There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:
Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies
Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.
Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.
Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.
Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.
Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.
Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.
Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.
Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.
From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.
But there are two areas of desperate need:
1) Data on effective treatments.
2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.
Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.
Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.
More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.
However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.
For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.
(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)
HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.
I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.
If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.