Alberto Trinidad, APRN-CNS received his Master’s degree from Liberty University as an Acute Care Clinical Nurse Specialist after completing a Bachelor of Science degree in Nursing from Centro Escolar University in Manila, Philippines. He began his career as a Registered Nurse with intensive care experience. Alberto holds a national certification from the American Association of Critical Care Nursing as an Adult Health Clinical Nurse Specialist. He is active with critical care medicine focusing on pulmonary.

Candis L. Broadnax, APRN-CNS received her Master’s degree from the University of Oklahoma as an Acute Care Clinical Nurse Specialist after completing a Bachelor of Science degree in Nursing from Northeastern State University. She began her career as a Registered Nurse with intensive care experience specializing in trauma/surgical and medical-surgical intensive care patients. Candis is a current member with the American Association of Critical Care Nursing and maintains her certification of CCRN. She is active with interventional and noninvasive cardiology.

Eric received his Master’s degree from the University of Oklahoma-Tulsa as a Physician Associate after completing a Bachelor of Science degree from University of Arkansas in Fort Smith, AR. He has spent his healthcare career working in neuroscience with an emphasis on neurosurgery. Eric maintains his certification with the National Commission of Certified Physician Assistants and is licensed by the Oklahoma Medical Board.

Georgianne C. Tokarchik, APRN-CNS received her Master’s degree from the University of Oklahoma as an Acute Care Clinical Nurse Specialist after completing a Bachelor of Science degree in Nursing from The University of Tulsa. She began her career as a Registered Nurse with a primary focus in cardiology. Georgianne holds a national certification from the American Association of Critical Care Nursing as an Adult Health Clinical Nurse Specialist. She now serves as the coordinator of the Oklahoma Heart Institute Structural Heart and Valve Center.

Katie Owens, PA-C received her Master’s degree from the University of Oklahoma College of Medicine as a Physician Associate after completing a Bachelor of Science degree from Northeastern State University. She has spent her healthcare career working in Family Medicine and Cardiology with an emphasis in electrophysiology. Katie maintains her certification with the National Commission of Certified Physician Assistants. She is a current member of Oklahoma Academy of Physician Assistants.

Lisa Lee, APRN-CNS received her Master’s degree from the University of Oklahoma College of Nursing as an Acute Care Clinical Nurse Specialist after completing a Bachelor of Science degree in Nursing from Northeastern State University.  She began her career as a Registered Nurse in critical care experience specializing in cardiovascular nursing and has held academic positions within the University of Oklahoma College of Nursing. Lisa holds a national certification from the American Association of Critical Care Nursing. She is a member of the American Nurses Association, American Association of Critical Care Nursing and American Association of Heart Failure Nursing. Lisa is active with general cardiology with a focus on congestive heart failure.

Padma Achanta, PA-C received her Master’s degree in Dietetics from Avinashi Lingam Deemed University in Coimbattore, India before completing a Bachelor of Science degree in Physician Assistant from Marywood University in Scranton, Pennsylvania. She has spent her healthcare career working in CVICU providing immediate postoperative care in The Methodist Hospital, Texas Medical Center in Houston, Texas. Padma maintains her certification with the National Commission of Certified Physician Assistants and is licensed by the Oklahoma Medical Board.

An Interview with Dr. Edward Martin

Where does Oklahoma, or Tulsa to be more specific, rank in terms of heart disease-related deaths?

Dr. Martin: Heart disease is the leading killer of both men and women in the state of Oklahoma. The last detailed United States state rankings were from 2009 and showed that Oklahoma was 48 out of 50 states in cardiovascular deaths. The third worst. From a statewide standpoint, the last compiled statistics for Oklahoma were from 2004-2006. In those rankings, Tulsa County ranked 28 out of Oklahoma’s 77 counties for heart-related deaths. Oklahoma City was slightly better and ranked 25th. From an overall state perspective, heart-related deaths generally occurred more in the southeastern counties of Oklahoma and were lowest in the northwest counties.

What are the warning signs?

Dr. Martin: The most classic symptom for a heart attack is discomfort in the center of the chest that lasts more than a few minutes, or that goes away and comes back. It can feel like uncomfortable pressure, squeezing, fullness or pain. However other symptoms can include pain or discomfort in one or both arms, the back, neck, jaw or stomach. Other symptoms that may or may not occur include breaking out in a cold sweat, nausea or lightheadedness. As with men, a woman’s most common heart attack symptom is chest pain or discomfort. But women are somewhat more likely than men to experience some of the other common symptoms, particularly shortness of breath, nausea/vomiting, and back or jaw pain.

What is a person’s risk of having a heart attack or suffering from a heart-related condition?

Dr. Martin: The controllable risk factors that increase the risk of developing a heart attack or stroke are smoking, high blood pressure, high cholesterol, diabetes, overweight and obesity and physical inactivity. Additional risk factors include male gender and family history of heart disease. Multiple risk calculators exist to help the individual person calculate his or her own risk of having a heart attack or dying from coronary heart disease over the next 10 years. One of the better ones can be found at the American Heart Association (AHA) website at http://www.heart.org/HEARTORG/ Conditions/HeartAttack/HeartAttackToolsResources/ Heart-Attack-Risk-Assessment_ UCM_303944_Article.jsp. But, in general, the greater the number of risk factors you have, the greater the risk; especially if the risk factors are not well controlled.

What screenings are important to help someone learn their risks and what can the doctors at Oklahoma Heart Institute do to help people manage those risks?

Everyone should know their risk factors, including your cholesterol, blood pressure, blood sugar and hs-CRP blood test for inflammation. At OHI, we offer inexpensive screening tests to evaluate carotid arteries, cardiac function, peripheral artery disease and your risk for abdominal aneurysm. We also offer a cardiac calcium score to measure arterial plaque buildup, which can cause blockages and heart attacks. All of the tests are painless and literally can save your life and prevent heart attack and strokes.

What local resources are available to help people facing heart disease?

