Heart Attack

Heart Attack

What is a heart attack?
How common is a heart attack?
What are the symptoms of a heart attack?
What should be done if a heart attack is suspected?
What happens when a heart attack patient arrives in the ER?
How does "clot buster" treatment compare with angioplasty?
Why is primary angioplasty and stent not used in every case?
What happens after the patient is admitted to the hospital?
What happens after the first day?
What are the complications of a heart attack?
What medications will be prescribed after discharge?

What is a heart attack?  The heart is a muscular organ that pumps blood to the body at an average of 72 times per minute. The coronary arteries are responsible for supplying oxygen and nutrients to the heart muscle. A temporary decrease in blood supply can cause the muscle to "starve" for oxygen and result in chest discomfort or angina. A prolonged total loss of supply can cause irreversible damage of the heart muscle and produces a heart attack. To understand this, let us imagine that the heart is represented by a garden kept lush and green by water sprinkler system. The lawn is divided into three areas, each receiving water from a separate pipe or coronary artery, as shown on the left (below):

   Now imagine that one of these pipes is partially blocked by debris and rust. During a hot summer season, the rusty pipe is unable to keep up with the water needs of the garden. The area supplied by the partially blocked pipe begins to dry and turns brown, but is still alive, as shown on the right (above).. If the garden had symptoms, it would feel pain as it starves for water and nutrients.

   If water flow is now restored or increased, the garden once again turns green and the pain goes away. This is equivalent to angina. The big difference being that angina usually lasts only a few minutes, while the garden's "symptoms" occurs over a matter of weeks or months.

   Now let us imagine that the pipe becomes abruptly and totally blocked (above). Water supply to a section of the garden is completely and permanently interrupted. The grass turns brown and then dies. Once this happens, subsequent restoration of water supply will never return that section of the lawn to its original live, lush and green status. The plant life in one section of the garden has suffered the equivalent of a heart attack and turned into "scar tissue."

   The human heart, like the garden example, can experience prolonged "starvation" or angina before the affected muscle dies and turns into scar tissue. Scar tissue looses a muscle's power to pump. Thus, that portion of the pump becomes stiff, moves sluggishly and decreases the ability of the left ventricle (major pumping chamber of the heart) to efficiently pump blood to the body. The symptoms of chest pain preceding a heart attack can last from several minutes to a few hours.

    The pictures below demonstrate the different phases of atherosclerosis or blockage within a coronary artery. You may click on the left and middle button to stop and then play the slide show. The slides will "loop" continually. You may click on the "Rewind" button to restart the slide show from the beginning.

     The majority of heart attacks occur when a blockage plaque "ruptures" or develops a crack on the inner aspect of the blood vessel. Clot develops at this site and then grows to completely block the channel of the artery. This cuts off blood supply to the heart muscle supplied by that artery and results in a heart attack.

How common is a heart attack?: According to the AHA (American Heart Association; based on statistics from 1996) 1.1 million new and recurrent heart attacks occur per year in the United States. There are about 800,000 new heart attack survivors per year, according to the National Center for Health Statistics (NCHS). Following are additional important statistics provided by the AHA and NCHS:

• There are 12 million victims of angina, heart attack and other forms of coronary artery disease (CAD) living in the USA.
• 5.8 million are male and 6.1 million are female.
• Approximately 225,000 people die, including 125,000 who die suddenly or before they reach a hospital. Most of these deaths are due to lethal irregular heart beats.
• Heart Disease is the number one cause of death in the USA. This is followed by cancer, stroke, lung disease and accidents.
  from 1986 to 1996 the death rate from CAD declined approximately 25%

What are the symptoms of a heart attack? A heart attack may be the first symptom of coronary artery disease in many patients. In others, it may be preceded by days, weeks, months or even years of angina.

   Classic or commonest signals of a heart attack consists of pressure- like, squeezing, or tightness feeling in the center of the chest that may radiate or move to the left shoulder and arm. In some, it may move to both shoulders and arms, the jaw, or between the shoulder blades in the back. If this is merely an angina warning, the symptom may go away in a few minutes and then return.
   Once a coronary artery is totally blocked, a heart attack takes place and the chest discomfort becomes more intense and persistent. The chest discomfort or pain may be accompanied by shortness of breath, unexplained anxiety (a sense of impending doom), weakness, marked fatigue, cold sweats, paleness and a feeling of skipped heart beats. It must be recognized that only one or some of these symptoms may accompany the chest discomfort of heart attack. Also, the symptoms may not be typical in some cases and shortness of breath, cold sweats or marked and sudden fatigue may be the only symptom. 

How should be done if a heart attack is suspected? When a heart attack occurs, it is extremely important to recognize the symptoms and respond rapidly. Nearly 50% of patients suffering from a heart attack wait two or more hours before seeking medical help. This delay reduces the amount of heart muscle that can be salvaged with treatment, raises the amount of disability and increases the risk of sudden death.

   A person experiencing symptoms of a heart attack should be rushed to the nearest emergency room that offers round-the-clock cardiac care. Each person needs to recognize that their symptoms of heart pain may be different from the classical pattern described here and else where. If chest discomfort occurs during exertion, the activity should be stopped and the person be advised to lie down.

   If nitroglycerin tablets have been previously prescribed, a single tablet should be placed under the tongue and allowed to dissolve. if pain continues, take a second and third nitroglycerine tablet at five minute intervals. If pain is not completely relieved, 911 should be called. If time allows, notify the patient's physician so that he or she can make appropriate preparations for the patient's arrival in the emergency room.

What happens when a heart attack patient arrives in the ER? As noted earlier, a heart attack results when a coronary artery is abruptly and totally blocked. In the majority of cases, this occurs as a result of a blood clot. The goals of treatment are to quickly confirm the diagnosis, relieve the symptoms and open up the closed artery (with a "clot buster" medication or by means of angioplasty with or without stents).

