Posts for: July, 2018
Our bodies are large and complex. Cells are not concerned with complexity. They are simply needy. The broad sweeping narrative of normal cardiovascular function is delivery that is prompt, proportional and predictable. The normal heart and arteries deliver, regardless of circumstances and with little notice. Simple. There are, however, a few details.
James M. Wilson, MD The Heart Beat Houston MDs Neurology: 713-790-1775 Cardiology: 832-336-1530 Fax: 713-790-1605 Normal Cardiovascular Function Our bodies are large and complex. Cells are not concerned with complexity. They are simply needy. The broad sweeping narrative of normal cardiovascular function is delivery that is prompt, proportional and predictable. The normal heart and arteries deliver, regardless of circumstances and with little notice. Simple. There are, however, a few details. The Arteries The average cell needs to be bathed and refreshed constantly. Cells enjoy just such a bath that moves in a gentle to and fro, sent out from arteries and collected by veins. A heartbeat lasts a very short time, only about 1/5th of a second. In that time, roughly 4 tablespoons of blood are sent out to the arteries for delivery and the pressure in the arteries rises from 70 to 105 mmHg. Were arteries and veins simple plumbing, every bit of blood in the body would be required to move in unison in the short time of a heartbeat. The strength required to accomplish this feat would be so great that a human heart would have to have the strength of a bull. Arteries stretch and rebound. They are smarter than plumbing.
In the short time of a heartbeat, blood is shoved into the largest artery (Aorta). Blood already sitting there is pushed forward. At the same time, the artery stretches out to make more room. Instead of moving all of the blood in unison, from the heart to the smallest artery, pressure builds. Afterward, while the heart is relaxed and refilling, blood continues to be jostled about by arterial walls that are like a stretched spring. Up and down the line of arteries, stretched walls vibrate their encouragement to keep blood moving. All of the work moving blood does not have to be done in the blink of a heartbeat. Because of artery's rubber-like behavior, much of it the work accomplished during the time in between.
There is an aphorism about organizations. Sergeants run the army. Nurses run the hospital and secretaries run the world. Arterioles run the circulation. (Figure 1) They are the faucets governing flow and respond to strategic direction from nerves and hormones. For example, adrenalin makes many arterioles tighten severely so that blood will be diverted to where it is most needed. However, most of the decisions about blood flow to a tissue are made locally, without direction from nerves and hormones. Arterioles are the entry, controlling flow into the large, thin walled network of capillaries. Sitting upstream from all of the cells that they supply, arterioles can somehow sense how much blood is needed. Capillaries weep much of the fluid part of blood across their cheesecloth-like walls. The part of blood that can't cross the wall stays inside the vessel and moves along to a pool of low-pressure venules, the microscopic beginnings of the veins. There, because of the lower pressure, fluid seeps back inside of the vessel. That fluid contains waste from the cells.
Tissue waste that includes Carbon Dioxide (CO2), adenosine and a few other things that are carried with the fluid back into blood vessels make microscopic veins relax. Relaxed veins grow larger and blood speeds away more quickly, as though running down a steeper hill. Easier out from the veins means faster flow in the capillaries and, in turn, faster flow in the arteriole. The lining of the arteriole feels the tug of the torrent and releases Nitric oxide. Nitric oxide relaxes the wall of the arteriole, opening the channel for more blood to pass. (Figure 2). This process is called autoregulation.
Large arteries absorb and distribute the blow from the heart while small arteries regulate where and how much blood may pass. Changing either of these behaviors can cause disease. More commonly, these aspects of artery function are changed in the course of a disease. For example, high blood pressure has many causes. In any individual with high blood pressure, there is rarely a single fault, but many combined. Arteries, both large and small, adapt to elevated blood pressure by increasing stiffness and thickness of their walls. The result is perpetuation of rising blood pressure regardless of its root cause(s). Meanwhile, many of the medicines that lower blood pressure act by changing either stiffness of large arteries, the opposition of small arteries or both.
Our heart is actually two muscular pumps joined side-by-side and twisted together like a work from Escher. The two pumps are referred to as right and left for simplicity. On each side, an upper chamber (atrium) receives blood from veins and a lower chamber (ventricle) discharges it with enthusiasm into an artery. There are two sets of blood vessels connected to the heart. Both sets of vessels include both arteries and veins.
