The Fibrillating Heart

Fibrillation is a word used to describe rapid, uncoordinated, wormlike wriggling of muscle fibers. Heart muscle fibrillation is the most common cause of cardiac “arrest.” Many people have seen devices called cardiac defibrillators and heard campaigns urging education in their use. Some people have even seen people rescued from imminent death by the electrical shock of a defibrillator. But many people also know friends and family members who have a heart condition called atrial fibrillation – one with which they live normally. Why is fibrillation sometimes lethal and sometimes simply a chronic heart condition? The answer lies in the heart’s muscular and electrical anatomy.


An electrically driven pump

The heart is a pump made from muscle and driven by an electrical system. Normal heart muscle contraction begins with electrical activity in the atria, the two upper chambers of the heart. There, the  “sinus node,” the body’s inborn pacemaker, begins generating a rhythmical electrical signal three to four weeks after the human egg is fertilized. An orderly wave of electrical activity and muscular contraction spreads through the atria to the lower chambers, the left and right ventricles. The muscle contraction pushes blood from atria through valves into the two ventricles below. The wave of contraction in the ventricles pushes blood from the right ventricle into the lungs and from the left ventricle out to the body. You feel each contraction of the ventricles as your pulse. Once the heart has emptied, it relaxes and blood passively accumulates in the atria, coming from throughout the body through big veins in the abdomen and the neck. After fraction of a second, the sinus node fires again and the pump goes into another round of action.

When the sinus node is no longer in charge

When atrial muscle fibrillates and the contraction of the atria no longer follows an orderly path, the atria no longer squeeze and push blood – but  most of the atrial blood still falls through the valves into the ventricles. Some decline in exercise capacity might result from incomplete emptying of the atria, but life goes on.  The disordered electrical activity from the atria often stimulates much too rapid, but still well-ordered activation of the ventricles and pulse rates as high as 170-200. When this happens the ventricles don’t have enough time to fill with blood between contractions, making symptoms worse and rate controlling drugs necessary. More on this later.

Ventricular fibrillation – an intolerable situation

When ventricular muscle fibrillates and there is no longer any coordinated pumping action to push blood out to the lungs and the body. Consciousness promptly fails, and the victim loses muscle tone. Technically the heart has not stopped, but its pumping action has. While there is still electrical activity, as there is in fibrillating muscle, an external shock can restore orderly heart muscle activity, which is why defibrillators work.

The origins of fibrillating heart muscle

Why does heart muscle fibrillate? The reasons are many and varied, but all are related to the fact that the primitive cells that formed the heart all possessed the ability to produce spontaneous electrical activity. Some of these, by virtue of their location in the developing heart, became the dominant pacemakers and conductors of electrical current. In the aging adult, changes in the heart’s structure wrought by both age and disease disturb the tidiness of the electrical conduction system, particularly in the thin walled, expandable atria. Some of the original electrical excitability of muscle returns and disordered patterns of muscle contraction result.

Who Fibrillates

Atrial fibrillation (AF) is a relatively common problem. It is age related, and more common in men than women. Underlying problems with coronary arteries, with heart valves, with high blood pressure, congestive heart failure and diabetes seem to trigger it. Transient atrial fibrillation is common after heart surgery, particularly valve surgery. It is also associated with binge drinking and stimulant use, and with use of prescription strength non-steroidal anti-inflammatory drugs (no study has been done yet to see if the same association is present in users of over-the-counter NSAIDS). AF is more common in people with long histories of high level endurance exercise (Nordic skiers), possibly because years of high volume demand on the heart stretch its muscular and electrical architecture. Hyperthyroidism can trigger AF and people with sleep apnea or lung diseases may develop it. Lone atrial fibrillation is the name applied when no risk factors are present. In these cases, abnormal electrical activity appears to originate near the pulmonary veins.

Ventricular fibrillation is almost always the result of underlying scarring in the heart, from prior heart attacks, from heart infections, or from deprivation of blood flow to the ventricular muscle during an acute heart attack. Other causes include congenital heart disease which affects electrical conduction pathways, cocaine and methamphetamine use and severe electrolyte imbalances such as seen in anorexia nervosa.

What does fibrillation feel like?

Atrial fibrillation may occur in brief episodes before it becomes a chronic heart rhythm. The cardinal symptom is an irregular pulse. Some beats are stronger than others. Sometimes the pulse is very rapid as well as irregular. While the normal, orderly electrical activity of the heart responds to physical demands via some complex physiology, the fibrillating atria do not allow that to happen and the predictable increase in pulse demanded by exercise such as climbing stairs can’t be met. In people who have fibrillating atria, shortness of breath with exertion is a common first symptom. An electrocardiogram shows a characteristic abnormal electrical activation pattern.

Symptoms of ventricular fibrillation are immediate and devastating – consciousness is lost within 30 seconds or less. Brain cells begin to die in 4 minutes. Ventricular fibrillation can be preceded by a very high pulse rate called ventricular tachycardia, often accompanied by lightheadedness and shortness of breath, or by premature or “ectopic” heartbeats which cause a sensation of skipped heart beats followed by very strong beats. They warrant medical attention.

