Triggers and timing of cardiac events
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| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
1996
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| Schriftenreihe: | Cardiology clinics
14,2 |
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| Online-Zugang: | Inhaltsverzeichnis |
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| 245 | 1 | 0 | |a Triggers and timing of cardiac events |c Prakash C. Deedwania ..., guest ed. |
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Datensatz im Suchindex
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| adam_text | IRK.;c;i KS AM) TIMINC; OI: CARDIAC I:VI[VIS
CONTENTS
Foreword ix
Michael H. Crawford
Preface xi
Prakash C. Deedwania and Geoffrey H. Tofler
Epidemiologic Aspects of Orcadian Patterns of Cardiovascular
Disease and Triggers of Acute Cardiac Events 175
Robert J. Goldberg
An appreciation of the existence of circadian variation in association with
the onset of acute coronary disease and of the public health and clinical
implications of this temporal nonrandom disease occurrence with possible
precipitating factors has been gained only over the past decade. Data
providing support for the existence of circadian variation in the onset of
acute coronary heart disease and the role of acute triggers are reviewed.
Circadian Patterns and Triggers of Sudden Cardiac Death 185
Robert W. Peters
Sudden cardiac death and other acute cardiovascular events have been
demonstrated to occur in certain temporal patterns. The study of these
patterns may yield important clues to the pathophysiology of the disease
process. Most studies of the timing of onset of sudden cardiac death have
revealed a prominent midmorning peak, thought to be related to a surge
in catecholamines associated with arising and assuming the upright pos¬
ture, that is blunted or eliminated by beta blockers. In addition, some
studies have also shown a secondary peak in late afternoon or early
evening of uncertain cause. The development of third generation im
plantable cardioverter defibrillators with memory capabilities offers a
unique opportunity to accurately define event chronology.
Triggers for Sudden Cardiac Death in the Athlete 195
Barry J. Maron
Sudden death on the athletic field is usually due to underlying cardiovas¬
cular disease. Coronary artery disease is most common in older athletes,
CARDIOLOGY CUNICS ; . , ,;,: _
VOLUME 14 • NUMBER 2 • MAY 1996 V
and a variety of congenital cardiovascular malformations predominate in
young competitive athletes. Of these lesions, the most common in North
America is hypertrophic cardiomyopathy. A variety of coronary artery
anomalies are next in frequency, with the most important being anomalous
origin of left main coronary artery from the anterior sinus of Valsalva.
Pathophysiology and Inflammatory Aspects of Plaque Rupture 211
Anne Pauline Schroeder and Erling Falk
Endothelial dysfunction, lipid accumulation, growth of smooth muscle
cells, and chronic inflammation are main pathogenic features of coronary
atherosclerosis. The composition rather than the size of the atherosclerotic
plaques determines their stability. Soft atheromatous plaques with a core
of extracellular lipid are vulnerable, as the fibrous cap covering the core
may rupture, exposing highly thrombogenic material to the circulating
blood. External factors might trigger plaque disruption, provided a vulner¬
able plaque is present. What makes plaque disruption dangerous is the
ensuing thrombotic response.
Role of Plaque Size and Degree of Stenosis in Acute
Myocardial Infarction 221
William C. Little and Robert J. Applegate
Angiographically apparent coronary artery stenoses limit coronary flow,
produce symptomatic ischemia, and can be targeted for revascularization.
Severe stenoses are more likely to occlude than segments without signifi¬
cant stenoses. Coronary angiography underestimates the extent of coro¬
nary atherosclerosis. Arterial segments without severe stenoses are much
more common, and their risk of occlusion is not zero. Thus, the majority
of myocardial infarctions are due to occlusion of arteries that do not
contain obstructive coronary stenoses. Consequently, coronary angiogra¬
phy is not able to accurately predict the site of a coronary artery occlusion
that subsequently will produce myocardial infarction.
