New Therapies And Potential Claims For Cardiologic Malpractice

New Therapies And Potential Claims For Cardiologic Malpractice

Anatomy and Normal Operation

Very simply, the heart is a hollow muscular pump which propels blood throughout the body. The lungs are bellows which suck in oxygen, deposit it in the bloodstream, remove carbon dioxide from the blood and expel it into the atmosphere. In terms of their combined operation, they are strikingly similar to an internal combustion engine. However, rather than analogizing to an automobile, think of a gasoline driven pump that supplies fuel to numerous other engines in a factory. Most importantly it pumps to itself the fuel which drives it. The fuel for the heart itself travels through the coronary arteries which are a parallel for a fuel injection system or carburetor. The lungs function like the air intake manifold not just for the pump but all of the engines (organs, tissues and structures) in the body.

All analogies have their limitations. An important feature of our cardiovascular system which defies analogy is that it is a closed loop system. What goes around comes around, thus the term circulation. The fuel consists of nutrients, most significantly glucose (sugar) and electrolytes. Since glucose produces the energy it is, logically, the key component of the fuel. The blood carries glucose from the digestive system and oxygen from the lungs throughout the body. As in the engine, where fuel and oxygen are needed for combustion, in the body sugar and oxygen are needed to produce energy. When the energy is released the glucose and oxygen are converted to carbon dioxide and water. The former and some of the latter are exhaled from the lungs and the latter is excreted from the kidneys as urine or secreted out the pores as sweat. The urine and sweat also rid the body of excess electrolytes, impurities and by-products. In essence the lungs (on expiration), kidneys and pores serve as our exhaust system. This process of converting sugar and oxygen to carbon dioxide and water, as well as the delivery and use of nutrients and electrolytes and removal of by-products and waste, is what we call metabolism in general terms.

Circulation in our closed vascular system starts with the heart and ends with it. The heart consists of four chambers. It is divided by a vertical wall, called the septum which runs roughly down the middle. Each side has two chambers with an atrium or auricle on top and a ventricle below. These chambers are separated by valves. Blood from the venous side of the system flows into the right atrium. Then the heart muscle contracts and the valve opens forcing the blood into the right ventricle. Immediately the valve closes, the muscle of the ventricle contracts and the blood flows into the pulmonary arteries and from there into the lungs. Next the blood is dispersed throughout the alveolar membrane where carbon dioxide is released and the hemoglobin in the blood picks up oxygen. From the alveolar membrane blood collects into the pulmonary veins. It is significant to note that the pulmonary artery is the only artery in the body that carries nonoxygenated blood and the pulmonary vein is the only vein that carries oxygenated blood.

From the pulmonary veins blood flows into the left atrium and like on the right side it is transferred to the ventricle and propelled out through the arterial side of the system by the contracting of muscle and the opening and closing of the valve. As with an engine, the moving parts of the heart must operate in a coordinated manner in order to be efficient. On a gasoline engine a timing wheel regulates the flow of electrical current to the spark plugs which in turn trigger the actions of the pistons. The pistons then take turns compressing and expanding which in turn smoothly converts energy into motion. The heart has an electrical system called the Purkinje system. Like a timing wheel the S.A. (sinus) node (pacemaker) regulates the flow of electrical impulses released by the A.V. nodes. The Purkinje fibers are the equivalent of spark plugs and they cause the heart muscle to contract and relax. The coordination of these electrical impulses and the resulting heart action is called its rhythm. The valves primarily operate based upon pressure. Forward pressure from the atrium opens the valve and back pressure from the ventricle closes it. A complete cycle of all four chambers opening and closing, which we recognize as a heartbeat, is like a revolution on a piston engine. We speak of heart rate, or pulse, in beats per minute much like we refer to engine performance in revolutions per minute.

On the arterial side, blood is transported from the left ventricle into the aorta. This vessel arches over the heart and follows the spinal column through the diaghram into the abdomen. Through the course of the aorta arteries branch off and travel to all of the structures of the body in a network. Within the various structures they branch off further and gradually become smaller structures referred to as arterioles and even smaller ones called capillaries. The vessels of the arterial system are musclar tubes. The sympathetic and parasympathetic nervous systems cause them to dilate or constrict depending upon blood flow supply and demand. The capillaries spread blood filled with oxygen and nutrients through the capillary beds to the cells. The process of delivering blood from the left ventricle down to the capillaries and into the tissue is called perfusion. The level of force at which the blood flows is called blood pressure. Normally we measure arterial pressure but sometimes it is important to determine venous pressures. The first number in a blood pressure reading is the systolic which reflects pressure from the heart under stress. The second one is the diastolic, which measures pressure from the heart at rest. The term cardiac output identifies the volume of blood exiting the left ventricle.