A large artery called the aorta carries blood away from the heart and on through all the needy tissues, such as the brain, muscles, intestines and kidneys. The blood collects in large veins (Vena Cava) and returns to the heart, but to the part that will send blood to the lungs. The vena cavae (there are two) is connected to the right atrium, where blood rests briefly before moving to the ventricle for discharge to the lungs. The second set of blood vessels carries blood away through the pulmonary artery, travels through the lungs and returns in pulmonary veins. Pulmonary veins are attached to the left atrium where blood rests briefly before moving to the ventricle for discharge to all points distal. Between each of the atria and their ventricles, and between each ventricle and its artery, is a valve that ensures blood will only move in one direction. Together, both sets of arteries and veins make a grand loop in a figure eight, with the heart at its center: Aorta to Vena Cava to Heart to Pulmonary Artery to Pulmonary Vein to Heart and repeat. The left ventricle is usually the principle focus of interest as the pump supplying the body. It moves blood forcefully in increments, one-quarter cup with each beat. (Figure 3)
Individual heart muscle cells function simply. They shorten and relax. Laid end to end, the tiny contraction of each cell adds up to a movement of some distance. Laid side by side, their contraction has leverage that generates pressure. Archimedes claimed that, given a lever and a place to stand, he could move the world. For the heart, the shape of the pumping chamber and the thickness of the heart muscle are the lever and the place to stand. Two familiar animals offer examples of how form affects function. The frog lives life mostly prone, often in water, and minimally challenged by gravity. Its left ventricle is thin-walled and spherical, a mostly end-to-end orientation made to move large amounts of blood at low pressure. In contrast, the giraffe has a head sitting atop a long neck. This neck provides reserved seating for the finest dining, but keeps the brain at dizzying heights. In order to maintain blood flow to the brain, the heart must provide sufficient pressure to overcome the effects of gravity. As a result, its left ventricle is thick-walled with a chamber, shaped like a cylinder that is good for gripping. Although ill prepared to move large quantities, it is a very efficient pressure generator. The design of the human left ventricle lies somewhere between the cylinder and the sphere, resembling an American football.
Configuration (shape combined with muscle thickness) and the intrinsic ability of individual cells determines the heart's leverage for generating pressure and capacity to move large amounts of blood. However, each cell of the heart must follow direction. Should each tiny muscle cell act alone, the result would be a heart in wriggling chaos, without moving any blood.
Arm and leg muscles receive direction from the brain. Heart muscle cells receive direction from their neighbor. A small area of the right atrium called the sinus node awakens approximately 100 times each minute. Its awakening is a change in its electrical charge that spreads like the chime from a clock tower. As each cells feels the change, its machinery contracts even as it begins a rapid effort to return to normal. The sinus node has no other responsibility save to initiate the heartbeat.
The lights come on in the sinus node and the electrical charge moves through atrial muscle cells like a brush fire. Ventricles do the real work of sending blood out of the heart. Their contraction depends upon the spread of the same electrical charge that went through the atria. Although, the cells of the atria and ventricles lie in close proximity, they do not communicate directly. A point at the very center of the heart, where all four chambers are adjacent to one another, contains a small group of cells that bridge the communication gap. Like the sinus node, this is their only purpose. This small group of cells is the communication ?junction? between the atria and the ventricles, also known as the AtrioVentricular (AV) node. The junction was not designed for speedy communication. Its cells communicate with one another like a large group of people passing a message through a crowded room. The time required for the junction to pass along a message creates a pause between the awakening of the atria and the real work that follows in the ventricles.
Within the ventricles there are so many muscle cells that communication, one to another, would take a very long time to make all of them move. The heart awakened in such a fashion would only suggest blood move on, rather than ejecting it. Therefore, a few muscle cells, like the cells of the sinus node and junction, have forsaken contraction and live only to pass along a message. They are arranged in long filaments. Groups of these cells, like communication cables, are called fibers. Near the junction, fibers are tightly clustered into bundles, one to the right ventricle (Right Bundle Branch) and another to the left (Left Bundle Branch). Out near the intended point of communication with working muscle, groups of these cells are called Purkinje fibers. This communication network spreads the electrical charge so quickly that all points of the ventricle move almost simultaneously. The effect is like the coordinated movement of both hands together in a clap.