Panoramic View of the Cardiac Section of an Emergency Room:

     Move your move cursor within the picture to pan left and right or pause the rotation. You may also do so by placing the mouse cursor within the image and moving it left and right or up and down. Each open door reveals a typical room with ready availability of emergency devices and medications.

   The initial evaluation of a patient with a suspected heart attack is usually accomplished within 10 - 20 minutes of arrival to the Emergency room.

Initial evaluation and treatment usually consists of:

• History of illness is obtained by interviewing the patient and family. This helps the physician determine the likelihood and duration of the heart attack.
• Physical Examination is performed, including recordings of the pulse rate, blood pressure, respiration rate and temperature.
• EKG or electrocardiogram is a useful test in indicating the presence of a heart attack.
• An intravenous line is placed.
• Oxygen is started.
• A nitroglycerin (NTG) tablet is placed under the tongue if the blood pressure is not too low. and the patient is continuing to have chest pain. Intravenous NTG may also be used in these cases.
• Pain medication is delivered, usually via an i.v. line.
• Aspirin is given by mouth.
• Blood is drawn and sent "stat" to the laboratory. This helps confirm the early indication of a heart attack.
• The safety and feasibility of using an intravenous "clot buster" medicine versus taking the patient to the cardiac
  catheterization laboratory (if promptly available) is quickly assessed. If not contraindicated one or the other form of treatment is used in the majority of patients.
• A portable chest x-ray is commonly obtained, particularly if the patient is having shortness of breath. In some cases, an echocardiogram may be obtained in the emergency room to asses the size of a heart attack.

     All the above measures may not be performed or needed in every case, and is individualized on the basis of the patient's symptoms and urgency of the situation.

    The video shown above was taken, during cardiac cath in a patient with angina. It shows a 70% blockage in the proximal or beginning portion of the right coronary artery (RCA) as shown by the arrow. The patient desired medical treatment and did well for a year.. You can also switch between the gray scale and a colorized version by clicking on the button.

    A year later, the same patient was admitted through the emergency room with a heart attack, Unfortunately, the patient continued to smoke and neglected his diet and exercise for several months. He was taken from the emergency room to the cardiac catheterization laboratory where the x-ray films showed total blockage of the right coronary artery. Click on the green arrow button to see how the blockage was treated in the laboratory. 

How does "clot buster" treatment compare with emergency angioplasty and coronary stenting? This is an excellent question for which there is no easy answer. Let us first look at intravenous thrombolytic (clot buster) treatment which became one of the more important advances in the treatment of heart attacks since its introduction. It offers the following advantages (Reference: ACC/AHA Guidelines for Patients with Acute Myocardial Infarction: Executive Summary, Circulation, Nov 1, 1996):

• In comparison with standard medical treatment, thrombolytic therapy reduces the 35-day mortality (death rate) by 21%
  This corresponds to an overall reduction of 21 deaths per 1000 patients treated in this manner.
•  Time is of essence with the use of thrombolytic treatment. Higher benefits are achieved when it is given within 6 hours of the onset of heart attack symptoms. Best results are observed within two to three hours but continues to be beneficial even if started within 12 hours.
• 35 per 1000 lives are saved when it is used within the first hour of symptoms. This drops to 16 lives saved per thousand if treatment is delayed for 7 to 12 hours.
• Thrombolytic therapy benefits the patient regardless of age, sex or presence of risk factors for coronary artery disease.
• Disadvantages include a small risk of a stroke (2%) with a little over half of them (1.1%) being due to bleeding. To place this in the proper perspective, the risk of a stroke due to thrombolytic treatment is far outweighed by the number of lives that are saved

   Next, let us examine the advantages of angioplasty performed as a primary procedure in the treatment of a heart attack. According to the recommendations of the American College of Cardiology and the American Heart Association Guidelines (above), primary angioplasty may be performed as an alert native to thrombolytic therapy in the following circumstances:

• It can be accomplished in a timely manner by skilled and experienced staff.
• There is prompt access to coronary bypass graft surgery.

   Advantages of Primary Angioplasty:

• About half the patients treated with thrombolytic therapy continue to have a significant blockage (since the treatment breaks up blood clots but does nothing for the underlying blockage) and reduced blood flow in the affected artery. In comparison, blood flow is brisk and a mild or no blockage is left behind in over 90% of cases treated with primary angioplasty with or without stenting.
• The mortality or death rate with primary angioplasty is 60% lower (Reference: JAMA 278:2093, 1997) than that achieved with thrombolytic therapy (4.4% compared to 6.5%).
• The risk of stroke is reduced by more than 50%, compared to thrombolytic therapy.
• The probability of having an open artery at 6 months with thrombolytic therapy alone is 59%. The odds improve to 87-91% at 3-6 months with primary angioplasty (References: NEJM: 328, 1993 and Circulation 90:156, 1994).
• In studies where patients were randomized to thrombolytic therapy versus primary angioplasty, those treated with thrombolytic therapy required subsequent PTCA or bypass surgery in 30% of cases. In contrast, only 5% of patients treated with primary angioplasty required a subsequent procedure or surgery during the 3-6 month follow-up (Reference: Circulation 10[Suppl A] 12A, 1998).
• With Primary Stenting in heart attacks, the success rate of the procedure is increased to >95% with less than 1% (0.8%) mortality (death rate) within the hospitalization period (Reference: Cathet Cardiovasc Diag 44, 118, 1998).
• The restenosis rate (chance of blockage returning at same site) is around 25% at 7 months in cases of primary stenting for heart attacks (Reference: J Am Coll Cardiol 31, 23, 1998).

