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Bateeilee blog admin will share Coronary Artery Disease. Coronary artery disease (CAD) is a condition in which plaques build up in the walls of the coronary arteries (the vessels that supply blood to the heart muscle). These plaques can gradually obstruct the artery, or they can suddenly rupture, causing a more acute obstruction. Because the heart muscle requires a continuous supply of oxygen and nutrients to survive, obstruction of a coronary artery rapidly leads to significant problems.

CAD is caused by atherosclerosis. Atherosclerosis is a chronic, progressive disorder of the arteries in which deposits of cholesterol, calcium, and abnormal cells (that is, plaques) build up on the inner lining of the arteries.

These plaques can cause a gradual but progressive narrowing of the artery, and as a result, blood flow through the artery becomes more difficult. When the obstruction becomes large enough, the patient may experience angina.

"Angina" refers to the symptoms a patient experiences any time the heart muscle is not getting enough blood flow through the coronary arteries. Angina is usually felt as a discomfort (often a pressure-like pain) in or around the chest, shoulders, neck or arms.

"Stable angina" is angina that occurs in a nearly predictable fashion, for instance, with exertion or after a big meal. Stable angina generally means that a plaque has become large enough to produce a partial obstruction of a coronary artery.

When a person with stable angina is at rest, the partially blocked artery is able to meet the needs of the heart muscle. But when that person exercises, (or has some other stress that makes the heart work harder), the obstruction prevents an adequate increse in blood flow to the heart muscle, and angina occurs. So stable angina usually means there that there is a significant plaque in a coronary artery that is partially obstructing the flow of blood.

In addition to causing obstruction by a gradual increase in their size, plaques are also subject to sudden rupture, which can produce a very sudden obstruction. The medical conditions caused by the rupture of a plaque are referred to as Acute Coronary Syndrome (ACS). ACS is always a medical emergency.

“Unstable angina” is one type of ACS. Unstable angina occurs when a plaque has partially ruptured, causing a sudden worsening of the blockage in the artery. In contrast to stable angina, symptoms in unstable angina occur unpredictably, (that is, they are not particularly related to exertion or stress), and notably, tend to occur at rest. (Another name for unstable angina is "rest angina.") Patients with unstable angina are at high risk of developing a total occlusion of the coronary artery, leading to a myocardial infarction.

Myocardial infarction, or heart attack, is a more dire form of ACS. Here, the ruptured plaque causes a total (or near total) occlusion of the coronary artery, so that the heart muscle supplied by that artery dies. A heart attack, therefore, is death of heart muscle. The seriousness of a myocardial infarction depend largely on how much heart muscle has died. A small heart attack is one in which only a small portion of the heart muscle dies. A large heart attack is one in which a large portion of heart muscle dies.

If a patient receives medical attention within a few hours of the onset of a heart attack, the size of the heart attack can be greatly reduced by administering “clot-busting drugs," or by performing an immediate angioplasty (and most often, stenting) to open up the blocked artery.

After surviving a heart attack, the patient is still at risk. Further heart attacks are possible if more plaques are present in the coronary arteries. Also, depending on the amount of heart muscle that has been damaged, the patient can develop heart failure. Furthermore, damaged heart muscle can cause a permanent instability in the heart's electrical system, which can lead to sudden cardiac arrest. So after a heart attack, all of these risks need to be carefully evaluated, and steps need to be taken to reduce each of these risks to the greatest extent possible. Here is more information on reducing risk after surviving a heart attack.

The best way to deal with coronary artery disease, of course, is to prevent it. All of us should do everything we can to reduce our CAD risk factors.

For those who already have CAD, reducing these same risk factors becomes even more important, in order to slow the progression of the disease. In addition, several avenues are available for treating CAD, including drug therapy, surgical therapy, and angioplasty and stenting. The treatment of CAD always needs to be individualized, and optimal therapy depends on careful consideration of all the options, by both the doctor and the patient.

Bateeilee blog admin will post What Is Peripheral Artery Disease?. Peripheral artery disease (PAD) is a condition in which one or more of the arteries supplying blood to the legs (or arms) becomes blocked or partially blocked, usually because of atherosclerosis. If the blood flow to the limbs is no longer sufficient to keep up with the demand, a person with PAD may experience symptoms.

What Are the Symptoms of PAD?

