Antiphospholipid Antibody Syndrome also known as APL, APLA, APS & Hughes Syndrome
Primary APLA: no underlying systemic disorder
Secondary APLA: presence of an underlying disease, most commonly SLE.
Antiphospholipid Antibody Syndrome is a disease which involves the immune system. Common to autoimmune diseases, auto-antibodies are proteins produced by the body to attack itself, rather than invading viruses and bacteria.
Normally antibodies are good and they help fight germs or viral infections from outside, however, occasionally the immune system makes the wrong kind – a type that acts against the body itself. These unusual auto-antibodies in APLA are detected by a blood test and when they are present make a person more likely to get specific problems.
APLA doesn’t make you feel unwell or stop your immune system from working to fight disease. You can’t catch it or give it to someone else and it certainly isn’t a terminal disease or anything like that. Many people go throughout life without even knowing their body makes these antibodies. Its just that there’s more chance of certain problems. APLA is associated with systemic lupus erythematosis (SLE) and other autoimmune diseases.
It is only recently that these antibodies were discovered and their significance understood, so the information available is somewhat limited, but more research is being carried out on this all the time. We still don’t know exactly how the antibodies bring about the effects described below, although we have some good ideas.
Patients with antiphospholipid antibody syndrome can develop abnormal symptoms while having antiphospholipid antibodies detectable in the blood. The antiphospholipid antibody syndrome involves abnormal clotting. Antiphospholipid antibody syndrome is also referred to as Hughes syndrome in honor of the doctor who first described it.
It is important to note that antiphospholipid antibodies can also be found in the blood of individuals without any disease process. In fact, antiphospholipid antibodies have been reported in up to 2 percent of the normal population. Harmless antiphospholipid antibodies can be detected in the blood for a brief period occasionally in association with a wide variety of conditions, including bacterial, viral (hepatitis, HIV), and parasite (malaria) infections. Certain drugs can cause antiphospholipid antibodies to be produced in the blood, including antibiotics, cocaine, hydralazine, procainamide, and quinine.
Neverthelss, the antiphospholipid antibody (a protein) is not considered a normal blood protein and has been found in patients with a number of illnesses. These illnesses include abnormal clotting (thrombosis) of arteries and/or veins, phlebitis, premature miscarriages (spontaneous abortions), abnormally low blood platelet counts (thrombocytopenia), slowly progressing memory problems/dementia, strokes, optic changes, Addison’s disease, and skin rashes (purplish mottling discoloration of the skin-livedo reticularis), migraine headaches, a rare form of inflammation of the nervous tissue of the brain or spinal cord, called transverse myelitis and a form of “atypical multiple sclerosis”. Antiphospholipid antibodies have been detected in over half of patients with the immune disease systemic lupus erythematosus.
How common is APLA?
The auto-antibodies are found in about 2% of women. Not all of these will have had one of the associated problems, so they do not necessarily have the disease. The levels of antibody can go up and down, and even disappear, so to definitely say someone has APLA, the blood tests need to repeated at least 8 weeks from the first and still be positive. The decision on treatment at a particular time (such as pregnancy) depends upon the levels and what previous medical problems there were. APLA may run in families, although not all members are necessarily affected. It isn’t exactly clear to what extent this happens, but it is certainly suggestive, for example, if several people have had a series of miscarriages or thromboses.
Who Gets Apla?
About 30-50% of patients with SLE (lupus) will have APLA. These antibodies can also be found in patients with other autoimmune diseases. Patients without lupus or other autoimmune disease can have symptomatic APLA (“Primary APLA syndrome”). Children will often develop transient APLA after viral infections. These often come to clinical attention during pre-operative evaluation for tonsillectomy. Up to 30% of patients with HIV infection will also develop APLA.
The infection associated APLA are not associated with thrombosis. Medication may also induce APLA. Chlorpromazine is the most common but APLA have also been associated with procainamide, dilantin and quinidine. In screening studies of blood donors, up to 8% of normal people will have APLA. However the APLA in these people are usually low titer and most often occur in young women.