Diagnosis and treatment of atrial fibrillation

Diagnosis of atrial fibrillation is important because not only for relief of symptoms, but also for preventing strokes. A fibrillating atrium is often dilated, with blood flow inside slow and sludgy. Clots may form in the nooks and crannies of the atrial chambers, later to be dislodged and sent upstream to the brain. It is estimated that 20-25% of strokes are caused by AF and sometimes a stroke is the symptom which brings the heart problem to attention. Because AF can be intermittent, it may not show up on one EKG. A monitor which can be worn for several days at home may be required to pick up episodes.

Shocking treatments: cardioversion and radio frequency ablation

A fibrillating atrium can be shocked back into a normal contraction pattern, in a controlled laboratory situation. This treatment is called cardioversion and is usually accompanied by drugs to prevent recurrence of fibrillation, and also drugs to control rate of ventricular contraction should atrial fibrillation recur. Surgical procedures using radio frequency ablation of sites of overactive electrical activity on the surface of the heart can be very successful in terminating AF and in preventing its recurrence, especially in cases of lone AF.

Preventing strokes

Blood thinners are necessary, temporarily, for patients being cardioverted or undergoing ablation surgery, to make certain that no clot is present in the heart at the time of conversion of the heart rhythm. Once it is clear that normal rhythms are holding, anticoagulants may be stopped. In chronic AF patients, however, blood thinners are always necessary.


A variety of cardiac drugs, called anti-arrhythmics, are prescribed prevent abnormal heart rhythms in people who are at risk for ventricular fibrillation, usually people who have known heart disease. They are the same as or similar to similar the drugs used to keep the heart rate from becoming too fast in people who already have AF.  careful control of other medical problems like diabetes is important. recognition and treatment of AF early may help prevent the development of chronic atrial fibrillation.

The biggest controllable risk factor: alcohol

While doctors know that excessive alcohol use is one of the leading risk factors for atrial fibrillation and realize that most patients underreport their alcohol consumption, they often do not emphasize the value of drastically cutting alcohol consumption once atrial fibrillation has occurred. Some of the other risk factors for atrial fibrillation, like aging, are beyond control, but alcohol consumption requires lifting the glass to the lips and swallowing. That is a choice and one well worth avoiding when the heart muscle has protested.

Broken Heart Syndrome: The Octopus Trap

“Doctoring her seemed to her as absurd as putting together the pieces of a broken vase. Her heart was broken. Why would they try to cure her with pills and powders?”  Leo Tolstoy, writing about Kitty’s heartbreak over Vronsky in Anna Karenina


Sometimes people say that a spouse who dies unexpectedly within hours to weeks after the partner’s death has “died of a broken heart,” though a variety of different medical conditions are responsible for the increased death rate among grieving partners, who are often elderly. In 1990 a paper appeared in the Japanese medical literature that described a peculiar heart problem, documented by modern technology, that the popular press seized upon as a possible explanation for the correlation between grief or fright or other emotional stress and sudden, unexpected death. The cardiomyopathy the authors described was an abnormality in the heart muscle of the left ventricle, the chamber of the heart that pumps blood out to the body. That part of the heart acted as if it had been “stunned” into inactivity and caused pain and other symptoms commonly associated with heart attacks, but the patients did not have any coronary artery disease.  These facts seemed fit neatly into the concept of a “broken heart.”

Why an octopus trap?

The ventriculograms, or dye studies, of the hearts of the Japanese patients described in the 1990 paper showed peculiarly dilated left ventricles, ballooned at their tips so that they resembled octopus traps – narrow-necked, flask-shaped contraptions that are easy for the tentacled animals to enter but hard to escape. In the Japanese language an octopus trap is a takot-subo and by the mid-2000s the name Takotsubo cardiomyopathy, or TCM, was widespread and many more cases had been described. Risk factors for the stress-induced cardiomyopathy were both physical and mental and included stays in ICUs, near drownings, major physical injuries, bad medical or financial news, legal problems and natural disasters, and, of course, unexpected death of a loved one. Cases have also been attributed to cocaine and methamphetamine use, as well as to exercise stress testing. These patients who acted as if they had had a heart attack were most often women and they had no history of heart problems prior to the events that hospitalized them.

Who is at risk? What are the symptoms?

Takotsubo syndrome is not common, but also not rare. It accounts for 1-2% people who have symptoms initially thought to be caused by regular coronary artery disease. In women, some people estimate that as many as 5% of heart attacks are actually TCM.  Most TCM patients are Asians or Caucasian, over 90% are post-menopausal women and most cases come to attention because of heart attack-like symptoms such as acute chest pain and shortness of breath.  But unusual presentations also occur as a result of the effects of the poor heart muscle function. When it’s pump action fails, the heart sends hormonal signals that affect water and salt balance in the body.  Fluid retention occurs in some people. Low sodium levels cause symptoms of profound fatigue in others. Clots may form in the poorly contracting ventricle, break loose and cause strokes. Lethal complications such as ventricular fibrillation and actual rupture of the impaired ventricle are very rare, but have occurred.

