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In 3 patients with a congenital aneurysm of the membranous portion of the ventricular septum diagnosis could be made by angiography. One of these patients was clinically asymptomatic, while the two other patients were transferred for surgery because of right ventricular outflow tract obstruction or intracardiac left-to-right shunt. These both patients underwent successful open heart corrections. Aneurysms with a different intracardiac localization could be found. One of the cases represents an unusual association with corrected transposition of the great vessels.

Although left ventricular aneurysmectomy (LVA) is a common surgical procedure, the late functional and hemodynamic results have not been well defined. This presentation describes our results with LVA in 135 patients operated between 1969 and 1979. Associated procedures were performed in 57 (42%) including coronary bypass grafting in 50, valve replacement in 5, closure of ventricular septal defect in 2, or combinations of these in 3 patients. One hundred four of the 122 hospital survivors were followed from 2 to 107 months (mean = 37 months). There were 13 hospital deaths (9.6%), 12 late deaths (9.8%) and an actuarial 5-year survival rate of 77%. Clinical improvement of preoperative heart failure occurred in 82%, and of angina in 70%. Only 33 patients (30%) returned to normal work. Bicycle exercise testing in 70 patients showed normal working capacity in 41 (59%). Recatheterization in 49 patients showed no significant changes in left ventricular end-diastolic pressure or cardiac index, and a borderline reduction of the total ejection fraction. Ventricular arrhythmias were detected by long-term ECG in 70% of all patients after surgery. Of those with preoperative life-threatening arrhythmias, rhythm improvement was noted in 50%, but only 2 of 13 patients were free of arrhythmias after operation. This study demonstrates a greater frequency of postoperative symptomatic and functional improvement as compared to hemodynamic and ECG improvement. Ventricular tachyarrhythmias originating from post-infarct scars increased intra- and postoperative risk and aneurysmectomy alone is considered insufficient for treatment of these disturbances. Further electrophysiologic investigations are needed and additional surgical measures may be necessary to improve the subset of patients with life-threatening arrhythmias.

Pulmonary arteriovenous fistula is not a rare congenital malformation, but obviously most often it is a very late diagnosis. Moreover the disease is associated with a high risk of serious complications, namely cerebrovascular accidents. Two patients, an one month old infant and an 8 years old boy with typical symptoms and signs are presented. Both of them were operated upon successfully. It is concluded, that the diagnosis of solitary pulmonary arteriovenous fistula should lead to immediate operation, which is technically easy and of low risk only, even in infancy. Conservative surgery is recommended without sacrifice of healthy lung tissue, i.e. local excision or segmental resection in subpleural lesions and lobectomy for deep-seated fistulas.

The clinical syndrome of paraplegia following acute occlusion of the infrarenal aorta may be caused by either ischemic spinal cord damage or ischemia of the cauda equina and sacral nerve roots and ganglia. The neurologic manifestations are similar and therefore specific anatomic diagnosis is difficult. From October 1972 to February 1975 a total of 31 patients with infrarenal aortic occlusion were treated at the Medizinische Hochschule in Hannover. In nine cases the occlusion up to the renal arteries was acute. Three of these patients presented beside acute ischemic manifestations on both legs and the lower abdominal wall, neurologic symptoms of paraplegia. The anatomic and hemodynamic aspects of ischemic spinal cord damage and those of ischemic lesions of the cauda equina and peripheral nerves are discussed. There appear to be three main mechanisms responsible for vascular paraplegia following acute infrarenal occlusion of the aorta: 1. it may be caused by thrombotic occlusion of a major radicular artery which arises below the level of occlusion. 2. it may be produced by thrombosis of a lumbar collateral acting as major supply to the cord when arteriosclerotic narrowing of the major radicular artery is present. Especially in states of severe hypotension critical interference of blood supply to the spinal cord will result. 3. Paraplegia by ischemia of the cauda and peripheral nervous tissue may also follow prolonged interruption of circulation to this area supplying spinal vessels from low lumbar and sacral arteries.