Strokes: APLA is found 10-46% of young patients with strokes and in 10% of stroke patients overall. Stroke patients with APLA tend to be younger (42 years vs 62 years). These patient also have a recurrence rate of 6-30%/year and a mortality rate of 10%/year. Certain groups of patients appear to be at even higher recurrence rates. These would include SLE patients with APLA and patients with Sneddon’s syndrome (described below).
Early-Onset Dementia is becoming a more recognized and feared feature of APLA. Thirty-five patients with APLA and dementia are followed at OHSU and dozens are reported in the literature. The dementia is multi-infarct in nature and occurs often without a history of major stroke episodes. APLA-related dementia on the average occurs a decade earlier (52 years) than non-APLA dementia. Sneddon’s syndrome is a combination of livedo reticularis and cerebral ischemic events. It is a form of APLA that often results in major morbidity and mortality. The skin involvement in Sneddon’s may be severe enough to result in ulceration. Patients with Sneddon’s syndrome seem also to have a higher incidence of thrombocytopenia.
Venous Thrombosis was the first described manifestation of APLA and still one of the most clinically predominant. Overall, retrospective studies show that 31% of patient with APLA have venous thrombosis. Patients with lupus and SLE have a thrombosis rate of 42% while those with infections and drug-induced APLA the rate is less then five percent. Patients with APLA are over represented in young patients with deep vein thrombosis. Prospective studies have demonstrated a relative risk for venous thrombosis of 5.3 for patients with IgG ACLA. Patients with APLA venous thrombosis can be difficult to treat. Many patients (?1/3-1/2) are resistant to low intensity warfarin (INR 2.0-3.0) and need to be treated with high intensity warfarin therapy (INR= 2.5-3.5) or chronic subcutaneous heparin. These patients have high rates of recurrent thrombosis if anticoagulation is stopped with recurrence rates of 20-50%/year of repeat thromboses have been reported if therapy is stopped. Rarely patients may be refractory to warfarin and will need to be on long-term heparin therapy.
Arterial Disease: APLA are increased in young patients with myocardial infarctions and strokes. They are also found in higher proportion in patients with peripheral vascular disease and may predict graft failure. Prospective studies have demonstrated that patients have APLA have higher rates of saphenous by-pass vein occlusion and re-occlusion of PTCA. One confounding factor is that anticardiolipin antibodies will cross-react with oxidized-LDL. Since raised levels of ox-LDL are found in patients with atherosclerosis the anticardiolipin antibodies sometimes found in these patients may be an epiphenomenon of their atherosclerosis.
Neurological Disease: A variety of neurological disorders have been associated with APLA. The underlying cause of these symptoms appear to be thrombosis. Some patients have large vessel disease while many patient have small vessel involvement. Patients with APLA often will have multiple MRI abnormalities consistent with small white matter infarcts. The neurological diseases include:
Ocular Events: Amaurosis fugax, retinal artery and vein thrombosis have been reported in multiple case reports to be a part of the APLA syndrome.
Other: APLA are found in as many as 50% of patients who get migraines. As will be discussed below, patients may have encephalopathy as part of severe APLA.
Fetal Loss is seen in 38% of SLE patients with APLA. The incidence of fetal loss in non-SLE APLA is controversial. When women who have recurrent fetal loss (>3) are screened the incidence of APLA is 30%. The pathophysiology is thought to be due to micro-thrombosis in the placenta.
Thrombocytopenia: Certain APLA will react with activated platelets leading to thrombocytopenia. Since it is only activated platelets that expose the proper epitopes, often it is the patients with the thrombotic manifestations of APLA who will also get the thrombocytopenia. The treatment of these patients is clinically challenging since the thrombocytopenia often occurs in patients who are anticoagulated for thrombosis. Danazol appears to be uniquely effective for these patients.
Hypoprothrombinemia Patients with APLA (almost always ones with lupus inhibitors) may have an elevated prothrombin time (PT) for 2 reasons. One is that the APLA are present in such high titer that will also interfere with the PT test. The other is that 10% of patients with lupus inhibitors will develop non-neutralizing antibodies to prothrombin.
