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One of the organs affected by SARS-CoV-2 is the heart. Cardiac manifestations of SARS-CoV-2 include acute coronary syndrome, endocarditis, myocarditis, pericarditis with pericardial effusion, heart failure, Takotsubo syndrome, arrhythmias, intra-ventricular thrombus formation, and cardiogenic shock. If COVID-19 patients present with cardiac complications, they require thorough cardiologic work-up, including coronary angiography if myocardial infarction or Takotsubo syndrome is suspected. Since patients with prosthetic valves and those carrying devises are prone to experience cardiac complications from a SARS-CoV-2 infection, they require particular attention and surveillance. If myocarditis is suspected, the diagnosis should be established by cardiac MRI with contrast medium or endo-myocardial biopsy.

Circulating fatty acids (FA) have an endogenous or exogenous origin and are metabolized under the effect of many enzymes. They play crucial roles in many mechanisms: cell signaling, modulation of gene expression, etc., which leads to the hypothesis that their perturbation could be the cause of disease development. FA in erythrocytes and plasma rather than dietary FA could be used as a biomarker for many diseases. Cardiovascular disease was associated with elevated trans FA and decreased DHA and EPA. Increased arachidonic acid and decreased Docosahexaenoic Acids (DHA) were associated with Alzheimer’s disease. Low Arachidonic acid and DHA are associated with neonatal morbidities and mortality. Decreased saturated fatty acids (SFA), increased monounsaturated FA (MUFA) and polyunsaturated FA (PUFA) (C18:2 n-6 and C20:3 n-6) are associated with cancer. Additionally, genetic polymorphisms in genes coding for enzymes implicated in FA metabolism are associated with disease development. FA desaturase (FADS1 and FADS2) polymorphisms are associated with Alzheimer’s disease, Acute Coronary Syndrome, Autism spectrum disorder and obesity. Polymorphisms in FA elongase (ELOVL2) are associated with Alzheimer’s disease, Autism spectrum disorder and obesity. FA-binding protein polymorphism is associated with dyslipidemia, type 2 diabetes, metabolic syndrome, obesity, hypertension, non-alcoholic fatty liver disease, peripheral atherosclerosis combined with type 2 diabetes and polycystic ovary syndrome. Acetyl-coenzyme A carboxylase polymorphisms are associated with diabetes, obesity and diabetic nephropathy. FA profile and genetic variants of proteins implicated in FA metabolism could be considered as disease biomarkers and may help with the prevention and management of diseases.

Objective: This study aims to determine whether genetic variants in ACE I/D and AGT M235T are associated with overweight-obesity and body mass index (BMI) in a Tunisian population. Methods: We designed an age- and sex-matched case-control study. The height and weight were measured and BMI was calculated. A total of 259 overweight-obese patients and 369 healthy controls were genotyped for the ACE I/D and AGT M235T genes using polymerase chain reaction and restriction fragment length polymorphism. Results: ACE I/D and AGT M235T genes were associated with BMI, waist circumference and overweight-obesity (p⩽0.001). In an additive model, the I and the M alleles in ACE and AGT variants, respectively, were associated with a lower BMI: –1.45 and −2.29 units, respectively. ACE I/D genotypes were associated with dyslipidemia; AGT M235T genotypes with dyslipidemia and total cholesterol. Conclusion: These data suggest that variations in ACE I/D and AGT M235T affect the risk of overweight-obesity, BMI and dyslipidemia, and could point to a key molecular pathway of metabolic syndrome and its related comorbidities.

Olive oil is a very versatile product. It has distinctive virtues in the fields of health and nutrition. For this reason olive oil quality has attracted attention and become the focus of many studies. Olive oil quality depends on several factors such as ripening, extraction method, soil type, climatic conditions, harvesting time, varieties and storage conditions. Quality assessment of olive oil is linked to an important series of physicochemical parameters including free fatty acid content, peroxide value and sensory evaluation. The main objective of this study is to investigate using statistical analysis, the main factors influencing the quality of Tunisian olive oils. Physicochemical analysis of 89 samples of olive oil produced in the region of the Sahel and central Tunisia. This study demonstrates that the main factors influencing Tunisian olive oil quality are: olive ripening, harvesting methods, olive pre-processing storage, olive washing, leaf removing, mixing, separation systems and crushing time. The data also shows that the commercial qualitative parameters of virgin olive oil such as free fatty acids, peroxide value, specific spectrophotometric absorptions in the UV region and sensorial assessment depend on the cultivar and quality of olives before processing. The application of good olive-growing practices complemented by studies similar to this would improve the quality of olive oil produced in Tunisia. This will contribute to the promotion and value of these oils as a regional product.