 

The most common symptom of PAD is "claudication." Claudication is pain, cramping or discomfort - which can vary from merely annoying to quite severe - that occurs in the affected limb. Typically, claudication occurs during exercise, and is relieved by rest.

Since PAD most commonly affects the legs, claudication most typically manifests as leg pain when walking. Depending on where in the leg artery the blockage is located, leg claudication can affect the foot, calf, thigh or buttocks. People who have PAD in one of the arteries that supply the upper extremities can experience claudication in the arm or shoulder; and some can even experience neurological symptoms during arm exercise, a condition called "subclavian steal syndrome."

Sometimes PAD will cause persistent claudication even at rest. Resting claudication often means that the arterial blockage is relatively severe, and the affected limb is not receiving sufficient bloodflow even at rest.
Because claudication does not always follow the typical pattern - that is, pain during exertion, with relief during rest - the diagnosis of PAD should be considered any time a person over 50 years of age, who has risk factors for atherosclerosis, experiences unexplained pain in the arms or legs.

Very severe PAD can lead to ulceration and even gangrene of the affected limb.

What Causes PAD?

In the large majority of cases, PAD is caused by atherosclerosis. This means that the same kinds of risk factors that produce coronary artery disease (CAD) - especially elevated cholesterol levels, smoking, hypertension and diabetes - also produce PAD. In fact, because PAD and CAD are caused by the same disease process, when PAD is diagnosed, very often it means that CAD is also present.

More rarely, PAD can be seen in people who do not have atherosclerosis. For instance, PAD can be caused by trauma to the limbs, exposure to radiation, and certain drugs (the ergotamine drugs) used to treat migraine headaches.

How Is PAD Diagnosed?

 

PAD can be diagnosed with non-invasive testing. In some cases, PAD can be detected by physical examination, when a reduced pulse is noticed in the affected limb. More often, however, one of several specific tests is required to diagnose PAD.

Diagnosing PAD in the legs can be done using the "ankle-brachial index," or ABI, in which the blood pressure is measured and compared in the ankle and the arm. A low ABI index indicates a reduced blood pressure in a leg artery, indicating that PAD is present.

"Plethysmography" is another technique used for diagnosing PAD. With this test, air is pumped into a series of cuffs placed along the leg, and the pulse pressure of the artery beneath each cuff is estimated. A blockage somewhere in the artery will result in a reduced pulse pressure beyond the area of blockage.

"Duplex ultrasonography" is a special ultrasound test which provides an estimate of blood flow at various levels within an artery. A sudden drop in blood flow suggests a partial blockage at the area of the drop.
If your doctor suspects PAD, one or more of these non-invasive tests is usually sufficient to make a diagnosis. Today, the ABI is the test used most commonly.

How Is PAD Treated?

 

While mild or moderate PAD can be treated with medication and lifestyle changes, more severe cases often require bypass surgery or angioplasty to relieve the blockages.

Bateeilee blog admin will share What is Atherosclerosis?. Atherosclerosis is a chronic, progressive disease in which plaques (consisting of deposits of cholesterol and other lipids, calcium, and large inflammatory cells called macrophages) build up in the walls of the arteries.

These plaques can cause several problems. First, plaques can protrude into the artery, eventually causing a partial or complete obstruction to blood flow. Second, plaques can suddenly rupture, causing a thrombus (blood clot) to form, leading to sudden occlusion of the artery. (This condition is called arterial thrombosis.) Third, plaques can weaken the wall of the artery causing a ballooning out of the artery to form what is called an aneurysm. The rupturing of an aneurysm often produces severe internal bleeding.

What causes atherosclerosis?

 

The fundamental underlying cause of atherosclerosis has not been fully established. However, many factors that contribute to atherosclerosis have been identified, including:

• Genetic predisposition - the propensity for atherosclerosis clearly runs in families. Anybody whose close relatives (parents, sibs, uncles and aunts) have had atherosclerosis ought to take every opportunity to reduce their own risk factors.
• Cholesterol abnormalities - high blood levels of LDL cholesterol, and low levels of HDL cholesterol, are associated with atherosclerosis.
• Hypertension
• Smoking
• Sedentary lifestyle
• Obesity, especially abdominal obesity
• Diabetes

In Western cultures, arteries commonly show early changes of atherosclerosis even in childhood and adolescence. This is a disease that develops over a period of decades before it ever begins to produce symptoms.

