Prelim (sir syenes)

Cardiovascular System FunctionThe cardiovascular system function is considered to be one of the most important functions of the human body. Knowing about the cardiovascular system function and structure will help you a great deal in keeping it healthy for it to function appropriately. Read on for more information on cardiovascular system functions.

The cardiovascular system, the most important of the human body systems, consists of organs that are responsible for carrying out many of the important cardiovascular system functions. The system consists of organs like the heart, the spleen and the blood vessels that are spread throughout the body. The cardiovascular system is a complex system and understanding its functions will help understand the overall human physiology better.

Functions of the Cardiovascular System

The cardiovascular system functions can be categorized into three main functions: transport, regulation and protection. The organs of the system carry out these functions in coordination with the functions of the other systems for the proper functioning of the body. These are the main functions of the cardiovascular system and they are explained in detail below.

Transport: The cardiovascular system transports oxygen from the lungs to the various cells of the body. The primary function of the cardiovascular system is to transport nutrients from the intestines to the lungs and other parts of the body, and carbon dioxide from the cells to the lungs. Hormones from the various endocrine glands and heat from the cells are also transported by this system. Removal of waste products like carbon dioxide and nitrogen from the body is also performed by this system. This function of transport is mainly carried out by the blood and the network of blood vessels present in the cardiovascular system.

Protection: The cardiovascular system performs the function of protecting the body and its organs from infection and diseases by providing white blood cells that have the ability to fight against them. Proteins and antibodies required for destroying viruses, bacteria and disease causing germs are also provided by this system to the various parts of the body. Another important function of this system is to protect the body from excessive blood loss through the process of blood clotting during an injury. 

Regulation: Another important cardiovascular system function is the regulation of the concentration of hydrogen ions (pH) in the body, the body temperature and body heat, and the regulation of the salt and water content of the cells in the body.

Cardiovascular System Function and Structure

It is important to know and understand the structure of the cardiovascular system to understand its functions better. As mentioned before, the cardiovascular system is made up of the heart, the blood vessels, the spleen and blood. Each of these perform individual functions to make the overall functioning of the system possible.

The Heart: The human heart is situated at the center of the chest and is approximately the size of a clenched fist. It performs the function of a muscular pump, wherein it expands and contracts to pump blood into the blood vessels and the rest of your body. it consists of four chambers, the upper two are known as the left and the right atria and the lower two are known as the left and right ventricles. The deoxygenated blood is carried to the right side of the heart which pumps it into the lungs where blood absorbs more oxygen. This oxygenated blood moves to the left side of the heart which pumps it into the blood stream and is carried to the various body parts. Read more on a labeled diagram of the human heart.

Blood Vessels: There are three different types of blood vessels in the human body, the arteries, the capillaries and the veins. The arteries are of three types, the pulmonary artery, the aorta and the coronary arteries. They perform the function of carrying oxygenated blood from the heart to the other parts of the body, but the pulmonary artery carried deoxygenated blood from the heart to the lungs. The capillaries carry oxygen and nutrients to the tissues and cells of the body and the veins carry deoxygenated blood from the various organs of the body to the heart. 

The Spleen: The spleen is a large organ situated below the diaphragm and performs an important function of storing blood.

How does the Cardiovascular System Function?

By now you must have got an idea of how the cardiovascular

system functions. To sum it up, deoxygenated blood is carried by the veins to the right side of the heart which pumps it into the lungs for oxygen absorption. Once the oxygen has been absorbed, the blood is pumped into the left side of the heart and from here the arteries carry it to the other parts of the body. The capillaries distribute the oxygen and nutrients supplied to them by the arteries and remove waste products from the blood stream. You may also find some useful information about the cardiovascular system in cardiovascular system facts.

For more information, you can also refer to how does the heart pump blood.

Now that you know about the cardiovascular system function, it will be easier for you to understand its importance and how essential it is to protect this system from damage. To keep it healthy, it is essential to eat right, exercise and follow a healthy lifestyle.

Cardiovascular System (Simplified)

The cardiovascular system includes the heart and the blood vessels. The heart pumps blood, and the blood vessels channel and deliver it throughout the body. Arteries carry blood filled with nutrients away from the heart to all parts of the body. The blood is sometimes compared to a river, but the arteries are more like a river in reverse. Arteries are thick-walled tubes with a circular covering of yellow, elastic fibers, which contain a filling of muscle that absorbs the tremendous pressure wave of a heartbeat and slows the blood down. This pressure can be felt in the arm and wrist - it is the pulse. Eventually arteries divide into smaller arterioles and then into even smaller capillaries, the smallest of all blood vessels. One arteriole can serve a hundred capillaries. Here, in every tissue of every organ, blood's work is done when it gives up what the cells need and takes away the waste products that they don't need. Now the river comparison really does apply. Capillaries join together to form small veins, which flow into larger main veins, and these deliver deoxygenated blood back to the heart. Veins, unlike arteries, have thin, slack walls, because the blood has lost the pressure which forced it out of the heart, so the dark, reddish-blue blood which flows through the veins on

its way to the lungs oozes along very slowly on its way to be reoxygenated. Back at the heart, the veins enter a special vessel, called the pulmonary arteries, into the wall at right side of the heart. It flows along the pulmonary arteries to the lungs to collect oxygen, then back to the heart's left side to begin its journey around the body again.

Anatomy of the heart

Human Anatomy

Picture of the Heart

© 2009 WebMD, LLC. All rights reserved.The heart is a muscular organ about the size of a fist, located just behind and slightly left of the breastbone. The heart pumps blood

through the network of arteries and veins called the cardiovascular system.The heart has four chambers:

The right atrium receives blood from the veins and pumps it to the right ventricle.

The right ventricle receives blood from the right atrium and pumps it to the lungs, where it is loaded with oxygen.

The left atrium receives oxygenated blood from the lungs and pumps it to the left ventricle.

The left ventricle (the strongest chamber) pumps oxygen-rich blood to the rest of the body. The left ventricle’s vigorous contractions create our blood pressure.

The coronary arteries run along the surface of the heart and provide oxygen-rich blood to the heart muscle. A web of nerve tissue also runs through the heart, conducting the complex signals that govern contraction and relaxation. Surrounding the heart is a sac called the pericardium.Heart Conditions

Coronary artery disease : Over the years, cholesterol plaques can narrow the arteries supplying blood to the heart. The narrowed arteries are at higher risk for  complete blockage from a sudden blood clot (this blockage is called a heart attack).

