I am an attorney.  I represent a widow whose husband died due to a
heart attack (myocardial infarction).  The basic facts are as follows:
 Husband works for an electric utility company as a "line worker." 
His basic job is to climb up the electric poles and repair lines when
they are blown down due to high winds and other storm conditions.  The
Husband was studying to become a supervisor and had to pass a written
test to qualify for the promotion.  There are several witnesses that
indicate that the Husband was very nervous about taking this test.  On
the day of his death, the Husband woke up early (around 6:00 am) and
took the exam prior to starting his regular work day.  He then worked
a 16 hour work day, the extra time necessitated by a storm that had
caused several problems with the power lines.  He worked most of the
day outside, in the rain.  There is evidence that he may have thrown
up while at work.  When he arrived home at 10:00 pm, he immediately
went to the bathroom and vomited violently.  His wife then demanded
that he go to the hospital.  She drove him there (about a 5 minute
trip) and he was immediately taken to the emergency room where he died
approximately 30 minutes later.

There is a "workers compensation" law that allows the widow to recover
certain benefits if her husband's work was a "substantial contributing
factor" to his heart attack and eventual death.  The Husband was a
smoker and did have high cholesterol, so he did have risk factors for
a heart attack.  The legal impact of these factors is unclear, though
the law does not require that the Husband be in perfect health. 
Probably the best way to put the legal question for the court to
determine is:  Would this man have still had the heart attack and died
was he to spend the day sitting at home on the couch, as opposed to
working the 16 hour day and being stressed because of his test?  If he
would have had the heart attack anyway, then the widow gets no
benefits.  But if he wouldn't have had the heart attack, but for the
work, then she does get benefits.

That said, my question is:

What research and/or scholarly articles (preferably US - the Courts
prefer US medical research) is/are available that discuss whether -
and to what extent - environmental factors (i.e., physical strain,
psychological stress, etc.) can lead to a heart attack?  In
particular, I am looking for research that explains the causation of
these factors on the heart and cardiovascular system.  Correlative
articles (i.e., people that work construction jobs are more likely to
have a heart attack than librarians) are not particularly helpful.

I hope I have provided you enough information to get the idea of what
I am looking for.  Feel free to contact me with any questions.  I hope
that we are able to help this woman.  Thank you for your time.

---

Request for Question Clarification by pafalafa-ga on 27 Sep 2005 15:49 PDT

smtm-ga,

Are you looking ONLY for scientific studies on this topic?

I ask, because there is a good body of case law as well on
occupationally-related heart attacks, and some of these cases
acknowledge stress as a contributing factor.

You are probably familiar with these already, but I just wanted to double check.


Also, most of the scientific literature on this topic is, in fact,
epidemiological in nature, or correlative, as you put it.  However, it
is still well-regarded, and well-recognized research.

The findings on the links between exaggerated work-place stress and
heart attacks are still in the research stage I would label
'suggestive', but they have been suggestive enough to have been
accepted by the courts on numerous occasions.

Again, should I include these?  Or only focus on studies of causation
rather than correlation?


Let me know.

pafalafa-ga

---

Clarification of Question by smtm-ga on 28 Sep 2005 06:51 PDT

pafalafa-ga

Thank you for your questions.  You are correct that we have already
done a fair amount of research in the case law in our jurisdiction. 
If however, there are cases that provide detailed discussions of the
effect of workplace strain and stress on a heartattack, particularly
if they reference testifying experts.

If there are epidemiological studies that have been recognized
favorably by the courts, I would be interested in both those cases and
the studies recognized.  Otherwise, I think we should concentrate on
non-epidemiological research.


Thanks again.

---

Request for Question Clarification by pafalafa-ga on 28 Sep 2005 06:53 PDT

OK.  I'm on it.

If you'd care to identify your jurisdiction, that would be useful.

But if not, I'll just cast around broadly for the most relevant information.


paf

---

Clarification of Question by smtm-ga on 28 Sep 2005 07:07 PDT

paf:

Sounds good.  Let's just go for the broad search.

Thanks.

smtm

smtm-ga,

I found what look to me to be a number of useful studies for your case.  

I generally focused on providing studies from the US with a strong
biological (rather than correlative) component.  However, I also
included a number of studies that were non-US, or were correlative,
where they seemed to have a particularly compelling story to tell.

I also concentrated on scientific studies, rather than case law, since
there is so much compelling and very recent literature on the topic,
that I don't think most of it has had an opportunity to yet be
considered by the courts.