This leads to increased clearance of prothrombin from the plasma and hypoprothrombinemia. Since patients with hypoprothrombinemia can present with hemorrhagic complications, it is important to check for this when one is faced with an APLA patient with an elevated PT. This can be done by doing a 50:50 mix on the PT and measuring the plasma level of prothrombin. Plasma infusions and steroids are effective in raising the prothrombin levels in patients with prothrombin antibodies.
Other Associated Diseases: Patients with APLA may have an assortment of skin findings included livedo, Raynaud’s phenomena, ulcers, and superficial thrombophlebitis. Up to 26% of patients with SLE and APLA have cardiac valve vegetations and mitral regurgitation. Rarely patient have had valve destruction so extensive as to have required valve replacement. Myocardial dysfunction is seen in 5% of SLE-APLA patients. Primary pulmonary hypertension has been associated with APLA. Ten percent of patients with chronic thromboembolic pulmonary hypertension have APLA. Adrenal insufficiency from microvascular thrombosis has been seen also in APLA patients.
Rarely patients with APLA can present with fulminate multiorgan system failure. This is cause by widespread microthrombi in multiple vascular fields. These patient will present with renal failure, encephalopathy, ARDS (often with pulmonary hemorrhage), cardiac failure, dramatic livido reticularis, and thrombocytopenia. Many of these patients have pre-existing autoimmune disorders. It appears that the best therapy for these patients is aggressive immunosuppression with plasmapheresis then (perhaps) IV cyclophosphamide monthly. Early recognition of this syndrome can lead to quick therapy and resolution of the multiorgan system failure.
How is APS treated?
Each manifestation of the antiphospholipid antibody syndrome, and each individual patient with the condition, is treated uniquely. The discovery of the syndrome has made treatment decision much more precise. Many organs can be affected by APS/Hughes syndrome. Simple blood testing can point to much more appropriate treatment with anticoagulants where sticky blood is felt to be the cause. The three drugs most commonly used are aspirin, warfarin or heparin. Aspirin has long been known to make the blood platelets less ‘sticky’. In turn this has improved the outcome for people who have thrombosis. Low dose aspirin is now used throughout the world in patients who have suffered heart attacks or strokes.
Aspirin is clearly beneficial in milder cases (comparative trials are still going on). In recurrent miscarriage, the addition of aspirin alone has improved the success rate dramatically. In our combined lupus pregnancy clinic within St Thomas’ Hospital in London, for example, the success rate for pregnancy in patients with the syndrome has risen over the past five years from 19% to over 70% successful pregnancies. Whilst there are certainly many factors in this success, the addition of aspirin has been crucial
Heparin is less widely used, being administered by injection. It does have two potential advantages over warfarin: Its anticoagulant effects can easily be reversed and is therefore useful around the time of an operation. It can be used throughout pregnancy whereby warfarin cannot always be used.
Warfarin is an effective treatment for the Hughes’ Syndrome. It is the standard treatment for thrombosis and is relatively free from side effects, provided the blood thickness is regularly tested. In many patients it dramatically improves symptoms.
It is now fifteen years since the clinical description of the syndrome. In that time, it has become an ‘established’ medical condition, meriting articles, textbook chapters, research, conferences and so on. More important, it has provided, by means of simple blood tests, a whole new approach to treatment. In those patients in whom Hughes’ Syndrome is diagnosed and treated early, the outlook has dramatically changed for the better. In main, the treatment for Hughes’ Syndrome (Antiphospholipid Syndrome) is to thin the blood i.e. with aspirin, warfarin or heparin.
Difficulties in Monitoring Anticoagulation
Since APLA react with phospholipid both the aPTT and the protime can be affected. If one uses standard heparin to anticoagulate patients with APLA one needs to monitor with heparin levels (0.35 – 0.70 anti-Xa units 6 hours after the shot). The predictable dosing and anticoagulant effect is one advantage of using LMW heparin acutely for thrombosis in APLA patients. One should measure LMW heparin levels in patients with APLA for long term therapy (0.7 – 1.0 anti-Xa units) or those patients with renal failure.