From the capillary beds blood then enters the venous system in order to remove carbon dioxide, water, by-products and waste. The blood flows into a network of venules and from there into a larger network of veins. Within the torso the veins tie into either the superior vena cava or the inferior vena cava. These vessels then enter the right atrium and complete the cycle called circulation. The components of the venous system are all muscular tubes, however, because they are on the low pressure side of the vascular system, they lack the muscular development strength and elasticity of the arteries.

It is important to understand that the cardiovascular system strives for stability. Relatively constant blood pressure, circulating volume, heart rate and rythym are certainly best for the system. However, it has compensatory mechanisms which allow it to respond to special circumstances. If we exercise vigorously and our muscles demand additional oxygen and glucose, our respiration and heart rate will quicken and our arteries dilate so that greater volumes of these substances will be delivered. If we introduce too much fluid into our system, the kidneys will increase their performance and produce more urine to restore a balance. On the other hand, if we become dehydrated, blood vessels will constrict so that adequate pressure can be maintained with less volume. As long as the compensatory mechanisms are not overwhelmed or disrupted by disease states, or extrinsic factors they will function effectively.

Although the operation of the pulmonary system should already be relatively obvious, some points bear further mention. The lungs consist of five lobes, three on the right and two on the left. The lungs are enclosed in a lining, called the pleura. In breathing, air passes from the oral and nasal airways in the larynx, through the pharynx and down the trachea. Once inside the lungs it branches off into the bronchi and from there into the alveolar sacs. Within the membranes of the sacs the O2/C02 exchange occurs. It should be noted that CO2 is not just a by-product of metabolism. In fact it triggers the involuntary action of respiration by chemical mediation in the medulla.

Last but not least, the fuel and fuel media in the circulatory system are vitally important. As stated above the fuel consists of oxygen, nutrients and electrolytes. Several electrolytes affect cardiovascular function. High sodium (hypernatremia) causes fluid retention which increases circulatory volume and blood pressure. Potassium impacts heart rhythm. Low potassium (hypokalemia) can provoke arrhythmia and even cardiac arrest. Elevated potassium can cause an arrest. Magnesium affects heart rhythm as well. The fuel media consists of erythrocites (red blood cells), leukocytes (white blood cells) and platelets (thrombin). Red blood cells contain hemoglobin which binds with oxygen in the lungs. Anemia is an abnormally low concentration of erythrocites (also decreased hematocrit and hemoglobin levels) and diminishes the body’s ability to deliver oxygen. Leukocytes fight infection. Platelets are essential to clot formation. A low level of platelets (thrombocytopenia) can lead to uncontrollable bleeding. In short, the components of the blood need to be in balance for the circulatory system to function properly.

Pathology

Heart Disease

The four major components of the heart are:

1. Arteries
2. Muscle
3. Electrical System
4. Valves

Heart disease can involve any one of the components but may involve several. Disease originating in one component can progress to damage others.

Atherosclerosis: This term refers to the accumulation of plaque on the lumen (inner wall) of arteries. It can develop on any arterial structure. Some, but not all, causes of atherosclerosis have been identified. Genetics, smoking, fatty diet, elevated lipids, inactivity and diabetes are several known pre-disposing factors. The effect of atherosclerosis is that it occludes the vessel, which means that it narrows and can ultimately block off the passageway. Since this occurs in a pressurized pumping system, it has an effect similar to squeezing or kinking a garden hose. Restriction of the passageway creates resistance to flow. This in turn has three direct effects. If the pressure in the system remains constant, perfusion of tissue beyond the occlusion will be reduced (Ischemia). The system will respond to the lack of perfusion by increasing pressure within the system to unacceptable levels (Hypertension). The combination of resistance and elevated pressure will cause back pressure which may ultimately stress the entire system. This back pressure is analogous to the bulging of a soft hose that occurs when flow is restricted. These effects can produce or interact with other changes in the system to cause additional problems.

