The purpose of this clinical study was to (1) evaluate mortality rates after surgical interventions for patients in cardiogenic shock (CS) secondary to acute coronary occlusion, acute ventricular septal defect (VSD) or acute valvular heart disease, (2) determine the pre-operative regional wall motion, and (3) ascertain the recovery of preoperative regional wall motion abnormalities after surgical intervention. The hospital records of twenty-five consecutive patients in CS were reviewed retrospectively. Regional wall motion was assessed preoperatively by ventriculography and postoperatively by 2D echocardiography (Sonotron Kardio VUE 60) after 1 and 3 days and at the day of discharge from the surgical ward (7-10 days). The left ventricle was divided in three segments according to the blood supply: LAD artery (antero-lateral wall), circumflex artery (lateral wall), and right coronary artery (inferior and basal wall). Regional wall motion was analyzed with the use of a scoring system in which grading was from 0 to 4 according to the following criteria: 0 = hyperkinesia, 1 = normokinesia, 2 = hypokinesia, 3 = dyskinesia, 4 = akinesia. Postmortem examination was performed in 8/9 patients. Data are presented as mean ± SD. Significant differences were defined as probabilities for each test of p < 0.05. The hospital mortality was higher for patients with acute coronary occlusion as compared to those with acute valvular disease or VSD (54.5%, 27.3%, 0%, resp.). The cause of death was cardiac in 7/9 patients. However, postmortem examination revealed loss by infarction of only moderate quantities of myocardium which could not explain the severe postoperative heart failure in those patients. Previous myocardial infarctions and preoperative cardiac arrest were significant risk factors for hospital mortality. In all patients with acute coronary occlusion (11/11) at least one region of the left ventricle was either a- or dyskinetic in the region supplied by the acute occluded vessel. In addition five patients had akinetic regions due to previous infarctions. The remaining remote myocardium was hypocontractile due to significant stenosis in coronary arteries supplying remote areas. Of 10 dyskinetic segments before surgical intervention, 5 were akinetic postoperatively, and only 5 developed slight hypokinetic contractions. The overall hypokinetic regions were not different as compared to the preoperative data (36.4% vs 39.4%). The normokinetic segments increased from 9.1% to 33.% (p < 0.05). All patients with an acute VSD had an akinetic segment (3/3) in the region supplied by the occluded vessel. The remote myocardium was hypokinetic in 2/3 patients whereas a normal contractility was observed in 1 patient. Postoperatively the hypokinetic areas resumed normal contractility, whereas the scars remained akinetic. Preoperatively, 4 of 11 (36%) patients with acute valvular disease had global left ventricular hypokinesis and 7 of 11 patients (64%) showed a normokinetic left ventricle. Postoperatively, hypokinesia was replaced by normokinesia in 2/4 patients. One patient with purulent myocarditis stayed hypocontractile and one patient developed an acute infarction of the entire left ventricle. We conclude from our data that a successful operative treatment for patients in cardiogenic shock requires (a) technically successful operative procedures (relieve the hemodynamic burden of valvular heart disease, closure of VSD, complete revascularization) and (b) immediate return of contractility in segments with previously abnormal wall motion. After normal blood reperfusion there is a delay in return of segmental contractility and this represents the cause of death in the majority of patients with cardiogenic shock. This clinical report confirms our experimental observations of the regional contractility in CS and provides further evidence for the importance of immediate reversal of regional wall motion abnormalities. The evolution and application of surgical principles to avoid stunning of the myocardium and careful selection of patients will improve the results of surgical treatment in patients with preoperative cardiogenic shock. Die vorliegende Studie wurde durchgeführt, um (1) die Mortalitätsrate von Patienten im kardiogenen Schock (kS) nach den auslösenden Ursachen aufzuschlüsseln, (2) die präoperativen regionalen Wandbewegungsstörungen zu erforschen und (3) die Reversibilität der präoperativen regionalen Wandbewegungsstörungen nach chirurgischer Therapie aufzuzeigen. 25 konsekutive Patienten mit kS wurden retrospektiv untersucht. Präoperativ wurde die regionale Wandbewegung durch Ventrikulographie erfaßt, postoperativ durch 2D-Echokardiographie (Sonotron Kardio VUE 60) nach 1 und 3 Tagen sowie kurz vor der Entlassung (7-10 Tage). Der linke Ventrikel wurde in 3 Zonen - entsprechend der Koronarversorgung - eingeteilt: RIA (antero-lateral), Circumflexa (lateral) und rechte Kranzarterie (inferior und posterior). Die regionale Wandbeweglichkeit erfolgte durch einen Score von 0 bis 4:0 = Hyperkinesie, 1 = Normokinesie, 2 = Hypokinesie, 3 = Dyskinesie, 4 = Akinesie. Von den 9 verstorbenen Patienten konnten 8 seziert werden. Die Daten werden als Durchschnittswerte ± SD angegeben. Signifikanzen werden ab einem p-Wert von < 0,05 angegeben. Die Krankenhaus-Mortalität war für Patienten mit akutem Koronarverschluß höher als für Patienten mit akuter Klappendysfunktion oder VSD (54,5%, 27,3%, 0%, resp.). Eine kardiale Ursache lag in 7/9 Patienten vor. Bei der postmortalen Untersuchung fanden sich jedoch nur mittelgroße Myokardinfarkte, die die postoperative Herzinsuffizienz nicht erklären konnten. Als signifikante Risikofaktoren der Mortalität fanden sich alte Myokardinfarkte und die Notwendigkeit zur präoperativen Wiederbelebung. In der Gruppe mit akutem Koronarverschluß war mindestens eine...