BMC Cardiovascular Disorders最新文献

Background: This study employed four-dimensional automated left atrial quantitative analysis (4D Auto LAQ) technology to assess left atrial structure and function in patients with H-type hypertension and to investigate the impact of serum homocysteine (Hcy) level on the left atrium in patients with primary hypertension.

Methods: A total of 173 patients with primary hypertension newly diagnosed between December 2023 and December 2024 were enrolled and divided into two groups: H-type hypertension (n = 85) and non-H-type hypertension (n = 88). Additionally, 60 healthy volunteers were recruited as the control group.

Results: The results showed that compared with the non-H-type hypertension group and the control group, the H-type hypertension group exhibited statistically significant differences in Hcy, total cholesterol, triglycerides, estimated glomerular filtration rate (eGFR), and uric acid (p < 0.05). Additionally, there was a decrease (p < 0.05) in left atrial reservoir systolic longitudinal strain (LASr), left atrial systolic longitudinal strain (LASct), left atrial reservoir systolic circumferential strain (LASr-c), and left atrial systolic circumferential strain (LASct-c). Multiple linear regression analysis identified plasma Hcy levels as an independent associated factor for decreased left atrial strain parameters, including LASr (β=-0.246, p < 0.001), LASct (β=-0.279, p < 0.001), LASr-c (β=-0.333, p < 0.001), and LASct-c (β=-0.303, p < 0.001).

Conclusions: In conclusion, patients with H-type hypertension have decreased left atrial strain parameters, and when serum Hcy levels rise, the degree of strain dysfunction gradually gets worse. This suggests that these parameters could be used as an early indicator of left atrial myocardial injury in patients with H-type hypertension.

Background: Amyloidosis is increasingly recognized as a contributor to heart failure, particularly among older adults and patients with heart failure with preserved ejection fraction (HFpEF). Despite advances in diagnostic imaging and disease-modifying therapies, amyloidosis remains underdiagnosed in many settings, and population-level data examining its co-occurrence with cardiovascular disease on death certificates are limited. This study examined two decades of national mortality data to evaluate deaths co-coded with amyloidosis and cardiovascular disease (CVD) in the United States and to assess temporal trends and demographic disparities in age-adjusted mortality rates.

Methods: A retrospective analysis was conducted using mortality data from the CDC WONDER database spanning 1999-2020. Age-adjusted mortality rates (AAMRs) per 1,000,000 persons were calculated, and trends were assessed using Average Annual Percentage Change (AAPC) and Annual Percent Change (APC) using Joinpoint 5.0.2.

Results: Between 1999 and 2020, 26,391 amyloidosis and CVD-related deaths occurred among adults aged 25 years and older in the United States. The overall AAMR for deaths co-coded with amyloidosis and CVD increased from 4.40 in 1999 to 9.31 in 2020, with an AAPC of 3.49 (p < 0.001). The most pronounced increase occurred between 2018 and 2020 (APC: 13.60). Rates were higher among men than women, with both sexes showing a marked increase in the last decade. African American or Black individuals had the highest rates (11.40), followed by White (5.11) and Hispanic (3.86) individuals. Rates were highest in the Northeast region (6.71). Metropolitan areas had higher rates than non-metropolitan areas (5.73 vs. 4.76), with a more pronounced increase in metropolitan regions.

Conclusions: Age-adjusted mortality rates for deaths co-coded with amyloidosis and cardiovascular disease have increased over time, likely reflecting improved recognition and documentation. Higher rates of co-coded deaths were noted among men, African Americans, and individuals in the Northeast region, highlighting potential disparities in diagnostic access and recognition.

Arterial calcification represents a major burden in chronic kidney disease (CKD) and is an independent risk factor for cardiovascular diseases (CVD). Rodent models are essential for preclinical research on arterial calcification mechanisms and potential therapeutic interventions, permitting longitudinal analysis of disease progression, which is ethically unfeasible in humans. In this study, we specifically focused on rat models as representative rodent models, given their well-established use in cardiovascular research. Through systematic literature screening, we identified 470 studies employing rat models to investigate arterial calcification, with these models designed to simulate various pathological conditions. Our analysis revealed that arterial calcification was predominantly induced through kidney impairment, vitamin D overload, or mechanical and chemical vessel damage. Female rats were significantly underrepresented across studies, highlighting a considerable sex bias in experimental design. Particular emphasis was given to CKD-associated arterial calcification models, which accounted for about 60% of the identified studies. A meta-analysis of 67 CKD-related studies identified several significant factors influencing arterial calcification. Dietary phosphate concentration, male sex, and the use of Sprague-Dawley rats were associated with enhanced arterial calcification development. Nephrectomy-based approaches demonstrated superior efficacy and reliability in arterial calcification induction compared to adenine-based models. However, the analysis was limited by substantial heterogeneity across studies, potential publication bias, and inconsistent reporting of experimental parameters.These findings underscore the critical need for standardized reporting of experimental procedures and results to enhance the applicability of animal studies in meta-analyses and improve their translational value.