Coronary Artery Disease: When atherosclerosis involves the arteries that supply oxygenated blood to the heart muscle itself to any significant degree, this is referred to as coronary artery disease. Without a doubt, this is the major culprit in cardiopulmonary pathology. It is lethal not only because of its direct impact on the heart muscle but also because of its indirect effect on the operation of the heart and other organs.

Ischemia, which is simply a lack of blood perfusion to the tissue, can occur throughout the body, but is particularly ominous in the heart. When atherosclerotic occlusion of coronary arteries reduces perfusion of parts of the heart muscle, this causes the pain known as angina pectoris. If a coronary artery becomes completely occluded, blood supply to a portion of the heart will cease and if the condition is not corrected promptly heart tissue will die. This event is called a myocardial infarction and is commonly known as a heart attack. Usually coronary arteries become completely occluded because a clot forms in an area of reduced flow or a fragment of plaque breaks free and blocks a narrow area. However, an infarct may also occur because of vasospasm, a hemorrhagic event or vascular collapse secondary to a rapid drop in pressure (Hypotension).

If ischemia affects multiple coronary arteries this can lead to heart failure. It may precipitate a myocardial infarction but death can occur from failure alone without infarct.

Diagnosis and Treatment of Coronary Artery Disease

A. Risk Factors:

1. Male
2. Family History
3. Obesity
4. Sedentary Lifestyle
5. Elevated Cholesterol
6. Smoking
7. Diabetes
8. Hypertension
9. Stress

B. Symptoms:

1. Dyspnea: (shortness of breath)
   Cause: coronary insufficiency (heart muscle starved for oxygen). Can be angina equivalent, especially in women.
   
   
2. Chest Pain or Discomfort: Angina
   
   Chest discomfort with exertion is angina until ruled out. Only objective testing can rule it out. Pain frequently radiates to shoulders, neck, jaw or arms (primarily the left).
   
   Heartburn (epigastric burning pains) can be either angina or esophagitis. These are indistinguishable based on patient’s report of symptoms because the same nerve provides sensation to both the heart and esophagus.
   
   Unstable Angina: Chest discomfort occurring without exertion.

C. Testing:

1. Resting EKG: Usually will be normal unless there is active ischemia or underlying heart disease (muscle, valves or electrical system). Ischemia in progress can cause EKG changes such as ST segment depression or inverted U waves.
   
   Whenever possible EKG’s should be compared to earlier ones. Ordinarily a person’s EKG will remain essentially unchanged until old age. Nonspecific changes in an EKG may warrant further investigation.
   
   Holter Monitoring: Continuous outpatient monitoring and recording of heart rhythm to detect transient arrhythmias.
   
   
2. Exercise EKG (Stress Test) Exercise increases the heart’s demand for oxygen. Diseased coronary arteries cannot meet the demand, resulting on or several of the following: dyspnea, angina or EKG changes.
   
   
3. Echo Stress Test: Whereas the Exercise EKG shows how the electrical system performs under stress, this test shows visually how the heart muscle performs under stress.
   
   
4. Nitroglycerin (NTG): Administration of NTG usually relieves angina therefore it has a diagnostic value, but it also relieves esophageal symptoms.
   
   
5. Cardiolite or Thalium Stress Test: The same as the exercise EKG except nuclear contrast is injected when a target heart rate is achieved allowing visualization of coronary perfusion under stress.
   
   
6. Coronary Angiography: A catheter is inserted into the arterial system and threaded back to the heart where it enters the coronary arteries. Contrast material is injected and produces a radiographic visualization of the arteries.

Treatment:

1. Prophylactic
   
   a. Aspirin
   b. Antihypertensives if HBP.
   c. Statins for elevated lipids.
   d. Smoking cessation.
   e. Diabetes management.
   
   
2. Syptomotic (Angina)
   
   a. NTG
   b. Beta Blockers
   c. ACE Inhibitors
   d. Calcium Channel Blockers
   
   
3. Coronary Revascularization
   
   a. Balloon angioplasty
   b. Stents
   c. Coronary artery bypass grafting (CABG)

E. Unstable Angina/Acute Coronary Syndrome

Chest pain and dyspnea unrelated to exertion and not secondary to AMI.
See the treatment algorithm.

