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    Categories: Food & Health

How to prevent heart disease

Heart Disease – An infographic by GeriatricNursing.org

 

Every year over 1.2 million people suffer from a heart attack due to coronary heart disease. The probability that a person may die from heart attack is 40 out of 100. According to the latest estimations, more than 335,000 of these heart attack patients are estimated to die even before reaching the hospital or the emergency ward. In the United States alone, more than 7 million people have had a heart attack incident at least once in their lifetime. This data comes from the American Heart Association which monitors heart disease in the United States. Heart disease has become very common nowadays due to lifestyle changes. The fact that heart disease does not manifest its symptoms until it strikes calls for extra care on the patient’s part.

RISK FACTORS FOR HEART DISEASE

There are many factors responsible for the development of heart disease. Some of them can be controlled whereas others cannot. The factors that can be controlled are linked with lifestyle and making suitable changes to one’s lifestyle reduces his/her chances of getting heart disease. Some of the controllable factors are:

SMOKING:

Smoking is known to increase the risk of heart disease. In fact, smokers are at two times more risk of getting a heart attack than non-smokers. The probability of heart attack being fatal is greater  in active smokers. It is better to never start smoking at all in first place than try to quit smoking after becoming addicted. Quitting smoking helps reduce the risk of coronary heart disease.

DIET:

Increased consumption of fats in the diet is known to increase the risk of heart disease. Reducing the consumption of fats reduces heart disease. Junk foods should be avoided at all costs.

BLOOD PRESSURE:

Lowering blood pressure helps reduce the risk of a heart attack. Blood pressure can be controlled by avoiding excessive sodium in the diet, eliminating stress and relaxing.

OBESITY:

Obesity is one of the leading causes of heart disease. Obesity can be controlled by avoiding junk foods and proper exercise.

SUGAR LEVELS:

Diabetics should take extra care to control their blood sugar levels. Higher blood sugar levels are known to increase the risk of heart disease.

STRESS AND ANGER:

Stress and anger increase ones chances of heart disease. They should be avoided.

Uncontrollable factors are the ones that are beyond our reach. These include:

SEX:

Males are more prone to heart disease.

AGE:

Older people are more susceptible to heart disease.

HEREDITY:

People who have a family history of heart disease run a higher risk of getting it.

MENOPAUSE:

The risk of heart attack increases in women in the post-menopausal period.

ETHNICITY OR RACE:

The incidence of heart disease in certain races is more as compared to others. For example, American Africans and Mexican Americans have a higher incidence rate of heart disease relative to Caucasians.

LIFESTYLE:

Lifestyle change can significantly prevent heart disease. While it cannot be said with confidence that lifestyle changes can sthetop  disease, it is clear that certain changes do improve health in other ways. Many of the risk factors are interlinked and making changes that decrease a particular risk factor may also decrease other related ones, such that heart disease may be effectively controlled.

HOW DOES THE HEART WORK?

The circulatory system of the body is a one-way road that travels from the heart out to the organs and extremities and back to the heart. The heart itself has a unidirectional pathway that ensures that blood flow continues traveling in the same direction. By examining the structures of the inner heart, it becomes understandable why this organ is so vital to maintaining blood flow to the rest of the human body.

The heart is divided into four sections, or chambers. The two chambers on the top of the heart are the right and left atria. The right atrium receives blood that has been circulated throughout the body, and the left atrium receives freshly oxygenated blood from the lungs.

The two lower chambers are the ventricles. In order for the blood that has been received in the atria to get to the ventricles, the blood must first pass through a door, or valve, that divides the atrium on each side of the heart from the corresponding ventricle beneath. The valve on the left side of the heart is the bicuspid, and the valve on the right is the tricuspid. Once the blood passes through these valves, it is now in the ventricles and ready to be pumped outside of the heart. There is one more set of valves that leads out of the ventricles called semi-lunar valves. Blood from the right atrium will be sent to the lungs to pick up oxygen, and blood from the left will be sent out to all other areas of the body.

The pumping of the heart is controlled by special cells in its muscular walls. These cells, known as the SA Node, are the pacemakers of the heart. They start an electrical signal that travels through the right atrium to another concentration of special cells called the AV Node, which will cause the two atria to contract. Once the signal reaches this node, it then gets sent down the septum of the heart, a muscular area that divides the heart into right and left halves. Upon exiting the septum, the signal then travels up both sides of the lower ventricles which causes these two chambers to contract, sending blood outside the heart to the lungs or the rest of the body.

Human survival is dependent upon the heart being able to function properly. Delivering nutrient and oxygen-rich blood to the body’s cells and tissues ensures that the organs made up of cells and tissues are kept healthy.