Stable angina pectoris : Narrowed coronary arteries cause predictable chest pain or discomfort with exertion. The blockages prevent the heart from receiving the extra oxygen needed for strenuous activity. Symptoms typically get better with rest.

Unstable angina pectoris : Chest pain or discomfort that is new, worsening, or occurs at rest. This is an emergency situation as it can precede a heart attack, serious abnormal heart rhythm, or cardiac arrest.

Myocardial infarction (heart attack): A coronary artery is suddenly blocked. Starved of oxygen, part of the heart muscle dies.

Arrhythmia  (dysrhythmia): An abnormal heart rhythm due to changes in the conduction of electrical impulses through the

heart. Some arrhythmias are benign, but others are life-threatening.

Congestive heart failure : The heart is either too weak or too stiff to effectively pump blood through the body. Shortness of breath and leg swelling are common symptoms.

Cardiomyopathy : A disease of heart muscle in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart's ability to pump blood is weakened.

Myocarditis: Inflammation of the heart muscle, most often due to a viral infection.

Pericarditis : Inflammation of the lining of the heart (pericardium). Viral infections, kidney failure, and autoimmune conditions are common causes.

Pericardial effusion : Fluid between the lining of the heart (pericardium) and the heart itself. Often, this is due to pericarditis.

Atrial fibrillation : Abnormal electrical impulses in the atria cause an irregular heartbeat. Atrial fibrillation is one of the most common arrhythmias.

Pulmonary embolism : Typically a blood clot  travels through the heart to the lungs. 

Heart valve disease : There are four heart valves, and each can develop problems. If severe, valve disease can cause congestive heart failure.

Heart murmur : An abnormal sound heard when listening to the heart with a stethoscope. Some heart murmurs are benign; others suggest heart disease.

Endocarditis : Inflammation of the inner lining or heart valves of the heart. Usually, endocarditis is due to a serious infection of the heart valves.

Mitral valve prolapse : The mitral valve is forced backward slightly after blood has passed through the valve. 

Sudden cardiac death : Death caused by a sudden loss of heart function (cardiac arrest).

Cardiac arrest : Sudden loss of heart function.

The purpose of the heart is to pump the blood that bathes every organ of the body. The blood carries oxygen and nutrients to the tissues, and removes waste products from the tissues. If the pumping action of the heart is disrupted, the body’s organs begin to fail very quickly. Therefore, life itself is dependent on the efficient operation of the heart.

Heart chambers and heart valves

The heart has four chambers. The two ventricles (right and left) are muscular chambers that propel the blood out of the heart (the right ventricle to the lungs, and the left ventricle to all other organs). The two atria (right and left) hold the blood returning to the heart, and at just the right moment empty into the right and left ventricles.

The four heart valves (tricuspid, pulmonic, mitral and aortic) keep the blood moving in the right direction through the heart.

How the heart pumps blood

It is helpful to visualize the heart as two separate pumps, working in series – the right heart pump, and the left heart pump.

The right heart pump

Figure 1: The right heart pump consists of the right atrium (RA), tricuspid valve (TV), right ventricle (RV), pulmonic valve (PV), and pulmonary artery (PA).Poorly oxygenated blood returning to the heart from the body's organs enters the right atrium, and is stored there until the right atrium contracts.

Figure 2: When the right atrium contracts, the tricuspid valve opens, allowing the blood to enter the right ventricle.

Figure 3: Then, when the right ventricle contracts, the pulmonic valve opens, and the blood is propelled into the pulmonary artery. The pulmonary artery carries the blood to the lungs, where it picks up oxygen.

Sponsored LinksCardiovascular BiologyRecent advances in the field Read the Insight in Naturewww.nature.com/natureEnvironmental sound pumpsCheck out A-labeled Grundfos pump. Save significantly on energy.PoweredBy.Grundfos.comPiranha Slurry PumpsSlurry pumps for sand, mud, gravel or anywhere that sediment gatherswww.piranhapump.com

Heart Health Center Ads Heart Disease Heart Health Open Heart Surgery Valves of the Heart Heart Attack Signs Women

(Continued from Page 1)

Figure 4: The left heart pump consists of the left atrium (LA), mitral valve (MV), left ventricle (LV), aortic valve (AV), and aorta (Ao). Well oxygenated blood returning to the heart from the lungs enters the left atrium, and is stored there until the left atrium contracts.Page 3 - The left heart pump (continued)

Figure 5: When the left atrium contracts, the mitral valve opens, allowing the blood to enter the left ventricle

Figure 6: Then, when the left ventricle contracts, the aortic valve opens, and the blood is propelled into aorta, the main artery of the body. The aorta then carries the blood throughout the body.

Coronary circulationFrom Wikipedia, the free encyclopedia

Coronary circulation

An anterior left coronary artery.

Base and diaphragmatic surface of heart.

MeSH Coronary+Vessels

Coronary circulation is the circulation of blood in the blood vessels of the heart muscle (themyocardium). The vessels that deliver oxygen-rich blood to the

myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins.

The coronary arteries that run on the surface of the heart are called epicardial coronary arteries. These arteries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the needs of the heart muscle. These relatively narrow vessels are commonly affected by atherosclerosis and can become blocked, causing angina or a heart attack. (See also: circulatory system.) The coronary arteries that run deep within the myocardium are referred to as subendocardial.

The coronary arteries are classified as "end circulation", since they represent the only

source of blood supply to the myocardium: there is very little redundant blood supply,

which is why blockage of these vessels can be so critical.

Contents

[hide]

1 Coronary anatomy o 1.1 Variations

o 1.2 Coronary artery dominance

2 Blood supply of the papillary muscles

3 Coronary flow

4 Anastomoses

5 See also

6 References

[edit]Coronary anatomy

Coronary arteries labeled in red text and other landmarks in blue text.

Schematic view of the heart

Both of these arteries originate from the left side of the heart at the beginning (root) of the aorta, immediately above the aortic valve. As discussed below, the left coronary artery originates from the leftaortic sinus, while the right coronary artery originates from the right aortic sinus.

[edit]VariationsFour percent of people have a third, the posterior coronary artery. In rare cases, a person will have one coronary artery that runs around the root of the aorta.

Occasionally, a coronary artery will exist as a double structure (i.e. there are two arteries, parallel to each other, where ordinarily there would be one).

[edit]Coronary artery dominance

The artery that supplies the posterior descending artery (PDA)[1] (a.k.a. posterior interventricular artery) determines the coronary dominance.[2]

If the posterior descending artery (PDA) (a.k.a. posterior interventricular artery) is supplied by the right coronary artery (RCA), then the coronary circulation can be classified as "right-dominant".

