Chapter 5
Coronary Heart Disease
“ W I T H R E S P E C T TO T H E T R E AT M E N T O F T H I S C O M P L A I N T ( A N G I N A P E C TO R I S ) … I
K N E W O N E W H O S E T H I M S E L F A TA S K O F S AW I N G W O O D F O R H A L F A N H O U R
E V E RY D AY, A N D WA S N E A R LY C U R E D . ”
WILLIAM HEBERDEN, 1818
P-96
CHD is usually a disease of high-income countries, but also in low and middle-income countries.
Recorded history of CHD dates to AD 150.
Children, mummies, etc. CHD #1 cause of mortality of mankind.
Angina Pectoris---chest pain due to lack of O2 (in blood).
Heart disease (CHD, hypertensive heart disease, rheumatic heart disease is the # 1 cause of mortality in the USA since the
1920’s.
Rheumatic heart disease is the most dreaded complication of rheumatic fever. The term "rheumatic heart disease" refers
to the chronic heart valve damage that can occur after a person has had an episode of acute rheumatic fever. This valve
damage can eventually lead to heart failure.
Reduced smoking by adults, better hypertension meds, greater public awareness about a healthy diet and better medical
treatment have all helped lower the % of mortality from heart disease.
Currently, about 17.6 million people from age 20 to older in the USA have CHD.
The annual # of CHD deaths is about 425,000. About every 25 seconds an American will have a cardiac event and about
every 60 seconds one American will die from it.
CHD Risk Factors
Major risk factors for CHD: genetic susceptibility, male sex, elevated serum cholesterol, low levels of HDL, smoking, high BP, obesity, diabetes and
being sedentary.
Major Modifiable CHD Risk Factors:
1.
Tobaccos Smoke
2.
High blood cholesterol
3.
High BP
4.
Physical inactivity
5.
Diabetes mellitus
6.
Obesity
7.
Stress
8.
High triglycerides
9.
ETOH abuse---moderate use, 1-2 drinks a day, reduces risk)
Contributing factors include: inflammation abnormalities in regulatory proteins of the hemostatic system (blood clotting) & possibly elevated
homocysteine (associated with vascular injury).
CHD Etiology
Starts with atherosclerosis which is a form or arteriosclerosis—characterized by atheromas (fatty
deposits)—which contribute to narrowing of med to large arteries.
Thrombosis—clot formation.
Ischemia—blockage/shortage of blood and O2.
All this begins in childhood---due to level of cholesterol (& type). LDL increases this where HDL
retards it. Smoking, high BP and high intake of sat fat and cholesterol increase the chance. In
contrast, physical activity decreases risk via its positive effects on LDL through HDL and
reducing BP.
Atherogenesis
Begins with lesion of the intima (innermost lining) of coronary artery. This injury is from damage to
endothelium—could be physical or from smoking.
Atherogenesis: “Formation of atheromatous deposits, especially on the innermost layer of arterial walls.” “The
formation of subintimal plaques in the lining of arteries.”
atheroma /ath·er·o·ma/ (ath″er-o´mah) a mass or plaque of degenerated thickened arterial intima, occurring in
atherosclerosis.
Picture on P-98.
Renegade LDL contributes to atheromas are free radicals. (P-97).
Inflammation (P-98): Atherosclerotic disease involves inflammatory processes. Major risk factors for CVD
including dyslipidemia, hypertension, diabetes and obesity all have pro-inflammatory features, as do bacterial and
viral infection.
The anti-inflammatory effect of physical activity may be mediated through beneficial changes in body weight.
C-reactive protein (CRP) is a protein found in the blood, the levels of which rise in
response to inflammation (i.e. C-reactive protein is an acute-phase protein). Its
physiological role is to bind to phosphocholine expressed on the surface of dead or
dying cells (and some types of bacteria) in order to activate the complement system via
the C1Q complex.
C-reactive protein, or CRP, a sign of inflammation and potential risk factor for heart disease.
