In controlled, randomized trials and in genetically-driven studies (the two most powerful tools that we have to assess causality), almost all factors that reduce LDL-cholesterol lead to reduced ischemic heart disease and death.
Your commentary about statins being primary useful for secondary prevention (in those who have already had a heart attack) was true until a couple decades ago, but there is now evidence demonstrating that statins reduce primary events (though at a high NNT depending on the population's risk). Naturally, the higher risk the population, the more benefit and lower NNT you will see from any intervention.
A classic genetic study, for example, is that of Hobbs and Cohen looking at PCSK9 variants [1]. People with loss of function mutations in PCSK9 have lower LDL-cholesterol. These people have an even lower risk of ischemic heart disease than you would expect based on the degree of LDL-cholesterol lowering. This is surmised to be due to the lifelong exposure to low LDL-C, though the actual reason is not currently known with certainty.
The real question is, though, is drug therapy something that should be pushed on otherwise healthy (non-FHC/high risk) individuals in order to reduce mortality. The PCSK9 research paper you linked has the percentage dead after 15 years (starting at an average of 55 yr/o) at 10.7% for those without the mutation and 8.3% for those with it.
Assuming they actually work identically to the mutation, maybe one could argue that the $$$ cost of the new PCSK9 targeting drugs will be worth it to save 2.4%, but we have zero long term data on their safety. There is certainly some evidence [1] that the risk for diabetes could be higher...much like the current statins.
I don't think we have anything even approaching a complete picture on the interplay between CHD, cholesterol, and overall mortality. Until the picture becomes clearer, it doesn't seem prudent to push drug therapy as strongly as it typically is.
To rephrase the exact same data, 15-year mortality is ~30% higher among those with the normal variant compared to those with the cholesterol-lowering variant. That is an enormous mortality effect.
Based on the mechanism by which statins are postulated to cause diabetes (and LDLR-dependent mechanism), PCSK9 inhibitors may also cause diabetes, though it's not yet known. From a mortality perspective, this is irrelevant because we know that statins (and PCSK9 mutations) reduce mortality despite (probably) causing diabetes.
The timing of statins falling off patent is essentially uncorrelated with anything - there was a multi-year gap with atorvastatin off patent before the PCSK9 inhibitors were approved, which makes no sense if you would like to invoke a patent conspiracy. With the advent of genetically-informed early phase research, you will continue to see new drugs come out at an increasing frequency (reversing the trend over the past few decades of fewer approvals).
The link from cholesterol -> CHD -> mortality is as clear as anything in biology (clear enough for the basis for this work to have won a Nobel prize decades ago).
Your commentary about statins being primary useful for secondary prevention (in those who have already had a heart attack) was true until a couple decades ago, but there is now evidence demonstrating that statins reduce primary events (though at a high NNT depending on the population's risk). Naturally, the higher risk the population, the more benefit and lower NNT you will see from any intervention.
A classic genetic study, for example, is that of Hobbs and Cohen looking at PCSK9 variants [1]. People with loss of function mutations in PCSK9 have lower LDL-cholesterol. These people have an even lower risk of ischemic heart disease than you would expect based on the degree of LDL-cholesterol lowering. This is surmised to be due to the lifelong exposure to low LDL-C, though the actual reason is not currently known with certainty.
1 = http://www.nejm.org/doi/full/10.1056/NEJMoa054013