If the posterior descending artery (PDA) is supplied by the circumflex artery (CX), a branch of the left artery, then the coronary circulation can be classified as "left-dominant".

If the posterior descending artery (PDA) is supplied by both the right coronary artery (RCA) and the circumflex artery, then the coronary circulation can be classified as "co-dominant".

Approximately 70% of the general population are right-dominant, 20% are co-dominant, and 10% are left-dominant.[2] A precise anatomic definition of dominance would be the artery which gives off supply to the AV node i.e. the AV nodal artery. Most of the times this is the right coronary artery.

[edit]Blood supply of the papillary muscles

The papillary muscles together the mitral valve (the valve between the left atrium and the left ventricle) and the tricuspid valve (the valve between the right atrium and the right ventricle) to the wall of the heart. If the papillary muscles are not functioning properly, the mitral valve may leak during contraction of the left ventricle. This causes some of the blood to travel "in reverse", from the left ventricle to the left atrium, instead

of forward to the aorta and the rest of the body. This leaking of blood to the left atrium is known as mitral regurgitation. Similarly, the leaking of blood from the right ventricle through the tricuspid valve and into the right atrium can also occur, and this is described as tricuspid insufficiency or tricuspid regurgitation.

The anterolateral papillary muscle more frequently receives two blood supplies: left anterior descending (LAD) artery and the left circumflex artery (LCX).[3] It is therefore more frequently resistant to coronary ischemia (insufficiency of oxygen-rich blood). On the other hand, the posteromedial papillary muscle is usually supplied only by the PDA.[3] This makes the posteromedial papillary muscle significantly more susceptible to ischemia. The clinical significance of this is that a myocardial infarction involving the PDA is more likely to cause mitral regurgitation.

[edit]Coronary flow

During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high intraventricular pressures. However, the epicardial coronary vessels (the vessels that run along the outer surface of the heart) remain patent. Because of this, blood flow in the subendocardium stops. As a result most myocardial perfusion occurs during heart relaxation (diastole) when the subendocardial coronary vessels are patent and under low pressure. This contributes to the filling difficulties of the coronary arteries. Compression remains the same. Failure of oxygen delivery caused by a decrease in blood flow in front of increased oxygen

demand of the heart results in tissue ischemia, a condition of oxygen debt. Brief ischemia is associated with intense chest pain, known as angina. Severe ischemia can cause the heart muscle to die from hypoxia, such as during a myocardial infarction. Chronic moderate ischemia causes contraction of the heart to weaken, known as myocardial hibernation.

In addition to metabolism, the coronary circulation possesses unique pharmacologic characteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of vasculature in the body constricts to norepinephrine, a sympathetic neurotransmitter the body uses to increase blood pressure. In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation. Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.

[edit]Anastomoses

There is some anastomoses between branches of the two coronary arteries. However the coronary arteries are functionally end arteries and so these meetings are referred to as anatomical anastamoses, which lack function, as opposed to functional or physiological anastomoseslike that in the palm of the hand. This is as blockage of one coronary artery generally results in death of the heart tissue due to lack of sufficient blood supply from the other branch. When two arteries or their branches join, the area of the myocardium receives dual blood supply. These junctions

are called anastomoses. If one coronary artery is obstructed by an atheroma, the second artery is still able to supply oxygenated blood to the myocardium. However this can only occur if the atheroma progresses slowly, giving the anastomoses a chance to proliferate. Under the most common configuration of coronary arteries, there are three areas of anastomoses. Small branches of the LAD (left anterior descending/anterior interventricular) branch of the left coronary join with branches of the posterior interventricular branch of the right coronary in the interventricular groove. More superiorly, there is an anastomosis between the circumflex artery (a branch of the left coronary artery) and the right coronary artery in the atrioventricular groove. There is also an anastomoses between the septal branches of the two coronary arteries in the interventricular septum. The photograph shows area of heart supplied by the right and the left coronary arteries.(Right = yellow, left = red) http://commons.wikimedia.org/wiki/File:Coronary_Arteries.tif[edit]

Cardiac striated muscleFrom Wikipedia, the free encyclopedia

  (Redirected from Cardiac muscle)

Cardiac striated muscle

Cardiac muscle

Dog Cardiac Muscle 400X

Latin textus muscularis striatus cardiacus

Code TH H2.00.05.2.02001

Cardiac muscle is a type of involuntary striated muscle found in the walls and histologic foundation of the heart, specifically the myocardium. Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle. The cells that comprise cardiac muscle, called myocardiocyteal muscle cells, are mononuclear, like smooth muscle cells.[1]

Coordinated contractions of cardiac muscle cells in the heart propel blood out of the atria andventricles to the blood vessels of the left/body/systemic and right/lungs/pulmonary circulatory

systems. This complex of actions makes up the systole of the heart.

Cardiac muscle cells, like all tissues in the body, rely on an ample blood supply to deliver oxygen and nutrients and to remove waste products such as carbon dioxide. The coronary arteries fulfill this function.

Contents

[hide]

1 Metabolism 2 Appearance

o 2.1 Striation

o 2.2 T-Tubules

o 2.3 Intercalated discs

3 Role of calcium in contraction

4 Regeneration of heart muscle cells

5 See also

6 References

7 External links

[edit]MetabolismCardiac muscle is adapted to be highly resistant to fatigue: it has a large number ofmitochondria, enabling continuous aerobic respiration via oxidative phosphorylation, numerous myoglobins (oxygen-storing pigment) and a good blood supply, which provides nutrients and oxygen. The heart is so tuned to aerobic metabolism that it is unable to pump sufficiently inischaemic conditions. At basal metabolic rates,

about 1% of energy is derived from anaerobic metabolism. This can increase to 10% under moderately hypoxic conditions, but, under more severe hypoxic conditions, not enough energy can be liberated by lactate production to sustain ventricular contractions.[2]

Under basal aerobic conditions, 60% of energy comes from fat (free fatty acids and triglycerides), 35% from carbohydrates, and 5% fromamino acids and ketone bodies. However, these proportions vary widely according to nutritional state. For example, during starvation, lactate can be recycled by the heart. This is very energy efficient, because one NAD +  is reduced to NADH and H+ (equal to 2.5 or 3 ATP) when lactate is oxidized to pyruvate, which can then be burned aerobically in the TCA cycle, liberating much more energy (ca 14 ATP per cycle).

