Western-type diet with high salt and sugar, sedentary behavior, obesity, tobacco and alcoholism are important risk factors for hypertension. This review aims to highlight the role of western diet-induced oxidative stress and inflammation in the pathogenesis of hypertension and the role of various types of diets in its prevention with reference to dietary approaches to stop hypertension (DASH) diet. It seems that it is crucial to alter the western type of diet because such diets can also predispose all CVDs. Western diet-induced oxidative stress is characterized by excessive production of reactive oxygen species (ROS) with an altered oxidation-reduction (redox) state, leading to a marked increase in inflammation and vascular dysfunction. Apart from genetic and environmental factors, one important cause for differences in the prevalence of hypertension in various countries may be diet quality, deficiency in functional foods, and salt consumption. The role of the DASH diet has been established. However, there are gaps in knowledge about the role of some Indo-Mediterranean foods and Japanese foods, which have been found to decrease blood pressure (BP) by improving vascular function. The notable Indo-Mediterranean foods are pulses, porridge, spices, and millets; fruits such as guava and blackberry and vegetables, which may also decrease BPs. The Japanese diet consists of soya tofu, whole rice, in particular medical rice, vegetables and plenty of fish rich in fish oil, fish peptides and taurine that are known to decrease BPs. Epidemiological studies and randomized, controlled trials have demonstrated the role of these diets in the prevention of hypertension and metabolic diseases. Such evidence is still meager from Japan, although the prevalence of hypertension is lower (15–21%) compared to other developed countries, which may be due to the high quality of the Japanese diet. Interestingly, some foods, such as berries, guava, pumpkin seeds, carrots, soya beans, and spices, have been found to cause a decrease in BPs. Omega-3 fatty acids, fish peptide, taurine, dietary vitamin D, vitamin C, potassium, magnesium, flavonoids, nitrate and l-arginine are potential nutrients that can also decrease BPs. Larger cohort studies and controlled trials are necessary to confirm our views.

The exact pathophysiology of heart failure (HF) is not yet known. Western diet, characterized by highly sweetened foods, as well as being rich in fat, fried foods, red meat and processed meat, eggs, and sweet beverages, may cause inflammation, leading to oxidative dysfunction in the cardiac ultra-structure. Oxidative function of the myocardium and how oxidative dysfunction causes physio-pathological remodeling, leading to HF, is not well known. Antioxidants, such as polyphenolics and flavonoids, omega-3 fatty acids, and other micronutrients that are rich in Indo-Mediterranean-type diets, could be protective in sustaining the oxidative functions of the heart. The cardiomyocytes use glucose and fatty acids for the physiological functions depending upon the metabolic requirements of the heart. Apart from toxicity due to glucose, lipotoxicity also adversely affects the cardiomyocytes, which worsen in the presence of deficiency of endogenous antioxidants and deficiency of exogenous antioxidant nutrients in the diet. The high-sugar-and-high-fat-induced production of ceramide, advanced glycation end products (AGE) and triamino-methyl-N-oxide (TMAO) can predispose individuals to oxidative dysfunction and Ca-overloading. The alteration in the biology may start with normal cardiac cell remodeling to biological remodeling due to inflammation. An increase in the fat content of a diet in combination with inducible nitric oxide synthase (NOSi) via N-arginine methyl ester has been found to preserve the ejection fraction in HF. It is proposed that a greater intake of high exogenous antioxidant restorative treatment (HEART) diet, polyphenolics and flavonoids, as well as cessation of red meat intake and egg, can cause improvement in the oxidative function of the heart, by inhibiting oxidative damage to lipids, proteins and DNA in the cell, resulting in beneficial effects in the early stage of the Six Stages of HF. There is an unmet need to conduct cohort studies and randomized, controlled studies to demonstrate the role of the HEART diet in the treatment of HF.

The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. In a double blind, randomized, placebo-controlled, parallel group study (a retrospective analysis of an earlier trial) in 55 patients with left ventricular ejection fraction <50% after AMI, the effects of coenzyme Q10 (120 mg/day) or placebo were studied for 24 weeks. Two-dimensional echocardiography was performed at discharge, (approximately 5–10 days after admission) and at 6 months after AMI. The results revealed that wall thickness opposite the site of infarction decreased from (mean ± standard deviation (SD)) 12.2 ± 2.0 mm to 10.0 ± 1.8 mm with coenzyme Q10 compared with 12.8 ± 2.2 mm to 13.3 ± 2.3 mm with placebo (p < 0.01). Left ventricular mass changed from 236 ± 72 g to 213 ± 61 g with coenzyme Q10 compared with 230 ± 77 g to 255 ± 86 g with placebo (p < 0.01). Treatment with coenzyme Q10 also prevented alteration of sphericity index which is a ratio of the long and short axis of the left ventricle (which changed from 1.61 ± 0.28 to 1.63 ± 0.30 with coenzyme Q10 compared with 1.61 ± 0.32 to 1.41 ± 0.31 with placebo (p < 0.05)). Coenzyme Q10 also prevented alteration of the wall thickening abnormality at the infarct site, which changed from 9.4 ± 3.0 cm² to 9.1 ± 2.8 cm² compared with 10.1 ± 3.1 to 13.7 ± 4.2 cm² with placebo (p < 0.05). End diastolic and systolic volumes also showed significant reduction with coenzyme Q10 compared to placebo. The serum level of ACE showed significant decline in the coenzyme Q10 group compared to the control group. Treatment with coenzyme Q10 early after AMI causes attenuation of left ventricular remodeling and decreases the serum ACE level in patients with left ventricular dysfunction.