Since the articles and abstracts are copyright, I can only provide
excerpts here, but I've selected text that should readily give you the
gist of the results.

A number of the articles cited provided contact information for the
primary author, and where this was available, I included it as well.


I trust the information below fully answers your question.

However, please don't rate this answer until you have everything you
need.  If there's anything more I can do for you, just post a Request
for Clarification, and I'm happy to assist you further.

pafalafa-ga



===============


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9153365&dopt=Abstract
JAMA. 1997 May 21;277(19):1521-6

Effects of mental stress on myocardial ischemia during daily life
Gullette EC et al
Department of Psychiatry and Behavioral Sciences, Duke University
Medical Center, Durham, NC 27710, USA. gulle002@mc.duke.edu

OBJECTIVE: To determine the relative risk of myocardial ischemia
triggered by specific emotions during daily life

SUBJECTS: From a sample of 132 patients with coronary artery disease
and recent evidence of exercise-induced ischemia who underwent 48
hours of ambulatory ECG monitoring, 58 patients exhibited ambulatory
ischemia and were included in the analysis.

CONCLUSIONS: Mental stress during daily life, including reported
feelings of tension, frustration, and sadness, can more than double
the risk of myocardial ischemia in the subsequent hour.

==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15687136&query_hl=4
Circulation. 2005 Feb 1;111(4):472-9

Acute and reversible cardiomyopathy provoked by stress in women from
the United States
Sharkey SW et al
Minneapolis Heart Institute Foundation, Minneapolis, Minn 55407

BACKGROUND: A clinical entity characterized by acute but rapidly
reversible left ventricular (LV) systolic dysfunction and triggered by
psychological stress is emerging, with reports largely confined to
Japan

METHODS AND RESULTS: Over a 32-month period, 22 consecutive patients
with this novel cardiomyopathy were prospectively identified within a
community-based practice in the Minneapolis-St. Paul, Minn, area

CONCLUSIONS: A reversible cardiomyopathy triggered by psychologically
stressful events occurs in older women and may mimic evolving acute
myocardial infarction or coronary syndrome. This condition is
characterized by a distinctive form of systolic dysfunction that
predominantly affects the distal LV chamber and a favorable outcome
with appropriate medical therapy.

==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12237162&query_hl=4
Cardiovasc Res. 2002 Oct;56(1):15-21

Molecular and cellular interface between behavior and acute coronary syndromes
Gidron Y, et al
Department of Sociology of Health, Faculty of Health Sciences,
Ben-Gurion University, Be'er Sheeba, Israel. yorig.@bgumail.bgu.ac.il


This review article integrates empirical findings from various
scientific disciplines into a proposed psychoneuroimmunological (PNI)
model of the acute coronary syndrome (ACS...

...The ACS is triggered by three stages...

(1) Plaque instability: Pro-inflammatory cytokines...induce leukocyte
chemoattraction to the endothelium...Acute stress, hostility,
depression and vital exhaustion (VE) have been associated with
elevated pro-inflammatory cytokines and leukocyte levels and their
recruitment...

(2) Extra-plaque factors promoting rupture...Hostility/anger and acute
stress can lead to vasoconstriction and elevated BP via
catecholamines...

(3) Superimposed thrombosis at a ruptured site...Increases in
coagulation factors and reductions in anticoagulation factors (e.g.
protein C) induced by inflammatory factors enhance platelet
aggregation, a key stage in thrombosis. Hostility, depression and VE
have been positively correlated with platelet aggregation...


==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15963652&query_hl=10
Psychoneuroendocrinology. 2005 Nov;30(10):1017-21.

Stress hormones in health and illness: the roles of work and gender
Lundberg U.
Department of Psychology, Centre for Health Equity Studies, Stockholm
University, Stockholm, Sweden. ul@psychology.su.se

Two neuroendocrine systems are of specific interest in the study of
stress and health; the sympathetic adrenomedullary system with the
secretion of epinephrine and norepinephrine, and the hypothalamic
pituitary adrenocortical (HPA) system with the secretion of cortisol.
These hormones have often been used as objective indicators of stress
in the individual.

...stress responses have been important for human and animal survival
and for protection of the body. However, in modern society, some of
these bodily responses may cause harm rather than protection.

