Background: Rates of cardiovascular disease and its risk factors seem to be increasing in American Indian populations, yet these changes have received little documentation.

No abstract

Left atrial appendage aneurysm (LAAA) is a rare condition caused by congenital dysplasia of the atrial muscles. Patients usually present with atrial tachyarrhythmias as a result of ectopic foci of atrial rhythm generation or systemic thromboembolism. We report a case of a 38-year-old Native American female presenting with 1-month history of cough, in sinus rhythm, and found to have a large cyst-like structure next to the left ventricular lateral wall on transthoracic echocardiography. This structure was later confirmed as a LAAA on cardiac magnetic resonance imaging. Patient underwent aneurysmectomy without any complications.

Early recognition of acute myocardial infarction (MI), followed by prompt emergency care, improves patient outcomes. Among rural American Indian (AI) populations there are disparities in access to care for MI and processes of care, resulting in poor MI-related health outcomes compared to the general population. We sought to gain an understanding of barriers related to MI time-to-treatment delays using a qualitative approach. We conducted semi-structured interviews and focus groups with AI key informants and community members in three Indian Health Service regions. Major barriers to care included long travel distance to care and lack of supporting infrastructure; distrust of the health care system; low overall literacy and basic health literacy; priority of family care-giving; and lack of specialized medical facilities and specialists. Findings suggest that improved time-to-treatment facilitators include educating the local community about the causes and consequences of MI and culturally-sensitive health communication, as well as addressing the quality of local systems of care and the community's perception of these systems. Pursuing these strategies may improve quality of care and reduce MI-related morbidity and mortality in rural AI populations.

The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophing in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.