Dr. Seth Bilazarian - News, Information, Publications, Research
Dr. Seth Bilazarian leads Pentucket Medical's Cardiovascular Research Program.
For more information on current enrolling trials, click here.
Instructor of Medicine, Harvard Medical School
Treatment Advances for Artery Blockages [+]
By Seth Bilazarian, MD, FACC, FSCAI, RPVI
Clinical and Interventional Cardiologist
Coronary artery disease is the #1 killer of both men and women in our country, and more than 50% of Americans die as a result of problems with artery blockages. During the past decade however, we have seen tremendous advances in percutaneous coronary intervention (PCI) otherwise known as stents or angioplasty used to fix blocked arteries.
Coronary artery blockages develop for a variety of reasons.
The five most common risk factors are: high blood pressure (hypertension), high cholesterol, diabetes, cigarette smoking and a family history of heart disease. Other contributors include lack of exercise, a diet rich in fat or sugar, and being overweight.
What treatments are available for coronary artery disease?
For over a decade, physicians have been able to treat coronary artery disease and fix blockages without surgery. These catheter-based treatments use small, thin tubes placed in the groin artery and inserted into the heart. In the early 1990’s, balloon angioplasty was introduced, allowing the physician to insert small balloons that stretched the arteries and opened blockages. This, and bypass surgery (CABG or coronary artery bypass graft) were really the only options available to patients with arterial blockages.
In the mid 1990’s, stents became available. These thin, stainless steel metal coils have become very effective in helping to reduce the risk of re narrowing, or restenosis, after the procedure. About 40% of patients experience re-narrowing of the arteries within 6 months of treatment with balloon angioplasty alone. The degree of this renarrowing often necessitated repeat treatment. With the introduction of stents, the risk of renarrowing was reduced to about 30% during the 4-6month period following treatment.
In May 2003, the USA FDA approved a new innovation - a drug eluting stent.
The Cypher stent is made by Johnson & Johnson, and is coated with a drug called sirolimus. The re-narrowing risk has been shown to be as low as 8%-9% with the sirolimus-coated stent as opposed to a stent without a drug coating. A second drug eluting stent, made by Boston Scientific, will be released in early 2005, and many other manufactures are expected to bring new products to market in the coming years.
Drug eluting stents are a major innovation that has revolutionized stenting and the treatment of patients with coronary
artery disease. Like any new device or treatment, clinicians and patients need to be cautious and watchful in identifying potential problems. For example, one issue that is being watched very carefully by the medical community is the potential risk for clotting which may occur with this new drug eluting stent. However, at this point, physicians are using these stents with cautious enthusiasm in appropriate patients.
In summary, there are several important innovations that are occurring with percutaneous coronary intervention (PCI) or stenting. These new innovations are reducing the risk of recurrence and need for repeated treatments for patients and may change the evolution of future treatment options. Some patients, who might have been candidates for bypass surgery in the past, may now be able to be treated with stents given the reduced risk of renarrowing.
If you have additional questions about coronary artery disease or these treatment options, contact your doctor or cardiologist.
Atrial Fibrillation [+]
By Seth Bilazarian, MD, FACC, FSCAI, RPVI
Clinical and Interventional Cardiologist
Atrial fibrillation is a common heart condition, and in fact, is the most common type of arrhythmia disorder. Atrial fibrillation, sometimes called A Fib, affects 2 million Americans; six percent of Americans over age 65 experience it; and it is responsible for about 15% of all strokes. In this area, atrial fibrillation is the second most common cause for admission at the Merrimack Valley Hospital. Many things cause atrial fibrillation. The most common causes are hypertension (high blood pressure) as well as valvular and other cardiac disorders. Alcohol can also be a cause - in fact some have nick named atrial fibrillation the “holiday heart syndrome,” as it is sometimes associated with alcohol consumption during holiday celebrations. Atrial fibrillation can also be caused by pulmonary and thyroid conditions.
What are the symptoms of atrial fibrillation?
Patients with atrial fibrillation experience a number of symptoms including an inappropriately fast and irregular heart rate, dizziness and chest pain. If these symptoms occur, patients should seek immediate treatment in a hospital emergency room.