If Primary Angioplasty and Stenting is so good why is it not used in every patient with a heart attack? Excellent question! Since only 18% of hospitals are equipped to perform emergency angioplasty and stenting in patients with heart attacks, this form of treatment is not available in the remaining 82% of hospitals that admit patient's with chest pain. Remember that time is of essence in getting rid of obstructing blood clots and salvaging heart muscle. In most cases, the patient is far better off in receiving a "clot buster" medication in the emergency room if access to a hospital with a cardiac cath lab is not readily available.

   The x-ray video on the left shows a normal left ventricle as it fills and empties. The study was obtained during cardiac catheterization. Note how the top (anterior wall) and bottom (inferior wall) move towards each other as the heart pumps blood to the body.

    The video on the right shows the same left ventricle after a heart attack involving total blockage of the right coronary artery (RCA). Compared to the video above, please note that the inferior (bottom) wall, which is supplied by the RCA, is now barely moving.

What happens after the patient is admitted to the hospital with a heart attack? As noted earlier, most patients who are admitted to an ER (emergency room) in the US are considered for treatment with a "clot buster" medication or emergency angioplasty (with or without a stent). The exact form of treatment has to be individualized on the basis of each case, location of the ER and the duration of time in getting the patient to a cardiac catheterization laboratory. In some cases, because of a patients age and coexisting disease (terminal cancer, etc.), the family and patient may decide to use neither approach.
The first 24 hours in the hospital are usually spent in a coronary care unit (CCU) where the patient's heart rhythm is continuously monitored and the diagnosis of a heart attack is confirmed by a series of EKGs and blood tests. Most deaths from heart attacks occur during the first 24 hours and close observation is usually best provided in a CCU. Here, the patient receives appropriate medications by mouth and through an intravenous line.

Panoramic View of a Coronary Care Unit (CCU) Room:
You may move your mouse within the picture to pan left and right or pause the rotation. 

What are the possible complications of a heart attack and how are they managed? As noted earlier, the first 24 hours of a heart attack are the most critical. With the use of modern day interventions, the death rate from a heart attack has been brought down to around 5% in patients who are hospitalized with a heart attack. depending upon the location of the heart attack and the delay in seeking medical attention, the following complications may be seen:

• Very slow heart beat or heart block (where electrical impulses from the upper chambers of the heart does not make it down to the lower ones). This is usually treated by using a temporary pacemaker.
• Ventricular arrhythmias originating from the lower chambers of the heart. This usually responds to medications but may require an electrical shock to regulate. In some patients with serious and persistent irregular heart beats, an AICD (a specialized device that detects and corrects serious irregular heart beats and looks like a large pacemaker) may be needed to reduce the risk of sudden death).
• Heart failure, where the pumping capability of the heart is significantly reduced by a large heart attack. This is more likely to occur in patients who have had one or more prior attacks. Heart failure (also known as congestive heart failure or CHF) is treated with oxygen and diuretics (a medication that increases the flow of urine and helps the patient get rid of excess fluids). Medications are also used to help reduce the workload of the heart and improve the strength of muscle contraction.
  Shock may occur when a very large amount of heart muscle is damaged by a heart attack. It is a more severe form of heart failure. Depending upon the situation, this may be treated with intravenous medicines, insertion of an intra-aortic balloon pump It consists of a special balloon catheter that is inserted via the groin artery. The inflation and deflation of the balloon pump is timed by the patient's heart beat and helps support the circulation and gives the patient's heart to recover. The treatment of cardiogenic or heart shock may require that the pressure within the heart be monitored with the use of a special (Swan-Ganz) catheter. This is usually inserted through a little needle hole in the groin, or under the collar bone.

    A Swan-Ganz catheter and temporary pacemakers may be inserted in a special procedure room that is equipped with x-ray equipment and is shown below. A Swan-Ganz catheter can also be inserted in the CCU room without the use of x-ray.

Recurrent closure of a coronary artery after it has been opened up with "clot buster" medication or emergency angioplasty. Such patients are usually taken to a cardiac cath lab on an emergency basis and the artery reopened. In some cases, emergency coronary bypass surgery may be needed. The video above shows a surgeon suturing a bypass graft to a coronary artery.

   Other complications can include pericarditis (inflammation of the lining of the heart, heart rupture and a tear within the lower partition of the heart or of the muscle attached to a valve. The latter two complications usually require heart surgery for correction. 

What happens in the hospital after the first 24 hours of a heart attack? Depending upon how well the patient is doing, transfer to a "telemetry" floor is usually arranged on the second day. Unstable patients may remain in the CCU for one or more additional days.
If the patient is recovering nicely, he or she is ambulated in the hallway and may be seen by the cardiac rehabilitation team. The patient and spouse or family are provided with information that helps them understand what happened during the heart attack and what preventive measures are needed to avoid a second one. Instructions about dietary restrictions and an exercise regimen are also given. Depending upon the severity of the heart attack and promptness with which treatment was received, many patients are discharged in 2 to 4 days. Smokers are encouraged to quit tobacco use and supportive measures are recommended.

What medications are prescribed after a heart attack? Many of the patient's home medicines (for example those used to treat high blood pressure, diabetes, etc) are continued. Traditionally, the majority of patients also receive daily aspirin and nitroglycerine for "PRN" or as needed use. If there are no contraindications, most patients are also discharged on a "beta-blocker" medicine. This helps reduce the risk of a second heart attack and sudden death. However, a beta-blocker may not be used in patients with very slow heart beat, asthma and heart failure. Instead, patients with heart failure or reduced heart function may be sent home on a medicine known as an "ACE inhibitor" that helps reduce the workload of the heart. Patients with a high cholesterol level may be sent home on a medication to help control this problem.
Upon discharge, the patient will be given a follow-up appointment with the physician.

