Urbanization and cardiovascular health among Indigenous groups in Brazil.

BACKGROUND: We described the prevalence of cardiovascular risk factors in groups of Brazilian Indigenous people at different degrees of urbanization. METHODS: The Project of Atherosclerosis among Indigenous populations (Projeto de Aterosclerose em Indígenas; PAI) is a cross-sectional study conducted in Northeast Brazil between August 2016-June 2017. It included three populations: Fulni-ô Indigenous people (lowest degree of urbanization), Truká Indigenous people (greater urbanization), and a highly urbanized non-Indigenous local cohort (control group). Participants were assessed to register sociodemographic, anthropometric, as well as clinical and laboratory-derived cardiovascular (CV) risk parameters. Age-adjusted prevalence of hypertension was also computed. Nonparametric tests were used for group comparisons. RESULTS: Here we included 999 participants, with a predominance of females in all three groups (68.3% Control group, 65.0% Fulni-ô indigenous group, and 60.1% Truká indigenous group). Obesity was present in 45.6% of the urban non-Indigenous population, 37.7% Truká and in 27.6% Fulni-ô participants. The prevalence of hypertension was 29.1% (n = 297) with lower prevalence in the less urbanized Fulni-ô people (Fulni-ô - 18.2%; Truká - 33.9%; and Control - 33.8%; p < 0.001). In the elderly male population, the prevalence of hypertension was 18.7% in the Fulni-ô, 45.8% in the Truká, and 54.5% in the control group. Of the 342 participants that self-reported hypertension, 37.5% (n = 68) showed uncontrolled blood pressure (BP). Uncontrolled BP was more prevalent among Truká people when compared to Fulni-ô people and non-Indigenous participants (45.4%, 22.9%, and 40.7%, respectively; p < 0.001). CONCLUSIONS: We found a higher cardiovascular risk in communities with a higher degree of urbanization, suggesting that living in towns and cities may have a negative impact on these aspects of cardiovascular health.

The lifestyles and environments of traditional indigenous and city-living communities differ. We compared rates of obesity and hypertension in members of two under-studied Indigenous groups in Northeast Brazil and a nearby urbanized group. We found higher rates of obesity and hypertension amongst members of the more urbanized community, suggesting that living in towns and cities may have a negative impact on these aspects of cardiovascular health. These results suggest those living in the city should modify their lifestyle and monitor their cardiovascular health more carefully if possible.

Knockdown of transglutaminase-2 prevents early age-induced vascular changes in mice1.

PURPOSE: To determine whether the absence of transglutaminase 2 enzyme (TG2) in TG2 knockout mice (TG2-/-) protect them against early age-related functional and histological arterial changes. METHODS: Pulse wave velocity (PWV) was measured using non-invasive Doppler and mean arterial pressure (MAP) was measured in awake mice using tail-cuff system. Thoracic aortas were excised for evaluation of endothelial dependent vasodilation (EDV) by wire myography, as well as histological analyses. RESULTS: PWV and MAP were similar in TG2-/-mice to age-matched wild type (WT) control mice. Old WT mice exhibited a markedly attenuated EDV as compared to young WT animals. The TG2-/-young and old mice had enhanced EDV responses (p<0.01) as compared to WT mice. There was a significant increase in TG2 crosslinks by IHC in WT old group compared to Young, with no stain in the TG2-/-animals. Optical microscopy examination of Old WT mice aorta showed thinning and fragmentation of elastic laminae. Young WT mice, old and young TG2-/-mice presented regularly arranged and parallel elastic laminae of the tunica media. CONCLUSION: The genetic suppression of TG2 delays the age-induced endothelial dysfunction and histological modifications.