Adipose tissue expresses all the renin-angiotensin system (RAS) components that play an important role in the adipogenesis, lipid and glucose metabolism regulation in an auto/paracrine manner. The classical RAS has been found to be over-activated during the adipose tissue enlargement, thus elevated Generation of Angiotensin II (Ang II) may contribute to the obesity pathogenesis. Obesity rates continue to increase worldwide. The question arises whether obesity is truly perceived as a risk factor and a disease. Then, the association between angiotensin converting enzyme (ACE) gene I/D polymorphism and the risk of overweight/obesity remains controversial. We investigated the possible relationship between ACE gene I/D polymorphism and obesity in Tunisian type 2 diabetes mellitus (T2DM) patients. In this study, obesity was defined as a body mass index (BMI) value ≥ 25 kg/m2 and subjects were classified into 4 groups (lean, normal, overweight, and obese). ACE genotyping was determined by PCR. Finding of 47.9% of hypertensives among the subjects having DD genotype and BMI ≥ 30 kg/m2 is consistent with an additive effect of DD genotype and obesity. In conclusion, the present study implies that genotyping of the ACE gene I/D polymorphism could in the future become an important part of the clinical process of risk identification for T2DM in Tunisian population.

Because acute myocardial infarction (ami) frequently occurs suddenly without any preceding clinical symptoms, the prediction of ami is clinically of great importance. the principal element of the pathogenesis of ami is the rupture of coronary atherosclerotic plaques rather than gradual progression of atherosclerosis to complete occlusion. Identification of factors concerned with plaque rupture should therefore enable to predict the risk of AMI. Two hundred AMI patients compared to 250 healthy controls. Higher diastolic blood pressure (DBP), systolic blood pressure (SBP), triglyceride, total cholesterol, LDL-cholesterol, HDL-cholesterol and fasting glucose were also shown in AMI patients group. In logistic regression analysis, smoking, hypertension (HTA) and diabetes were significant independent predictors of AMI. The patients with 1VD with multi-vessel disease with stenoses in one coronary vessels were the most frequent (33.3%), and approximately 90% of patients had a critical arterial occlusion (>90%) in coronary vessels. Due to our limited sample size our findings require confirmation in larger cohortes.

Mitochondria play critical roles in both the life and death of cardiac myocytes. Pathogenic mitochondrial DNA (mtDNA) mutations leading to mitochondrial dysfunction can cause cardiomyopathies (CMPs). Our aim was to investigate the underlying mitochondrial defect in a patient with hypertrophic cardiomyopathy (hCMP). A detailed clinical and molecular genetic analysis was performed. Total DNA was extracted from lymphocytes in a 14-year-old index male patient with hCMP, preexcitation syndrome, and severe ventricular arrhythmias. Direct sequencing of the PCR fragments was performed. To distinguish deleterious from functionally neutral variants, the ClustalW program, RNAfold software, and PolyPhen algorithm were applied, which predict the pathogenicity of a particular variant by using a set of empirical rules based on the nature of the mutation, the phylogenetic conservation of the variant, and the physicochemical property of the amino acid. The mutational analysis of mtDNA genes revealed four variants. The m.4395A>G transition (C6G) in the MT-TQ gene, which altered an evolutionary conserved nucleotide, with a conservation index of 85.7 % and affected a highly conserved U.G base pair in the secondary structure of MT-TQ. Additionally, the previously reported polymorphisms m.14757T>A, m.15236A>G, and m.15314G>A resulting in the replacement of amino acid residues in the MT-CYB gene were detected. The m.4395A>G variant was scored as possibly pathogenic and may exert a negative effect on heart function to generate hCMP.

Background. Previously it has been shown that various types of hypertrophic and dilative cardiomyopathy (hCMP, dCMP) can be attributed to disturbed mitochondrial oxidative energy metabolism. Several studies described mutations in mitochondrial DNA-located genes encoding for subunits of respiratory chain complexes, including the cytochrome b gene (MT-CYB), causing CMPs.Methods and Results. In the present study the MT-CYB gene was analysed in 30 patients with hCMP, 40 patients with dCMP, and 50 controls for alterations. Altogether, 27 MT-CYB variants were detected. Twenty-four of them were single nucleotide polymorphisms defining common haplogroups. The variant m.15434C>A was found in a single patient with severe dCMP and assessed as novel mutation, since it was not found in healthy controls or available data sets, and was nonhaplogroup associated with Phylotree. This variant altered an amino acid (L230I) with a high interspecific amino acid conservation index (CI=97.7%) indicative of the functional importance of the residue.Conclusions. Though the L230I mutation seems to play a causative role for dCMP, prospective studies on yeast or transgenic mice models with defined mutation are warranted to study the pathogenetic impact of this mutation.