Hemodynamic Changes as Triggers of Cardiovascular Events 229
Prakash C. Deedwania
Although a large number of clinical studies during the past decade have
documented that myocardial ischemia, acute myocardial infarction, and
sudden cardiac death have definite circadian patterns, recently published
work suggests that it is not necessarily a specific time of the day but the
sleep/wake cycle and postural changes as well as the balance between
triggers and protective factors that determine the onset of cardiovascular
events. A clear understanding of the pathophysiologic processes responsi¬
ble for ischemic events and the specific roles played by various triggers
would be helpful in better defining the therapeutic strategies designed for
the prevention and treatment of acute cardiac events. Because changes in
hemodynamic parameters are of paramount importance in initiating an
ischemic event, it is critical to review their role and relationship in the
pathogenesis of acute coronary events.
Hemostatic Factors as Triggers of Cardiovascular Events 239
Guido B. Aranha Rosito and Geoffrey H. Tofler
A growing body of evidence supports a role for hemostatic factors in
triggering cardiovascular events. Fibrinogen has been identified as an
independent cardiovascular risk factor that is as powerful a predictor as
cholesterol. Factor VII, fibrinolytic potential, von Willebrand s factor, and
platelet reactivity also have been linked to increased incidence of cardio¬
vascular disease. Further characterization of these factors may lead to
improved risk assessment and the development of new therapies for
prevention.
vi CONTENTS
Practical Implications of Circadian Variations in Thrombolytic
and Antithrombotic Activities 251
Peter B. Kurnik
It recently has been demonstrated that thrombolytic therapy has a circa¬
dian pattern of efficacy, as assessed by the ability to rapidly provide
coronary patency. A study of 692 patients receiving intravenous tPA
and undergoing acute coronary arteriography demonstrated a substantial
diurnal pattern in patency with a peak at 8:00 pm. The heightened tendency
for a coronary artery to be opened in the evening correlates well with the
substantial tendency demonstrated in the same study and in multiple
other studies for coronary arteries to thrombose and cause myocardial
infarction in the morning hours. Circadian variations have been defined
for a number of hemostatic and physiologic factors that would predispose
toward clotting in the late morning, and converse circadian patterns have
been described for a number of factors associated with thromborysis that
would predispose towards enhanced fibrinolysis in the evening hours.
Methods by which efficacy of lytic therapy potentially could be enhanced
include development of tPA variants or adjunctive agents that eliminate
the circadian nadirs of efficacy, modification of dosage or choice of lytic
agent as a function of time of treatment, and selection between pharmaco
logic lysis and direct angioplasty as a function of time of day.
Physical Exertion as a Trigger of Myocardial Infarction and
Sudden Cardiac Death 263
Murray A. Mittleman and David S. Siscovick
Physical exertion can trigger the onset of nonfatal myocardial infarction
and sudden cardiac death. Although the transient increase in risk during
acute episodes of physical exertion may be high, the absolute risk is
actually quite small. Regular exercise reduces the risk of myocardial in¬
farction and sudden cardiac death during periods of heavy physical exer¬
tion. Thus, evidence that the benefits of regular physical exertion outweigh
the transient increase in risk during exertion provides further support for
encouragement of regular exercise as recommended by the American
Heart Association.
Mental Stress as a Trigger of Myocardial Ischemia and Infarction 271
David S. Krantz, Willem J. Kop, Helen T. Santiago, and John S. Gottdiener
Recent research on the effects of behavioral activities on myocardial ische¬
mia in coronary artery disease patients has provided a pathophysiologic
model for understanding the mechanisms by which mental stress can
trigger clinical cardiovascular events. This article reviews epidemiologic
research implicating psychosocial stress as an acute trigger of myocardial
infarction in patients with pre existing coronary artery disease, and evi¬
dence for the pathophysiologic effects of acute mental stress in individuals
with pre existing coronary artery disease. Via its actions on the central and
autonomic nervous systems, stress can produce a cascade of physiologic
responses in vulnerable individuals that may lead to myocardial ischemia,
ventricular fibrillation, plaque rupture, or coronary thrombosis. Also re¬
viewed are field and laboratory studies that suggest important causal links
between mental stress and myocardial ischemia, and evidence suggesting
clinical significance for vulnerability to mental stress induced ischemia.