Which arteries are affected?

 

Atherosclerosis commonly affects the coronary arteries, leading to angina and myocardial infarction (heart attack); the cerebrovascular circulation (brain arteries), leading to stroke; the renal arteries, leading to kidney disease; the aorta, leading to aortic aneurysm; and the blood vessels of the arms and (especially) the legs, leading to claudication, ulceration, skin changes, and slow-healing.

In the United States, atherosclerosis causes more death and disability than any other disease.

Bateeilee blog admin will share Medical Treatment for Angina.  If you have coronary artery disease (CAD), you can develop cardiac symptoms for two general reasons. First, it is possible to have acute coronary syndrome (ACS), which is a sudden deterioration caused by the formation of a blood clot within a coronary artery. ACS causes unstable angina and myocardial infarctions (heart attacks).

Second, you can have angina caused by the gradual development of partial blockages in a coronary artery. In this case, you can experience episodes of cardiac ischemia during periods of cardiac stress (such as exercise), when your heart muscle is demanding more oxygen than a partially blocked coronary artery can provide. The oxygen-starved (ischemic) heart muscle often causes the painful or uncomfortable sensation which we refer to as angina. Because this kind of angina is due to a blockage that is changing only gradually, and because the angina it produces occurs relatively predictably (that is, during a certain amount of exercise), we call it stable angina.

There are two general approaches to treating stable angina. The first approach is to use so-called "invasive therapy" -- that is, to use either bypass surgery or angioplasty and stenting to relieve specific blockages. You can read here about bypass surgery, angioplasty, and stents.

The second approach is to use medical therapies, also referred to as "non-invasive" therapies, including drugs and other non-surgical approaches. Medical therapies tend to work by reducing the "oxygen demand" of the heart muscle, that is, to reduce the amount of oxygen the heart muscle requires, so that even a partially blocked can deliver an adequate amount. The rest of this article reviews medical therapies for stable angina.

Drug Therapy For Stable Angina

Three categories of drugs are commonly used to lower the oxygen demand of the heart muscle, and to treat or prevent episodes of stable angina. These categories are nitrates, beta blockers, and calcium channel blockers. A few new drugs that are not in any of these categories are also being developed.
Nitrates: Nitrates cause dilation of blood vessels, which reduces stress on the heart muscle, thereby reducing the cardiac demand for oxygen.

Beta blockers: Beta blockers reduce the effect of adrenaline on the heart muscle, which reduces the heart rate and the force of heart muscle contraction, thus reducing the oxygen demand of the heart. These drugs also improve survival in some patients with CAD.

Calcium blockers: Calcium blockers reduce the influx of calcium into the heart muscle, also into the smooth muscle of blood vessels. This results in blood vessel dilation, lowers heart rate, and reduces the forcefulness of the heart beat -- all of which lower the oxygen demand of the heart.

Other anti-anginal drugs: Ranexa (ranolazine) is a new type of anti-angina drug that appears to work by blocking what is called the "late sodium channel" in heart cells which are suffering from ischemia. Blocking this sodium channel improves the metabolism in ischemic heart cells, reducing damage to the heart muscle, and also reducing angina symptoms.

How are these drugs used? In general, if you have angina your doctor usually will first give you a beta blocker, and also nitroglycerin (one of the nitrates) to treat any acute episodes you may have. If you still have episodes of angina, your doctor may next give you either a long-acting form of nitrate therapy or a calcium channel blocker (or both). Ranexa, being a new drug, is usually given as a third or fourth drug when necessary -- but some cardiologists have found it to be useful when added earlier. Finally, almost all patients with angina should be placed on aspirin, 81 to 325 mg/day. If your doctor does not do this, you should bring it up yourself.

Other Non-invasive Therapy for Stable Angina

Exercise therapy: Exercise training is an effective method of reducing episodes of angina in people with stable angina. Chronic, low-intensity aerobic exercise (for instance, walking or cycling) "trains" your cardiovascular system and the skeletal muscles to become more efficient. This means you will be able to maintain higher levels of exercise without experiencing angina.

If you have CAD you should usually begin an exercise program under medical supervision. Your doctor may perform a formal stress test to measure your exercise capacity, and to evaluate the level of exercise that begins to produce cardiac ischemia. You will then be given an exercise "prescription," advising you to maintain a heart rate during aerobic exercise that is 60% to 75% of your highest "safe" heart rate, as measured during the exercise test.