Hemostasis: (factors that regulate blood clotting) are risk factors for CVD.
Hematocrit: (the % of blood volume occupied by cells) is a risk factor for CVD. High hematocrit
is associated with increased blood thickness and coagulability ( characteristics which increase the
contacts between platelets and endothelial cells which can promote aggregation).
Blood clotting factors are associated with increased risk of ischemic heart attack and stroke—
people who are active tend to have lower levels of clotting factors.
Homocysteine: Homocysteine is a common amino acid (one of the building blocks that make up
proteins) found in the blood and is acquired mostly from eating meat. High levels of
homocysteine are related to the early development of heart and blood vessel disease. In fact, it is
considered an independent risk factor for heart disease. High homocysteine is associated with low
levels of vitamin B6, B12, and folate and renal disease. Research has shown, however, that
reducing your homocysteine levels with vitamins does not reduce the risk of heart disease.
Physical Activity and CHD
P-100
On average, physical activity cuts risk of CHD by 30% to 40% for both men and women.
Physical inactivity is recognized by the American Heart Association (et al.) as a major
independent risk factor for CHD.
Occupational Activity and CHD Risk: Studies include—San Francisco Longshoremen; Railroad
switchmen and Israeli workers.
Leisure-Time Physical Activity and CHD Risk: In general, findings have been consistent in
showing an inverse relationship between physical activity and CHD risk.
Sedentary Behavior and CHD Risk
Sedentary behavior may be an independent risk factor for CHD, ---separate from physical
activity. P-107.
In other words, you may exercise (even vigorously) but if you spend a lot of the rest of the
day sitting, being inactive—you still carry the risk for getting CHD! You might exercise 2hrs
a day but that still leaves 22 to be sedentary!
Even among people active enough to meet exercise guidelines those spending more time sitting
were at increased risk of CVD mortality compared with those sitting less.
Physical inactivity contributes substantially to the public health burden. Eliminating inactivity
would have an impact on reducing excess mortality as great as, or greater than, eliminating other
major CHD risk factors.
Physical Fitness and CHD Risk
While physical fitness has a genetic basis—regular physical activity also contributes to higher
levels of physical fitness.
Low physical fitness is associated with increased risk of CVD & CHD. Cardio is the heart and –
vascular the veins and arteries it pumps blood to. Coronary heart disease is a problem with the
veins and arteries that distribute blood to the heart itself to keep it working properly.
The true size of the protective effect of physical activity against CHD is probably underestimated
by the current methods used to measure physical activity, which undoubtedly misclassify some
inactive people as active and some active people as inactive.
Although cardiorespiratory fitness is partly explainable by genetics, a high proportion of the
variation in cardio fitness is explained by physical activity habits. The agreement of studies is
that: Either physical activity or physical fitness supports the hypothesis of a causal relationship
between regular physical activity and reduced risk of CHD.
Strength of the Evidence
After seeing if the roles of chance, bias and confounding we can reasonably conclude that physical activity and fitness with lower CHD
exists---are these observations causal?
We must now apply the 5 main criteria to see if the observations are causal? These criteria are Mill’s canons are :1-temporal sequence, 2strength of association, 3-consistency of results, 4-biological plausibility and 5-dose response.
1.
Temporal Sequence: activity/fitness is measured first—before the outcome appears—higher activity—lower CHD risk. Thus, proper
temporal sequence.
2.
Strength of Association: CHD mortality is about twice as high for the sedentary as compared to active—or conversely, the active have
about half the risk for CHD as the sedentary.
3.
Consistency of Results: Data consistent for men and women---many studies yield similar results.
4.
Biological Plausibility: The biological mechanisms that explain the protective effects of activity against CHD are not fully known but
include factors related to myocardial O2 supply and demand and myocardial electrical stability. Also—better levels of HDL, decreased
body weight and BP, improved glucose tolerance, better hemostatic variables, & decreased inflammation.