Knockdown of transglutaminase-2 prevents early age-induced vascular changes in mice

Abstract Purpose: To determine whether the absence of transglutaminase 2 enzyme (TG2) in TG2 knockout mice (TG2-/-) protect them against early age-related functional and histological arterial changes. Methods: Pulse wave velocity (PWV) was measured using non-invasive Doppler and mean arterial pressure (MAP) was measured in awake mice using tail-cuff system. Thoracic aortas were excised for evaluation of endothelial dependent vasodilation (EDV) by wire myography, as well as histological analyses. Results: PWV and MAP were similar in TG2-/-mice to age-matched wild type (WT) control mice. Old WT mice exhibited a markedly attenuated EDV as compared to young WT animals. The TG2-/-young and old mice had enhanced EDV responses (p<0.01) as compared to WT mice. There was a significant increase in TG2 crosslinks by IHC in WT old group compared to Young, with no stain in the TG2-/-animals. Optical microscopy examination of Old WT mice aorta showed thinning and fragmentation of elastic laminae. Young WT mice, old and young TG2-/-mice presented regularly arranged and parallel elastic laminae of the tunica media. Conclusion: The genetic suppression of TG2 delays the age-induced endothelial dysfunction and histological modifications.

Urbanization is Associated with Increased Trends in Cardiovascular Mortality Among Indigenous Populations: the PAI Study / Urbanização Associa-se com Tendência a Maior Mortalidade Cardiovascular em Populações Indígenas: o Estudo PAI

Abstract Background: The cardiovascular risk burden among diverse indigenous populations is not totally known and may be influenced by lifestyle changes related to the urbanization process. Objectives: To investigate the cardiovascular (CV) mortality profile of indigenous populations during a rapid urbanization process largely influenced by governmental infrastructure interventions in Northeast Brazil. Methods: We assessed the mortality of indigenous populations (≥ 30 y/o) from 2007 to 2011 in Northeast Brazil (Bahia and Pernambuco states). Cardiovascular mortality was considered if the cause of death was in the ICD-10 CV disease group or if registered as sudden death. The indigenous populations were then divided into two groups according to the degree of urbanization based on anthropological criteria:9,10 Group 1 - less urbanized tribes (Funi-ô, Pankararu, Kiriri, and Pankararé); and Group 2 - more urbanized tribes (Tuxá, Truká, and Tumbalalá). Mortality rates of highly urbanized cities (Petrolina and Juazeiro) in the proximity of indigenous areas were also evaluated. The analysis explored trends in the percentage of CV mortality for each studied population. Statistical significance was established for p value < 0.05. Results: There were 1,333 indigenous deaths in tribes of Bahia and Pernambuco (2007-2011): 281 in Group 1 (1.8% of the 2012 group population) and 73 in Group 2 (3.7% of the 2012 group population), CV mortality of 24% and 37%, respectively (p = 0.02). In 2007-2009, there were 133 deaths in Group 1 and 44 in Group 2, CV mortality of 23% and 34%, respectively. In 2009-2010, there were 148 deaths in Group 1 and 29 in Group 2, CV mortality of 25% and 41%, respectively. Conclusions: Urbanization appears to influence increases in CV mortality of indigenous peoples living in traditional tribes. Lifestyle and environmental changes due to urbanization added to suboptimal health care may increase CV risk in this population.

