Friday, December 11, 2009
This video says that ancient mummies had heart disease even though they had a very different life-style.
Thursday, December 4, 2008
Wednesday, July 9, 2008
This meta-study shows that forty minutes of exercise four times per week is very effective
Investigators from Tokyo published results in the May 28 issue of the Archives of Internal Medicine from a meta-analysis they performed to evaluate the effect of exercise on HDL levels. Their meta-analysis included data from 35 randomized trials assessing the effect of exercise on HDL levels in adults. While exercise regimens varied among these studies, on average patients in these studies exercised for 40 minutes, three to four times per week, and the effect on HDL was measured after eight to 27 weeks.
Across the studies, participants had increases in HDL cholesterol averaging about 2.5 mg/dL. This increase in HDL cholesterol was only modest, but was statistically significant. Furthermore, since cardiac risk is thought to drop by two to three percent for each 1 mg/dL increase in HDL, a 2.5 mg/dL rise in HDL amounts to a substantial reduction in risk.
Perhaps the most interesting finding from this study is the observation that the duration of exercise sessions - and not the frequency or intensity of exercise - correlated the best with rises in HDL levels. The investigators report that in research subjects exercising for at least 20 minutes, each additional 10-minute increase in exercise duration increased HDL levels by an additional 1.4 mg/dL.
Since Health Plus is no longer allowing nuclear stress test, this summary is very interesting to my case.
What are the implications of the new way?
While actual blockages can and do cause angina and heart attacks and while treating specific blockages is often important, therapy aimed at these blockages within the coronary arteries is often neither necessary nor sufficient to adequately treat CAD. Evidence is building that with intensive medical therapy -- largely based on statins but also including aggressive risk-factor modification -- CAD can be halted or even reversed, and plaques can be "stabilized" to reduce the odds that they will rupture. In these individuals, exercise, smoking cessation, weight loss, blood pressure control and cholesterol control (aiming for LDL cholesterol levels of 100 mg/dL and HDL levels of at least 40 mg/dl) is especially important.
The key, then, is to decide whether an individual is likely to have active CAD, that is, whether plaques are likely to be present, and then direct therapy accordingly. To a large extent, deciding whether plaques are likely to be present can be accomplished noninvasively. Begin with a simple assessment of risk to decide whether your risk is low, intermediate or high. ( Here's how to assess your risk simply and easily.) People in the low-risk categories probably need no further intervention. People in the high-risk categories should be treated aggressively (with statins and risk-factor modification), as they are very likely to have plaques. People in the intermediate risk category should consider noninvasive testing with EBT scanning (calcium scans): if calcium deposits are present on the coronary arteries, then they have plaques and should be treated aggressively.
When should blockages be looked for?
Blockages in the coronary arteries are still important. Most experts think that people in the high-risk category should have a stress thallium test. If this test is suggestive of a major blockage, cardiac catheterization should be considered. A stress test or cardiac catheterization should also be strongly considered in anybody (whatever their apparent level of risk) who has symptoms of angina. Relieving blockages by surgery or stenting can be extremely effective in treating angina and, in some circumstances, can improve survival.
Our thinking about CAD has changed significantly over the past decade or so. It is not simply a disease of blockages that ought to be treated with stents. Treatment aimed at halting or reversing chronic CAD and at stabilizing plaques to reduce the odds that they will rupture, is very important, whether "significant" blockages are present or not.
Sunday, April 27, 2008
Obstructed blood vessels and clogged or blocked arteries typically are treated through angioplasty, the mechanical widening of a vessel, or bypass surgery. Some patients, however, have numerous small blockages that cannot be treated through traditional approaches. In most cases, they are sent home with a predicted life expectancy that, no matter how it’s phrased, sounds like a death sentence.
A new approach to the problem called therapeutic coronary angiogenesis is creating hope through the injection of human fibroblast growth factor protein into affected areas. Improvements with the procedure may arise from the use of mutant forms with increased stability.
Blaber and his research team are creating artificial “mutant’’ proteins in their College of Medicine laboratory that mimic the human proteins used in angiogenic therapy, and with enhanced stability properties. So far, the mutant proteins engineered at the College of Medicine have exhibited potency in stimulating cell growth while simultaneously maintaining greater stability under conditions common to angiogenic therapy.
Overweight people have a higher risk of heart attacks, strokes and other problems that arise from clogged, hardened arteries. Now, a new study in mice gives the first direct evidence of why this link might exist – and a tantalizing look at how it might be broken.