Heart failure (HF) has become a public health problem, but exact pathophysiology is still unknown. Western diet characterised with high sugar, high fat, red meat and processed meat, eggs, fried foods and sweetened beverages, may cause oxidative stress and inflammation, leading to oxidative dysfunction and adverse effects on cardiac-ultra-structure. However, only little is known about oxidative function of the of the myocardium and how oxidative dysfunction predispose Ca-overloading resulting in to physio-pathological remodelling leading to HF. Antioxidants such as flavonoids and polyphenolics, omega-3 fatty acids, vitamins, minerals as well as essential and nonessential amino acids that are rich in Indo-Mediterranean type of diets, may have protective roles in maintaining oxidative functions of the heart. The cardiac cells use fatty acids and glucose for the metabolic functions depending upon physiological and metabolic requirements. Apart from glucotoxicity, lipotoxicity is also damaging to cardiac cells which worsen in presence of deficiency of endogenous antioxidants and lower exogenous antioxidants in the diet. There is increased production of ceramide, advanced glycation end products (AGE) and triamino-methyl-N-oxide (TMAO) due to high sugar and high fat diets, leading to oxidative dysfunction and Ca-overloading. The biological changes may begin with physiological remodelling to pathological remodelling due to oxidative damages. High fat diet in combination with inducible nitric oxide synthase (NOSi) via N-arginine methyl ester has been found to preserve ejection fraction in a mouse model of HF. It is possible that increased supplementation of High Exogenous Antioxidant Restorative Treatment (HEART) diet; polyphenolics and flavonoids, vitamins, minerals, arginine, with omega-3 fatty acids, and cessation of red meat and egg may further improve the oxidative function of cardiac cells, resulting in the prevention and improvement in the earliest of the Six Stages of HF. Cohort studies and randomised, controlled trials would be necessary for demonstration of the role of HEART diet in the management of HF.

Background and Objectives: Metabolic syndrome (MS) represents several diseases encompassing a heterogeneous group of biochemical and physiological abnormalities characterized by structural and functional alterations in the myocardium, including the endothelium of the coronary arteries. MS also affects a substantial portion of the global population. Understanding the risk factors, the development and treatment associated with MS are of paramount importance for early identification, treatment and prevention. This study was designed to evaluate the role of the supplementation of omega-3 polyunsaturated fatty acids (n-3 PUFAs) on endothelial function in patients with MS. Materials and Methods: A total of 80 patients with MS were enrolled in two groups. The study evaluated endothelial function (EF) in subjects before and after a three-month treatment with n-3 PUFAs in a dose of 2.4 g daily (800 mg, three times a day) vs. placebo, using an Endo-PAT2000 device (Itamar Medical Ltd., Caesarea, Israel) measuring the reactive hyperemia index (a parameter of EF) and augmentation index (a parameter of arterial stiffness). Plasmatic levels of glutathione peroxidase, homocysteine, apolipoprotein B and lipoprotein were also evaluated for comparison. Results: The results showed that the average value of reactive hyperemia index before the treatment with n-3 PUFAs was 1.62 ± 0.42, compared to 1.96 ± 0.62 at the end of the study (p < 0.005). The augmentation index changed from 14.66 ± 19.55 to 9.21 ± 15.64 after the treatment (p = 0.003) with n-3 PUFA. The results also revealed a statistically significant decrease in apolipoprotein B (0.94 ± 0.36 vs. 1.13 ± 0.35, p = 0.001) and homocysteine (19.31 ± 5.29 vs. 13.78 ± 3.05, p = 0.001) and an increase in glutathione peroxidase plasma levels (41.65 ± 8.90 vs. 45.20 ± 8.01), p = 0.001. Conclusions: The results of this prospective study showed a significant improvement in EF in subjects with MS treated with n-3 PUFAs in a dose of 2.4 g daily.

Today, there are many parameters used for cardiovascular risk quantification and to identify many of the high-risk subjects; however, many of them do not reflect reality. Modern personalized medicine is the key to fast and effective diagnostics and treatment of cardiovascular diseases. One step towards this goal is a better understanding of connections between numerous risk factors. We used Factor analysis to identify a suitable number of factors on observed data about patients hospitalized in the East Slovak Institute of Cardiovascular Diseases in Košice. The data describes 808 participants cross-identifying symptomatic and coronarography resulting characteristics. We created several clusters of factors. The most significant cluster of factors identified six factors: basic characteristics of the patient; renal parameters and fibrinogen; family predisposition to CVD; personal history of CVD; lifestyle of the patient; and echo and ECG examination results. The factor analysis results confirmed the known findings and recommendations related to CVD. The derivation of new facts concerning the risk factors of CVD will be of interest to further research, focusing, among other things, on explanatory methods