Angina

Angina

Coronary Artery Disease Medical Treatment of Angina Heart Attack

    Angina (pronounced an-ji-na) or angina pectoris is produced when the supply of oxygen that is carried by blood is unable to meet the demands of the heart muscle. The decreased supply of blood is created by an obstruction within the coronary artery which impedes blood flow across it. Atherosclerosis is the commonest cause of obstruction. However, obstruction may also result from coronary artery spasm or the use of "crack" cocaine. Angina pectoris is a recurring symptom and usually occurs in the form of chest discomfort (tightness, fullness, squeezing, heaviness, burning or pain) in the center of the chest and /or over the left breast). The discomfort may move to the left shoulder and arm (although it may move to both shoulders/arms, throat, jaw, or even the lower portion of the chest or upper abdomen). It may be accompanied by shortness of breath, sweating, weakness, dizziness or nausea, or numbness in the shoulders, arms and hands. When the build up of plaque is gradual, the patient's symptoms are relatively predictable and stable. Such patient's usually have symptoms that are provoked by specific levels of exercise. They are generally brief, last only 2-3 minutes, and subside promptly with cessation of exercise or following the use of a nitroglycerin tablet. This pattern of pain is known as stable angina. The partial and temporary decrease in oxygen supply to the heart muscle does not generally cause permanent damage (unlike a heart attack).

  

   Some patients may have atypical (not typical) symptoms. For example, the pain may be confined to left shoulder, throat, jaw, or between the shoulder blades. Others may have shortness of breath or sudden weakness, while approximately 10% may have no symptoms, even when the heart is severely stressed or undergoing a heart attack. Such patients are said to have a defective warning system. Diabetic patients are more prone to have atypical or no symptoms.

  Because there are several causes of chest pain that are unrelated to the heart, many patients tend to ignore their symptoms attributing it to heartburn, mitral valve prolapse, a gall bladder attack, muscle sprain, etc. If you have risk factors for coronary artery disease and are having unusual symptoms suggestive of angina or a heart attack, make sure that you consult your doctor about your complaints.

 The following section will walk you through the various phases of atherosclerosis. The following "lecture" describes various phases of the disease. The pictures will change automatically during the audio presentation. You can play, stop, and rewind the animation/narration by clicking on the buttons below.

   Atherosclerosis begins with the deposition of fatty streaks on the inner lining of the artery. Additional deposits lead to a bulky atheroma that begins to encroach into the channel of the coronary artery. Fibers begin to grow into the atheroma causing harder plaques. The plaque of atherosclerosis may develop a crack on its surface. This is known as plaque rupture which can result in the deposit of a blood clot at the site of the blockage. If the blood clot totally blocks flow to the heart muscle, a heart attack usually results.

  However, if the clot causes a partial blockage, the patient may develop unstable angina. Such patients have prolonged, frequent and more severe episodes of angina. The discomfort may be the patient's first symptom (in which case it is called new onset angina). In other cases, stable angina gradually or suddenly changes into a pattern of unstable angina.

  The chest discomfort of unstable angina may become more frequent, last longer, be more intense, be brought on by lesser degrees of exertion (compared to prior symptoms), appear at rest or even awaken the patient from a sound sleep. It is called unstable angina because many untreated patients end up having a heart attack. Unstable angina may also occur in the absence of a blood clot if the severity of the blockage (due to the atheroma and plaques) becomes severe enough to cause a drastic decrease in blood supply to the heart muscle.

As mentioned earlier, angina occurs when the coronary artery is unable to supply the demands of the heart muscle. Thus, it seems logical that the patient's symptoms would improve only if one was able to increase blood supply or decrease the oxygen needs of the heart muscle, or achieve a combination of the two. Listed below are medications commonly used in the treatment of angina:

Nitroglycerin and long acting nitrates: Nitroglycerin (NTG) tablets placed under the tongue (known as sublingual; sub=under and lingua=tongue), is a very effective means of treating angina. The tablet dissolves under the tongue and may have a slightly sharp, burning or tingling taste. Tablets which have this taste when fresh but subsequently become tasteless may indicate loss of effectiveness and potency. They need to be replaced by a fresh supply when they pass the expiration date printed on the bottle label; usually a few months after purchase. NTG is also available in the form of a spray. This spray pump has the advantage of maintaining its potency for years instead of months.

   NTG placed under the tongue dissolves quickly and demonstrates a beneficial effect within a minute or two. It works by dilating the coronary artery and thus improving the supply of blood and oxygen to the heart muscle. NTG also dilates (opens up) the veins and arteries of the body. Dilated veins decrease the filling of the left ventricle (LV), which in turn reduces its workload. On the other hand, dilated arteries of the body reduces the blood pressure and the resistance that the LV has to overcome in pumping blood through those arteries. A single NTG tablet should be placed under the tongue if angina persists beyond a few minutes after stopping activity. If the pain is unrelieved, a second tablet is used after 5 minutes. This is repeated at 5 minute intervals, if pain persists. It is wise to seek medical attention if angina is not completely resolved by the fourth tablets. Consecutive tablets of NTG may cause dizziness if it significantly lowers the blood pressure. In such cases, the patient should sit or lie down. Persistence of angina after the use of four NTG tablets at 5 minute intervals should prompt a phone call to your doctor. Most patients with established or suspected coronary artery disease will be advised to go to the emergency room or a physician's office, depending upon the specific case.

    NTG tablets placed under the tongue are short acting and lasts only 5 to 10 minutes, which is usually a sufficient amount of time to relieve angina. However, a different form of NTG is needed for preventing angina from coming on. They are known as long acting nitrates. Long acting nitrates are available in the form of pills that are taken one to three times a day (depending upon the type that is prescribed) , a patch that is applied to the skin in the morning and removed at night, or an ointment that is placed on the skin three to four times a day. Patients on long acting nitrates will need to continue using NTG under the tongue if angina occurs.

