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Achieving cholesterol targets by individualizing starting doses of statin according to baseline low-density lipoprotein cholesterol and coronary artery disease risk category: the CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (CanACTFAST) study.

https://arctichealth.org/en/permalink/ahliterature145456
Source
Can J Cardiol. 2010 Feb;26(2):80-6
Publication Type
Article
Date
Feb-2010
Author
Ehud Ur
Anatoly Langer
Simon W Rabkin
Cristina-Dana Calciu
Lawrence A Leiter
Author Affiliation
University of British Columbia, Vancouver, BC, Canada.
Source
Can J Cardiol. 2010 Feb;26(2):80-6
Date
Feb-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Canada
Cholesterol, LDL - blood - drug effects
Coronary Artery Disease - blood - etiology - prevention & control
Dose-Response Relationship, Drug
Female
Follow-Up Studies
Heptanoic Acids - administration & dosage
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - administration & dosage
Hypercholesterolemia - blood - complications - drug therapy
Male
Middle Aged
Pyrroles - administration & dosage
Risk factors
Treatment Outcome
Abstract
Despite an increasing body of evidence on the benefit of lowering elevated levels of low-density lipoprotein cholesterol (LDL-C), there is still considerable concern that patients are not achieving target LDL-C levels.
The CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (CanACTFAST) trial tested whether an algorithm-based statin dosing approach would enable patients to achieve LDL-C and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio targets quickly.
Subjects requiring statin therapy, but with an LDL-C level of 5.7 mmol/L or lower, and triglycerides of 6.8 mmol/L or lower at screening participated in the 12-week study, which had two open-label, six-week phases: a treatment period during which patients received 10 mg, 20 mg, 40 mg or 80 mg of atorvastatin based on an algorithm incorporating baseline LDL-C value and cardiovascular risk; and patients who achieved both LDL-C and TC/HDL-C ratio targets at six weeks continued on the same atorvastatin dose. Patients who did not achieve both targets received dose uptitration using a single-step titration regimen. The primary efficacy outcome was the proportion of patients achieving target LDL-C levels after 12 weeks.
Of 2016 subjects screened at 88 Canadian sites, 1258 were assigned to a study drug (1101 were statin-free and 157 were statin-treated at baseline). The proportion of subjects who achieved LDL-C targets after 12 weeks of treatment was 86% (95% CI 84% to 88%) for statin-free patients and 54% (95% CI 46% to 61%) for statin-treated patients. Overall, 1003 subjects (80%; 95% CI 78% to 82%) achieved both lipid targets.
Algorithm-based statin dosing enables patients to achieve LDL-C and TC/HDL-C ratio targets quickly, with either no titration or a single titration.
Notes
Cites: CMAJ. 2000 May 16;162(10):1441-710834048
Cites: Atherosclerosis. 2007 Mar;191(1):135-4616643923
Cites: JAMA. 2001 May 16;285(19):2486-9711368702
Cites: Am Heart J. 2001 Jun;141(6):949-5611376309
Cites: Am J Med. 2001 Aug 15;111(3):185-9111530028
Cites: JAMA. 2002 Jul 24-31;288(4):462-712132976
Cites: Am J Cardiol. 2003 Jul 1;92(1):79-8112842255
Cites: CMAJ. 2003 Oct 28;169(9):921-414581310
Cites: JAMA. 2004 Mar 3;291(9):1071-8014996776
Cites: Lancet. 1994 Nov 19;344(8934):1383-97968073
Cites: N Engl J Med. 1996 Oct 3;335(14):1001-98801446
Cites: J Am Coll Cardiol. 1998 Sep;32(3):665-729741509
Cites: Am Heart J. 2004 Dec;148(6):1028-3315632889
Cites: Am Heart J. 2005 Jan;149(1):e115660024
Cites: N Engl J Med. 2005 Apr 7;352(14):1425-3515755765
Cites: Lancet. 2005 Oct 8;366(9493):1267-7816214597
Cites: Can J Cardiol. 2005 Nov;21(13):1187-9316308595
Cites: Am J Cardiol. 2006 Jan 1;97(1):61-716377285
Cites: Am Heart J. 2006 May;151(5):969-7516644313
Cites: Am J Med. 2006 Aug;119(8):676-8316887414
Cites: Can J Cardiol. 2006 Sep;22(11):913-2716971976
Cites: Circulation. 2007 Feb 13;115(6):700-717283260
Cites: Atherosclerosis. 2000 Oct;152(2):489-9610998478
PubMed ID
20151053 View in PubMed
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[Atherosclerotic lesion of the vessels in patients with stable coronary artery disease: relations with concentration of C-reactive protein].