A program of aerobic exercise has many benefits in addition to reducing episodes of angina, including promoting weight control, improving vascular health, improving muscle and joint strength, and creating a better mindset for achieving other favorable lifestyle modifications such as diet control and smoking cessation.

Enhanced external counterpulsation (EECP): EECP is a unique treatment for angina that can be quite effective in some patients, but which most cardiologists studiously ignore.

Bateeilee blogs admin will share What is Unstable Angina?. Unstable angina is a pattern of angina that occurs randomly or unpredictably, and is unrelated to any obvious trigger (such as physical exertion or emotional stress). Unstable angina is a form of Acute Coronary Syndrome (ACS), and like all ACS, unstable angina should be considered a medical emergency.

What is Unstable Angina?

 

Angina is considered to be "unstable" when it no longer follows the predictable patterns typical of "stable angina."

Unstable angina is called "unstable" for two reasons.
First, in contrast to stable angina, symptoms occur in a more random and unpredictable fashion. While in stable angina, symptoms typically are brought on by exertion, fatigue, anger, or some other form of stress, in unstable angina symptoms can (and often do) occur without any apparent trigger. In fact, unstable angina often occurs at rest, and can even wake people from a restful sleep. Furthermore, in unstable angina, the symptoms often persist for more than just a few minutes, and nitroglycerin often fails to relieve the pain. So: unstable angina is "unstable" because symptoms may occur more frequently than usual, without any discernible trigger, and may persist for a long time.

Second, and more importantly, unstable angina is "unstable" because, as with all forms of ACS, it is most often caused by the actual rupture of a plaque in a coronary artery. In unstable angina, the ruptured plaque, and the blood clot that is almost always associated with the rupture, are producing partial blockage of the artery. The partial blockage may take a "stuttering" pattern (as the blood clot grows and shrinks), producing angina that comes and goes in an unpredictable fashion. If the clot should cause complete obstruction of the artery (which happens commonly), the heart muscle supplied by that affected artery is in grave danger of sustaining irreversible damage. In other words, the imminent risk of a complete myocardial infarction is very high in unstable angina. Obviously, such a condition is quite "unstable," and for this reason is a medical emergency.

When Should You Suspect You Might have Unstable Angina?

 

Anybody with a history of coronary artery disease should suspect unstable angina if their angina begins to occur at lower levels of physical exertion than normal, if it occurs at rest, if it persists longer than usual, if it is more difficult to relieve with nitroglycerin, or especially if it wakes them up at night.

People without any history of coronary artery disease can also develop unstable angina. Unfortunately these people seem to be at higher risk of a heart attack because, unfortunately, they often don’t recognize the symptoms as being angina. The classic symptoms of angina include chest pressure or pain, sometimes squeezing or “heavy” in character, often radiating to the jaw or left arm. Unfortunately, many patients with angina do not have classic symptoms. Their discomfort may be very mild, and may be localized to the back, abdomen, shoulders, or either or both arms. Nausea, breathlessness, or merely a feeling of heartburn may be the only symptom. What this means, essentially, is that anyone middle aged or older, especially anyone with one or more risk factors for coronary artery disease, should be alert to symptoms that might represent angina.

If you think there is any possibility you might have unstable angina, you need to go to your doctor, or to an emergency room, immediately.

How Is Unstable Angina Diagnosed?

 

Symptoms are critically important in making the diagnosis of unstable angina, or indeed, any form of ACS. In particular, if you have one or more of the following three symptoms, your doctor should take that as a strong clue that one type or another of ACS is occurring:

• Angina at rest, especially if it lasts more than 20 minutes at a time
• New onset angina that markedly limits your ability to engage in physical activity
• An increase in prior stable angina, with episodes that are more frequent, longer lasting, or occur with less exertion than previously

Once your doctor suspects ACS, he should immediately get an ECG and blood tests for cardiac enzyme testing. If the portion of the ECG known as "ST segments" are elevated (which indicates that the artery is completely blocked), and the cardiac enzymes are increased (which indicates cardiac cell damage), a "large" myocardial infarction (MI) is diagnosed (also called an "ST-segment elevation MI," or STEMI).

If the ST segments are not elevated (indicating that the artery is not completely blocked), but the cardiac enzymes are increased (indicating that cell damage is present), a "smaller" MI is diagnosed (also called a "non-ST segment MI," or NSTEMI).

