Familial Atherosclerosis Treatment Study (FATS): Difference between revisions

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{{High density lipoprotein}}
{{High density lipoprotein}}


{{CMG}}
{{CMG}}; {{AE}} {{Rim}}
 
==Official Title==
 
 
==Objective==
==Objective==
To compare the effects of two intensive [[lipid]] altering therapies in men with [[familial combined hyperlipidemia]] as assessed by [[arteriography]].  
To compare the effects of two intensive [[lipid]] altering therapies in men with [[familial combined hyperlipidemia]] as assessed by [[arteriography]].  


==Methods==
==Sponsor==
Familial Atherosclerosis Treatment Study (FATS) is a randomized, double blinded, [[placebo]] controlled study wherein 146 men with one coronary [[stenosis]] of greater than 50 percent or three lesions of greater than 30 percent were enrolled and randomized into three groups. The groups included:
 
* Placebo plus low dose [[colestipol]] (if needed, to lower [[LDL]])
 
* [[Niacin]] (1 g QID) plus colestipol (10 g TID)
==Timeline==
* [[Lovastatin]] (20 mg BID) plus colestipol (10 g TID)
{| class="wikitable" border="1" style="background:WhiteSmoke" width="40%"
The primary endpoint was a measure of change in the severity of disease in the proximal coronary arteries as measured by quantitative arteriography.
|-
| Colspan="2" style="background:Gainsboro" align="center"|'''Timeline'''
|-
| Style="width:30%"| '''Start Date'''||Style="width:70%"|
|-
| '''End Date'''||
|-
| '''Status'''||
|-
|}
<span style="font-size:85%">The previous information was derived from ClinicalTrials.gov on 08/18/2014 using the identification number NCT00136981.</span>
 
==Study Description==
 
{| class="wikitable" border="1" style="background:WhiteSmoke" width="40%"
|-
| Colspan="2" style="background:Gainsboro" align="center"|'''Study Description'''
|-
| Style="width:30%"|'''Study Type'''|| Style="width:70%"|
|-
| '''Study Phase''' ||
|-
| Colspan="2" style="background:Gainsboro" align="center"|'''Study Design'''
|-
| '''Allocation'''||
|-
| '''Endpoint'''||
|-
| '''Interventional Model'''||
|-
| '''Masking'''||
|-
| Colspan="2" style="background:Gainsboro" align="center"|'''Study Details'''
|-
| '''Primary Purpose'''||
|-
| '''Condition'''||
|-
| '''Intervention'''||
|-
| '''Study Arms'''||
|-
| '''Population Size'''||
|-
|}
 
<span style="font-size:85%">The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT00136981.</span>
 