A case of intramyocardial calcification is presented. The etiology can neither be explained by history, nor by clinical or histological examination. The diagnosis was made by cardiac catheterization and angiocardiography. This showed that the calcification had occurred mostly in the myocardium of the left ventricle and interventricular septum. Because of chronic heart failure surgery was indicated and large amounts of the calcified mass were removed by means of an open heart operation. One and a half years later the patient is much improved though clinical signs of heart failure persist. Possible causes of myocardial calcification are discussed and the problems of surgical intervention outlined.

The results of 100 patients with primary active infective endocarditis treated surgically are presented. Hospital and late mortalities as well as postoperative complications in patients operated electively and not showing paravalvular infection approach those of routine procedures while frank circulatory failure and uncontrolled sepsis were associated with high death and complication rates. Paravalvular extension of the infection was associated with frequent postoperative leakage, reoperations and mortality. The present operative choices in eradicating paravalvular disease are described and the great importance of early operation is stressed.

11 patients were studied 6 to 12 months after aortic valve replacement with Lillehei-Kaster-prosthesis (LKP). We found pressure gradients (deltaP) at rest of 31 mmHg (7 to 52 mmHg), 37 mmHg (8 to 69 mmHg during exercise and 8 mmHg during ventricular pacing delta P was influenced by stroke volume and valve size, but not by the width of the aorta. The opening angle alpha of the disc was only 62degrees and depended on stroke volume and on the orientation of the value within the aorta. The blood passed the valve ring only through the larger part of the orifice, the opening area was only 50% of the given area. Thus in practice the LKP does not perform to manufacturers specification.

Die chirurgische Korrektur angeborener Herzanomalien wird durch das Bestehen eines Hochdrucks im Lungenkreislauf erheblich kompliziert. Um einer Losung dieses Problems naherzukommen, wurde im Tierversuch bei Hunden eine pulmonale Hypertension kunstlich erzeugt, indem zwischen der Arteria subclavia und einer Lappenarterie der linken Lunge eine End-zu-End-Anastomose angelegt wurde. Dies fuhrte zur Erhohung des Drucks in diesem arterialisierten Lappen auf durchschnittlich das Doppelte des normalen Drucks. Die mit Hilfe eines elektromagnetischen Flowmeters gemessene Durchblutung stieg in Abhangigkeit von der Weite der Anastomose bis zum Dreifachen der Norm an. Gleichzeitig wurde ein Druckanstieg im linken Vorhof festgestellt. Die sechs Monate nach der ersten Operation vorgenommene Rekatheterisierung ergab bei sieben von zehn Hunden einen weiteren Anstieg des Blutdrucks im Lungenkreislauf. Bei weiten Anastomosen entstand ein Lungenodem oder es kam durch den erhohten Druck zu einer Schadigung der Lungengefase. Diese Versuche, die noch nicht abgeschlossen sind, haben bereits gezeigt, das eine Drucksteigerung auf das Doppelte der Norm ausreicht, um die Lungengefase so zu schadigen, das es zur Steigerung des Gefaswiderstands kommt. Eine Ubersicht uber die Literatur ergibt, das es auf dem Gebiet der Herz-Kreislauf-Dynamik gerade die pulmonale Hypertension ist, deren Ursprung noch ungeklart ist und welche weiterer Erforschung bedarf. The surgical correction of congenital heart disease is complicated by the presence of pulmonary hypertension. To shed more light in this phenomenon pulmonary hypertension has been produced experimentally in dogs by establishing an end to end anastomosis between the subclavian artery and one lobe artery of the left lung. Generally mean pressures in this arterialized lobe increased more than twofold the normal level; blood flow, measured by means of electromagnetic flowmetry, increased threefold depending upon the size of the anastomosis. There was a simultaneous rise of left atrial pressure. On recatheterization 6 months after the first operation a further increase of pulmonary pressure could be recorded in 7 out of 10 dogs. Large shunts produced lung edema or destruction of the pulmonary vessels by the high pressure impact. These experiments, which are still in progress, have shown that an increase of pressure of twice the normal level is enough to produce changes of the pulmonary vascular bed, which results in an increase of pulmonary vascular resistance. Discussion of the literature reveals, that the origin of pulmonary hypertension remains a moot point in cardiovascular dynamics and requires further investigations. La chirurgie reparatrice d'anomalies cardiaques congenitales se complique considerablement par suite de l'existence d'une hyperpression de la petite circulation. Pour solutionner ce probleme supplementaire nous avons provoque artificiellement une hypertension pulmonaire chez des chiens. Une anastomose bout a bout est placee entre une artere du poumon gauche et l'artere sous-claviere. Ceci conduit a une augmentation de pression dans le territoire de cette artere. Cette augmentation de pression est en moyenne le double de la pression normale. Nous mesurons l'irrigation sanguine au moyen d'un flowmeter electromagnetique. Cette irrigation sanguine monte au triple de la normale sur tout le parcours de l'anastomose. En meme temps on remarque une augmentation de la pression de l'oreillette gauche. Apres six mois nous procedons a un nouveau catheterisme. 6 chiens sur 7 presentent une hyperpression de la petite circulation. Dans les larges anastomoses apparait un oedeme pulmonaire ou des lesions des vaisseaux pulmonaires suite a la haute pression. Ces essais, qui ne sont pas encore termines, ont deja montre qui une augmentation de pression du double de la normale suffit pour endommager les vaisseaux des poumons. Cela apparait comme une augmentation de resistance des vaisseaux. Un coup d'oeil sur la litterature montre que c'est justement dans le domaine de la dynamique de la circulation et du coeur qu'apparait l'hypertension pulmonaire dont l'origine n'est pas encore eclairci. Le besoin de pousser plus loin les investigations est hautement souhaitable.

