjected to 30min of cardiac ischemia followed by 2h of reperfusion, with or without prior OzoneOP (100μg/kg/day) for 5 days. Antioxidant capacity, myocardial apoptosis and mitochondrial damage were evaluated and compared at the end of reperfusion. OzoneOP was found to increase antioxidant capacity and to protect the myocardium against IRI by attenuating mitochondrial damage and myocardial apoptosis. The study suggests a potential role for OzoneOP in protecting the heart against IRI during cardiovascular surgery, cardiopulmonary bypass procedures or transplantation.

As one of the most serious complications of diabetes, diabetic cardiomyopathy (DCM) imposes a huge burden on individuals and society, and represents a major public health problem. It has long been recognized that physical exercise has important health benefits for patients with type 2 diabetes, and regular physical exercise can delay or prevent the complications of diabetes. Current studies show that physical exercise has been regarded as an importantly non-pharmacological treatment for diabetes and DCM, with high efficacy and low adverse events. It can inhibit the pathological processes of myocardial apoptosis, myocardial fibrosis, and myocardial microvascular diseases through improving myocardial metabolism, enhancing the regulation of Ca, and protecting the function of mitochondria. Eventually, it can alleviate the occurrence and development of diabetic complications. Describing the mechanisms of physical exercise on DCM may provide a new theory for alleviating, or even reversing the development of DCM, and prevent it from developing to heart failure.

It is now well established that after menopause cardiometabolic disorders become more common. Recently, resistance exercise has been recommended as a complement to aerobic (combined training, CT) for the treatment of cardiometabolic diseases. The aim of this study was to evaluate the effects of CT in hypertensive ovariectomized rats undergoing fructose overload in blood pressure variability (BPV), inflammation, and oxidative stress parameters. Female rats were divided into the following groups (n = 8/group): sedentary normotensive Wistar rats (C), and sedentary (FHO) or trained (FHOT) ovariectomized spontaneously hypertensive rats undergoing and fructose overload. CT was performed on a treadmill and ladder adapted to rats in alternate days (8 wk; 40-60% maximal capacity). Arterial pressure (AP) was directly measured. Oxidative stress and inflammation were measured on cardiac and renal tissues. The association of risk factors (hypertension + ovariectomy + fructose) promoted increase in insulin resistance, mean AP (FHO: 174± 4 vs. C: 108 ± 1 mmHg), heart rate (FHO: 403 ± 12 vs. C: 352 ± 11 beats/min), BPV, cardiac inflammation (tumor necrosis factor-α-FHO: 65.8 ± 9.9 vs. C: 23.3 ± 4.3 pg/mg protein), and oxidative stress cardiac and renal tissues. However, CT was able to reduce mean AP (FHOT: 158 ± 4 mmHg), heart rate (FHOT: 303 ± 5 beats/min), insulin resistance, and sympathetic modulation. Moreover, the trained rats presented increased nitric oxide bioavailability, reduced tumor necrosis factor-α (FHOT: 33.1 ± 4.9 pg/mg protein), increased IL-10 in cardiac tissue and reduced lipoperoxidation, and increased antioxidant defenses in cardiac and renal tissues. In conclusion, the association of risk factors promoted an additional impairment in metabolic, cardiovascular, autonomic, inflammatory, and oxidative stress parameters and combined exercise training was able to attenuate these dysfunctions.

This article provides an overview of the current literature relating to the efficacy of dietary nitrate (NO) ingestion in altering aspects of cardiovascular and metabolic health and exercise capacity in healthy and diseased individuals. The consumption of NO-rich vegetables, such as spinach and beetroot, have been variously shown to promote nitric oxide bioavailability, reduce systemic blood pressure, enhance tissue blood flow, modulate muscle Outilisation and improve exercise tolerance both in normoxia and in hypoxia, as is commonly observed in a number of disease states. NOingestion may, therefore, act as a natural means for augmenting performance and attenuating complications associated with limited Oavailability or transport, hypertension and the metabolic syndrome. Recent studies indicate that dietary NOmight also augment intrinsic skeletal muscle contractility and improve the speed and power of muscle contraction. Moreover, several investigations suggest that NOsupplementation may improve aspects of cognitive performance both at rest and during exercise. Collectively, these observations position NOas more than a putative ergogenic aid and suggest that increasing natural dietary NOintake may act as a prophylactic in countering the predations of senescence and certain cardiovascular-metabolic diseases.

Background Oxidative stress plays a critical role in the pathogenesis and progression of type 2 diabetes and diabetic-associated cardiovascular complications. This study investigated the impact of crocin combined with voluntary exercise on heart oxidative stress indicator in high-fat diet-induced type 2 diabetic rats.