WHAT ARE THE TYPES OF HEART DISEASE?

Heart disease is a broad term that encompasses true heart-related diseases, particularly acute myocardial infarction, cerebrovascular disease (strokes), and peripheral vascular disease.  Each of these is a disorder ultimately caused by atherosclerosis.  Atherosclerosis is an abnormality of the blood vessels that causes a narrowing of the arteries leading to the heart, the brain, or the extremities. The end result is a lack of blood flow to a crucial body area and possible death from heart damage or brain damage. People with peripheral vascular disease tend not to die from their disorder but will have an increased risk of amputation.

THE ACUTE MI

The acute myocardial infarction or MI is a major cause of death throughout the world. An MI stems directly from coronary artery disease and the blockage of the coronary blood vessels, leading to myocardial cell death from poor oxygenation of the heart.  At a critical low threshold, the heart muscle cells begin to die off and form a permanent scar on the muscle.  The most common cause of an MI is occlusion of the coronary arteries from atherosclerosis, but spasms of unoccluded arteries can also lead to an MI in less common circumstances.

MIs can be transmural (going through the entire heart muscle) or non-transmural (affecting less than the full thickness of the heart muscle wall).  The least easily-perfused areas of the heart are the endocardial cells and the sub-endocardial cells, as these tend to be more affected by ischemia to the heart.

Another classification of myocardial infarction comes from the acute ECG changes seen in a heart attack.  A STEMI is also referred to as an ST-segment elevation myocardial infarction because the ST segment is elevated in the acute phase of the heart attack.  The other is called a NSTEMI or a non-ST segment elevation myocardial infarction.  This is a simple designation, but it doesn’t necessarily tell if the MI is transmural or not and doesn’t indicate differences in the size of the MI.  The biggest difference between the two is that the STEMI is associated with a greater mortality in the short term (but not in the long term).

An MI is the leading cause of death in developed countries throughout the world, with almost half a million patients succumbing per year from the disorder in the US.  Fortunately for those patients that make it to the hospital, about 95 percent of patients survive their infarction.  The mean age at the time of myocardial infarction is 65 years of age.

CAUSES OF AN ACUTE MI

Things that can precipitate an MI include intense physical activity, which increases the myocardial oxygen demand, severely high blood pressure, which stresses the heart muscle, and severe aortic valve stenosis, which inflicts extra work on the heart.  Any condition causing a low cardiac output will underperfuse the coronary arteries and will decrease the amount of oxygen and blood that gets to the heart muscle.

There are several significant risk factors for having an MI.  These include having a family history of MI, using tobacco, being male, having diabetes mellitus, being hypertensive, and having elevated lipid levels.  Each of these can contribute to the major cause of an MI, which is atherosclerosis.

With hyperlipidemia, an elevation of LDL cholesterol, total cholesterol, and triglycerides each raises the risk of atherosclerosis and MI.  Low HDL levels have also been linked to a higher risk of MI.  In diabetic patients, worsened glycemic control and persistent elevations of the hemoglobin A1c are linked to a greater chance of atherosclerosis and myocardial infarction.  Worsened control of blood pressure stresses the heart and predisposes a person to developing an MI.

Compounds found in tobacco smoke cause considerable damage to the lining of the blood vessels that supply the heart. This damage leads to atherosclerotic buildup on the inside of the blood vessels, which adds to a greater risk of thrombosis formation in smokers.

The actual plaque develops over many years or decades.  Plaque contains lipids and fibrous material that can become disrupted, causing a thrombus to form in the area of the plaque.  Thrombus ultimately results in myocardial infarction, occurring relatively suddenly over a few minutes or a couple of hours. Those myocardial cells most distal to the site of the blockage tend to get the least amount of oxygen and will die off first.  The endocardium dies off before the myocardium and the epicardium.

Some myocardial cells are simply injured in the MI and are not yet dead.  These are the cells that can be salvaged in treating an MI by reperfusing the injured part of the heart.  Things like tissue plasminogen activator (TPA) and emergency angioplasty can salvage the injured cells, decreasing the overall size of the infarcted area.

MI severity depends on the degree of occlusion in the affected coronary artery, the time the affected artery was occluded before revascularization, and the presence or absence of helpful collateral circulation. Proximal thrombi tend to cause a more severe infarct as compared to distal thrombi.  Larger infarcts are associated with a higher chance of CHF and sudden cardiac death.  STEMI is usually secondary to a complete arterial blockage in the coronary artery, while a NSTEMI involves a bigger plaque but a lesser degree of occlusion at the time of infarct.

