5 Steps to prevent Heart Disease

Wednesday, March 26, 2014

Dr. Dayspring's analysis of recent Niacin trials

Have your Doctor read this before he stops your Niacin.

Dr. Dayspring on recent niacin trials link
This article no longer appears on Dr. Dayspring's site 


"On December 22nd a world class cardiologist, lipid thought leader, Michael Davidson, tweeted that the baseline lipids(in HPS2 THRIVE) were LDL-C = 63, TG = 120 and HDL-C 44 mg/dL with the comment “Why treat?” Bingo – whenever a trial produces a certain outcome, that outcome pertains only to patients who have the characteristics of the population that was studied. So this study shows that in patients with stable coronary artery disease who happen to have on-treatment lipids at goal, indeed exemplary values, why would anyone add any additional lipid therapy. So I could not more strongly agree with my friend and colleague’s statement! 

This study almost looks like a re-run of the AIM-HIGH trial in which adding niacin to statin or statin/ezetimibe also struck out – but once again LDL-C, non-HDL-C and apoB goals had been achieved at baseline with use of high dose simvastatin or simvastatin plus ezetimibe. Of course in AIM-HIGH study the baseline HDL-C was still low and at least you can make the case that this study was well designed to show whether niacin induced-raising of HDL-C in high-risk persons with at-goal apoB (LDL-C, non-HDL-C) has any clinical benefit.
 Clearly it does (did) put to bed the idea that niacin’s mechanism has anything to do with HDL-cholesterol. Niacin is primarily an apoB lowering drug.
 Paradoxically niacin raises HDL-C without raising HDL-P which it would suggest niacin is simply increasing HDL size and perhaps reducing HDL-TG.

HPS2-THRIVE makes no statement about what benefit niacin/laropiprant might bring when added to on-treatment persons not at goal of therapy. It also makes no statement about what niacin monotherapy or niacin/fibrate combo therapy or niacin bile acid sequestrant therapy might do. 
So all we really know right now is when treating high risk patients who are at goal additional lipid modulation with niacin is not needed. 
However in my mind, I would not hesitate to add high dose niacin (cannot prescribe laropiprant in US):
1- to a statin or statin/ezetimibe regimen if the patient were not at apoB (LDL-C, non-HDL-C) goal
2- or use niacin in statin-intolerant persons."
Niacin's anti-inflammatory effect

Niacin treatment in hypercholesterolemic patients with low HDL levels caused a significant decrease in their oxidative stress status. These results indicate an additional beneficial effect of niacin beyond its ability to affect the lipid profile. 

"Further, baseline TG was 125 mg/dL and HDL-C was 44 mg/dL, so HPS2-THRIVE tested a drug in patients who, on average, had no indication to take it. "
"Thus, ERNL has net harm in Chinese patients when added to simvastatin.

"In contrast, however, among Europeans (likely largely Caucasian) there was net MVE benefit, as well as less myopathy.

Finally, it remains possible that the use of laropiprant in the niacin arm of the study increased adverse events and/or reduced benefits."

Meanwhile, we believe that niacin
1- remains a valuable adjunct to statin treatment for LDL-C lowering,
2- a valuable statin alternative in statin intolerant patients.
3-Further, in agreement with current NCEP ATP III Guidelines, we believe that niacin should continue to be considered for use as a statin adjunct in patients with persistent low HDL-C and high TG."


Saturday, March 22, 2014

March 2014, 16:398

HDL Hypothesis: Where Do We Stand Now?


"patients who are unable to achieve their LDL-C (or non-HDL-C)goals

  on a statin should continue to be considered for combination therapy 

  with fibrates, fish oil, and niacin."

Friday, March 21, 2014

New Study Validates Endur-acin in Tubby Theory

This trial validates my experience with Endur-acin described in my book from Tubby Theory from Topeka 2010

I have no financial interest in Endur-acin nor Slo-Niacin nor Niaspan.  

I am a retired lipidologist and have tried to bring attention to a low cost, safe, low side effect combination treatment which can be used to prevent 100,000 Sudden Coronary Deaths in America.  50% of these deaths have death as first sign of the disease.  We need to do CIMT's and CAC' and LDL-P's on everyone with one risk factor for cardiac events.  If plaque present we need to Rx with combo Rx Endur-acin (or Slo-niacin) with low dose Atorvastatin to prevent the rupture of plaque that causes sudden death.  

Monday, March 17, 2014

New expert text on cholesterol (lipids) 

Niacin Therapy: Impact on Dyslipidemia and Cardiovascular Events in Diabetic Patients



Patients with diabetes mellitus often have deleterious changes in the lipoprotein profile leading to accelerated atherogenesis and increased risk of cardiovascular disease. Niacin (nicotinic acid) was the first pharmacologic agent demonstrated to lower serum cholesterol. It remains the most clinically efficacious drug available to increase serum HDL-C and lower triglycerides.

 Several clinical trials that included patients with diabetes have demonstrated modest clinical benefits with niacin therapy.

 The characteristic flushing after niacin administration limits its tolerability; however, niacin-induced hyperglycemia and hepatotoxicity must also be considered. Although the reduction of LDL-C with statins is the cornerstones of current antilipidemic therapy, niacin therapy may still be clinically beneficial as adjuvant therapy

NOLA is the place you get free cabbage at the St. Patrick Day parade.

Saturday, March 1, 2014

Update on HDLc, HDLp, HDL functonality

Benjamin J. Ansell, MD, FACP, FACC, FNLA
Professor of Medicine
Division of Cardiology and General Internal Medicine
UCLA School of Medicine
Los Angeles, CA
The last eight years have tempered the enthusiasm directed toward development and clinical utility of HDL-based therapies to mitigate CVD risk.
 In clinical trials employing contemporary statin treatment, high-risk patients with CHD have not been shown to benefit from the addition of niacin, fenofibrate, and two CETP-inhibitors, all of which significantly raise HDL-C.
 Studies of other developmental compounds have been similarly underwhelming, in some cases limited by study size, practicality of the approach, and possibly patient selection.

 While HDL-C, and even better, HDL-P and/or ApoA-1 levels have demonstrated clear utility in identifying individuals at increased risk for CVD, their role as targets of therapy remains elusive.

 A greater understanding of HDL’s role in
1-innate immunity, and as
2-a target and mediator of systemic inflammation,
 has led to an appreciation that HDL functionality in modulating
1- lipid transport,
4- thrombosis,
5-glycemia, and
6-endothelial function
 may be as or even more important than quantitative measures of HDL. 

However, there is no consensus as to which function(s) of HDL is/are most relevant or how they are best measured.
 Several potential therapeutic pathways involving HDL remain the subject of active clinical investigation, and these will be discussed. (At NLA Spring meeting)