Atherosclerosis is the technical term for "hardening of the arteries," a process that can eventually culminate in a heart attack. The process starts with an infusion of LDL into the artery wall and ends with a rapid cascade of events leading to plaque rupture and the subsequent release of clotting agents that cause the artery to be completely blocked. As a consequence, the section of the heart supplied by the artery becomes nutrient starved, and it quickly becomes non-functioning and is converted to inert scar tissue. The remainder of the heart then has to work harder to pump blood throughout the body. However, plenty of people survive a minor heart attack and go on living for many years with no obvious disability.
The most clear and unambiguous benefit of statin drugs is that they reduce the incidence of nonfatal heart attacks in men in their 50's. The mechanism by which they achieve this outcome is surely directly tied to their ability to reduce the concentration of LDL in the blood. In careful studies of atherosclerosis, it has been determined that cholesterol in LDL plays a critical role in all stages of the atherosclerotic process. When the supply of LDL is reduced, the entire process is slowed down and the heart attack is delayed or possibly even arrested.
This is surely a good thing? Well, it seems to me that the atherosclerotic process is so intricate and so purposeful that it is hard to believe it plays no role in sustaining health. An excellent and widely referenced article written in 1995 on atherosclerosis  provides a fascinating account of all that happens in between the time that the LDL first penetrates the vessel wall and the time of the acute event triggering the heart attack.
Under normal circumstances, the cholesterol enters and leaves the artery wall at the same pace, and no fatty streak accumulates. However, sometimes the LDL "decides" to linger in the wall and also transforms to a weakly oxidized state. This oxidation is a signaling device that encourages white blood cells to join the party. They in turn release chemicals which further oxidize the LDL and trigger an inflammatory response. The newly arrived white blood cells are converted into macrophages, and the LDL, which had been hanging in the extracellular matrix, now take up semi-permanent residence inside the macrophages that are being steadily recruited from the blood supply. Once the LDL becomes highly oxidized it can even become toxic to the macrophages. They release their lipid (fat) droplets which are then consumed by nearby smooth muscle cells lining the artery wall. Over time, the resulting lesion grows outward until it eventually reaches the adventitia, the outermost layer of the artery wall. This situation is deemed a crisis condition, presumably because any further expansion in that direction would penetrate into the heart muscle.
Highly oxidized LDL penetrating all the way to the adventitia triggers a remarkable series of events intent on closing off the artery. High concentrations of "tissue factor" are released from the macrophages, and this tissue factor induces blood clotting by the platelets. The oxidized LDL also inhibits vasodilation, causing the vessel to constrict and furthering the goal of complete closure. Plaque rupture ensues, and more platelets are recruited to the wound site to further encourage a blood clot. In short, systematic biological mechanisms have been preprogrammed to shut down and isolate this segment of the heart.
What could possibly be a good reason to want to kill off a segment of the heart? The article that so beautifully laid out the sequence of events leading to a heart attack never mentioned the idea of an infective agent. However, the entire process would suddenly make sense if you imagine that, when LDL first entered the artery wall, it encountered an infective agent such as a bacterium or a virus, and it was this that triggered it to linger in the artery wall and enter the mildly oxidized state. The macrophages were then recruited to release toxic chemicals with the intent of disabling or even killing the viruses, and then to consume their debris. Meanwhile, the LDL could work on the parallel task of neutralizing toxins released by the infective agents. Further penetration towards the outer wall of the artery was necessitated because the viruses or bacteria were advancing in that direction. Once the enemy reached the outer wall, a crisis ensued because the next step would be penetration of the virus or bacterium into the heart muscle. Such an infection of the heart itself, myocarditis, was something to be avoided at all cost. A minor heart attack, which would essentially turn this segment of the heart into necrotic tissue, would also isolate the infective agent, a preferred outcome to the alternative of letting the infective agent grow unchecked within the heart muscle, leading directly to heart failure.