SIGNS AND SYMPTOMS OF AN ACUTE MI

There can be several signs and symptoms associated with having a myocardial infarction.  The main symptoms suggestive of an MI include pressure-like or crushing chest pain, radiation of the pain to either the arms, jaw, or back, shortness of breath at rest, sweating (diaphoresis), dizziness or outright syncope, or altered cognitive function. Half of all patients who have an MI will have a history of angina pectoris that indicates a past risk for having an MI.

The actual signs and symptoms of an MI vary from person to person.  Some symptoms are so slight that the patient doesn’t recognize the severity of the disease. Other patients will die suddenly without the chance to display any obvious symptoms.  Asymptomatic MIs are more common among diabetics, who may have a serious MI without any major symptoms.

Typical symptoms include the following:

  • Sudden or gradual onset of pressure in the chest, sometimes described as a squeezing or fullness in the midportion of the chest anterior
  • Radiation of the chest discomfort to the jaw, teeth, shoulder, back, or arms
  • Epigastric discomfort with or without feeling nauseous
  • Being sweaty or diaphoretic
  • Having a syncopal or near syncopal episode
  • Having a cognitive impairment that comes on suddenly

Myocardial infarctions can happen at any time but are more common with physical activity and in the early morning hours.  About half of all patients will have some type of warning, such as angina or similar symptoms, before actually having their infarction.

DIAGNOSIS OF AN ACUTE MI

In general, the first diagnostic test used to confirm the presence of an MI is the ECG, which will often show ST segment elevation or other stress on the heart.  ST segment depression can also be seen in an ECG evaluation.  The next confirmatory test is the serum troponin level, which is the first enzyme to be elevated in an acute MI.  Later elevations in the CPK, SGOT, and LDH can be seen after the MI.  The serum troponin level predicts morbidity and mortality in an MI.

TREATMENT OF AN ACUTE MI

The treatment of an acute MI can be medical or interventional.  The overall goal is to restore blood flow to the heart muscle as soon as possible after a blockage.  If a patient presents soon enough to the hospital and the MI is detected early, those parts of the heart muscle that are ischemic but not necrotic have the potential to be salvaged through treatment.

Chewable aspirin has been found to decrease the overall mortality in an acute MI situation.  It is given as soon as an MI is suspected, in the ambulance if possible. It works within minutes to stop platelet activation and further thrombosis but doesn’t break down the clot that has already formed. Other antiplatelet agents like clopidogrel have added effectiveness in preventing complications from an MI when aspirin is given at the same time. A total of 325 mg of aspirin is given on admission to the emergency department or in the ambulance as a chewable medication.

Oxygen is another treatment modality for acute myocardial infarction.  It should be done for low O2 sats or pulmonary edema. It allows for maximum oxygenation to reach the heart.  It can provide oxygen to those areas of the heart that aren’t necrotic but are ischemic.  Oxygen must be given to patients with symptoms of an MI, evidence of pulmonary edema, or with pulse oximetry readings less than 90 percent saturation. The recommended duration of oxygen supplementation in an acute myocardial infarction is 2 to 6 hours after admission, but can be given for longer periods of time if the patient is in congestive heart failure or has an arterial oxygen saturation less than 90 percent.

IV nitrates are important for ongoing ischemia, CHF, hypertension, or for a significant anterior wall MI.  It directly vasodilates the arteries, decreasing both the preload and the afterload, decreasing the myocardial oxygen demand. By dilating the coronary arteries, more blood gets to the poorly oxygenated areas of the heart.  There can be constriction in the thrombosed areas, which is reversed with nitrates.

Nitroglycerin acts very quickly and can be used in the first 48 hours after admission.  Low blood pressure, headache, and secondary tachycardia can be side effects that limit the use of nitroglycerin. Nitrates like nitroglycerin must not be given to patients who have taken a phosphodiesterase inhibitor for erectile dysfunction within the previous 24 hours before the infarction or suspected infarction.

Pain control is important to decrease anxiety and tachycardia.  The mainstay of pain control is IV morphine. The drug is given initially intravenously at doses of 2-4 mg IV given at 5 to 15-minute intervals. It can be used on patients receiving coronary angiography, angioplasty, or stent placement to reduce pain.  Morphine is not a first-line therapy for an acute MI because it can mask ongoing ischemic symptoms.

Beta blockers are recommended within 12 hours of an MI. They are known to decrease the incidence of ventricular arrhythmias and the chance of reinfarction, and can decrease infarction size.  This can reduce oxygen demand in the heart. Beta blockers include carvedilol, atenolol, and metoprolol. The most dangerous side effect of beta blocker therapy is CHF, bradycardia, and wheezing.