Beta Blockers: The heart rate and blood pressure are elevated when the body releases increased amounts of adrenaline under moments of exertion and emotional stress. Adrenaline the left ventricle contracts more vigorously to provide the body with more blood flow during the period of activity and stress. The increased blood pressure, faster heart rate and more forceful pumping of the left ventricle all increase the need of oxygen by the heart. In patients with coronary artery disease, angina occurs if the supply of oxygen and blood cannot keep up with this increased demand

   A class of medications known as beta blockers partially "insulates" the heart and blood vessels from the effects of adrenaline. This lowers the blood pressure, slows the heart and decreases the force with which the heart contracts. This in turn reduces the oxygen needs of the heart and thus helps in preventing the occurrence of angina. There are over a dozen available beta blockers with similar activities. They have also shown to be benefit in reducing the risk of a heart attack. Beta blockers are often avoided or used with great caution in patient's with slow heart beat and obstructive lung disease (emphysema, bronchitis and asthma). Fatigue, sleepiness, depression and decreased sexual libido may be experienced by some patients. Some of these symptoms may improve by changing the dose or type of beta blocker, or with the passage of time (weeks or months).

Calcium Channel Blockers: Calcium channel blockers decrease blood pressure and can dilate coronary arteries. For these reasons, it is of value in the treatment of patient's with angina; particularly in patients with high blood pressure or in those who have not responded to a combination of nitrates and beta blockers.

Aspirin: Aspirin is one of the least expensive and most valuable medication in the treatment of coronary artery disease. Platelets are small cells that float around in our blood stream. They are the "beavers" of the body that rush to seal any break or breach in the dam. When there is any type of damage or tear in the wall of a blood vessel, platelets collect in that area, clump together and attract formation of a clot. This seals the damage and stops bleeding when a person is injured.

   Unfortunately, the same mechanism comes into play when the coronary artery develops minor cracks in the inner lining of the coronary artery (plaque rupture). This can result in a blood clot that seals the artery, cuts off blood supply to the heart muscle and leads to a heart attack. Aspirin reduces the activity of platelets, decreases the tendency to form clots and is thus extremely valuable in lowering the incidence of heart attacks in patients with coronary artery disease. Aspirin should be avoided in patients with an allergy to the drug. In such cases, alternative medications may be employed.

Preventive Measures, risk factor modification, dietary restrictions, smoking cessation and a structured exercise program are an important cornerstone in the treatment of coronary artery disease.

Coronary Artery Disease

Coronary Artery Disease

Angina Medical Treatment of Angina Heart Attack

   The heart is a muscular organ that pumps blood to the body at an average of 72 times per minute. Oxygen and nutrients serve as a fuel supply to the pump and are carried to heart in the form of blood that flows through the coronary arteries. Thus, the coronary arteries serve as fuel pipe lines to the heart muscle.

   The three major coronary arteries (Left Anterior Descending (LAD), Circumflex (Circ) and Right Coronary Artery (RCA)) and their respective branches each supply a designated portion of the heart, as follows: The LAD supplies blood to the front (anterior) portion of the heart and the septum (muscle partition that separates the Left Ventricle (LV) and Right Ventricle (RV)). The Circ supplies the back (posterior) portion of the LV. The RCA supplies the bottom (inferior) portion of the ventricle and also the RV in 90% of cases. In the other 10%, the Circ sends a branch to the inferior wall of the LV.

   Coronary arteries have muscle fibers within their walls. By contracting the muscle, the artery can reduce blood flow; relaxing the muscle increases flow. In this way, the coronary arteries can regulate blood flow to different portions of the heart. Occasionally, the muscle within a coronary artery may go into spasm and markedly reduce blood flow to the heart muscle. This condition is known as coronary spasm. Typically, the chest discomfort of coronary artery spasm occurs at rest, and usually during the early morning hours. When the spasm is relieved (spontaneously or with the use of medications), the blood vessel goes back to its normal appearance and function. A temporary decrease in blood supply can cause chest discomfort while a persistent decrease can result in permanent muscle damage or a heart attack.

   Atherosclerosis is by far the commonest cause of coronary artery blockage. Unlike coronary spasm which creates a temporary blockage, atherosclerosis results in a fixed blockage. Occasionally, atherosclerosis may be accompanied by coronary spasm. The diagrams below show the various stages of progression of atherosclerosis and development of coronary artery blockages. The round picture on the left of each illustration is a cross-sectional view of the coronary artery, while the picture on the right is a longitudinal section at the same level.

   The inner lining of the normal coronary artery is smooth and free of blockages or obstructions.

    However, as we get older, lipids or fatty substances (cholesterol and triglycerides) are deposited as fatty streaks. The streaks are only minimally raised and thus do not produce any obstruction or symptoms.

   Patients with one or more risk factors for CAD are susceptible to the increased buildup of fatty layers, known as atheroma (pronounced athe-a-roma). This buildup of material begins to encroach upon the inner channel and starts to interfere with the free flow of blood through the coronary artery.

Major risk factors for developing CAD include:

• Hyperlipidemia (high cholesterol level, particularly the "bad" component known as Low-Density Lipoprotein (LDL))
• High blood pressure
• Diabetes
• Cigarette smoking
• Strong family history of CAD
• Male gender, obesity, age above 50 years, lack of exercise, stress and tension can also predispose to the development of atherosclerosis

The deposit of atheroma within the inner lining of arteries is called atherosclerosis (pronounced ath-row-sklee-rosis). It is estimated that 1/3 of adult Americans develop some form of CAD.
Significant atherosclerosis may be confined to the coronary arteries or may be associated with blockages within the arteries of the neck and those supplying blood to the lower limbs (legs)

   As atherosclerosis progresses, fibers begin to grow into and around the fatty layers of atheroma, causing the blockage to harden and turn into a plaque (pronounced plak). The enlarging plaque (above) increases the encroachment into the inner channel of the coronary artery. When the channel is reduced by more than 50% (of the diameter) the artery may become obstructed enough to decrease blood flow to the heart muscle during times of increased need (exercise, emotional stress, etc.). During such times, the blood pressure and heart rate are both elevated and increase the need of oxygen and nutrients by the heart muscle.
The imbalance between the supply and demand of oxygen can cause chest discomfort (tightness, fullness, heaviness or pain) in the center of the chest and/or over the left breast). This is known as angina (pronounced an-ji-na) or angina pectoris. When the coronary artery blockage is severe enough to completely cut off the supply of oxygen and nutrients to the heart muscle, a heart attack can result. However, atherosclerosis may maintain a stable pattern for several years or even decades if the plaques grow slowly or remain relatively stationary. These patients may not notice worsening of angina during the time of stability and are said to have stable angina.