Resumo Fundamento: O risco cardiovascular das diversas comunidades indígenas não está bem estabelecido e pode ser influenciado pelo processo de urbanização a que se submetem esses povos. Objetivos: Investigar o perfil da mortalidade cardiovascular (CV) das populações indígenas durante o rápido processo de urbanização altamente influenciado por intervenções governamentais de infraestrutura no Nordeste do Brasil. Métodos: Avaliamos a mortalidade de populações indígenas (≥ 30 anos) do Vale do São Francisco (Bahia e Pernambuco) no período de 2007-2011. Considerou-se mortalidade CV se a causa de morte constasse no grupo de doenças CV do CID-10 ou se tivesse sido registrada como morte súbita. As populações indígenas foram divididas em dois grupos conforme o grau de urbanização baseado em critérios antropológicos: Grupo 1 - menos urbanizadas (Funi-ô, Pankararu, Kiriri e Pankararé); e Grupo 2 - mais urbanizadas (Tuxá, Truká e Tumbalalá). Taxas de mortalidade de cidades altamente urbanizadas (Petrolina e Juazeiro) nas proximidades das áreas indígenas foram também avaliadas. A análise explorou tendências na porcentagem de mortalidade CV para cada população estudada. Adotou-se o valor de p < 0,05 como significância estatística. Resultados: Houve 1.333 mortes indígenas nas tribos da Bahia e de Pernambuco (2007-2011): 281 no Grupo 1 (1,8% da população de 2012) e 73 no Grupo 2 (3,7% da população de 2012), mortalidade CV de 24% e 37%, respectivamente (p = 0,02). Entre 2007 e 2009, houve 133 mortes no Grupo 1 e 44 no Grupo 2, mortalidade CV de 23% e 34%, respectivamente. Entre 2009 e 2010, houve 148 mortes no Grupo 1 e 29 no Grupo 2, mortalidade CV de 25% e 41%, respectivamente. Conclusões: A urbanização parece influenciar os aumentos de mortalidade CV dos povos indígenas vivendo de modo tradicional. Mudanças no estilo de vida e ambientais devidas à urbanização somadas à subótima atenção à saúde podem estar implicadas no aumento do risco CV nos povos indígenas.

Urbanization is Associated with Increased Trends in Cardiovascular Mortality Among Indigenous Populations: the PAI Study.

BACKGROUND: The cardiovascular risk burden among diverse indigenous populations is not totally known and may be influenced by lifestyle changes related to the urbanization process. OBJECTIVES: To investigate the cardiovascular (CV) mortality profile of indigenous populations during a rapid urbanization process largely influenced by governmental infrastructure interventions in Northeast Brazil. METHODS: We assessed the mortality of indigenous populations (≥ 30 y/o) from 2007 to 2011 in Northeast Brazil (Bahia and Pernambuco states). Cardiovascular mortality was considered if the cause of death was in the ICD-10 CV disease group or if registered as sudden death. The indigenous populations were then divided into two groups according to the degree of urbanization based on anthropological criteria:9,10 Group 1 - less urbanized tribes (Funi-ô, Pankararu, Kiriri, and Pankararé); and Group 2 - more urbanized tribes (Tuxá, Truká, and Tumbalalá). Mortality rates of highly urbanized cities (Petrolina and Juazeiro) in the proximity of indigenous areas were also evaluated. The analysis explored trends in the percentage of CV mortality for each studied population. Statistical significance was established for p value < 0.05. RESULTS: There were 1,333 indigenous deaths in tribes of Bahia and Pernambuco (2007-2011): 281 in Group 1 (1.8% of the 2012 group population) and 73 in Group 2 (3.7% of the 2012 group population), CV mortality of 24% and 37%, respectively (p = 0.02). In 2007-2009, there were 133 deaths in Group 1 and 44 in Group 2, CV mortality of 23% and 34%, respectively. In 2009-2010, there were 148 deaths in Group 1 and 29 in Group 2, CV mortality of 25% and 41%, respectively. CONCLUSIONS: Urbanization appears to influence increases in CV mortality of indigenous peoples living in traditional tribes. Lifestyle and environmental changes due to urbanization added to suboptimal health care may increase CV risk in this population.

Tissue Transglutaminase Modulates Vascular Stiffness and Function Through Crosslinking-Dependent and Crosslinking-Independent Functions.