Heparin is an anticoagulant indicated in the treatment of MI.  it is used until the clot has completely gone away.  It can be given for a minimum of 48 hours and is usually given as an IV drug to hospitalized patients, titrated to a PTT of between 50 and 70 seconds. It is beneficial because it addresses the clotting process in an entirely different way than with aspirin.

Low molecular weight heparin is used in patients who don’t tolerate regular heparin.  Lab testing of the PTT Isn’t necessary.  It is given every few hours by subcutaneous means. There are two main types of LMWH, usually called enoxaparin and dalteparin.  Treatment with warfarin is not a first-line treatment for acute MI except in cases of a thrombus in the left ventricle, left ventricular aneurysm, atrial fibrillation, or an ejection fraction of less than 30 percent. Warfarin is given for a minimum of three months.

Reducing blockages can be done using fibrinolytic agents, such as a tissue plasminogen activator.  This will restore coronary blood flow in up to 60 percent of patients with a STEMI infarction within 12 hours of taking the drug.  It can’t be used in situations where a secondary bleeding complication may occur.  It must be given within 90 minutes of presentation to the hospital.  They are most effective when given within an hour of symptom onset.  Time from the onset of symptoms to receiving a fibrinolytic drug is the most crucial aspect when giving this class of drugs.

ACE inhibitors should be used in all STEMI patients and NSTEMI patients who are diabetic, hypertensive, or have a low ejection fraction.  Every MI patient should ultimately be discharged with it. In such patients, the ACE inhibitor needs to be given within 24 hours of admission and continued indefinitely to prevent a recurrence. It can’t be given to patients with poor kidney function. The most common ACE inhibitors used are lisinopril, captopril, ramipril, and captopril. For patients who can’t take ACE inhibitors, angiotensin receptor blocker (ARB) therapy may be used instead.

Statin drugs should be started on all MI patients before getting out of the hospital.  They lower the risk of another heart attack by decreasing the LDL and total cholesterol levels.  The drug of choice is atorvastatin, which is given at 80 mg per day.

Glycoprotein IIb/IIIa antagonists can be used as a relatively new treatment option in an acute MI.  They block the glycoprotein IIb/IIIa receptors located on platelets.  These receptors bind to fibrinogen as the last step in platelet aggregation.  These can be used during a percutaneous coronary intervention procedure, in MI cases, and in acute coronary syndrome cases.  They improve mortality and decrease the rate of MI recurrence.  They are used in NSTEMI patients for up to 72 hours, particularly in  who arthosee not undergoing PCI. The three medications of this class include abciximab, eptifibatide and tirofiban.

TREATMENT INTERVENTIONS

Interventionist procedures after an MI include percutaneous coronary intervention or an angioplasty procedure.  It should be done on STEMI patient within 90 minutes of hospital arrival on NSTEMI patients with an elevation of cardiac enzymes or a new bundle branch block.  It should be done by an experienced operator at a well-equipped coronary intervention unit.  If it cannot be done, then fibrinolytic therapy should be started. The PCI procedure generally includes diagnostic angiography first, followed by angioplasty, and, usually, stenting.   It successfully restores blood flow in up to 95 percent of patients.

Research has shown that PCI has an advantage over fibrinolysis when it comes to short-term mortality, and bleeding and reinfarction rates. However, the short-term mortality advantage does not last, with PCI and fibrinolysis showing similar survival rates over the long term. Stenting is helpful because it decreases the chance of another thrombotic event in the same area.

Emergency coronary artery bypass grafting or CABG is done when PCI has failed in all patients stable enough to have surgery.  It should also be done when there are cardiac complications of an MI that require surgery (such as a ventricular septal defect, free wall rupture, or mitral regurgitation).  If done within three hours of symptom onset, it can reduce the size of the infarct but carries a higher risk of short-term mortality.  It improves long-term survival in patients who have had an MI. An elective CABG procedure improves long-term survival rates in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease when PCI is contraindicated.

An implantable cardiac defibrillator (ICD) should be used in cases where the patient is at risk for an arrhythmia after an MI.  It is used in patients who have an MI and a reduced ejection fraction.  They are not recommended for severe heart failure patients.  There is about a thirty percent risk in all-cause death when an ICD is used.  A period of 40 days evaluation and waiting time is recommended after the MI to see if the patient truly needs the defibrillator.

