Description / Table of Contents: Zusammenfassung Die Muskelmassenbestimmung bei Patienten mit dilatativer Kardiomyopathie (DCM) mittels der herkömmlichen Algorithmen der ein- (1D) und zweidimensionalen (2D) Echokardiographie gilt aufgrund der individuellen Konfiguration der vergrößerten Herzen bei diesen Patienten als unzuverlässig. Die echokardiographische Muskelmassenbestimmung (MMB) im transthorakal dreidimensionalen (3D) Verfahren läßt diesbezüglich exaktere Ergebnisse erwarten. Dies soll im Vergleich zur MMB mittels der Magnetresonanztomographie (MRT) überprüft werden. Untersucht wurden 36 Patienten (Alter 18–74 Jahre) mit DCM mittels herkömmlicher transthorakaler ein- und zweidimensionaler Echokardiographie sowie durch eine transthorakale 3D-Datenakquisition. Zudem wurden die Patienten einer MRT-Untersuchung des Herzens unterzogen. Eindimensional wurde die Muskelmasse nach Devereux bestimmt, zweidimensional nach der Flächenlängenmethode. Der 3D-Datensatz wurde durch manuelle Konturierung des Endo- und Epikards in 3 orthogonalen Schnittebenen “scheibchenweise” rekonstruiert, um dann aus dem algorithmisch bestimmten Muskelvolumen die linksventrikuläre Muskelmasse zu bestimmen. Diese wurde aus den MRT-Daten anhand von maximal 15 Kurzachsenschnitten durch Markierung der Endo- und Epikardgrenzen ermittelt. Hiernach zeigt sich, daß die MMB mittels des Algorithmus der 1D-Echokardiographie (r = 0,42, n. s.) nicht signifikant mit den Ergebnissen der Muskelmassenbestimmung durch die MRT korreliert. Dahingegen zeigt sich für die 2D-Echokardiographie (r = 0,64, p 〈 0,01) sowie die Berechnung aus dem 3D-Datensatz (r = 0,78, p 〈 0,01) bei Patienten mit DCM eine befriedigende Korrelation mit den Ergebnissen der MRT. Die echokardiographischen 1D- (MW: 399,2 g, p 〈 0,01) und 2D- (MW: 285,9 g, p 〈 0,01) Verfahren überschätzen die durch die MRT (MW: 199,1 g) bestimmte linksventrikuläre Muskelmasse, wohingegen die 3D-Analyse (MW: 172,6 g, n. s.) diesen Ergebnissen am nächsten kommt. Die Interobservervariabilität lag für die 3D-Muskelmassenbestimmung bei 5,1% (1D: 11,2%, 2D: 9,1%).

Description / Table of Contents: Summary Dobutamine stress echocardiography (DSE) leads to strong hypercontraction, tachycardia, and peripheral vasodilatation. In previous studies systolic obstruction of the left ventricular outflow tract (LVOT) was observed as a result of these factors. To evaluate left ventricular function and morphology in patients (pts) with induced systolic LVOT obstruction, we used continuous wave (CW) doppler registrations in combination with quantitative 2-D-echocardiography in 100 pts during routinely performed DSE (5–40 μg/kg/min). In addition left ventricular wall thickness was measured. Symptoms were registrated using a standardised questionaire and cardiac arrhythmias were counted over a two minute intervall at rest and during the maximal heart rate of each patient. During DSE dynamic flow acceleration with late systolic peak velocity above 2 m/second (s) was considered to represent LVOT obstruction in pts with normal flow profiles in the LVOT before infusion of dobutamine. For invasive studies pts were investigated with femoral catheterisation by the method of Judkins. A greater than 50% stenosis was judged to be significant. Results: Examinations in 73 pts provided data of sufficient quality for echocardiographic and Dopplersonographic evaluations. 39 pts, 26 men, 13 women, mean age 64 ± 8 years, developed late systolic flow velocities above 2 m/s and therefore formed the obstructive group (grp A). Grp B consisted of 34 pts, 26 men and 8 women, mean age 66 ± 10 years, who showed normal time velocity integrals during DSE. In 41 pts invasive data provided information concerning the existence and severity of coronary artery disease. There were no significant differences in the increase of heart rate, the product of maximal systolic blood pressure and maximal heart rate or the percentage of pts, who reached their age corrected submaximal heart rate during DSE. Obstructive pts (group A) showed late systolic dynamic acceleration of systolic flow with a mean maximal speed of 315.4 ± 139.8 cm/s, which peaked 0.12 ± 0.04 s after the R-wave. From the velocities we calculated a mean pressure gradient of 47.5 ± 39.7 mm Hg using the modified Bernoulli equation. Group B patients showed lower and earlier maximal speeds with a mean value of 158.2 ± 37.6 cm/s, 0.09 ± 0.04 s after the R-wave, corresponding to a pressure gradient of 10.6 ± 4.9 mm Hg (p 〈 0.001). Ejection fractions were higher (p 〈 0.001) before the test in grp A: 68.2 ± 8% compared to 55.7 ± 10.4% in B. This difference increased during peak stress: 74.1 ± 7.7% compared to 59.5 ± 12.8%. Enddiastolic (EDVI) and endsystolic volume indexes (ESVI) were lower in grp A (p 〈 0.001). During DSE, the decrease in ESVI was somewhat stronger for pts in grp A. Left ventricular hypertrophy was more often seen with obstruction. Septal thickness was increased in A: 1.45 ± 0.34 cm compared to 1.13 ± 0.27 cm in B (p 〈 0.001). Left ventricular posterior wall measured 1.03 ± 0.28 cm in A and 0.83 ± 0.23 cm in B (p 〈 0.01). 27 pts in grp B and only 9 in grp A had a history of previous myocardial infarction. Showing no difference at rest, wall motion score indexes raised under DSE in both groups and developed significantly higher scores in grp B at peak stress: 1.30 (1.0–1.90) compared to 1.18 (1.0–1.90) compared to 1.18 (1.0–1.75) in A. We observed typical chest pain more often in grp B. Unspecific symptoms and arrhythmogenic complications were not statistically different, with the exception of ventricular bigeminy which was more often observed in grp B. A decline in the diastolic blood pressure was observed in pts with very severe obstruction (〉 3.5 m/s, p 〈 0.05). Sensitivity of DSE was 84%, specificity 79%. No significant differences between pts with and without obstruction were observed. Summary: Intraventricular obstructions during DSE are often observed in pts with normal systolic function at rest and during peak stress, especially in the case of left ventricular hypertrophy. This flow pattern is not regularly correlated to clinical signs, symptoms or complications. It did not impair diagnostic accuracy concerning the detection of significant coronary artery disease in our pts.