Materials and methods Rats were divided into four groups: diabetes, diabetic-crocin, diabetic-voluntary exercise, diabetic-crocin-voluntary exercise. Type 2 diabetes was induced by high-fat diet (4 weeks) and injection of streptozotocin (intraperitoneally, 35 mg/kg). Animals received crocin orally (50 mg/kg); voluntary exercise was performed alone or combined with crocin treatment for 8 weeks. Finally, malondialdehyde (MDA), activity of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were measured spectrophotometrically.

Results Treatment of diabetic rats with crocin and exercise significantly decreased the levels of MDA (p < 0.001) and increased the activity of SOD, GPx, and CAT compared with the untreated diabetic group. In addition, combination of exercise and crocin amplified their effect on antioxidant levels in the heart tissue of type 2 diabetic rats.

Conclusion We suggest that a combination of crocin with voluntary exercise treatment may cause more beneficial effects in antioxidant defense system of heart tissues than the use of crocin or voluntary exercise alone.

Cardiovascular diseases (CVDs) are disorders of the heart and blood vessels and include coronary heart diseases, cerebrovascular diseases, rheumatic heart diseases, and other conditions. CVDs are one of the most major causes of morbidity and mortality around the world, taking the lives of 17.9 million people every year. Several investigations have shown the influence of Ganoderma lucidum (G. lucidum, Lingzhi) on some metabolic markers, such as low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), blood pressure, and oxidative damage. G. lucidum potentially reduces the risk of suffering cardiovascular diseases. Some studies found that G. lucidum prevented from heart damage in a variety of disease models, such as streptozotocin (STZ)-induced diabetic, high-fat-diet-induced diabetic, isoprenaline (ISO)-induced myocardial hypertrophy, acute ethanol-induced heart toxicity, and transverse aortic constriction (TAC) models. This chapter summarizes putative preventive and therapeutic effects of G. lucidum on cardiovascular diseases and the potential clinical use of G. lucidum involved in these effects.

To investigate the effect and possible mechanism of berberine (Ber) on myocardial injury induced by exhaustion exercise (Ee).Forty healthy male SPF Sprague-Dawley rats were randomly divided into 5 groups using the random unit group design method: control group, Ee group and Ee plus Ber group (low: 50 mg·kg(-1)·d(-1), medium: 100 mg·kg(-1)·d(-1) and high dose: 150 mg·kg(-1)·d(-1),8 each). Ber (1.5 ml) or equal volume saline was given per gavage for 14 days. Rats assigned to Ee groups underwent Ee swimming once daily and rats in control group remain sedentary. After 14 days, echocardiographic measurements were performed and left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), left ventricular diastolic diameter (LVIDd) and left ventricular systolic diameter (LVIDs) were obtained. The morphological structure of heart was detected by HE and Masson staining. Serum superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by enzyme-linked immunosorbent assay. Cardiomyocytes apoptosis was detected by TUNEL method. The protein expression of myocardial hypertrophy marker protein B-type natriuretic peptide (BNP) and apoptotic marker protein (Bcl-2, Bax) in rat myocardial tissue was detected by Western blot.(1) Both LVFS and LVEF were significantly lower, and LVIDs and LVIDd were significantly larger in Ee group than those in control group (all0.01). The LVFS and LVEF in medium dose of Ber and high-dose Ber groups were significantly higher, and the LVIDs and LVIDd were significantly smaller than those in Ee group (all0.01). (2) The results of HE staining showed that the myocardial cells in control group were closely arranged, regular, normal in morphology, clear in structure, and uniform in staining. The myocardial cells of rats in Ee group were disarranged, cell staining was uneven, and vacuoles appeared in the cytoplasm. The disorder of myocardial cell arrangement and unequal staining in the medium dose of Ber were attenuated than in Ee group. The Masson staining results showed that the myocardial cells in control group were closely arranged, regular, normal in shape, clear in structure, and rarely blue-stained (fibrosis). Myocardial cells in rats in Ee group showed obvious fibrosis. The myocardial cell fibrosis in rats with medium dose of Ber was significantly reduced than exercise group. (3) MDA content in myocardial tissue of rats in Ee group was significantly higher than that of control group, and MDA content in myocardial tissue of rats in medium dose of Ber group was significantly lower than in Ee group (0.01). The SOD activity of myocardial tissue in rats was significantly lower than that of control group, while that of rats with medium dose of Ber was significantly higher than that of rats in Ee group (0.01). (4) TUNEL staining results showed that only a small amount of apoptosis myocardial cells were seen in control group, and a large number of apoptosis myocardial cells were seen in rats in Ee group. However, the number of apoptotic cardiomyocytes in medium dose of Ber was significantly lower than that in Ee group. The AI of rat cardiomyocytes was significantly higher than that of control group (0.01), and the AI of rat cardiomyocytes in median dose of Ber group was significantly lower than in Ee group (0.01). (5) BNP and Bax protein expression in the myocardial tissues of rats in Ee group were significantly higher than in control group (0.01). BNP and Bax protein expression in the myocardial tissues in median dose of Ber group were significantly lower than that of Ee group (0.01). The myocardial protein expression level of Bax was significantly higher, and the myocardial protein level of Bcl-2 was significantly lower in Ee group than in control group (both0.01), treatment with median dose of Ber could partly reverse above changes (both0.01).Ber can attenuate exhaustion exercise induced myocardial injury and remodeling in rats, and the beneficial effects of Ber might possibly be mediated by reducing free radical release and cardiomyocytes apoptosis.