CEREBROVASCULAR DISEASE AND STROKE

Cerebrovascular disease, or brain-related heart disease, will lead to an ischemic stroke. When this happens, there is a lack of adequate blood flow to the brain, resulting in intracerebral cell death.  While there is more than one kind of stroke (ischemic, embolic, and hemorrhagic), the ischemic type is directly related to the same underlying conditions that cause acute myocardial infarctions.  The signs and symptoms that occur from a stroke are often immediate at the time of blood vessel blockage and may gradually improve over time.

The definition of a stroke is a neurological deficit in the brain that lasts longer than 24 hours or causes death prior to 24 hours. The time of 24 hours is arbitrary and defines a “stroke” versus a “transient ischemic attack”, an ischemic event that lasts for a shorter duration of time.  Nowadays, a stroke is a medical emergency that can be managed urgently so as to affect the outcome and minimize brain tissue loss.

SIGNS AND SYMPTOMS OF A STROKE

As mentioned, stroke symptoms begin relatively quickly after the onset of cerebral ischemia.  The symptoms tend not to progress after the first few minutes. The more of the brain involved, the more severe the symptoms.  With ischemic infarcts, there can be wide range of symptoms, from facial paralysis, hemiparesis, numbness of the arms, face, or legs, aphasia, hemineglect, memory deficits, apraxia, disorganized thoughts, dysarthria, sensory deficits, and visual disturbances.  The symptoms affect just one side of the body, usually on the opposite side as the stroke in the brain.  Brainstem strokes can involve the cranial nerves.

The problem is ultimately secondary to a blood clot (thrombus) that develops near the atherosclerotic plaque. While the atherosclerotic parts of the blood vessels develop gradually over time, the thrombus itself is relatively sudden.  The thrombus can remain in the plaque area or can break off, forming an “embolic stroke”.  The disease can involve the large vessels to the brain (carotid arteries and vertebral arteries) or the small vessels (branches of the larger arteries).

DIAGNOSIS OF STROKE

There are many ways to document a stroke.  A neurological examination will help support the diagnosis; a CT or MRI scan will show abnormalities in the brain and arteriography will show the actual site of the thrombosis and arterial blockages.  The CT scan without contrast will be 16 percent sensitive and 96 percent specific.  The MRI exam is slightly better in evaluating the brain for a stroke, being 83 percent sensitive and 98 percent specific. SPECT scans can help because they show cerebral blood flow deficits.

Other imaging tests that may help in diagnosing a stroke include an ultrasound or Doppler study of the carotid arteries, an echocardiogram (to look for vegetations), electrocardiogram (to look for arrhythmias), angiogram (to evaluate the vessels inside the brain), and blood tests to look for things like diabetes and blood cholesterol elevation.

MANAGEMENT OF ISCHEMIC STROKE

Aspirin decreases the chance of recurrences by 13 percent and can help in the first few hours of the onset of the stroke.  The definitive treatment involves mechanically moving the clot in the initial stage of the stroke or thrombolysis (the chemical breakdown of the clot).  Lowering blood pressure and blood sugar are not recommended at the time of a stroke.

The mainstay of the treatment of thrombotic strokes includes tissue plasminogen activator (tPA).  It must be given between three hours of symptoms with a ten percent benefit (leading to life without disability).  Unfortunately, tPA does not reduce mortality rates.  Benefits do not happen if tPA is given further out than four and a half hours. The main problem with tPA is a bleeding complication, known particularly in extremely large infarcts.  The use of tPA can be improved by directly injecting it into the affected artery using a catheter. This is called intra-arterial fibrinolysis.

Surgery can be done within seven hours of the onset of symptoms.  It is primarily done with an anterior stroke and a known clot in the affected artery.  While it doesn’t alter the overall mortality rate, surgery to remove the clot (called a thrombectomy) can improve functional outcome. Thrombolysis is often used along with the thrombectomy procedure to maximize the outcome.

After the stroke, patients undergo stroke rehabilitation or recovery, a process that helps the stroke patient return to normal life and relearn skills lost. The rehabilitation team includes speech therapists, occupational therapists, physical therapists, pharmacists, psychologists and social workers.  About a third of all patients will have post-stroke depression, requiring psychological and possibly psychiatric intervention. Patients will use assistive devices like canes and wheelchairs to help them ambulate and get around after the stroke. Stroke rehabilitation needs to start as soon as possible and may last for more than a year.  The return of function happens within a few months, with a falling-off of improvements after that.  Improvements in writing, talking, and large motor skills have been found to occur many months after the initial stroke.