What kind of treatment is used for atrial fibrillation?
When a patient with atrial fibrillation comes to an emergency room, the first goal of the medical team is to slow down the patient’s heart rate and to restore a normal heart rhythm. To do this, patients usually receive a medication called Cardizem or diltiazem intravenously. The second goal of the emergency room team is to reduce the patient’s risk of blood clotting. The patient is usually given a blood thinning medication such as heparin. Patients with atrial fibrillation are then usually admitted to the hospital for observation and monitored on a telemetry unit where the nurses can closely watch the heart rates and rhythms. Some physicians may also order studies such as an echocardiogram (heart ultrasound) or thyroid function blood work to determine the cause of the atrial fibrillation. Long-term care may include continued medication for rate control and blood thinning. For many patients however, no medications or follow-up treatment is needed.
Atrial fibrillation is a very common heart disorder.
People experiencing an inappropriately fast heart rate, dizziness and chest pain should seek immediate treatment at a hospital emergency room. Under a physician’s care, there are several treatment options available, and long term treatment and prognosis for most patients is very good.
If you have questions about atrial fibrillation or other heart-related concerns, contact your primary care physician or cardiologist.
Metabolic Syndrome [+]
By Seth Bilazarian, MD, FACC, FSCAI, RPVI
Clinical and Intervential Cardiologist
What is the Metabolic Syndrome?
The Metabolic Syndrome is a collection of five problems that greatly increase a person’s risk for
stroke, heart attack and diabetes. These five characteristics are:
Hypertension (On treatment for high blood pressure
or blood pressure greater than 130 without medication)
Abnormal Blood Sugar (over 100 when fasting)
Abnormal Triglycerides (over 150 when fasting)
Low levels of HDL “good cholesterol”(less than 40 for
men and 50 for women)
Obesity with fat especially in the abdominal area (waistline
of 40 inches or more for men and 35 inches or more for
women measured across the belly)
A physician generally makes this diagnosis if three of these five problems are present.
How big a problem is it?
The Metabolic Syndrome has become increasingly common in the United States, and it’s estimated that over 50 million Americans have it. According to a national health survey, more than one in five Americans has metabolic syndrome and the number is increasing. The Metabolic Syndrome increases with age, affecting more than 40% of people in their 60s and 70s.
Who typically has Metabolic Syndrome?
According to the American Heart Association, three groups of people often have metabolic syndrome:
People with diabetes who cannot maintain a proper level of glucose (glucose intolerance)
People without diabetes who have high blood pressure and who also secrete large amounts of insulin (hyperinsulinemia) to maintain blood glucose levels
Heart attack survivors who have hyperinsulinemia without glucose intolerance
What causes the Metabolic Syndrome?
Conditions associated with the Metabolic Syndrome include the body’s inability to metabolize insulin efficiently. This problem of insulin resistance is at the heart of the problem. Contributing factors also may include physical inactivity, aging, hormonal imbalance and family history, but being overweight is the most important aspect of the problem.
Why is it important?
The Metabolic Syndrome is a strong predictor of diabetes and vascular problems like stroke and heart attack. Consistently high levels of insulin and sugar increase health risks by:
- Damage to the lining of arteries, a key step in the development of heart disease or stroke
- Changes in the kidneys' ability to remove salt, leading to high blood pressure, heart disease and stroke
- Increase in triglyceride levels, resulting in an increased risk of developing cardiovascular disease
- Increased risk of blood clot formation, which can block arteries and cause heart attacks and strokes
Slowing of insulin production, which can signal the start of type 2 diabetes
How can the risk be reduced?
Physical inactivity and excess weight are the main contributors to metabolic syndrome development, getting more exercise and losing weight reduces the complications. Your doctor may prescribe medications to manage some of the underlying problems to reduce your risk:
Lose weight --
Moderate weight loss, in the range of 5 - 10 % of body weight, can reduce your body's resistance to insulin and reduce complications.
Increased activity alone can improve insulin levels. A 30-minute walk daily can reduce weight, improved blood pressure and cholesterol and reduce the risk of developing diabetes.
