[Myocardial changes in acute pulmonary artery embolism--an experimental study]

Massive pulmonary embolism usually causes acute right ventricular hypertension. Structural and hemodynamic effects of right ventricular overloading were studied in piglets (weight 17-22,5 kg). Pulmonary arterial obstruction (PAO) was achieved by temporary banding of the main pulmonary artery, the external diameter of the vessel being reduced to one-third (Group I) or by half (Group II) of the original size. In Group I PAO caused a twofold increase of systolic right ventricular pressure (RVP), whereas the systolic left ventricular pressure decreased to 30% of its original value; PAO was terminated after 25 seconds. After PAO, no changes of right or left ventricular function were observed in Group I. Electron microscopy revealed mitochondrial alterations and fragmentations of the sarcomeres. In Group II, PAO was maintained for 60 minutes. Due to PAO, the systolic RVP increased to twice the original value and the systolic aortic pressure decreased by 10%. During the PAO period, a continuous increase of enddiastolic RVP was observed in Group II. After termination of PAO, contractility parameters for the right ventricle were reduced, and right ventricular diameters (RVD) and enddiastolic RVP were increased in comparison to the pre-PAO values. As hemodynamic alterations increased corresponding to the duration of PAO, it is concluded that in case of acute pulmonary embolism early relief of right ventricular overloading may be important.