Acute Myocardial Infarction (AMI)

A. Symptoms and Signs

1. Shortness of breath
2. Chest Pain
3. Diaphoresis (Cold sweat; clammy)
4. Nausea and Vomitting
5. Panic symptoms: sense of impending doom, dizziness, weakness, diarrhea, palpitations.
6. Bradycardia, Tachycardia or Premature ventricular beats.

B. EKG: Q wave, ST elevation, and T wave inversion are classic.

C. Labs

1. Cardiac Enzymes
   
   a. Trapanin
   b. CK – MB
   c. LDH

D. Echo: May show abnormal wall motion consistent with MI.

F. Treatment Options

1. Acute Care
   
   a. O2 (Always)
   b. NTG (Vasodilation)
   c. Aspirin & other blood thinners
   d. Morphine (pain and anxiety)
   e. Beta Blockers (O2 demand and pain relief)
   f. ACE Inhibitors
   g. Electrolytes (Potassium)
   h. Heparin
   
   
2. Repurfusion
   
   a. Angioplasty/Stenting
   b. Thrombolytics – Timing from onset of symptoms is important.

Cardiogenic Shock with AMI: Hypotension and Hypoperfusion

1. Prognosis poor
   
   
2. Treatment
   
   a. Correct rhythm to sinus
   b. Fluids
   c. Inotropics (Dopamine and Neosynephrine)
   d. Intraaortic Balloon Pump

Heart Failure: In lay terms this refers to the heart’s inability to function properly as a pump. When the pump fails completely this produces cardiac arrest. Generally heart failure is divided into acute failure and chronic failure. Chronic failure results from long term damage to the heart and lungs such as cardiomyopathy, mitral valve prolapse, obstructive pulmonary disease and atherosclerosis. Acute heart failure refers to failure which develops rather quickly because of a precipitating event such as a cardiac ischemic episode, myocardial infarction, pulmonary emboli and tamponade. In failure either the entire heart or one of the ventricles encounters resistence which it cannot overcome. Initially the heart adjusts by elevating its rate excessively (Tachycardia) until the heart loses the fight and then the rate drops too low (Bradycardia). Heart failure is often called congestive heart failure because one of the key manifestations of failure is effusion. This generally occurs in the lungs but sometimes arises in the pericardial sac which surrounds the heart. Effusion occurs because increased resistance coupled with elevated pressure and a rapid heart rate causes fluid to leak out of the vascular system. The development of heart failure in connection with other major events such as infarction greatly reduces survivability. The mechanism for failure secondary to tamponade bears some mention. Tamponade refers to the constrictive pressure produced by fluid accumulating in a closed space. In the event of hemorrage within the chest, blood can collect in the pericardium, the mediastinum or the thorax. Eventually it may create pressure and resistance on the heart muscle which prevents it from expanding the chambers to accept blood flow and failure will occur. To understand this try blowing up a balloon under water. Tamponade can also cause pulmonary failure which will lead to respiratory arrest.

1. Acute heart failure: Can develop rapidly following AMI or acute rhythm disturbance.
   
   a. Left Ventricular Failure: Fluid backs up in the lungs or pericardial sac.
   b. Right Ventricular Failure: Back pressure in the venous system producing abnormal liver or kidney function levels and peripheral edema.
   c. Uncorrected LVF will lead to RVF.
   
   
2. Chronic heart failure: Can be related to disease affecting any of the four components of the heart.
   
   a. Ischemia (50% of the cases)
   b. Hypertension
   c. Rhythm disorders
   d. Cardiomyopathy
       1) Congenital
       2) Alcohol or drug abuse
       3) Past M.I.
   
   e. Valve disease.
   f. Idiopathic
   g. Other obscure causes
   
   
3. Diagnosis:
   
   a. Physical exam
   
       1) Chest auscultation (stethoscope) demonstrates rales
       2) Peripheral edema
       3) Neck vein distention
   
   b. CXR shows effusion in lungs or cardiomegaly
   c. Tachycardia
   d. Symptoms
   
       1) dyspnea
       2) exercise intolerance (fatigue and weakness)
   
   
4. Treatment:
   
   a. Diuretics
   b. Therapy to address the underlying cause if known.
   c. ACE Inhibitors
   d. Beta blockers
   e. Vasodilators
   
       1) NTG
   
   f. Calcium Channel Blockers (but not for acute failure post MI); is also an antiarrhythmic.
   g. Digitalis (Lanoxin) for arrhythmia.