In the condition of diabetes, more fat and less carbohydrate is used due to the reduced induction of GLUT4 glucose transporters to the cell surfaces. However, contraction itself plays a part in bringing GLUT4 transporters to the surface.[3] This is true of skeletal muscle as well, but relevant in particular to cardiac muscle due to its continuous contractions.

[edit]Appearance

[edit]StriationCardiac muscle exhibits cross striations formed by alternating segments of thick and thin protein filaments. Like skeletal muscle, the primary structural proteins of cardiac muscle are actin and myosin. The actin filaments are thin causing the lighter appearance of the I bands in striated muscle, while the myosin filament is thicker lending a darker appearance to the alternating A bands as observed with electron microscopy. However, in contrast to skeletal muscle, cardiac muscle cells may be branched instead of linear and longitudinal.

[edit]T-TubulesAnother histological difference between cardiac muscle and skeletal muscle is that the T-tubules in the cardiac muscle are larger, broader and run along the Z-Discs. There are fewer T-tubules in comparison with skeletal muscle. Additionally, cardiac muscle forms diads instead of the triads formed between the T-tubules and the sarcoplasmic reticulum in skeletal muscle. T-tubules play critical role in excitation-contraction coupling (ECC). Recently, the action potentials of T-tubules were recorded optically by Guixue Bu et al.[4]

[edit]Intercalated discsMain article: intercalated disc

Intercalated discs (IDs) are complex adhering structures which connect single cardiac myocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development) and are mainly responsible for force transmission during muscle contraction. Intercalated discs also support the rapid spread of action potentials and the synchronized contraction of the myocardium. IDs are described to consist of three different types of cell-cell junctions: the actin filament anchoring adherens junctions (fascia adherens), the intermediate filament anchoring desmosomes (macula adherens) and gap junctions. Gap junctions are responsible for electrochemical and metabolic coupling. They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. However, novel molecular biological and comprehensive studies unequivocally showed that IDs consist for the most part of mixed type adhering junctions named area composita (pl.areae compositae) representing an amalgamation of typical desmosomal and fascia adhaerens proteins (in contrast to various epithelia)[citation needed]. The authors discuss the high importance of these findings for the understanding of inherited

cardiomyopathies (such as Arrhythmogenic Right Ventricular Cardiomyopathy, ARVC).

Under light microscopy, intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section.[5]

[edit]Role of calcium in contractionIn contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle,the initiation and upshoot of the action potential in ventricular muscle cells is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur under normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which initiate extracellular fluid and intracellular stores, and skeletal muscle, which is only activated by calcium stored in the sarcoplasmic reticulum.

[edit]Regeneration of heart muscle cellsUntil recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief.[6] Olaf

Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 when nuclear bomb testing caused elevated levels of radioactive carbon 14 in the Earth's atmosphere. They found that samples from people born before 1955 did have elevated carbon 14 in their heart muscle cell DNA, indicating that the cells had divided after the person's birth. By using DNA samples from many hearts, the researchers estimated that a 20-year-old renews about 1% of heart muscle cells per year and about 45 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.

Cardiac electrophysiology

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Drawing of the ECG, with labels of intervals

Cardiac electrophysiology is the science of elucidating, diagnosing, and treating the electrical activities of the heart. The term is usually used to describe studies of such phenomena by invasive (intracardiac) catheter recording of spontaneous activity as well as of cardiac responses to programmed electrical stimulation (PES). These studies are performed to assess complex arrhythmias, elucidate symptoms, evaluate abnormal electrocardiograms, assess risk of developing arrhythmias in the future, and design treatment. These procedures increasingly include therapeutic methods (typically radiofrequency ablation) in addition to diagnostic and prognostic procedures. Other therapeutic modalities employed in this field include antiarrhythmic drug therapy and implantation of pacemakers and automatic implantable cardioverter-defibrillators (AICD).[1]

The cardiac electrophysiology study (EPS) typically measures the response of the injured or cardiomyopathic myocardium to PES on specific pharmacological regimens in order to assess the likelihood that the regimen will successfully prevent potentially fatal sustained ventricular tachycardia (VT) or ventricular fibrillation VF(VF) in the future. Sometimes a series of EPS drug trials must be conducted to enable the cardiologist to select the one regimen for long-term treatment that best prevents or slows the development of VT or VF following PES. Such studies may also be conducted in the presence of a newly-implanted or newly-replaced cardiac pacemaker or AICD.[1]

A specialist in cardiac electrophysiology is known as a cardiac electrophysiologist, or (more commonly) simply an electrophysiologist. Cardiac electrophysiology is considered a subspecialty of cardiology in most countries and usually requires two or more years of fellowship training beyond a general cardiology fellowship. In early 2011, the Centers for Medicare and Medicaid Services (CMS) promoted cardiac electrophysiology to its own specialty category in the United States. Cardiac electrophysiologists are trained to perform interventional cardiac electrophysiology studies (EPS) as well as surgical device implantations.[1]

Cardiac electrophysiology is a relatively young subdiscipline of cardiology and internal medicine. It was developed during the mid-1970s jointly by Mark E. Josephson, of the University of Pennsylvania School of Medicine in Philadelphia, Pennsylvania, now of Beth Israel Deaconess Medical Center at Harvard Medical School in Boston, Massachusetts, and Hein J. J. Wellens, of the Academic Hospital in Maastricht, Netherlands.[2]

The Heart Rhythm Society, founded in 1979, promotes education and advocacy for cardiac arrhythmia professionals (including cardiac electrophysiologists) and patients. It is the largest society of its kind.

Coronary artery diseaseFrom Wikipedia, the free encyclopedia

Coronary artery disease

Classification and external resources

Micrograph of a coronary artery with the most common form of coronary artery

disease(atherosclerosis) and marked luminalnarrowing. Masson's trichrome.

ICD-10 I20.-I25.

ICD-9 410-414, 429.2

eMedicine radio/192

MeSH D003324

Coronary Artery Disease (CAD or atherosclerotic heart disease) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries[1] that supply themyocardium (the muscle of the heart) with oxygen and nutrients. It is sometimes also calledcoronary heart disease (CHD), although CAD is the most common cause of CHD, it is not the only one.

CAD is the leading cause of death worldwide.[2] While the symptoms and signs of coronary artery disease are noted in the advanced state of disease, most individuals with coronary artery disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arises. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death,[3] and is also the most common reason for death of men and women over 20 years of age.[4] According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old women.[5]According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CAD. By contrast, the Maasai of Africa have almost no heart disease.

As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary artery disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.

A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of blood supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.

An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary artery disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).

