The previous one century has seen exceptional changes in the commonness and clinical results of hypertension internationally yet remarkably in Africa and creating economies by and large. This paper audits the current image of target organ harm and cardiovascular confusions in Africa utilizing accessible writing just as meta-examinations. Critical perceptions show that around 66% of people with hypertension overall live in non-industrial nations. Projections for 2025 see an expansion in this extent to 75 percent. Low mindfulness levels, late introduction, and low treatment and control levels add to the higher predominance of target organ harm and other cardiovascular entanglements in hypertensive subjects in Africa. Coordinated endeavors are prescribed to battle this scourge in Africa and other non-industrial nations all around the world. Hypertension is frequently asymptomatic and recording pulse is shrewd. A significant number of these patients are ignorant of their condition and consequently, stay untreated. Untreated or ineffectively controlled hypertension and left ventricular hypertrophy (LVH) are hazard factors for cardiovascular sicknesses (CVD), a significant reason for grimness and mortality, and abrupt demise. The absence of familiarity with the infection brings about more awful results. Various hypertensive may introduce unexpectedly with target-organ harm (TOD) including different organs. Hence at starting determination, they as of now have a hypertensive coronary illness (HHD); some with LVH, while some have a straightforward congestive cardiovascular breakdown (CHF). CHF is a deadly sickness with a helpless guess and decreased future. It forces huge wellbeing, financial, and social weight on the patient, his/her family, and the network everywhere, and it for the most part influences guys and females in their gainful center years. Significant TOD of hypertension, for example, LVH, diastolic brokenness, CHF, ischaemic coronary illness (IHD), stroke, and renal disappointment have been archived by different laborers in Nigeria and these were generally emergency clinic-based investigations. Post-mortem examination contemplates affirmed that the commonest reason for abrupt, unforeseen demise in Nigerians is hypertension. In Nigeria, little is thought about the encounters of guardians and care-chasing rehearses concerning hypertension and components affecting late introduction with TOD. A portion of the undiscovered hypertensive is distinguished unexpectedly throughout the board for other clinical conditions or during calamitous occasions. The test to the doctor along these lines is early identification and treatment of hypertension before movement 

For cell therapy on myocardial infarction, many kinds of cells have been studied. In our experience since 2001, the implant of mesenchyme stem cells CD34+ obtained from peripheral blood showed inconsistent improvement in the contractile function of infarcted myocardial tissue, but better survival in long term. For improved cell therapy, in 2014 we characterized the kind of cells that were mobilized to peripheral blood in patients with acute myocardial infarction, which were identified as a response of bone marrow to myocardial insult. In 2015, we began a clinical trial with CXCR4-stem cells and specific cell markers in patients with old myocardial infarction and reduced LVFE. Cells with specific markers were separated with immune-magnetic auto MACS Pro Separator machine and implanted on infarcted myocardial tissue guided by epicardial ultrasound.

Marfan syndrome is the most common genetic disorder of connective tissue. One complication that threatens the lives of patients is progressive dilatation of the ascending aorta with the development of aortic valve regurgitation or the emergence of dissection, often leading to sudden death. Until now, these patients were operated on only after dilatation of the ascending aorta causing hemodynamically significant regurgitation of the aortic valve. The surgery consisted of the replacement of the ascending aorta and aortic valve or valve-sparing procedure. This new method is a preventive operation. The method involves creating a custom made external support of the root and the ascending portion of the aorta. Based on the CT examination, a prosthesis Extent is created. The surgery is performed from the longitudinal median sternotomy without cardiopulmonary bypass. The entire aortic root is dissected to its origin from the left ventricle, Ostia of the coronary arteries are encircled, the prosthesis is pulled underneath and fixed to the root and then sutured longitudinally. It is interesting that the prosthesis was developed and as the world’s first have it sewn on himself (Mr. Tal Golesworthy), 13 years ago in Oxford. Neither he nor the other 100 patients operated in this department with this disease had dilation or dissection throughout the study. It is because the prosthesis grows over time into the aortic wall thereby enforces it while maintaining the elastic properties of the wall. At our institute, we have so far experience with operations of 20 patients, with good results. This operation moves the care of patients with Marfan syndrome to a qualitatively higher level.

Introduction: The common life-threatening cardiac arrhythmias, Long QT (LQTS type 1-13) and Brugada (BrS type 1-12) present with syncope/palpitations/ seizures/aborted cardiac arrest. They have incomplete penetrance and variable expressivity. The three common genes (KCNQ1, KCNH2, and SCN5A) account for 75% of all LQTS cases and the SCN5A gene in BrS accounts for 25% of all cases.