==Eligibility Criteria==
===Inclusion Criteria===
 
===Exclusion Criteria===
 
==Outcomes==
===Primary Outcomes===
 
==Publications==
===Results===


==Results==
===Conclusion===
Both the intensive lipid lowering therapies were equally effective. Both reduced the frequency of progression of coronary lesions (21% and 25% versus 46% in the control group), increased the frequency of regression (32% and 39% versus 11%), and reduced the incidence of cardiovascular events in men with coronary artery disease who were at high risk for cardiovascular events.<ref name="pmid2215615">{{cite journal |author=Brown G, Albers JJ, Fisher LD, ''et al.'' |title=Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B |journal=N. Engl. J. Med. |volume=323 |issue=19 |pages=1289–98 |year=1990 |month=November |pmid=2215615 |doi=10.1056/NEJM199011083231901 |url=}}</ref><ref name="pmid8252687">{{cite journal |author=Zhao XQ, Brown BG, Hillger L, ''et al.'' |title=Effects of intensive lipid-lowering therapy on the coronary arteries of asymptomatic subjects with elevated apolipoprotein B |journal=Circulation |volume=88 |issue=6 |pages=2744–53 |year=1993 |month=December |pmid=8252687 |doi= |url=}}</ref><ref name="pmid23168285">{{cite journal |author=Phan BA, Muñoz L, Shadzi P, ''et al.'' |title=Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment Study (HATS), Armed Forces Regression Study (AFREGS), and Carotid Plaque Composition by MRI during lipid-lowering (CPC) study |journal=Am. J. Cardiol. |volume=111 |issue=3 |pages=352–5 |year=2013 |month=February |pmid=23168285 |doi=10.1016/j.amjcard.2012.09.034 |url=}}</ref><ref name="pmid8106695">{{cite journal |author=Stewart BF, Brown BG, Zhao XQ, ''et al.'' |title=Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol |journal=J. Am. Coll. Cardiol. |volume=23 |issue=4 |pages=899–906 |year=1994 |month=March |pmid=8106695 |doi= |url=}}</ref><ref name="pmid7695184">{{cite journal |author=Brown BG, Hillger L, Zhao XQ, Poulin D, Albers JJ |title=Types of change in coronary stenosis severity and their relative importance in overall progression and regression of coronary disease. Observations from the FATS Trial. Familial Atherosclerosis Treatment Study |journal=Ann. N. Y. Acad. Sci. |volume=748 |issue= |pages=407–17; discussion 417–8 |year=1995 |month=January |pmid=7695184 |doi= |url=}}</ref><ref name="pmid7500507">{{cite journal |author=Maher VM, Brown BG, Marcovina SM, Hillger LA, Zhao XQ, Albers JJ |title=Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a) |journal=JAMA |volume=274 |issue=22 |pages=1771–4 |year=1995 |month=December |pmid=7500507 |doi= |url=}}</ref><ref name="pmid10208998">{{cite journal |author=Zambon A, Hokanson JE, Brown BG, Brunzell JD |title=Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density |journal=Circulation |volume=99 |issue=15 |pages=1959–64 |year=1999 |month=April |pmid=10208998 |doi= |url=}}</ref>
Both the intensive lipid lowering therapies were equally effective. Both reduced the frequency of progression of coronary lesions (21% and 25% versus 46% in the control group), increased the frequency of regression (32% and 39% versus 11%), and reduced the incidence of cardiovascular events in men with coronary artery disease who were at high risk for cardiovascular events.<ref name="pmid2215615">{{cite journal |author=Brown G, Albers JJ, Fisher LD, ''et al.'' |title=Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B |journal=N. Engl. J. Med. |volume=323 |issue=19 |pages=1289–98 |year=1990 |month=November |pmid=2215615 |doi=10.1056/NEJM199011083231901 |url=}}</ref><ref name="pmid8252687">{{cite journal |author=Zhao XQ, Brown BG, Hillger L, ''et al.'' |title=Effects of intensive lipid-lowering therapy on the coronary arteries of asymptomatic subjects with elevated apolipoprotein B |journal=Circulation |volume=88 |issue=6 |pages=2744–53 |year=1993 |month=December |pmid=8252687 |doi= |url=}}</ref><ref name="pmid23168285">{{cite journal |author=Phan BA, Muñoz L, Shadzi P, ''et al.'' |title=Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment Study (HATS), Armed Forces Regression Study (AFREGS), and Carotid Plaque Composition by MRI during lipid-lowering (CPC) study |journal=Am. J. Cardiol. |volume=111 |issue=3 |pages=352–5 |year=2013 |month=February |pmid=23168285 |doi=10.1016/j.amjcard.2012.09.034 |url=}}</ref><ref name="pmid8106695">{{cite journal |author=Stewart BF, Brown BG, Zhao XQ, ''et al.'' |title=Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol |journal=J. Am. Coll. Cardiol. |volume=23 |issue=4 |pages=899–906 |year=1994 |month=March |pmid=8106695 |doi= |url=}}</ref><ref name="pmid7695184">{{cite journal |author=Brown BG, Hillger L, Zhao XQ, Poulin D, Albers JJ |title=Types of change in coronary stenosis severity and their relative importance in overall progression and regression of coronary disease. Observations from the FATS Trial. Familial Atherosclerosis Treatment Study |journal=Ann. N. Y. Acad. Sci. |volume=748 |issue= |pages=407–17; discussion 417–8 |year=1995 |month=January |pmid=7695184 |doi= |url=}}</ref><ref name="pmid7500507">{{cite journal |author=Maher VM, Brown BG, Marcovina SM, Hillger LA, Zhao XQ, Albers JJ |title=Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a) |journal=JAMA |volume=274 |issue=22 |pages=1771–4 |year=1995 |month=December |pmid=7500507 |doi= |url=}}</ref><ref name="pmid10208998">{{cite journal |author=Zambon A, Hokanson JE, Brown BG, Brunzell JD |title=Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density |journal=Circulation |volume=99 |issue=15 |pages=1959–64 |year=1999 |month=April |pmid=10208998 |doi= |url=}}</ref>


