Effect of atrial fibrillation on the dynamics of mitral annular area.

BACKGROUND AND AIMS OF THE STUDY: The mitral annulus shows dynamic changes in shape and size during the cardiac cycle. A smaller size in end-diastole is attributed to the sphincteric action of atrial systole, and this may be important for functional integrity of the mitral valve. However, the effect of atrial fibrillation (AF) on dynamic changes in mitral annular size in humans is not known. METHODS: Mitral annular diameters in apical four- and two-chamber views were measured using echocardiography in 25 patients in atrial fibrillation, and in 37 subjects in normal sinus rhythm at mid-diastole, end-diastole and end-systole. Mitral annular area was computed assuming elliptical geometry. RESULTS: Patients in sinus rhythm showed a significant increase in mitral annular area of 25.9 +/- 12.8% with ventricular systole compared to its area in end-diastole (p < 0.0001), and a 10.5 +/- 8.4% reduction with atrial systole compared to mid-diastole (p < 0.001). Patients in AF had larger mitral annuli which showed non-significant changes in size between these three phases of the cardiac cycle. Percent reduction in mitral annular area in the latter half of diastole correlated significantly with left atrial (LA) diameter (r = -0.54, p < 0.0001), LA volume (r = -0.50, p < 0.0001), left ventricular (LV) fractional shortening (r = 0.37, p = 0.0036), mitral annular area in mid-diastole (r = -0.41, p = 0.0011) and mitral annular area in end-diastole (r = -0.64, p < 0.0001). That is, atrial sphincteric action on the mitral annulus was less in the presence of larger left atrium or the mitral annulus. Stepwise multiple regression analysis showed rhythm and mitral annular size to be independent predictors of dynamic changes in mitral annular area. CONCLUSION: It is concluded that AF blunts or eliminates the phasic changes in mitral annular size during the cardiac cycle with loss of its presystolic sphincteric action; this may have implications in the genesis and surgical correction of mitral regurgitation.

Predictors of recurrent restenosis after coronary stenting: an analysis of 197 patients.

One of the major limitations in coronary stenting is in-stent restenosis. This study was aimed to identify clinical, angiographic, and procedural factors that may be related to recurrent in-stent restenosis. We analyzed consecutive 197 patients who underwent coronary stenting. Follow-up angiography was available in 170 patients and repeat balloon angioplasty was performed for in-stent restenosis. These patients were subdivided into 3 groups: group A consisted of 100 patients that were never restenosed, group B had 49 patients restenosed once, and in group C were 21 patients restenosed more than twice. Group C was more often female (48%) and included diabetes mellitus patients (52%). Lesion location, reference vessel size and diameter stenosis were similar for all groups. However, the incidence of calcified lesions tended to be higher (50% vs. 29%; p = 0.07), and lesion length was longer in group C than in group A (11.9+/- 5.4 mm vs. 9.0+/- 3.9 mm; p < 0.01). Diameter stenosis after predilation as well as after stenting was significantly higher in group C than in group A (50+/- 10% vs 39+/- 10%; p < 0.01, 32+/- 8% vs. 19+/- 10%; p < 0.01). The incidence of diffuse type of in-stent restenosis was significantly higher in group C than in group B (62% vs. 14%; p < 0.01). Multivariate logistic regression analysis identified diameter stenosis after stenting (p = 0.0022), female (p = 0.0135), and diameter stenosis after predilatation (p = 0.0233) as the significant correlate of recurrent in-stent restenosis. In conclusion, the major recurrent in-stent restenosis predictors identified included female gender, final diameter stenosis, and diameter stenosis after predilatation.

Left Atrial Systolic Performance in the Presence of Elevated Left Ventricular End-Diastolic Pressure: Evaluation by Transesophageal Pulsed Doppler Echocardiography of Left Ventricular Inflow and Pulmonary Venous Flow Velocities.