What’s the cause?

Diagnosis of Takotsubo syndrome requires new abnormalities in the electrocardiogram, absence of coronary artery disease and no evidence of heart inflammation from an infection or autoimmune disease. While the enzyme markers for a heart attack may rise, they do so earlier and fall back to normal more quickly than they do in a routine heart attack. In addition, the muscle abnormalities in the left ventricle can’t be mapped to the territory supplied by one coronary artery as they can when a blockage is responsible for the damage. Doctors who make a TCM diagnosis must also make certain the patient does not have a tumor called a pheochromocytoma, which produces stress hormones.

Most patients recover completely

By now TCM is known to be transient, with supportive care leading to complete recovery within 1-2 months in over 95%of patients. Recurrence is extremely rare. However, the actual cause, or mechanism by which the transient heart damage occurs, remains unknown. A number of theories have been proposed and all of them have something to do with a temporary derangement in function of the cells of the inside layer of cells of the left ventricular chamber of the heart. In these cells normal energy production from fatty acids is halted. The area of the heart involved happens to have a high concentration of receptors for catecholamines (adrenaline like hormones), perhaps making it susceptible to overstimulation and damage by severe stress. The high preponderance of postmenopausal women in case reports suggests that perhaps sex hormones are somehow protective factors.

Do people really die from broken hearts?

But is the Takotsubo syndrome responsible for deaths that seem to come from emotionally broken hearts? The mortality rate in cases of Takotsubo syndrome that come to medical attention is low. Recovery rates are high. Broken heart deaths most often occur in older people who have multiple health problems which might play a role. For example, when singer/actress Debbie Fisher died as she was planning her daughter Carrie Fisher’s funeral this year, a NYT reporter speculated about the cause of death being the Takotsubo syndrome. But Debbie Fisher had suffered several strokes in recent years and had high blood pressure. Later stories attributed her death to a fatal stroke related to high blood pressure.

Grief and stress do raise the risks of dying for the bereaved, but the causes of death are many and varied and mostly related to longstanding health problems.  The pills and powders Kitty scorned for her broken heart in Anna Karenina have a place in the treatment of the many other problems that occur in the setting of grief, especially depression. While it is tempting to attribute sudden, unexpected deaths in emotionally stressed people to an odd and mysterious heart problem named after an octopus trap, science requires objectivity and evidence.  So far the evidence about sick hearts that resemble octopus traps suggests that, at least in the people in whom the diagnosis is made, death is a very rare outcome and complete recovery is the rule.

Chilly Treatment

Large scale studies of survival after cardiac arrest have produced dismal statistics, with survival to hospital discharge of 17.6% when the patient is already in the hospital at the time of the arrest and only 6.1% when the arrest occurs outside the hospital.  The development and widespread deployment of portable automatic external defibrillators (AEDS) in public places has increased the number of people who make it to the hospital after cardiac arrest.  However, the survivor’s longer term outcome depends in large part on how much brain damage occurs during the arrest and whether or not the restoration of circulation damages the brain further, a phenomenon called reperfusion injury.  Because the odds of initial survival have improved, and because lowering the core temperature of the body appears to lessen reperfusion injury, the subject of hypothermia has emerged as a vibrant area of research and therapeutics.

Therapeutic hypothermia is an old idea

Hippocrates (460-370B.C.) recognized the value of cold temperatures in the outcome of soldiers with head injuries and in people suffering from tetanus. In the 1800s, Napoleon’s surgeon used ice to prepare limbs for amputation because it numbed pain and reduced bleeding. Over much of history, miraculous recoveries were reported in victims of cold water submersion. But not until the late 1950s did therapeutic hypothermia become a routine part of some surgical care, when experiments in animals demonstrated its value in protecting the brain during the open-heart surgery.  Despite some attempts to cool patients for other problems such as cardiac arrest, strokes and head injuries, the number of problems encountered in during cooling and in the re-warming phase put a damper on the use of the technique. Now, however, we are in the middle of a revival of interest in therapeutic hypothermia.

How does cold help?

Cold protects the brain because the biochemical reactions that sustain life are influenced by temperature. If the heart stops, the brain runs out of fresh supplies for energy production in two minutes. A downward spiral toward brain cell death begins unless blood flow is restored within the next two minutes. When blood flow is restored (reperfusion), a cascade of potentially damaging chemical reactions begins in cells that have been deprived of oxygen. The longer the period of arrested circulation was, the more damaging these reactions are.

The body at different temperatures

Changing the body’s temperature changes the speed and efficiency of its chemical reactions.  At temperatures over 105 many processes fail completely. As body temperature falls below normal, chemical reactions slow down.  Between 92 and 89.6  the damaging chemical responses that come after blood flow returns are blunted enough to improve outcomes significantly.  By 90, pulse and respirations slow and peripheral circulation shuts down. By 86 the patient may still be alive, but looks dead. This level of deep hypothermia is used for some long, difficult cardiac and neurosurgical procedures.

