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Background: Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear. Objective: To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach. Results: Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability. Conclusion: Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate which one among possible risk factors are independently related to first nonfatal myocardial infarction (MI) in Belgrade population. Case-control study was conducted in Belgrade during the period 2005-2006. Case group comprised 100 subjects 35-80 years old who were hospitalized because of first nonfatal MI at the coronary care unit in Urgent Center, Belgrade. Control group consisted of 100 persons chosen among patients treated during the same period at the Institute of Rheumatology, Institute for Gastroenterology, and Clinic for Orthopedics, Belgrade, Serbia. Cases and controls were individually matched by sex, age (+/- 2 years) and place of residence (urban/rural communities of Belgrade). According to the multivariate analysis risk factors for MI occurrence were "good" socioeconomic conditions (OR = 2.76), total alcohol consumption (OR = 2.62) and consumption of brandy (OR = 6.73), stressful life events taken together (OR = 3.13) and stress because of close relative Ns death (OR = 3.35), great financial problems (OR = 31.64) and small financial problems (OR = 8.47), hypertension (OR = 2.39), MI among all relatives (OR = 3.66), MI in father (OR = 6.24), and low level of high density lipoprotein cholesterol (OR = 152.41). Amateur sport activity in the past was negatively associated with MI development. The results obtained are mainly in accordance with other studies results and can be of help in development of strategy for coronary heart disease prevention in Serbia.

Introduction. Angiotensin-converting enzyme (ACE) inhibitors reduce cardiovascular events in patients with established vascular disease and heart failure (HF). ACE-inhibitors have important effects on fibrinolytic balance, which may be the underlying mechanism for a reduction in cardiovascular events.Although angiotensin-receptor blockers (ARBs) offer greater tolerability than ACE-inhibitors, the major ARB trials have demonstrated a lack of reduction in myocardial infarction (MI) occurrence and mortality in contrast to ACE-inhibitors. In this study, we investigated the combined effects of ARBs and ACE-inhibitors on fibrinolytic and inflammatory parameters in patients with uncontrolled hypertension.Methods. Twenty-four patients with uncontrolled hypertension despite taking adequate doses of ACE-inhibitor therapy were selected. Patients were started on Candesartan 16 mg once a day. Plasma plasminogen activator inhibitor (PAI-1) antigen (Ag), tissue plasminogen activator (t-PA) Ag, thrombin-activatable fibrinolysis inhibitor (TAFI) % activity and high sensitivity C-reactive protein (hsCRP) levels, were measured during low salt intake at baseline and two weeks after therapy with an ARB.Results. Addition of ARB to the regimen reduced systolic (155±17 R vs. 139±13, p<0.001), and diastolic (91±9 vs. 81±8, p<0.001) blood pressures (BP). No significant changes were observed in PAI-1 Ag (66±51 vs. 68±52, p=0.9), t-PAAg (12.6±5.3 vs. 13.3±4.7, p=0.3),TAFI % activity (119±30 vs. 118±32, p=0.9) and hsCRP (3.9±3.4 vs. 3.6±3.6, p=0.7) levels after adding an ARB.Conclusions. Combined ARB and ACE-inhibitor use provide better BP control without any detrimental effect in plasma inflammatory and fibrinolytic parameters. [ABSTRACT FROM PUBLISHER]