Dietary changes --
Keep carbohydrates to less than 50 percent of total calories. Eat complex carbohydrates, such as whole grain bread (instead of white), brown rice (instead of white), and avoid refined sugars ( for example candy and pastry). Increase fruits and vegetables and reduce intake of red meats and poultry. Consume healthy fats such as those in canola oil, olive oil, flaxseed oil and nuts.
Limit alcohol --
Consume no more than one drink a day for women or two drinks for men.
See your doctor –
“Knowing your numbers” – blood pressure; cholesterol, blood sugar and ideal weight can be the first step
The primary goals of treatment plans include steps to reduce cardiovascular risk. Patients are encouraged to stop smoking, reduce LDL cholesterol and blood pressure and to monitor blood sugar. Diet and exercise are the best initial strategy, but medications may also be prescribed.
Most patients can reduce their risk for serious medical complications later in life through lifestyle changes alone.
Homocysteine — Folate or Folic Acid and B Vitamins Are No Longer
Recommended for Cardiovascular Risk Reduction [+]
By Seth Bilazarian, MD, FACC, FSCAI, RPVI
Homocysteine has long been recognized as an abnormality that is elevated in some patients with vascular diseases such as stroke or heart attack or venous clots. Treatment with B vitamins, especially folate, can be used to lower the level of the chemical homocysteine found in blood.
Many physicians have recommended that the homocysteine level be checked as part of a multi marker strategy to assess the risk for vascular disease. Evaluation of homocysteine in addition to cholesterol levels and glucose levels and hs-CRP can help define a patient’s overall risk. By defining the risk in patients, more intense treatments can be used for higher risk patients and lower risk patients can receive less treatments. The rationale for treatment of elevated homocysteine with folate has been recommended for several years by many cardiologists because:
- Folate definitely lowers the level of homocysteine and higher levels correlate with a greater risk of vascular disease
- Folate is inexpensive and available without a prescription
- Folate is a water-soluble vitamin and vitamin supplementation is felt to be safe, although megadoses can cause irreversible peripheral neuropathy
- Many patients prefer a natural or non-pharmaceutical approach to prevention
- Cardiovascular diseases such as stroke and heart attack causes significant disability and death for patients so physicians and patients are often highly motivated to reduce risk
Because of these reasons many physicians, including me, have recommended a vitamin supplementation approach. This strategy has changed thanks to important new clinical trial date. In the New England Journal of Medicine, in April 2006, 2 large clinical trials were published which investigated this topic.
The trials title and summaries are:
Homocysteine lowering and cardiovascular events after acute myocardial infarction
N Engl J Med. 2006; 354(15):1578-88 by Bønaa KH et al
BACKGROUND: Homocysteine is a risk factor for cardiovascular disease. We evaluated the efficacy of homocysteine-lowering treatment with B vitamins for secondary prevention in patients who had had an acute myocardial infarction. METHODS: The trial included 3749 men and women who had had an acute myocardial infarction within seven days before randomization. Patients were randomly assigned, in a two-by-two factorial design, to receive one of the following four daily treatments: 0.8 mg of folic acid, 0.4 mg of vitamin B12, and 40 mg of vitamin B6; 0.8 mg of folic acid and 0.4 mg of vitamin B12; 40 mg of vitamin B6; or placebo. The primary end point during a median follow-up of 40 months was a composite of recurrent myocardial infarction, stroke, and sudden death attributed to coronary artery disease. RESULTS: The mean total homocysteine level was lowered by 27 % among patients given folic acid plus vitamin B12, but such treatment had no significant effect on the primary end point (risk ratio, 1.08; 95 % confidence interval, 0.93 to 1.25; P=0.31). Also, treatment with vitamin B6 was not associated with any significant benefit with regard to the primary end point (relative risk of the primary end point, 1.14; 95 % confidence interval, 0.98 to 1.32; P=0.09). In the group given folic acid, vitamin B12, and vitamin B6, there was a trend toward an increased risk (relative risk, 1.22; 95 % confidence interval, 1.00 to 1.50; P=0.05). CONCLUSIONS: Treatment with B vitamins did not lower the risk of recurrent cardiovascular disease after acute myocardial infarction. A harmful effect from combined B vitamin treatment was suggested. Such treatment should therefore not be recommended.
Homocysteine lowering with folic acid and B vitamins in vascular disease.
