Estudio de prevalencia, conocimiento y control de la hipertensión arterial en barrios vulnerables de Argentina / Prevalence, knowledge and control of arterial hypertension in vulnerable neighborhoods of Argentina: A Cross-sectional Study

Introducción: La hipertensión arterial (HTA) representa el principal factor de riesgo individual, con mayor carga a nivel mundial de enfermedades cardiovasculares (ECV). En nuestro país, algunos trabajos epidemiológicos han mostrado marcadas diferencias en las prevalencias de estos factores de riesgo de acuerdo con la población evaluada. Sin embargo, no hay estudios epidemiológicos de evaluación de factores de riesgo cardiovascular exclusivos referentes a barrios vulnerables con muy bajos recursos económicos, socioculturales y poca accesibilidad a los sistemas de salud. Materiales y métodos: Estudio observacional de corte transversal multicéntrico en habitantes de comunas vulnerables de muy bajos recursos, como asentamientos populares y barrios carenciados con muestreo aleatorizado simple de casas. Se realizaron tomas de presión arterial (PA), medidas antropométricas, así como cuestionarios epidemiológicos, económicos y socioculturales. Se describen los hallazgos: prevalencia, conocimiento y control de la PA en las distintas regiones. Se efectuó una regresión logística para determinar las variables independientes a los resultados principales. Resultados: Se analizaron 989 participantes. La prevalencia de HTA global fue de 48,2%. Un total de 82% tenía un índice de masa corporal (IMC) >25 kg/m2. De estos pacientes, 45,3% tenían menos de seis años de educación. Este último aspecto se asoció a mayor prevalencia de HTA de forma independiente. De los hipertensos, 44% desconocían su padecimiento y solo en 17,2% estaba controlado, asociándose esto a tener obra social (OS) y mayor nivel educativo. Únicamente 24% estaban bajo tratamiento combinado. Conclusión: La prevalencia de HTA en barrios vulnerables es elevada, superando a la de otros estratos sociales con niveles de conocimiento, tratamiento y control de la HTA bajos, similar a otras poblaciones. Se detectó un uso insuficiente de la terapia combinada.

Introduction: Hypertension (HTN) represents the primary individual risk factor, contributing significantly to the global burden of cardiovascular diseases (CVD). In our country, epidemiological research has highlighted substantial variations in the prevalence of these risk factors across different populations. However, there is a lack of epidemiological studies assessing exclusive cardiovascular risk factors within vulnerable neighborhoods characterized by extremely limited economic resources, sociocultural challenges, and inadequate healthcare access. Methods: A multicenter cross-sectional observational study was conducted among individuals residing in economically deprived and marginalized communities, including informal settlements and underprivileged neighborhoods. Simple random sampling of households was employed. Blood pressure measurements, anthropometric assessments, and epidemiological, economic, and sociocultural questionnaires were administered. Results encompass prevalence rates, awareness levels, and blood pressure control across diverse regions. Logistic regression was utilized to identify independent variables influencing primary outcomes. Results: A total of 989 participants were analyzed. The overall prevalence of hypertension was 48.2%. About 82% had a body mass index (BMI) >25. Approximately 45.3% had less than 6 years of formal education. Independent association was established between education levels below 6 years and higher hypertension prevalence Among hypertensive individuals, 44% were unaware of their condition, with only 17.2% achieving control, correlated with having health insurance and a higher educational background. Merely 24% were receiving combined therapy. Conclusion: The prevalence of hypertension within vulnerable neighborhoods is alarmingly high, surpassing rates in other social strata. Knowledge, treatment, and control levels of hypertension are suboptimal, comparable to other populations... (AU)

[Prevalence, knowledge and control of arterial hypertension in vulnerable neighborhoods of Argentina: A Cross-sectional Study]. / Estudio de prevalencia, conocimiento y control de la hipertensión arterial en barrios vulnerables de Argentina.