https://arctichealth.org/en/permalink/ahliterature150806
Source
Kardiologiia. 2009;49(4):40-5
Publication Type
Article
Date
2009
Author
E V Paniugova
E N Aleksandrova
E L Nasonov
Iu A Karpov
Source
Kardiologiia. 2009;49(4):40-5
Date
2009
Language
Russian
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Atherosclerosis - blood - complications - epidemiology
C-Reactive Protein - metabolism
Coronary Angiography
Coronary Artery Disease - blood - etiology - radiography
Female
Follow-Up Studies
Humans
Incidence
Male
Middle Aged
Prognosis
Risk factors
Russia - epidemiology
Abstract
To study value of C reactive protein (CRP) in development of atherosclerotic lesion of vascular wall and its relation to extent of pathological process in patients with stable coronary artery disease.
We studied 307 patients with stable coronary artery disease (278 men, 29 women) aged 33 - 80 years (mean age 58 years) with arterial atherosclerosis of various severity and extent. All patients were subjected to clinical, biochemical, and instrumental examination. Coronary angiography was performed when indicated. Analysis of traditional risk factors was also carried out. CRP was measured with high sensitivity method.
Elevated CRP level (> 3 mg/1) was found in 34% of patients. Patients who had atherosclerotic changes (stenosing plaques) in carotid, pelvic or leg arteries, celiac trunk, renal and mesenteric arteries (group 2, n=37) had significantly higher CRP concentrations (p=0.002) than patients who had only atherosclerosis in coronary arteries (group 1, n=270). CRP concentration did not correlate with number of stenosed coronary vessels according to coronary angiographic findings. Patients with hypertension, type 2 diabetes and smokers had significantly higher CRP concentrations ( =0.013, =0.002, =0.004, respectively).
In patients with stable coronary artery disease combination of coronary and peripheral atherosclerosis is associated with increased CRP concentration. CRP and data of coronary angiography in patients with stable coronary artery disease are essentially independent factors. Elevated CRP level is associated with traditional risk factors of coronary artery disease (smoking, hypertension, type 2 diabetes).
PubMed ID
19463117 View in PubMed
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Cascade plasma filtration during the first year after CABG in patients with hyperlipidemia refractory to statins.

https://arctichealth.org/en/permalink/ahliterature116814
Source
Atheroscler Suppl. 2013 Jan;14(1):101-5
Publication Type
Article
Date
Jan-2013
Author
Marat V Ezhov
Larisa N Il'ina
Maya S Safarova
Olga I Afanasieva
Irina Yu Adamova
Ruslan V Atanesyan
Gennadiy A Konovalov
Renat S Akchurin
Sergei N Pokrovsky
Author Affiliation
Cardiology Research Center, 15a, 3rd Cherepkovskaya Street, 121552 Moscow, Russia.
Source
Atheroscler Suppl. 2013 Jan;14(1):101-5
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biological Markers - blood
Blood Component Removal - methods
Chi-Square Distribution
Cholesterol, LDL - blood
Combined Modality Therapy
Coronary Angiography
Coronary Artery Bypass - adverse effects
Coronary Artery Disease - blood - etiology - radiography - surgery
Drug resistance
Graft Occlusion, Vascular - etiology - physiopathology - prevention & control - radiography
Heptanoic Acids - therapeutic use
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Hyperlipidemias - blood - complications - diagnosis - therapy
Male
Middle Aged
Prospective Studies
Pyrroles - therapeutic use
Risk factors
Russia
Time Factors
Treatment Outcome
Vascular Patency
Abstract
To evaluate the effect of a 12-month course of weekly lipid apheresis on vein graft patency after coronary artery bypass grafting (CABG) in patients with hyperlipidemia refractory to statins.
In a 12-month prospective controlled clinical trial we enrolled 34 male patients (mean age 57 ± 8 years) who passed through successful CABG and low-density lipoprotein cholesterol (LDL-C) level >2.6 mmol/L prior to the operation despite statin treatment. Patients were allocated into 2 groups: active (n = 17, weekly apheresis by cascade plasma filtration (CPF) plus atorvastatin), and control (n = 17, atorvastatin alone). Graft patency was evaluated by multislice computed tomography at 3 months and by angiography at 12 months after an operation.