The notion of heart disease being due to an infective agent was proposed over two decades ago, and is gaining increased traction in recent times. One clear possibility is the extremely common herpes virus, also known as HCMV (Human Cytomegalovirus), which is estimated to infect from 60 to 99 percent of the world's population . Several distinct observations are strongly suggestive of a role played by these viruses . One such observation is that they are capable of triggering many of the steps involved in the above process of atherosclerosis. Another line of evidence comes from a clinical study that showed that patients with high titres of CMV antibodies were at greater risk to atherosclerosis. Direct evidence of their existence in atherosclerotic lesions has been found in the form of HCMV nucleic acids, detected in 90% of the severe atherosclerotic lesions that were examined. A final line of evidence comes from transplant patients --those who tested positive for HCMV infection were at much higher risk to arterial blockage.
A compelling argument for a relationship between an infective agent and atherosclerosis is in the case of children who were infected with typhoid fever. As early as 1911, Klotz and Manning  observed that atherosclerosis was particularly pronounced in children who had died from typhoid fever. They concluded that the production of fatty tissue in the arterial wall was the result of a direct irritation of that tissue by the presence of infection or toxins. Many studies have implicated a variety of other common infective agents as being cofactors in causing arterial disease. These include Chlamydia pneumoniae (a common source of pneumonia), Helicobacter pylori (the bacterium that causes stomach ulcers), and HSV and CMV (the one discussed above), both of which cause Herpes .
Another indirect argument for the relationship between infection and heart disease is that people who experience an acute heart attack or stroke have disproprortionately just recovered from an infectious disease. These diseases include tuberculosis, sepsis, HIV, chickenpox, tooth infections, and infections of the urinary tract. People with heart disease are encouraged to take steps to prevent gum disease, due to the observed correlation between infections in the gum and atherosclerosis.
A strong proponent of the theory that heart disease is the result of an infective agent is Uffe Ravnskov, a Swedish doctor who has been a tireless advocate of cholesterol as a much-abused and vital biological substance. In his recent book on cholesterol , the next-to-last chapter, titled simply "The Real Cause," argues persuasively for the point of view that atherosclerosis is the direct result of infective agents, and also makes a case for LDL's critical role in plaque build-up to protect against the infective agents. Oxidation is the usual way that macrophages destroy bacteria and viruses. Thus the presence of intense oxidation in the plaque is very suggestive of an attempt to neutralize a pathogen. LDL is able to bind and neutralize the alfa-toxin produced by staphylococcus baceteria, and, as we have seen before, it also neutralizes lipopolysccharide, another common bacterial endotoxin. By subsequently changing their structure to induce the macrophages to consume them, the LDL particles effectively render inert the bacteria and their harmful products.
The endotoxins that are released by bacteria are thus clearly implicated in heart disease. Since LDL can bind with and neutralize bacterial endotoxins, one reason why it might settle in the arterial wall, then, is to be available to neutralize the endotoxins of resident bacteria. It has also been shown that bacterial endotoxin stimulates the expression of tissue factor by macrophages (cells that were derived from the white blood cells) . As we have seen from the above discussion on atherosclerosis, tissue factor is probably the single most contributory component for initiating the final cascade in a heart attack. This would presumably occur because the presence of unneutralized endotoxin indicates that the body's defenses have lost the battle against the bacteria at this site. Statins have been shown to inhibit the migration of white blood cells to inflammatory sites , which would reduce the bioavailability of tissue factor and therefore possibly prevent the heart attack, but would allow the bacteria and their endotoxin to remain in place and continue to do harm to the surrounding tissues, eventually invading the heart muscle itself.
Thus, the observed rapid rise in the incidence of heart failure subsequent to widespread statin usage may not be just due to the fact that statins may directly harm heart muscle cells, but also to the possibility that they indirectly put them in harm's way to the bacteria and viruses that have broken through the protective arterial wall.