Lowering temperature is now routine, sometimes

Since 2005, the American Heart Association has recommended therapeutic hypothermia as a routine part of patient care after a cardiac arrest in circumstances that depend on the reason for the cardiac arrest, the speed of the resuscitation, and the state of the patient after circulation is restored.  Some medical centers are also experimenting with the technique in the treatment of certain types of strokes and head injuries.

How do you lower someone’s core temperature?

How do you cool a body that normally maintains a constant temperature that hovers within a few tenths of a degree of 98.6?  Any environment with a temperature less than body temperature provides a gradient for heat loss.  Deliberately making someone hypothermic means increasing that temperature gradient. In the presence of a gradient, heat radiates away from the body. Heat is also conducted away when the body is in contact with any colder substance; when the colder substance such as air or water is in motion, heat is lost even faster, by convection.  Heat is also drawn away by evaporation of perspiration on the skin’s surface, where the sweat keeps the microclimate humidity at 70% even when you think you are dry.   Heat also dissipates when warm moist air is exhaled from the lungs.

Several internal and external ways of changing the temperature gradient  exist: ice packs applied to the head, neck, axillae, groin, where large blood vessels are close to the surface; cooling blankets that house cold water circuits; closed catheters through which cold saline circulates inserted into large blood vessels; ice water balloons in the bladder.    These methods are directed at the core temperature of the body – the temperature of the internal organs and the brain. They do not cause problems like frostbite, seen commonly with accidental hypothermia, because the ambient temperature is not freezing and the skin is protected from direct exposure to ice packs being used for cooling.

The body resists lowering the temperature

Normally, we protect ourselves from falling temperatures by putting on more clothes and increasing activity, and by shaking and shivering, which produce heat.  A patient who has suffered a cardiac arrest will not engage in the normal behavioral responses, but he will shiver and perhaps become agitated, both of which are counterproductive to getting the temperature down. Sedation and even muscle paralysis are therefore necessary for the period of cooling.

Despite problems,  therapeutic hypothermia is here to stay

Current therapeutic hypothermia protocols call for maintenance of temperature between 32-34 (89.6-93.2) for 18-24 hours, followed by passive re-warming over the next 24 hours. Overshooting and undershooting of temperature are both common, as are difficulties maintaining electrolyte and sugar balance. Some complications like pneumonia and bleeding problems are more common than in similar patients not being treated with cold temperatures. Much work remains to determine the best timing for induction and maintenance of hypothermia after cardiac arrest, but it is clear that “the sooner the better” is the general rule and that the revival of interest in therapeutic hypothermia is here to stay.

Heart Failure: The Price of Success

In 1953, surgeon John Gibbon undertook the first successful open heart surgery using a heart-lung machine, a pump that performs both heart and lung functions while the heart is stopped for repairs.  The pump ushered in a new era of cardiac surgery and made it possible to correct heart problems that had up until then caused premature disability and death.

In the years that followed Dr. Gibbon’s groundbreaking surgery, materials science, technology and pharmacology advanced rapidly, allowing surgery and medication to be used to treat a wider variety of heart problems, including heart attacks. Today we live in an age of coronary artery bypass surgery, clot-busting drugs,  and stents that prop open diseased coronary arteries. Advancements such as these have reduced death rates from heart attacks substantially; nonetheless, heart disease remains the number one killer of men and women in the United States, and heart failurethe constellation of symptoms that come from poorly contracting heart muscle –  is now the leading cause of hospitalization for patients over the age of sixty-five. With all of the progress that has been made in cardiovascular care, how can this be?

Why is there more heart failure now than in the past?

The answer is simple. Mortality rates are lower in the immediate aftermath of heart attacks because of the ability to dissolve clots and prop arteries open. Drugs and lifestyle management may be slowing the progression of the coronary artery disease that causes heart attacks. As a result of these advances, people no longer die as often in the earlier phases of a very long disease process which often ends in failure of the heart muscle to contract as strongly as it needs to.

If you liken cardiovascular care to home repairs, then the major advances in care ­­­have taken place in areas roughly equivalent to plumbing and electrical maintenance. Angioplasties, coronary artery bypasses, and stents are used to keep the pipes open; electronic pacemakers provide power, triggering muscle contractions in an organized fashion, while defibrillators restart the power when there are outages. A house with functional plumbing and electrical systems remains habitable remains habitable long enough for the underlying structural elements of the building, like the roof, ceilings, walls, and floors, to begin to fail. In the heart, the underlying structural element is muscle. When the muscular structure of the heart begins to fail, the signs and symptoms of heart failure appear.

Signs and symptoms

Heart muscle fibers that begin to contract less efficiently reduce the heart’s pumping capacity, preventing adequate blood flow to the major organs. The body reacts to this deficient blood flow by increasing the volume of blood in the body. It accomplishes this by retaining more salt and water, but when this happens, the blood’s increased volume stretches the failing heart muscle and damages it even further. The more the heart stretches, the less efficiently it pumps; the less efficiently it pumps, the more the body tries to boost blood flow by retaining fluids.