Both groups were comparable in clinical and biochemical characteristics. During each CPF procedure, LDL-C level decreased by 64 ± 9%, apoB - by 65 ± 8%, Lp(a) - by 52 ± 15%,; these changes were significant compared to baseline and the control group. Mean net difference in LDL-C level between apheresis and control groups was 1.1 ± 0.3 mmol/L. Vein graft patency at study end was 88.2% (45 of 51) in the apheresis group versus 72.7% (40 of 55) in the control group (p = 0.05). Use of apheresis was associated with decreased vein graft occlusions by 46%: relative risk 0.54; 95% confidence interval 0.27 to 1.02; p = 0.05.
Our data suggest that the use of lipoprotein apheresis with CPF results in a better vein graft patency during the first year after CABG in patients with hyperlipidemia refractory to statins.
PubMed ID
23357150 View in PubMed
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NT-proBNP, echocardiographic abnormalities and subclinical coronary artery disease in high risk type 2 diabetic patients.

https://arctichealth.org/en/permalink/ahliterature126442
Source
Cardiovasc Diabetol. 2012;11:19
Publication Type
Article
Date
2012
Author
Henrik Reinhard
Peter R Hansen
Niels Wiinberg
Andreas Kjær
Claus L Petersen
Kaj Winther
Hans-Henrik Parving
Peter Rossing
Peter K Jacobsen
Author Affiliation
Steno Diabetes Center, Niels Steensenvej 1, DK-2820 Gentofte, Denmark. hrhl@dadlnet.dk
Source
Cardiovasc Diabetol. 2012;11:19
Date
2012
Language
English
Publication Type
Article
Keywords
Aged
Albuminuria - etiology
Asymptomatic Diseases
Biological Markers - blood
Coronary Angiography - methods
Coronary Artery Disease - blood - etiology - ultrasonography
Cross-Sectional Studies
Denmark
Diabetes Complications - blood - etiology - ultrasonography
Diabetes Mellitus, Type 2 - complications - therapy
Echocardiography, Doppler
Female
Heart Atria - ultrasonography
Humans
Hypertrophy, Left Ventricular - blood - etiology - ultrasonography
Linear Models
Logistic Models
Male
Middle Aged
Multivariate Analysis
Myocardial Perfusion Imaging
Natriuretic Peptide, Brain - blood
Odds Ratio
Peptide Fragments - blood
Predictive value of tests
Risk assessment
Risk factors
Tomography, X-Ray Computed
Ventricular Dysfunction, Left - blood - etiology - ultrasonography
Abstract
Intensive multifactorial treatment aimed at prevention of cardiovascular (CV) disease may reduce left ventricular (LV) echocardiographic abnormalities in diabetic subjects. Plasma N-terminal (NT)-proBNP predicts CV mortality in diabetic patients but the association between P-NT-proBNP and the putative residual abnormalities in such patients are not well described. This study examined echocardiographic measurements of LV hypertrophy, atrial dilatation and LV dysfunction and their relation to P-NT-proBNP levels or subclinical coronary artery disease (CAD) in type 2 diabetic patients with microalbuminuria receiving intensive multifactorial treatment.
Echocardiography including tissue Doppler imaging and P-NT-proBNP measurements were performed in 200 patients without prior CAD. Patients with P-NT-proBNP > 45.2 ng/L and/or coronary calcium score = 400 were stratified as high risk patients for CAD(n = 133) and examined for significant CAD by myocardial perfusion imaging and/or CT-angiography and/or coronary angiography.
LV mass index was 41.2 ± 10.9 g/m2.7 and 48 (24%) patients had LV hypertrophy. LA and RA dilatation were found in 54(27%) and 45(23%) patients, respectively, and LV diastolic dysfunction was found in 109(55%) patients. Patients with increased P-NT-proBNP levels did not have more major echocardiographic abnormalities. In 70(53%) of 133 high risk patients significant CAD was demonstrated and patients with LV hypertrophy had increased risk of significant CAD(adjusted odd ratio[CI] was 4.53[1.14-18.06]).
Among asymptomatic type 2 diabetic patients with microalbuminuria that received intensive multifactorial treatment, P-NT-proBNP levels is not associated with echocardiographic abnormalities. LV diastolic dysfunction was frequently observed, whereas LV hypertrophy was less frequent but associated with significant CAD.