Cardiomyopathy:Disease involving the heart muscle itself. By definition cardiomyopathy excludes muscle damage caused by ischmia. The term “ischemic cardiomyopathy” is used but the condition is not categorized as a true cardiomyopathy.

The causes of cardiomyopathy are too numerous to list or discuss here.

Arrest: cessation of coronary performance, respirations or both.

1. Cardiac v. Respiratory. One will quickly produce the other, but it is important to determine which came first as it effects the focus of resuscitative measures. Legally the distinction may be paramount.
   
   Factors:
   
   a. Was the heart still beating after respirations stopped?
   b. Rhythm strips shortly before and after the code.
   c. Pulse oximetry before and ABG’s after the code.
   d. Underlying medical condition.
   e. Therapies shortly before the code
       1) Drugs
       2) Respiratory therapy.
   
   
2. Sudden Cardiac Arrest
   (outside the hospital) Has a very poor prognosis.
   eg. Widowmaker

Rhythm Disorders: These are disruptions of the electrical conduction system that coordinates heart activity. They develop secondary to significant cardiopulmonary or cerebral insults. They can also be congenital and arise secondary to toxic exposure.

Heart Rhythm refers to the electrical activity initiated by the sinus node which triggers the coordinated muscle activity of the heart. In a healthy heart an electrical emission will cause both the right and left atria to contract simultaneously then relax and an instant later both ventricles will contract and relax. This creates an electrical wave pattern which an EKG demonstrates graphically as a normal sinus rhythm. In the absence of disease this wave pattern should remain essentially unchanged until old age. Therefore EKG’s should always be compared to earlier ones. Even non-specific changes can be significant for the particular patient. EKG’s can vary considerably from one person to the next and yet still be normal. Non-specific findings on an EKG are aberrations from the norm that may nor may not reflect disease. They are not diagnostic.

Arrhythmias refer to pathologic changes in the heart rhythm that impact the functioning of the heart. Time does not permit discussion of the numerous types of arrhythmias. They are quite complicated so they are best addressed by consulting a text such as Practical Electrocardiography by Marriott.

Other Vascular Disorders

Stroke: The precise medical term for this is cerebral vascular accident (CVA). The same mechanisms that produce coronary artery disease, myocardial infarction and ischemia, operate to produce stroke in the brain. The brain and particularly the eyes are very sensitive to blood pressure abnormalities. Surprisingly, sudden hypotension is more lethal than hypertension but fortunately it is much less likely. The vast majority of strokes are ischemic, usually because of a thrombo-embolic event. A small percentage are hemorrhagic.

Peripheral Vascular Disease: Wherever arteries travel they are susceptible to atherosclerotic occlusion. The degree of pathology depends upon the sensitivity of the organ served to reduced perfusion. The kidneys are very dependent upon a good perfusion. Occlusion of a renal artery can cause the kidney to infarct. Chronic uncontrolled hypertension or severe hypotension can result in kidney failure. In diabetics, their extremities, particularly the feet, are especially susceptible to ischemic injury. To a lesser degree smokers and heavy drinkers have similar risks.

Hypertension: This is increased circulatory pressure which develops because of resistence in the vascular system. Although coronary artery disease is a major culprit in hypertension, it certainly is not alone. Atherosclerotic occlusion throughout the vascular system can cause hypertension. Moreover, hypertension exacerbates atherosclerosis. Kidney impairment and dietary factors are other known causes, but often times the actual cause cannot be specified. Hypertension is generally chronic but certain events can provoke acute episodes. Depending upon the location of the resistance this may determine the site of the hypertension. For example left sided heart failure will cause back pressure that produces pulmonary hypertension. Similarly, right sided heart failure will produce hypertension in the venous system, such as vena cava syndrome. As indicated above, hypertension is the leading cause of stroke. It also causes hypertrophy (enlargement) of the heart and the aorta.