BACKGROUND: The structural elements of the vascular wall, namely, extracellular matrix and smooth muscle cells (SMCs), contribute to the overall stiffness of the vessel. In this study, we examined the crosslinking-dependent and crosslinking-independent roles of tissue transglutaminase (TG2) in vascular function and stiffness. METHODS AND RESULTS: SMCs were isolated from the aortae of TG2-/- and wild-type (WT) mice. Cell adhesion was examined by using electrical cell-substrate impedance sensing and PicoGreen assay. Cell motility was examined using a Boyden chamber assay. Cell proliferation was examined by electrical cell-substrate impedance sensing and EdU incorporation assays. Cell micromechanics were studied using magnetic torsion cytometry and spontaneous nanobead tracer motions. Aortic mechanics were examined by tensile testing. Vasoreactivity was studied by wire myography. SMCs from TG2-/- mice had delayed adhesion, reduced motility, and accelerated de-adhesion and proliferation rates compared with those from WT. TG2-/- SMCs were stiffer and displayed fewer cytoskeletal remodeling events than WT. Collagen assembly was delayed in TG2-/- SMCs and recovered with adenoviral transduction of TG2. Aortic rings from TG2-/- mice were less stiff than those from WT; stiffness was partly recovered by incubation with guinea pig liver TG2 independent of crosslinking function. TG2-/- rings showed augmented response to phenylephrine-mediated vasoconstriction when compared with WT. In human coronary arteries, vascular media and plaque, high abundance of fibronectin expression, and colocalization with TG2 were observed. CONCLUSIONS: TG2 modulates vascular function/tone by altering SMC contractility independent of its crosslinking function and contributes to vascular stiffness by regulating SMC proliferation and matrix remodeling.

Inferior gluteal artery pseudoaneurysm related to intramuscular injection.

INTRODUCTION: Gluteal artery pseudoaneurysms are rare, yet the most common in cases involving the superior gluteal artery. Pseudoaneurysms of the inferior gluteal artery are uncommon and are often related to blunt or penetrating trauma, infections and fractures of the pelvis. PRESENTATION OF CASE: The authors present a case of pseudoaneurysm of the inferior gluteal artery related to an iatrogenic injury due to intramuscular injection of medication, which was treated with selective embolization of the artery during angiography. DISCUSSION: The most common manifestation of an inferior gluteal artery pseudoaneurysm is the presence of a painful mass in the buttock that may or may not be associated with neurological symptoms due to compression of the sciatic nerve. Ultrasound with color Doppler and computerized tomography with multi-detectors are useful non-invasive tools for diagnosis. However, both diagnosis and therapy are facilitated by catheter angiography. CONCLUSION: This case cautions that although pseudoaneurysms are rare, pseudoaneurysms of the inferior gluteal artery require a high index of suspicion and careful physical examination by the physician in order to avoid misdiagnosis. It also illustrates the usefulness of a minimally invasive modality for treatment of these lesions.

Hemobilia após trauma abdominal: relato de 3 casos / Hemobilia after abdominal trauma: report of 3 cases

Hemobilia é rara e potencialmente fatal. A suspeita de sangramento em trato biliar é maior em casos recentes de trauma hepático ou cirurgia hepatobiliar. Ruptura de pseudoaneurisma de artéria hepática é causa comum de hemobilia. Relatamos 3 casos de hemobilia em indivíduos jovens, acometidos por trauma abdominal, que evoluíram com ruptura de pseudoaneurisma e necessidade de embolização angiográfica de vaso sangrante.

Hemobilia is rare and potentially fatal. Suspect bleeding in the biliary tract is higher in recent cases of liver trauma or hepatobiliary surgery. Rupture of hepatic artery pseudoaneurysm is a common cause of hemobilia. We report 3 cases of hemobilia in young individuals suffering from abdominal trauma, who developed pseudoaneurysm rupture and need for angiographic embolization of bleeding vessel.

Contribution of arginase activation to vascular dysfunction in cigarette smoking.