3 cases of coronary reoperations are described in which a leftsided thoracotomy offered considerable advantages. This approach is recommended for certain types of reoperations on the left coronary system.

Adequate surgical relief of left ventricular outflow obstruction (LVOO) in transposition of the great arteries (TGA) with atrio-ventricular concordance and intact ventricular septum, may to a significant degree depend on the severity of the lesion and the anatomic location of the ventricular septum and the mitral valve. A new approach to resection of subpulmonary obstruction in TGA through the left atrium and the retracted mitral valve is described. In contrast to dynamic stenosis, transmitral resection of a fixed subpulmonary narrowing will usually lead to a significant decrease of LVOO in TGA, with good clinical results.

In the Fontan operation and numerous of its modifications for hemodynamic correction of tricuspid atresia, extraanatomical conduits placed anteriorly are inevitably at particular risk of obstruction. This report describes the construction of a direct retroaortic left atriopulmonary anastomosis supplemented by an intraatrial rerouting of the systemic venous return. Hemodynamic considerations and growth potential may render this method suitable for primary intracardiac repair at all ages.

In this review the present state of cardiac valve replacement is summarized on the basis of the literature and personal experience in approximately 1500 cases, using various prosthetic models. Durability, hemodynamic performance at rest and during exercise, and thromboembolic risk are considered in particular and our choice of the various valve models is discussed on these grounds. The long-term durability has been significantly improved and has possibly been solved in the more advanced mechanical valves, while this question is still open in the present biological prostheses. Hemodynamic performance is considered less than optimal in all conventional mechanical prostheses and in the xenografts. Pressure gradients are abnormal in all mechanical as well as in stented biological prostheses, the latter being less likely to solve the problem of a narrow aortic root. The significantly lower incidence of thromboembolism and total valve thrombosis and the absence of anticoagulation accidents in patients with bioprostheses has tipped the balance for the present in favor of the latter, particularly in mitral valve replacement and certainly in all those patients in whom anticoagulation in impossible, unlikely, or undesirable.