Often patients with APLA will have minor elevations of their protime. Those few patients with elevated protimes due to the inhibitor can be very difficult to manage with warfarin. One option is to perform prothrombin and proconvertin times (“P&P”) to follow anticoagulation. The P&P is less dependent on phospholipids and one can monitor therapy. The other option is to use long-term heparin.
One difficult issue it what to do with the patient with APLA but no thrombotic manifestations. Although some of these patients are at risk, especially those with SLE, many will never develop thrombosis. The current recommendation would be to do very careful search for thrombosis. This would include a brain MRI in patients with SLE and in patients with any neurological symptom. If this work-up is negative then the patient is followed very closely.
Treatment to Prevent Thrombosis
Treatment of patients with aPL Antibody is controversial. The problem seems to be mainly an abnormal hypercoagulable state that predisposes to thrombosis of arteries rather than true vasculitis. Asymptomatic patient with Antiphospholipid Ab: reduce risk factors for vascular disease. Those with high titers: avoid oral contraceptive. Life style change: maintain ideal weight, cholesterol level and physical activity. Control blood pressure, avoid smoking.
Tests For Antiphospholipid Antibodies (Apla)
There are two main groups of tests for APLA’s: testing for presence of antibodies to cardiolipin and the coagulation based tests for APLA.
Coagulation Based Tests: As you recall, APLA react with phospholipid. Phospholipids are used in coagulation tests to provide a surface for the coagulation reaction to occur. The basis for all these tests is that if there are antibodies binding to the phospholipid, it will interfere with the coagulation reaction and prolong the clotting time.
Platelet Neutralization Test: This test takes a reaction that is prolonged by plasma which does not correct with a 50:50 mix and adds extracts of platelet. If it corrects to normal this is very specific for APLA.
Hexagonal Phase Phospholipid: Same principles as the platelet neutralization test but used hexagonal phase phospholipids. This is the only valid test for lupus inhibitors when patients are on anticoagulants.
Anticardiolipin Antibodies: This is an ELISA test for antibodies to cardiolipin. Therefore, unlike the coagulation based tests, it can be performed on plasma which has been anticoagulated.
Unfortunately there is no one test that can screen a patient for APLA. One must do the whole panel on patients suspected with APLA. A good screen is to perform the hexagonal phospholipid assay and ACLA assay. If these are negative and one is very suspicious then one order further tests. These would include 1) Anticardiolipin antibodies, 2) Kaolin clotting time 3) dRVVT 4)”Lupus Inhibitor Screen” (different aPTT reagents).
One of the largest obstacles to emergency treatment is that many people don’t
even know it when they are having a stroke.
The very word “stroke” indicates that no one is ever prepared for this sudden, often catastrophic event. Stroke survivors and their families can find workable solutions to most difficult situations by approaching every problem with patience, ingenuity, perseverance and creativity.
- 10 percent of stroke survivors recover almost completely
- 25 percent recover with minor impairments
- 40 percent experience moderate to severe impairments requiring special care
- 10 percent require care in a nursing home or other long-term care facility
- 15 percent die shortly after the stroke.
A stroke or “brain attack” occurs when a blood clot blocks a blood vessel or artery, or when a blood vessel breaks, interrupting blood flow to an area of the brain. When a stroke occurs, it kills brain cells in the immediate area. Doctors call this area of dead cells an infarct. These cells usually die within minutes to a few hours after the stroke starts.
When brain cells in the infarct die, they release chemicals that set off a chain reaction called the “ischemic cascade.” This chain reaction endangers brain cells in a larger, surrounding area of brain tissue for which the blood supply is compromised but not completely cut off. Without prompt medical treatment this larger area of brain cells, called the penumbra, will also die. Given the rapid pace of the ischemic cascade, the “window of opportunity” for interventional treatment is about six hours. Beyond this window, reestablishment of blood flow and administration of neuroprotective agents may fail to help and can potentially cause further damage.