A complex metabolic condition referred to as Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance (IR) and decreased insulin production. Obesity, dyslipidemia, hypertension, and chronic inflammation are just a few of the cardiometabolic illnesses that people with T2DM are more likely to acquire and results in cardiovascular issues. It is essential to comprehend the mechanistic insights into these risk variables in order to prevent and manage cardiovascular problems in T2DM effectively. Impaired glycemic control leads to upregulation of De novo lipogenesis (DNL), promote hepatic triglyceride (TG) synthesis, worsening dyslipidemia that is accompanied by low levels of high density lipoprotein cholesterol (HDL-C) and high amounts of small, dense low-density lipoprotein cholesterol (LDL-C) further developing atherosclerosis. By causing endothelial dysfunction, oxidative stress, and chronic inflammation, chronic hyperglycemia worsens already existing cardiometabolic risk factors. Vasoconstriction, inflammation, and platelet aggregation are caused by endothelial dysfunction, which is characterized by decreased nitric oxide production, increased release of vasoconstrictors, proinflammatory cytokines, and adhesion molecules. The loop of IR and endothelial dysfunction is sustained by chronic inflammation fueled by inflammatory mediators produced in adipose tissue. Infiltrating inflammatory cells exacerbate inflammation and the development of plaque in the artery wall. In addition, the combination of chronic inflammation, dyslipidemia, and IR contributes to the emergence of hypertension, a prevalent comorbidity in T2DM. The ability to target therapies and management techniques is made possible by improvements in our knowledge of these mechanistic insights. Aim of present review is to enhance our current understanding of the mechanistic insights into the cardiometabolic risk factors related to T2DM provides important details into the interaction of pathophysiological processes resulting in cardiovascular problems. Understanding these pathways will enable us to create efficient plans for the prevention, detection, and treatment of cardiovascular problems in T2DM patients, ultimately leading to better overall health outcomes. Plain Language Summary: Understanding the factors that increase the risk of type 2 diabetes: Exploring how the body works Type 2 diabetes mellitus (T2DM) is a complex condition where the body struggles to use insulin properly and doesn't produce enough of it. This often leads to other health issues like obesity, high cholesterol, high blood pressure, and chronic inflammation. These problems increase the risk of heart and blood vessel diseases in people with T2DM. To tackle these issues effectively, it's crucial to understand the underlying mechanisms. When blood sugar levels are not controlled, the body starts making more fat and storing it in the liver, leading to high triglycerides and low levels of good cholesterol. This process can block arteries, causing heart problems. High blood sugar also damages blood vessel linings, making them inflamed and less functional. This inflammation, combined with other factors like high cholesterol and insulin resistance, can lead to high blood pressure. Chronic inflammation, where the body's defense system stays active for too long, worsens these problems. In T2DM, inflammation occurs in fat tissues, making the situation even worse. Inflammatory cells infiltrate blood vessel walls, promoting plaque buildup and further worsening heart issues. Understanding these processes helps us develop better strategies to prevent, detect, and treat heart problems in people with T2DM. By targeting these mechanisms, doctors can create more effective plans to improve the overall health of individuals with diabetes and reduce the risk of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

To determine whether pretreatment plasma renin activity (PRA), without accompanying 24-h urine sodium, can predict myocardial infarction (MI), the PRA levels of 2,902 hypertensive patients [white (38%), male (65%), median age 55 years], with mean entry blood pressure (BP) of 150/97 mm Hg were examined. During an average 3.6 years follow-up (87% > or = 9 months), there were 55 MIs, 21 strokes, and 16 other cardiovascular disease (CVD) deaths. Classification of PRA levels into 3 renin strata [high (H) PRA > or = 4.5 (n = 354), normal (N) 0.75 to 4.49 (n = 1,622), and low (L) < 0.75 (n = 926) ng/mL/h] yielded subgroups that did not differ in LVH (9% v 11%) or smoking prevalence (26% v 25%) but high versus low PRA subjects included more aged < 55 years (64% v 53%); white (49% v 25%); men (79% v 52%); cholesterol > or = 6.3 mmol/L (33% v 25%); all P values < .01. MI rates per 1,000/year were H: 9.3, N: 5.5, L: 2.5 (H v L, RR = 3.8, 95% CI: 1.7 to 8.4). A similar relationship was seen with total CVD (H: 12.5, N: 9.3, L: 5.2; RR = 2.4, 95% CI: 1.3 to 4.5) and all-cause mortality (H: 7.0, N: 6.2, L: 2.5; RR = 2.8, 95% CI: 1.2 to 6.8) but not CVA (H: 1.6, N: 2.0, L: 1.9). In a Cox survival analysis only renin, age, sex, smoking, LVH, and cholesterol were significantly (P < .02) related to MI occurrence. There was, for every 2 unit increase in PRA, an overall 25% increase in MI incidence. Among hypertensive subjects, PRA level (without urine sodium), is independently and directly associated with the incidence of MI.