...The catecholamines have been linked to cardiovascular disorders
such as hypertension, myocardial infarction and stroke, cortisol to
cardiovascular disease, Type 2 diabetes, reduced immune function and
cognitive impairment. An adequate balance between catabolic
(mobilization of energy) and anabolic processes (growth, healing) is
considered necessary for long term health and survival...


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15961212&query_hl=10
Biol Psychol. 2005 Jun 13

Hemodynamic, hemostatic, and endothelial reactions to psychological
and physical stress in coronary artery disease patients
Bacon SL, et al
School of Sport and Exercise Sciences, University of Birmingham,
Birmingham B15 2TT, UK; Centre de Recherche, Hopital du Sacre-Coeur de
Montreal, Montreal, Que., Canada H4J 1C5; Department of Psychology,
McGill University, Montreal, Canada H3A 1B1

Episodes of psychological and physical stress may elicit thrombotic
cardiac events, such as myocardial infarction. These events are
triggered when there are concurrent hemodynamic, hemostatic, and
endothelial abnormalities.

Hemodynamic, hemostatic, and endothelial reactions of 72 (15 women, 57
men) coronary artery disease patients to psychological and physical
stress were examined. Blood pressure, electrocardiography, and
impedance cardiography were recorded during rest, mental arithmetic,
and exercise.

...This pattern of hemodynamic, hemostatic, and endothelial reactions
suggests that acute psychological and physical stress influence the
thrombotic system differently in these high risk patients. Future
research is needed to investigate how these stress responses are
prospectively related to acute cardiac events.


==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15916668&query_hl=10
Acta Physiol Scand. 2005 Jun;184(2):87-94

Electrocardiographic characterization of stress-induced myocardial
infarction in atherosclerotic mice
Hemdahl AL, et al
Center for Molecular Medicine L8:03 and Department of Medicine,
Karolinska Institutet, Stockholm, Sweden.
anne-louise.hemdahl@fyfa.ki.se


We have previously shown that mental and hypoxic stress can trigger
the development of myocardial infarction (MI) in atherosclerotic
apoE(-/-) x LDLR(-/-) mice

The purpose of the present study was to characterize the interval
between stress and MI and determine whether electrophysiological
changes precede the precipitation of an infarct

CONCLUSION: This is the first mouse model showing that increased
STU-area variability is indicative of MI development in
atherosclerotic mice following ischaemic stress. Furthermore, our
findings suggest a two-phase pathway for the infarction development:
an initial phase comprising a transient ischaemic response which
triggers a delayed second phase of ischaemia and MI.


==========


http://content.nejm.org/cgi/content/abstract/352/6/539
New England Journal of Medicine
Volume 352:539-548  February 10, 2005  Number 6

Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress
Ilan S. Wittstein, M.D, et al
Division of Cardiology, Johns Hopkins Hospital, Carnegie 568, 600 N.
Wolfe St., Baltimore, MD 21287, or at iwittste@jhmi.edu.


...Plasma catecholamine levels at presentation were markedly higher
among patients with stress-induced cardiomyopathy than among those
with Killip class III myocardial infarction

...Conclusions Emotional stress can precipitate severe, reversible
left ventricular dysfunction in patients without coronary disease.
Exaggerated sympathetic stimulation is probably central to the cause
of this syndrome.


==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15598722&query_hl=1
J Epidemiol Community Health. 2005 Jan;59(1):23-30

Work related stressful life events and the risk of myocardial
infarction. Case-control and case-crossover analyses within the
Stockholm heart epidemiology programme (SHEEP).
Moller J, et al
Karolinska Institutet, Department of Public Health Sciences, Division
of Social Medicine, Norrbacka, SE-171 76 Stockholm, Sweden.
jette.moller@phs.ki.se


...Recent changes in labour market conditions and in the organisation
of work in developed societies have increased exposure to work related
stress. The question is whether this also implies an increased risk of
myocardial infarction, either through the triggering effect of acute
stress, or through accumulation of stress over several months

...MAIN RESULTS: The case-crossover analysis showed triggering effects
of sudden, short term situations of increased work load or work
competition. Having "had a high pressure deadline at work" entailed a
sixfold increase in risk of myocardial infarction (OR = 6.0 95% CI
(1.8 to 20.4)) during the next 24 hours. The importance of work
related life events as risk factors for myocardial infarction was
supported by the case-control analysis.