Dr. Martin: Because of the internet, these days it is not as important as it used to be to have local resources available. A wealth of information can be garnered online. Multiple resources are available at the American Heart Association website at http://www.heart.org/ HEARTORG/. There you’ll find information on diet, exercise, weight loss, nutrition, research, smoking cessation and much more. However local resources do exist. In Oklahoma, the following resources are available: The Oklahoma State Department of Health’s Heart Disease and Stroke Prevention Program has resources available at http://www.ok.gov/health/Disease,_Prevention,_ Preparedness/Chronic_Disease_Service/ Heart_Disease_and_Stroke_Prevention_ Program/index.html. Smoking cessation help from the Oklahoma Tobacco Settlement Endowment Trust is available at 1(800) quit-now and at http://www.ok.gov/tset/Programs/Helpline. html. Additional smoking cessation help Dr. Martin is a noninvasive cardiologist with specialty expertise in noninvasive imaging. He is Director of Cardiovascular Magnetic Resonance Imaging at Oklahoma Heart Institute and Hillcrest Medical Center. In addition, he is a Clinical Associate Professor of Medicine at the University of Oklahoma College of Medicine — Tulsa. Dr. Martin has specialty training in Nuclear Medicine, as well as additional training dedicated to Cardiovascular Magnetic Resonance Imaging. He completed his Cardiology Fellowship at the University of Alabama. Dr. Martin’s Internal Medicine Internship and Residency training were performed at Temple University Hospital in Philadelphia. He received his medical degree from the Medical College of Ohio. Dr. Martin completed his Master of Science degree in mechanical engineering at the University of Cincinnati and his Bachelor of Science degree in physics at Xavier University. He is a founding member of the Society of Cardiovascular Magnetic Resonance and is an editorial board member of the Journal of Cardiovascular Magnetic Resonance. Understanding Heart Disease By Elaine Burkhardt An Interview with Edward T. Martin, MD, FACC, FACP, FAHA Oklahoma Heart Institute 19 and resources can be found under the Oklahoma State Plan for Tobacco Use Prevention and Cessation at http://www.ok.gov/health/ Disease,_Prevention,_Preparedness/Tobacco_ Use_Prevention_Service/. Tips on weight control, nutrition and physical activity can be found at Get Fit Eat Smart Oklahoma at http://www.ok.gov/h3andhealthy/%3Ci%3EGet_Fit_Eat_ Smart%3C_i%3E_State_Plan/index.html. Finally, local hospital websites can be loaded with useful information on preserving heart health. Take a look at www.oklahomaheart.com

How can we all reduce our risks? Are there nutrition and exercise tips?

Dr. Martin: Certain lifestyle modifications can help you reduce your risk of developing coronary heart disease. Most are simple to start but require dedication to implement completely.

• Exercise. The AHA recommends 30 minutes of moderate exercise a day at least five days per week. Or 15 minutes per day of vigorous activity. A simple positive change you can make to effectively improve your heart health is to start walking. A walking program is flexible and boasts high success rates because people can stick with it.
• Reduce the amount of “bad fats” or saturated fats and trans-fatty acids in your diet. These fats are bad and raise the bad or LDL cholesterol levels in the blood. They are commonly found in animal meats and dairy products and in many baked goods, fried foods and snack foods.
• Eat more fish. At least two times per week. They provide omega 3 fatty acids, which may help prevent heart disease and heart arrhythmias. Omega-3 fatty acids are one of the “better fats”. These are the monounsaturated and polyunsaturated fats. You should try to replace the bad fats with the better fats. These fats are commonly contained in canola oil, olive oil, peanut oil, sunflower oil, avocados, many nuts and seeds and oily fish (salmon, tuna, mackerel, herring and trout).
• A heart healthy diet should include a variety of fruits, vegetables, grains, legumes, fat-free or low-fat dairy products, fish, poultry and lean meats.
• Reduce your salt intake. High-sodium diets are linked to an increase in blood pressure and a higher risk for heart disease and stroke. Americans on average consume 3,436 mg of sodium daily. Many experts now believe that lowering daily consumption to no more than 1,500 mg of sodium daily would be an effective way to prevent or lower high blood pressure.
• If you are overweight, lose weight. Losing as few as 10 pounds can lower your heart disease risk. Last year 32% of Oklahoma adults were classified as obese. That is having a Body Mass Index (BMI) of 30 or higher. BMI is a numerical value of your weight in relation to your height. BMIs are good indicators of healthy or unhealthy weights for adult men and women, regardless of body frame size. A BMI of less than 25 indicates a healthy weight. A BMI of less than 18.5 is considered underweight. A BMI between 25 and 29.9 is considered overweight. BMI calculators can be found at multiple websites. However The National Heart Lung and Blood Institute has many resources in addition to a BMI calculator at http://www.nhlbisupport.com/bmi/.
• If you smoke, stop. Smokers are 4 times more likely to develop coronary heart disease. One in four Oklahoma adults, or 650,000 people, currently smoke. Smoking cessation is the most important lifestyle modification that one can make to reduce the risk of heart disease and stroke. If you can only make one change, this should be it.

If a person does have heart disease, what treatment options are available?

Dr. Martin: The treatment options will vary depending on the nature and severity of the coronary heart disease. The options will range from medical therapy to possibly angioplasty or heart stent to coronary artery bypass surgery. Once you have been affected with coronary heart disease. it is important to try and prevent it from getting worse to improve overall quality of life and extend survival. This is called secondary prevention. The goals for secondary prevention are:

• Complete smoking cessation.
• Blood pressure under 140/90 mmHg and under 130/80 mmHg in people with diabetes or chronic kidney disease.
• Exercise 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking, on most but preferably all days of the week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work). High risk patients (e.g., recent acute coronary syndrome or revascularization, heart failure) benefit from medically supervised cardiac rehabilitation programs.
• Weight management with a Body Mass Index (BMI) between 18.5–24.9 kg/m2 and waist circumference less than 40 inches in men and less than 35 inches in women.
• Start dietary therapy. Reduce intake of saturated fat (to less than 7 percent of calories) trans-fatty acids, and cholesterol (to less than 200 mg dietary cholesterol per day). Add plant stanol/sterols (2 grams/day) and viscous fiber (more than 10 grams/day) to further lower LDL cholesterol blood levels. Increased intake of omega-3 fatty acids in the form of fish or in capsule form (1 gram/day) for risk reduction. For treating elevated triglycerides, higher doses are usually necessary for risk reduction.
• In diabetics HbA1c less than 7 percent.
• Aspirin therapy 75-162 mg/day in all patients unless contraindicated.
• Reduce LDL cholesterol levels to less than 100 mg/dL and ideally less than 70 mg/dL. These are the essential secondary prevention guidelines. Consult with your physician or cardiologist to individualize additional medical therapy and lifestyle changes.