Although the human heart sees 1,800 gallons of blood going by every day, it can't drink a drop. It must be supplied by its own set of arteries. These arise from the aorta, very near its attachment to the left ventricle. From their origin, the arteries that feed the heart immediately drop down onto its surface, giving the appearance of a crown, or corona, at the base. Thus, they are known as the coronary arteries. There are two coronary arteries, one for the left side of the heart and one for the right side. They don't distribute exactly to the left and right sides and they vary from person to person, like fingerprints. (Figure 4)
Before technology extended the capacity of observation, the workings of the body were understood through the theory of humors. Energy, animation and all the stuff of life was governed by varying mixtures of basic humors. The humors were endowed with specific powers and characteristics. They could be either hot or cold and wet or dry. Illness arose from imbalance. Their origins differed but the mixture came together in blood as the heat of life. The heat of life was understood to penetrate and enliven all tissues. Altogether, given the limits of our senses and the information available at the time, the scenario is quite reasonable. In fact, some of the conceptual imagery persists today. Something that incites waste of one's vital heat makes the blood boil. Somehow snatching that vital heat away to stop the heart makes blood run cold. There is little doubt that blood carries the stuff of life. Our understanding of that stuff is just made more sophisticated by available technology. Blood is actually a mixture of about 1/2 saltwater with dissolved substances and 1/2 suspended solids. Suspended means separates when still. In a clear tube, the sunken part is mostly dark red and the top part as a clear fluid that is golden to straw-colored. The clear, golden part, called plasma, is full of salts and proteins with a specific job to do. The parts that sink are just too large to stay water-born while sitting still for any period. Most of the sinkable part is cells or pieces of cells that are big enough to be seen under a microscope.
The most abundant cell is the red blood cell. Its job is to carry oxygen, like a boxcar on a train carries cargo. Oxygen is necessary for most basic functions, most importantly harvesting energy from food. We use almost 8 ounces of oxygen every minute, but the amount that dissolves in water is very small. Red blood cells are packed with hemoglobin, a protein that is folded around an iron atom like a catcher's mitt. In its folds, oxygen sits comfortably, making the iron just a bit more red. Red blood cells are discoid and deformable, easing their movement through the crowed spaces of small arteries and capillaries.
Fewer in number but larger in size are a group of cells with no coloring. When mixed in with the red cells, they invisible to the naked eye. All alone, their lack of coloring leaves them appearing white. These white blood cells are responsible for the body's defense. Last of the visible elements is the platelet. Where all blood cells are made, in the bone marrow, a cell devoted to sealing wholes in blood vessels grows to a great size. Pieces of it break of to enter the blood stream and perform their function. These small cell remnants are like fragments of a shattered plate, giving them their name. (Figure 4).
Nature would invade and destroy with no mercy without the constant patrol of the immune system. It is amazingly complex, precise, and effective. Immunity is pervasive. It consists of cells and dissolved proteins found in every tissue. The system was once thought to be centered on a body fluid management system called the lymphatic system. Lymph is clear fluid. Along the system's pathways are small nodules that were referred to as lymph nodes. Lymph nodes are full of cells identical to roughly half of the white blood cells found in circulation. Stained and examined under a microscope, these cells have a large, round nucleus with smooth, blue surroundings. Their resemblance to the cells populating lymph nodes gave them the name lymphocytes. Although uniform in appearance, there are a great many types of lymphocytes. They are responsible for direction, coordination and some enforcement of the immune system.
One type of lymphocyte is responsible for making antibodies. Antibodies are water loving proteins found in plasma. They are capable of recognizing virtually anything foreign to the body. Where they attach, the enforcement of the immune system is targeted, including sequestration, removal and destruction. A separate white blood cell, found in circulation, is distinguished by a sandy or granular outer appearance and a nucleus that looks like splatter (shown in Figure 4). These are destructive enforcers called granulocytes. One other type of white blood cell looks like a lymphocyte, but is much larger. In blood, it is called a monocyte. Once out among tissues, it becomes even larger and performs all enforcement functions. In tissues it is called a macrophage. Immune function participates in several heart illnesses, most notably the disease of heart valves known as Rheumatic Fever. Macrophage behavior is very important to the development and progression of atherosclerosis.
