Lionel H. Opie – författare

Living Longer: The heart-mind connection is written for all those who strive for optimal long-term health and the maximal functioning of their hearts and minds. Today's problem for the health-conscious individual is information overload - new health studies pour out almost daily from newspapers, radio stations and television networks. Many of the reports are contradictory and often misleading. In this book, Professor Opie sifts through the available information on the vast number of possible health promotion changes, varying from increased exercise to aspirin to green tea, and diets from Atkins to the vegetarian, with the aim of grading the validity of the evidence, asking questions such as, "Just how true are the studies" and "Just how compelling are the facts they claim"? Living Longer guides the reader through this morass of information with the message that just five key steps taken now will promote long-term health benefits for heart and mind and give protection from future heart disease and brain deterioration.

Stunning is potentially an important complication of myocardial reperfusion. In contrast, hibernation is an important complication of myocardial ischemia. This book presents different viewpoints on these subjects, taken from a series of peer-reviewed articles which first appeared in "Cardiovascular Drugs and Therapy", and now in this book. In addition, a certain number of articles were directly invited for the book. The introductory article is by Eugene Braunwald, who with Kloner introduced the term "myocardial stunning" in 1982. The experimental phenomenon had first been described by Heyndrickx et al. This important concept of stunning is examined from a number of points of view in a series of articles which clarify the experimental causes and the clinical implications. The section on hibernation is introduced by Tubau and Rahimtoola, the latter having first propounded the concept in 1989. The difference between stunning and hibernation is that stunning is essentially a post-ischemic dysfunction of the myocardium, temporary in nature, occurring at a time when coronary blood flow is apparently normal or supranormal.Hibernation, on the other hand, is a condition of reduced contractile activity, the direct result of chronic ischemia and hence a sign of a tolerable reduction in blood flow. Possibly, the reduction in contractile activity of the hibernating heart balances the reduction in the oxygen availability (the "smart heart" of Rahimtoola). This non-contractile heart is hibernating, awaiting the return of summer after winter, and willing to contract normally again whenever warm coronary blood is restored. It is certain that the concepts of stunning and hibernation are here to stay, that they have or will have clinical relevance, and that the search for the most appropriate diagnosis and therapy for each condition is now under way. Hence, a greater understanding of the experimental work which underlies these two conditions is highly appropriate.

"Drug Evaluation in Angina Pectoris" has two fundamental aims: the first is to review the methodological aspects of drug evaluation in stable and unstable angina pectoris; the second is to provide a logical and methodological background for future studies aimed at assessing the ability of medical treatment to improve prognosis. Part I updates the pathophysiology, clinical presentation and prognosis of angina pectoris. Part II aims to "put in numbers" the symptoms and signs of myocardial ischemia, starting from a revision of the currently used parameters. It is important to quantify the variability of the disease for the correct design of clinical trials, a subject dealt with in Part III, which also discusses some clinico-pharmacological aspects of therapy. Part IV is a review of the drugs currently used for the treatment of stable and unstable angina, and particularly considers some important unresolved issues concerning their use.The current FDA and EC guidelines for the evaluation of antianginal drugs are briefly discussed in Part V, giving clinical investigators insight into how antianginal drugs are evaluated by regulatory agencies and what is considered as proof of a valid efficacy/tolerability ratio. "Drug Evaluation in Angina Pectoris" aims to assist discerning cardiologists, pharmacologists and advanced students of cardiology, as well as innovative pharmaceutical companies, all of whom need to understand what angina is, how to evaluate treatment, and how to judge the agents used in its treatment.

The chief current clinical indications for the use of nitrates remain ischemic heart disease in all its manifestations, and as adjuvant therapy in congestive heart failure. One study has shown a 17% fall in mortality when IV nitrates are combined with the ACE inhibitor lisinopril. Nitrates alone had no effect, and lisinopril alone reduced mortality by 12%, so it is logical to propose that the ACE inhibitor reduces or minimizes nitrate tolerance. Second, it has recently been suggested that concurrent treatment with hydralazine avoids or lessens nitrate tolerance in the treatment of congestive heart failure, thus explaining the sustained effect exerted by nitrates when given concurrently with hydralazine. This review of current research in th euse of nitrates as cardiovascular drugs covers such topics as: mechanisms of action of nitrates; Short and long-acting oral nitrates for stable angina pectoris; Nitrates in myocardial infarction; and nitrates in congestive heart failure.

Calcium antagonists are now regarded as the most important advance in cardiac drug therapy since the advent of beta-adrenergic blocking agents. Acting ba­ sically as vasodilators-though with many other com­ plex mechanisms especially in the case of the anti­ arrhythmic calcium antagonists, these agents have grown in importance to become among the therapeutic agents of first choice for angina pectoris and hyper­ tension. The major aim of the present book is to present the clinician with the information needed for the practical use of calcium antagonists. What do all the numerous and often conflicting trials say? Do these agents really work? If so, which agent and in what dose? How do the three front runners, verapamil, nifedipine and diltia­ zem compare in the efficacy and side-effects with each other? How do the new second generation agents, now entering the North American market, slot in and com­ pare with the three first-liners? When the gloss is taken away from the advertisements, what is really left? The strong clinical bias of the present book should be complimented by further reading of books slanted towards fundamentals. One of the most important and recent of these is that by Dr Winifred Nayler (Calcium Antagonists, Academic Press, 1988). That book should be basic for essential background knowledge in the area of calcium antagonists. The important basic contribu­ tions of Fleckenstein deserve emphasis.

Nitrates remain among the most commonly used therapeutic agents in cardiology. That they can re­ lieve pain in angina pectoris has been known at least since 1867, when Lauder Brunton described their clinical use. Now, almost 130 years later, we are constantly learning more about their optimal use in anginal syndromes. For example, there is no doubt that nitrate tolerance occurs, but equally no doubt that certain drug dosages help to attenuate such toler­ ance. Thus, our understanding of nitrate tolerance has been taken further by the advent of new nitrate preparations and by studies at a basic science level. The current intense interest in nitrates has been rekindled by the growing emphasis on the role of the endothelium in the production of nitric oxide, a basic cardiovascular regulator. If nitric oxide is vasodilator and protects the vascular endothelium, then nitrates should also have similar properties. Hence this book starts off with the role of the endothelium and ni­ trates in vasodilation. Next, the mechanisms of ac­ tion of nitrates are considered with emphasis on the role of cyclic GMP. The chief limitation to the use of nitrates lies in nitrate tolerance. After carefully looking at all the evidence, the authors of the third chapter conclude that the mechanism is likely to be multifactorial. The mechanism responsible for the tolerance still remains unknown. In vitro tolerance may be due to enhanced production of vascular superoxide [1].