By Paul J. Rosch, M.D., M.A., F.A.C.P.
The appreciation that emotional factors can have a powerful influence on the heart, and the acknowledgment of some intimate, although poorly understood, heart-mind connection, is certainly not new.
Toward the end of the 19th century, Sir William Osler, an astute clinician, succinctly but accurately described the coronary-prone individual as a "keen and ambitious man, the indicator of whose engines are set at 'full speed ahead.'"
In the 1930s, the Menningers suggested that coronary heart patients tended to have strongly aggressive behavior, and a decade later, Flanders Dunbar, who introduced the term "psychosomatic" into American medicine, characterized such individuals as being authoritarian with an intense drive to achieve unrealistic goals.
Fierce ambition and compulsiveness to achieve power and prestige were emphasized by many subsequent investigators, and over 50 years ago, the rising incidence of coronary heart disease in England was attributed to increased stress, especially in the workplace.
All of these 19th and 20th century physicians were describing various aspects of what is now called Type A behavior, a term coined by Meyer Friedman and Ray Rosenman 50 years ago.
Type A individuals are apt to be very competitive and are usually in a hurry, so they eat, talk, and do most other activities as quickly as possible. They generally try to do too many things at the same time, are frequently concerned with what they are going to do next, and are often so preoccupied with work that they tend to have few other interests.
Around the same time, Stewart Wolf independently but similarly noted that coronary disease was often due to the constant striving to achieve unrealistic goals, adding that even when successful, such individuals were unable to relax and enjoy the satisfaction of their labors.
He called this the "Sisyphus Syndrome", since in Greek mythology, Sisyphus had been condemned to roll a huge boulder up a hill, which, as soon as it reached the top, always rolled down to the bottom, and he repeatedly was forced to start all over again.
Type A was acknowledged by the National Institutes of Health ( NIH ) to be a powerful risk factor for heart attack. In that regard, the large, long term MRFIT study showed that lowering the standard risk factors of cholesterol, hypertension and cigarette smoking failed to show any reduction in heart attacks or coronary deaths in those who achieved these goals.
In contrast, two other intervention trials conducted during this same period were so successful that they had to be halted prematurely so controls would not be denied their benefits. One was a trial designed to modify and lessen Type A traits and the other was administration of propanolol (Inderal) a drug that blocks the damaging effects of stress hormones associated with Type A behavior.
Attempts to study the mechanisms whereby emotional states could produce cardiovascular damage and sudden death received tremendous impetus as a result of the investigations of Walter Cannon at Harvard University in the early part of the last century.
Cannon's studies showed that the response to the stress of acute fear resulted in a marked increase in sympathetic nervous system activity and an outpouring of adrenaline, which assisted the animal in life saving "fight or flight" activities.
His subsequent studies of voodoo deaths and lethal spells due to "bone pointing" by witch doctors in primitive societies also implicated a flooding of the system with adrenaline as the most likely cause of a fatal arrhythmia.
In the late 1940s, Hans Selye's formulation of his General Adaptation Syndrome, and Diseases of Adaptation provided further insights into stress induced heart disease in animals that he believed also applied to humans.
Selye's subsequent research in the 1950s included the experimental production of cardiac necrosis due to stress, in which direct biochemical injury to heart muscle rather than occlusion of a coronary vessel was the most important factor. He demonstrated the important influence of sodium, potassium, magnesium, and calcium in modulating this response. His results were subsequently corroborated in humans and now form the basis of various therapeutic strategies and pharmacologic approaches.
Selye's emphasis on the pituitary-adrenal cortex dominated stress research in the 1950s and 1960s, but subsequent advances led to a recognition that human responses to stress involved a vast repertoire of hormonal secretions including other pituitary and target gland hormones, the renin-angiotensin system, prostaglandins, and brain peptides such as serotonin, dopamine, melatonin, prolactin, and the endorphins.
Attention was also being focused on central nervous system mechanisms that initiate and transmit the stress signal, with evidence suggesting that both heart rhythm and force of contraction are regulated by the same centers in the frontal cortex of the brain that stimulate sensory receptors during acute fear.
