Erschienen:
[Erscheinungsort nicht ermittelbar]: University of New South Wales. Clinical School - South Western Sydney, 2012
Sprache:
Englisch
Entstehung:
Hochschulschrift:
Dissertation, University of New South Wales. Clinical School - South Western Sydney, 2012
Anmerkungen:
Beschreibung:
The thin walled left atrium (LA) is sensitive to diastolic changes within the left ventricle (LV), enabling it to be a robust marker of cardiovascular function and outcomes. However, there remain significant limitations in our understanding of atrial function. This research aimed to evaluate phasic atrial function by analysis of volumes and strain in normal subjects and in patients with cardiovascular conditions associated with LV diastolic dysfunction.LA volumes and strain were examined in normal subjects from decade three to eight. LA volume increased with age, but only became significant in the eighth decade. Therefore, any significant increase in LA size that occurs before advanced age likely represents latent or undiagnosed cardiovascular pathology. Additionally, with normal aging, changes in atrial strain and strain rate occurred earlier than changes in volume measurements, suggesting that strain changes may be a sensitive indicator of subclinical atrial dysfunction.In patients with non-ST elevation myocardial infarction (NSTEMI), LA volumes were significantly greater than normal controls at baseline, and continued to increase at 12 months. Thus the measurement of LA volumes post NSTEMI may be useful to monitor chronic diastolic dysfunction resulting from ischaemia.The predictors of LA appendage thrombus in patients with persistent atrial fibrillation were examined. The significant univariate predictors included ischaemic heart disease, LV mass and LA and right atrial spontaneous echo contrast (SEC). Increased LV mass was the strongest predictor of thrombus, supporting the link between hypertension and the development of atrial fibrillation and consequent thrombus formation.Mild or moderate hypertension resulted in increased LA volumes as early as decade four. Thus, hypertension accelerates the normal aging process of LA remodelling which may then result in the development of atrial fibrillation.Patients with Fabry disease had significantly increased LA volumes and reduced atrial reservoir function, independent of LV hypertrophy. Conduit function was selectively reduced only in Fabry patients with hypertrophy. These results suggest that Fabry disease results in fibrosis of the LA as well as the LV.The increased understanding of both physiological and pathological changes in LA function may be useful to predict adverse cardiovascular outcomes and target and monitor therapy in these specific high risk groups of patients with cardiovascular involvement.