   In other cases, plaques within the inner lining of the coronary artery may develop a slight crack or rupture. Note that the rupture involves only the surface and does not go through the wall of the artery. It is similar to a superficial crack on the plaster of a swimming pool lining, and blood does not escape out of the artery. Plaque rupture stimulates the production of blood clots that tries to seal off the superficial crack. The clot also gets into the crack and causes it to rise and further obstruct the channel of the artery. The sudden increase in the obstruction caused by the raised ruptured plaque and associated clot can transform a mild blockage into a critical one within a matter of hours (above). The decrease in blood flow to the heart muscle is severely reduced and the patient begins to have severe and prolonged chest pain that occurs at rest and may even awaken him or her from a sound sleep. This is known as unstable angina. If the clot does not fully close off the channel of the artery (as in the example above) enough blood flow is maintained to the heart muscle, and a heart attack may not develop if appropriate and prompt treatment is employed.

   However, the clot may continue to grow in many cases. This can completely fill the open channel of the artery (above) and cut off blood flow to the part of the heart muscle that it supplies. Without oxygen and nutrients, the patient suffers from a heart attack and the involved heart muscle can get permanently damaged. The good news is that there are several forms of treatment that can get rid of the blood clot and restore flow across the artery. However, this can only be employed if the patient is rushed to the emergency room of the nearest hospital. Every minute counts in salvaging heart muscle.
Coronary artery blockages and heart attacks may also be seen in patients who use "Crack" cocaine. This is becoming the commonest cause of heart attacks in young adults who are treated in emergency rooms in the USA.

The Heart

 The Heart

The heart is the pump station of the body and is responsible for circulating blood throughout the body. It is about the size of your clenched fist and sits in the chest cavity between two lungs. Its walls are made up of muscle that can squeeze or pump blood out every time that the organ "beats" or contracts.
Fresh, oxygen-rich air is brought to the lungs through the trachea (pronounced tray-kee-ya) or windpipe every time that you take a breath. The lungs are responsible for delivering oxygen to the blood, and the heart circulates the blood to the lungs and different parts of the body.

   The heart is divided into FOUR chambers or "rooms". You can compare it to a Duplex apartment that is made up of a right and a left unit, separated from each other by a partition wall known as a SEPTUM (pronounced sep-tum).

    Each "duplex" is subdivided into an upper and a lower chamber. The upper chamber is known as an ATRIUM (pronounced ay-tree-yum) while the lower chamber is referred to as a VENTRICLE (pronounced ven-trickle).
The right atrium (RA) sits on top of the right ventricle (RV) on the right side of the heart while the left atrium (LA) sits atop the left ventricle (LV) on the left.

    The right side of the heart is responsible for sending blood to the lungs, where the red blood cells pick up fresh oxygen. This OXYGENATED blood is then returned to the left side of the heart. From here the oxygenated blood is transported to the whole body supplying the fuel that the body cells need to function. The blood cells of the body extract or removes oxygen from the blood. The oxygen-poor blood is returned to the right atrium, where the journey began. This round trip is known as the CIRCULATION of blood.

 

The figure shown above is a section of the heart, as viewed from the front. It demonstrates the four chambers. You will also notice that there is an opening between the right atrium (RA) and the right ventricle (RV). This is actually a valve known as the TRICUSPID (pronounced try-cus-pid) valve. It has three flexible thin parts, known as leaflets, that open and shut. The figure below shows the mitral and tricuspid valves, as seen from above, in the open and shut position.

    When shut, the edge of the three leaflets touch each other to close the opening and prevent blood from leaving the RV and going back into the RA. Thus, the tricuspid valve serves as a trapdoor valve that allows blood to move only in one direction - from RA to RV. Similarly, the MITRAL valve (pronounced my-trull) allows blood to flow only from the left atrium to the left ventricle. Unlike the tricuspid valve, the mitral valve has only two leaflets.

In the top diagram, you will also notice thin thread like structures attached to the edges of the mitral and tricuspid valves. These chords or strings are known as chordae tendineae (do not even try to pronounce it. However, if you really must, it is chord-ee tend-in-ee). They connect the edges of the tricuspid and mitral valves to muscle bands or papillary (pronounced pap-pill-lurry) muscles. The papillary muscles shorten and lengthen during different phases of the cardiac cycle and keep the valve leaflets from flopping back into the atrium.

The chords are designed to control the movement of the valve leaflets similar to ropes attached to the sail of a boat. Like ropes, they allow the sail to bulge outwards in the direction of a wind but prevents them from helplessly flapping in the breeze. In other words, they provide the capability of a door jamb that allows a door to open and shut in a given direction and NOT beyond a certain point.

When the three leaflets of the tricuspid bulge upwards during contraction or emptying of the ventricles, their edges touch each other and close off backward flow to the right atrium. This important feature allows blood to flow through the heart in only ONE direction, and prevents it from leaking backwards when the valve is shut. The two leaflets of the mitral valve functions in a similar manner and allows flow of blood from the left atrium to the left ventricle, but closes and cuts off backward leakage into the left atrium when the left ventricle contracts and starts to empty.

Confused? Continue to hang in there. We will clarify this further in the next few pages. Please note that the repetition is intentional! Rephrasing and repeating an explanation often enhances the understanding and retention of key concepts. Skip areas that are redundant to you.