Contents

[hide]

1 Pathophysiology 2 Angina

3 Characteristics of coronary artery disease

o 3.1 Special Pathophysiology

o 3.2 Symptoms

o 3.3 Therapy

4 Risk factors

5 Prevention

6 Exercise

7 Preventive diets

8 Aspirin

9 Omega-3 fatty acids

10 Secondary prevention

o 10.1 Anti-platelet therapy

11 Therapy - Principles of Treatment

12 Recent research

13 See also

14 References

15 External links

[edit]PathophysiologyLimitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. Myocardial cells may die from lack of oxygen and this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage,heart muscle death and later myocardial scarring without heart muscle regrowth. Chronic high-grade stenosis of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into ventricular fibrillation leading to death.

CAD is associated with smoking, diabetes, and hypertension. A family history of early CAD is one of the less important predictors of CAD. Most of the familial association of coronary artery disease are related to common dietary habits. Screening for CAD includes evaluating high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels. Despite much press, most of the alternative risk factors including homocysteine, C-reactive protein (CRP), Lipoprotein (a), coronary calcium and more sophisticated lipid analysis have added little if any additional value to the conventional risk factors of smoking, diabetes and hypertension.

[edit]AnginaAngina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with betablocker therapy such as metoprolol or atenolol. Nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It may be treated with oxygen, intravenous nitroglycerin, and aspirin. Interventional procedures such asangioplasty may be done.

[edit]Characteristics of coronary artery disease

[edit]Special PathophysiologyTypically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis, the artery's lining becomes hardened, stiffened, and swollen with all sorts of "grunge" - including calcium deposits, fatty deposits, and abnormal inflammatory cells - to form a plaque. Deposits of calcium phosphates (hydroxyapatites) in the muscular layer of the blood vessels appear to play not only a significant role in stiffening arteries but also for the induction of an early phase of coronary arteriosclerosis. This can be seen in a so-called metatstatic mechanism of calcification as it occurs in chronic kidney disease and haemodialysis (Rainer Liedtke 2008). Although these patients suffer from a kidney dysfunction, almost fifty percent of them die due to coronary artery disease. Plaques can be thought of as large "pimples" that protrude into the channel of an artery, causing a partial obstruction to blood flow. Patients with coronary artery disease might have just one or two plaques, or might have dozens distributed throughout their coronary arteries. However, there is a term in medicine called “Cardiac Syndrome X”, which describes chest pain (Angina pectoris) and chest discomfort in people who do not show signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed.[6]

No one knows exactly what causes “Cardiac Syndrome X” and it is unlikely to have a single cause. Today, we speculate that the major contributing factor to “Cardiac Syndrome X” is “microvascular dysfunction”.[who?] The term “microvascular” refers to very small blood vessels and, in this case, very small arteries (arterioles, capillaries) of the heart. Studies have also shown that people with “Cardiac Syndrome X” have enhanced pain perception, meaning they feel chest pain more intensely than the average person.

The large majority of women have the garden variety of coronary artery disease. Rarely, women with “Cardiac Syndrome X” have typical anginal syndromes that are not associated with the presence of atherosclerotic plaques; that is, the localized blockages are absent. Scientists speculate that the blood vessels in these women are diffuse abnormal. Some have falsely claim that the entire lining of the arterybecomes thickened throughout, making the plaques flush with the wall of the artery without any scientific proof. On cardiac catheterizationtheir coronary arteries appear smooth-walled and normal, though they may look "small" in diameter. By the way: in general, female coronary arteries (like all arteries) are somewhat smaller than in males.

Coronary angiogram of a man

Coronary angiogram of a woman

“Cardiac Syndrome X” have never been shown to cause acute heart attacks (myocardial infarction) despite much speculation. The prognosis with syndrome-X coronary artery disease is also known to be better than with typical coronary artery disease, but this is not a benign condition since it can be quite disabling. It is not completely clear why women are more likely than men to suffer from "Syndrome X"; however, hormones and other risk factors unique to women may play a role.[7]Women’s blood vessels are exposed to changing levels of oestrogen throughout their lives, first during regular menstrual cycles and later during and after menopause as oestrogen levels decline with age. Oestrogen affects how blood vessels narrow and widen and how they respond to injury, so changes in oestrogen levels mean changes in the reactivity of the blood vessels. Women’s vessels may be “programmed” for more changes than men’s vessels, which could increase the risk of having problems in the lining of the arteries (endothelial cells) and the smooth muscle cells in the walls of the arteries. The endothelial dysfunction is likely to be multifactorial in these patients and it is conceivable that risk factors such as hypertension, hypercholesterolemia,diabetes mellitus and smoking can contribute to its development. Most patients with Syndrome X are postmenopausal women and oestrogen deficiency has been therefore proposed as a

pathogenic factor in female patients. In addition to changing hormone levels, there are several other risk conditions for blood vessel problems that are unique to women, such as preeclampsia (a problem associated with high blood pressure during pregnancy) and delivering a low-birth weight baby. Of course, despite these issues women, the female gender as a whole is protective against coronary artery disease.

[edit]SymptomsCardiac Syndrome X often is a diagnosis of exclusion where the presence of typical chest pains is not accompanied by coronary artery narrowings on angiography. In considering Syndrome-X, it is important to understand that about 80% of chest pains have nothing to do with the heart. Therefore, the characteristics of typical chest pains must be carefully documented to avoid unnecessary labelling patients with heart disease:

Chest pain or Angina pectoris with physical stress; the pain may spread to the left arm or the neck, back, throat, or jaw. There might be present a numbness (paresthesia) or a loss of feeling in the arms, shoulders, or wrists

Coronary angiography demonstrates “normal” coronary arteries, i.e. no blockages or stenoses can be detected in the larger epicardialvessels

No inducible coronary artery spasm present during cardiac catheterization

Characteristic ischemic ECG changes during exercise testing

ST segment depression and angina in the presence of left ventricular wall perfusion abnormalities during thallium or other stress perfusion test

Consistent response to sublingual nitrates.

Postmenopausal or menopausal status

The diagnosis of “Cardiac Syndrome X” - the rare coronary artery disease that is more common in women, as mentioned, an “exclusion” diagnosis. Therefore, usually the same tests are used as in any patient with the suspicion of coronary artery disease:

Baseline electrocardiography (ECG) Exercise ECG – Stress test

Exercise radioisotope test (nuclear stress test, myocardial scintigraphy)

Echocardiography (including stress echocardiography)

Coronary angiography

Intravascular ultrasound

Magnetic resonance imaging (MRI)

[edit]TherapyA variety of drugs are used in the attempt to treat the Syndrome-X coronary artery disease: nitrates, calcium channel antagonists, ACE-inhibitors, statins, imipramine (for analgesia), aminophylline, hormone replacement therapy (oestrogen), even electrical spinal cord stimulationare tried to overcome the symptomatology -all with mixed results. Quite often the quality of life for these women remains poor.