Several metals including barium (Ba) known as environmental pollutants provoke deleterious effects on human health. The present work pertains to the potential ability of selenium (Se) and/or vitamin C, used as nutritional supplements, to alleviate the toxic effects induced by barium chloride (BaCl2) in the heart of adult rats. Animals were randomly divided into seven groups of six each: group 1, serving as negative controls, received distilled water; group 2 received in their drinking water BaCl2 (67 ppm); group 3 received both Ba and Se (sodium selenite 0.5 mg kg(-1) of diet); group 4 received both Ba and vitamin C (200 mg kg(-1) bodyweight) via force feeding; group 5 received Ba, Se, and vitamin C; and groups 6 and 7, serving as positive controls, received either Se or vitamin C for 21 days. The exposure of rats to BaCl2 caused cardiotoxicity as monitored by an increase in malondialdehyde, hydrogen peroxide, and advanced oxidation protein product levels, a decrease in Na(+)-K(+) adenosine triphosphatase (ATPase), Mg(2+) ATPase, and acetylcholinesterase activities and in antioxidant defense system (catalase, glutathione peroxidase, superoxide dismutase, glutathione, and nonprotein thiols). Plasma lactate dehydrogenase and creatine kinase activities, total cholesterol, triglyceride, and low-density lipoprotein-cholesterol levels increased, while high-density lipoprotein-cholesterol level decreased. Coadministration of Se and/or vitamin C restored the parameters indicated above to near control values. The histopathological findings confirmed the biochemical results. Se and vitamin C may be a promising therapeutic strategy for Ba-induced heart injury.

BACKGROUND:Raisins are a significant source of dietary fiber and polyphenols, which may reduce cardiovascular disease (CVD) risk by affecting lipoprotein metabolism and inflammation. Walking represents a low intensity exercise intervention that may also reduce CVD risk. The purpose of this study was to determine the effects of consuming raisins, increasing steps walked, or a combination of these interventions on blood pressure, plasma lipids, glucose, insulin and inflammatory cytokines.

RESULTS:Thirty-four men and postmenopausal women were matched for weight and gender and randomly assigned to consume 1 cup raisins/d (RAISIN), increase the amount of steps walked/d (WALK) or a combination of both interventions (RAISINS + WALK). The subjects completed a 2 wk run-in period, followed by a 6 wk intervention. Systolic blood pressure was reduced for all subjects (P = 0.008). Plasma total cholesterol was decreased by 9.4% for all subjects (P<0.005), which was explained by a 13.7% reduction in plasma LDL cholesterol (LDL-C) (P<0.001). Plasma triglycerides (TG) concentrations were decreased by 19.5% for WALK (P<0.05 for group effect). Plasma TNF-alpha was decreased from 3.5 ng/L to 2.1 ng/L for RAISIN (P<0.025 for time and group x time effect). All subjects had a reduction in plasma sICAM-1 (P<0.01).

CONCLUSION:This research shows that simple lifestyle modifications such as adding raisins to the diet or increasing steps walked have distinct beneficial effects on CVD risk.

BACKGROUND:Dietary habits play an important role in the development of atherosclerosis, the most important cause of morbidity and mortality in the world. The objective of this study was to verify if vegetarian (VEG) diet could be related a better profile of subclinical vascular disease evaluated by arterial stiffness and functional and structural properties of carotid arteries, compared to omnivorous (OMN) diet.

METHODS:In this cross-sectional study, 44 VEG and 44 OMN apparently healthy men≥35years of age, in order to not have confounding risk factors of subclinical atherosclerosis, were assessed for anthropometric data, blood pressure, blood lipids, glucose, C reactive protein (CRP), and arterial stiffness determined by carotid-femoral pulse wave velocity (PWV). Also, carotid intima-media thickness (c-IMT) and distensibility were evaluated.