A coagulum is the gelatin like mass that forms from blood held in a glass tube. The blood components that create a coagulum work in circulating blood to seal fissures or fractures in blood vessels. The coagulation system works like a magic glue that moves about, sealing only when and where necessary. Some fast acting, industrial strength adhesives or glues are made of components that are so reactive with one another that they are kept physically apart until needed. When mixed, the combination is activated to its working and final state. The proteins dissolved in plasma work in a similar fashion but do not have to be physically separated before their activation. Meanwhile, once changed to their final state, they are a bell that cannot be unrung.
The components that will become biological cement mingle constantly in flowing blood. If the system were to simply be turned on and allowed to react all over, we would become a large collection of gelatin very quickly. Fortunately, the system is tightly regulated.. Coagulation proteins are washed away if they have nowhere to sit. Unprotected, they are quickly disarmed. Platelets, the small bits of cells floating about, are a special sanctuary where the glue-making coagulation proteins can get together. After platelets attach to a break in a blood vessel, they can then link together. On the surface of these platelets, the clotting system turns into glue, like masonry mortar. The mass that forms is a blood clot. In a normally functioning vessel, a clot should not form. In order to keep the clotting system from performing its task, blood is kept moving in an orderly fashion; no breaks are exposed AND the surface of a healthy blood vessel helps to disarm any wayward proteins and platelets.
Atherosclerosis, the disease responsible for heart attacks, triggers the coagulation system by exposing the underbelly of artery walls. Events like heart attack and some forms of stroke begin with platelet attachment and progress from there. Although treatment for atherosclerosis frequently employs a medicine to blunt platelet function, the fault lies in the breakdown of the artery wall, rather than with the platelets.
Energy is trapped in food, thankfully. It can?t be burned like coal to run a steam engine. So, when energy is released from food, it must be harnessed in a very particular fashion. The parts of food used for energy are carbohydrate (sugar) and lipid. Sugar is a grab bag term for substances that have a specific type of construction. They dissolve easily in water; are generally sweet to taste; may be found in different forms in many types of foods, and have names that end in ?ose, like sucrose, fructose and lactose. The sugar in milk is different from the sugar in an apple or in sugar cane. Glucose is the sugar used by the body. Burning any fuel requires oxygen. Burning the body's fuel requires oxygen to be most efficient. However, glucose can be used to release energy without oxygen. This mechanism is fast, brief and very inefficient. It is like trying to warm a room with a match.
Lipid is a broad term that encompasses fats, oils, waxes and the like. However, in this discussion, any mention of lipids is in reference to fatty acids, triglyceride and cholesterol. A fatty acid is a long molecule with one end that likes to associate with water and an oily tail that is shaped like a pipe cleaner bent into a zigzag. The long oily tails are none to fond of water, but love one another. They are stored by attaching fatty acid to a sugar-like molecule called glycerin. There are only three places to add a fatty acid to glycerin. Therefore, the complex is called a Tri-glyceride. Dietary sources of fatty acid and triglyceride abound, including meat, dairy, and plant fats.
The liver coordinates energy storage and distribution. It processes triglyceride from the diet. However, it may also convert surplus glucose to fatty acid and attach surplus fatty acid to glycerin. Glucose is distributed easily because it is soluble in water. Fats float, making transportation through the watery bloodstream difficult. Therefore, the liver packages them in special capsules whose outside lining has an affinity for water. The capsules, called lipoproteins are complex. Mixed into the surface coating are a group of handles that cells use to recognize the lipoprotein and extract its contents. (Figure 6)
Cholesterol is a chain of carbon atoms folded into shapes instead of long oily tails. The shapes make cholesterol useful in the construction of hormones and cell membranes. Most of the body's cholesterol is made in the liver rather than being taken in through diet. However, like triglycerides, it interacts poorly with water and must be transported to cells in a lipoprotein capsule.
The capsules are named based upon where they land after a trip through a centrifuge. The force applied to blood placed in a centrifuge is enormous. Contents exposed to that force order themselves according to size and density, softballs at the top and golf balls at the bottom. The capsules that carry lipid out of the liver are large and fluffy. They have the very clever name, Very Low Density Lipoprotein (VLDL). After a tour of the body, VLDL gives away some of its triglyceride. It becomes the smaller, denser, Low Density Lipoproteins (LDL) that still has plenty of cholesterol. LDL continues to make deliveries and is eventually taken back by the liver. The smallest and densest capsule is called High Density Lipoprotein (HDL). HDL is sent from the liver virtually empty. Its task is to bring lipid to the liver.