PERIPHERAL VASCULAR DISEASE

Peripheral vascular disease or peripheral arterial disease (PAD) involves a narrowing of the arteries in the periphery of the body, particularly the legs and sometimes the arms.  It is highly related to coronary artery and cerebrovascular disease as it basically has the same pathophysiology—the gradual narrowing of the arteries with atherosclerotic plaques and secondary thromboses that lead to arterial occlusion.  The classic symptom of early disease is intermittent claudication, although some people can have bluish skin coloration, poor hair/nail growth, cold skin, and ischemic skin ulcers. These things can lead to soft tissue death that can, without proper treatment, lead to an amputation. Up to half of all patients with PAD have no symptoms.

SIGNS AND SYMPTOMS

Patients with symptoms of peripheral vascular disease have two types. The first is intermittent claudication that involves muscle pain while walking that resolves during rest.  This is because activity causes an increase in muscle oxygen demand that cannot be met in the exercising body.   The second is critical limb ischemia, which involves pain at rest (especially with elevated feet) and tissue loss (sores and wounds that don’t heal, leading to gangrene).

The signs of PAD include a bluish coloration of the skin and coolness of the affected extremity.  There will be pallor and redness when changing body positions and a noticeable decreased growth of both hair and nails in the affected leg (or arm).

RISK FACTORS FOR PAD

The risk factors for PAD are identical to those for atherosclerosis. The most crucial and modifiable cause of PAD is smoking. There is a dose-response effect so that people who smoke more will have greater degrees of atherosclerotic disease.  Second-hand smoke will also contribute to the disease process.  More than 80-90 percent of patients with PAD have a history of smoking at some point in their lives.

Diabetes mellitus will increase the risk of PAD by 2-4 times.  High blood sugar will cause dysfunction of the endothelial and smooth muscle cells of the peripheral vessels, leading to an increased risk of PAD, dependent upon the severity of diabetes and the length of time the person has had the disease.

Patients with a high LDL cholesterol and a low HDL cholesterol (and elevated triglyceride levels and total cholesterol levels) will have a greater incidence of peripheral vascular disease.  People who take statins or other drugs to decrease cholesterol levels will show improvements in their risk for PAD.  Hypertension also increases the risk of PAD and other atherosclerotic heart diseases.  It will increase the risk of intermittent claudication by 2.5-fold in men and 4-fold in women.  Age is a factor in developing PAD as is being male, having a prior stroke or heart attack, and being obese.

DIAGNOSIS OF PAD

Peripheral vascular disease can be assessed with an ankle-brachial index (ABI), which is the first test that needs to be done when this disorder is suspected. It involves taking the blood pressure in the brachial artery and the ankle. A comparison of these two blood pressures is the ankle-brachial index.  The normal ABI is about 1 to 1.4.  Patients don’t get diagnosed with PAD until the ABI is 0.9 or less, with levels that are 0.91 to 0.99 being borderline.  An ABI that is higher than 1.4 means the arteries cannot be compressed.  Moderate PAD involves an ABI of between 0.41 and 0.9 while an ABI of less than 0.4 means the person has severe PAD.

If the patient’s ABI measurement is completely normal at rest, but the disease is still suspected, there can be further testing. The patient can be evaluated first at rest with an ABI measurement. They are then instructed to walk on a treadmill until they have their typical claudication pain or until they have exercised for a total of five minutes.  The ABI is then measured again.   If the ABI decreases by a minimum of 15-20 percent, the patient likely has peripheral vascular disease. If there is severe vessel wall calcification, the ABI will be higher than 1.40, which is a falsely negative test that requires further evaluation.

An abnormal ABI measurement usually means that further evaluation is necessary.  A lower leg Doppler ultrasound is performed to see what the flow is like inside the arteries.  This is a special ultrasound test that specifically measures blood flow.  The flow is evaluated in the femoral area, the popliteal area, and the vessels below the popliteal artery.  Decreased or absent flow means there is a high probability of peripheral vascular disease.

An angiography is the gold standard test of peripheral vascular disease. The physician places a catheter inside the femoral artery which is guided to the various vessels in the extremity.  A radiocontrast dye is injected into the artery and an x-ray is taken, which shows the caliber of the artery and any areas of partial or complete stenosis.  During this procedure, an atherectomy can be performed, angioplasty is possible, and stents in the arteries can be inserted.

There are two newer ways of evaluating the vessels that are accurate and less invasive than angiography. A CT scan can evaluate the lower extremities with radiocontrast dye used to highlight the inner aspect of the arteries.  MRA or medical resonance angiography is another way of getting a three-dimensional image of the arteries of the lower extremities. Either of these can be used when the patient or doctor does not want to do an invasive test.