Lindsey received her Master’s degree from the University of Oklahoma as an Acute Care Clinical Nurse Specialist after completing a Bachelor of Science degree in Nursing from The University of Tulsa. She began her career as a Registered Nurse in the operating room with experience as a circulating & scrub nurse. Lindsey holds a national certification from the American Nurse Credentialing Center as an Adult Health Clinical Nurse Specialist.

Dillon received his Master’s degree from the University of Oklahoma as a Family Nurse Practitioner after completing a Bachelor of Science degree in Nursing from The University of Arkansas Fort Smith. He began his career as a Registered Nurse in critical care experience specializing in cardiovascular nursing. Dillon holds his certification through American Academy of Nurse Practitioners.

Holiday tunes on the radio, strings of lights brightening the neighborhood and a scent of pine and cinnamon transport us to one of the “most wonderful times of the year.” The holidays are the time we see more evergreen, spiced lattes and booked nights on the calendar. They are also the time of the year health care providers see more people suffering from what is now known as “holiday heart syndrome” as more patients present to the hospital with episodes of atrial fibrillation (AFib). For those familiar with the irregular heartbeat or quivering, and even those who have never felt their heart flip-flop or skip beats, AFib tends to be that unwelcomed guest during the holidays, causing heart palpitations, shortness of breath, chest pain, dizziness and raising the risk of stroke and heart failure.

First coined Holiday Heart Syndrome in 1987 following a study of patients going to the hospital with AFib, the condition is one that can strike otherwise healthy people who tend to overindulge in the season’s offerings – caffeine, alcohol, fatty and salty foods and decadent desserts. The main culprit, health care providers believe, is alcohol and too much of it during the holidays. But this differs for everyone depending on how his or her heart responds to alcohol. For those susceptible to the effects of alcohol, any amount of alcohol is believed to weaken the heart muscle, increasing pressure on the heart and causing the upper chambers of the heart to stretch, triggering an AFib episode. For most of us, however, drinking too much is the main cause. For women, this could be seven or more drinks in one week (or more than three in one sitting) and more than 14 drinks per week for men (or more than four drinks in one sitting).

As mentioned, there are other causes of AFib during the holidays – eating too much, high salt intake, fatty foods and caffeine. As the social calendar gets booked with festivities, our regular diet, exercise and sleep routine tend to take a back seat to squeezing in as much fun as we can between Thanksgiving and New Year’s Day. Poor diet, sleeping less, all but wiping exercise off the calendar for a month and refueling on high-caffeinated lattes to keep us going spells a perfect recipe for AFib and even a heart attack. In fact, December 25 ranks number one as the deadliest day for heart attacks, followed by December 26.

Don’t Let AFib or a Heart Attack Crash Your Party

This holiday season, take care of your heart and the holiday season by staying more in line with what you have been doing the previous 11 months of this year. Eat a clean low-fat, low-sodium diet, keep exercise a priority (even if you only have 20 to 30 minutes each day), stay as close to your regular sleep schedule as possible (catching up on weekends doesn’t count), stay hydrated especially in this colder weather, and treat yourself to only an occasional limited-time-only holiday latte. Also, talk to your health care provider about any changes you notice during this time. If you feel like your heart is starting to act abnormally, have it checked out.

Looking for a perfect heart-warming stocking stuffer? Oklahoma Heart Institute Life-Saving Screenings can save lives and prevent a heart attack and stroke. Click here to learn more about the screenings beginning at $40. 

Heart Attack?
Ways to Reduce Your Risk
By Wayne N. Leimbach, MD, FACC, FSCAI, FCCP, FAHA

The disease that kills the most Americans each year is actually preventable in the majority of cases. It’s heart disease, and it causes heart attacks in about 1.2 million people in the United States each year. If heart disease is treatable for most people and can be diagnosed early, why are so many of us having heart attacks?

Many people don’t know they are at risk. Others who actually know their risk factors don’t treat them. Still others who know their risk factors do not seek testing to assess whether or not they already have significant heart disease that needs treating.

WAYS TO PREVENT A HEART ATTACK
Heart attacks can be prevented by treating the known risk factors that lead to your having one.

First, you should know your blood cholesterol and triglyceride levels (lipids).

Second, you should know your blood pressures and blood sugar. If these levels are elevated, blockages are probably being made in the blood vessels that provide blood supply to the heart. We now know blockage formation can start as early as in the teenage years. The formation of blockages in the blood vessels to the heart can also be caused by smoking, chronic inflammation as measured by a blood test called the high sensitivity–CRP (hs-CRP), and a sedentary lifestyle.

Your risk of having a heart attack increases as blockages continue to develop in the blood vessels supplying the heart muscle. In most cases, blockage material (plaque) in the blood vessels to the heart muscle ruptures, and a blood clot forms on the ruptured plaque, causing the blood vessel to become completely blocked. This causes heart muscle to die. If a large amount of heart muscle dies, the person will die.

WAYS TO TREAT YOUR RISK FACTORS
Preventative cardiology is important. Here’s why. If blockages in the blood vessels to the heart are never made, then blockages cannot rupture, and a blood clot cannot form on the ruptured plaque to block the blood supply to the heart muscle. Thus, a heart attack is prevented.

The goal, then, to preventing heart attacks is preventing blockage formation in the blood vessels to the heart.

You can do this by treating your major risk factors: high lipids (cholesterol and triglycerides), high blood pressures, high blood sugars, cigarette smoking, high hs-CRP (marker of inflammation) and sedentary lifestyle.

KNOW YOUR NUMBERS
What are good cholesterol levels? For people at mild risk, LDL cholesterol (the bad cholesterol) should ideally be less than 130. For people with known blockages of the blood vessels and/or with diabetes, the LDL cholesterol levels should be definitely less than 100 and, if possible, less than 70.

What should your blood pressure be? Ideal blood pressures are less than 120/80. The goal for most people is blood pressures at rest consistently to be less than 140/90.

What should your blood sugars be? For most people fasting blood sugars should be less than 110, and ideally less than 100. The blood test called a high sensitivity-CRP is a marker of inflammation. It also indicates increased risk of blockage formation. The hs-CRP should be less than 2, and ideally less than 1.

