Transcript HeartStress2001

PSYCHOLOGICAL
STRESS
ACUTE PSYCHOLOGICAL
STRESS
Confront a Bear
arouses
Fear
elicits
Adaptive Responses
Cardiovascular Responses
heart rate, contractile force
Preparatory and serve to increase cardiac output
to supply additional blood to skeletal muscles
BEAR
Sudden Cardiac Death
EMOTION AND SUDDEN
CARDIAC DEATH
BIBLE - BOOK of ACTS
When Ananias was charged by Peter “you
have not lied to man but to God,” he fell dead;
as did Sapphira, his wife, when told that “the
feet of them which have buried thy husband
are at the door and shall carry thee out”
George Engel (1971). Life Settings in
which Sudden Death Occurred
• On impact of the collapse and death of a loved
one (21%)
• During acute grief (20%)
• Threat of loss of a loved one (9%)
• During mourning or anniversary of death of
loved one (3%)
• Loss of status or self-esteem (6%)
• Personal danger or threat of injury (27%)
• After the danger is over (7%)
Engel - (cont)
• Reunion, triumph or happy ending (6%)
Common Thread - Events were
impossible for the victims to
ignore.
Trichopoulus et al. 1983.
Psychological stress and the
fatal heart attack: the
Athens (1981) earthquake
natural experiment.
Trichopoulus et al. - 1983
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February 24-11:00 p.m.
Earthquake
February 25
February 26
February 27
Aftershocks
February 28
March 1
Trichopoulus et al. - (cont.)
• Death Certificates at time of earthquake
• Death Certificates from Control Periods 1980, 1981,1982
• Immediate cause of death due to sudden
cardiac event
Trichopoulus et al. - Results
• Daily Number of Deaths due to Cardiac Event
• Control Period Mean = 7.1
• Quake Period:
Feb. 25 = 9
Feb. 26 = 11
Feb. 27 = 14
Mean = 10.4
Feb. 28 = 9
Mar. 1 = 9
Meisel et al. (1991). Effect of
Iraqi missile war on incidence
of acute myocardial infarction
and sudden death in Israeli
Civilians.
Meisel et al.(1991)
• Gulf War SCUD Missile attacks on Tel Aviv.
• Sapir Medical Center
• First week of the war – Jan. 17-25, 1991
- Number of patients who were seen/died from
acute myocardial infarction (heart attack)
- Compared to number of patients during
control periods
Meisel et al.,(1991)- Results
Sapir Medical Center Patients Seen*
Out of hospital Sudden Deaths
n = 41 First week of the war
n = 22 Jan. 17-25, 1990
Loer et al. (1996). Sudden
death triggered by an
Earthquake
The Northridge, California earthquake
Kawachi et al. (1994).
Prospective study of phobic
anxiety and risk of coronary
heart disease in men.
Kawachi et al.(1994)
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Studied 2000 men from 1961 to 1993
1961 – Physical exam
Questionaire – Five Questions
Do strange people or places make you afraid?
Are you considered to be a nervous person?
Are you constantly keyed-up or jittery?
Do you often become scared for no good reason?
Do you often break out in a cold sweat?
QUESTIONAIRE RESULTS - 89% scored a 0,
8.9% scored a 1, 1.9% scored a 2 or more.
Kawachi et al. (1994) – cont.
• From 1961- 1993
1. Every three years
- Medical history
- Physical exams
- Lab tests
2. Cause of death monitored in deceased men
• RESULTS – Those men who scored a 2 or higher
on the questionaire were 4 times more likely to die
of sudden cardiac death than those who scored a 0.
That is, phobic anxiety is a risk factor for sudden
cardiac death.
