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Emergency department (ED) visits for conditions unrelated to the Coronavirus Disease 2019 (COVID-19) pandemic decreased during the early pandemic, raising concerns about critically ill patients forgoing care and increasing their risk of adverse outcomes. It is unclear if Hispanic and Black adults, who have a high prevalence of chronic conditions, sought medical assistance for acute emergencies during this time. This study used 2018-2020 ED visit data from the largest safety net hospital in Los Angeles County to estimate ED visit differences for cardiac emergencies, diabetic complications, and strokes, during the first societal lockdown among Black and Hispanic patients using time series analyses. Emergency department visits were lower than the expected levels during the first societal lockdown. However, after the lockdown ended, Black patients experienced a rebound in ED visits while visits for Hispanics remained depressed. Future research could identify barriers Hispanics experienced that contributed to prolonged ED avoidance.

Chagas disease is an infection caused by the protozoan Trypanosoma cruzi, affecting 6-8 million people worldwide. Only two drugs are available for its treatment, having a limited efficacy and adverse side-effects. Estafietin is a sesquiterpene lactone isolated from Stevia alpina with in vitro activity against T. cruzi and low cytotoxicity against mammalian cells. The aim of this work was to predict the toxicologic profile of estafietin by in silico methods and assess its in vivo activity on a murine model of Chagas disease. Estafietin showed low toxicity according to pkCSM web tool and passed the PAINS filter from PAINS-remover web server. The treatment of infected mice with 1 mg/Kg/day of estafietin for five consecutive days administrated by intraperitoneal route significatively decreased parasitemia levels and reduced inflammatory infiltrates and myocyte damage on muscle tissue. These results suggest that estafietin had effect both on acute and chronic stages of the infection. [ABSTRACT FROM AUTHOR]

Introduction: The principles of justice, beneficence, and nonmaleficence are prescriptions of the Hippocratic Oath. To fulfill them, physicians are obligated morally to lifelong learning; yet, there is little evidence that the relationship of beneficence to lifelong learning or to continuing medical education (CME) is expressed in medical oaths. Methods: We analyzed 48 medical oaths written from the first century Ce through the present day, searching for a commitment to lifelong learning and for specification of a relationship to the principle of beneficence. Thirteen ancient and medieval and 35 modern and contemporary oaths were inventoried for source, such as corresponding to a medical school. They were sorted by those that mention the commitment toward lifelong learning and to determine their relationship with the principle of beneficence. Results: Of the 48 medical oaths analyzed, only 20 manifest the commitment to lifelong learning. However, most of the oaths that contain this commitment do not pertain to medical schools, with the exception of the Declaration of Geneva. Of this group, 16 also indicate the principle of beneficence. Of these 16, only 3 establish a link between both. One medical oath indicated this commitment, and none of them analyzed the relation with the principle of beneficence. Discussion: The commitment toward CME should not be absent in the present medical oaths. It is a duty and right of all physicians, and in turn, society should recognize this obligation in order to offer opportunities for the achievement of the principle of beneficence that will result in better health care.

Hemodynamic parameters and natriuretic peptide levels were evaluated in cardiac hypertrophy produced by sequentially applied renovascular (RV) and deoxycorticosterone acetate-salt (DS) models of hypertension. We studied hypertensive rats by RV or DS treatment at 2 and 4 wk, as well as by the combination of 2 wk of each treatment in an inverse sequence: RV 2 wk/DS 2 wk (RV2/DS2) and DS 2 wk/RV 2 wk (DS2/RV2). The in vivo cardiac function, interstitial fibrosis, and synthesis and secretion of types A (ANP) and B (BNP) natriuretic peptides were monitored in hypertensive models compared with their corresponding sham (Sh2, Sh4). There were no differences in relaxation parameters among RV or DS groups and combined treatments. Left ventricular +dP/[dt.sub.max] increased only in RV4 (P < 0.01 vs. Sh4), and this increase was abolished in RV2/DS2. Interstitial collagen concentration increased after 4 wk in both RV4 and RV2/DS2 groups. Although there were no changes in collagen concentration in either DS2 or DS4 groups, clipping after 2 wk of DS (DS2/RV2) remarkably stimulated interstitial fibrosis (P < 0.01 vs. DS2). Plasma BNP increased in RV treatment at 4 wk (P < 0.001 vs. Sh4), but not in DS. Interestingly, RV applied after the 2 wk of DS treatment induced a marked increase in BNP levels (P < 0.001 vs. Sh4). In this regard, plasma BNP appears to be a reliable indicator of pressure overload. Our results suggest that the second stimulus of mechanical overload in combined models of hypertension determines the evolution of hypertrophy and synthesis and secretion of ANP and BNP. cardiac hypertrophy; natriuretic peptides; renovascular hypertension; deoxycorticosterone acetate-salt hypertension doi: 10.1152/ajpheart.00911.2009.

