All entries posted by Dr. Micah Eimer
When patients are diagnosed with atherosclerotic disease (plaque in the arteries) they frequently ask me if this can ever get better. A new study published in the New England Journal of Medicine sheds some light on this subject.
Investigators from the Cleveland Clinic studied over 1,000 patients with coronary artery disease using a tiny ultrasound probe which fits inside coronary arteries and can measure the amount of plaque very accurately. Patients underwent an initial measurement of their “plaque burden” and then were randomized to one of two statin medications – either atorvastatin (Lipitor) 80mg daily or rosuvastatin (Crestor) 40mg daily. The ultrasound was then repeated about two years later to see if there was any change in the plaque levels.
At the beginning of the trial, the patients in both groups had an average LDL (bad cholesterol) of 120mg/dL. After two years of therapy the LDL had gone down significantly – the Lipitor group had an LDL of 70mg/dL and the Crestor group was slightly lower at 63 mg/dL. The HDL (good cholesterol) was 45mg/dL in both groups to start and increased to 49mg/dL in the Lipitor group and 50mg/dL in the Crestor group.
Regarding the amount of plaque in the coronary arteries, both groups saw an average decrease in the amount of plaque by about 1%. Looking at it another way, 63% of the patients in the Lipitor group and 69% of patients in the Crestor group had regression of their plaque burden in the coronary artery.
Despite the high doses of powerful cholesterol lowering medications, the incidence of side effects was quite low. Nonetheless approximately 20% of patients in both groups discontinued the study medication.
It should be noted that this study was not able to prove that reducing plaque results in less heart attack, stroke or death. However, it is encouraging to know that the majority of patients that achieve an LDL less than 70mg/dL using Crestor or Lipitor will experience a regression of their atherosclerosis.
Just like haircuts and clothing, vitamins will from time to time become fashionable in maintaining health and preventing disease. Vitamins E, C and folate seem to have had their time and the focus lately has been on Vitamin D. The body’s requirement for Vitamin D is met in two ways – 95% is derived from the exposure to ultraviolet B radiation, which creates Vitamin D in the skin, while the remainder is obtained from foods. Many foods are fortified with Vitamin D including dairy products, cereals and orange juice. A potent natural source of Vitamin D is oily fish such as salmon, mackerel, tuna and sardines. Depending on the normal cut-off value for Vitamin D, it is estimated that 25-60% of the United States population is deficient in Vitamin D. Risk factors for deficiency include increased distance from the equator ( the atmosphere filters the needed ultraviolet radiation), lack of sunshine, darker pigmentation, smoking, obesity, physical inactivity and certain medications. Originally recognized for its importance in bone development, it has recently been discovered that Vitamin D acts more like a hormone in that there are Vitamin D receptors located throughout the body; including white cells, nerve cells, heart cells and the pancreas cells that release insulin. The exact role of Vitamin D in these non-bone cells is the subject of much current research. Most of the available data on the consequence of Vitamin D deficiency is derived from population based observation studies in which Vitamin D levels were correlated with various outcomes including cardiovascular disease and death. For example, in the NHANES III study, patients with the lowest 25% of Vitamin D levels had a 26% higher risk of dying in the 9 years of follow up. In the Intermountain study, patients with low Vitamin D levels had an increased risk of having diabetes, high blood pressure, high cholesterol and also an increased risk of heart attack or stroke. Another recent study looking at patients who came to the hospital with heart attacks found that 96% were deficient in Vitamin D. While these are interesting findings they do not answer the key question- does giving Vitamin D reduce these risks? That requires a prospective, randomized double blind trial in which neither patients or investigators know who is receiving Vitamin D. One obvious obstacle is that it is impossible to restrict Vitamin D in the placebo arm as sunlight is everywhere. Nonetheless, about 18 studies have attempted to do just this with varying results. When the studies are pooled together, Vitamin D does appear to impart a modest (7%) reduction in the risk of dying. Is there any harm in having too much Vitamin D? The answer at this time appears to be yes. The population based studies demonstrate that there is a “U shaped” curve for Vitamin D, meaning that at high levels it may increase the risk of dying. There is currently a major trial sponsored by the NIH called the VITAL study which seeks to answer many of these questions. Until those results are released it seems prudent to try and maintain Vitamin D levels in a physiologic range by consuming foods rich in Vitamin D, living a healthy lifestyle as well as ensuring adequate exposure to sunlight.
People frequently ask me what foods they can eat to help lower cholesterol. A recent study in the Journal of the American Medical Association tested two diets for their ability to lower cholesterol, providing patients with some much needed guidance on the subject.
While several foods and food groups have been known to favorably impact cholesterol, these researchers put together a “portfolio” of some of the most effective foods. Patients were either placed on a control diet which was described as “low saturated fat” or a diet that included a portfolio of plant sterols, soy protein, viscous fibers and nuts.