Almost everyone’s blood pressure, cholesterol levels and blood sugars can be normalized today.

WATCH YOUR DIET
You should also follow a low-cholesterol, low-saturated fat diet to reduce cholesterol levels. A low-sodium diet will help reduce blood pressures. A low simple carbohydrate diet helps reduce the risk of diabetes and lowers triglycerides. Weight loss in overweight patients significantly reduces the risk of diabetes. If your risk factors cannot be normalized with dietary changes and lifestyle modification, then medications should be used.

Studies have shown that if risk factors are normalized, not only can blockage formation be stopped, but also reversal of already existing blockages can occur.

TESTING
For people who are having symptoms suggestive of heart disease or for people with multiple untreated risk factors, tests should be considered that screen for the presence of already severe blockages in the blood vessels to the heart. These include stress tests, calcium CT scans or CT angiograms. If severe blockages are present, they can be treated before a heart attack occurs.

HEART ATTACK INTERRUPTED
Finally, if you are having symptoms that may be those of a heart attack, call 911, so you can be taken immediately to the hospital.

If the diagnosis is confirmed at the hospital, the heart attack can be interrupted by emergency cardiac catheterization and balloon angioplasty and/or stenting. Most heart attacks can be interrupted, if the patient gets to the hospital early enough. This not only prevents death, but also minimizes the amount of damage done to the heart, so that the person can return to their normal lifestyle.

TAKING ACTION
It is important that we take an active role in our healthcare by knowing our risk factors for heart attacks, aggressively treating those risk factors and making sure symptoms suggestive of heart disease are evaluated.

Only in this way can you reduce your personal risks, thus reducing the number one cause of death in the United States.

Peripheral Arterial Disease
Is Your Leg Pain Related to Cardiovascular Disease?
By Raj H. Chandwaney, MD, FACC, FSCAI, FSVM

Are you having leg pain but don’t know what’s causing it? It could be lower extremity peripheral artery disease (PAD), which, actually, is very common. Just what is PAD?

Lower extremity PAD disease refers to the presence of plaque accumulation in the blood vessels that deliver blood to the feet. These blood vessels may include the distal abdominal aorta, iliac arteries, common femoral arteries, superficial femoral arteries, popliteal arteries, and/or infrapopliteal arteries. The plaque accumulation in these blood vessels is due to a disease called atherosclerosis. Atherosclerosis is also the disease that causes heart attacks when the plaque accumulates in the blood vessels that feed the heart. Atherosclerosis causes strokes if the plaque accumulates in the blood vessels that feed the brain.

PREVALENCE
Lower extremity PAD is present in 25-30% of people over age 70. The disease is also present in 25-30% of high-risk individuals over age 50. Individuals who have a history of diabetes or tobacco use are considered to be at high risk for developing lower extremity peripheral arterial disease.

SYMPTOMS
The classic symptom of lower extremity peripheral artery disease is called claudication, described as a tightness that occurs in the thighs or calves while walking. Interestingly, claudication only occurs in 10% of patients who have lower extremity peripheral arterial disease.

Atypical leg symptoms refer to any other type of leg discomfort that may occur in patients with lower extremity peripheral arterial disease. Atypical leg symptoms occur in 30% of patients with lower extremity peripheral arterial disease. Sixty percent of patients with lower extremity peripheral arterial disease are asymptomatic. Despite the fact that the majority of patients with lower extremity peripheral arterial disease are asymptomatic, it is very important to diagnose the disease in these asymptomatic individuals.

MORTALITY
Mortality rates are four times greater amongst individuals with lower extremity peripheral arterial disease compared to individuals without the disease. The increased risk of death is equally present in lower extremity peripheral arterial disease patients with or without symptoms. The five-year mortality rate for patients with lower extremity peripheral arterial disease is 25% (one of four patients with the disease are dead in 5 years if not treated).

Seventy-five percent of the deaths that occur in patients with lower extremity peripheral arterial disease are cardiovascular deaths (predominantly heart attack and stroke). Patients with lower extremity peripheral arterial disease are at high risk for heart attack and stroke because individuals with plaque accumulation in the lower extremity arteries are very likely to have plaque accumulation in the arteries that feed the heart and brain. Atherosclerosis is a systemic disease. This means it is usually present throughout the body rather than in just one area of the body.

RISK FACTORS
The risk factors for lower extremity peripheral arterial disease are similar to the risk factors for heart attack and stroke. These risk factors include: tobacco use, diabetes, high blood pressure, high cholesterol, family history of atherosclerosis, and advanced age. For unclear reasons, tobacco use and diabetes carry a much higher risk for lower extremity peripheral arterial disease than the other risk factors. The risk of developing lower extremity peripheral arterial disease is equal amongst men and women. Certain races are at higher risk for developing lower extremity peripheral arterial disease, such as African Americans.

DIAGNOSIS
The diagnosis of lower extremity peripheral arterial disease is readily established with the use of the Ankle-Brachial Index (ABI). The ABI is the perfect screening test because it is safe, cheap, accurate, and readily available. The ABI can be measured with the use of a simple hand-held Doppler by obtaining the systolic blood pressure in the ankle and brachial (arm) arteries. In my opinion, the ABI is the ideal test to establish the diagnosis of atherosclerosis, in asymptomatic individuals. Experts suggest performing a screening ABI on all individuals over age 70, and high-risk individuals over age 50. Screening ABIs facilitate the early diagnosis of systemic atherosclerosis in asymptomatic individuals.

When patients have symptoms that are concerning for lower extremity peripheral arterial disease, more sophisticated diagnostic tests may be required to diagnose and treat the patient’s symptoms. These diagnostic tests include duplex ultrasound, magnetic resonance angiography, CT angiography, and invasive angiography.

TREATMENT
The treatment of patients with lower extremity peripheral arterial disease is best summarized with the Lower Extremity PAD  Treatment Triangle. The most important priority in the care of patients with lower extremity peripheral arterial disease involves addressing the high risk of cardiovascular mortality. This priority is emphasized on the Lower Extremity PAD Treatment Triangle by the placement of this priority at the top of the triangle. Strategies used to address the high risk of cardiovascular mortality in patients with lower extremity peripheral arterial disease include:
• Smoking cessation
• Antiplatelet therapy (aspirin or clopidogrel)
• Cholesterol control
• Hypertension control
• Diabetes control
• Therapeutic Lifestyle Changes (heart healthy diet, routine exercise, weight loss)
• Flu shot annually

The next priority to be addressed in patients with lower extremity peripheral arterial disease is protecting the feet from amputation.