This vicious cycle results in what is known as congestion. Congestion occurs when the tissues, including the lungs, becoming filled with excess fluid. This fluid buildup causes swelling in the legs and abdomen and a shortness of breath. Fatigue and an inability to tolerate exercise are the heart failure patient’s constant companions. Gravity causes fluid to collect in the lower half of the body while the patient is standing or sitting, and when he lies down, it becomes redistributed, accumulating in the lungs where it can cause a telltale shortness of breath that is symptomatic of a deteriorating heart.


Age is an important contributing factor in the development of heart failure because the longer people live, the more time there is for coronary artery disease and the problems that contribute to it to take their toll on the heart muscle. Coronary artery disease deprives areas of the heart of blood and oxygen, leaving behind damaged muscle that contracts poorly and moves blood inefficiently. Smoking, excessive alcohol use, diabetes, hypertension, obesity, and lack of exercise contribute not only to coronary artery disease, but also to weakening the heart muscle directly. Less common factors involved in heart failure include viral infections that affect the heart and a variety of rare metabolic conditions that disrupt heart muscle fibers. Heart valve disease, when left untreated, can ultimately damage the heart by dilating it or causing it to thicken. However, valve disease is much less prevalent since the development of successful antibiotic treatments for childhood streptococcus infections.


The quality and length of life heart failure patients can expect depends on how closely they adhere to the treatment plans provided by their doctors. Salt-restricted diets are a very important part of a heart failure treatment plan, and the mainstays of drug treatment plans are medications that prevent salt retention, get rid of excess water, improve the ability of the heart muscle to contract, and decrease blood pressure. Heart failure treatment treads a fine line between causing the patient’s body to retain too much and too little fluid. Drying a heart failure patient out too much can push the kidneys into failure. Too little and the lungs are liked soaked sponges, unable to exchange carbon dioxide for oxygen efficiently.  The margin of error in fluid balance gets smaller and smaller as the disease progresses and this tightening window contributes to high hospital readmission rates for congestive heart failure patients.  Physicians must monitor their patients’ weight, symptoms, electrolytes, and kidney functions more and more closely and start adding tests like chest X-rays and echocardiograms.

A variety of innovative devices and surgical procedures have been designed to cinch up dilated, failing hearts but have not succeeded in producing adequate results. Some success is being reported from the use of multiple pacemakers, which allow different segments of the heart to be stimulated in a defined order that improves the sequence of muscular contraction enough to generate greater cardiac output. Currently, bi-ventricular pacing—the separate pacing of both sides of the heart–is the most promising addition to the heart failure treatment arsenal. Cardiac transplantation remains the most difficult, expensive, and uncommon solution for a heart that has reached the end of its functional life.

Heart failure may eventually be overcome by artificial pumping devices or methods of stimulating the production of new cardiac muscle, but in the meantime, prevention is still the most desirable treatment option. Not smoking, maintaining a healthy weight and good exercise habits, sticking to a balanced diet of fresh foods, getting adequate sleep, and managing stress well are all cheap and valuable ways to invest in your heart’s health.


Torn Aortas: Saving Life Depends on Recognizing Symptoms

“There is no disease more conducive to clinical humility than aneurysm of the aorta.”   William Osler, 1849-1919

    John Ritter, star of television’s Three’s Company, died unexpectedly at age fifty-four from aortic dissection, a catastrophic event which starts as a small tear in the lining of the aorta, the largest blood vessel in the body. His tear, like most aortic dissections, occurred in the part of the aorta that exits the heart and ascends toward the head, but dissections can anywhere along the course of the aorta as it turns and then descends along the back wall of the chest and abdomen. Actor Alan Thicke’s recent death has also been attributed to an aortic tear. In neither case was the cause of death confirmed by autopsy, presumably because diagnosis was made clinically and by imaging studies once the men reached medical care. Diagnosis in both cases came too late for their lives to be saved. The first step in saving the life of someone with an aortic dissection is recognition of the symptoms. As Osler accurately stated, this is not necessarily easy. 

Upper Aortic Symptoms 
Symptoms of aortic tears vary according to the part of the aorta involved. In the upper aorta, as in Ritter’s case, the tear appears without warning. The first symptoms, such as severe chest pain, confusion, dizziness, nausea and vomiting, come from blood tunneling its way into the tear and under the aortic lining, separating it from the thick outer wall of the blood vessel. Heartbeat by heartbeat, the tunnel enlarges and a growing clot of blood extends around the inner circumference of the aorta and along its length, stretching from the ascending part of the thoracic aorta into the curved aortic arch branches where large arteries branch off and carry blood to the head and arms. 

The differences between dissection and heart attack symptoms

    Sadly, like John Ritter, almost 40 percent of people with upper aortic dissection who get to medical attention are not diagnosed in time for doctors to attempt surgical repair. Within forty-eight hours, half of them are dead. Diagnosis depends on recognition of subtle and qualitative characteristics of symptoms that differ from similar heart attack symptoms. Chest pain is severe from the beginning and sometimes described as ripping or tearing. Its most distinctive quality is sudden onset of maximally severe pain . Often people report a sense of impending doom. The pain may radiate up the neck or into the back, as it can in a heart attack. As the dissection progresses, clotting blood can block the openings to the aortic arch branches and even work its way backwards to damage the coronary arteries that nourish the heart. The aortic valve may be damaged and begin to leak. 