While not enough is known about Syndrome-X coronary artery disease to list specific prevention techniques, adopting heart-healthy habits can be a good start.[citation needed] These include monitoring cholesterol and blood pressure levels[citation needed], maintaining a low-fatdiet[citation needed], exercising regularly[citation needed], quitting smoking, avoiding recreational drugs[citation needed], and moderating alcohol intake. However, there might be a new option for women suffering from “Cardiac Syndrome X”: Protein based Angiogenesis.[8] This newprotein-based angiogenic

therapy - using fibroblast growth factor 1 (FGF-1) - might be used as sole therapy as well as adjunct to bypass surgery – thus overcoming the limitations of conventional bypass surgery.

Neo-angiogenesis in a woman's heart after FGF-1 treatment

Beyond drug therapy, interventional procedures, and coronary artery bypass grafting, angiogenesisnow offers a new, specific and – so far as we know from three human clinical trials – effective treatment targeted for women’s coronary artery disease.[9]

[edit]Risk factorsThe following are confirmed independent risk factors for the development of CAD:

1. Hypercholesterolemia (specifically, serum LDL concentrations)[citation needed]

2. Smoking[citation needed]

3. Hypertension (high systolic pressure seems to be most significant in this regard)[citation needed]

4. Hyperglycemia (due to diabetes mellitus or otherwise)[citation

needed]

5. Type A Behavioural Patterns, TABP. Added in 1981 as an independent risk factor after a majority of research into the

field discovered that TABP's were twice as likely to exhibit CAD as any other personality type.[citation needed]

6. Hemostatic Factors:[10] High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD. Factor VII levels are higher in individuals with a high intake of dietary fat[citation needed]. Decreased fibrinolytic activity has been reported in patients with coronary atherosclerosis.

7. Hereditary differences/genetic polymorphisms in such diverse aspects as lipoprotein structure and that of their associated receptors, enzymes of lipoprotein metabolism such as cholesteryl ester transfer protein (CETP) and hepatic lipase (HL) [11], homocysteine processing/metabolism, etc.[citation needed]

8. High levels of Lipoprotein(a),[12][13][14] a compound formed when LDL cholesterol combines with a substance known as Apoliprotein (a).

Significant, but indirect risk factors include:

Lack of exercise Consumption of alcohol

Stress

Diet rich in saturated fats[citation needed]

Diet low in antioxidants

Obesity

Men over 60; Women over 65[15]

Risk factors can be classified as

1. Fixed: age, sex, family history

2. Modifiable: smoking, hypertension, diabetes mellitus, obesity, etc.

There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL cholesterol, tobacco smoking and systolic blood pressure.[16]

[edit]PreventionCoronary artery disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension, avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. There is some evidence that lowering homocysteine levels may contribute to more heart attacks (NORVIT trial). In diabetes mellitus, there is little evidence that very tight blood sugar control actually improves cardiac risk although improved sugar control appears to decrease other undesirable problems like kidney failure and blindness. Some recommend a diet rich in omega-3 fatty acids and vitamin C. The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary artery disease although this remains without scientific cause and effect proof.[17]

An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Patients with CAD and those trying to prevent CAD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of Low density lipoproteins (LDLs), triacylglycerol and apolipoprotein-B. [18] [19] [20]

[21] [22] It is also important to keep blood pressure normal, exercise

and stop smoking. These measures reduces the development of heart attacks. Recent studies have shown that dramatic reduction in LDL levels can cause regression of coronary artery disease in as many as 2/3 of patients after just one year of sustained treatment.

Menaquinone (Vitamin K2), but not phylloquinone (Vitamin K1), intake is associated with reduced risk of CAD mortality, all-cause mortality and severe aortic calcification.[23][24][25]

CAD has always been a tough disease to diagnose without the use of invasive or stressful activities. The development of the Multifunction Cardiogram (MCG) has changed the way CAD is diagnosed. The MCG consists of a 2 lead resting EKG signal is transformed into a mathematical model and compared against tens of thousands of clinical trials to diagnose a patient with an objective severity score, as well as secondary and tertiary results about the patients condition. The results from MCG tests have been validated in 8 clinical trials which resulted in a database of over 50,000 patients where the system has demonstrated accuracy comparable to coronary angiography (90% overall sensitivity, 85% specificity). This level of accuracy comes from the application of advanced techniques in signal processing and systems analysis combined with a large scale clinical database which allows MCG to provide quantitative, evidence-based results to assist physicians in reaching a diagnosis. The MCG has also been awarded a Category III CPT code by the American Medical Association in the July 2009 CPT update.

[edit]ExerciseSeparate to the question of the benefits of exercise; it is unclear whether doctors should spend time counseling patients to exercise. TheU.S. Preventive Services Task Force (USPSTF), based on a systematic review of randomized controlled trials, found 'insufficient evidence' to recommend that doctors counsel patients on exercise, but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease,

morbidity and mortality", it only examined the effectiveness of the counseling itself.[26] However, the American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.[27]

[edit]Preventive dietsMain article: Diet and Heart Disease

It has been suggested that coronary artery disease is partially reversible using an intense dietary regimen coupled with regular cardio exercise.[28]

Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.[29]

Cretan Mediterranean diet: The Seven Countries Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, and goat cheese.[30][31][32]However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet inCorfu, another region of Greece, which had higher death rates.[citation needed]

The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development ofendothelial dysfunction, a precursor to atherosclerosis.[33] The consumption of trans fatty acids has been shown to increase the risk of coronary artery disease[34]

Foods containing fiber, potassium, nitric oxide (in green leafy vegetables), monounsaturated fat, polyunsaturated fat, saponins, or lecithin are said to lower cholesterol levels. Foods high in grease, salt, trans fat, or saturated fat are said to raise cholesterol levels.