...CONCLUSION: Specific work related stressful life events seem to be
potential triggers of the onset of myocardial infarction


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15310721&query_hl=1
Heart. 2004 Sep;90(9):e52

Stress, myocardial infarction, and the "tako-tsubo" phenomenon
Connelly KA, et al
Department of Cardiology, St Vincent's Hospital Melbourne, Fitzroy,
Victoria, Australia. connelka@svhm.org.au

...Emotional distress as a trigger for acute myocardial infarction is
beginning to gain credibility as it is recognised that traditional
risk factors can account for only half of all myocardial infarctions.
Here, three cases of myocardial infarction are presented in the
setting of an acute emotional stressor, with coronary angiography
showing only minimal coronary artery disease. In all cases striking
wall motion abnormalities, mimicking a "tako-tsubo", were noted...


========== 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15189477&query_hl=1
Psychophysiology. 2004 Jul;41(4):541-51

Mental stress-induced hemoconcentration: Sex differences and mechanisms.
Veldhuijzen van Zanten JJ, et al
School of Sport and Exercise Sciences, University of Birmingham,
Birmingham, UK. jjv016@bham.ac.uk

...Given the possible role of hemoconcentration in myocardial
infarction and apparent sex differences in susceptibility, three
studies examined sex differences in mental stress-induced
hemoconcentration, and explored possible underlying mechanisms. Blood
pressure, heart rate, and hematocrit were monitored at rest and in
response to a mental stress task that was contrived to be increasingly
provocative across the three studies.

...Blood pressure reactivity was a strong and consistent predictor of
stress-induced hemoconcentration. These findings may help to explain
sex differences in susceptibility to myocardial infarction.

==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15087554&query_hl=1

Stroke. 2004 Jun;35(6):1294-8. Epub 2004 Apr 15
Stress-induced blood pressure reactivity and silent cerebrovascular disease.
Waldstein SR, et al
Department of Psychology, University of Maryland, Baltimore County,
1000 Hilltop Circle, Baltimore, MD 21250, USA. waldstei@umbc.edu

...Exaggerated blood pressure (BP) responses to mental stress, an
index of autonomic dysregulation, have been related to enhanced risk
for stroke. This study examined cross-sectional relations of
stress-induced BP reactivity to silent cerebrovascular disease
assessed by magnetic resonance imaging (MRI) in healthy older adults.

...results indicate that greater stress-induced BP reactivity is
associated with enhanced silent cerebrovascular disease on MRI in
healthy asymptomatic older adults independent of resting BP levels.
Exaggerated stress-induced BP reactivity warrants further examination
as a potential biobehavioral risk factor for cerebrovascular disease.



==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12972107&query_hl=1
Am J Cardiol. 2003 Sep 15;92(6):687-91.

Effects of mental stress on flow-mediated brachial arterial dilation
and influence of behavioral factors and hypercholesterolemia in
subjects without cardiovascular disease.
Gottdiener JS, et al
Division of Cardiology, St. Francis Hospital, 100 Port Washington
Boulevard, Roslyn, NY 11516, USA. gottdien@ziplink.net

Mental and emotional arousal are known to trigger coronary events. The
relation between hypercholesterolemia, behavioral factors, and mental
stress-induced alterations in endothelial function are not well
defined.

...Flow-mediated brachial arterial vasodilation has been established
as a measure of arterial endothelial function. High-resolution
ultrasound was used to measure mental stress-mediated, flow-mediated,
and the combination of mental stress- and flow-mediated brachial
artery dilation in 38 subjects

...Under mental stress, participants with hypercholesterolemia showed
less vasodilation than participants without hypercholesterolemia, even
after adjustment for age and the magnitude of blood pressure response
to mental stress. Mental stress attenuated flow-mediated brachial
arterial vasodilation.

...Thus, hypercholesterolemia is associated with impaired vasodilation
in response to mental stress. Mental stress inhibits flow-mediated
vasodilation in normal subjects and those with hypercholesterolemia.


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12688407&query_hl=1
J Cardiovasc Pharmacol. 2003 Jan;41 Suppl 1:S115-8

Molecular mechanism of emotional stress-induced and
catecholamine-induced heart attack
Ueyama T, et al
Department of Anatomy and Cell Biology, Wakayama Medical University,
Wakayama, Japan. tueyama@wakayama-med.ac.jp

...Emotional or physical stress triggers 'tako-tsubo' cardiomyopathy
or 'transient left ventricular apical ballooning', but the
pathogenesis is unclear. In response to the immobilization stress of
rats, a useful model of emotional stress, rapid activation of p44/p42
mitogen-activated protein kinase was observed in the heart, followed
by a transient upregulation of immediate early genes in the smooth
muscle cells of coronary arteries, the endothelial cells and the
myocardium.