If the ST segments are not elevated and the enzymes are normal (meaning the artery is not completely blocked and no cell damage is present), unstable angina is diagnosed.

Notably, unstable angina and NSTEMI are similar conditions. In each condition, a plaque rupture has occurred in a coronary artery, but the artery is not completely blocked so at least some blood flow remains. In both of these conditions, the symptoms of unstable angina are present. The only difference is that in an NSTEMI enough heart cell damage has occurred to produce an increase in cardiac enzymes. Because these two conditions are so similar, their treatment is identical.

What Is the Treatment For Unstable Angina (and NSTEMI)?

 

If you have either unstable angina or NSTEMI, you will be treated with one of two general approaches: a) treat aggressively with drugs to stabilize the condition, then evaluate non-invasively, or b) treat aggressively with drugs to stabilize the condition, and schedule early invasive intervention (generally, angioplasty and stenting).

Bateeilee blog admin will share about What's Unstable Angina or Stable Angina?. Angina is the name given to the symptoms (usually chest pain or chest discomfort) produced when the heart muscle is in a state of ischemia - that is, when the heart muscle is not getting enough blood supply. In unstable angina, ischemia occurs unpredictably and suddenly, usually because a blood clot has suddenly formed within a coronary artery, temporarily limiting blood flow to the heart muscle.

Unstable angina is often exacerbated by the formation of temporary blood clots within the coronary arteries. If the blood clots persist, a heart attack can occur. It's not surprising, then, that unstable angina often occurs before a heart attack, and should be treated aggressively.

Stable Angina is the name given to the symptoms (usually chest pain or chest discomfort) produced when the heart muscle is in a state of ischemia - that is, when the heart muscle is not getting enough blood supply. Stable angina occurs when there is a partial blockage in a coronary artery that limits the maximum blood flow to the heart muscle.

Patients with stable angina usually have no symptoms during rest or with mild activity, since blood flow to the heart muscle is adequate under these conditions. However, during periods of exercise or other conditions of stress in which the heart muscle requires more oxygen, the partial blockage prevents an adequate increase in blood flow. This lack of sufficient blood flow under these circumstances produces ischemia, thus leading to angina.

This condition is called "stable" angina because the symptoms occur in a predictable fashion - that is, they occur only under conditions such as exercise or other stresses that require the heart to work harder.
In contrast, in unstable angina symptoms occur unpredictably, most often at rest.

Bateeilee blogs admin will post How the Blood Clots?. The clotting mechanism is one of the most important and complex of physiologic systems. Blood must flow freely through the blood vessels in order to sustain life. But if a blood vessel is traumatized, the blood must clot to prevent life from flowing away. Thus, the blood must provide a system that can be activated instantaneously – and that can be contained locally – to stop the flow of blood. This system is called the clotting mechanism.

To treat or prevent abnormal blood clotting, doctors must understand the multifaceted aspects of the clotting mechanism. The following explanation is greatly simplified, but is designed to provide a basic understanding of how the many drugs used to treat clotting problems work, and some basis for assessing the treatments your doctor may prescribe for you.

How does the blood clot?

 

There are two major facets of the clotting mechanism – the platelets, and the thrombin system. The platelets are tiny cellular elements, made in the bone marrow, that travel in the bloodstream waiting for a bleeding problem to develop. When bleeding occurs, chemical reactions change the surface of the platelet to make it “sticky.” Sticky platelets are said to have become “activated.” These activated platelets begin adhering to the wall of the blood vessel at the site of bleeding, and within a few minutes they form what is called a “white clot.” (A clump of platelets appears white to the naked eye.)

The thrombin system consists of several blood proteins that, when bleeding occurs, become activated. The activated clotting proteins engage in a cascade of chemical reactions that finally produce a substance called fibrin. Fibrin can be thought of as a long, sticky string. Fibrin strands stick to the exposed vessel wall, clumping together and forming a web-like complex of strands. Red blood cells become caught up in the web, and a “red clot” forms.

A mature blood clot consists of both platelets and fibrin strands. The strands of fibrin bind the platelets together, and “tighten” the clot to make it stable.

In arteries, the primary clotting mechanism depends on platelets. In veins, the primary clotting mechanism depends on the thrombin system. But in reality, both platelets and thrombin are involved, to one degree or another, in all blood clotting.