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[[Category:HDL]]
[[Category:HDL]]
[[Category:Clinical trials]]
[[Category:Clinical trials]]
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Official Title

Objective

To compare the effects of two intensive lipid altering therapies in men with familial combined hyperlipidemia as assessed by arteriography.

Timeline

Timeline
Start Date
End Date
Status

The previous information was derived from ClinicalTrials.gov on 08/18/2014 using the identification number NCT00136981.

Study Description

Study Description
Study Type
Study Phase
Study Design
Allocation
Endpoint
Interventional Model
Masking
Study Details
Primary Purpose
Condition
Intervention
Study Arms
Population Size

The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT00136981.

Eligibility Criteria

Inclusion Criteria

Exclusion Criteria

Outcomes

Primary Outcomes

Publications

Results

Conclusion

Both the intensive lipid lowering therapies were equally effective. Both reduced the frequency of progression of coronary lesions (21% and 25% versus 46% in the control group), increased the frequency of regression (32% and 39% versus 11%), and reduced the incidence of cardiovascular events in men with coronary artery disease who were at high risk for cardiovascular events.[1][2][3][4][5][6][7]

References

  1. Brown G, Albers JJ, Fisher LD; et al. (1990). "Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B". N. Engl. J. Med. 323 (19): 1289–98. doi:10.1056/NEJM199011083231901. PMID 2215615. Unknown parameter |month= ignored (help)
  2. Zhao XQ, Brown BG, Hillger L; et al. (1993). "Effects of intensive lipid-lowering therapy on the coronary arteries of asymptomatic subjects with elevated apolipoprotein B". Circulation. 88 (6): 2744–53. PMID 8252687. Unknown parameter |month= ignored (help)
  3. Phan BA, Muñoz L, Shadzi P; et al. (2013). "Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment Study (HATS), Armed Forces Regression Study (AFREGS), and Carotid Plaque Composition by MRI during lipid-lowering (CPC) study". Am. J. Cardiol. 111 (3): 352–5. doi:10.1016/j.amjcard.2012.09.034. PMID 23168285. Unknown parameter |month= ignored (help)
  4. Stewart BF, Brown BG, Zhao XQ; et al. (1994). "Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol". J. Am. Coll. Cardiol. 23 (4): 899–906. PMID 8106695. Unknown parameter |month= ignored (help)
  5. Brown BG, Hillger L, Zhao XQ, Poulin D, Albers JJ (1995). "Types of change in coronary stenosis severity and their relative importance in overall progression and regression of coronary disease. Observations from the FATS Trial. Familial Atherosclerosis Treatment Study". Ann. N. Y. Acad. Sci. 748: 407–17, discussion 417–8. PMID 7695184. Unknown parameter |month= ignored (help)
  6. Maher VM, Brown BG, Marcovina SM, Hillger LA, Zhao XQ, Albers JJ (1995). "Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a)". JAMA. 274 (22): 1771–4. PMID 7500507. Unknown parameter |month= ignored (help)
  7. Zambon A, Hokanson JE, Brown BG, Brunzell JD (1999). "Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density". Circulation. 99 (15): 1959–64. PMID 10208998. Unknown parameter |month= ignored (help)