When brain cells die, control of abilities which that area of the brain once controlled are lost. This includes functions such as speech, movement, and memory. The specific abilities lost or affected depend on where in the brain the stroke occurs and on the size of the stroke (i.e., the extent of brain cell death). For example, someone who has a small stroke may experience only minor effects such as weakness of an arm or leg. On the other hand, someone who has a larger stroke may be left paralyzed on one side or lose his/her ability to express and process language. Some people recover completely from less serious strokes, while other individuals lose their lives to very severe strokes.
Stroke is a “Brain Attack”. Stroke happens in the brain rather than the heart. Stroke is an emergency! “Time is brain”
The symptoms of stroke should have the same alarming significance in identifying a brain attack that acute chest pain has in identifying a heart attack.
The public misperception that nothing can be done about stroke has prevailed for too long. With the use of the term “brain attack,” we give stroke a definitive name and a unique face for the first time. Of all the images we use to identify stroke, “brain attack” is the most descriptive, realistic and powerful call to action. The appropriate response to a brain attack is emergency action, both by the person it strikes and the medical community.Brain Attack Means Medical Emergency
Educating the public to treat stroke as a brain attack and to seek emergency treatment is crucial because every minute lost, from the onset of symptoms to the time of emergency contact, cuts into the limited window of opportunity for intervention. The majority of patients don’t report to the emergency room until more than 24 hours after the onset of stroke symptoms. The longer the delay in patient presentation, the more damage a stroke can do and the less recovery can be achieved.
The Five Most Common Stroke Symptoms Include:
- Sudden numbness or weakness of face, arm or leg, especially on one side of the body
- Sudden confusion, trouble speaking or understanding
- Sudden trouble seeing in one or both eyes
- Sudden trouble walking, dizziness, loss of balance or coordination
- Sudden severe headache with no known cause
Call 911 if you see or have any of these symptoms. Treatment can be more effective if given quickly. Every minute counts!
Other Important but less Common Stroke Symptoms Include:
- Sudden nausea, fever and vomiting distinguished from a viral illness by the speed of onset (minutes or hours vs. several days)
- Brief loss of consciousness or period of decreased consciousness (fainting, confusion, convulsions or coma)
Our notions about stroke and its treatment are being revolutionized. This truly is the “Decade of the Brain” for stroke. The new stroke interventionalists (neurologists, neuroradiologists, emergency medicine physicians and their colleagues) are dedicated to emergent stroke treatment. Time to presentation is a monumental obstacle. Recent studies have found that 42 percent of stroke patients wait as long as 24 hours before presenting, with 13 hours as the average. One study reported that the main factors which cause patients to present earlier are:
Recognizing stroke symptoms
Realizing that the symptoms require emergency treatment Current statistics indicate that there are nearly 4 million people in the United States who have survived a stroke and are living with the after-effects. These numbers do not reflect the scope of the problem and do not count the millions of husbands, wives and children who live with and care for stroke survivors and who are, because of their own altered lifestyle, greatly affected by stroke.
There’s still so much we don’t know about how the brain compensates for the damage caused by stroke. Some brain cells may be only temporarily damaged, not killed, and may resume functioning. In some cases, the brain can reorganize its own functioning. Sometimes, a region of the brain “takes over” for a region damaged by the stroke. Stroke survivors sometimes experience remarkable and unanticipated recoveries that can’t be explained.
General recovery guidelines show:
Rehabilitation actually starts in the hospital as soon as possible after the stroke. In patients who are stable, rehabilitation may begin within two days after the stroke has occurred, and should be continued as necessary after release from the hospital.
Depending on the severity of the stroke, rehabilitation options include:
- A rehabilitation unit in the hospital
- A subacute care unit
- A rehabilitation hospital
- Home therapy
- Home with outpatient therapy
- A long-term care facility that provides therapy and skilled nursing care
The goal in rehabilitation is to improve function so that the stroke survivor can become as independent as possible. This must be accomplished in a way that preserves dignity and motivates the survivor to relearn basic skills that the stroke may have taken away – skills like eating, dressing and walking.