   Let us now follow the circulation of blood through the heart. As noted earlier, oxygenated blood is pumped by the left ventricle to all parts of the body, other than the lungs. The body tissue removes much of the oxygen for its own need. The blood, which is now carrying less oxygen, returns to the heart. Blood from the head, neck and arms return to the right atrium (RA) via the SVC or SUPERIOR VENA CAVA. On the other hand, blood from the lower portion of the body returns to the RA via the IVC or INFERIOR VENA CAVA (pronounced vee-nah cave-ah).

    The RA contracts when filling is completed. This builds up pressure within that chamber and pushes the tricuspid valve open. Blood now rushes from the RA to the right ventricle (RV). When the RV is filled, the walls begin to contract and raises pressure within the RV. The increased pressure shuts the tricuspid valve and pumps blood into the pulmonary (pronounced pull-mun-narey) artery through the pulmonic valve (PV, pronounced pull-mon-nick) which is pushed open by the increased pressure. The diagram below once again shows the four heart valves as viewed from the top, standing in front of the heart, i.e., we are looking down at the two ventricles with the right atrium and left atrium removed.

    The pulmonic valve is made up of three cusps or flexible cup like structures. When the pressure in the right ventricle is low (as is the case during the filling phase of the chamber) the three cusps are full of blood and their sides touch each other to close the opening. This prevents blood from leaking into the pulmonary artery while the RV is filling.
When the RV contracts to empty, the pressure within the chamber rises above that of the pulmonary artery. This forces open the three cusps of PV and blood rushes through the pulmonary arteries and is sent to the lungs. Here the red blood cells pick up oxygen

    The oxygenated blood from the lungs now returns to the left atrium (LA) via four tubes that are known as pulmonary veins. They empty into the back portion of the LA. When the LA contracts after it is completely filled. This opens the mitral valve and forces blood into the left ventricle (LV).
When the LV is completely filled, it starts to empty its contents by contacting the walls. This increases pressure within the chamber, shuts the mitral valve and opens the aortic valve (AV, pronounced a-ortic). The sequence is similar to that described for the RA, RV and pulmonic valve.

Blood now rushes through the aorta (pronounced a-or-tah). The aorta is the main "highway" blood vessel that supplies blood to the head, neck, arms, legs, kidneys, etc. Thus, blood is brought to each of these organs and limbs via branches that originate from the aorta. The cells within each part of the body pick up oxygen and nutrients from the blood. The oxygen-poor blood then returns to the RA, via the superior and inferior vena cava, and the beat goes on!!

    The animation above demonstrates the flow of blood through the heart and lungs, as explained above. Notice that the mitral and the right side of the heart works in synchrony with the left, but that each atria contracts while the ventricle fills

Less confused? Good! Continue to hang in there as we further clarify these concepts

The various parts of the heart, including its chambers, valves and arteries are shown in the figures displayed below.

  The diagram on the right shows a longitudinal (cut from top to bottom) section of the heart. The flow of blood is represented by arrows. The narration will describe different phases of the cardiac circulation.
    The animation will serve as a revision or reinforcement of the various stages or steps of the circulation, with arrows and labels serving as a reminder of what takes place. You may click on the stop, rewind and play buttons to control the animation.

    The pictures below represent a heart that is cut along the horizontal axis. The picture on the left shows the plane along which the heart is cut. That is, the top of the heart, including the right and left atria (atria is plural for atrium), the pulmonary artery and aorta are removed on the picture on the right (below). It shows the heart as you would look down at it from the front. The tricuspid and mitral valves are represented right and left, respectively (you can see the right and left ventricles through the two valves). The aortic and pulmonic valves are shown up and down, respectively, in the bottom half of the picture. The heart size increases and decreases during the filling (DIASTOLE, pronounced die-as-tull-ee) and contraction or emptying (SYSTOLE, pronounced sis-tull-ee) of the heart chambers.

The animation on the bottom left shows a longitudinal section of the beating heart, together with valve structures that open and shut to let blood pass through the atria, ventricles and the great vessels. The animation on the right shows a cross-sectional view of the heart.

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    The mitral and tricuspid valves open and the aortic and pulmonic valves are shut while the ventricles fill during diastole. In contrast, the mitral and tricuspid valves shut while the aortic and pulmonic valves open during ventricular systole. This sequence ensures that the ventricles are filled to capacity before the aortic and pulmonic valves are opened. At this time, the mitral and tricuspid valves are shut so that blood does not leak back into the the two atria. Yes, the heart is an ingenious device that could have inspired design of the modern day mechanical pump and integrated valves.

Did you stop and wonder why each side of the heart has two pumping chambers (atrium and ventricle)? Why not just have a ventricle to receive blood and then pump it straight out? The reason is that the atrium serves as a "booster pump" that increases the filling of the ventricle. Filling a normal ventricle to capacity translates to more vigorous contraction or emptying. You can compare this to a strong spring, and imagine that the heart muscle is made up of tiny little "springs" known as ACTIN and MYOSIN. Within reasonable limits, the more you stretch a spring, the more vigorously will be its contraction or recoil. In medical terms, this is known as "Frank-Starling's" law.

Next, we will show you the heart sections in the frontal and top views again. However, the labels and arrows will be removed so that you can use your imagination to follow the flow of blood through the heart. As you visualize the flow, name the various chambers, valves, arteries and veins. Remember that ARTERIES (pronounces art-trees) carry blood away from the heart. The pulmonary arteries carry oxygen-poor blood to the lungs, while the AORTA (pronounced ay-or-ta) carries oxygen rich blood to the rest of the body. The tubes that return blood to the heart are known as VEINS (pronounced vaynes). The pulmonic (pronounced pull-monic) veins return oxygenated blood from the lungs to the left atrium. They connect into the back of the left atrium.