The plants sterols were ingested in the form of an enriched margarine such as Smart Balance. The soy proteins were consumed both as soy beverages and tofu. The psyllium was consumed though oats, barley and as psyllium itself (Metamucil). The nuts (tree nuts and peanuts) were typically eaten with the morning and afternoon snacks.
The patients were followed for 6 months with their cholesterol measured at baseline and at the end of the study. In addition, their blood pressure and body weight were followed.
All patients in the study were instructed to eat 6 times daily – 3 meals and 3 snacks. Each of the meals and snacks in the study group incorporated some of the portfolio components.
At the end of the study, both groups lost about 5 pounds. The control group had a reduction in the LDL (bad cholesterol) of 3.5% while the study group had a 14% reduction in the LDL. There was no significant change in the HDL (good cholesterol) or triglycerides.
I think there are several take home points from this study- first, dietary changes can significantly reduce LDL cholesterol. Further, this study shows that a diet rich in specifically plant sterols, soy protein, viscous fiber and nuts is considerably more effective at reducing cholesterol than a typical low saturated fat diet. However, the magnitude of the change in LDL (14% reduction) is modest in comparison to medications like statins, some of which can reliably lower LDL by over 50%.
Nonetheless, there are patients whose LDL cholesterol is borderline and dietary changes such as these may be all that is needed. Also, it is estimated that every 1% reduction in LDL translates into a 1% reduction in the risk for heart disease, so even patients already on cholesterol medication could benefit from these dietary changes.
For more information on the specifics of the dietary components, feel free to email me at email@example.com
Those of you that have been checking and following your cholesterol numbers over the years have probably felt confused at some point about what the optimal values are or even what values to follow. The basic components of the cholesterol panel have not changed- total cholesterol is a sum of HDL (good cholesterol) + LDL (bad cholesterol) and Triglycerides. What has changed is which of these entities is the primary focus of our attention and where to set the goals for these values.
Initially, patients were told that an ideal cholesterol level meant a total cholesterol less than 200. This approach fell out of favor as it was then appreciated that HDL cholesterol was protective and that high levels of HDL (which raised the total cholesterol) was associated with a lower risk of heart disease. Likewise, patients with low HDL (which would result in a lower total cholesterol) were at increased risk of heart attack.
The focus then shifted to primarily worrying about the level of LDL cholesterol as many large studies suggested that the level of LDL cholesterol was the most important predictor of a person’s risk for heart disease. Once there was general consensus that the LDL was the most important measure, researchers sought to define the optimal level of LDL cholesterol. The optimal level of LDL for patients with heart disease has dropped from 130 to 100 and now to 70 based on data that each subsequent reduction further reduces the risk for heart attack.
However, there are several problems with an “LDL-centric” approach to cholesterol. First, patients with low LDL are still at some risk of heart attack which has been termed “residual risk” suggesting that LDL is not the whole story. Second, there is currently an epidemic of patients who are overweight with diabetes (“metabolic syndrome”) who are clearly at high risk for heart disease, despite a relatively normal LDL. In addition to normal LDL these patients will typically have elevated triglycerides and low HDL.
An idea that is gaining traction in the cardiovascular prevention community is to simply dichotomize cholesterol into good and bad. In other words, if HDL is the only good cholesterol then everything else (termed “non-HDL” cholesterol) must be increasing the risk of heart attack. Non-HDL also includes cholesterol particles that are not routinely assessed like very low density LDL or VLDL. In fact, many large studies have already proven that non-HDL is actually better than LDL at predicting the risk of heart disease.
In terms of what the ideal non-HDL level should be, guidelines suggest that a level 30 points higher than your goal LDL (which can be determined by your doctor) is probably optimal.
Predicting and reducing a patient’s risk of having heart disease is the cornerstone of preventive cardiology. Doctors have many options on how to do this including tabulating risk factors like diabetes, smoking, high blood pressure, high cholesterol and family history. However, some patients will go on to develop heart disease with few or no risk factors. In fact, the majority of heart attacks occur in patients who would be deemed “low risk”.
A recent study in the New England Journal of Medicine examined the ability of carotid ultrasound (an ultrasound study of the main artery in the neck) to predict an individual’s risk of developing heart disease.
Nearly 3000 healthy patients with an average age of 58 underwent an ultrasound examination and then were followed for seven years. The ultrasounds were evaluated for the presence or absence of plaque as well as the thickness of the arterial wall (cIMT).
Patients with even minimal plaque in the neck arteries were noted to have double the risk of heart disease compared to those who did not have plaque. A similar relationship was also found with patients who had thickening of the arterial wall which is a very early sign of plaque build up.
Carotid ultrasound testing can be performed in a doctor’s office, is relatively inexpensive and involves no radiation. This study demonstrates that the findings of a carotid ultrasound gives doctors a powerful tool to predict, and thus reduce, a patient’s future risk of heart disease.
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