The final priority to be addressed in patients with lower extremity peripheral arterial disease is the treatment of leg pain that may be due to claudication. This priority is demonstrated on the Lower Extremity PAD Treatment Triangle located at the right lower corner of the triangle. Claudication symptoms can be treated with exercise rehabilitation, pharmacologic therapy, and/or revascularization.

Formalized exercise rehabilitation programs lasting 3 to 6 months have been proven to increase patient walking distances 100-150%. Rehabilitation sessions typically last 35 to 60 minutes. Patients are instructed to walk at an intensity that causes pain in 3 to 5 minutes, followed by rest until pain resolution, followed by walking again.

Pharmacologic therapy for claudication involves the prescription of cilostazol at a dose of 100 mg twice daily. Cilostazol has been proven to increase patient walking distances by 50%. Cilostazol has limited use with many lower extremity peripheral arterial disease patients because of common side effects that include headache, diarrhea, dizziness, and palpitations. Also noteworthy is that cilostazol has a black box warning contraindicating its use in patients with a history of congestive heart failure.

Finally, revascularization (restoration of blood flow) may be required in patients with lower extremity peripheral arterial disease who do not achieve adequate symptom relief with exercise rehabilitation or pharmacologic therapy. Revascularization strategies include endovascular techniques (balloon angioplasty, stents, atherectomy, or laser) and surgical techniques (bypass surgery).

CONCLUSIONS
Lower extremity peripheral arterial disease is a disease with a high prevalence. Most patients with lower extremity peripheral arterial disease are asymptomatic or have atypical symptoms. Patients with lower extremity peripheral arterial disease have significantly higher mortality rates (25% five year mortality) compared to the general population. Patients with lower extremity peripheral arterial disease die of cardiovascular diseases such as heart attack and stroke. Lower extremity peripheral arterial disease can easily be diagnosed in most patients with a cheap, safe, and simple screening test in the office (ABI). Treatment of all patients with lower extremity peripheral arterial disease should primarily focus on lowering their risk of cardiovascular death. Patients with lower extremity peripheral arterial disease require routine foot exams and diligent foot care. Some patients with lower extremity peripheral arterial disease will require treatment to improve claudication symptoms (exercise, pharmacologic, and/or revascularization). A smaller minority of patients will require revascularization to treat critical limb ischemia or acute limb schemia.

Heart Failure:
Signs, Symptoms and Treatment Options
By Alan M. Kaneshige, MD, FACC, FASE

Heart failure (HF) is a major healthcare issue for the United States. Because of the aging population, HF is one of the three cardiac conditions increasing in prevalence, the others being degenerative valvular heart disease and atrial fibrillation. There are 5.8 million patients with symptomatic HF in the United States and an estimated 23 million patients worldwide. Patients between the ages of 40 to 80 have a one in five chance for developing HF during their lifetime. Approximately 670,000 patients will be diagnosed with HF this year and 283,000 deaths will be attributed to HF. Acute decompensated HF will account for 1.1 million hospital admissions. In 2010, total HF costs amounted to $39.2 billion of which $21 billion was for hospitalizations alone.

To emphasize the severity of HF, it is believed that 20% of patients will die within one year of their diagnosis.

WHAT IS HEART FAILURE?
Heart failure is a cardiac syndrome, a collection of symptoms that occurs when the heart is not able to meet the metabolic needs of the body. In most cases, HF occurs when the heart is not able to pump enough blood to meet the demands of the body (reduced ejection fraction).

Normal hearts will pump out about 60% of the blood that fills the left ventricle with each heartbeat (ejection fraction 60%). Hearts with ejection fractions of less than 50% are considered impaired.

About half of HF cases are due to diastolic dysfunction, the inability of the left ventricle to fill with blood due to increased wall stiffness. In this condition, symptoms of HF occur even with normal pump function. Because of the inability of the heart to keep up with the demands of the organ systems, powerful neurohormones such as epinephrine, norepinephrine, endothelin, and aldosterone are released to maintain adequate perfusion. Persistently high levels of these neurohormones cause progressive cardiac dysfunction and ultimate failure.

WHAT CAUSES HEART FAILURE?
The causes of HF are numerous. The most common cause of HF today is coronary artery disease. Other common causes of HF include hypertension and valvular heart disease, particularly degenerative aortic and mitral valve disease.

Risk factors that contribute to the development of HF include cigarette smoking, diabetes, and obesity and obstructive sleep apnea. Prevention of HF requires early detection and treatment of these conditions.

WHAT ARE THE SYMPTOMS?
The most common symptom caused by HF is shortness of breath (dyspnea). A patient with HF will initially notice dyspnea with exertion. The effort required to cause dyspnea becomes less as HF progresses. Dyspnea may eventually occur at rest. Fatigue is another common symptom associated with HF.

Over time, the HF patient will need to keep his or her head elevated when lying down in order to breathe comfortably and not feel smothered. This symptom is known as orthopnea. The patient may suddenly awaken at night from a sound sleep with a sense of breathlessness, even panic, as lung congestion occurs because of HF. That sensation is known as paroxysmal nocturnal dyspnea.

With later stages of HF, patients will notice discomfort in the right upper quadrant of their abdomen due to swelling of the liver, leading to nausea, anorexia, and the feeling of fullness before consuming a complete meal. Abdominal bloating and lower extremity swelling are late signs of HF as these represent fluid retention and dysfunction of the right ventricle. Another sign of HF is the onset of palpitations and dysrhythmias and may lead to loss of consciousness (syncope) and possibly sudden death.

HOW IS HEART FAILURE TREATED?
Treatment for HF is based on a multi-level approach involving lifestyle changes, education, medical therapy, and close follow-up with specialists, as well as a HF specialty clinic.

Lifestyle Changes
Lifestyle changes are important to the successful treatment of HF. Adjustments include sodium/salt restriction to two grams or less a day, diet, regular exercise, and weight reduction. Diet therapy encompasses the American Heart Association low fat diet, the Mediterranean diet, and the DASH diet as ways to maintain adequate nutrition. Regular exercise, such as moderate paced walking 30 minutes a day, five days a week, prevents deconditioning and weight gain.