Abnormal energy metabolism traps many of its components in circulating blood. Excess glucose impairs tissue function throughout the body. It may also attach itself to a variety of proteins, furthering its dysfunctional influence. Lipoproteins in excess accumulate where they do not belong. The attemps to clear them away is one of the driving forces behind the development of atherosclerosis and heart attack. This is a brief, general description of basic functions affecting and affected by the heart and arteries. Each function is important in the pursuit of basic health maintenance as well as understanding most of the common forms of heart disease.
Heart valve failure is a mechanical problem. Of course, that is like saying that can't run is a leg problem. It's painting with a broad brush. Some valves get stiff and can't move. Some get floppy and don't close well. Some, touched by illness, don't heal well so that the corners stick together, pursed in a perpetual whistle. The last bit of attractive imagery is what happens in Rheumatic Fever, fortunately a rarity in developed countries today.
Regardless, the treatment for a valve that won't work in a heart that can't handle it is to remodel part of the valve or replace it. Nothing man-made can recreate Nature's design for the interaction between blood and the structures containing it. Sutures, sewing rings and struts of human design offer locations for clots to form and sometimes find freedom.
Therefore, when a man-made valve is placed, the self-solidifying capacity of blood is bridled by an anticoagulant. Replacements made of biological tissue are eventually accepted by the body and felt to require little in the way of "help" to retard clots as long as the heart rhythm remains normal. However, their mechanical counterparts require assistance throughout their lifetime. Without anticoagulation, their associated stroke risk is 4%/year.(1) The windsock mitral valve created by Rheumatic Fever leaves the left atrium like a balloon about to pop. As a result, the conciseness of sinus rhythm frequently degenerates into atrial fibrillation. Pooling blood in a quivering chamber with restricted outlet is a recipe for clot formation and stroke.
People with the combination of mitral stenosis and atrial fibrillation see a stroke risk of almost three out of ten every year. Therefore, when valve and stroke are considered together, it is the mitral valve that is feared most whether deformed by disease or mechanical design. Warfarin or dicoumarol is the drug of record used for protection from stroke in atrial fibrillation and from artificial heart valves. It reduces the stroke risk with a mechanical heart valve to 1%/year.(1) Neither design nor inherent virtue led to warfarin's ascendancy for long-term anticoagulation. Rather, it was the only practical anticoagulant available when the need arose. Long experience has refined its use though it remains problematic and virtually every valve recipient who uses it longs for something better. Something better is promised in a group of designed anticoagulation drugs whose behavior is far more predictable than warfarin. To the relief of all to whom they have proven valuable, they do not require periodic blood testing to guide their use. These drugs, given abbreviated references surely created by the US Army (DOAC, NVKA, etc.), have proven useful for people with blood clots in veins or who fear blood clots in veins and in the setting of atrial fibrillation. All valve owners wonder of their potential use for them.
Warfarin survived baptism by fire, a path that no drug can take to regular use today. Its alternatives require trials to prove their utility. Meanwhile, the specter of the mitral valve looms over all valve disease when combined with atrial fibrillation. Therefore, proof of value in the setting of atrial fibrillation labeled "non-valvular" leaves a question in many minds. Why not valvular and just what is non-valvular? (2)The logical first step of the makers of warfarin's better looking cousins was to dip their toes in atrial fibrillation first. Early on, an attempt with one of the new drugs to protect after valve replacement went poorly. It convinced no one that the alternatives won't work. Therefore, there is an inkling of hope in the observations made in a small number of people who helped with The ENGAGE AF-TIMI 48 trial (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation Thrombolysis in Myocardial Infarction 48).(2) This trial was designed to examine one of the warfarin alternatives, edoxaban in comparison to warfarin in people with atrial fibrillation and an increased risk of stroke. Out of the 21,105 people who participated, 191 had a prosthetic valve (about 2/3 mitral and 1/3 aortic). People with mechanical valves, quite reasonably, could not get into the trial.
