RESUMEN
The left atrium (LA) is a vital component of the cardiovascular system, playing a crucial role in cardiac function. It acts as a reservoir, conduit, and contractile chamber, contributing to optimal left ventricle (LV) filling and cardiac output. Abnormalities in LA function have been associated with various cardiovascular conditions, including heart failure, atrial fibrillation, valvular heart disease, and hypertension. Elevated left ventricular filling pressures resulting from impaired LA function can lead to diastolic dysfunction and increase the risk of adverse cardiovascular events. Understanding the relationship between LA function and LV filling pressures is crucial for comprehending the pathophysiology of cardiovascular diseases and guiding clinical management strategies. This article provides an overview of the anatomy and physiology of the LA, discusses the role of LA mechanics in maintaining normal cardiac function, highlights the clinical implications of elevated filling pressures, and explores diagnostic methods for assessing LA function and filling pressures. Furthermore, it discusses the prognostic implications and potential therapeutic approaches for managing patients with abnormal LA function and elevated filling pressure. Continued research and clinical focus on left atrial function are necessary to improve diagnostic accuracy, prognostic assessment, and treatment strategies in cardiovascular diseases. It will explore the importance of assessing LA function as a marker of cardiac performance and evaluate its implications for clinical practice. In accordance with rigorous scientific methodology, our search encompassed PubMed database. We selected articles deemed pertinent to our subject matter. Subsequently, we extracted and synthesized the salient contents, capturing the essence of each selected article.
RESUMEN
OBJECTIVE: Patients with unstable angina (UA) and high C-reactive protein (CRP) have increased cardiovascular risk. Whether genetic factors such as the synonymous 1059G/C polymorphism within the exon 2 of the human CRP gene determine CRP levels and outcome is unclear. METHODS: In 105 consecutive patients with UA, we assessed the CRP 1059G/C polymorphism, CRP plasma levels and interleukin-6 production after in-vitro stimulation of whole blood with lipopolysaccharide (1 ng/ml). Coronary events during a 24-month follow-up were recorded. RESULTS: CRP levels (median, range) were significantly lower among C-allele carriers (2.3 mg/l, 0.5-26.9) than among GG homozygotes (5.9 mg/l, 0.8-72.12, P=0.009). Interleukin-6 production was lower in C-allele carriers (1645 pg/ml, 832.0-9522) than in GG homozygotes (3929 pg/ml, 670.8-10 582), (P=0.085). At follow-up, 1059C-allele carriers experienced fewer coronary events than 1059GG homozygotes (13 vs. 47%, P=0.021). At multivariable analysis, a CRP level >3 mg/l, but not the 1059G/C polymorphism, was an independent predictor of coronary events (odds ratio 10.04, 95% confidence interval 2.84-35.44, P=0.0002). CONCLUSION: This study shows that the CRP synonymous 1059G/C polymorphism affects CRP levels. No independent association was, however, observed between this polymorphism and clinical outcome in UA.