Current thinking on cholesterol/heart disease

[Bikewer]

They've covered this topic quite a bit on NPR over the last week, including the Science Friday show. Recent studies have indicated some new information on the cholesterol/heart attack connection, it's treatment, and the effects of the new statin-type drugs.

Seems the previous model was that with high levels of LDL cholesterol, one's heart arteries gradually became more and more occluded, resulting eventually in angina or even heart attack.
The surgical response to this was to re-open or bypass the blocked artery or arteries, using bypass surgery or stents.
This resulted in quite dramatic temporary relief in many cases, but long term studies showed little effect on life-span or sudden death from further attacks.

Now, it seems, the model is somewhat different. Plaques built up of the LDL (low-density lipoprotein) can suddenly rupture, causing a massive heart attack. The cause of the ruptures are still under investigation, but include the fragile nature of the LDL plaques, and the other new culprit, inflammation.
Seems that chronic inflammation may cause a lack of adherence to the artery walls, increasing the risk of ruptured plaques.

The new generation of statin drugs are a double whammy, it appears, since they not only lower the LDL levels, but reduce inflammation as well. Putting heart patients on relatively heavy doses of statins, to bring LDL levels down to as low as 60 and under, has show to have a very beneficial effect on a large number of already-being-treated patients.

Interesting stuff for me, 57 and found to have a total cholesterol level of over 300 about 7 years ago, despite being a 100 mile-a-week cyclist!
The drugs are keeping my levels in the good range, so I'm keeping up on this research.

 

[Rolfe]

a total cholesterol level of over 300 ....

That (I hope) would be 300 mg/100ml.

The rest of the world gave up on those ancient, creaky gravimetric units in about 1975.

Non-Merikans should therefore multiply this figure by 0.026, to derive an understandable figure in the universally-accepted (except for Merika) SI unit of mmol/l. Comes to 7.8 mmol/l.

Glad to hear you've got that down now, Bikewer!

Rolfe. (See my sig, by the way! )

 

[sickstan]

Seems the previous model was that with high levels of LDL cholesterol, one's heart arteries gradually became more and more occluded, resulting eventually in angina or even heart attack.

Angina can result in gradual plaque buildup that leads to occlusion. Progressive, symptomatic occlusion is called unstable angina and is treated like a heart attack. However, most acute infarctions (actual muscle death due to blockage of coronary flow) occur in non-clinically significant occlusions (<90%).

The surgical response to this was to re-open or bypass the blocked artery or arteries, using bypass surgery or stents.
This resulted in quite dramatic temporary relief in many cases, but long term studies showed little effect on life-span or sudden death from further attacks.

tPA (tissue plasminogen activator) was also used to "bust clots". A quick review of abstracts from medline suggests that PTCA (Percutaneous transluminal coronary angioplasty) has improved morbidity and mortality. Further studies with anti-platelet and anti-coagulation therapy and drug-eluting stents promise further reductions in reocclusion rates. I don't know how they concluded that CABG (bypass) and PTCA don't affect mortality.

Now, it seems, the model is somewhat different. Plaques built up of the LDL (low-density lipoprotein) can suddenly rupture, causing a massive heart attack. The cause of the ruptures are still under investigation, but include the fragile nature of the LDL plaques, and the other new culprit, inflammation.
Seems that chronic inflammation may cause a lack of adherence to the artery walls, increasing the risk of ruptured plaques.

Yes, some people are pointing to an infectious cause of the inflammation. People who had been treated within a certain period with certain antibiotics (macrolides, tetracyclines) had a reduction in the risk of heart disease. Chlamydia pneumonia has been a putative agent, but periodontal disease, with its gram negative agents has also been pushed as another risk factor. It's still unknown if low-dose aspirin has enough anti-inflammatory effect to be a significant protective mechanism.

Again, it may be startling to realize this, but most acute MIs occur in people with nonsignificant occlusions. The stability of plaques is hard to determine, but appears to be the controlling factor for MI risk. Certainly, inflammation and dyslipidemia make plaques unstable.

The new generation of statin drugs are a double whammy, it appears, since they not only lower the LDL levels, but reduce inflammation as well. Putting heart patients on relatively heavy doses of statins, to bring LDL levels down to as low as 60 and under, has show to have a very beneficial effect on a large number of already-being-treated patients.

How low can you go? Well, according to some cardiologists, lower is better. Did they mention the Pravastatin vs. atorvastatin study that was done by the maker of pravastatin? Pravastatin was showed to be less effective at reducing risk than the more potent atorvastatin. The new drug on the market, rosuvastatin, is even more potent, and has positive effects on HDL and triglycerides as well. It may be what Baycol should have been without all the death and fulminant hepatic failure.

Has anybody read about the super-HDL that a few people from Limone sul Garda have? here's a link:
http://www.cedars-sinai.edu/6189.html