N Engl J Med. 2006; 354(15):1567-77 by Lonn E et al
BACKGROUND: In observational studies, lower homocysteine levels are associated with lower rates of coronary heart disease and stroke. Folic acid and vitamins B6 and B12 lower homocysteine levels. We assessed whether supplementation reduced the risk of major cardiovascular events in patients with vascular disease. METHODS: We randomly assigned 5522 patients 55 years of age or older who had vascular disease or diabetes to daily treatment either with the combination of 2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12 or with placebo for an average of five years. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, and stroke. RESULTS: Mean plasma homocysteine levels decreased by 2.4 micromol per liter (0.3 mg per liter) in the active-treatment group and increased by 0.8 micromol per liter (0.1 mg per liter) in the placebo group. Primary outcome events occurred in 519 patients (18.8 %) assigned to active therapy and 547 (19.8 %) assigned to placebo (relative risk, 0.95; 95 % confidence interval, 0.84 to 1.07; P=0.41). As compared with placebo, active treatment did not significantly decrease the risk of death from cardiovascular causes (relative risk, 0.96; 95 % confidence interval, 0.81 to 1.13), myocardial infarction (relative risk, 0.98; 95 % confidence interval, 0.85 to 1.14), or any of the secondary outcomes. Fewer patients assigned to active treatment than to placebo had a stroke (relative risk, 0.75; 95 % confidence interval, 0.59 to 0.97). More patients in the active-treatment group were hospitalized for unstable angina (relative risk, 1.24; 95 % confidence interval, 1.04 to 1.49). CONCLUSIONS: Supplements combining folic acid and vitamins B6 and B12 did not reduce the risk of major cardiovascular events in patients with vascular disease.
In the USA, the FDA is often criticized for taking a conservative and cautious approach to allowing claims of benefit from drug manufacturers. In 1999, the FDA evaluated data for and against the claim that B vitamins were of benefit. Evidence showed that folic acid and, to a lesser extent, cyanocobalamin and pyridoxine, did lower homocysteine. Yet, at that time, there were insufficient data to prove any link between elevated homocysteine levels and increased risk of vascular disease. The agency was therefore unwilling to allow any claims about B vitamins and cardiovascular risk in 1999. Shortly thereafter, the FDA initiated a new review of over 35 more recent studies. Suggestive (not conclusive) evidence indicated that elevated homocysteine levels are associated with the risk of vascular disease, based on prospective, case-control, and cross-sectional research. This research did not answer whether some other unidentified variable affects both and thus could not conclusively confirm whether lowering homocysteine would reduce the risk of vascular disease.
Due to the limitations of existing data, the FDA allowed a qualified health claim for folic acid, pyridoxine, and cyanocobalamin: "It is known that diets low in saturated fat and cholesterol may reduce the risk of heart disease. The scientific evidence about whether folic acid, vitamin B6 and vitamin B12 may also reduce the risk of heart disease and other vascular diseases is suggestive, but not conclusive. Clearly the FDA’s cautious position has been vindicated and this lesson is useful for patients and physicians alike as we consider other therapies in the future.
The point of these two studies for patients and clinicians goes beyond the specific findings of the lack of benefit from these “logical strategies”. These two trials of over 9000 patients not only failed to demonstrate a benefit but suggest harm from the use of these vitamins. This data adds to our knowledge that another vitamin strategy Vitamin E is not effective and is probably harmful for cardiovascular event reduction. The “take home” message is that patients and clinicians should be cautious about all health strategies regardless of how sensible or logical or safe it may appear until it has been assessed in a well conducted clinical trial that can be reviewed by health care professionals and shared with patients.
|"Intervention in Peripheral Vascular Disease" from The Journal of Invasive Cardiology
Dr. Bilazarian has also been published on a number of additional topics listed below. If you would like any additional information on any of these, please contact his office at (978) 521-3288.
• Bilazarian. SD. Taylor, AJ; Brezinski, D; Hochberg, Me; Guarinier, T; Provost, TT; High grade atrioventricular heart block in adult RNP (Ul RNP) antibodies, a case report, and review of the literature. Arthritis & Rheumatism, 1989; 32:1170-1174.