INTRODUCTION: Hypertension (HTN) represents the primary individual risk factor, contributing significantly to the global burden of cardiovascular diseases (CVD). In our country, epidemiological research has highlighted substantial variations in the prevalence of these risk factors across different populations. However, there is a lack of epidemiological studies assessing exclusive cardiovascular risk factors within vulnerable neighborhoods characterized by extremely limited economic resources, sociocultural challenges, and inadequate healthcare access. METHODS: A multicenter cross-sectional observational study was conducted among individuals residing in economically deprived and marginalized communities, including informal settlements and underprivileged neighborhoods. Simple random sampling of households was employed. Blood pressure measurements, anthropometric assessments, and epidemiological, economic, and sociocultural questionnaires were administered. Results encompass prevalence rates, awareness levels, and blood pressure control across diverse regions. Logistic regression was utilized to identify independent variables influencing primary outcomes. RESULTS: A total of 989 participants were analyzed. The overall prevalence of hypertension was 48.2%. About 82% had a body mass index (BMI) >25. Approximately 45.3% had less than 6 years of formal education. Independent association was established between education levels below 6 years and higher hypertension prevalence. Among hypertensive individuals, 44% were unaware of their condition, with only 17.2% achieving control, correlated with having health insurance and a higher educational background. Merely 24% were receiving combined therapy. CONCLUSION: The prevalence of hypertension within vulnerable neighborhoods is alarmingly high, surpassing rates in other social strata. Knowledge, treatment, and control levels of hypertension are suboptimal, comparable to other populations. Inadequate use of combination therapy was observed. This study underscores the urgent need for targeted interventions addressing cardiovascular risk factors in poor areas to mitigate the burden of CVD.

Gap junctional hemichannels in the heart.

Upon contacting each other, cells form gap junctions, in which each cell contributes half of the channel linking their cytoplasms, enabling them to share their metabolome up to a molecular weight of 1000. Each hemichannel (or connexon) is randomly inserted into the plasma membrane and then migrates to the site of cell-to-cell contact before pairing with the neighbouring cell's hemichannel to form a communicating conduit. This review summarizes the evidence for hemichannels in heart ventricular myocytes. Morphological findings are summarized describing how hemichannels are inserted into the plasma membrane. Once in the plasma membrane, hemichannels can be functionally detected electrophysiologically or by dye uptake assays. Each technique reveals specific aspects of hemichannel function. Using dye uptake studies, it is possible to investigate the biological regulation of hemichannels in vivo. Evidence is summarized which indicates that hemichannels are normally kept closed in the presence of normal extracellular Ca because they are phosphorylated at residues in the C-terminus regulated by the MAPK signalling pathway. When hemichannels are dephosphorylated, the channels open and allow dye uptake into the cells, as well as potentially deleterious ion exchange. Biological stresses, such as hyperosmolarity and metabolic inhibition, open hemichannels by this mechanism through activating phosphatases. The resulting ion fluxes may have important roles in heart physiology and pathophysiology.

Experimental autoimmune myocarditis produced by adoptive transfer of splenocytes after myocardial infarction.

One possible mechanism for neurohumoral activation after myocardial infarction may be the generation of an immune response against cardiac self-antigens. We hypothesize that if there is a T cell-mediated reaction to self-antigens, the transfer of splenic lymphocytes from postinfarct rats into syngeneic rats with normal hearts should result in a T cell-mediated autoimmune myocarditis in the healthy syngeneic rats. Rats were killed 6 weeks after coronary ligation. Splenocytes from animals with large and small infarcts were purified from spleens, activated with concanavalin A, and injected in varying doses into normal syngeneic rats. These recipient rats were killed 6 weeks later, and histopathological studies were performed. Our results demonstrate in vivo evidence of lymphocyte-mediated myocardial injury by adoptive transfer of sensitized lymphocytes from rats who developed congestive heart failure after acute myocardial infarction. The amount of infiltrate and necrosis in the recipient rats appeared directly related to the size of the infarct from the donor rats. This suggests that larger infarcts lead to a greater inflammatory response as well as a greater propensity for alteration of cardiac surface antigens or the emergence of previously sequestered antigens. None of the other organs (kidney, liver, lung, or brain) had evidence of infiltrates. Two-dimensional echocardiography did not reveal systolic dysfunction. This study provides direct evidence of autoimmune myocardial injury produced by adoptive transfer of concanavalin A-activated splenocytes after myocardial infarction. We propose that neurohumoral activation early in the postinfarction period triggers a series of specific inflammatory and immunological events that lead to formation of specific clones of T cells. When these are activated and transferred into normal rats, cardiac-specific cellular infiltration occurs, occasionally accompanied by myocardial necrosis. This model should help to further explore the link between neurohumoral activation after myocardial infarction and the subsequent immune alterations that might be associated with the development and/or progression of congestive heart failure. Additionally, this might be a useful model in which to study other immune-mediated cardiomyopathies.

