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Biomedical subjects

A M Katz

Publications and source records attributed to A M Katz.

At least 19 recordsLinked to original sources
PubMed1999

Interval-force relation is unaffected by the presence of cardiomyopathy or coronary artery disease in patients with atrial fibrillation.

BACKGROUND: We tested the hypothesis that cycle length-dependent cardiac contractility in atrial fibrillation is primarily governed by the negative interval-force relation in patients with normal and depressed systolic function. METHODS AND RESULTS: We performed two-dimensional guided M-mode echocardiography in 41 patients (mean age, 69 +/- 4 years; range, 48 to 92 years; 19 men, 11 women). Twelve patients had objective evidence of left ventricular systolic dysfunction (CMP; mean ejection fraction, 37% +/- 7%) in the absence of coronary artery disease (CAD), 13 patients had documented CAD (mean ejection fraction, 43% +/- 6%), and 16 patients had normal resting left ventricular systolic function (mean ejection fraction, 58% +/- 7%). Simultaneous beat-to-beat blood pressure, end-systolic and end-diastolic dimension, circumferential velocity of fiber shortening (Vcf), and end-systolic wall stress (ESWS) were calculated for all patients. All three groups showed a significant linear relation between beat-to-beat Vcf and Vcf corrected for afterload (represented as the Vcf/ESWS ratio) and preceding cycle length. There was, however, no significant difference in the relation between either of these variables and cycle length among the three groups. There was also no difference in the rate of change in either Vcf or Vcf corrected for afterload (Vcf/ESWS ratio) from beat-to-beat among the three groups. Control patients with normal systolic function showed greater Vcf at any given cycle length compared with patients with CMP or CAD. CONCLUSION: Our data show that, for each beat in atrial fibrillation, Vcf and Vcf/ESWS ratio are decreased after shorter cycle lengths and increased after long cycles, but there is no significant attenuation of this effect in patients with systolic dysfunction with or without coronary disease compared with controls. Thus, the negative interval-force relation, the predominant determinant of beat-to-beat variation in contractility in atrial fibrillation, is preserved in patients with CAD or reduced left ventricular systolic function.

Aged↗
PubMed1998

Is the failing heart energy depleted?

This article takes three different approaches to the question of whether the failing heart is in an energy-starved state. A brief historical overview introduces the issue and points out problems in both models and methods. Second, current information regarding the energetic state of the failing heart is examined. Finally, the mechanistic and therapeutic implications of a defect in energy production are described.

Adenosine Diphosphate↗
PubMed1998

Behçet's disease: summary notes.

The intention of the Summary Notes section is to provide the practitioner and trainee with a current, concise reference source to dermatologic diseases and to serve as a form of Continuing Medical Education. Each installment will deal with a specific disease. When included, the pretest questions indicate some of the areas to be covered and will challenge your present knowledge of the material before reading further. The self-assessment post-test questions appear on page 89; the answers are on page 101.

Behcet Syndrome↗
PubMed1997

Molecular biology of calcium channels in the cardiovascular system.

Calcium ions are key intracellular messengers in the cardiovascular system. Calcium homeostasis is regulated by an extracellular cycle, which controls the entry and removal of calcium between the cytosol and extracellular space, and an intracellular cycle, which controls calcium fluxes between the cytosol and intracellular stores in the sarcoplasmic reticulum. Several protein families mediate these calcium fluxes including those that (1) regulate the entry of calcium into the cytosol; (2) recognize calcium within the cytosol; and (3) remove calcium from the cytosol. Intracellular calcium binding proteins (the "E-F hand" proteins) recognize the appearance of calcium in the cytosol; in the heart and vascular smooth muscle, these proteins initiate excitation-contraction coupling. Calcium efflux occurs via adenosine triphosphate (ATP)-dependent calcium pumps and sodium-calcium exchangers, while two families of channels--intracellular release calcium channels and plasma membrane calcium channels--regulate calcium entry into the cytosol. The plasma membrane calcium channels, which include the L- and T-type channels, are of the greatest clinical interest because they are targets for pharmacologic therapy. T-type calcium channels, which activate contraction in vascular smooth muscle but have little or no role in cardiac excitation-contraction coupling, appear to be involved in signal transduction pathways that promote cell growth and proliferation. Calcium channel blockers that selectively block T-type calcium channels, therefore, offer a novel approach to cardiovascular drug therapy.

Calcium↗
PubMed1997

Evolving concepts of heart failure: cooling furnace, malfunctioning pump, enlarging muscle--Part I.