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Background and aims: Hypertension is one of the most common and important risk factors of cardiovascular diseases. This phenomenon, if not cured, causes lots of problems in vital organs of the body like kidneys, brain, eyes, and heart. The aim of the current study was to identify factors which affect the time until myocardial infarction (MI) in hypertension patients using truncated Cox regression. Methods: This study was a population retrospective cohort and its statistical population included patients with hypertension symptoms, who had MI for the first time in Sari. A decision was made based on continuing the study as a nested case and control study because the number of MI incidents was low (7%) in the studied sample. In addition, the Cox's model and truncated Cox were used for determining the factors affecting the patients' survival. Results: The median and mean survival times in this sample were equal to 57 and 66.44 months, respectively. Considering time truncation, family history (HR=1.70) and the age at diagnosis (HR=0.99) were statistically significant in the Cox's model (P< 0.05). Conclusion: Overall, using the Akaike criterion for comparing the survival time without the effect of truncation, the Cox's model demonstrated better fitness by controlling the truncation effect. These results show the importance of controlling the truncation in those diseases in which it is impossible to distinguish the time of the appearance from the symptoms. [ABSTRACT FROM AUTHOR]

Take home figure View large Download slide Adapted from Bärtsch and Gibbs 2 Physiological response to hypoxia. Life-sustaining oxygen delivery, in spite of a reduction in the partial pressure of inhaled oxygen between 25% and 60% (respectively at 2500 m and 8000 m), is ensured by an increase in pulmonary ventilation, an increase in cardiac output by increasing heart rate, changes in vascular tone, as well as an increase in haemoglobin concentration. BP, blood pressure; HR, heart rate; PaCO2, partial pressure of arterial carbon dioxide. Take home figure View large Download slide Adapted from Bärtsch and Gibbs 2 Physiological response to hypoxia. Life-sustaining oxygen delivery, in spite of a reduction in the partial pressure of inhaled oxygen between 25% and 60% (respectively at 2500 m and 8000 m), is ensured by an increase in pulmonary ventilation, an increase in cardiac output by increasing heart rate, changes in vascular tone, as well as an increase in haemoglobin concentration. BP, blood pressure; HR, heart rate; PaCO2, partial pressure of arterial carbon dioxide. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular diseases are the leading causes of mortality and morbidity in Western countries. The possible synergistic effect of poor adherence to a Mediterranean diet (MD) and other risk factors for acute myocardial infarction (AMI) such as hypertension, cholesterol, ever smoker, BMI> 25, diabetes, has not been deeply studied. Design: Case-control study. Methods: Patients with first AMI and controls from four tertiary referral Italian centers were screened for enrolment. Dietary information was collected through a questionnaire and a MD adherence score was calculated. Physical activity and smoking habits were also registered. The Synergy Index was calculated according to Rothman. Results: 127 cases and 173 controls were enrolled. The analysis was conducted using a dichotomous variable for the MD score with values ≥7 representing good adherence. Multivariate analysis showed the following variables associated to AMI: ever smoker (OR = 2.08), diabetes (OR = 1.42), hypertension (OR = 2.08), hypercholesterolemia (OR = 2.47), BMI> 25 (OR = 1.99), while a protective effect emerged both in subjects scoring > 7 on the MD score (OR = 0.55) and in subjects resident of Southern Italy (OR = 0.38). A synergistic effect does exist between poor adherence to the MD and the following risk factors: hypertension, hypercholesterolemia, BMI >25, diabetes and being a resident in central and northern Italy. Conclusion: Synergy between heart disease risk factors and MD underlines the need to enlarge the list of known modifiable cardiovascular risk factors to include and promote adherence to Mediterranean dietary habits. [ABSTRACT FROM AUTHOR]

Hypertension significantly contributes to the increased cardiovascular morbidity and mortality, thus leading to rising healthcare costs. The objective of this study was to quantify the clinical and economic benefits of optimal systolic blood pressure (SBP), in a setting under severe financial constraints, as in the case of Greece. Hence, a Markov model projecting 10-year outcomes and costs was adopted, in order to compare two scenarios. The first one depicted the “current setting”, where all hypertensives in Greece presented an average SBP of 164 mmHg, while the second scenario namely “optimal SBP control” represented a hypothesis in which the whole population of hypertensives would achieve optimal SBP (i.e. <140 mmHg). Cardiovascular events’ occurrence was estimated for four sub-models (according to gender and smoking status). Costs were calculated from the Greek healthcare system’s perspective (discounted at a 3% annual rate). Findings showed that compared to the “current setting”, universal “optimal SBP control” could, within a 10-year period, reduce the occurrence of non-fatal events and deaths, by 80 and 61 cases/1000 male smokers; 59 and 37 cases/1000 men non-smokers; whereas the respective figures for women were 69 and 57 cases/1000 women smokers; and accordingly, 52 and 28 cases/1000 women non-smokers. Considering health expenditures, they could be reduced by approximately €83 million per year. Therefore, prevention of cardiovascular events through BP control could result in reduced morbidity, thereby in substantial cost savings. Based on clinical and economic outcomes, interventions that promote BP control should be a health policy priority. [ABSTRACT FROM AUTHOR]

