Statins Promote Alternative Blood Supply
Statins Promote Alternative Blood Supply to Heart Muscle Threatened by Coronary Artery Disease
What is the problem and what is known about it so far?
The three main arteries (blood vessels) that supply oxygen rich blood to the heart muscle do not connect with each other at their ends. Therefore, when there is an obstruction in one blood vessel (e.g. atherosclerosis/cholesterol plaque), the decreased or absent blood flow to the heart muscle results in cell injury and death to the region of the heart supplied by that blood vessel. However, although the three main coronary arteries are not connected, there is a network of small vessels that provide another route of circulation to the under-supplied portion of the heart muscle. Increasing these alternate blood vessels to the heart can be important for the treatment of coronary artery disease.
Statins are a class of drugs that can decrease the level of LDL or "bad" cholesterol and raise levels of HDL or "good" cholesterol. Animal studies have shown that statins can also promote new blood vessel growth and collateralization, or the development of alternate pathways for blood flow.
Why did the researchers do this particular study?
The purpose of this study was to investigate the effect of statins on collateral circulation in patients with severe coronary artery disease independent of their effect on cholesterol.
Who was studied?
94 patients who had an occlusion or a >95% narrowing of at least one major coronary artery. 51 of these patients were taking statins before they began participating in this study and 43 patients were not.
How was the study done?
The amount of coronary artery collateralization was evaluated by angiography, a technique that uses x-ray and dye to picture blood vessels. The angiographer had no previous knowledge of the patient's medical history. Collateralization was graded on a scale of 0 to 3 based on the filling of small arteries supplying the heart wall muscle. The dose of statins each person was taking was changed to a standard amount for the purpose of the study. Other factors that could influence heart muscle blood supply or heart function were also considered. These included a history of hypertension, history of high cholesterol, aspirin use, medications for treatment of hypertension, heart failure, and angina [beta-blocker, angiotensin converting enzymer inhibitor, calcium channel blocker, long-acting nitroglycerin], and left ventricular function,
What did the researchers find?
Statins increased the formation of collaterals, small arteries that network to supply blood to the heart. No relationship was found between the development of collaterals and LDL cholesterol levels or the dose of the statins. Furthermore, the group using statins had much better left ventricular (heart muscle) function than those not using them.
What were the limitations of the study?
Because of the way this study was designed there may be factors (e.g socio-economic, environmental) that were not taken into account. Also, this study was performed within a specific time frame, so the progression of collateralization over time was not studied. Likewise, the duration of statin or dose of therapy required to produce the observed increase in collateral formation is unknown.
What are the implications of the study?
Statins may stimulate collateral formation thereby creating an alternative blood supply to heart tissue affected by coronary artery disease and lead to the improvement of left ventricular function. This appears to occur independently of the effects of cholesterol on the heart.
Summarized by Winifred Lee, College of Medicine, University of Vermont
Summarized from "Statin Use Is Associated with Enhanced Collateralization of Severely Diseased Coronary Arteries". Pourati, Isaac et al. American Heart Journal, November 2003, Volume 146, Number 5, Pages 876-881.