Avoiding nonsteroidal anti-inflammatory medications (NSAIDs) is important as these medications, both prescription and non-prescription, contribute to salt retention, swelling, and kidney dysfunction, all poorly tolerated by the HF patient. Advanced HF patients will even have to follow a fluid restriction of two liters or less a day to avoid fluid retention and progression of symptoms.

Medical Therapy
Medical therapy for the HF patients is a cornerstone for maintaining quality of life and to increase lifespan, as well as slow disease progression. Diuretics mobilize salt and water from the body. Angiotensin converting enzyme inhibitors (ACE inhibitors), angiotensin receptor blockers (ARBs), beta-blockers, and aldosterone inhibitors block the effects of harmful neurohormones that lead to HF progression. Physicians try to maximize these medications to approach the dosages that have shown benefit in large clinical trials.

Advanced Therapies
When HF patients show progression of symptoms and failure to respond to conventional lifestyle and medical treatments, more advanced therapy can be instituted. For some patients, biventricular pacing devices improve heart function. Ultrafiltration is utilized in volume-overloaded HF patients not responding to diuretic therapy. With ultrafiltration, fluid can be removed at a controlled rate so as not to significantly impact kidney function or blood pressure.

Surgical treatment for advanced HF includes high-risk coronary artery bypass surgery to attempt to improve pump function. For HF patients with severe mitral regurgitation, mitral valve repair can reshape the failing left ventricle and improve symptoms. Left ventricular assist devices (LVADs) are now approved for select refractory end-stage HF patients for prolonging life without the possibility of transplant (called destination therapy). These LVADs are also used to bridge advanced HF patients to transplant.

The ultimate surgical therapy at this time is a cardiac transplant. Because of limited organ supply, this option is only available to very select, advanced, end-stage HF patients. The totally artificial heart remains investigational.

CONCLUSION
Heart failure is a costly and growing problem for our healthcare system. Aggressive medical therapy, lifestyle changes, and education, as well as close medical following are key features to effective treatment. Advanced treatment is available to patients with progressive disease. A combined effort is needed to adequately provide a good quality of life and survival of the HF patient.

Sudden Cardiac Death: The Dangers of Rapid Heart Rhythms
Understanding Ventricular Tachycardia and Premature Ventricular Complexes
By Craig S. Cameron, MD, FCC, FACC

Sudden cardiac death is the leading cause of death in the United States. It accounts for more deaths than stroke, lung cancer, and breast cancer combined. When the normal electrical activation of the heart is interrupted by a rapid heart rhythm in the bottom chamber of the heart (ventricular tachycardia), sudden cardiac death occurs. Symptoms of ventricular tachycardia, VT, may include palpitations, light-headedness, dizziness, loss of consciousness, or seizures. VT is diagnosed using an electrocardiogram or heart monitor, and may indicate significant underlying heart disease.

Individuals with a prior heart attack and reduced “pump function,” are at particularly high risk for sudden cardiac death from VT.

For this reason, patients with VT usually require additional cardiac testing to assess the risk of sudden death and to determine treatment options. Such testing may include an echocardiogram, stress test, cardiac MRI, cardiac CT, or heart catheterization.

IMPLANTABLE CARDIOVERTER - DEFIBRILLATORS (ICDs)
The cornerstone of treatment for VT is to electrically shock the heart and reset its electrical activity. Unfortunately, most cases of sudden cardiac death progress too rapidly to allow sufficient time for emergency medical services to arrive and administer a life-saving shock. Thus, the implantable cardioverter-defibrillator (ICD) was developed and has revolutionized the prevention of sudden cardiac death. Current ICD models are capable of diagnosing and treating VT within seconds. While ICDs are highly effective at treating VT and saving lives, they do not address underlying heart disease and thus do not prevent VT from occurring. Furthermore, ICD shocks are painful and may result in reduced quality of life and psychological stress. ICD patients who have frequent VT often require either medications or a procedure called catheter ablation to reduce the burden of VT and likelihood of receiving electrical shocks.

ANTIARRHYTHMIC MEDICATIONS
Antiarrhythmic medications have demonstrated limited benefit for VT. Such “heart rhythm medications,” have not been shown to prevent sudden death and are only modestly effective at reducing VT burden and preventing ICD shocks. Additionally, antiarrhythmic medical therapy is often limited by drug interactions and extensive side effects. In some cases, antiarrhythmic medications may actually cause VT! Alternatively, catheter ablation is rapidly becoming a suitable and often superior therapy for preventing ICD shocks.

CATHETER ABLATION
Catheter ablation of VT is a minimally invasive procedure performed by an electrophysiologist (“heart rhythm doctor”) at specialized centers across the country, including Oklahoma Heart Institute.

It is performed in the electrophysiology procedure room under sedation or general anesthesia using a variety of tools which include X-ray fluoroscopy, intracardiac ultrasound, and 3-dimensional mapping systems. Small catheters are introduced from blood vessels in the groin and positioned within the heart.  These catheters are then used to record the heart’s electrical activity and determine the source for the VT. Once identified, the abnormal tissues in the heart are targeted for radiofrequency ablation to eliminate VT.

The procedure generally lasts for 3-6 hours depending upon the number of abnormal electrical circuits identified and how easily they are eradicated. Overall, catheter ablation successfully reduces VT burden by more than 75%, thereby reducing ICD shocks. Despite the critically ill nature of many patients, VT ablation is generally well tolerated with a 1.5% risk of major complications.

Patients without heart disease who have VT are said to have “idiopathic VT.” Such patients are usually considered low-risk for sudden cardiac death and treatment is thus directed at controlling individual symptoms. Within this group of patients, isolated “extra beats,” from the bottom chamber of the heart called premature ventricular complexes (PVCs) are typically more common than actual VT. PVCs may cause palpitations, fatigue, shortness of breath, and lightheadedness. Individuals with very frequent PVCs (>10-20% of total beats on a 24 hour heart monitor) are at risk for developing a PVC-induced cardiomyopathy or “weakening of the heart’s pump function.” Thus, in addition to assessment of cardiac structure, such patients should also be considered for heart monitoring to quantitate their PVC burden. In some patients, lifestyle modification (e.g., caffeine reduction) is effective at reducing symptoms. Others require additional therapy with medications or catheter ablation.

