Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage [antikvár]

FOREWORD In our age of expeditious information, any book of some volume which would take a while to read is in itself somewhat antiquated; it is especially so for a treatise devoted to such a wonted problem as protecting the heart from stress and ischemia. Therefore the author feels a need to explain himself going back to the good old days when a manuscript submitted for judgment to a respectable university used to be prefaced with a brief listing of the basic propositions, "theses" that had not theretofore been set forth in other works. I believe that just as in the past, this enables the reader to decide whether to spend time on further reading or to make better use of it. Hence I state that this book has been written to substantiate the following ideas concerning heart damage and heart protection. 1. Stress and ischemia, and most often combinations thereof, are of paramount importance in the development of major heart diseases, and nevertheless these two factors are deeply unequal both in their place in cardiac pathology and in the extent of previous study. Indeed, genetic defects in the hepatic cholesterol-eliminating systems and excess cholesterol in food with ensuing atherogenic dyslipidemia and stenosing coronary atherosclerosis, are generally recognized as the key link in the pathogenesis of ischemic heart disease (IHD).* The position of stress in heart pathology proves to be less definite. On the one hand, an excessively long and strong stress reaction is known to provoke atherosclerosis, spasm, thrombosis, overloading of the heart, and other conditions engendering or aggravating ischemia. On the other hand, are there indeed self-contained, noncoronarogenic, not ischemia-linked, direct stress damages to the heart? What are the concrete regulatory, biochemical, morphological, and physiological substrata of such damage? Can such damage to the heart evolve because of stress disorders in other organs? Finally, what is the clinical significance of such nonischemic stress heart damages, in particular, for the pathogenesis of noncoronarogenic cardiosclerosis, arrhythmias, and sudden cardiac death? Diagnoses such as **stress heart" and "stress arrhythmic heart disease" are not found in the accepted nosology. Yet the thought that cardiac stress damage is a reality in many a patient and not at all need be associated with ischemic disease is most obviously present in the minds of more than a few cardiologists. The idea haunts the clinics and conferences. Therefore, Chapter 1 of this monograph is devoted to analyzing the noncoronarogenic stress damage to the heart, and considering their probable role in the pathogenesis of chronic stress cardiopathies, nonischemic arrhythmias, and sudden cardiac death. In other words, in this Chapter we sought to unfold the concept of "primary stress damage of the heart" and to bring it into use in modem cardiology. 2. The decisive role of coronary atherosclerosis in the pathogenesis of ischemic heart disease does not at present raise any doubt, but still leaves open some important questions. Thus, it has been shown that at the same degree of coronary stenosis, the clinical manifestations of IHD can be vivid — or altogether lacking. The fatal sequelae of IHD — myocardial infarction or sudden cardiac death — may occur in moderate coronary atherosclerosis that is of no such consequence for other persons. Moreover, these dramatic events happen even when the coronary arteries are intact. Facts of this kind make inevitable the question of the weight of the stress factor, first, in the pathogenesis of dangerous arrhythmias, fibrillation, and sudden cardiac death, and second, in the formation of atherosclerosis, thrombosis, and spasm, i.e., in the pathogenetic progression of the ischemic disease proper. Therefore, Chapter 2 deals consecutively with these matters, using experimental, epidemiological, and some clinical data to discriminate, on the one hand, the stress arrhythmic disease of the heart from the ischemic disease as such, and to demonstrate, on the other hand, that the two conditions are interconnected. * References to all works used in this Foreword are given at the end of the relevant Chapters. y.i;.'-/