Experimental animals that would normally succumb to ventricular fibrillation due to severe psychological stress are protected if the nerve pathways from the frontal cortex to the brain are severed or temporarily blocked by freezing, and the search began for a drug that might replicate this.
Here are a half dozen of the numerous other mechanisms that link stress to coronary heart disease:
1. For those who still believe in elevated cholesterol, stress has a far greater effect than fatty foods as demonstrated in tax accountants as April 15 approaches, students on the eve of an important exam and several other studies. Stress also contributes to other risk factors such as smoking, hypertension, diabetes and obesity.
2. Stress can cause constriction of the coronary vasculature and increased platelet stickiness and clumping that promote clot formation.
3. Stress increases homocysteine, CRP and fibrinogen, all of which are risk factors or risk markers for coronary heart disease.
4. Stress causes increased deep abdominal fat deposits that contribute to insulin resistance and metabolic syndrome with its varied and sometimes deadly cardiovascular consequences.
5. In addition to Type A behavior, hostility, excessive anger, stressful life events, depression, and anxiety, have all been demonstrated to cause coronary heart disease.
6. It has been proposed that unstable atherosclerotic plaque might actually represent a "microabscess" that resulted from an infection. There is surprising support for this theory, and it is well established that stress can increase susceptibility to infections.
Uffe Ravnskov and Kilmer McCully suggest that atherosclerosis and unstable plaque may be due to infection rather than cholesterol deposits. They point out that lipoproteins are part of a nonspecific immune defense system that binds and inactivates microbes and their toxins by the formation of complexes.
This would explain why vulnerable plaque contains lipids and microbes in the arterial wall, why neutrophils are seen in the myocardium following an infarct, as well as the frequent occurrence of fever, diaphoresis, elevated inflammatory markers and even bacteremia in acute myocardial infarction.
There is considerable supportive evidence. The presence of cholesterol in human atheroma was first described in 1856 by Rudolph Virchow. He termed it endarteritis deformans to emphasize it resulted from an inflammatory process that injured the intimal lining of arteries, as follows
"We cannot help regarding the process as one which has arisen out of irritation of the parts stimulating them to new, formative actions; so far therefore it comes under our ideas of inflammation, or at least of those processes which are extremely nearly allied to inflammation." In other words, atherosclerotic plaque in humans was a response to injury or inflammation. The cholesterol deposits came later.
A variety of microbes have been identified in atherosclerotic plaque and Chlamydia pneumoniae has been cultured from the atherosclerotic plaque of patients with unstable angina. This organism is a fairly harmless pathogen that causes a mild flu like illness, but unlike most other bacteria, it lives not on the surface of cells but within them, and is frequently found in the coronary arteries of heart disease patients, but not others.
While this might not produce any signs or symptoms, it can continue to stimulate immune system components designed to attack foreign microorganisms. These chemicals are attracted to sites on the inner lining of blood vessels where Chlamydia pneumoniae is frequently located, which can produce a smoldering, low-grade inflammatory response that results in the steady growth of plaque.
One study reported that a protein on chlamydia cell walls was almost identical to one found in heart tissue and suggested that when the immune system attacks chlamydia, it accidentally attacks the heart protein as well. In experimental animals, the resultant microscopic changes are very similar to those seen in human myocardial infarctions.
Most people probably harbor chlamydia, as well as Helicobacter pylori, which causes peptic ulcer and many with the tubercle bacillus also have no signs or symptoms of their presence. It is only when stress reduces resistance to these pathogens that clinical disease surfaces.
Excerpted, with permission, from: Health and Stress, The Newsletter of The American Institute of Stress. ( www.stress.org )
Paul J. Rosch, M.D., M.A., F.A.C.P.
President of The American Institute of Stress,
Clinical Professor of Medicine and Psychiatry at New York Medical College,
Honorary Vice President of the International Stress Management Association and Chairman of its U.S. branch.