[edit]AspirinAspirin, in doses of less than 75 to 81 mg/d,[35] can reduce the incidence of cardiovascular events.[36] The U.S. Preventive Services Task Force 'strongly recommends that clinicians discuss aspirin chemoprevention with adults who are at increased risk for coronary artery disease'.[37] The Task Force defines increased risk as 'Men older than 90 years of age, postmenopausal women, and younger persons with risk factors for coronary artery disease (for example, hypertension, diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'. More specifically, high-risk persons are 'those with a 5-year risk ≥ 3%'. A risk calculator is available.[38]

Regarding healthy women, the more recent Women's Health Study randomized controlled trial found insignificant benefit from aspirin in the reduction of cardiac events; however there was a significant reduction in stroke.[39] Subgroup analysis showed that all benefit was confined to women over 65 years old.[39] In spite of the insignificant benefit for women <65 years old, recent practice guidelines by the American Heart Association recommend to 'consider' aspirin in 'healthy women' <65 years of age 'when benefit for ischemic stroke prevention is likely to outweigh adverse effects of therapy'.[40]

[edit]Omega-3 fatty acidsThe benefit of fish oil is controversial with conflicting conclusions reached by a negative meta-analysis on studies using traditional omega-3 products[41] of randomized controlled trials by the international Cochrane Collaboration and a partially positive systematic review[42] by theAgency for Healthcare Research and Quality. Since these two reviews, a randomized controlled trial reported a remarkable reduction on coronary events in Japanese hypercholesterolemic patients,[43] and a later subanalysis suggested that the protective effect of highly purified

EPA (E-EPA) is even more pronounced in Japanese diabetics even though their intake of fish is high.[44]

Omega-3 fatty acids are also found in some plant sources including flax seed oil, hemp seed oil, and walnuts. The plant omega-3 (ALA) is biologically inferior to marine omega-3, as ALA needs to be converted in the liver to EPA, but only about five per cent is converted.

[edit]Secondary preventionSecondary prevention is preventing further sequelae of already established disease. Regarding coronary artery disease, this can mean risk factor management that is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation, and blood pressure and cholesterol management. Beta blockers may also be used for this purpose.[45]

[edit]Anti-platelet therapyA meta-analysis of randomized controlled trials by the international Cochrane Collaboration found "that the use of clopidogrel plus aspirin is associated with a reduction in the risk of cardiovascular events compared with aspirin alone in patients with acute non-ST coronary syndrome. In patients at high risk of cardiovascular disease but not presenting acutely, there is only weak evidence of benefit and hazards of treatment almost match any benefit obtained.".[46]

[edit]Therapy - Principles of TreatmentTherapeutic options for coronary artery disease[47] today are based on three principles:

1. Medical treatment - drugs (e.g. cholesterol lowering medications, beta-blockers, nitroglycerin, calcium antagonists, etc.);

2. Coronary interventions as angioplasty and coronary stent-implantation;

3. Coronary artery bypass grafting (CABG - coronary artery bypass surgery).

Recent research efforts focus on new angiogenic treatment modalities (angiogenesis) and various (adult) stem cell therapies.

[edit]Recent researchFurther information: atheroma and atherosclerosis

A 2006 study by the Cleveland Clinic found a region on Chromosome 17 was confined to families with multiple cases of myocardial infarction.[48]

A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[49] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[citation needed]Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[50]

Since the 1990s the search for new treatment options for coronary artery disease patients, particularly for so called "no-option" coronary patients, focused on usage of angiogenesis[51] and (adult) stem cell therapies. Numerous clinical trials were performed, either applyingprotein (angiogenic growth factor) therapies, such as FGF-1 or VEGF, or cell therapies using different kinds of adult stem cell populations. Research is still going on - with first promising results particularly for FGF-1[52][53] and utilization of endothelial progenitor cells.

Myocardial infarctionFrom Wikipedia, the free encyclopedia

"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).

Myocardial infarction

Classification and external resources

Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct)

after occlusion (1) of a branch of the (left coronary artery = LCA, right coronary artery = RCA).

ICD-10 I 21. -I 22.

ICD-9 410

DiseasesDB 8664

MedlinePlus 000195

eMedicine med/1567 emerg/327 ped/2520

MeSH D009203

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as aheart attack, is the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) andwhite blood cells (especially macrophages) in the wall of an artery. The resulting ischemia(restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations,sweating, and anxiety (often described as a sense of impending doom).[1] Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.[2] Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms.

Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram(ECG), echocardiography, and

various blood tests. The most often used markers are thecreatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin.[3]

Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable, or in a few emergency cases, bypass surgery may be an option.

Heart attacks are the leading cause of death for both men and women worldwide.[4] Importantrisk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein) and low levels of high density lipoprotein(HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress levels.[5][6]

Contents

[hide]

1 Classification 2 Signs and symptoms

3 Causes

o 3.1 Risk factors

4 Pathophysiology

5 Diagnosis

6 Prevention

7 Management

8 Complications

9 Prognosis

10 Epidemiology

11 Legal implications

12 Research

13 References

14 External links

[edit]Classification

There are two basic types of acute myocardial infarction:

Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart

muscle and are usually a result of complete occlusion of the area's blood supply.[7]

Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart's blood supply and is more susceptible to this type of pathology.[7]

Clinically, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes.[8]

The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is the stopping of the heartbeat, andcardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily.[citation needed]

A 2007 consensus document classifies myocardial infarction into five main types:[9]

Type 1 – Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection

Type 2 – Myocardial infarction secondary to ischaemia due to either increased oxygen demand or

decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension

Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood

Type 4 – Associated with coronary angioplasty or stents:

Type 4a – Myocardial infarction associated with PCI

Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy

Type 5 – Myocardial infarction associated with CABG

[edit]Signs and symptoms

Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest).

Back view.

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.[10] Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due toischemia (a lack of blood

and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm,[not in citation given] back, and epigastrium, where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.[11]

Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating),[1] weakness, light-headedness, nausea,vomiting, and palpitations. These symptoms are likely induced by a massive surge ofcatecholamines from the sympathetic nervous system [12]  which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.[citation needed]

Women and older patients report atypical symptoms more frequently than their male and younger counterparts.[13] Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men).[13] The most common symptoms of MI in women includedyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring

symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.[14]

Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.[15] These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. A silent course is more common in the elderly, in patients with diabetes mellitus [16]  and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.[17] In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[16]

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.[18]

The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other non-catastrophic differentials includegastroesophageal reflux and Tietze's syndrome.[19]

[edit]Causes

Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs.[20] Quantitatively, the period

of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit.[20]For those in poor physical condition, the rate differential is over 35-fold higher.[20] One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.[20]

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[21] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[21] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[22]

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m.[23][24][25] Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.[26]

[edit]Risk factorsRisk factors for atherosclerosis are generally risk factors for myocardial infarction:[citation needed]

Diabetes  (with or without insulin resistance) – the single most important risk factor for ischaemic heart disease (IHD)

Tobacco smoking

Hypercholesterolemia  (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein)

Low HDL

High Triglycerides

High blood pressure

Family history of ischaemic heart disease (IHD)

Obesity [27]  (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).

