Echocardiographic assessment of atrioventricular plane displacement, Clinical application in patients with coronary artery disease, atrial fibrillation and aortic stenosis

Sammanfattning: Left atrioventricular plane displacement (AVPD) has been shown to correlate well with left ventricular (LV) systolic function measured as ejection fraction (EF). AVPD has also been shown to be related to diastolic performance. Other factors related to AVPD include age, heart rate, LV and atrial dimensions, myocardial thickness, bodysurface, and afterload. In this thesis the left AVPD was studied in relation to some specific clinical conditions. In study I, left AVPD at rest was shown to be related to the degree and extent of CAD, independent of prior myocardial infarction (MI), in 159 patients with coronary angiography verified stable CAD. The AVPD decrease was more pronounced the more widespread the coronary disease. Left AVPD and EF are different measures of LV function. AVPD reflects systolic and diastolic performance whereas EF only is a measure of LV systolic function. The observation in study II underscores this. AVPD was independently correlated with both LV systolic function and diastolic filling in patients with stable CAD. The more pronounced the diastolic filling impairment, the lower the AVPD. The degree of displacement decrease has a prognostic value in patients with heart failure and in post MI patients. Studies III and IV show that AVPD has a prognostic value regarding mortality in cardiac events in patients with stable CAD and in patients with chronic atrial fibrillation. AVPD correlates independently with mortality in patients with CAD. However, AVPD is related to prognosis in patients with atrial fibrillation but the discriminative value of AVPD decrease is limited since the difference in AVPD between those who died in cardiac events and survivors is rather small. In patients with aortic stenosis, the hemodynamic load with increased afterload causes a rise in LV wall stress. Myocardial hypertrophy develops in response to this. The LV hypertrophy initially leads to diastolic dysfunction. In late stages, reduced LV systolic function can occur as a result of myocardial fibrosis. However, prior to that, increased wall stress can cause LV systolic dysfunction. In study V, in patients with aortic stenosis, AVPD independently correlates to the degree of aortic valve obstruction, whereas LVEF does not. Our results indicate that AVPD may be affected earlier than LVEF by the hemodynamic consequences of aortic stenosis. AVPD may therefore be a more sensitive marker of LV dysfunction in aortic stenosis than LVEF. In summary, this thesis suggests that AVPD is a sensitive marker of LV function. AVPD is already decreased at mild ischemia and is influenced by small changes in diastolic filling impairment. AVPD is also more sensitive than LVEF to increased afterload, as seen in aortic valve obstruction since, AVPD is already affected at slightly increased LV filling pressures. Furthermore, it seems that AVPD is a better predictor of mortality than LVEF, patients with CAD, heart failure and atrial fibrillation in earlier stages of these heart diseases.