Symptoms From the Descending Aorta

     While the involvement of so many other structures in an upper aortic dissection can produce a host of symptoms that manifest themselves in the heart, the brain, the neck, the face, and the extremities, sometimes confusing physicians, descending aortic symptoms are more straightforward. Pain from dissection in the descending thoracic aorta bores through to the back. In the abdominal aortic segment dissection pain may be felt in the flank, lower back, or groin. Because the descending aorta is more tightly bound to surrounding structures, tears may be more confined and symptoms less severe. 

Dissections and Aneurysms

   Sometimes a dissection begins in an aortic wall already weakened enough to have ballooned out into an aneurysm, which is a distended spot in an artery wall. Ninety-five percent of aortic aneurysms are located in the abdominal aorta, and aortic dissections in the abdomen are often triggered by the prior development of an aneurysm. A tear in the wall of an aneurysm can cause the aorta to rupture completely causing internal bleeding, with mortality rates between 75 percent and 90 percent of aortic aneurysms Fortunately, aneurysms are often found incidentally on imaging tests for other problems, or as part of an investigation of vague abdominal or back pain or of a pulsating sensation in the lower abdomen allowing time for surgical repair of the damaged artery before rupture occurs. 

Who’s at Risk
    Most upper aortic dissections occur in people between the ages of forty and seventy, with men affected three times as often as women. In otherwise healthy and relatively young people like John Ritter, the tear begins because the aortic wall is weakened by genetic processes that are often poorly understood. Pregnancy and cocaine use are also risk factors below age 40. In older people and in smokers high blood pressure, atherosclerosis are responsible for the breakdown in the aortic lining, but even in these patients, dissections tend to run in families. 

     While smoking, hypertension, and atherosclerosis are risk factors in all types and locations of aortic disease, the abdominal aorta is particualry susceptible to their degenerative effects. Abdominal aortic disease is far more common than the forms of aortic disease that affect younger people and most aneurysms of the abdominal aorta reflect age-related (over age sixty) vascular degeneration. An estimated 5 percent of men over age sixty-five have some degree of degenerative abdominal aortic dilatation. 

The importance of family history
Assessment of a patient’s family history is very important in diagnosing aortic diseases like aortic dissection because genes control the proteins that make up the connective tissue of the thick aortic wall, and there can be a hereditary predisposition to dissection and aneurysm formation, particularly in younger people like John Ritter. One relatively common condition (1 in 5000 people), which can affect the connective tissue and lead to aortic dissection, is Marfan’s syndrome. The Olympic volleyball star Flo Hyman had Marfan’s syndrome, which accounted for her six feet five stature and long arms and fingers. She died at age thirty-two of aortic dissection. Dissections can also occur in people with congenital heart abnormalities, particularly those that affect the aortic valve.  

Surgical repair of aortic aneurysms and dissections is a serious and complicated undertaking. Incidentally discovered abdominal aneurysms and aneurysms found by screening programs should be followed carefully with ultrasound or computerized tomography scans because the risk of rupture is correlated with the size of an aneurysm. Surgical repair is far less dangerous when done before dissection or rupture but carries risk enough to warrant waiting if the aneurysm is less than five centimeters in diameter. 

    Once a dissection has begun, the outcome of surgical repair rests heavily on the condition of the patient going into surgery, on the experience of the surgical team and hospital involved, and on the complexity of the procedure required. In recent years, radiologists and cardiologists have developed procedures to repair the inside of the aorta by deploying stents and grafts via catheters inserted though the arms or legs and guided by x-ray. Initially, these procedures were only used on patients who were too frail or sick to undergo the rigors of open surgery. Increasingly, though, these less invasive procedures are gaining favor and are even being used to repair dissections of the descending thoracic aorta, which have traditionally been treated by careful control of blood pressure. More research will have to be done to assess the long-term outcome of stent and graft treatments. 

Not even recent technological advances would have helped John Ritter, however, because the proper diagnosis was not made prior to his death. His family has since set up an educational foundation called the John Ritter Foundation for Aortic Health ( with the goal of increasing knowledge and awareness about a disease which is still a very humbling clinical problem for the medical professio

Cholesterol Phobia

Cholesterol research is difficult, esoteric and accessible in journals that seldom make it beyond their target audience – other people doing the same type of work. One theory about the relationship of cholesterol and heart disease has dominated medical practice for over half a century, but there has always been dissension in the ranks of scientists, some of whom labor away in obscurity, slowly building a case that may one day topple the current dogma. I have attempted to make this subject accessible to a non-medical audience because the current paradigms for thinking about heart disease and treating it affect everyone who sees a doctor, listens to the news or reads the popular press – even children, because they eat what their parents believe is healthy for them.   
Cholesterol phobia: is the end in sight?