Therefore, all of the prosthetic valves were biological. Of that number, eight people out of seventy, taking warfarin had a stroke as opposed to seven out of one hundred twenty-one on edoxaban. http://circ.ahajournals.org/content/135/13/1273
This observation will relax the minds of many concerned by the broadly drawn proscription on considering atrial fibrillation with any valve disease in the same light as other people with atrial fibrillation. In addition to other types of valve problems (mostly minor and not a narrowing deformity) that have benefited from the new drugs, this may push a change of reference from the oft-mentioned "non-valvular" atrial fibrillation. The burning question is now the use of these designed anticoagulants for people with mechanical valves that have been in place for some time, particularly in the mitral position.
1. Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. 1994;89(2):635-41.
2. Carnicelli AP, De Caterina R, Halperin JL, Renda G, Ruff CT, Trevisan M, et al. Edoxaban for the Prevention of Thromboembolism in Patients With Atrial Fibrillation and Bioprosthetic Valves. Circulation. 2017;135(13):1273.
Keywords: Stroke, Atrial Fibrillation, Anticoagulant, Heart Valve
Stent, the Saxon sobriquet, is a monosyllabic moniker for the strutted savior of the disease-ravaged coronary artery. Surgery proved to the world that crippling coronary artery disease could be treated but not everyone wanted or warranted an operation. A less traumatic option came from tackling the problem from the inside out but angioplasty was troubled by cave-in. In response, a 2000 year-old mining concept was applied to arteries. Supports for sink shafts became struts for arteries. In truth, the idea was used before the development of angioplasty to prevent sutures attaching two arteries from being tied too tight.(1) When a cave-in could be prevented, angioplasty became safer. Adoption of stents as an addition to angioplasty was rapid and almost universal. But, as each difficult artery fell, the next one loomed larger and the stents seemed too thick, too bulky, too stiff or too weak. They were too likely to renarrow, too hard to see on X-ray and they lasted too long. Despite a designer stent for every occasion, none overcame the fact that they were made of metal. Thus was born the idea of a stent that would be absorbed by the body like stitches that didn't have to be removed. Once it was gone, what was left would be just the artery but one that is reformed.
There have been some very good ideas for stents that get absorbed by the body after placement. In amazing feats of engineering, they could get where they needed to go, give the support that was needed to prevent cave-in and just fade away. The question posed was how they compare to the metal versions that are used routinely.
In several hospitals in the Netherlands, about 2000 people who were having something done to their coronary arteries agreed to have a reabsorbable stent if they were chosen. The ease with which the stent could be used, problems with its placement and how it held up long term were recorded. Generally, the reabsorbable version was a little harder to place. Once in place, both the routinely used version of a stent and the reabsorbable one held up about the same with one major difference. When the test version ran aground, it did so in the least desirable manner possible. It clotted.
Impact and analysis
The observations from this study are quite a blow to the stent being studied. It is not the end of an idea but it places a hurdle before similar stents that will come after. The observations made through the development of this stent may be re-examined as part of a post-mortem to see why a clot was a more frequent mode of failure than with the standard metal version. In the interim, this will have no major impact on the current model for when and where a stent is the right treatment option.
Keywords: Stent, Thrombosis, Coronary Artery Disease, Cardiovascular Disease
1. Hall Rj Fau - Khouri EM, Khouri Em Fau - Gregg DE, Gregg DE. Coronary-internal mammary artery anastomosis in dogs. Surgery. 1961;50(0039-6060 (Print)):560-7.
It is said that there are two kinds of coaches in professional sports, those that have been fired and those that will be fired; Pithy and generally true. The same argument can be applied to the treatment of Coronary Artery Disease. There are two types of arteries in someone having a heart attack, the one causing the problem and the ones that may cause the next one. So, the approach to heart attack can be summarized as Rescue from the one that's here. Prepare for the one that's coming and Prevent it if you can. There was no rescue until clot busting drugs (thrombolytics) and they don't work all that well. Balloon angioplasty made all the difference. However, the tools and techniques of the early version were primitive and not completely reliable. Therefore, the prevailing behavior was to follow Royal's Law. You dance with the one what brung you. The site in the artery that is causing a heart attack and leave the other narrowings, that you may happen upon, alone. Time and technology have moved on. The success and reliability of reforming diseased arteries are such that some physicians argue for repair of all potential problems in the same setting. Therefore, if heart attack has brought you to attention, "fix" all other narrowings that are found at the same time. On the surface, this may seem to be a simple decision. Find narrowings. Fix narrowings. Rescue and prevent at the same time. Unfortunately, as usual, simple is misleading and essentially incorrect. The knowledge that coronary artery disease is present is like a mountain road with the sign, beware falling rocks. Attacking the rocks found on the road doesn't protect anyone from the next one to fall. So too, treating a narrowed segment of artery that is not the source of current difficulty is not likely to prevent anything. It just makes the road easier to pass. The other side of the argument is that the narrowings present are a source of danger if another heart attack comes along. The heart muscle that they are restricting by their presence may not be able to give its all should it be needed. People who have a heart attack may be in danger of another. Therefore, the rocks fallen or the narrowing present should be cleared if it can be done safely.