Age : Men acquire an independent risk factor at age 45, Women acquire an independent risk factor at age 55; in addition individuals acquire another independent risk factor if they have a first-degree male relative (brother, father) who suffered a coronary vascular event at or before age 55. Another independent risk factor is acquired if one has a first-degree female relative (mother, sister) who suffered a coronary vascular event at age 65 or younger.

Hyperhomocysteinemia  (high homocysteine, a toxic blood amino acid that is elevated when intakes of vitamins B2, B6, B12 and folic acidare insufficient)

Stress  (occupations with high stress index are known to have susceptibility for atherosclerosis)

Alcohol  Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack

Males are more at risk than females.[20]

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.[28] Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.[20]

Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation may also contribute to the risk of MI.[29] To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.[29]

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.[30]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[31] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes.[31] Moreover, some drugs for MI

might also reduce CRP levels.[31] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease.[32] Whether CRP plays a direct role in atherosclerosis remains uncertain.[31]

Inflammation in periodontal disease may be linked to coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.[33] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.[34] Periodontitis tends to increase blood levels of CRP, fibrinogenand cytokines;[35] thus, periodontitis may mediate its effect on MI risk via other risk factors.[36] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.[37]

[38] A role for specific periodontal bacteria has been suggested but remains to be established.[39] There is some evidence that influenza may trigger an acute myocardial infarction.[40]

Baldness, hair greying, a diagonal earlobe crease (Frank's sign [41] ) and possibly other skin features have been suggested as independent risk factors for MI.[42] Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.[43]

Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies

have shown that coronary calcium can provide predictive information beyond that of classical risk factors.[44][45][46]

The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version.[47]

[edit]Pathophysiology

See also: Acute coronary syndrome

A myocardial infarction occurs when anatherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophicthrombus formation, totally occluding the artery and preventing blood flow downstream.

Drawing of the heart showing anterior left ventricle wall infarction.

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently (but not always) a manifestation of coronary artery disease.[8] The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery.[48]

[49]Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall ofarteries (in this case, the coronary arteries), typically over decades.[50] Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis.[51] Plaques can become unstable, rupture, and additionally promote athrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).[48][49]

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly throughnecrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[52] As a result, the patient's heart will be permanently damaged.

This Myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

[edit]Diagnosis

Main article: Myocardial infarction diagnosis

The diagnosis of myocardial infarction can be made after assessing patient's complaints and physical

status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels.[53] At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to anemergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist.[54] In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress.[54]

[55] Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.[56]

WHO criteria[57] formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

1.Clinical history of ischaemic type chest pain lasting for more than 20 minutes

2.Changes in serial ECG tracings

3.Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.[58] According to the new guidelines, a cardiac troponinrise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

[edit]Prevention

The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions,congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:[59][60]

Antiplatelet drug  therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.[61]

Beta blocker  therapy such as metoprolol or carvedilol should be commenced.

[62] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.[63] β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.

ACE inhibitor  therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.[64]

Statin  therapy has been shown to reduce mortality and morbidity post-MI.[65][66] The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.[67]

The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.[68] Spironolactone is another option that is sometimes preferable to eplerenone due to cost.

Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease.[69] Omega-3 fatty acids, commonly found in fish, have

been shown to reduce mortality post-MI.[70] While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation.[71] However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.[72][73]

Blood donation may reduce the risk of heart disease for men,[74] but the link has not been firmly established.

A Cochrane review found that giving heparin to people who have heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of suffering from minor bleeding.[75]

[edit]Management

Main article: Myocardial infarction management

An MI is a medical emergency which requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, thus the phrase "time is muscle".[76] Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI.[77] A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.[78]

[79] Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.

[edit]Complications

Main article: Myocardial infarction complications

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to adequately pump blood around the body; aneurysm or rupture of the myocardium; mitral regurgitation, particularly if the infarction causes dysfunction of the papillary muscle; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

[edit]Prognosis

The prognosis post myocardial infarction varies greatly, depending on a person's health, the extent of the heart damage and the treatment given. For the period 2005 – 2008 in the United States the median mortality at 30 days was 16.6% with a range from 10.9% to 24.9% depending on the hospital.[80] Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found that 0.4% of patients with a low risk profile died after 90 days, whereas in high risk people it was 21.1%.[81]

Some of the more reproduced risk stratifying factors include: age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular

disease and elevation of cardiac markers.[81][82]

[83] Assessment of left ventricular ejection fraction may increase the predictive power.[84] The prognostic importance of Q-waves is debated.[85] Prognosis is significantly worsened if a mechanical complication such as papillary muscleor myocardial free wall rupture occur.[86] Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.[87]

[edit]Epidemiology

Myocardial infarction is a common presentation of ischemic heart disease. The WHO estimated in 2002, that 12.6 percent of worldwide deaths were from ischemic heart disease[4] with it the leading cause of death in developed countries, and third to AIDS and lower respiratory infections in developing countries.[88] Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[89]

Coronary heart disease is responsible for 1 in 5 deaths in the United States. It is becoming more common in the developing world such that in India, cardiovascular disease (CVD) is the leading cause of death.[90] The deaths due to CVD in India were 32% of all deaths in 2007 and are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010.[91] Although a relatively new epidemic in India, it has quickly become a major health issue with deaths due to CVD expected to double during 1985–2015.[92]

[93] Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the

highest CVD related mortality estimates.[94] State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).[92]

[edit]Legal implications

At common law, a myocardial infarction is generally a disease, but may sometimes be an injury. This has implications for no-fault insurance schemes such as workers' compensation. A heart attack is generally not covered;[95] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[96] Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.[97]

[edit]Research

Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after a myocardial infarction (MI) show improvements in left ventricular ejection fraction and end-diastolic volume not seen with placebo. The larger the initial infarct size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to ST elevation MI are proceeding.[98]

There are currently 3 biomaterial and tissue engineering approaches for the treatment of MI, but these are in an even earlier stage of medical research, so many questions and issues need to be addressed before they can be applied to patients. The first involves polymeric left ventricular restraints in the prevention of heart failure. The second utilizes in vitro engineered cardiac tissue, which is subsequently implantedin vivo. The final approach entails injecting cells and/or a scaffold into the myocardium to create in situ engineered cardiac tissue.[99]

[edit]