Essential hypertension (HTA) is the clinical expression of a disordered interaction between the genetic, physiological, and biochemical systems that under usual conditions maintain cardiovascular homeostasis. We studied the effects of the angiotensinogen M235T, angiotensin converting enzyme insertion/deletion (ACE I/D), and angiotensin II receptor 1 (AT1R) A1166C gene polymorphisms on the risk of HTA and to evaluate the relationship between these polymorphisms and obesity. We performed AGT, ACE and AGTR genotyping in 142 hypertensive patients and 191 control subjects using PCR-RFLP methods and PCR, respectively. The three polymorphisms were significantly associated with HTA. Individuals carrying the mutated TT of AGT, DD of ACE and CC of AT1R genotypes had an 1.67 (P = 0.032), 3.09 (P < 0.001) and 3.45 (P < 0.001)-fold increased risk of HTA. After adjustment for sex, smoking, diabetes, dyslipidemia, BMI, triglycerides and DD, TT and CC genotypes, BMI was independent risk factor of HTA (OR = 3.14; P < 0.001). An association of BMI with ACE gene polymorphism (P = 0.035), whereas no association with AGT and AT1R gene polymorphisms was obtained. The proportion of hypertensives is as high as 21.8 and 13.4% in the overweight and the obese DD group. The present study implies that the genotyping for the variants of RAS gene could in the future become an important part of the clinical process of risk identification for HTA.

Introduction Excess of total homocysteine (tHcy) and decrease of thiolactonase activities (HTase) have been proposed as risk factors for coronary artery diseases (CAD). Objectives We evaluated the relationship of tHcy and HTase with paraoxonase 1 (PON1) gene polymorphism according to CAD severity. Design and methods 118 healthy volunteers and 91 CAD patients were compared. Results Serum levels of tHcy and oxidized LDL (ox-LDL) increased significantly by 26% and 48% in CAD patients and were associated with significantly lower levels of HDL cholesterol (p = 0.02) and 42% of decrease in HTase activities (p

Background. Previously it has been shown that various types of hypertrophic and dilative cardiomyopathy (hCMP, dCMP) can be attributed to disturbed mitochondrial oxidative energy metabolism. Several studies described mutations in mitochondrial DNA-located genes encoding for subunits of respiratory chain complexes, including the cytochrome b gene (MT-CYB), causing CMPs. Methods and Results. In the present study the MT-CYB gene was analysed in 30 patients with hCMP, 40 patients with dCMP, and 50 controls for alterations. Altogether, 27 MT-CYB variants were detected. Twenty-four of them were single nucleotide polymorphisms defining common haplogroups. The variant m.15434C>A was found in a single patient with severe dCMP and assessed as novel mutation, since it was not found in healthy controls or available data sets, and was nonhaplogroup associated with Phylotree. This variant altered an amino acid (L230I) with a high interspecific amino acid conservation index (CI = 97.7%) indicative of the functional importance of the residue. Conclusions. Though the L230I mutation seems to play a causative role for dCMP, prospective studies on yeast or transgenic mice models with defined mutation are warranted to study the pathogenetic impact of this mutation.

Cardiovascular disease (CVD) is the predominant cause for morbidity and mortality in diabetes mellitus (DM). Patients with diabetes mellitus have two to three times the incidence of atherosclerotic disease compared to the general population (Kannel & McGee, 1979). Several etiologic factors increase susceptibility to CVD in DM including insulin resistance, dyslipidemia, endothelial dysfunction, prothrombosis, and increased protein glycation (Baynes & Thorpe, 1999). Plasma homocysteine levels are elevated in patients with diabetes, particularly in patients with type 2 diabetes as well as in individuals in prediabetic states who exhibit insulin resistance. Homocysteine (Hcy) is a non-essential amino acid that is produced from demethylation of methionine. Hcy can be remethylated into methionine by means of vitamin B12-dependent methionine synthase and 5-methyltetrahydrofolate as a methyl donor. Hcy can be also catabolized into cysteine (the transsulfuration pathway) via cystathionine beta synthase and cystathioninase, both enzymes being vitamin B6dependent. A third way to remove Hcy is conversion to S-adenosylhomocysteine (SAH). The last reaction is mediated by SAH-hydrolase and favors the SAH formation in case of increased Hcy concentrations. S-Adenosyl methionine (SAM) is a universal methyl donor that is formed from methionine and converted into SAH after donating its methyl group. SAH is a potent inhibitor of most known methyltransferases (Kloor & Osswald, 2004). Among the main determinants of tHcy levels in non-diabetic subjects are age, sex, renal function, several diseases, drugs, coffee and chronic alcohol consumption, smoking and physical inactivity (Refsum et al., 2006). Genetic factors and nutritional deficiencies of folate

