What are your risks?

Heart Disease and Stroke in Women "Preventing the First Attack”

What Causes a Heart Attack or Stroke?

• Over 90% of heart attacks and strokes are due to an inflammatory disease within the walls of arteries supplying blood to the vital organs of the body.
• This disease is called atherosclerosis or ‘hardening of the artery’. Atherosclerosis occurs when there is inflammation in the wall of an artery. LDL or ‘bad’ cholesterol is deposited within the inflamed area. The body’s defense mechanisms attempt to reverse the process. However, during the healing process LDL cholesterol continues to be deposited and eventually a fibrin cap is formed to cover the inflamed areas resulting in a cholesterol plaque.
• When there is a rupture of the thin capsule on the surface of the plaque, a significant and sudden event occurs: a blood clot is formed causing a potential blockage of the blood flow and oxygen supply.
• When this occurs in the coronary arteries of the heart, the result is a heart attack. When it occurs in the carotid arteries supplying the brain a stroke occurs. The size and location of the clot determines the severity of the attack, including death.

What is the Role of Cholesterol?

• Cholesterol is an essential building block for the normal metabolism of the body.
• Cholesterol is a lipid (fat). The liver produces 90% of the body’s cholesterol (usually during sleep);
  only 10% comes from food.
• Problem: Lipids cannot circulate alone in the blood stream (fat and water do not mix). They require a transport system.
• Solution: ‘Water-soluble’ proteins called lipoproteins transport cholesterol in the blood. Think of ‘dump trucks’ designed to carry specific types of cholesterol. The amount of these lipoprotein ‘dump trucks’ determines how much cholesterol can be transported.
• There are three main types of lipoproteins that transport cholesterol:
• HDL – high-density lipoprotein. Referred to as “good” cholesterol, because it removescholesterol from arterial plaque and transports it back to the liver to be metabolized.
• LDL – low-density lipoprotein.  Referred to as “bad” cholesterol, because it deposits cholesterol into the inflamed plaque of the artery wall.
• VLDL - very low-density lipoprotein.  This lipoprotein is directly related to the level of triglycerides.
• Total cholesterol is the sum of all three types of lipoproteins.  Measuring these and the triglyceride level produces a lipid profile. The ratio is the total cholesterol divided by the HDL level.
• Women are frequently told that their cholesterol and “ratio” are normal. Or, if abnormal, their ‘good’ cholesterol is ‘OK’.  The problem with this message is the fact that 50% of women who suffer their first heart attack or stroke have ‘normal’ cholesterol levels, according to the American Heart Association criteria.

What is the Role of CRP-HS?

• CRP-HS (C-Reactive Protein - Highly Sensitive) is a normal protein produced in the liver and   circulates in the blood stream. It rises and falls in the presence or absence of inflammation occurring somewhere in the body, such as infections, inflammatory diseases (e.g. rheumatoid arthritis), cancers, diabetes, hypertension and Alzheimer’s disease. It remains elevated as long as the inflammation is present, including the walls of arteries.
• Environmental factors such as smoking, poor diet, lack of exercise and obesity also leads to increased CRP-HS levels.  Whereas, avoiding tobacco, eating less saturated fat, and exercising 5 times a week can reduce CRP-HS levels.
• Many studies have shown that this simple blood test is the most sensitive predictor of a future heart attack or stroke, even more so than the cholesterol level.
• Jupiter Study.  This study confirmed the important role of CRP-HS.
• Released in November 2008, it included nearly 18,000 apparently healthy patients with normal cholesterol numbers, but had elevated levels of CRP-HS.
• Patients who had received a statin (cholesterol lowering and anti-inflammatory medication) for 2 years had 50% fewer heart attacks and strokes than the placebo group.
• Study explains why cholesterol levels are “normal” in 50% of women who experience a heart attack.
• Strongly suggests that when CRP-HS levels remain elevated, despite lifestyle changes (discussed below), a statin medication is indicated.

How is atherosclerotic plaque detected?

• Atherosclerotic plaque is a dynamic inflammatory process with cholesterol being deposited in the artery wall by the LDL lipoproteins and removed by the HDL lipoproteins. During this active phase the plaque is soft and subject to rupture. During the healing phase the soft plaque becomes hard or calcified.
• Calcified plaque: Detected by X-Ray, such as a CT-Scan of the heart and referred to as ‘hardening of the arteries’. However, CT-Scans do NOT detect the presence of any soft plaque.
• Soft plaque: Detected with vascular ultrasound. Vascular (Doppler) Ultrasound is a simple, non-invasive, safe and very accurate method for detecting both soft and calcified plaque in arteries. It is used for the carotid arteries in the neck (stroke risk), abdomen (aneurysm risk) and femoral arteries (peripheral vascular risk). Note: Coronary artery ultrasound requires the invasive insertion of a special ultrasound catheter in the femoral (thigh) artery and is not recommended as a screening test.

What determines your risk of heart attack or stroke?