Thrombosis and Pulmonary Emboli: On the venous side of the vascular system the major pathology involves thrombosis and pulmonary emboli. A thrombosis is a blood clot that adheres to the wall of a blood vessel. When the clot breaks free and enters the bloodstream it is an embolus. Most clinically significant thrombi develop in the large veins of the pelvis and leg. Stasis (reduced venous flow), hypercoagulable states and pelvic injury predispose to thrombus formation. When the clot embolizes it travels along the vena cava into the right side of the heart and then into the arterial system of the lungs. If the embolus is large enough it will block off or infarct an artery. Multiple emobli can infarct many or all of the pulmonary arteries. If the flow of blood to the lungs decreases, the flow of oxygenated blood away from the lungs will also fail and ischemia occurs. Also the resistance to blood flow creates back pressure which will produce pulmonary edema (effusion) and right sided heart failure. Pulmonary edema can then lead to collapsed lung lobes (Atelectasis). Needless to say, without effective treatment, the condition has a high incidence of mortality.

Respiratory Distress: This is an impairment of respiration. Usually it is the result of a failure of ventilation (respiration) and is secondary to obstruction (eg. choking) or pharmacological depression. The lack of oxygen in the lungs is hypoxia. The ensuing failure of O2/CO2 exchange is asphyxia. From that point the lack of oxygen in the blood is hypoxemia and the failure to perfuse the tissue with oxygenated blood is ischemia. When ischemia develops in any tissue of the body this interferes with the complete break down of sugar. This incomplete chemical reaction then produces carbolic acid. This state is characterized as metabolic acidosis. An acidic condition kills sensitive cells, especially in the brain, heart and kidneys. Brain injury/death, blindness, cardiac arrest, respiratory arrest and kidney failure can ensue very quickly.

Pulse oximetry is a simple test to discover hypoxemia. Arterial Blood Gases allow an assessment of hypoxia, hypoxemia, respiratory acidosis, metabolic acidosis and alkalosis.

Anemia: The most common type consists of decreased circulating volume of red blood cells because of hemorrhage or chronic blood loss. Severe anemia can cause hypotension, angina, myocardial infarction and respiratory distress.

Syncope: sudden loss of consciousness because of ischemia related to hypotension or bradycardia (vasovogal syncope).

Causes: infection, trauma, hemorrhage, choking, severe pain, nausea.

Query: Did he get drunk, pass out and hit the coffee table or did he choke on a pretzel?

Recent and Prospective Areas of Cardiovascular Malpractice

The general subject areas that give rise to medical malpractice claims pertaining to cardiovascular disease have not really changed. They are as follows:

1. Failure to consider coronary artery disease.
2. Failure to appropriately work-up suspected coronary artery disease.
3. Failure to diagnose acute myocardial infarction
4. Failure to treat acute myocardial infarction in a timely and aggressive manner.
5. Improper management of heart failure .
6. Improper management of hypertension.
7. Failure to diagnose pulmonary emboli.

There are, however, several evolving or fertile areas where we will see litigation in the future.

Coronary Artery Disease/Coronary Heart Disease

Disease Risk Factors

The long recognized major risk factors are still valid. Northwestern University researchers reviewed the records of almost 400,000 people and found that just about everyone who had a myocardial infarction or other major coronary event had at least one of the four well-established risk factors: high cholesterol, high blood pressure, cigarette smoking or diabetes. A fifth risk factor, obesity, is also very important because it contributes to cholesterolemia, hypertension and diabetes.

Global Risk Assessment

In 2001 the American College of Cardiology received the Adult Treatment Panel III (ATPIII) guidelines. Unfortunately many cardiologists have failed to implement the guidelines in their practices.

The features of the ATP III are as follows:

Focus on multiple risk factors:
Raises persons with diabetes without CHD, most of whom have multiple risk factors, to the risk level of CHD risk equivalent.

Uses Framinghaqm 10-year risk projections to identify certain patients with multiple (2+) risk factors for more intensive treatment.

Identifies person with metabolic syndrome as candidate for intensified therapeutic lifestyle changes.

Modifications of lipid and lipoprotein classification:
Identifies LDL<100 mg/dl as optimal; raises categorical low HDL from <35 mg/dL to <40 mg/dL.

Lowers triglyceride classifications to give more attention to moderate elevations.

Recommends a complete lipoprotein profile rather than total cholesterol and HDL alone as the preferred initial test.

Recommends treatment beyond LDL lowering when triglycerides are >200 mg/dL.

Diabetes: Is a more serious risk factor for CHD than smoking.

Diabetes is equivalent to CHD even in diabetics with no evidence of CHD.

Statin therapy should be considered routinely for all diabetic patients irrespective of their cholesterol levels.

65% of diabetics will due from either an M.I. or stroke. Physicians are well aware of the link but are not adequately educating patients.