    The superior vena cava brings oxygen-poor blood from the head, neck and arms to the right atrium, while the inferior vena cava returns oxygen-poor blood to the same chamber from lower portions of the body. Remember that both the superior and inferior vena cavae (cavae is plural for cava and is pronounced cay-veeh). Yup! us docs have our own secret language that originate from the Latin roots of medical terminology. That is why the plural for cava is "cavae" and not "cavas." Go figure!!
The superior vena cava connects to the top of the right atrium (and hence the term superior) while the inferior vena cava connects to the bottom of the chamber.

    Shown below is the same figure that was presented to you a few pages ago. It shows the circulation of blood through the heart and lungs.
    Once again, no labels are provided. If we have done our job, you should not have any problems following the flow of blood. If we have failed to clarify it for you, please accept our apologies and go through the previous sections again - if you so desire.
The aorta is the major blood vessel that arises from the left ventricle and is separated from it by the aortic valve. The left main coronary artery arises from above the left portion of the aortic valve and then usually divides into two branches, known as the left anterior descending (LAD) and the circumflex (Circ) coronary arteries. In some patients, a third branch arises in between the LAD and the Circ. This is known as the ramus (pronounced ray-muss), intermediate , or optional diagonal coronary artery.

    The LAD travels in the groove (known as the inter-ventricular groove) that runs in the anterior or front portion the heart. It sits between the right and the left ventricles or the two lower chambers of the heart.
The LAD gives rise to the following two sets of branches:

• The diagonals are branches of the LAD that runs diagonally away from the LAD and towards the left edge in front of the heart.
• The septal perforators (SP) runs into the septum (partition that separates the two ventricles) and provides its blood supply. 

Circumflex Coronary Artery

    The Circumflex (Circ) coronary artery is a branch of the left main coronary artery. It travels in the left atrio-ventricular groove that separates the left atrium from the left ventricle. The Circ moves away from the LAD and wraps around to the back of the heart. The major branches that it gives off in the proximal or initial portion are known as obtuse (pronounced Ob-tews) marginal or OM coronary arteries. As it makes its way to the back or posterior portion of the heart, it gives off one or more left postero-lateral (PL) branches.

   In 85% of cases, the Circ terminates at this point and is known as a non-dominant left coronary artery system. In the other 15% of cases, a dominant Circ supplies the PDA or posterior descending artery, which run in the bottom of the heart within a groove that separates the left from the right ventricle.

Right Coronary Artery 

The right coronary artery or RCA travels originates above the right portion of the aortic valve and runs in the groove that separates the right atrium from the right ventricle, as it moves towards the bottom or inferior portion of the heart.

    The acute marginal coronary artery is given off in the proximal or early course of the artery. While the terminal or distal portion of the RCA gives off the posterior descending artery or PDA. The PDA runs in the bottom of the heart in a groove that separates the left and right ventricles, as it supplies branches to the lower portion of the septum (partition between the two ventricles. In 15% of cases, RCA is "non-dominant" and the Circ supplies the PDA branch.

    The RCA also supplies the postero-lateral artery or PLA to the lower back portion of the left ventricle and the right ventricular branch to the right ventricle.

Heart Electrical Activity

 The heart has a natural pacemaker that regulates the pace or rate of the heart. It sits in the upper portion of the right atrium (RA) and is a collection of specializes electrical cells known as the SINUS or SINO-ATRIAL (SA) node.

   Like the spark-plug of an automobile it generates a number of "sparks" per minute. Each "spark" travels across a specialized electrical pathway and stimulates the muscle wall of the four chambers of the heart to contract (and thus empty) in a certain sequence or pattern. The upper chambers or atria are first stimulated. This is followed by a slight delay to allow the two atria (atria is plural for atrium and pronounced ay-tree-ya) to empty. Finally, the two ventricles are electrically stimulated.
   In an automobile, the number of sparks per minute generated by a spark plug is increased when you press the gas pedal or accelerator. This revs up the motor. In case of the heart, adrenaline acts as a gas pedal and causes the sinus node to increase the number of sparks per minute, which in turn increases the heart rate. The release of adrenaline is controlled by the nervous system. The heart normally beats at around 72 times per minute and the sinus node speeds up during exertion, emotional stress, fever, etc., or whenever our body needs an extra boost of blood supply. In contrast, it and slows down during rest or under the influence of certain medications. Well trained athletes also tend to have a slower heart beat.

   The sequence of electrical activity within the heart is displayed in the diagrams above and occurs as follows:
As the SA node fires, each electrical impulse travels through the right and left atrium. This electrical activity causes the two upper chambers of the heart to contract. This electrical activity and can be recorded from the surface of the body as a "P" wave" on the patient's EKG or ECG (electrocardiogram).
   The electrical impulse then moves to an area known as the AV (atrio-ventricular) node. This node sits just above the ventricles. Here, the electrical impulse is held up for a brief period. This delay allows the right and left atrium to continue emptying it's blood contents into the two ventricles. This delay is recorded as a "PR interval." The AV node thus acts as a "relay station" delaying stimulation of the ventricles long enough to allow the two atria to finish emptying.

   Following the delay, the electrical impulse travels through both ventricles (via special electrical pathways known as the right and left bundle branches). The electrically stimulated ventricles contract and blood is pumped into the pulmonary artery and aorta. This electrical activity is recorded from the surface of the body as a "QRS complex". The ventricles then recover from this electrical stimulation and generates an "ST segment" and T wave on the EKG.

    In summary, the heart constantly generates a sequence of electrical activity with every single heart beat. This can be recorded on paper or displayed on a monitor by attaching special electrodes to a machine that can amplify and record an EKG or ECG (electrocardiogram). The animation (above) shows the sequence of electrical activity throughout the heart. Note how the chambers of the heart contract when they are electrically stimulated. This in turn makes the heart valves open and shut.
Click on the NEXT button below to move to the EKG section . .