Beneficial effects of intermittent home administration of the inotrope/vasodilator milrinone in patients with end-stage congestive heart failure: a preliminary study.

BACKGROUND: End-stage congestive heart failure (CHF) is associated with a high mortality rate and is often refractory to standard medical treatment. Although parenteral inotropes have been beneficial in hospitalized patients, their use in outpatients has been limited by toxicity and tachyphylaxis. METHODS AND RESULTS: To determine whether patients with end-stage CHF could safely tolerate intermittent outpatient inotropic therapy and demonstrate both symptomatic and functional improvement with these agents, we studied the effects of low-dose, intermittent home infusions of the inotrope/vasodilator milrinone in 10 patients with end-stage CHF. After showing hemodynamic improvement with milrinone while hospitalized, central lines were placed and patients were given the drug at home with small portable infusion pumps, starting at 3 days a week for 6 hours at a time over a 3-month period. Patients tolerated the drug well, with no deaths and a fourfold decrease in hospitalizations during the study. Arrhythmias were minimal and angina decreased in two patients. Mean total, physical, and emotional scores on the Minnesota Living with Heart Failure Questionnaire reflected a general trend of symptomatic improvement throughout the infusion period. The mean number of reported hours of improvement after infusion progressively increased throughout the study, producing a mean of 25 hours of postinfusion improvement during the final week (p < 0.01). Repeat hemodynamic study at the end of the 3-month period showed trends toward improvement in cardiac function. CONCLUSIONS: This is the first study to demonstrate safety, efficacy, hemodynamic, and functional improvement in patients receiving low-dose, intermittent outpatient milrinone therapy. We believe this improvement partly relates to a "training" effect on the heart or peripheral muscles and circulation. These promising results suggest that given appropriately, inotropes have an important therapeutic role in the outpatient treatment of end-stage CHF.

Effects of enalapril on T and B cell function in rats after myocardial infarction.

The cellular mechanisms following myocardial infarction remain poorly characterized. It is believed that an inflammatory and immunologic process may be involved and that the beneficial effects of enalapril on remodeling may, in part, work through an immune mechanism. To characterize the effect of enalapril on immune alterations in the late phase of ventricular remodeling after myocardial infarction, rats underwent left coronary artery ligation followed by 6 weeks of either enalapril or placebo treatment. Infarct sizes, heart weights, and volumes were compared. Peripheral and splenic leukocyte and lymphocyte subsets, along with T cell blastogenesis, were quantified in enalapril treated rats 6 weeks after coronary ligation and compared to untreated control rats. Additionally, antibody production to a de novo antigen, keyhole limpet hemocyanin, was assessed with and without treatment. Average infarct size was equivalent among enalapril-treated myocardial infarction rats and untreated infarct rats. There was, however, less left and right ventricular hypertrophy in the enalapril treated group. Enalapril completely prevented the 42% increase in white blood count, the 88% increase in neutrophils, and the 28% increase in lymphocyte count seen in untreated infarct rats. Both untreated and enalapril treated rats tended toward a decrease in T helper:suppressor ratio. All rats treated with enalapril, however, had a significant increase in the T helper:suppressor ratio versus untreated control rats (F = 3.6, P = .018). Blastogenesis was markedly increased in T cells from infarcted animals. This was mitigated by treatment with enalapril. Additionally, immunoglobulin G antibody production was significantly lessened in rats treated with enalapril. The results of this study suggest that alterations in immunoregulatory cell type and function occurs following myocardial infarction. The beneficial effects of the angiotensin-converting enzyme inhibitor enalapril may be, in part, due to its mitigating effects on immune cell release and activation following myocardial infarction.