To characterize the temporal activation of the renin-angiotensin system after myocardial infarction (MI) in rabbits, we examined cardiac ANG II type 1 receptor ([AT.sub.1]R) expression and ANG II levels from 3 h to 35 days. The effects of losartan (12.5 mg x [kg.sup.-1] x [day.sup.-1]) on functional and histomorphometric parameters when treatment was initiated early (3 h) and late (day 15) post-MI and maintained for different periods of time [short term (4 days), midterm (20 days), and long term (35 days)] were also studied. [AT.sub.1]R expression increased in the MI zone at 15 and 35 days (P < 0.05). ANG II levels increased (P < 0.05) in the non-MI zone at 24 h and in the MI zone as well as in plasma at 4 days and then progressively decreased until 35 days. The survival rate was significantly lower in untreated MI and early long-term-treated animals. Diastolic pressure-volume curves in MI at 35 and 56 days shifted to the right (P < 0.05). This shift was even more pronounced in long-term-treated groups (P < 0.05). Contractility decreased (P < 0.05 vs. sham) in the untreated and long-term-treated groups and was attenuated in the midterm-treated group. The early administration of losartan reduced RAM 11-positive macrophages from 4.15 [+ or -] 0.05 to 3.05 [+ or -] 0.02 cells/high-power field (HPF; P < 0.05) and CD45 RO-positive lymphocytes from 2.23 [+ or -] 0.05 to 1.48 [+ or -] 0.01 cells/HPF (P < 0.05) in the MI zone at 4 days. Long-term treatment reduced the scar collagen (MI: 70.50 [+ or -] 2.35% and MI + losartan: 57.50 [+ or -] 2.48, P < 0.05), determined the persistency of RAM 11-positive macrophages (3.02 [+ or -] 0.13 cells/HPF) and CD45 RO-positive lymphocytes (2.77 [+ or -] 0.58 cells/HPF, P < 0.05 vs. MI), and reduced the scar thinning ratio at 35 days (P < 0.05). Consequently, the temporal expressions of cardiac [AT.sub.1]R and ANG II post-MI in rabbits are different from those described in other species. Long-term treatment unfavorably modified post-MI remodeling, whereas midterm treatment attenuated this harmful effect. The delay in wound healing (early reduction and late persistency of inflammatory infiltrate) and adverse remodeling observed in long-term-treated animals might explain the unfavorable effect observed in rabbits. angiotensin II type 1 receptor blockers

Background/Aims: Aging is accompanied by progressive and adverse cardiac remodeling characterized by myocardial hypertrophy, fibrosis, and dysfunction. We previously reported that galectin-3 (Gal-3) is a critical regulator of inflammation and fibrosis associated with hypertensive heart disease and myocardial infarction. Nevertheless, the role and mechanism of Gal-3 in age-related cardiac remodeling have not been previously investigated. We hypothesized that Gal-3 plays a critical role in cardiac aging and that its deficiency exacerbates the underlying mechanisms of myocardial hypertrophy and fibrosis. Methods: Male C57BL/6 (control) (n=24) and Gal-3 knockout (KO) (n=29) mice were studied at 24 months of age to evaluate the role of Gal-3 in cardiac aging. We assessed 1) survival rate; 2) systolic blood pressure (SBP) by plethysmography; 3) myocardial hypertrophy, apoptosis, and fibrosis by quantification of histological and immunohistochemical analysis; 4) cardiac expression of angiotensin (Ang) II, Ang (1–7) by Radioimmunoassay; 5) transforming growth factor-β (TGF-β), sirtuin (SIRT) 1, SIRT 7 and metalloproteinase 9 (MMP-9) by RT-qPCR and 6) ventricular remodeling and function by echocardiography. Results: We found that aged Gal-3 KO mice had a lower survival rate and exhibited exacerbated myocardial hypertrophy and fibrosis without changes in SBP. Similarly, myocardial apoptosis and MMP-9 mRNA expression was significantly increased in the hearts of Gal-3 KO mice compared to controls. Additionally, cardiac Ang II and TGF-β expression were higher in aged Gal-3 KO mice while SIRT1 and SIRT7 expression were reduced. Conclusion: Our findings strongly suggest that Gal-3 is involved in age-related cardiac remodeling by regulating critical mechanisms associated with the development of pathological hypertrophy. The gene deletion of Gal-3 reduced the lifespan and markedly increased age-dependent mechanisms of myocardial hypertrophy, apoptosis, and fibrosis, including Ang-II, TGF-β, and MMP-9. At the same time, there was diminished cardiac-specific expression of SIRT1 and SIRT7, which are extensively implicated in delaying age-dependent cardiomyopathies. [ABSTRACT FROM AUTHOR]

Abstract: The aims of the present study were to determine whether the transitory systolic overshoot (TSO) that occurs in the early reperfusion (R) of the stunned myocardium is accompanied by [...]

Open in new tab Download slide Open in new tab Download slide OBJECTIVES Cardiopulmonary bypass (CPB) use is an essential strategy for many cardiovascular surgeries. However, its use and duration have been associated with a higher rate of postoperative complications, such as low cardiac output syndrome due to myocardial oedema and dysfunction. Though Aquaporin water channels have been implicated in myocardial water balance, their specific role in this clinical scenario has not been established. METHODS In a consecutive study of 17 patients with severe aortic stenosis undergoing aortic valve replacement surgery, 2 myocardial biopsies of the left ventricle were taken: 1 before and 1 after CPB use. Sociodemographic, clinical and laboratory data were collected. Western blot and immunohistochemistry studies were performed. RESULTS After CPB use, there was a mean increase of ∼62% in Aquaporin 1 protein levels (P  = 0.001) and a mean reduction of ∼38% in Aquaporin 4 protein levels (P  = 0.030). In immunohistochemistry assays, Aquaporin 1 was found lining small blood vessels, while Aquaporin 4 formed a circular label in cardiomyocytes. There were no changes in the localization of either protein following CPB use. During the observed on-pump time interval, there was a 1.7%/min mean increase in Aquaporin 1 (P  = 0.021) and a 2.5%/min mean decrease in Aquaporin 4 (P  = 0.018). Myocardial interstitial oedema increased by 42% (95% confidence interval 31–54%) after CPB use. Patients who developed low cardiac output syndrome were in the upper half of the median percentage change of Aquaporin expression. CONCLUSION Time-dependent changes in cardiac Aquaporin expression may be associated with myocardial oedema and dysfunction related to CPB use. [ABSTRACT FROM AUTHOR]