       Cholesterol earned a villain’s reputation because it got caught at many criminal scenes where victims succumbed to heart attacks. It was found lurking in the walls of arteries too narrowed by “plaques” to allow blood passage. Even in young healthy men, cholesterol- laden “fatty streaks” were surprise findings at autopsy after accidental or war-related death. Experimentally, fat choked arteries were easy to produce in experimental animals by feeding them food pellets saturated with fat – even olive oil worked. The laboratory work bolstered attempts to show that different populations consuming different amounts of fat had different rates of heart disease. Though both the laboratory and epidemiology studies were fraught with contradictory results, and the dietary cholesterol theory of heart disease was initially rejected by the American Heart Association, the personalities and scientific politics involved eventually catapulted the theory into the lives of all Americans, over 20 million of whom are now on potent drugs to combat the evil substance. 

The dietary theory of heart disease

       After more than half a century of war on cholesterol, the dietary theory remains just that – a theory – no matter how many commercials remind you that you need to lower your cholesterol. You may be surprised to hear that cholesterol could be absolved of its villainous status, within your lifetime. But don’t expect your doctor to agree, at least not yet. The cholesterol theory has a grip on our culture that is almost religious. The current dogma, advertised everywhere, is simple: there is good cholesterol, labeled HDL, and bad cholesterol, labeled LDL and anyone who cares a whit about his health will do whatever it takes to get those numbers in line with the current recommendations of the American Heart Association –eat a low fat diet, exercise, and take the right drugs. 

Inconvenient facts

Inconvenient facts have always dogged the theory. Cholesterol levels plummet in seizure patients treated with high fat, no carbohydrate diets. Heart attacks occur despite normal cholesterol levels. Low fat diets raise cholesterol levels -President Eisenhower was one of the most famous examples. And buried in the literature of the last half century are many clues pointing a blaming finger away from cholesterol and toward the complex lipoproteins that ferry it around the body. As more and more questions are raised about the efficacy and dangers of drugs that reduce cholesterol, more attention may turn to these lipoproteins. After all, like cholesterol, they have been part of the statistic most closely associated with heart disease – the LDL (low-density lipoprotein) cholesterol. 

What are lipoproteins? 

       Total cholesterol measures cholesterol attached to lipoproteins. Lipoproteins are combinations of phospholipids (fats that dissolve in water) and specialized proteins that fit like keys into receptors on cells. Lipoproteins function like cargo ships, carrying fats to cells for fuel, to fat tissue for storage, and back to the liver for reprocessing when demanded. More or less cholesterol crowds aboard each boat depending on the number of boats available. The size of the fleet, in turn, depends on the amount of triglycerides (another type of fat), awaiting shipment. 

Triglycerides rule

        Triglycerides and cholesterol are very different fats. Triglycerides provide the fatty acids that fuel most cells and are stored in fat tissue for later energy demands. Cholesterol yields no energy at all. It is a building block, used in the construction of all cell membranes and in the making of hormones and bile. Not all cholesterol comes from fat in the diet. The brain makes its own, and the liver and skin make whatever the body needs – raising production whenever dietary intake is low. Cholesterol and triglycerides attached to lipoproteins are like citizens of two different countries travelling together on one of the country’s boats. That country that builds the boats belongs to the triglycerides. The more triglycerides present in the body, the more lipoproteins in the fleet.    

The varying density of lipoproteins 

Lipoproteins fully loaded with cholesterol and triglycerides are fluffy and buoyant (fat floats) and called very low density lipoproteins, VLDL for short. They dock at cells in need of fuel or cholesterol, unload some cargo, lose some buoyancy, and become a little denser. Eventually they become low-density lipoproteins (LDL) and , with no energy or building material left to give up, they return to the liver for recycling. Another particle type called high-density lipoprotein (HDL) is even less buoyant – and less well understood. In contrast to cholesterol bound to LDL and VLDL, the cholesterol carried by HDL particles, like the cholesterol carried away from the intestines by chylomicrons (very large lipoproteins) does not contribute to the storage of fat in any tissues so is not associated with plaque formation in arteries. 

What do the anti-cholesterol drugs do? 

       The widely prescribed statin drugs block the body’s ability to make cholesterol, which makes less cholesterol available to be loaded on to the lipoprotein boats. But boat make proceeds apace because it is driven by the amount of triglyceride awaiting transport- and the triglycerides, remember, come from dietary carbohydrates. Lowering cholesterol manufacture does not lower  lipoprotein production  – the lipoprotein boats will simply carry less cholesterol per lipoprotein particle, making each particle smaller and denser. Will this magically keep cholesterol out of artery walls? Not a good bet. Lipoprotein research labs have identified seven different particle types within the LDL fraction of total cholesterol. Heart risk appears to be correlated with the smallest and densest sub-fraction – the kind carrying the least amount of fat per molecule. (The anti-cholesterol drugs do have an independent anti-inflammatory effect which may be the way they diminish risk of a cardiac event in people with heart disease.) 

Take-away message

       So how does this complicated information change your life? Triglycerides, the stimulus for VLDL and LDL production, are a product of carbohydrate processing – especially of sugars and refined grains. Lowering VLDL production and hence LDL production requires lowering dietary carbohydrates – not fat, not cholesterol. Blood cholesterol isn’t even a good marker for total body cholesterol, which includes cholesterol squirreled away in artery walls. Cholesterol in arteries behaves much like cholesterol stored in fat tissue. It is responsive to the entire array of interconnected feedback loops involve not only fats, but carbohydrates and insulin and all the other hormones. It is time to respect its complexity and quit expecting that coaxing the body to make less cholesterol by taking drugs to block its production, or by eliminating it form the diet will end the scourge of heart disease. 