The ability to define the world and our place in it distinguishes our humanity. Stroke forever alters this world-making capacity. The stroke patient’s world, once comprehensible and manageable, is transformed into a confusing, intimidating and hostile environment. The skills of intellect, sensation, perception and movement, which are honed over the course of a lifetime and which so characterize our humanity are the very abilities most compromised by stroke. Stroke can rob people of the most basic methods of interacting with the world.
The specific abilities that will be lost or affected by stroke depend on the extent of the brain damage and most importantly where in the brain the stroke occurred. The brain is an incredibly complex organ, and each area within the brain has responsibility for a particular function or ability. The brain is divided into four primary parts: the right hemisphere (or half), the left hemisphere, the cerebellum and the brain stem.
The right hemisphere of the brain controls the movement of the left side of the body. It also controls analytical and perceptual tasks, such as judging distance, size, speed, or position and seeing how parts are connected to wholes.
A stroke in the right hemisphere often causes paralysis in the left side of the body. This is known as left hemiplegia. Survivors of right-hemisphere strokes may also have problems with their spatial and perceptual abilities. This may cause them to misjudge distances (leading to a fall) or be unable to guide their hands to pick up an object, button a shirt or tie their shoes. They may even be unable to tell right-side up from upside-down when trying to read.
Along with their impaired ability to judge spatial relationships, survivors of right-hemisphere strokes often have judgment difficulties that show up in their behavioral styles. These patients often develop an impulsive style unaware of their impairments and certain of their ability to perform the same tasks as before the stroke. This behavioral style can be extremely dangerous. It may lead the left hemiplegic stroke survivor to try to walk without aid. Or it may lead the survivor with spatial and perceptual impairments to try to drive a car.
Survivors of right-hemisphere strokes may also experience left-sided neglect. Stemming from visual field impairments, left-sided neglect causes the survivor of a right-hemisphere stroke to “forget” or “ignore” objects or people on their left side.
Finally, some survivors of right-hemisphere strokes will experience problems with short-term memory. Although they may be able to recount a visit to the seashore that took place 30 years ago, they may be unable to remember what they ate for breakfast that morning.
The left hemisphere of the brain controls the movement of the right side of the body. It also controls speech and language abilities for most people. A left-hemisphere stroke often causes paralysis of the right side of the body. This is known as right hemiplegia.
Someone who has had a left-hemisphere stroke may also develop aphasia. Aphasia is a catch-all term used to describe a wide range of speech and language problems. These problems can be highly specific, affecting only one component of the patient’s ability to communicate, such as the ability to move their speech-related muscles to talk properly. The same patient may be completely unimpaired when it comes to writing, reading or understanding speech.
In contrast to survivors of right-hemisphere stroke, patients who have had a left-hemisphere stroke often develop a slow and cautious behavioral style. They may need frequent instruction and feedback to complete tasks.
Finally, patients with left-hemisphere stroke may develop memory problems similar to those of right-hemisphere stroke survivors. These problems can include shortened retention spans, difficulty in learning new information and problems in conceptualizing and generalizing.
The cerebellum controls many of our reflexes and much of our balance and coordination. A stroke that takes place in the cerebellum can cause abnormal reflexes of the head and torso, coordination and balance problems, dizziness, nausea and vomiting.
Brain Stem Stroke
Strokes that occur in the brain stem are especially devastating. The brain stem is the area of the brain that controls all of our involuntary, “life-support” functions, such as breathing rate, blood pressure and heartbeat. The brain stem also controls abilities such as eye movements, hearing, speech and swallowing. Since impulses generated in the brain’s hemispheres must travel through the brain stem on their way to the arms and legs, patients with a brain stem stroke may also develop paralysis in one or both sides of the body.
Stroke Risk Factors & Their Impact
Stroke is one of the most preventable of all life-threatening health problems. The two primary types of risk factors for stroke are those that are controllable and those that are not. It’s important to remember that having one or more uncontrollable stroke risk factors DOES NOT MAKE A PERSON FATED TO HAVE A STROKE. With proper attention to controllable stroke risk factors, the impact of uncontrollable factors can be greatly reduced.