There are several stages of PAD that help doctors decide on the severity of the disease. In fact, there are several “Fontaine stages” that identify chronic leg ischemia. In stage I, the patient is entirely asymptomatic but has blood vessel obstruction.  In stage II, the patient has mild claudication.  Stage IIA involves claudication only after walking more than 200 meters, while Stage IIB involves claudication after walking less than 200 meters.  Stage III disease involves rest pain in the feet and stage IV disease entails gangrene or tissue necrosis in the legs.

The Rutherford classification can also be done as used by the Society for Vascular Surgery. Grade O is asymptotic; grade I (category 1) is mild claudication; grade 1 (category 2) is mild claudication; grade 1 (category 3) is severe claudication.  Patients with Grade II (Category 4) disease have pain at rest, while patients with Grade III (category 5) disease involves tissue loss of the digits only. The most serious grade is grade IV (category 6), which involves major tissue loss and possible gangrene.  People with a high grade disease are said to have critical limb ischemia that can easily lead to gangrene and amputation.

TREATMENT OF PERIPHERAL VASCULAR DISEASE

The treatment of PAD depends on how serious the patient’s disease is.  The patient will first need to identify and treat those lifestyle changes that have contributed to the disease process. This means quitting smoking as continuation will only cause disease progression.  Diabetics need to manage their blood sugars and people with hypertension must maintain good blood pressure control. High cholesterol should be treated with statin drugs; antiplatelet drugs will help prevent further thrombosis.  Exercise, even in severely affected patients, will open alternate small arteries for an improvement in PAD symptoms.

Drugs and medications often used in the management of peripheral vascular disease include aspirin (an anti-platelet drug), clopidogrel (an anti-platelet drug), drugs for blood pressure and diabetes, and statin drugs, which prevent the progression of disease by decreasing the total and LDL-cholesterol.  There are no drugs as yet that have been found to reverse existing atherosclerotic lesions. Patients with symptoms may have decreased symptoms with pentoxifylline and Cilostazol; however, the use of these drugs doesn’t mean there will be a prolongation of life or a decrease in atherosclerotic cardiovascular events.

When the disease is severe, medications alone are not going to be effective in managing symptoms and complications. The mainstay of permanent treatment involves being referred for revascularization procedures by a vascular surgeon or endovascular surgeon.  Procedures have the potential to reverse the degree of stenosis so the limb can be re-perfused.

One of the most common invasive procedures for PAD is an angioplasty or PTA (percutaneous transluminal angioplasty).  It is often done on large vessels, such as the popliteal artery or a femoral artery. The downside of this treatment is that it is not always a permanent solution.  Patency rates remain relatively high for iliac artery angioplasties but they decrease as one progresses more distally. The length of the lesion plays a role in whether or not an angioplasty will be successful and patients with multiple lesions at many levels have decreased long-term success rates. PTA is sometimes used along with stent placement to keep the blood vessel open; however, this doesn’t mean that the vessel will stay open any longer than if a stent were not used.

An atherectomy involves scraping the plaque off the inside of the arterial wall. While this does improve blood flow, the procedure doesn’t work any better than an angioplasty. As an alternative, vascular surgeons will take the great saphenous vein and use it to bypass the diseased artery. This is used for patients with long lesions or multiple severe lesions along the same blood vessel. If there is no vein available, the patient can have a Gore-Tex or a PTFE graft, made from artificial materials. If the patient already has gangrene, an amputation is necessary to avoid deep tissue infections and septicemia.  In the event that a thrombosis occurs, a thrombectomy or embolectomy may be required to restore sudden losses of perfusion that threaten the survival of the limb.

KEEPING YOUR HEART HEALTHY

Even though heart disease is the number one killer out there, it does not mean that there is nothing you can do to lower your risk. While there are risk factors you can do nothing about (like your age, sex or family history), there are many things can be change, to keep your heart beating longer! WHO estimates that nearly 80% of strokes and heart attacks are preventable. So why not change some of your bad habits today and start some good ones!

EXERCISE

Just a few minutes of exercise that raises your heart rate ultimately lowers daily blood pressure and cholesterol levels. Exercise is the key to plenty of improvements in your body including a healthy heart.

AVOID OBESITY OR EXTRA WEIGHT

Extra pounds put extra stress on the heart to make sure an increased waistline has enough blood to survive. Keeping your weight within a reasonable amount helps relieve the heart and avoids exertion on its ability to maintain homeostasis. For the best healthy heart probabilities, keep your weight under control.

CUT OUT THE SMOKING

Smoking is one of the worst things for not only your heart but your entire body. Smoking decreases the lungs’ ability to remove harmful microbes and increases the chances for respiratory diseases and emphysema. Decreased lung capacity to pump enough oxygen to the blood makes it harder for your heart. To keep a healthy heart, decrease or abandon daily smoking.