...Activation of alpha-adrenoceptors and beta-adrenoceptors is the
primary trigger of emotional stress-induced molecular changes in the
heart.


==========



Again, if there's anything else you need, just let me know.


pafalafa-ga



search strategy:  Searched Google and several medical databases along
with PubMed, but the best results, by far were from a PubMed search on
[ stress and infarction ]

---

Request for Answer Clarification by smtm-ga on 29 Sep 2005 09:17 PDT

paf:

The studies you found look very interesting.  You seem to have found a
lot of material on the effect of psychological stress on MI. 
Probably, the more compelling factor in our case will be to what
extent physical strain can lead to a heart attack.  It appears that
some of the studies you cited touch on this as well, but I was
wondering if you found more information on triggers as a result of
physical activity (i.e, shoveling snow, etc.).  If it may be that such
medical information is more rudimentary (i.e, more available in texts)
and not ground breaking reasearch, but is more simple and recognized. 
Such commonplace information is not necessarily a bad thing.

Thanks.

---

Clarification of Answer by pafalafa-ga on 29 Sep 2005 12:48 PDT

Happy to add some more references.  I must say, though, that given the
conventional wisdom that sudden exertion can bring on a heart attack,
there did not appear to be nearly as much research on this topic as I
would have anticipated.

However, there's certainly enough to help build a case.

Again, let me know if there's anything else you need.


paf


===============



http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15308957&query_hl=17
Epidemiology. 2004 Sep;15(5):573-82

The risk of acute myocardial infarction: interactions of types of
physical activity.
Fransson E, et al
Division of Cardiovascular Epidemiology, Institute of Environmental
Medicine, Karolinska Institutet, Stockholm, Sweden.
eleonor.fransson@imm.ki.se

We estimated the influence of exercise, occupational physical
activity, and household work with regard to risk of acute myocardial
infarction (MI).

Exercise, walking or standing at work, and doing demanding household
work were all associated with decreased risk of acute MI;

In contrast, lifting or carrying at work, and an occupational workload
perceived to be strenuous, were related to an increased risk of MI

CONCLUSION: Aerobic physical activities such as exercise or walking at
work seemed to reduce the risk of MI, whereas anaerobic activities
such as heavy lifting at work were related to increased risk of MI


===

http://www.epidem.com/pt/re/epidemiology/fulltext.00001648-200409000-00015.htm;jsessionid=D8bc11fPlJZh5UkFJ6KCyE8B20mmN5vq1Epq5fEJLvLjUgMkpVX7!-1383460204!-949856144!9001!-1
[full text of the above article]


==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10693072&dopt=Abstract
J Occup Environ Med. 2000 Feb;42(2):127-35

Association of physical activity at work with mortality in Israeli
industrial employees: the CORDIS study.
Kristal-Boneh E, et al
Epidemiology Unit, Occupational Health and Rehabilitation Institute,
Raanana, Israel.


The objective of this study was to evaluate the association of
physical activity at work with the risk of all-cause cardiovascular
disease and cancer mortality.

We found that the hazard ratio of all-cause mortality in workers with
a high physical workload was 1.82 (95% confidence interval, 1.18 to
2.81) compared with workers having a low workload. A similar trend was
noted for cardiovascular disease and cancer mortality. We concluded
that a high physical workload is associated with increased mortality
rates.


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15784781&query_hl=29
Psychosom Med. 2005 Mar-Apr;67(2):179-86

Behavioral and emotional triggers of acute coronary syndromes: a
systematic review and critique.
Strike PC, Steptoe A.
Department of Epidemiology and Public Health, University College
London, London WC1E 6BT, UK.

There is consistent evidence that physical exertion (particularly by
people who are not normally active), emotional stress, anger, and
extreme excitement can trigger acute myocardial infarction and sudden
cardiac death in susceptible individuals. Many triggers operate within
1 to 2 hours of symptom onset.

Behavioral and emotional factors are probable triggers of acute
coronary syndromes in vulnerable individuals

[The full text of this article can be purchased online here:  
http://www.psychosomaticmedicine.org/cgi/content/abstract/67/2/179
It seems worth a look, and likely includes other valuable references
not listed by me]


==========


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15170392&query_hl=29
Pathophysiol Haemost Thromb. 2003 May-Jun;33(3):127-33.