Life Threatening Cardiovascular Consequences of Anger in
Patients with Coronary Heart Disease 289
Richard L. Verrier and Murray A. Mittleman
Anger is the affective state most commonly associated with myocardial
ischemia and life threatening arrhythmias. The scope of the problem is
CONTENTS Vii
sizeable—at least 36,000 (2.4% of 1.5 million) heart attacks are precipitated
annually in the United States by anger. The lethal cardiovascular conse¬
quences in ischemic heart disease are attributable to the unique physiology
of this state, which activates high gain central neurocircuitry and the
sympathetic nervous system, leading to acute sinus tachycardia, hyperten¬
sion, impaired myocardial perfusion, and a high degree of cardiac electri¬
cal instability. Exciting new tools have emerged from the fields of epidemi¬
ology, behavioral medicine, and cardiovascular physiology that offer
considerable promise in accelerating our understanding of the pathophysi
ology of anger and in developing means to sever the link between anger
and its life threatening consequences.
Prevention and Practical Aspects of Triggering of Cardiovascular Events 309
Geoffrey H. Tofler and James E. Muller
The recognition of the peak morning incidence of cardiovascular events
and the role of triggering mechanisms can lead to some practical sugges¬
tions. For instance, adequate pharmacologic coverage over the full 24
hour period, in particular during the morning period of increased risk, is
desirable among individuals taking antihypertensive and anti ischemic
medication. Although the absolute risk of an event occurring following a
single exposure to a potential trigger is in general too low to recommend
avoidance of the stressor, further research in this area may result in the
design of pharmacologic and nonpharmacologic means to prevent the
trigger from precipitating disease onset.
Special Article
The Treatment of Coronary Disease 313
Francis C. Wood
This article is reprinted from The Medical Climes of North America, volume
30, Philadelphia number, 1946; pp 1275 1285.
Index 323
Subscription Information Inside back cover
viii CONTENTS
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| physical | XII S., S. 175 - 326 Ill., graph. Darst. |
| publishDate | 1996 |
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| publisher | Saunders |
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| series | Cardiology clinics |
| series2 | Cardiology clinics |
| spellingShingle | Triggers and timing of cardiac events Cardiology clinics Herzkrankheit (DE-588)4024663-2 gnd Tagesrhythmus (DE-588)4078131-8 gnd Stressor (DE-588)4183681-9 gnd Komplikation (DE-588)4123547-2 gnd |
| subject_GND | (DE-588)4024663-2 (DE-588)4078131-8 (DE-588)4183681-9 (DE-588)4123547-2 (DE-588)4143413-4 |
| title | Triggers and timing of cardiac events |
| title_auth | Triggers and timing of cardiac events |
| title_exact_search | Triggers and timing of cardiac events |
| title_full | Triggers and timing of cardiac events Prakash C. Deedwania ..., guest ed. |
| title_fullStr | Triggers and timing of cardiac events Prakash C. Deedwania ..., guest ed. |
| title_full_unstemmed | Triggers and timing of cardiac events Prakash C. Deedwania ..., guest ed. |
| title_short | Triggers and timing of cardiac events |
| title_sort | triggers and timing of cardiac events |
| topic | Herzkrankheit (DE-588)4024663-2 gnd Tagesrhythmus (DE-588)4078131-8 gnd Stressor (DE-588)4183681-9 gnd Komplikation (DE-588)4123547-2 gnd |
| topic_facet | Herzkrankheit Tagesrhythmus Stressor Komplikation Aufsatzsammlung |
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