We recorded left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities by transesophageal pulsed Doppler echocardiography in 25 patients with a ratio of peak atrial systolic to early diastolic LVIF velocity of <1 and a left ventricular end-diastolic pressure (LVEDP) of 15 mmHg or greater, as well as in 30 normal subjects. The group consisted of 14 patients with prior myocardial infarction, 7 with dilated cardiomyopathy, and 4 with cardiac amyloidosis, and were divided into: (1) group A (n = 7): peak atrial systolic LVIF velocity of 40 cm/sec or greater; (2) group B (n = 7): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of 30 cm/sec or greater; and (3) group C (n = 11): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of <30 cm/sec. Although LVEDPs in groups B and C were significantly greater than in group A, there was no difference between groups B and C. The mean pulmonary capillary wedge pressure (mPCWP) in group C was significantly greater than in groups A and B, but there was no difference between groups A and B. The difference between LVEDP and mPCWP (LVEDP - mPCWP) in group B was significantly higher than in groups A and C. Dilatation of the left atrium (LA) was seen in all three groups, particularly in groups B and C. There were no differences in peak atrial systolic LVIF velocity and LA volume change during atrial contraction between group A and the control group, and there were no differences in LA volume change and peak second systolic PVF velocity between groups A and B. LA volume change and peak second systolic PVF velocity were significantly less in group C than in groups A and B. Among the four patients whose courses could be observed after medical treatment with diuretic and vasodilator, one changed from group B to A, one from group B to C, one from group C to A, and one remained in group C. Thus, recording of peak atrial systolic LVIF and PVF by transesophageal pulsed Doppler echocardiography permits detailed evaluation of LA systolic performance in the presence of elevated LVEDP. These two variables provide important information for less invasive differentiation of LA afterload mismatch from LA myocardial failure.

Three-Dimensional Echocardiographic Reconstruction of the Left Ventricle by a Transesophageal Tomographic Technique: In Vitro and In Vivo Validation of its Volume Measurement.

Accurate determination of left ventricular (LV) volume has important therapeutic and prognostic implications in patients with cardiac disease. Volume estimations by two-dimensional techniques are not very accurate due to geometric assumptions. OBJECTIVES: To validate LV volume determinations by a new transesophageal three-dimensional echocardiographic technique. We performed three-dimensional reconstruction of the LV using an echo-computed tomographic (CT) technique based on serial pullback parallel slice imaging technique in both in vitro and in vivo settings. Fourteen latex balloons with various sizes (30-235 mL) and shapes (conical, pear shaped, round, elliptical, and aneurysms in various locations) filled with known volumes of water were imaged in a water bath. From the static three-dimensional image, the LV long axis was defined and the LV was sectioned perpendicular to this axis into 2-mm slices. The volume of each slice was calculated with the observer blinded to the actual volume as the product of the slice thickness and the manually traced perimeter of the slice and the LV volume as the sum of the volumes of the slices (Simpson's method). The calculated LV volume closely correlated with the actual volume (r = 0.99, P < 0.0001, calculated volume = 1.06x - 11.3, Deltavolume = -5.7 +/- 10.0 cc). Using the same system, transesophageal echocardiographic (TEE) images of the LV were obtained in 15 patients gated to respiration and ECG. Satisfactory dynamic three-dimensional reconstruction of the LV was possible in ten patients. The three-dimensional LV volumes (systolic and diastolic) using Simpson's method correlated well with those obtained from biplane or multiplane TEE images using the area length method (r = 0.89, p < 0.0001, y = 12.7 + 0.84x, Deltavolume = 1.3 +/- 18.1 cc). The LV major-axis diameters by the two methods showed very close correlations as well (r = 0.86, P < 0.0001, y = 19 + 0.74x, Deltadiameter = 1.0 +/- 7.2 mm). We conclude that three-dimensional LV volume calculation by the echo-CT technique is intrinsically sound, is independent of LV geometry, and with some limitations, is applicable in vivo. (ECHOCARDIOGRAPHY, Volume 13, November 1996)