Assessment of cardiac energetics at the level of ATP-synthesis, chemomechanical energy transformation and whole organ dynamics as a function of haemodynamic load, ventricular configuration and oxygen- and substrates supply is basic to understanding cardiac function under physiological and pathophysiological (hypertrophy, hypoxia, ischaemia and heart failure) conditions. Moreover, cardiac energetics should be an important consideration in the choice and application of drugs especially in the case of vasodilators, inotropic agents and in cardioprotective measures. Only by considering energetics at the subcellular, cellular, and whole-heart level we can arrive at a better understanding of cardiac performance and ultimately better clinical judgement and drug therapy. Quantification of myocardial energetics will also help to determine the optimal time for surgical interventions such as valvular replacement or aneurysm resection. The present volume is the outcome of an international symposium on cardiac energetics held in Gargellen/Montafon (Austria), June 1986. The contributions will certainly help bridge the existing gap between basic research involving isolated structures and that involving the whole organ, on the one hand, and render the results derived from basic research applicable to clinical problems, on the other hand.

Alteration of excitation-contraction coupling in the failing human heart was deemed an interesting subject for a dialogue between basic scientists and clinical researchers in continuation of previous Gargellen Conferences concerned with the function of the normal and failing human myocardium. In 1987 basic mechanisms and clinical implications of then new insights into cardiac energetics was followed by a comprehensive review of inotropic stimulation and myocardial energetics in 1989. Here, we undertook a re-evaluation of the principles of inotropic stimulation and of its potential therapeutic value, based on new observa tions from experiments with human myocardium. In 1992 the risk due to myocardial phenotype change as a consequence of adaptation in heart failure was published. Here, alterations of subcellular structures and functions as a consequence of chronic heart failure, summarized as phenotype change, could be described as an essential characteristic of the failing human myocardium. This topic was discussed in greater depth in the volume "Cellular and Molecular Alterations in the Failing Human Heart," considering both the sarcolemma and the phosphodiesterases, as well as excitation-contraction coupling and contractile proteins, extracellular matrix, and mitrochondrial function."

Primary myocardial disease, nowadays referred to as congestive or, more re cently, dilating cardiomyopathy, comprises disorders of varied etiology. Most oftenly the pathogenetic mechanism or causative agent remains unknown. The significance of inflammatory processes, i.e. myocarditis in a wider sense as the etiologic factor has been debated for many years. In a few instances, especially in children and newborns viral infections can be incriminated. In adults this etiology can be ascertained only in rare instances. And it has remained entirely uncertain if, or under which circumstances, and how often virus myocarditis can lead to a chronic disorder of the heart, namely dilated cardiomyopathy. Although it would seem conceivable that an immunological response to an infectious agent might induce parenchymal damage with subsequent loss of cellular function and structural integrity of permanent nature, i.e. dilatation, functional deterioration and dysrhythmias, numerous attempts to establish such a pathogenetic mechanism have not yet furnished convinicing results. Therefore the reader will direct his attention specifically to the respective contribution in this volume. Morphologic studies have yielded a host of new and intriguing findings in cardiomyopathy, but have likewise failed to settle the basic question as to which etiology can be held responsible in a given case, especially if an inflam matory process can be incriminated. Specific processes such as sarcoidosis of the heart undoubtedly furnish examples of chronic inflammation as a cause of dilating cardiomyopathy. This disorder, however, as a specific inflammato ry myocardial affection, i.e. myocarditis, is encountered only infrequently."

Inspite of considerable progress in prevention, diagnosis, and treatment, pulmonary embolism has remained a threat to the patient and a challenge for the physician both in conservative, as well as in operative disciplines. Pulmonary embolism is according to pathology observations still the most frequently overlooked clinical diagnosis. In 1-5 per 100 autopsies, clinically unexpected pulmonary emboli are found. In addition, the sequelae of recurrent pulmonary emboli, the syndrome of pulmonary hypertension with or without right heart failure, continues to present a therapeutic dilemma - and no progress is in sight. In intensive care medicine pulmonary embolism, either acute, massive, and/or recur- rent, continues to be both a therapeutic as well as a preventive challenge mobilizing pharmacotherapeutic, catheter-interventional, and operative resources. Diagnostic, therapeutic, and preventive strategies are currently in use. Their basis, however, seems surprisingly thin, as far as our knowledge on the natural course of this chameleon-like illness with and without fibrinolytic, anticoagulative, catheter or opera- tive treatment is concerned. A large European multicenter register has been initiated by Professors Kasper and Geibel with the help of Boehringer Ingelheim Pharmaceutics, in order to better describe the natural course of pulmonary embolism under current treat- ment modalities. Furthermore, recently the clinical significance of the valve patent foramen ovale as a source of paradoxical emboli is beginning to be better understood. Many concepts therefore require revision.