Description / Table of Contents: Summary Pulmonary thromboendarterectomy (PTE) is a potentially curative procedure in chronic thromboembolic pulmonary hypertension. From June, 1989, to December, 1994, we performed PTE in 109 consecutive patients. Multiple changes in surgical approach and postoperative management have been implemented since January, 1995. We report the early results of 32 thromboendarterectomies performed from January, 1995, to January, 1997. Thirty-two patients (16 females, 16 males; mean age 55 years) were operated using cardiopulmonary bypass, deep hypothermia and circulatory arrest. Preoperative NYHA functional class was II in 21 and IV in 11 patients. Pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (mPAP) were elevated to 967 ± 238 dynes ˙ s ˙ cm-5 and 51 ± 11 mm HG respectively. The perioperative mortality rate was 9.3% (3 of 32). Twenty-nine survivors were weaned from mechanical ventilation and extubated after a mean of 35 hours (12 to 190 hours). PVR was reduced to 301 ± 151 dynes ˙ s ˙ cm-5 (p 〈 0.001) and mPAP was reduced to 28 ± 10 mm Hg (p 〈 0.001). Pulmonary thromboendarterectomy is an effective surgical procedure for chronic thromboembolic pulmonary hypertension. By means of modifications in surgical approach and postoperative management, early results can be improved and perioperative mortality can be decreased to less than 10%.

Description / Table of Contents: Summary Pulmonary thrombendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 ± 20 years) before and 18 ± 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 ± 18, postoperative 323 ± 280 dyn x s/cm5, p 〈 0.05; PAP preoperative 71 ± 40, postoperative 41 ± 40 mm Hg + right atrial pressure, p 〈 0.05). Enddiastolic and endsystolic RV area decreased from 33 ± 12 to 23 ± 8 cm2, respectively, from 26 ± 10 to 16 ± 6 cm2, p 〈 0.05. There was an increase in systolic RV fractional area change from 20 ± 12 to 30 ± 16% , p 〈 0.05. RV systolic pressure rise remained unchanged (516 ± 166 vs. 556 ± 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 ± 16 vs. 62 ± 12%). Echocardiographically determined cardiac index increased from 2.8 ± 0.74 to 4.1 ± 1.74 l/min/m2. A decrease in LV excentricity indices (enddiastolic: 1.9 ± 1 vs. 1.1 ± 0.3, endsystolic: 1.7 ± 0.6 vs. 1.1 ± 0.4, p 〈 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 ± 0.34 vs. 1.3 ± 0.8; p 〈 0.05); Peak E velocity: 0.51 ± 0.34 vs. 0.88 ± 0.28 m/sec, p 〈 0.05; Peak A velocity: 0.81 ± 0.36 vs. 0.72 ± 0.42 m/sec, ns; E deceleration velocity: 299 ± 328 vs. 582 ± 294 cm/sec2, p 〈 0.05; Isovolumic relaxation time: 134 ± 40 vs. 83 ± 38 m/sec, p 〈 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function – even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.