Understanding of the causes of dyspnea and anasarca, the cardinal features of heart failure, has changed dramatically since Greco-Roman times, when sputum and pleural effusions were thought to originate in the brain, and the heart was believed to heat and distribute the vital spirit. It was not until the seventeenth century, when Harvey demonstrated that the heart was a pump and autopsy descriptions revealed valve abnormalities that interfered with the circulation, that it became possible to identify the role of heart disease in causing shortness of breath and edema. Morgagni's recognition, toward the end of the eighteenth century, that overload caused the heart to enlarge was followed less than 50 years later by Corvisart's distinction between hypertrophy and dilation. Differences in the architecture of failing hearts focused attention of nineteenth-century clinical scientists on the myocardial response to overload, and by the end of this century overload-induced hypertrophy was recognized not only to have immediate adaptive effects, but also to cause progressive degeneration of the heart muscle. This focus on the failing myocardium ended in the early years of the twentieth century, when new discoveries in hemodynamic physiology shifted attention to pressure and flow abnormalities caused by the then prevalent rheumatic valvular heart disease. During the past decade, new emphasis on prognosis, along with realization that drugs intended to correct hemodynamic abnormalities often had adverse effects on survival, has led to a reexamination of the biology of the failing heart. As a result, the focus in heart failure research has returned to the myocardium. This article reviews some of the misconceptions and errors of early physicians, who, while often careful and intelligent observers, lacked the means to explain and treat heart failure. It is hoped an appreciation of the evolving concepts of heart failure will help the reader meet today's challenge of incorporating new information from molecular biology that holds the key to further progress in understanding the causes and therapy of this syndrome.

Cardiology↗
PubMed1996

Protein families that mediate Ca2+ signaling in the cardiovascular system.

Five protein families are known to participate in the signaling cascades that enable calcium ions (Ca2+) to regulate functions in the cardiovascular system. Ca2+ signaling is involved in muscle contraction, pacemaking, and perhaps cell growth and differentiation. Recent evidence about the molecular properties of Ca2+ regulatory proteins has suggested possibilities for new therapeutic agents, including T-type Ca2+ channel blockers for patients with cardiovascular disease. This article reviews new information about Ca2+ signaling in the heart, vascular smooth muscle, and other tissues.

Calcium↗
PubMed1996

Hearing the patient's 'voice': toward a social poetics in diagnostic interviews.

In this article we introduce a special practice that we have called the practice of a "social poetics", and explore its nature. The setting is a Primary Care Clinic at a large urban teaching hospital in the northeast of the U.S. As we describe it, the practice is at first conducted by a third person who occupies the position of a "cultural go-between" and who mediates between doctors and their patients in diagnostic interviews. Her task is to be open to being 'arrested', or 'moved' by, certain fleeting, momentary occurrences in what patients do or say. For sometimes in such moments, in our responding to the unfolding motions of their whole body and voice-as they respond to the circumstances in which they find themselves-we can begin to sense that the unique nature of their 'inner world of pain and suffering' is like for them. The practice of a social poetics entails a new relational attitude to the patient's use of words, an attitude that invites a creative, poetic sensibility, as well as a 'boundary crossing' stance that creates comparisons useful in relating what patients say to the rest of their lives. In elucidating the nature of such a practice further, we draw on the work of Wittgenstein, Bachelard, and Bakhtin. Together, these can lead to a new diagnostic practice that enables those involved in it to create, within the practice itself, both ways of talking that draw attention to the new possibilities for interaction the practice itself momentarily makes available, and ways of talking relevant to realizing these possibilities.

Anthropology, Cultural↗
PubMed1996

Calcium channel diversity in the cardiovascular system.

The flux of calcium ions (Ca2+) into the cytosol, where they serve as intracellular messengers, is regulated by two distinct families of Ca2+ channel proteins. These are the intracellular Ca2+ release channels, which allow Ca2+ to enter the cytosol from intracellular stores, and the plasma membrane Ca2+ channels, which control Ca2+ entry from the extracellular space. Each of these two families of channel proteins contains several subgroups. The intracellular channels include the large Ca2+ channels ("ryanodine receptors") that participate in cardiac and skeletal muscle excitation-contraction coupling, and smaller inositol trisphosphate (InsP3)-activated Ca2+ channels. The latter serve several functions, including the pharmacomechanical coupling that activates smooth muscle contraction, and possibly regulation of diastolic tone in the heart. The InsP3-activated Ca2+ channels may also participate in signal transduction systems that regulate cell growth. The family of plasma membrane Ca2+ channels includes L-type channels, which respond to membrane depolarization by generating a signal that opens the intracellular Ca2+ release channels. Calcium ion entry through L-type Ca2+ channels in the sinoatrial (SA) node contributes to pacemaker activity, whereas L-type Ca2+ channels in the atrioventricular (AV) node are essential for AV conduction. The T-type Ca2+ channels, another member of the family of plasma membrane Ca2+ channels, participate in pharmacomechanical coupling in smooth muscle. Opening of these channels in response to membrane depolarization participates in SA node pacemaker currents, but their role in the working cells of the atria and ventricle is less clear. Like the InsP3-activated intracellular Ca2+ release channels, T-type plasma membrane channels may regulate cell growth. Because most of the familiar Ca2+ channel blocking agents currently used in cardiology, such as nifedipine, verapamil and diltiazem, are selective for L-type Ca2+ channels, the recent development of drugs that selectively block T-type Ca2+ channels offers promise of new approaches to cardiovascular therapy.

Animals↗