High intensity exercise enhances platelet reactivity to shear stress
and coagulation during and after exercise.
Ikarugi H, et al
Laboratory of Health and Sport Sciences, University of Hyogo, Kobe,
Japan. ikarugi@econ.u-hyogo.ac.jp

Platelets play a crucial role in the pathogenesis of acute cardiac
events, such as angina, myocardial infarction and sudden death. It is
believed that regular low-intensity exercise can reduce, while
high-intensity exercise may provoke acute cardiac events. The aim of
the present study was to investigate the effect of acute exercise both
at low and high intensities on the ventilatory threshold (VT),
platelet reactivity and coagulation before and after exercise.

The present study suggests that high-intensity exercise-induced
platelet hyperreactivity and hypercoagulable state may pose an
increased risk for acute, sometimes fatal cardiac event.


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14980132&query_hl=29
Curr Sports Med Rep. 2004 Apr;3(2):59-61

Winter storm warning: snow removal may be hazardous to your (patient's) health
Franklin BA, et al
Preventive Cardiology/Cardiac Rehabilitation, William Beaumont
Hospital, 4949 Coolidge Highway, Royal Oak, MI 48073, USA.
bfranklin@beaumont.edu

[No abstract was available, but the article and author seemed worth
noting just the same]


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12024335&query_hl=29
Prog Cardiovasc Dis. 2002 Mar-Apr;44(5):369-80

Triggers of acute coronary syndromes.
Servoss SJ, et al
Cardiology Division, Department of Medicine, Massachusetts General
Hospital, Harvard Medical School, Boston, MA02114, USA

...approximately 50% of the deaths from coronary artery disease
continue to occur out of hospital, and many major cardiac events occur
in individuals not previously known to be at risk. These facts create
the need to identify the acute causes of myocardial infarction (MI)
and sudden death, which has led to a rapid growth in interest over the
last 15 years in the field of triggering research.

...triggering of MI by heavy exertion, sexual activity, anger, mental
stress, cocaine and marijuana use, and exposure to air pollution has
been demonstrated.


==========

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10443851&query_hl=29
J Am Geriatr Soc. 1999 Aug;47(8):923-9

Exercise-induced silent myocardial ischemia and future cardiac events
in healthy, sedentary, middle-aged and older men.
Katzel LI, et al
Department of Medicine, University of Maryland School of Medicine, and
Baltimore Veterans Affairs Medical Center Geriatrics Research,
Education, and Clinical Center, 21201

Before men older than age 45 participate in vigorous exercise
programs, the American Heart Association and the American College of
Sports Medicine recommend they undergo a screening maximal exercise
treadmill test.

We examined the predictive value for subsequent cardiac events of
exercise-induced silent myocardial ischemia (SI) during the exercise
treadmill test in healthy, sedentary, obese, middle-aged and older men

At baseline, 37 of the men (22%) had exercise-induced SI on their
treadmill tests. Seven-year follow-up data was obtained in 97% of the
patients. In the interim, 31 men had cardiac endpoints (sudden cardiac
death, myocardial infarction, angioplasty, coronary artery bypass
graft surgery, angina), and four had noncardiac deaths.

CONCLUSION: In a healthy population of obese, sedentary, middle-aged
and older men, exercise-induced SI and low VO2max were predictors of
incident CAD...


==========


Hope that helps.


paf

Consider searching for adrenaline/catecholamines and  associated risk
of heart attacks. It has been shown that surges of adrenaline loosen
arterial plaque, leading to heart attack. This came from the fact that
more heart attacks occur on Monday morning, as people dread going to
work.

"Chest pain or pressure is a common symptom of heart attack. Cardiac
chest pain is often vague, or dull, and may be described as a pressure
or band-like sensation, squeezing, heaviness, or other discomfort.
Heart attacks frequently occur from 4:00 A.M. to 10:00 A.M. due to
higher adrenaline amounts released from the adrenal glands during the
morning hours. Increased adrenaline in the bloodstream can contribute
to the above mentioned plaque rupture. Interestingly, heart attacks do
not usually happen during exercise, although exercise is commonly
associated with exertional angina. Approximately one quarter of all
heart attacks are silent, without chest pain. In diabetics, the
incidence of ?silent? heart attacks may be much higher."
http://www.seniorhousingnet.com/seniors/reading_room/health_well/heart_attack.jhtml