BackgroundWe aimed this study to test the hypothesis that short-term blood pressure (BP) variability and abnormal patterns of diurnal BP variation, evaluated by ambulatory BP (ABP), predicts risk of incident cardiovascular disease (CVD) in patients with type 2 diabetes (T2DM).MethodsABP monitoring (ABPM) was performed in 300 patients with uncomplicated T2DM without known CVD and without BP medications, who were followed for 54 ± 20 months. The relationships of different measures of BP variability, the presence of abnormal patterns of diurnal BP variation (nondipper, riser, or morning BP surge) and the standard deviations of awake and asleep ABP were determined. Cox proportional hazards models were used to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs) before and after controlling for various covariates.ResultsThe mean age was 67.8 ± 9.6 years, 48% were male, 253 (84%) had a diagnosis of hypertension, and the mean of the standard deviations of awake systolic BP/diastolic BP (SBP/DBP) were 18 ± 6/11 ± 4 mm Hg, and those of sleep SBP/DBP were 13 ± 5/9 ± 3 mm Hg. During follow-up, there were 29 cardiovascular events. In multivariable analyses, the standard deviations of sleep SBP (HR = 1.08; 95% CI, 1.01–1.16, P < 0.05) and sleep DBP (HR = 1.13; 1.04–1.23, P < 0.01) were independently associated with incident CVD. Neither the nondipper and riser patterns nor the morning BP surge were associated with incident CVD events independently of clinic and 24-h BP levels.ConclusionsAbnormal diurnal BP variation was not a predictor of CVD in patients with T2DM. Night time BP variability was an independent predictor of future incidence of CVD, suggesting that this measure could reflect pathophysiology of T2DM.American Journal of Hypertension (2009). doi:10.1038/ajh.2008.294American Journal of Hypertension (2009); 22, 1, 46–51. doi:10.1038/ajh.2008.294 [ABSTRACT FROM AUTHOR]

The calcium Sensing Receptor (CaSR) is a cell surface receptor belonging to the family of G-protein coupled receptors. CaSR is mainly expressed by parathyroid glands, kidneys, bone, skin, adipose tissue, the gut, the nervous system, and the cardiovascular system. The receptor, as its name implies is involved in sensing calcium fluctuations in the extracellular matrix of cells, thereby having a major impact on the mineral homeostasis in humans. Besides calcium ions, the receptor is also activated by other di- and tri-valent cations, polypeptides, polyamines, antibiotics, calcilytics and calcimimetics, which upon binding induce intracellular signaling pathways. Recent studies have demonstrated that CaSR influences a wide variety of cells and processes that are involved in inflammation, the cardiovascular system, such as vascular calcification, atherosclerosis, myocardial infarction, hypertension, and obesity. Therefore, in this review, the current understanding of the role that CaSR plays in inflammation and its consequences on the cardiovascular system will be highlighted. [ABSTRACT FROM AUTHOR]

Aim: To examine trends in the prevalence of myocardial infarction (MI) and conventional risk factors in Greek adults between 2002 and 2006. Design: Repeated cross-sectional study. Methods: Self-reported data from surveys given in Salamis during two election days in 2002 and 2006 were analysed. The same sampling method and procedures were used on both surveys. The study sample included 2805 and 3478 subjects (20 years) in 2002 and 2006, respectively, with similar age and sex distribution to the target population. Results: The prevalence of MI increased from 4.1% (men, 6.3%; women, 1.9%) in 2002 to 4.8% (men, 7.3%; women, 2.2%) in 2006 (P = 0.18). At the same time, prevalence rates of major risk factors were as follows: diabetes increased from 8.7% to 10.3% (P = 0.037), hypertension from 20.1% to 25.7% (P 240 mg/dl or the use of cholesterol-lowering medication) increased from 17.5% to 22.3% (P Conclusions: These findings show that, in the Greek population, prevalence of MI continues to rise (at ∼4% per year). This trend seems to be driven by a persistently high prevalence of smoking and the rapidly increasing burden of diabetes, hypertension and hypercholesterolemia. [ABSTRACT FROM AUTHOR]