Aim: To identify the causative variation in the associated genes responsible for causing cardiac channelopathies in Indian patients.

Materials & Methods: Hundred patients who fulfilled the inclusion criteria of the study were enrolled. Mutation analysis was performed in the most probable candidate gene by direct sequencing using primers flanking exon-intron boundaries. If a mutation was not identified, NGS was performed to identify mutations in other cardiac genes in patients. Parents and siblings were screened if a mutation was identified in the proband. Novel mutations were evaluated for pathogenicity using ACMG guidelines, bioinformatics, and molecular modeling software.

Results: Mutations were identified in 23 of 100 (23%) patients by Sanger sequencing, 20 had LQTS, and 3 had BrS. Among the LQT syndromes, mutations were identified in 17 in KCNQ1 (LQTS1), one in KCNH2 (LQTS2), and two in SCN5A (LQTS3). Among the LQTS1 patients, ten were identified with biallelic mutations. The three BrS patients had mutations in SCN5A (BrS1). Ten of 23 mutations were novel. NGS identified mutation in 22 (49%) of 45 patients negative for mutations by Sanger and with significant family history and/or strong clinical indication. Of which, 20 had LQTS and two had BrS. Out of these 46 mutations, 18 were novel. Cascade screening identified mutations in two symptomatic and forty asymptomatic family members. Genetic counseling was provided to the proband and family members.

Conclusion: Genotyping is important for confirming the type of LQTS/BrS, which has implications for management, cascade screening, and risk assessment.

Pathogenesis of atherosclerosis and the search for novel therapies and diagnostic markers remain major problems of modern medicine. Currently available therapeutic approaches are often not sufficiently effective, probably due to the complexity of the disease mechanisms. This review focuses on the evaluation of low-density lipoprotein (LDL) as risk factor for atherosclerosis. We summarize the current paradigm of LDL involvement in atherogenesis. We question the currently widely accepted hypothesis of the central role of oxidized LDL in atherogenesis and present an alternative concept of multiple modifications of LDL that confers its pro-atherogenic properties. According to a series of studies conducted with blood serum and LDL from atherosclerotic patients, desialylation is one of the earliest if not the first atherogenic modification of LDL. Desialylation occurs in the bloodstream and is followed by a cascade of other modifications, including the reduction of LDL particle size and increase of its density, acquisition of negative electrical charge, oxidation, and formation of highly atherogenic complexes.

Background: Salvia miltiorrhiza (SM) is a Chinese herb widely used for ischemic heart diseases (IHD), yet little is known about the cellular mechanisms. The aims of this study were to investigate the mechanisms of SM.

Methods: The rat A10 cells line, a vascular smooth muscle cells line isolated from rat thoracic embryonic aorta was as a study model. The SM roots aqueous extract, MTT assay, cytotoxicity assay, two-dimensional electrophoresis coupled with MALDI-TOF mass spectrometry, western blot analysis, and biological network analysis were applied for the elucidation of protein changes characterizing the response of the rat A10 cells into the homocysteine(Hcy) -induced oxidative stress.

Results: Our study showed that a low dose (0.015 mg/mL) of the SM significantly inhibited growth (>60%, p < 0.05) of the Hcy stimulated rat A10 cells. In addition, the concentration of intracellular reactive oxygen species obviously decreased in the rat A10 cells after its incubation with SM in terms of catalase increasing activity. Next, marked down-regulation of protein kinase C beta-1 and phosphorylated mitogen-activated protein kinase expression suggest that the observed inhibitory effect of the SM on the Hcy-induced growth of rat A10 cells was realized via the PKC/p44/42 MAPK- dependent pathway. The intensity changes of 10 protein spots in the response of the rat A10 cells to the Hcy-induced oxidative damage as alpha-4-tropomyosin, vimentin, F1F0- ATP synthase (beta subunit), glucose-regulated protein 75, actin (fragment), prohibitin, capping protein, plakoglobin, an endoplasmic reticulum protein 29, and peptidylprolyl isomerase A, were detected with statistical significance (p < 0.05). Meanwhile, it was shown that used here SM resists carbonylation of vimentin, alpha-4-tropomyosin, and GRP75, respectively, leading to phenotype transformations in the rat A10 cells.

Conclusion: These data suggest that SM may exert its protective effect in IHD through circulating ROS suppression and subsequent modulation of protein carbonylation in rat aortic smooth muscle cells.