The incident of adult onset diabetes is growing rapidly.

Obesity: Not only does obesity contribute to hypertension, hyperlipidemia and diabetes, it is a cardiac risk factor in and of itself.

Obesity is treatable both medically and surgically. Insurance will cover surgery for the morbidly obese but not medical therapy. Numerous safe and effective medications are available for treating obesity but physicians do not provide treatment because they are not reimbursed. Instead care amounts to little more than the ineffective advice to “move more and eat less”. Physicians treat the co-morbid states but ignore the major contributing factor, obesity, and its root causes. Unfortunately patients who go to weight loss clinics often do not receive the required cardiovascular evaluation and monitoring necessary for safe treatment.

Statins: Cholesterol lowering drugs are becoming recognized by the medical community as “the new aspirin”. Lowering LDL (Low density lipoprotein) reduces the risk of cardiovascular events by roughly 30%. This includes the risk of stroke. Numerous authorities recommend the use of statins in all high-risk patients regardless of their LDL concentration.

Female Patients: Many physicians still act as though CAD is a male disease. While men are more susceptible at an earlier age, women are by no means insulated from the risk.

Symptoms of CAD and even M.I. tend to be less pronounced and less specific in women. The classic male presentation is severe burning chest pain, pain radiating into the arm(s), shoulders, neck or jaw, or crushing chest pain. Women, in contrast, more often present with transient chest pain, upper abdominal pain, back pain, nausea, sweating or shortness of breath.

Because of the differing presentation and physician bias women are much more likely to be sent home with a diagnosis of anxiety or gastro-intestinal disease (gallbladder v. reflux). Consequently men are referred for cardiac catheterization much more frequently than women.

See Understanding Heart Disease in Female Patients, Susan Dennehy, Trial, August 2003.

Young Patients: Much like women, young patients are often sent home with undiagnosed CAD because physicians have a bias that heart disease begins during middle age. With increase in obesity and early onset of Type II diabetes coupled with decreased physical fitness, more and more young people are developing CAD.

Black Patients:
Hypertension and CVD (cardiovascular disease): The incidence of CVD is 29% higher among blacks. The risk of death from a stroke is 40% higher. There is disagreement as to whether blacks should receive different medication regimens for treating HBP and CVD.

Even though blacks are at greater risk of CVD they are less likely than whites to be treated with aspirin or statins.

Testing:
Electron Beam Computed Tomography: Although the American College of Cardiology and the American Heart Association do not recommend EBCT testing in asymptomatic patients, a recent study indicates that the test was more predictive than cholesterol levels, hypertension, body mass index, age or smoking for CAD events.

Acute Myocardial Infarction

A recent analysis of 86, 735 AMI patients at 1,085 U.S. Hospitals revealed the presence of a large and persistent gap between the AHA/ACC myocardial infarction guidelines and current community myocardial infarction care.

Angioplasty & Specialty Hospitals:

Angioplasty, usually with stent placement, is rapidly becoming the treatment of choice over thrombolytics for A.M.I. Consequently, patients receive optimum care at hospitals with an experienced cardiac catheterization team available 24 hours per day.

Specialty heart hospitals are opening. The question arises as to the adequacy of these facilities to address non-cardiac emergencies mistaken for cardiac events.

Testing:
Advanced MRI’s may replace EKG’s and blood enzyme tests as the best method for diagnosing an AMI or unstable angina.

Heart Failure: Beta Blockers are valuable tools for treating heart failure, yet only one-third of heart failure patients receive them.

Pulmonary Emboli: The American College of Chest Physicians has adopted guidelines to prevent blood clots in high risk hospital patients. The risk factors for DVT (deep veinous thrombosis) are as follows:

Hospitalization for a serious illness or surgery or other prolonged immobility.
Obesity
Stroke or paralysis
Trauma (abdomen, pelvis, hip and leg)
Major surgery (especially abdomen, pelvis, hip and leg)
Pregnancy or estrogen use
Age greater than 40
Previous history of blood clots
Cancer and its treatment
Varicose veins
Cardiac dysfunction

All such high risk patients should be treated with compression stockings and anti-coagulants.

Prevention of Recurrent P.E.: Currently P.E. patients receive full-dose coumadin for six months. Still 6% to 9% of such patients have recurrences following the completion of therapy. Long term low-dose coumadin can reduce this risk by 64%.