5.
Dose-Response: Does CHD risk decrease by a predictable dose response pattern with increasing levels of activity? Yes—a curvilinear
dose response between activity and CHD risk exists. How much is the question?
Regular physical activity reduces CHD risk independent of other risk factors, but it can also favorably
influence CV risk factors such as BP, body weight, blood lipids, blood clotting factors, and inflammatory
markers.
P-112
Myocardial O2 Supply & Demand: Activity lowers cholesterol & triglycerides which should decrease
arterial plaque and help maintain normal blood supply to the heart. Also a lower BP at rest & during
submax exercise.
Physically active men have larger lumens in coronary arteries (autopsy).—less complete occlusions of
arteries and less scarring from ischemic events—even with advanced atherosclerosis.
Regular exercise lowers the O2 demands of the heart during physical activity of a fixed intensity, thus
reducing the risk of ischemia during physical work.
Hemostatic & Inflammatory Biomarkers
Activity might reduce the risk of coronary thrombosis via favorable changes in hemostatic & inflammatory
biomarkers. Decreased hematocrit comes from physical activity. Exercise should lead to reduced viscosity
(thickness) of blood—which might reduce coagulability and platelet stickiness.
Regular activity may also decrease platelet aggregation via changes in metabolism of prostaglandins.
[Prostaglandins are a group of lipid compounds that are derived enzymatically from fatty acids and have
important functions in the animal body. Every prostaglandin contains 20 carbon atoms, including a 5-carbon
ring.
They are mediators and have a variety of strong physiological effects, such as regulating the contraction and
relaxation of smooth muscle tissue.[1] Prostaglandins are not endocrine hormones, but autocrine or paracrine,
which are locally acting messenger molecules. They differ from hormones in that they are not produced at a
discrete site but in many places throughout the human body. Also, their target cells are present in the
immediate vicinity of the site of their secretion (of which there are many).
The prostaglandins, together with the thromboxanes and prostacyclins, form the prostanoid class of fatty
acid derivatives, a subclass of eicosanoids].
Exercise and habitual moderately intense physical activity are associated with a favorable blood
clotting profile and lower levels of markers for chronic low-grade inflammation that are
predictors of sudden coronary death resulting from blood clots after ruptures of atheromas.
Responses to Exercise
P-114.
Responses to acute exercise: Acute exercise increases blood coagulability but that effect is offset
by a co-concurring increase in fibrinolysis.
[Fibrinolysis is a process that prevents blood clots from growing and becoming problematic.[1]
This process has two types: primary fibrinolysis and secondary fibrinolysis. The primary type is a
normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medicine,
a medical disorder, or some other cause.[1]
In fibrinolysis, a fibrin clot, the product of coagulation, is broken down.[2] Its main enzyme
plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments
that are cleared by other proteases or by the kidney and liver].
Response after chronic exercise: Some studies suggest that chronic exercise diminishes increased
coagulability during exercise while maintaining fibrinolytic activity.
Chronic exercise increases VO2.
Electrical stability of the myocardium: Animal studies have shown that increased O2 demand of
the heart during exercise increases the risk of ventricular fibrillation—the leading cause of sudden
cardiac death. BUT—the increased ration of 02 supply and demand during exercise should reduce
the risk of V fib in people who have CAD. The reduction in the sympathetic nervous system
activity and catecholamine secretion should reduce myocardial irritability and the risk of V-fib.
Ventricular fibrillation (VF) is a severely abnormal heart rhythm (arrhythmia) that can be
life-threatening.
How Much Physical Activity is Needed to Decrease CHD Risk?
150 min/week of mod intensity (brisk walking) or 75 min/week of vigorous intensity aerobic
activity or a combo of the two that offers the same energy expenditure is clearly associated with a
CHD reduction.
Does the intensity and frequency matter?—Even with the same caloric expenditure?
Whether the dose response between activity and CHD is linear or curvilinear is unclear.