Walking or Running For Fitness? Both.

Karl is a friend who hikes a local trail almost every day. The trail is not easy, ascending 300 feet in the first quarter mile alone. Uphill stretches push the pulse and breathing rates up; downhill stretches require strength, flexibility and balance. Karl is 83 and he has maintained his physical fitness with functional activities like hiking and skiing. His old friends in the valley no longer hike with him.  “It is sad,” he says, shaking his head. “They didn’t need to stop and now they can’t do it anymore.”  He is right – fitness requires doing.

Why bother staying fit?

Physical fitness is worth preserving. It makes aging easier and more enjoyable, prolongs independent living and accessibility to many pleasurable activities, and lessens dementia risk. It raises insulin sensitivity, reduces blood pressure, cuts weight and improves cardiovascular risk factors.  You needn’t be an athlete to be fit and, as Karl demonstrates, fitness does not require gym memberships, classes or travel to and from a sports facility. And as many researchers have demonstrated, simple activities such as walking and running have positive effects on body and mind.

What does running do for you?

Much information about the beneficial effects of running comes from studies done in high level athletes. This sports oriented literature can be bewildering, leading into a thicket of terms like periodization and lactate thresholds and specialized measurements like aerobic capacity and heart rate variability. But buried in the details of these studies are useful facts that, when simplified, provide guidance that will improve the fitness of beginners and people who already have a stable exercise habit.

Why walk too?

While running promotes faster weight loss than walking, both lower blood pressure and improve heart and lung function. Walking requires more of the shin muscles and running more of the gluteals and quadriceps. Both are worth incorporating into a fitness program because of these different patterns of leg muscle use. Balancing the strength of lower and upper leg muscles and improving flexibility of all of them lessens strain on knees.

How much of each?

The balance between walking and running in an exercise plan depends on beginning fitness level and on goals.  For a sedentary individual unaccustomed to exercise, regular walks will be enough to increase fitness, at least in the beginning. For someone who has run in the past but not recently, a combination of walking and running is a good way to start. And for someone who has a good level of fitness and a long running history but is getting older and accumulating aches and pains, the addition of walking balances leg muscle groups.

Short periods of intense effort pay off

For all groups, the introduction of short bouts of more intense walking or running into a regular exercise program is perhaps the most important aspect of maintaining and improving fitness. These “intervals” provide the challenge that the heart and lungs need to stimulate their capacity to provide blood to working muscle more efficiently. A recent study from Denmark provides good evidence that a very small amount of time spent running faster improves fitness. It also decreases blood pressure and makes routine running more efficient. In the study, the addition of an interval program of faster activity, performed twice a week, was not only well tolerated but study subjects stuck with it and benefited more than they did from other seemingly more difficult programs.

In the Danish program, a short warmup is followed by two five minute segments separated by a 2 minute rest, and followed by a short cool-down walk or run. The five minute segments consist of running comfortably for 30 seconds, harder for another 20 and as fast as possible for another 10 seconds, and repeating this pattern 4 more times. A walker could try the same pattern, with effort judged by breathing rate and difficulty and by the ability to complete the 5 minute segments. As improvement occurs the segments cover more distance.

Change the terrain

Other ways to increase effort include walking or hiking uphill and climbing stairs. The important thing is to build in some segments of exercise that require more effort and cause faster breathing into at least two periods of exercise a week. In addition, going “off-road” on dirt and rock and sand requires use of little balancing muscles and improves strength and balance.

How much is enough?

How much weekly exercise is necessary? One figure quoted frequently is 150 minutes – less than half an hour a day. The payoffs though, depend on demanding more of the heart and lungs during those times than during routine life. Ambling up the street at the same pace as you walk between the couch and the TV will have less effect than but walking briskly, to the point of feeling slightly short of breath.

Can people who have arthritis walk and run for exercise? For the most part stiff joints feel better with movement. If walking or running gets easier as the joint is “warmed up,” the joint stiffness and discomfort are most likely related to shortened muscles and tension on their tendons, not to joint pathology that will get worse with activity.

Make sure you remain able to get up and down from the ground

For overall fitness, some time also needs to be devoted to strength and flexibility exercises. Pilates exercises, yoga practices, weight lifting and core muscle strengthening exercises like the TRX programs all improve muscle strength and flexibility, enhance walking and running ability and contribute to improving balance. The ability to get up and down from the ground indicates a lot about these non-cardiovascular aspects of fitness, and every effort should be made to make certain this ability is preserved over time.

Mind over matter

The most difficult part of beginning or sticking to an exercise plan is often in the mind rather than the muscles. When Karl says his friends didn’t need to stop hiking, he means that they stopped pushing themselves before there were any compelling physical reasons to stop, and then one day they no longer had the ability which he has so far maintained. His example is inspiring.

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