RESULTS:VEG men had lower body mass index, systolic and diastolic blood pressures, fasting serum total cholesterol, LDL and non-HDL-cholesterol, apolipoprotein B, glucose and glycated hemoglobin values in comparison with OMN individuals (all p values<0.05). Markers of vascular structure and function were different between VEG and OMN: PWV 7.1±0.8m/s vs. 7.7±0.9m/s (p<0.001); c-IMT 593±94 vs. 661±128μm (p=0.003); and relative carotid distensibility 6.39±1.7 vs. 5.72±1.8% (p=0.042), respectively. After a multivariate linear regression analysis, a VEG diet was independently and negatively associated with PWV (p value 0.005).

CONCLUSIONS:A VEG diet is associated with a more favorable cardiovascular diseases biomarker profile and better vascular structural and functional parameters.

BACKGROUND: Yoga has potential for benefit for patients with coronary artery disease though objective, angiographic studies are lacking. MATERIAL AND METHODS: We evaluated possible role of lifestyle modification incorporating yoga, on retardation of coronary atherosclerotic disease. In this prospective, randomized, controlled trial, 42 men with angiographically proven coronary artery disease (CAD) were randomized to control (n = 21) and yoga intervention group (n = 21) and were followed for one year. The active group was treated with a user-friendly program consisting of yoga, control of risk factors, diet control and moderate aerobic exercise. The control group was managed by conventional methods i.e. risk factor control and American Heart Association step I diet. RESULTS: At one year, the yoga groups showed significant reduction in number of anginal episodes per week, improved exercise capacity and decrease in body weight. Serum total cholesterol, LDL cholesterol and triglyceride levels also showed greater reductions as compared with control group. Revascularisation procedures (coronary angioplasty or bypass surgery) were less frequently required in the yoga group (one versus eight patients; relative risk = 5.45; P = 0.01). Coronary angiography repeated at one year showed that significantly more lesions regressed (20% versus 2%) and less lesions progressed (5% versus 37%) in the yoga group (chi-square = 24.9; P<0.0001). The compliance to the total program was excellent and no side effects were observed. CONCLUSION: Yoga lifestyle intervention retards progression and increases regression of coronary atherosclerosis in patients with severe coronary artery disease. It also improves symptomatic status, functional class and risk factor profile.

Mitochondrial diseases are rare metabolic disorders which can cause hypertrophic cardiomyopathy. We describe a 3-year-old girl who was diagnosed for mitochondrial disease (mutation m.5559A>G in the mitochondrial-tRNAgene (MT-TW)). Echocardiography showed left ventricular hypertrophy with an enlarged septum (9 mm, Z-score 3.26). Antioxidant supplementation associated with a high-fat ketogenic diet were introduced and improved, as expected, neurological status. In addition, heart parameters improved with a normalization of interventricular septum thickness at the age of six (6 mm, Z-score 1.05). This case report suggests that a ketogenic diet may improve hypertrophic cardiomyopathy in the context of mitochondrial disease.

The purpose of this study was to assess the synergistic effect of polydatin and vitamin C on attenuating cardiotoxicity induced by doxorubicin (DOX) in rats. Polydatin could significantly increase the activity of SOD and the heart rate, attenuate myocardial pathological damage, decrease MDA content, slightly increase arterial pressure and GSH-Px activity, reduce intervals of QRS, QT and ST, and lower FFA content. The combination of polydatin and vitamin C could significantly increase arterial pressure and heart rate, decrease QRS interval and slightly reduce ST and QT intervals, significantly attenuate myocardial pathological damage, increase the activities of GSH-Px,T-SOD, Na(+) K(+) -ATPase and Ca(2+) Mg(2+) -ATPase, and elevate PCr and ATP contents, slightly increase ADP and TAN contents and PCr/ATP, and significantly decrease the contents of MDA and FFA, when compared with those in the DOX group. Meanwhile, the improvement effects on FFA content, the activities of ATPase and SOD and contents of ATP and TAN in combination group were more obvious than those in polydatin group; and the improvement effects on arterial pressure, heart rate, interval of QRS, GSH-Px activity, and MDA, ADP and PCr contents in combination group were slightly obvious when compared with those in polydatin group. In addition, the mRNA expression levels of AMPK-α2 and PPAR-α were slightly improved in combination group. The results illustrate that the combination of polydatin and vitamin C has the ability to enhance the myocardial protective effects by its antioxidative effect and improving energy metabolism. This article is protected by copyright. All rights reserved.