Acute myocardial infarction (AMI) is a multifactorial disease influenced by environmental and genetic factors. The aim of this study was to assess the association of angiotensin II type 1 receptor (ATR1) gene polymorphisms with AMI as well as to evaluate the role of serum angiotensin-converting enzyme (ACE) activity and that of cardiac troponin I (cTnI) in Tunisian AMI patients. One hundred and eighteen AMI patients were compared to 150 healthy controls. ATR1 genotypes were determined by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The ATR1 A1166C polymorphism was significantly associated with AMI ( p = 0.024). CC genotype and C allele frequencies were associated with increased AMI risk [CC vs. AC and AA: OR = 2.06; p = 0.045; 95 % CI (1.02–4.18); C vs. A: OR = 1.68; p = 0.004; 95 % CI (1.17–2.41)]. By multivariate logistic regression analysis, CC genotype, hypertension, diabetes, serum ACE activity and peak-cTnI were significant independent predictors of AMI. Increased serum ACE activity and cTnI peak levels were associated with the CC genotype in AMI patients. In conclusion, the ATR1 A1166C polymorphism is associated with AMI and the CC genotype associated with increased ACE activity and cTnI levels appear to predispose for AMI risk.

Coronary artery diseases (CAD) are influenced by multiple genes of modest effect as the methylenetetrahydrofolate reductase (MTHFR) C677T gene polymorphism, related to MTHFR activity and total plasma homocysteine (tHcy) concentration. This study was designed to evaluate tHcy, oxidized low-density lipoprotein (LDL) (ox-LDL), high-sensibility C-reactive protein (Hs CRP) levels, and homocysteine thiolactonase (HTase) activities as new risk factors for CAD and to investigate an association between MTHFR polymorphism tHcy concentrations and coronary syndrome severity. Our results showed significantly higher levels of tHcy and ox-LDL in patients associated with lower HTase activities. These levels increased proportionally to disease severity. Total plasma Hcy levels were negatively correlated to HTase activities in patients where the TT genotype was significantly more frequent. In a multivariate analysis, tHcy level was the only independent factor affecting the coronary syndrome severity. High tHcy levels are associated with coronary syndrome severity and may be explained either by the elevated prevalence of TT genotype or by the diminished HTase activities.

Aims To explore the role of genetic variants of angiotensinogen (AGT M235T), angiotensin-converting enzyme (ACE I/D), and angiotensin type 1 receptor (AT1R A1166C) as predictors of diabetes risk and to examine their combined effects on type 2 diabetes mellitus (T2DM) patients. Main methods One hundred and fourteen T2DM patients were compared to 175 healthy controls with similar age and sex. Key findings The genotypic frequencies for all three genes alone were significantly associated with increased risk of developing diabetes. Logistic regression analysis of classic coronary risk factors and the genetic polymorphisms demonstrated that hypertension and ACE DD genotype were the most significant contributors to T2DM. For the renin–angiotensin system (RAS) genes, the risk of T2DM in individuals with one risk genotype was 1.9 (95%CI: 1.1–3.0, p = 0.017) higher than those with zero risk genotype. Individuals who carried two risk genotypes had a 4.0 (95%CI 1.7–9.4, p = 0.001) times higher risk of T2DM than those who did not carry any risk genotypes of the RAS genes. Most interestingly, the risk of T2DM for individuals with three risk genotypes was 26.2 (95%CI: 5.8–117.9, p Significance The results of the present study imply that genotyping of renin–angiotensin system genes could become an important part of the clinical process of risk identification for T2DM in Tunisian population.

The role of methylenetetrahydrofolate reductase (MTHFR) and angiotensin-converting enzyme (ACE) gene polymorphisms as being risk factors for diabetes is still controversial. The aim was to investigate the distribution of ACE and MTHFR genotypes as well as to evaluate the role of plasmatic total homocysteine levels (tHcy) and ACE activity in Tunisian patients with type 2 diabetes mellitus (T2DM).115 T2DM patients compared to 116 healthy volunteers.The ACE I/D polymorphism was significantly associated with diabetes (p0.0001). The DD genotype and D allele were more frequent in patients compared to control group [DD: OR=4.93; p0.0001; 95 % CI: 2.71-8.97; D: OR=3.08, 95% CI: 2.09-4.51 p0.0001]. MTHFR allele and genotype frequencies did not differ between patients and controls. The susceptibility to diabetes in individuals with genotypes DD+vTT was 13.39 and in the individuals with DD+CT was 6.57 times that of the controls. However, individuals with genotypes ID+CC or II+CT have a protective effect against diabetes. The DD and TT genotypes were associated with significantly higher ACE activity and tHcy levels in diabetics.Our data suggest that ACE ID polymorphism may act synergistically with MTHFR C677T polymorphism to assess diabetes risk.