Notes
Cites: Am J Physiol Heart Circ Physiol. 2000 May;278(5):H1500-610775127
Cites: Am J Cardiol. 2001 Nov 15;88(10):1163-811703964
Cites: Lancet. 2002 Apr 20;359(9315):1430-211978359
Cites: JAMA. 2003 Jan 8;289(2):194-20212517230
Cites: Angiology. 1972 Apr;23(4):211-75030556
Cites: Am J Cardiol. 1986 Feb 15;57(6):450-82936235
Cites: J Am Coll Cardiol. 1990 Mar 15;15(4):827-322407762
Cites: Diabet Med. 1997 Jul;14(7):538-469223391
Cites: Circulation. 1998 Jan 6-13;97(1):48-549443431
Cites: Diabetologia. 2005 Jan;48(1):156-6315619076
Cites: Am J Cardiol. 2005 Sep 15;96(6):832-616169372
Cites: QJM. 2005 Dec;98(12):879-8416272208
Cites: J Am Soc Echocardiogr. 2005 Dec;18(12):1440-6316376782
Cites: Eur J Echocardiogr. 2006 Jan;7(1):40-415886060
Cites: Eur J Echocardiogr. 2006 Mar;7(2):79-10816458610
Cites: Circulation. 2006 Mar 28;113(12):1588-9616534012
Cites: Diabetologia. 2006 Oct;49(10):2256-6216937127
Cites: Eur Heart J. 2006 Nov;27(21):2588-60517000623
Cites: Circulation. 2007 Jun 26;115(25):3213-2317592090
Cites: Eur Heart J. 2007 Oct;28(20):2539-5017428822
Cites: Clin Sci (Lond). 2008 Feb;114(4):313-2017916064
Cites: N Engl J Med. 2008 Feb 7;358(6):580-9118256393
Cites: J Am Soc Echocardiogr. 2009 Feb;22(2):107-3319187853
Cites: Nutr Metab Cardiovasc Dis. 2009 Jun;19(5):306-1219303268
Cites: J Cardiovasc Comput Tomogr. 2009 May-Jun;3(3):190-20419409872
Cites: Diabetes. 2009 Nov;58(11):2448-919875621
Cites: Circ Cardiovasc Imaging. 2010 Jan;3(1):24-3119846730
Cites: Cardiovasc Diabetol. 2010;9:220078898
Cites: Cardiovasc Diabetol. 2010;9:8921162718
Cites: J Am Coll Cardiol. 2011 Mar 22;57(12):1386-9521414536
Cites: Cardiovasc Diabetol. 2011;10:7121812947
Cites: Nephrol Dial Transplant. 2011 Oct;26(10):3242-921372253
PubMed ID
22390472 View in PubMed
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Tracking of serum total cholesterol during childhood: an 8-year follow-up population-based family study in eastern Finland.

https://arctichealth.org/en/permalink/ahliterature184997
Source
Acta Paediatr. 2003 Apr;92(4):420-4
Publication Type
Article
Date
Apr-2003
Author
R M Fuentes
I L Notkola
S. Shemeikka
J. Tuomilehto
A. Nissinen
Author Affiliation
Department of Public Health and General Practice, Faculty of Medicine, University of Kuopio, Kuopio, Finland. ricardo.fuentes@messi.uku.fi
Source
Acta Paediatr. 2003 Apr;92(4):420-4
Date
Apr-2003
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Child
Cholesterol - blood
Cohort Studies
Coronary Artery Disease - blood - etiology
Family Health
Female
Finland
Follow-Up Studies
Humans
Hypercholesterolemia - blood - complications
Infant
Longitudinal Studies
Male
Middle Aged
Risk factors
Rural Population
Time Factors
Abstract
To investigate the tracking of serum total cholesterol (TC) during childhood.
All children born during 1981-1982 in a rural community of eastern Finland were followed at 6 mo, 7 y and 15 y of age. The full follow-up period was completed by 138 out of 205 children, of whom 82 (33 girls) had TC measured at 7 y and 15 y of age (-7 y, -15 y). The main outcome measurement was TC (mmol/L).
TC-7 y was significantly associated with TC-15 y (r = 0.655; p-value or = 5.0 mmol/L in at least one parent) (beta = 0.58; p-value = 0.030). Birthweight had no significant association with TC during childhood.
The study confirmed the tracking of TC during childhood. The identification of children at risk of developing high TC during adolescence should take into consideration the child's previous TC values during childhood and parental TC status.
PubMed ID
12801106 View in PubMed
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