BACKGROUND: Cigarette smoke increases the risk of several cardiovascular diseases and has synergistic detrimental effects when present with other risks that contribute to its pathogenesis. Oxidative injury to the endothelium via reactive oxygen species (ROS) and nitric oxide (NO) dysregulation is a common denominator of smoking-induced alterations in vascular function. However, the mechanisms underlying ROS and NO dysregulation due to smoking remain unclear. We tested if arginase (Arg) activation/upregulation contributes to this phenomenon by constraining nitric oxide synthase (NOS) activity. METHODS: Arg2 knockout (Arg2(-/-)) and control C57BL/6J mice were either exposed to cigarette smoke, 6 h/day/2 weeks (Second Hand Smoking; SHS) or housed in normal environment (Non Smoking; NS). Arg activity, NO and ROS levels were determined by measuring urea production, fluorescent dye (DAF), and dihydroethedium (DHE) respectively in isolated mouse aorta. RESULTS: Arg activity and ROS levels were higher NO lower in SHS compared to NS mice. SHS failed to lower NO levels in Arg2(-/-) mice. Endothelial dependent vasodilation (EDV) was attenuated in SHS mice as compared to controls (78.80% ± 8 vs 46.58% ± 5). This impaired EDV was abolished in Arg2(-/-) mice (67.48% ± 7 in SHS vs. 78.80% ± 8 in NS). Vascular stiffness was increased in SHS mice as compared to NS controls but remained unchanged in Arg2(-/-) mice. CONCLUSION: Endothelial NOS is uncoupled by smoking exposure, leading to endothelial dysfunction and vascular stiffness, a process that is prevented by Arg2 deletion. Hence, we identify Arg2 upregulation as a critical pathogenic factor and target for therapy in oxidative injury following smoking exposure through reciprocal regulation of endothelial NOS.

Sildenafil citrate protects skeletal muscle of ischemia-reperfusion injury: immunohistochemical study in rat model.

PURPOSE: To investigate the effect of sildenafil citrate (SC) on skeletal muscle ischemia-reperfusion (IR) injury in rats. METHODS: Adult male Wistar rats were randomized into three groups: vehicle-treated control (CTG), sildenafil citrate-treated (SCG), and sham group (SG). CTG and SCG had femoral artery occluded for 6 hours. Saline or 1 mg/kg of SC was given 5.5 hours after occlusion. SG had a similar procedure without artery occlusion. Soleus muscle samples were acquired 4 or 24h after the reperfusion. Immunohistochemistry caspase-3 analysis was used to estimate apoptosis using the apoptotic ratio (computed as positive/negative cells). Wilcoxon rank-sum or Kruskal-Wallis tests were used to assess differences among groups. RESULTS: Eighteen animals were included in the 4h reperfusion groups and 21 animals in the 24h reperfusion groups. The mean apoptotic ratio was 0.18 ± 0.1 for the total cohort; 0.14 ± 0.06 for the 4h reperfusion groups and 0.19 ± 0.08 for the 24h groups (p<0.05). The SCG had lower caspase-3 ratio compared to the control groups at the 24h reperfusion time point (p<0.05). CONCLUSION: Sildenafil citrate administration after the onset of the ischemic injury reduces IR-induced cellular damage in skeletal muscle in this rat hindlimb ischemia model.

Sildenafil citrate protects skeletal muscle of ischemia-reperfusion injury: immunohistochemical study in rat model

PURPOSE: To investigate the effect of sildenafil citrate (SC) on skeletal muscle ischemia-reperfusion (IR) injury in rats. METHODS: Adult male Wistar rats were randomized into three groups: vehicle-treated control (CTG), sildenafil citrate-treated (SCG), and sham group (SG). CTG and SCG had femoral artery occluded for 6 hours. Saline or 1 mg/kg of SC was given 5.5 hours after occlusion. SG had a similar procedure without artery occlusion. Soleus muscle samples were acquired 4 or 24h after the reperfusion. Immunohistochemistry caspase-3 analysis was used to estimate apoptosis using the apoptotic ratio (computed as positive/negative cells). Wilcoxon rank-sum or Kruskal-Wallis tests were used to assess differences among groups. RESULTS: Eighteen animals were included in the 4h reperfusion groups and 21 animals in the 24h reperfusion groups. The mean apoptotic ratio was 0.18±0.1 for the total cohort; 0.14±0.06 for the 4h reperfusion groups and 0.19±0.08 for the 24h groups (p<0.05). The SCG had lower caspase-3 ratio compared to the control groups at the 24h reperfusion time point (p<0.05). CONCLUSION: Sildenafil citrate administration after the onset of the ischemic injury reduces IR-induced cellular damage in skeletal muscle in this rat hindlimb ischemia model.