As with VT in structural heart disease, antiarrhythmic medications have limited efficacy but may be useful in some patients. Idiopathic PVCs/VT tends to be a focal problem arising from predictable locations within the heart. As such, many of these patients are excellent candidates for catheter ablation. In the absence of significant heart disease, the success rate of catheter ablation for frequent PVCs or VT approaches 90%. Catheter ablation is therefore very effective at treating patient symptoms from idiopathic PVCs/VT. Also, weakening of the heart from a PVC-induced cardiomyopathy may be reversed by successfully ablating the culprit PVC.

CONCLUSION
In conclusion, sudden cardiac death is the leading cause of death in the United States and occurs as a result of ventricular tachycardia. Patients with VT should be assessed for underlying heart disease and risk of sudden death. ICDs are highly effective at preventing sudden death in at-risk individuals but do not address the underlying cause of VT. Thus, many patients with ICDs will ultimately require additional treatment to prevent ICD shocks. Likewise, many patients with idiopathic PVCs/VT may require treatment to address symptoms, or to prevent or reverse weakening of the heart’s pump function. Medications are often not effective or well tolerated in treating PVCs/VT. Thus, catheter ablation of PVCs/VT is offered at highly specialized centers such as the Oklahoma Heart Institute. Ablation is a safe and effective option to eliminate or significantly reduce VT in the majority of patients and should be considered early in the course of this disorder.

Varicose Veins:
How to Find Relief
By Robert L. Smith, MD, MSc, FACC, FSCAI

If you are plagued by painful varicose veins, heavy, swollen, discolored legs, or any form of venous disease read on to learn more about venous insufficiency and the treatment options available at the OHI Vein Clinic.

In 2009, Oklahoma Heart Institute began performing catheter ablations of incompetent saphenous veins, which are the underlying cause of painful, ropy varicose veins, as well as most other forms of symptomatic venous insufficiency. Since then, we have successfully treated hundreds of incompetent veins, and have expanded our practice to include adjunctive therapies like microsurgical phlebectomy (surgical removal of varicose veins through tiny incisions) and foam sclerotherapy of varicose veins and spider veins.

Patient satisfaction after treatment of venous insufficiency at Oklahoma Heart has been remarkably high, and our team of vein specialists has grown to include nurses, nurse practitioners, ultrasound technicians, and physicians alike. We have a brand new, state-of-the-art vein treatment center at our OHI SouthPointe office (92nd and Mingo).

Although recent years have brought about a greater awareness of the importance of diagnosing and treating peripheral arterial disease, pathology of the venous system has received little attention. Peripheral venous disease was first mentioned in the medical literature in 500 BC, when Hippocrates described an association between leg ulcers and varicose veins1. Despite longstanding recognition, understanding of issues surrounding venous hypertension and resultant venous incompetence has lagged.

Peripheral venous disease is four to five times more common than peripheral arterial disease (reference 1), and the clinical presentation of lower extremity venous incompetence spans a broad clinical spectrum from telangiectasias (spider veins) to long-standing and recalcitrant venous stasis ulcers. This spectrum of disease manifests from cosmetically displeasing lesions on the legs to threats of serious secondary illnesses, such as deep venous thrombosis (DVT), pulmonary embolism (PE), and infection from chronic ulceration.

Venous disease has a hereditary component, and children of patients with varicose veins are more likely to develop problems related to venous reflux (reference 2). Occupations characterized by inactivity, such as standing or sitting for long periods of time, also place patients at risk (reference 3).

Until recently, the treatment of varicose veins and venous incompetence consisted mainly of surgical “vein stripping” procedures, during which large veins from the superficial collecting system of the legs are ligated and/or removed under general anesthesia. These surgical procedures, while effective, are associated with the risks of general anesthesia, infection of surgical wounds, long recovery times, and considerable patient discomfort. Perhaps for these reasons, surgical treatment of venous disease has occupied a rather small niche, and many patients have chosen to live with the condition rather than opt for surgery.

During the last ten years, outpatient, catheter based treatments have revolutionized how this disease is treated.

In order to understand the physiology of venous reflux disease, one must understand that there are two distinct venous systems in the lower extremities: The deep venous system is comprised of veins that run parallel to the arteries. These veins are surrounded by muscle and encased in connective tissue, providing them with good mechanical support. The deep veins are responsible for returning >95% of the venous blood from the lower extremity back to the heart.

The superficial system, comprised primarily of the saphenous veins, lies just beneath the skin and is without the mechanical support of the deep system. These superficial veins collect blood from surrounding tissues and, in a healthy system, route blood into the deep system so that it may be returned to the heart. It is typically incompetence of the superficial system that gives rise to the symptoms and physical manifestations of venous reflux disease.

It is widely accepted that most varicose veins and other problems from venous reflux relate to incompetence of the largest superficial vein; the greater saphenous vein. In some cases, the small saphenous vein (previously referred to as the lesser saphenous vein) is also involved. These superficial veins are located about a centimeter beneath the skin and should be less than 3mm in diameter in a healthy patient, though they can dilate to greater than 10mm in a patient with venous reflux disease. Unlike the deep venous system, where contraction of the leg muscles plays an important role in “pumping” the venous blood back to the heart, the return of venous blood in the superficial systems is passive, and depends entirely upon a series of one-way valves that aid the flow of the superficially collected blood on its route back to the deep venous system. Once in the deep system, venous blood is actively propelled against gravity back to the heart, primarily through the action of the calf muscles. In a healthy system, the superficially collected blood enters the deep venous system at two critical anatomic locations: The small saphenous vein deposits blood into the deep system at the sapheno-popliteal junc- tion (near the knee) and the greater saphenous vein deposits blood into the deep system at the sapheno-femoral junction (near the groin). If the series of one-way valves in the superficial veins become incompetent, the superficial system becomes congested, and the flow of blood into the deep system (and subsequently toward the heart) stalls, resulting in swelling, pain, and other clinical sequelae.

When valvular function in the superficial system becomes sufficiently compromised, deoxygenated venous blood flows backwards, from the deep system into the superficial system, at these critical anatomic points, resulting in a blind loop, where deoxygenated blood cycles endlessly from the deep system to the superficial system, back to the deep system, and so forth, never making it back to the heart.