How the Blood Clots - using a coronary artery as an example.

 

Figure 1. A coronary artery is shown that has an atherosclerotic plaque ("AP") partially occluding the lumen (opening) of the artery. Platelets within the blood are shown ("P"). The flow of blood through the artery is indicated by the long arrow. The patient with this artery likely has stable angina.

Figure 2. The atherosclerotic plaque has developed an ulcer ("U").

Figure 3. The platelets have been activated (i.e., made "sticky") by their exposure to the ulcerated plaque. They begin to aggregate (to stick) to the surface of the ulcer.

Figure 4. The thrombin system has been activated (also by exposure of the blood to the surface of the ulcer), and fibrin strands begin to form, connecting the aggregated platelets, and drawing them together. 

Figure 5. A mature clot is now present, superimposed on the atherosclerotic plaque. This clot makes the partial obstruction of the coronary artery substantially worse. The arrow indicates the increased sluggishness and turbulence of blood flow through the artery. This patient most likely now has unstable angina, and if blood flow is sluggish enough, some of the heart cells supplied by this artery may die.

If the artery becomes totally occluded by a clot, a classic heart attack (myocardial infarction) will occur.

How can the clotting mechanism produce problems?

 

The clotting system, like all complex physiologic systems, can produce problems. Blood clots forming on atherosclerotic plaques in the arteries are the major cause of heart attack and stroke. Blood clots forming in the veins of the legs produce a painful condition called phlebitis, and when these venous blood clots break off (“embolize”) they move into the lungs and produce a dangerous condition called pulmonary embolus.

How can abnormal blood clotting be treated?

 

Drugs used for preventing or treating abnormal blood clotting can be aimed either at the platelets, or at the thrombin system. While they all have their own profile of side effects, one side effect common to all these drugs is excess bleeding. They must all be used with appropriate precautions.

Drugs aimed at the thrombin system.

 

Drugs that prevent further fibrin from forming. These drugs, which inhibit one or more of the proteins involved in the thrombin clotting system, are used for both arterial and venous clotting problems. Heparin. Heparin is an intravenous drug that has an immediate (within seconds) inhibitory effect on the thrombin system. Its dosage can be adjusted frequently, following the PTT blood test (the partial thromboplastin time) to achieve the desired effect.

Low molecular weight heparin: enoxaparin, dalteparin.  LMWH is a “purified” derivative of heparin. Its major advantages are that it can be given as a skin injection (which almost anyone can learn to do in a few minutes), and does not need to be closely monitored with blood tests. Thus, unlike heparin, LMWH can be administered safely on an outpatient basis.

Coumadin. Coumadin is an oral anti-thrombin drug that can be taken chronically. The dose must be carefully monitored by following the prothrombin time (PT), a blood test.

Drugs that “dissolve” fibrin – the fibrinolytic drugs. These powerful drugs actually dissolve fibrin strands that have already formed.

TPA, streptokinase, urokinase. These are the intravenous drugs that are administered acutely during the first few hours of an acute heart attack or stroke, to attempt to re-open an occluded artery, and prevent permanent tissue damage.

Drugs aimed at platelets.

 

These three groups of drugs, in one way or another, reduce the “stickiness” of platelets. They are used most commonly in preventing arterial clots from forming. Aspirin and diypyramidole. These drugs have a modest effect on platelet “stickiness,” but have few important side effects.

Ticlopidine (Ticlid) and clopidrogel (Plavix). These drugs are somewhat more powerful than the first group, but can be poorly tolerated and can have important side effects. They are generally used in patients who need, but cannot tolerate, aspirin.

IIb/IIIa inhibitors: abciximab (Reopro), eptifabitide (Integrilin), tirofiban (Aggrastat). The IIb/IIIa inhibitors are the most powerful group of platelet inhibitors. They inhibit a receptor on the surface of platelets (the so-called IIb/IIIa receptor) that is essential for platelet stickiness. Their chief usage is to prevent acute clotting after interventional procedures (such as angioplasty and stent placement), and in patients with acute coronary artery syndromes, such as unstable angina. These drugs are very expensive and (in general) must be given intravenously.

Bateeilee blog admin will share Preventing Acute Coronary Syndrome. Preventing acute coronary syndrome - ACS - should be one of your chief concerns if you have been told you have coronary artery disease (CAD).