Most cardiologists would agree that the doctor's eye alone should not be the arbiter of what narrowing needs attention. When that is the only guide available, a "stress test" of each narrowing that can be done at the same time as the angiogram (called Fractional Flow Reserve or FFR) reduces how often treatment is chosen and makes the whole process safer. So, the next logical question is, if the doctor has the angel of FFR on his or her shoulder, is it safe and useful to address more narrowings than just the one what brung me.
A group of physicians and institutions throughout Europe convinced almost 900 people having a heart attack to participate in a study.(1) The basics were that if one of the arteries not causing the heart attack exceeded 50% narrowing, they could participate. In those who did, FFR was measured and some had the artery repaired, the remaining did not. The headline is that with the guidance of FFR, people who had everything done at the same time benefited. The longer version starts with the fact that very few people who participated died of their heart attack. That is very reassuring. In the people who got everything done at the same time, there did not appear to be any harm done by the extra work. The only real benefit that they had was that fewer had to have something done later. Having everything done at the same time didn't change survival (it was too good to get much better) or prevent heart attacks.
Impact and analysis
If you're having a heart attack and in pretty good shape going in, your doctor can take care of any extra narrowings at the same time as long as there is proof that they need taking care of. More importantly, if he or she doesn't, you don't lose anything. The observation that some of the people who didn't get everything done at the same time got something done later is not very convincing. Not all that many ended up needing anything extra and it's hard to be certain that they really needed it. The take home message is that people having a heart attack who were getting timely treatment did very well. With respect to any other narrowings that may be present, there is neither compelling reason to do something nor to avoid it.
Keywords: Heart Attack, Myocardial Infarction, Stent, Cardiovascular Disease
1. Smits PC, Abdel-Wahab M, Neumann F-J, Boxma-de Klerk BM, Lunde K, Schotborgh CE, et al. Fractional Flow Reserve-Guided Multivessel Angioplasty in Myocardial Infarction. New England Journal of Medicine. 2017.
Why composition should take the place of weight.
The new addition to potboilers of how to lose 30 lb in 3 weeks or the one month cure for your risk of heart attack is that changing weight and complications of cardiovascular disease ride together.(1) As grabbers go, this is a winner and it could be the source of serious misunderstanding. It is not a mistake or fanciful finagling with numbers. The observation is real. It is meaningful. It raises a very important question about weight loss and diets but in no way suggests that lifestyle changes with weight loss in mind are bad.
Obesity is the problem for all seasons, linked to high blood pressure, diabetes mellitus, elevated cholesterol, sleep apnea as well as heart failure, atrial fibrillation and heart attack. The link to cardiovascular disease is such that body weight often takes center stage in efforts to treat illness.(2) From the association between body weight and the known risk factors for cardiovascular disease come estimates of the value of weight loss. Lose weight and blood pressure is easier to control. Risk factors improve. Therefore, it seems logical that virtually any effort that safely reduces body weight while maintaining essential nutrition is going to be valuable but there is a problem. A consistent observation from efforts to improve the lot of people with cardiovascular disease is that people with disease, who are on average heavier fare better over time.(3) The observation that heavy people get sick but sick, heavy people do better over time is referred to as the obesity paradox. When this thorny observation first attacked logic, a variety of explanations were offered but as yet, no one really knows why it is true, just that it is. Even faced with the paradox, most physicians do not question the need to reduce body fat when its known effects may be fueling identified vascular disease. However, it is possible that weight loss efforts may not provide the benefit that is expected of them. Specific regimens may lower weight without reducing fat. Worse, many diet and exercise regimens designed to address body weight often have brief success, only to see weight return, likely as fat.