Common clinical manifestations of these events are swelling, heaviness, throbbing, pain, varicosities (bulging tributaries of the overloaded superficial veins), and skin changes that occur as a result of the endless loop of oxygen and nutrient poor blood circulating throughout the lower extremity network of veins. At the extreme, refractory and painful venous ulcers develop.

Although incompetence of the one-way valves can occur at any point in the network, the most common site of incompetence is the sapheno-femoral junction. When incompetence of the sapheno-femoral junction occurs, venous blood from the deep system, en route to the heart, is diverted from the (deep) femoral vein back into the (superficial) greater saphenous vein. This is typically the starting point of the pathologic cycle, and causes the greater saphenous vein to become increasingly engorged, setting off a cascade of events where superficial valves, unaided by the pumping function of the leg muscles, fail in a top to bottom fashion until clinical manifestations develop. This is why surgical removal of a diseased greater saphenous vein has proven effective in the treatment of venous reflux disease: the most common site of retrograde flow from the deep to superficial system is eliminated and the blood has nowhere to go but up (and back to the heart).

Experience with surgical removal of the greater saphenous vein goes back many decades. During the last several years, less invasive alternatives to surgical vein stripping procedures have arisen, and have targeted treatment of greater saphenous and small saphenous veins. Endovenous laser ablation and radiofrequency ablation of diseased greater and small saphenous veins have largely replaced the more painful surgical procedures. In several trials, these minimally invasive procedures, which can be performed on an outpatient basis, have proven to be as effective as the surgical alternatives (references 7,8,9,10). While laser endovenous ablation of the greater saphenous vein and radio-frequency ablation of the greater saphenous vein are both as effective as surgery, radiofrequency ablation causes the least amount of patient discomfort, and is emerging as the minimally invasive procedure of choice (references 11,12).

During radiofrequency ablation of the greater saphenous vein, a tiny incision is made near the knee. Under ultrasound guidance, the greater saphenous vein is entered and a radiofrequency ablation catheter is advanced from the knee to the sapheno-femoral junction near the groin. Radiofrequency waves are then applied to the vein, causing the vein to fibrose and permanently close. In a matter of minutes, the vein is ablated, and the same functional outcome of the more painful surgical treatments is achieved. Although the benefit to the patients is the same as the surgical approach, patients may have this procedure performed on an outpatient basis (often in about 15 minutes) and will walk out of the office afterward, often experiencing dramatic results in hours to days after the procedure. When done properly, radiofrequency ablation of the saphenous veins is associated with little pain, speedy recovery times, and lasting results (references 11,12). Complications, which include infection, paresthesias, DVT/PE, skin burns, and lymphedema, are exceedingly rare (references 11,12).

Several clinical scenarios may lead to the recommendation of minimally invasive saphenous confirmed by ultrasound prior to consideration of any treatment. Ultrasound mapping studies are performed in order to rule out deep venous thrombosis in the deep venous system and to evaluate for dilation and reflux in the superficial system. Prior to minimally invasive saphenous vein ablation, conservative measures should be tried. These include compression with graded elastic stockings, leg elevation, exercise, and symptomatic pain management with NSAIDS. If the patient demonstrably fails a 3-6 month trial of conservative therapy, they may be considered for minimally invasive saphenous vein ablation. In cases where isolated saphenous vein ablation fails to entirely treat the problem, a host of adjunctive therapies, such as stab phlebectomy and sclerotherapy, are available.

Venous reflux disease results in painful and cosmetically displeasing derangements of normal venous anatomy. At the extreme, it leads to recalcitrant venous ulcers, which can themselves cause secondary health issues. In the modern era, this common disease can be effectively treated with a minimally invasive, office-based procedure, with pleasing results. Radiofrequency saphenous vein ablation results in less discomfort and risk to the patient than surgical alternatives, and is proven to have lasting benefit. If you are interested in learning more about the treatment of varicose veins and other forms of venous disease, please call for an evaluation in the OHI vein clinic: 918-592-0999.

REFERENCES

1 Poblete E, Elias S. “New Options in Treatment:Minimally Invasive Vein Surgery” Journal of the American College of Certified Wound Specialists.2009. 1:12-19

2 Cornu-Thenard A et al. “Importance of the familial factor in varicose disease. Clinical study of 134 families” J Dermatol Surg Oncol 1994

3 Santler, R., Ernst G., Weiel, B. “Statistisches uber der varikosen Symptomenkomplex” Hautarzt 1956; 10: 460-3

4 Jones L et al. “Neovascularization is the principal cause of varicose vein recurrence: results of a randomized trial of stripping the long saphenous vein” EurJ Endovasc Surg 1996; 12:442-5.

5 Rutgers PH et al. “Randomized trial of stripping versus high ligation combined with sclerotherapy in the treatment of the incompetent greater saphenous vein” Am J Surg 1994;168:311-15.

6 Dwerryhouse S, Davies B, Harradine K, Earnshaw JJ. “Stripping the long saphenous vein reduces the rate of reoperation for recurrent varicose veins: five-year results of a randomized trial” J Vasc Surg. 1999 Apr;29(4):589-92.

7 Rasmussen L et al. “Randomized trial comparing endovenous laser ablation of the great saphenous vein with high ligation and stripping in patients with varicose veins” J Vasc Surg 2007;46:308-15

8 Darwood RJ et al. “Randomized clinical trial comparing endovenous laser ablation with surgery for thetreatment of primary great saphenous

varicose veins” Br J Surg 2008;95:294-301

9 Kalteis M et al. “High ligation combined with stripping and endovenous laser ablation of the great saphenous vein: Early results of a randomized controlled study” J Vasc Surg. 2008;47:822-29

10 Ogawa T et al. “Endovenous Laser Ablation Compared With Stripping – Multi-Center RCT in Japan” Poster presentation at the American Venous Forum February 2008, Charleston, SC

11 Merchant et al. “Long-term Outcomes of Endovenous Radiofrequency Obliteration of Saphenous Reflux as a Treatment for Superficial

Venous Insufficiency” J Vasc Surg 2005;42:502-9.

12 Proebstle et al. “Treatment of the incompetent great saphenous vein by radiofrequency powered segmental thermal ablation: First clinical experience” J Vasc Surg 2008;47:151-6.