Acute coronary syndrome (ACS) occurs when a blood clot suddenly forms within a coronary artery. This usually happens when a plaque ruptures in the wall of the artery. The blood clot produces a sudden blockage of the artery, leading to ischemia (insufficient blood flow to the heart muscle).

The severity of ACS syndrome depends on whether the blood clot completely or only partially blocks the artery, and how long the clot lasts. (The body's protective mechanisms try to dissolve blood clots that form within blood vessels. Read more about how the blood clots here.) Clots that completely block an artery often cause myocardial infarction or even sudden death. Clots that only partially block an artery, or that persist for only a few minutes, produce unstable angina. In either case, ACS is a medical emergency.

Anyone with CAD can develop ACS. So everyone with CAD should take appropriate steps to reduce the risk of ACS. These preventative actions include steps to lower the risk of plaque rupture, and steps to reduce the risk of large or persistent blood clots if a rupture occurs.

Accordingly, if you have CAD you should do the following things:

• Stop smoking. You should think of smoking as a technique for actively irritating plaques within your coronary arteries. Even one cigarette can acutely increase the risk of ACS for up to a day or two. And when you quit smoking, your risk of ACS drops substantially within a few days.
• Ask your doctor about statin therapy. Statins can help to stabilize plaques to help keep them from rupturing. Statins also improve the function of the lining of arteries, reduce inflammation, and reduce blood clot formation -- all of which can help to prevent ACS.
• Make sure your blood pressure is normal blood pressure. High blood pressure increases the risk of plaque rupture.
• Ask your doctor about taking beta blockers. Beta blockers can help prevent plaque rupture by limiting the effect of stress and exertion on the blood vessels.
• Make sure your cholesterol measurements are adequate. High LDL cholesterol and low HDL cholesterol levels are thought to increase the risk of plaque rupture.
• Ask your doctor about taking aspirin. Aspirin therapy reduces the "stickiness" of blood platelets, and can reduce blood clot formation when plaque rupture occurs.

Taking these steps will go a long way toward preventing ACS.

Bateeilee blog admin will share What Is Acute Coronary Syndrome - ACS. Coronary artery disease (CAD) produces two broad categories of clinical syndromes - stable angina, and Acute Coronary Syndrome (ACS). If you have CAD, you probably know all about stable angina. But chances are, you don't know much about ACS. You need to know about ACS, though, because it is extremely important.

What is ACS?

ASC occurs when a blood clot suddenly forms within a coronary artery, usually due to the acute rupture of a plaque. Plaque rupture can occur at any time, and often completely without warning. The blood clot will often completely stop or significantly reduce the flow of blood to the heart muscle, and is considered a medical emergency. Any plaque can rupture, even small ones. This is why you will often hear of people who have a myocardial infarction (MI), or heart attack, shortly after being told their CAD is "insignificant."

Symptoms of ACS

 

The symptoms of ACS are similar to those of stable angina (i.e., chest pain or discomfort), but are often much more intense and persistent. The chest pain in ACS is often accompanied by other disturbing symptoms such as sweating, dizziness, nausea, extreme anxiety, and what is often described as a "feeling of impending doom." The chest pain is often untouched by nitroglycerin (which usually relieves stable angina). On the other hand, some people who have ACS will have only mild symptoms, or will fail to notice any symptoms at all - at least initially. Unfortunately, the permanent heart damage that often results from ACS will, sooner or later, produce symptoms.

The Three General Types of ACS.

 

Cardiologists divide ACS into three distinct clinical patterns. Two of them represent different forms of MI, and one represents a particularly severe form of angina, called "unstable angina." All three are caused by acute blood clots in the coronary arteries.

• If the blood clot persists for more than just a few minutes, some of the heart muscle cells begin to die. The death of heart muscle is what defines an MI. There are two types of MI, based on the pattern that appears on the ECG.
  
  • "ST-Elevation myocardial infarction" (or STEMI, so named because the "ST segment" on the ECG appears "elevated"), occurs when a coronary artery is completely blocked, so that a large proportion of the heart muscle being supplied by that artery is becoming damaged.
  • Non-ST-Elevation myocardial infarction (or NSTEMI, in which the "ST segment" is not elevated), occurs when the blockage in the coronary artery is not complete, so that a relatively small proportion of heart muscle is becoming damaged. 
• Sometimes the blood clot that occurs in ACS does not cause any permanent heart muscle damage, either because the degree of blockage it produces is not large enough, or because the clot doesn't persist long enough, to produce cell death. (The body's protective mechanisms try to dissolve blood clots that form within blood vessels. When an ACS occurs that does not actually cause heart muscle to die, it is termed unstable angina.

