Tomographic left ventricular volume determination in the presence of aneurysm by three-dimensional echocardiographic imaging. I: Asymmetric model hearts.

To improve the accuracy of measurements of left ventricular volume in the presence of an aneurysm, we used three-dimensional echocardiographic imaging to analyze the shape of left ventricles in 23 asymmetric model hearts with eccentric aneurysms of different sizes, shapes, and localizations. A standard 3.75 MHz ultrasound probe with a rotation motor device was used to obtain a three-dimensional data set. By rotating the probe stepwise 1 degree, 180 radial ultrasound pictures were digitized. On the basis of the three-dimensional data set, the following parameters were determined and compared with the dimensions of the model hearts obtained by direct measurement: total left ventricular volume (LVV), aneurysm volume, area of the aneurysm's base, the longest aneurysm long diameter, and the longest aneurysm cross diameter. In addition, quantification of LVV by three-dimensional echocardiography was compared with biplane two-dimensional echocardiographic measurement according to the disk method. Good agreements were found for LVV measured by both techniques, three-dimensional echocardiographic and direct measurement (mean of differences = 0.91 ml; SD of differences = +/- 6.23 ml; line of regression y = 1.07 x - 14.24 ml; r = 0.968; standard error of the estimate [SEE] = +/- 6.17 ml), aneurysm volume (mean of differences = 0.43 ml; SD of differences = +/- 2.14 ml; line of regression y = 1.05 x - 0.81 ml; r = 0.996; SEE = +/- 1.96 ml), area of the aneurysm's base (mean of differences = 0.24 cm2; SD of differences = +/- 1.72 cm2; line of regression y = 1.02 x - 0.02 cm2; r = 0.981; SEE = +/- 1.75 cm2), the longest aneurysm long diameter (mean of differences = -0.26 mm; SD of differences = +/- 1.60 mm; line of regression y = 0.97 x + 1.34 mm; r = 0.996; SEE = +/- 1.54 mm), and the longest aneurysm cross diameter (mean of differences = 1.35 mm; SD of differences = +/- 3.94 mm; line of regression y = 0.95 x + 3.17 mm; r = 0.941; SEE = +/- 3.99 mm). In contrast, in these extremely asymmetric-shaped model hearts, agreement between biplane two-dimensional echocardiographic and both direct LVV measurement (mean of differences = 7.8 ml; SD of differences = +/- 20.8 ml; line of regression y = 1.48 x - 92.45 ml; r = 0.874; SEE = +/- 18.36 ml) and three-dimensional echocardiographic measurements (mean of differences = -7.6 ml; SD of difference = +/- 18.1 ml; line of regression y = 0.59 x + 80.98 ml; r = 0.908; SEE = +/- 10.36 ml) was poor. Thus tomographic three-dimensional echocardiography allowed accurate volume determination of asymmetric model hearts in the shape of left ventricles with eccentric aneurysms.

Results of mitral valve reconstruction in mitral valve insufficiency.

In the last three years forty mitral valve reconstruction (MR) procedures were performed in case of mitral insufficiency (MI). In three cases, anatomical changes made reconstruction impossible for us. One patient had to be re-operated because of unsatisfactory valve function. There was no operative mortality. In twelve of the patients, mitral insufficiency was the only problem, while in twenty eight others additional cardiac procedures (CABG, AVR) were performed. The patients' age ranged from 17 to 77 years. The aortic cross-clamping time for mitral reconstruction without additional cardiac procedures ranged from 35 to 134 minutes. With one exception, the post-operative TEE indicated no, or very little, insufficiency. We concluded that the mitral valve insufficiency can be corrected with very good results and with a very low rate of complications. Such corrections ought therefore be taken into consideration before valve replacement.

Diagnosis and therapeutic consequences of intramural aortic hematoma.

The classical triad of sudden devastating chest pain, electrocardiographic absence of acute myocardial infarction, and identification of an upstream flap in the ascending aorta by transesophageal echocardiography (TEE) indicates aortic type A dissection requiring emergent surgery. Among 34 patients presenting with clinical signs and symptoms of an aortic dissection, three did not show the mandatory flap in the upstream aorta. The only echocardiographic finding was aortic wall thickening indicating an intramural hematoma. Two of these patients showed early aortic ectasia and one showed a pericardial effusion. Despite the missing flap echocardiographically, surgery was performed in all three patients. The surgical approach was the same as that for patients with a type A dissection. Two patients are doing well after the procedure, and one patient died after reoperation. The postoperative histologic work-up confirmed that there was no intimal tear or dissection of the intimal layer. We conclude that the echocardiographic finding of an intramural hematoma combined with typical clinical signs of chest pain, with myocardial infarction ruled out, requires emergent surgical intervention.

Differences in cardiodepressant effects of halothane and isoflurane after inotropic stimulation in guinea-pig papillary muscles.

The effects of halothane and isoflurane on action potentials and force of contraction were studied in guinea-pig isolated papillary muscles in order to investigate the cardiodepressant action of the anesthetics in the presence of clinically relevant inotropic drugs. In control conditions, equipotent concentrations of the two volatile anesthetics depressed force of contraction to a similar degree. Halothane (2%) slightly shortened the action potential duration, whereas isoflurane (2.8%) did not influence the shape of the action potential. The muscles were then treated with three different inotropes, digitoxin, amrinone and 3-isobutyl-1-methylxanthine (IBMX) prior to exposure to the anesthetics. After pretreatment with digitoxin and amrinone, halothane was significantly more cardiodepressant than isoflurane. With IBMX, no difference in negative inotropic effect was observed. Neither volatile anesthetic significantly changed the action potential duration after pretreatment with the inotropic drugs. We suggest that halothane is more cardiodepressant than isoflurane in the presence of drugs which enhance force of contraction both by an increase in calcium influx and calcium release because it impairs force of contraction not only via inhibition of the calcium current but also via interference with calcium release.

Combined effects of volatile anesthetics and phosphodiesterase inhibitors on contractile performance in guinea pig hearts.

The cardiotonic effects of the phosphodiesterase inhibitors amrinone, milrinone, and 3-isobutyl-1-methylxanthine were studied in Langendorff-perfused guinea pig hearts exposed to the cardiodepressant concentrations of halothane or isoflurane. Left ventricular pressure, rate of change of pressure (dP/dt), heart rate, and perfusion pressure were measured in the presence of increasing drug concentrations. Under control conditions, both (dP/dt)max and heart rate were increased most with 3-isobutyl-1-methylxanthine and least with amrinone. In isoflurane-pretreated hearts (1.3%, vol/vol), the phosphodiesterase inhibitors increased (dP/dt)max to a larger degree, whereas the increase in heart rate remained similar to that in the control hearts. After exposure to halothane (0.8%, vol/vol), however, amrinone and milrinone were less effective with respect to enhancement of contractile performance. There was no difference in the 3-isobutyl-1-methylxanthine-induced increase of (dP/dt)max between hearts exposed to isoflurane and those exposed to halothane. Our results suggest that contractile performance of isolated hearts is more easily stimulated by milrinone and amrinone in the presence of isoflurane than in the presence of halothane.