In people left to their own designs, does weight that is frequently changing correspond to any difference in the chance of having a heart attack or other problems related to cardiovascular disease.
The source of information was a study done to record heart attacks and complications of cardiovascular disease in more than 9500 people testing different doses of a cholesterol-lowering medication. What the investigators did with the information was to pay attention to something that is usually ignored, how much body weight changed each time it was measured during the study.(1) Over a period of several years, most participants had some variation in weight from visit-to-visit. In about 10-15% of people, the weight swings averaged more than five pounds for each visit. The swingers had an increased risk of complications even when all other things were taken into account. There were several methods of describing how much weight varied between visits. Regardless of how the difference was portrayed, people whose visit-to-visit weight varied more than others, not just in one direction but the amount that it swung in either direction, had a greater chance of encountering difficulty.
The study discovered an association between changing weight and complications but it couldn't address the next question. Why? Did one cause the other or are they just two faces of some other underlying problem? There is no way to tell from the information available. The set up above would suggest that the answer is obvious, dietary recidivism changes body composition to more fatty over time driving vascular disease. However, as often as not, the obvious answer proves to be wrong when put to the test. While we wait for more information, the things to think about are, pay more attention to your waistline than your weight. One of the problems with something like obesity is to make it into a number. Exactly what does it mean to be fat? Is it too much weight, too much weight for age, for height or both? Your total body weight reflects muscle, bone, organs as well as fluid and fat. Changes in weight lasting more than a few days are usually due to a change in either fat or what is referred to as lean body mass. Since your bones and organs are an unusual source of weight change, lean body mass really means muscle. If you diet to lose weight rapidly, there is a good chance that you will lose muscle at the same time. Should the weight later return, there is also a very good chance that what comes back will be fat. While net weight may be the same at the end of some time period, cycling weight change may shift body composition from muscle to fat. If you have vascular disease and lose muscle or gain body fat your chance of having complications of your disease is increased.(4, 5) Researchers examining diets and weight loss have used body composition or more importantly change in body fat to describe the impact of diets and exercise regimens for many years. The easiest method to measure a change in body fat is to use the skin folds around the belly, on the arms, back and elsewhere. For you and I, the easiest measure is the waistline. If it's shrinking, slowly and on purpose, any change in diet and activity is probably helping, even if weight hasn't changed greatly. An effort to lose body fat should be a permanent change of habit. Diet and exercise designed to keep muscle mass and lose fat is almost certainly beneficial. The lesson suggested by the new observations is that attempts to change body composition and weight secondarily should have goals set over six months to years with interventions that are long lasting, if not permanent. Does the type of diet or exercise influence the type of weight that is lost? In addition to seeking some evidence to show why changing weight and increased risk go together, my questions are, 1. What diet/exercise combination best sustains muscle while reducing fat? a. Generally b. In specific groups with physical limitations 2. Is there a rate of intentional, guided weight loss, targeting fat, at which muscle is sacrificed? Stated differently, if you're trying to lose fat and are losing weight, can the speed that it is coming off warn you that you may be losing muscle too? The worst possible conclusion to draw from this study is that a change in lifestyle geared to losing weight is bad. The goal remains laudable when the approach is a long-term change with a goal of reducing body fat but maintaining muscle.
Keywords: Obesity, Diet, Heart Attack, Weight loss
1. Bangalore S, Fayyad R, Laskey R, DeMicco DA, Messerli FH, Waters DD. Body-Weight Fluctuations and Outcomes in Coronary Disease. New England Journal of Medicine. 2017;376(14):1332-40.
2. Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX, et al. Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss. Circulation. 2006;113(6):898.
3. Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, et al. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. The Lancet. 2006;368(9536):666-78.
4. Allison DB, Zannolli R, Faith MS, Heo M, Pietrobelli A, VanItallie TB, et al. Weight loss increases and fat loss decreases all-cause mortality rate: results from two independent cohort studies. Int J Obes Relat Metab Disord. 1999;23(6):603-11.
5. Santanasto AJ, Goodpaster BH, Kritchevsky SB, Miljkovic I, Satterfield S, Schwartz AV, et al. Body Composition Remodeling and Mortality: The Health Aging and Body Composition Study. The Journals of Gerontology: Series A. 2017;72(4):513-9.