• Heredity. Family history is an important indicator of your future risks, especially if your father had a heart attack before the age of 45 or your mother before the age of 55.
• Personal.  Factors that contribute to an elevated LDL, an elevated CRP-HS, and the amount of atherosclerotic plaque within your arteries (determined by vascular ultrasound) include:
• Aging, existing heart disease, diabetes, high blood pressure, smoking, metabolic syndrome, obesity, stress, excessive alcohol, sedentary lifestyle, and poor nutrition. 
• All risk factors, except age, can be reduced with lifestyle changes and proper medical care.
• Estrogen deficiency (menopause) and low thyroid function will increase cholesterol levels.
• Atherosclerotic plaque in your arteries.

How is the Disease Treated?

• Goal: Prevent or reverse atherosclerotic plaque.
• Current research has demonstrated that the future risk of a heart attack appears to be significantly lower when the LDL is reduced to the levels of healthy newborns and infants (30–70mg).
• Our recommended target goals of medical treatment is as follows:
• HDL "Good" Cholesterol>60 mg
• LDL "Bad" Cholesterol<60 mg
• Triglycerides<60 mg
• CRP-HS<1.0

Reducing Your Risks

• The good news is there is overwhelming medical research that atherosclerosis is a dynamic inflammatory metabolic disorder that can be stabilized and even reversed. Studies have clearly demonstrated that by not smoking, controlling elevated blood pressure and blood sugar levels (diabetes), maintaining a normal weight with balanced nutrition, reducing stress factors and engaging in an aerobic exercise program (five days a week) can significantly reduce LDL and CRP-HS, thereby reducing your risk of atherosclerosis.
• In many patients modification of these lifestyle factors may not bring the levels of LDL and CRP-HS down within the goal or target range (listed above). It may be necessary to add medication such as statins to achieve your goal. Statins are chemicals that inhibit the liver’s production of cholesterol.  Statins also reduces the inflammation in the arteries, decreases plaque formation, stabilizes the fibrin cap and lowers the risk of plaque rupture.  Result: Plaque in the arteries can actually be reversed. The Jupiter study showed that when statins are used to reduce elevated CRP-HS levels, the incidence of heart attack and stroke is reduced by 50%.
• ‘Breaking News’: To date 28 patients treated under the Gunn Towbin Center Heart Healthy WOW Program and have had significant reduction or complete reversal of their carotid artery plaque. These are patients who had been previously diagnosed with carotid artery plaque. WOW!

How to Assess Your Risk for Developing Heart Disease or Stroke

• The goal in determining your risk is to diagnose the actual presence of atherosclerosis within the arteries of your body, especially your brain, heart, abdomen and legs.
• Our Wellness Overview for Women program or ‘WOW’ Analysis includes understanding your inherited genetic makeup (family history) as well as determining your personal lifestyle, medical history, physical examination, body fat composition, laboratory testing, carotid artery ultrasound (determines the actual presence of any atherosclerotic plaque in the carotid arteries in the neck), and EKG. Additional testing may include a 64-Slice CT scan of the heart.  
• Initial screening tests include:
• Family History
• Personal Medical History
• Complete Physical Examination
• Current Status of: Smoking, Alcohol Intake, Physical Activity, Medications
• Blood Pressure
• Pulse (to detect any irregularity of the heart rate)
• Resting EKG
• Body Mass Index (BMI)
• BodyStat Bioelectrical Impedance Analysis (BIA) of fat and lean body mass composition
• Waist / Hip Circumference Ratio
•  Laboratory Testing:
• Fasting Lipoprotein Profile (Total cholesterol, HDL, LDL, VLDL, Triglycerides)
• Cardiovascular Risk Markers (CRP-HS)
• Metabolic Profile for Diabetes, Liver, Kidney, Bone and Electrolytes
• Thyroid Function
• Complete Blood Count (CBC)
• Carotid Artery Ultrasound Screening for atherosclerosis and Stroke Risk
• Echo and Stress Echocardiograms, when indicated
• Holter Monitoring for evaluation of irregular heart beat, when indicated

Initial screening tests should be performed at the age of 18 and be repeated at least every two to five years, depending on age and test results. By implementing lifestyle changes and indicated medical treatments now available, the future risk of coronary artery disease and stroke due to atherosclerosis can be significantly reduced and probably prevented.

Learn more about your health and opportunities for prevention of this disease by enrolling in the
WOW Program at the Gunn Towbin Center of Gynecology.

References:

www.nhlbi.nih.gov/health/public/heart/index.htm
www.americanheart.org/presenter.jhtml?identifier=4704
www.nhlbi.nih.gov/guidelines/obesity/bmi_tbl.pdf
New England J. of Medicine: C-Reactive Protein Levels and Outcomes after Statin Therapy, Paul M Ridker, M.D. et al., Vol. 352:20-28, January 6, 2005
New England J. of Medicine: Statin Therapy, LDL Cholesterol, C-Reactive Protein, and Coronary Artery Disease, Steven E. Nissen, M.D. et al. Vol. 352: 29-38, January 6, 2005
J. Atherosclerosis: CAFES-CAVE Study, Belcaro et al. Vol. 156:379-387, 2001.
Amer. J. of Cardiology: Effect of Intensive Lipid Lowering on Progression of Coronary Atherosclerosis, the REVERSAL Trial, Steven E. Nissen, M.D., Vol. 96:61-68, Aug. 22, 2005
Jupiter Study: http://www.astrazeneca.com/pressrelease/5385.aspx

Revised: 11.24.08