Uncontrollable Stroke Risk Factors Include:
Age: The chances of having a stroke go up with age. Two-thirds of all strokes happen to people over age 65. Stroke risk doubles with each decade past age 55.
Gender: Males have a slightly higher stroke risk than females. But, because women in the United States live longer than men, more stroke survivors over age 65 are women.
Race: African-Americans have a higher stroke risk than most other racial groups.
Family history of stroke or TIA. Risk is higher for people with a family history of stroke or TIA. Also, people who have already had a stroke or TIA are at risk for having another. After suffering a stroke, men have a 42 percent chance of recurrent stroke within five years, and women have a 24 percent chance of having another stroke. TIAs are also strong predictors of stroke because 35 percent of those who experience TIAs have a stroke within five years.
Personal history of diabetes
People with diabetes have a higher stroke risk. This may be due to circulation problems that diabetes can cause. In addition, brain damage may be more severe and extensive if blood sugar is high when a stroke happens. Treating diabetes may delay the onset of complications that increase stroke risk. However, even if diabetics are on medication and have blood sugar under control, they may still have an increased stroke risk simply because they have diabetes.
Controllable Stroke Risk Factors
Treatable Medical Disorders that Increase Stroke Risk Include: High blood pressure
Having high blood pressure, or hypertension, increases stroke risk four to six times. It is the single most important controllable stroke risk factor. High blood pressure is often called “the silent killer” because people can have it a nd not realize it, since it often has no symptoms. Hypertension is a common condition, affecting approximately 50 million Americans, or one-third of the adult population. Blood pressure is high if it is consistently more than 140/90. Between 40 and 90 percent of all stroke patients had high blood pressure before their stroke. Hypertension puts stress on blood vessel walls and can lead to strokes from blood clots or hemorrhage.
The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
Atrial fibrillation and other heart diseases
Heart disease such as atrial fibrillation increases stroke risk up to six times. About 15 percent of all people who have a stroke have a heart disease called atrial fibrillation, or AF, which affects more than 1 million Americans. AF is caused when the atria (the two upper chambers of the heart) beat rapidly and unpredictably, producing an irregular heartbeat. AF raises stroke risk because it allows blood to pool in the heart. When blood pools, it tends to form clots which can then be carried to the brain, causing a stroke.
Normally, all four chambers of the heart beat in the same rhythm somewhere between 60 and 100 times every minute. In someone who has AF, the left atrium may beat as many as 400 times a minute. If left untreated, AF can increase stroke risk four to six times. Long-term untreated AF can also weaken the heart, leading to potential heart failure. The prevalence of AF increases with age. AF is found most often in people over age 65 and in people who have heart disease or thyroid disorders. Among people age 50 to 59, AF is linked to 6.7 percent of all strokes. By ages 80-89, AF is responsible for 36.2 percent of all strokes.
Coronary Heart Disease and High Cholesterol
High cholesterol can directly and indirectly increase stroke risk by clogging blood vessels and putting people at greater risk of coronary heart disease, another important stroke risk factor. A cholesterol level of more than 200 is considered “high.” Cholesterol is a fatty substance in the blood that our bodies make on their own, but we also get it from fat in the foods we eat. Certain foods (such as egg yolks, liver or foods fried in animal fat or tropical oils) contain cholesterol. High levels of cholesterol in the blood stream can lead to the buildup of plaque on the inside of arteries, which can clog arteries and cause heart or brain attack.
Sleep Disordered Breathing – Sleep Apnea
Sleep apnea is a major cardiovascular and stroke risk factor increasing blood pressure rates which may cause stroke or heart attack. Studies also indicate that people with sleep apnea develop dangerously low levels of oxygen in the blood while carbon dioxide levels rise, possibly causing blood clots or even strokes to occur. Diagnosing sleep apnea early may be an important stroke prevention tool. Click here for more information on Sleep Apnea and Stroke.
A stroke is an emergency…….call 911!