• Bilazarian, SD. Baughman, KL; Hutchins, DM; Hellman, DB. Systemic lupus erythematosus presenting as acute severe mitral regurgitation. American Journal of Medicine, 1990; 21: 103-5.
• Bilazarian, SD. Shemin, RJ; Mills, RM. Catheterization of a graft from the descending aorta. Catheterization and Cardiovascular Diagnosis, 1990; 21: 103-5.
• Bilazarian, SD. Pseudoinfarction pattern on electrocardiogram after coronary artery bypass. Chest, 1990; 98:1271-4.
• Bilazarian, SD. Brush, JE. Drug therapy for chronic stable angina pectoris. P&T, 1991; 16:20029.
• Bilazarian. SD. Jacobs, AK.; Fonger, JD; Faxon, DP. Case report of a coronary anomaly. Crossing Obtuse Margins. Catheterization and Cardiovascular Diagnosis, 1991; 23: 130-132.
• Bilazarian, SD. Faxon, DP; Jacobs, AK.. Coronary sinus retroperfusion; a critical review. Coronary Artery Disease, 1991; 2:638-645.
• Bilazarian, SD. Davidoff, R. Mitral regurgitation improves when aortic valve area increases significantly. (letter). American Journal of Cardiology, 1991; 68:567-8.
• BiIazarian. SD. Mittal, S; Mills, RM. The extrarenal hazards of intravascular contrast material. Journal of Critical Illness, 1991; 6:859-869.
• Podric, PJ, Bilazarian, SD. Fuch, TT. Prognostic importance of ventricular premature beats. Journal of Arrhythmia Management, Spring 1991; 32-48.
• Dubrey, SW; Bilazarian. SD. LaValley, M; Reisinger, J; Skinner, M; Falk, RH. Signal-averaged electrocardiography in patients with AL (primary) amyloidosis. American Heart Journal, 1997 December; 134 (6):994-1001.
• Podric, PJ; Bilazarian, SD. Fuch, IT. "Prognostic Importance of Ventricular Premature Beats" in Prognosis and Risk Assessment in Cardiovascular Disease, ed. Kapoor, AS; Singh, BN; Churchill Livingstone, New York, 1993.
• Bilazarian. SD. Jacobs, AK. "Percutaneous Support Techniques" in Practical Angioplasty, ed. Faxon, DP, Raven Press, New York, 1994.
• Bresee, SJ; Jacobs, AK.; Steenksite, A; Bilazarian, SD; Ruocco, NA; Detre, KM; Ryan, TJ; Faxon, DP; and Registry Investigators. Do coronaryrisk factors influence lesion morphology? A report from the 1985 - 1986 NHLBI PTCA Registry. Journal of the American College of Cardiology, 1990; 16:99A.
• Bilazarian. SD; Currier, JW; Haudenschild, CC; Heyman, D; Powell, J; Ryan, TJ; Faxon, DP. Angiotensin converting enzyme inhibition reduces restenosis in experimental angioplasty. Joumal of the American College of Cardiology, 1990; 16:2268A.
• Davidoff, R; Schoen, FJ; Ngoy, S; Bilazarian, SD; Apstein, CS. Angiotensin II rapidly induces L VH with asymmetric septal hypertrophy: An echo cardiographic-pathologic correlation.
• Landau, C; Jacobs, AK; Currier, JW; Bilazarian, SD; Leitschuh, ML; Ryan, TJ; Faxon, DP. One year followup of PTCA induced dissections treated with a perfusion balloon catheter. Cire 1991; 84:11-130.
• Bilazarian, SD; Mohammed A; Coats, M; Falk, RH. The signal-averaged electrocardiogram in amyloid heart disease. Journal of the American College of Cardiology. 1992; 19:324A.
• Bilazarian, SD, Currier, JW; Kakuta, T; Haudenschild, CC; Faxon, DP. AngiotenSin II antagonism does not prevent after rabbit iliac angioplasty. Circ 1992; 86:1234.
Dr. Seth Bilazarian has participated as collaborator/site investigator for many multicenter completed trials. To see a list of these trials, please click here. If you would like any additional information, please contact Dr. Bilazarian's office at (978) 521-3288.