FIND A RELEASE FOR STRESS

Stress is harmful to the body and soul. Decreased stress and proper rest and relaxation help your body release  tension and ultimately keeps blood pressure and heart beats at a normal rate. Stress ages us, lowers immune system efficiency and increases the chances of cardiovascular disease. Keep a healthy heart by exercising, relaxing, and eliminating stress from the body.

EVALUATE YOUR LIFESTYLE

Evaluate your lifestyle for a healthy heart. Poor eating habits, smoking, lack of exercise, and laziness all accumulate and lead to an unhealthy lifestyle that eventually affects your heart. Keep a healthy heart by watching areas in your life that can be changed to reduce the possibility of cardiovascular disease.

CHECK YOUR DENTAL HEALTH

Gum diseases such as gingivitis and decaying teeth leach harmful bacteria into the bloodstream where they travel throughout the body to the heart and vascular system. Here they cause inflammation and even infections that can weaken the immune system and eventually even the heart muscles. Dental health is very important for overall body health.

HEART HEALTHY DIET

It is important to eat to feed the heart; the right nutrition helps to maintain a healthy body weight and reduces high cholesterol and blood pressure (hypertension) levels. Individuals with diabetes are at higher risk and need to be especially careful of nutrition and exercise as well as blood glucose levels.

  • Eat more foods high in potassium and low in sodium (salt) such as unsalted nuts, legumes, and beans. High salt intake leads to water retention which increases the pressure on the blood vessels, causing hypertension.
  • Add plenty of fiber and fresh fruits and vegetables to your diet and reduce refined foods, especially sugar, flour and fatty products.
  • Garlic and onions naturally help to thin the blood and reduce the risk of blood clots.
  • Cayenne pepper acts to strengthen the heart, arteries, and capillaries and lowers cholesterol levels.
  • Research in Pakistan shows that consuming a tablespoon of cinnamon a day helped to lower cholesterol significantly.
  • Consuming a diet rich in omega-3 oils from fish or vegetable sources has reduced the risk of developing heart disease. Good sources are cold-water fish such as salmon, mackerel, halibut or herring and flax seed.
  • Nuts such as peanuts, walnuts, almonds, and pecans are packed with heart-healthy nutrients. Studies show that eating just a handful of nuts, about 140 grams, twice a week reduces the risk of a heart attack by up to 47 percent.
  • Reduce fat for a healthy heart. Some fatty acids are good for your health, but too much fat is actually detrimental to your heart. Increased saturated fats will affect your cholesterol level while polyunsaturated fats can actually reduce the amount of cholesterol that circulates in the body. Oils such as fish oil, sunflower seed and corn are good for a healthy heart.
  • Reduce salt intake. While sodium intake is important, too much causes high blood pressure. This puts stress on your heart to pump harder. To keep a healthy heart, make sure to eat salt in moderation.

ADDITIONAL RESOURCE:

American Heart Association 

The AHA offers information for patients, caregivers, and clinical and research professionals on cardiovascular health-related diseases, including tips on management and prevention. The site provides links to community events and resources, along with updates on recent medical findings. There is information in Spanish, Vietnamese, and Chinese.

National Heart, Lung, and Blood Institute Heart Disease page

The NHLBI is part of the National Institutes of Health and offers educational material on heart health, heart defects, blood pressure, cholesterol, obesity, and preventive measures such as physical activity. You can get this information on its website or order printed brochures. The site also contains links to health assessment tools.

Health finder Heart Disease page

This U.S. government group offers basic facts about many conditions including cardiovascular disease. The website provides risk calculator tips on how to help keep yourself healthy, as well as heart health news stories.

U.S. Centers for Disease Control and Prevention Heart Disease page

The CDC, best known for its work in the control of communicable diseases, also has information on heart health. You can find facts and statistics concerning heart disease, signs and symptoms, and risk factors, as well as preventive measures.

Society for Vascular Surgery

A professional organization for vascular surgeons, the SVS has pages on its website containing detailed descriptions of cardiovascular conditions, tests, and treatments, as well as images of various conditions, including varicose veins.

Heart Healthy Women

A collaborative project of three heart-focused organizations — the National Coalition for Women With Heart Disease, the Cardiovascular Research Foundation, and the Office on Women’s Health of the Department of Health and Human Services — offers consumer information and funds research on heart and blood vessel diseases that affect women.

Cardiosmart

A service of the American College of Cardiology Foundation, this website offers the latest cardiovascular health news, online videos on a variety of topics, and a blood pressure health tracker.


Also published on Medium.