Acute Psychological Stress
Ventricular Arrhythmias
(abnormal heart beats)
Ventricular Fibrillation
Sudden Death
Predisposition to Electrical
Instability
Digitalis
• Used to increase contractile force of the
heart
• Can cause arrhythmias at high doses
Amygdala
Cardioregulatory Nuclei
(Medulla)
Heart
Chronic Stress ? Cardiovascular
Disease
• Cardiovascular Stress Response
1. Cardiac Output - heart rate
contractile force
2. Changes in Blood Vessels
- constriction produces blood pressure
3. Changes in blood flow
- constriction of vessels to skin, kidney, viscera
- dilation of vessels in skeletal muscles
PSYCHOSOCIAL STRESS
AND ATHEROSCHLEROSIS
• Jay Kaplan – 1980’s ff
- cynomolgus monkeys
- in the wild
- mixed gender groups
- all male groups
- intrusions during the mating season
Kaplan et al. – Experiment 1
22 months duration
1. Unstable Social Condition
- Three groups of males
- n=5 per group
- Every 1-3 months
Redistribution
Each male is placed with 3-4 new males
2. Stable Social Condition
- Three groups of males
- No redistribution
UNSTABLE SOCIAL CONDITION
N=5
N=5
N=5
Redistribution every 1-3 months
Each male with 3 to 4 new males
STABLE SOCIAL CONDITION
N=5
N=5
No Redistribution
N=5
Kaplan et al. - Experiment 1(cont.)
• Fed a “North American Diet”
- moderately atherogenic (high fat, high
cholesterol)
• Routine evaluations
- Pathological Observations
- blood lipids, blood pressure, heart rate
- Behavioral Observations
- fighting behavior
- patterns of dominance
• Measured coronary artery atheroschlerosis
- at 22 months
Kaplan et al.- Expt.1
RESULTS
• When compared to subordinates, dominant
monkeys in unstable condition show
a. Increased heart rates
b. Increased atheroschlerotic lesions*
• No difference in atheroschlerosis and heart rates
between subordinate and dominant monkeys in
stable condition
Is the increased atheroschlerosis
due to increased sympathetic nervous
system activation?
Kaplan et al. - Experiment 2
• Male monkeys
• 22 months
• Unstable social condition
- Two Drug Conditions
a. Norepinephrine Beta receptor antagonist group
propranolol = antagonist
b. Placebo control group
Kaplan et al.- Experiment 2
Results
• Propranolol inhibited the development of
atheroschlerosis in dominant monkeys.
• Propranolol had no effect on subordinate
monkeys.
Kaplan et al. - Conclusions
Psychosocial Stress
activate
Sympathetic Nervous System
produces
Atheroschlerosis
How does sympathetic nervous
system innervation of the
vascular system produce
atheroschlerosis?
Blood Vessels
Bifurcations
Bends
Increased Force
Increased Turbulence
Increased Wear and Tear
Mechanics of Wear
1. Smooth inner lining of vessel tears and scars
2. Fatty acids and glucose work their way under
the layer and stick there
thickening plaques
Green = Atheroschler. plaque
Adrenal
Glands
Norepinephrine
Epinephrine
released with stress
Glucose, Fatty acids
Gender Differences in
Development of
Atheroschlerosis in Humans
• Expression of atheroschlerosis is delayed
in females by 10-15 years
• What contributes to this delayed onset?
Kaplan et al. - Experiment 3
• Female monkeys
• Male monkeys
- n=5-6 in stable social groups for 24 months
• Evaluation of ovarian function in females
- measurements of progesterone levels
• RESULTS:
Subordinate females
- enlarged adrenal glands*
- impaired ovarian function*
- greater incidence of atheroschlerosis*
Dominant
Subordinate
Progesterone levels
Luteal phase of
ovulatory cycle
8.89 ng/ml
3.79 ng/ml
Adrenal weights
168 mg/kg
201 mg/kg
Percentage cycles
with luteal phase
deficiencies
8.9
24.3
Does Impaired Ovarian
Function Contribute to
Atheroschlerosis?
Kaplan et al. - Experiment 4
• 24 months
• Ovarectomized females
• RESULTS :
- Ovarectomy increased atheroschlerosis in
dominant but not subordinate females
• CONCLUDE:
- Ovarian hormones are anti-atheroschlerotic
Kaplan et al. Expt 4. – cont.
Stress of Social Subordination
Impairment of Ovarian Function
Increased Risk of Atheroschlerosis
Kaplan et al. Experiment 5
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Exogenous estrogen treatment to female monkeys
Triphasil=exogenous estrogen
Measured iliac artery atheroschlerosis
RESULTS:
- triphasil protected subordinate females*
- in control group, the more dominant the monkey,
the less the atheroschlerosis*
Sparing of coronary heart
disease in pre-menopausal
women compared to men
• Delay of disease onset in women
CHD Death Rate – 40 year olds
Men
40 per 100,000/yr 5:1
Women
8 per 100,000/yr
Men
Women
CHD Death Rate – 60 yr olds
400 per 100,000/yr 2:1
175 per 100,000/yr