PATIENTS

We assessed 11 male patients that represented a subgroup of 19 previously reported2 patients who underwent successful PLV with technically satisfactory data for estimating pre- and postoperative left ventricular end systolic elastance. In eight patients end systolic elastance data could not be calculated because of technical reasons and they were not included in this analysis. (In seven patients only one adequate preoperative ventricular angiogram was obtained because of the following: four patients had extrasystoles, in two patients there was inadequate opacification of the left ventricle, and one patient had an inadequate pressure drop after glyceryl trinitrate. In one patient tachycardia occurred before the second postoperative angiogram.) All 11 patients had chronic heart failure caused by idiopathic dilated cardiomyopathy, severe left ventricular dilation (echocardiographic end diastolic dimension > 70 mm) with normal coronary arteries, normal valve morphology, and no history of alcohol abuse. Preoperative patient characteristics were similar between these patients and eight patients in whom end systolic elastance estimates could not be calculated. All patients were treated with digoxin, captopril, amiodarone, and frusemide (furosemide), both pre- and postoperatively. No patient was on inotropic support during pre- or postoperative catheterisation studies. The investigational status of PLV was explained to all patients, who signed informed consent forms both for the catheterisation studies and for the operation.

A control group comprised 11 patients with atypical chest pain and normal coronary arteries in whom data for calculation of end systolic elastance estimates were collected. None of these patients had a history of hypertension, while in all of them echocardiography showed normal left ventricular size (end diastolic diameter < 56 mm) with no signs of valvar heart disease or left ventricular hypertrophy (wall thickness < 11 mm).

SURGICAL AND ANGIOGRAPHIC PROCEDURES

The surgical technique used has been previously described.9 All operations were performed using cardiopulmonary bypass. In 2/11 patients beating heart technique was used, while in 9/11 patients surgery was performed during cardioplegic arrest. Mitral valve repairs were performed using a previously described modification.9 The procedure involved a diamond shaped resection of the left ventricular posterolateral wall confined by two papillary muscles. The resected myocardial specimen was 9.1 (2.5) cm long, 4.5 (1.3) cm wide, and 1.8 (0.7) cm thick. Additional valve procedures are presented in table1.

All patients underwent preoperative (15 (10) days before surgery) and postoperative (13 (3) days after surgery) catheterisation studies. The control group was evaluated using the same protocol as for the study patients. Cardiovascular medications were not withheld on the day of the procedure. After recording baseline intracardiac pressures and cardiac output, and performing coronary angiography, patients entered a modified version of previously reported protocols.10 ,11 A bipolar pacing catheter was placed into the right atrium (or into the right ventricle in patients with atrial fibrillation). Pacing was used to avoid differences caused by cycle length during ventricular angiographies. A 7 F pigtail catheter was inserted into the left ventricle through an 8 F femoral sheath. Single plane left ventricular angiography was performed in 30° right anterior oblique view using 35 mm film at a rate of 50 frames/s, after the injection of 40–50 ml of non-ionic contrast medium. Femoral artery pressure was recorded during left ventricular angiography using a side arm of a femoral sheath at a paper speed of 25 mm/s on a Mingograf 7 strip chart recorder (Siemens, Erlangen, Germany). After allowing for adequate recovery time to achieve a return of stable baseline haemodynamics, an intravenous glyceryl trinitrate bolus was administered into a femoral vein to decrease systolic arterial pressure by at least 20 mm Hg or to a level of 80 mm Hg.12 At that moment, a second left ventricular angiography was performed.

ANGIOGRAPHIC ANALYSIS PROCEDURES

For each ventricular angiogram, left ventricular volumes and femoral artery pressures of the first two heart cycles, which provided adequate left ventricular opacification and were not postextrasystolic, were averaged and used for the analysis. Left ventricular volumes were calculated by the area–length method using an appropriate regression equation.13 We previously reported the accuracy of single plane ventricular angiography for the assessment of left ventricular volumes in this patient population.2End diastolic and end systolic frames were defined as the frames with the largest and smallest ventricular silhouette, respectively.

Correlations between intraobserver variability of measurements of left ventricular end diastolic and end systolic volumes, and for the end systolic volume decrease after glyceryl trinitrate bolus in our patient group, were r = 0.97, 0.98, and 0.76, respectively. The correlation between interobserver variability of measurements of the same variables werer = 0.95, 0.96, and 0.72, respectively. The mean (SD) of absolute differences of intraobserver measurements of left ventricular end diastolic and end systolic volumes and for the end systolic volume decrease after the glyceryl trinitrate bolus were 19.0 (14.1) ml, 10.5 (11.0) ml, and 11.8 (10.1) ml, respectively; the mean of absolute differences of interobserver measurements of the same variables were 23.6 (20.7) ml, 17.3 (13.6) ml, and 11.1 (7.4) ml, respectively.

End systolic pressure was defined as the dicrotic notch of the femoral artery pressure tracing recorded during left ventricular angiography.2 Left ventricular end diastolic wall thickness was measured as the distance between epicardial and endocardial surfaces of the anterior free wall in its middle third, and the result was used for determination of ventricular mass.14

Left ventricular end systolic elastance was estimated by two methods. First, the matched points of end systolic pressure–volume relation were subjected to a linear regression. The regression slope was considered to be the first end systolic elastance estimate (Ees), while its intercept with the abscissa was considered to be the theoretical volume at zero pressure.6 ,10 ,11 The end systolic pressure was then replaced with peak systolic pressure and the method repeated, with a resulting regression slope considered as a second end systolic elastance estimate (Eps). Previous studies have shown a good correlation between these two estimates and more accurate measures of left ventricular end systolic elastance.15 To eliminate the impact of change of left ventricular size on end systolic elastance, we calculated corrected Ees by multiplying it with either left ventricular mass or end diastolic volume.16 ,17Arterial elastance was calculated as the ratio of end systolic pressure to stroke volume, and ventriculoarterial coupling was calculated by dividing arterial elastance with Ees.18

STATISTICS

All data are presented as mean (SD). Pairedt tests were used to compare patients' data before and after surgery and unpaired ttests were used for comparisons between controls and patients, using Bonferroni's correction for multiple comparisons. Simple linear regression was used to assess correlation between variables. The impact of correction of mitral regurgitation on Ees was assessed by repeated measures analysis of variance. A value of p ⩽ 0.05 was considered significant.