 

Making the Right Diagnosis in ACS

 

To summarize, once a blood clot forms in a coronary artery, then: if a lot of heart muscle damage occurs a STEMI is diagnosed; if a "little" heart muscle damage occurs, a NSTEMI is diagnosed; if no measurable heart muscle damage occurs, unstable angina is diagnosed. Because each type of ACS is treated differently, it is important to distinguish among the three.

If you are having ACS, usually your symptoms, physical examination, medical history and cardiac risk factors will immediately steer the doctor to strongly suspect the diagnosis. From that point, he or she will quickly examine your ECG and measure your cardiac enzymes. (Cardiac enzymes are released into the bloodstream by dying heart muscle cells, so an elevation in the cardiac enzymes means that heart cell damage is occurring.) The appearance of the ECG (i.e., the presence or absence of "elevation" in the ST segments) will distinguish between STEMI and NSTEMI. And the presence or absence of elevated cardiac enzymes will distinguish between NSTEMI and unstable angina.

The Significance of ACS

 

The three types of ACS actually represent the spectrum of the clinical conditions that can occur when a plaque ruptures within a coronary artery. In fact, there is actually no clear line that inherently divides STEMI, NSSTEMI, and unstable angina. Where cardiologists draw the line between a STEMI and an NSTEMI, or between an NSTEMI and unstable angina, is a relatively arbitrary decision. Indeed, the definitions of these three types of ACS have changed substantially over the years, as our knowledge - specifically our ability to interpret ECGS and detect heart cell damage with enzyme tests - have improved.

The important point is that every case of ACS (no matter how it is categorized) is a medical emergency, and requires imediate medical care to try to accomplish two things: 1) to limit the heart muscle damage being done acutely by the blood clot within the coronary artery, and 2) to limit the possibility that the plaque - which has now shown itself to be unstable and prone to rupture - will rupture again.

Bateeilee Blog admin will share What are the symptoms of lung cancer?. Since lung cancer survival is better the earlier it is caught, understanding some of the common symptoms of lung cancer is very important. Symptoms of lung cancer to be aware of can include:

 

Symptoms Related to Cancer in The Lungs

A cough that persists over time, or does not go away with treatment is a common warning sign of lung cancer. Other local symptoms that can be caused by lung cancer include:

• coughing up blood (hemoptysis)
• difficulty breathing – due to decreased airflow by a tumor obstructing the large airways or spread through the lungs
• wheezing – caused by the interference of airflow through an airway obstructed by a tumor
• pain in the chest, back, shoulder, or arm – when a lung tumor presses on nerves around the lungs
• repeated lung infections such as pneumonia or bronchitis
• hoarseness

 

No Symptoms

Roughly 25% of the time, lung cancer causes no symptoms at all. These tumors are usually found when a chest x-ray is done for another reason. Occasionally, lung cancer is found when a smoker or former smoker has a procedure to screen for lung cancer.

General Symptoms Associated With Lung Cancer

 

Lung cancer can sometimes present with vague symptoms. Concerns such as fatigue, unexplained weight loss, loss of appetite, and even depression can be a symptom of lung cancer as well as many other conditions. It is important to talk with your health care provider if you have any concerns such as these, especially if you have a history of smoking.

Symptoms Related to The Spread of Lung Cancer

 

Sometimes, the first symptoms of lung cancer are due to its spread (metastasis) to other regions in the body. With lung cancer, the most common places lung cancer spreads are to the liver, adrenal glands, brain, and bones. Symptoms commonly found include:

• bone - pain in the back, ribs, or hips
• brain - headaches, seizures, weakness on one side of the body, vision symptoms

 

Paraneoplastic Symptoms

 

Paraneoplastic symptoms are symptoms related to the production of hormones-like chemicals by some types of lung cancers. These often show up as unexplained findings on lab tests and can include:

• low sodium levels (hyponatremia)
• elevated calcium levels (hypercalcemia)
• anemia
• clubbing of the fingers (bulging of the fingernails)
• new bone formation seen on x-rays