Effect of Cholesterol-Lowering Therapy on Coronary Endothelial Vasomotor Function in Patients With Coronary Artery Disease

Vita, Joseph A.; Yeung, Alan C.; Winniford, Michael D.; Hodgson, John McB.; Treasure, Charles B.; Klein, Jacob; Werns, Steven W.; Kern, Morton J.; Plotkin, D.; Shih, Weichung J.; Mitchel, Yale; Ganz, Patricia A.

doi:10.1161/01.cir.102.8.846

Cited by 110 publications

(76 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similar to our findings, another study showed that 6 months of cholesterol-lowering therapy had no significant effect on coronary endothelial vasomotor function in a population of patients with CAD and mildly elevated cholesterol levels. 23 In that study, the authors also suggested the reason for the lack of improvement in endothelial function was attributable to a lower baseline LDL-C level and the mild degree of CAD. Therefore, these findings support the importance of adequate statin treatment for primary prevention.…”

Section: Discussionmentioning

confidence: 94%

“…Additionally, the proportion of subjects who normalized endothelial function (RHI ≥2) after atorvastatin and placebo treatment was not significantly different (40% vs 37%, P = 1.000) (Figure 3). The augmentation index after atorvastatin treatment was not different from that after placebo treatment (24 [IQR, [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] vs 29 [IQR 16-35], P = 0.922). In the subgroup analysis, these results were consistent both in subjects indicated for drug therapy (11 subjects, 31%) and subjects not indicated for drug therapy (24 subjects, 69%), according to the NCEP-ATP III guidelines.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Impact of Atorvastatin Treatment in First‐Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double‐Blind, Randomized, Placebo‐Controlled Crossover Trial

Hong

Chang

Park

et al. 2013

Clinical Cardiology

View full text Add to dashboard Cite

Background: A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events. Hypothesis: Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED. Methods: Thirty-five FDRs (median age, 52 years [interquartile range (IQR), 46-57 years], 21 male) of patients with premature CAD with ED were recruited in a prospective trial with a crossover double-blind design: 6 weeks of treatment with atorvastatin 40 mg/day followed by placebo, or vice versa. After each treatment, the digital pulse wave amplitude was determined by EndoPAT to obtain the reactive hyperemia index (RHI), a measure for endothelial function. The primary outcome was the difference of RHI between atorvastatin and placebo treatment.Results: Low-density lipoprotein cholesterol was lower after atorvastatin compared with placebo treatment (124 [102-145] mg/dL vs 67 [50-73] mg/dL, P < 0.001). However, RHI was not different after atorvastatin compared with placebo treatment (1.9 [1.5-2.4] vs 1.9 [1.6-2.2], P = 0.902). Also, the augmentation index was similar after each treatment. These results were observed both in subjects who had indications for statin treatment (31%) and those who did not (69%) according to National Cholesterol Education Program Adult Treatment Panel III guidelines. Conclusions: Despite improvement in the lipid profile, atorvastatin failed to improve ED in the FDRs of patients with premature CAD with ED. Although we identified those with ED in FDRs of patients with premature CAD as a high-risk group for future cardiovascular events, atorvastatin treatment may not be a beneficial primary prevention strategy for this population.

show abstract

Section: Discussionmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

Impact of Atorvastatin Treatment in First‐Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double‐Blind, Randomized, Placebo‐Controlled Crossover Trial

Hong

Chang

Park

et al. 2013

Clinical Cardiology

View full text Add to dashboard Cite

show abstract

“…[7][8][9][10][11][12][13][14] What this study adds Pravastatin 40 mg daily did not reduce blood pressure or pulse pressure at any time point in 4126 survivors of myocardial infarction who were followed for more than 5 years.…”

mentioning

confidence: 73%

“…6 For instance, statins reduce markers of inflammation such as C-reactive protein, 7 and may reverse endothelial dysfunction through their effects on nitric oxide synthase 8 or by other mechanisms, 9 although this is controversial. 10 Since these abnormalities are associated with hypertension, it is plausible that statin therapy might also reduce blood pressure. 11,12 Several previous experimental and retrospective studies suggest that statins reduce blood pressure in animals and humans with and without hypertension.…”

Section: Introductionmentioning

confidence: 99%

Effect of pravastatin on blood pressure in people with cardiovascular disease

et al. 2006

View full text Add to dashboard Cite

Experimental evidence and several small studies in humans suggest that HMG-CoA (3-hydroxy 3-methylglutaryl coenzyme A) reductase inhibitors (statins) reduce blood pressure, perhaps through effects on endothelial function or by reducing inflammation. We tested the hypothesis that pravastatin would reduce blood pressure at 3 months and the risk of developing new hypertension over a follow-up period of 5 years. This was a post hoc subgroup analysis of a randomized double-blind placebo-controlled trial of pravastatin 40 mg daily vs placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol o240 mg/dl (6.2 mmol/l). The primary outcome was the unadjusted change in mean arterial pressure (MAP) from baseline to 3 months. We also considered systolic and diastolic blood pressure (SBP and DBP) and pulse pressure. Analysis of covariance was used to calculate the adjusted effect of treatment on change in these outcomes at 3, 6, 12 and 24 months postrandomization, after controlling for potential confounders. Logistic regression was used to calculate the adjusted effect of treatment on incident hypertension (blood pressure X140/90 in those without known hypertension at baseline). This analysis included 4126/4159 (99.2%) participants for whom blood pressure was measured at baseline and during at least one follow-up visit. Median duration of follow-up was 57.8 months. The unadjusted and adjusted change in MAP, SBP, DBP or pulse pressure from baseline was not significantly different for pravastatin or placebo recipients at 3, 6, 12 or 24 months after randomization, or at last follow-up. Pravastatin did not reduce the adjusted risk of incident systolic hypertension (odds ratio 0.99, 95% CI 0.80-1.23), or incident diastolic hypertension (odds ratio 0.97, 95% CI 0.73-1.27). In summary, pravastatin 40 mg daily did not reduce blood pressure in survivors of myocardial infarction without overt hypercholesterolaemia.

show abstract

“…8,9 Thus, improved endothelium-dependent dilator responsiveness after statin therapy, demonstrated by provocative testing and clinically manifest as reduced ischemia during stress, has been viewed widely as a useful mechanistic surrogate for reduced cardiovascular risk by that therapy. However, in this issue of Circulation, 10 investigators of the Coronary Artery Reactivity After Treatment with Simvastatin (CARATS) study found no benefit of simvastatin 40 mg/d for 6 months to coronary artery epicardial or microvascular endothelial vasodilator function in 34 analyzable patients with mild to moderate coronary artery disease randomly assigned to this therapy, compared with 26 analyzable patients randomized to placebo in a double-blind clinical trial. Participants were mildly hypercholesterolemic (average LDL cholesterol 130 mg/dL) and had not been on cholesterollowering therapy for at least 6 weeks before study.…”

Section: See P 846 Endothelial Vasodilator Function Testing Myocardimentioning

confidence: 98%

Cardiovascular Benefit of Cholesterol-Lowering Therapy

Cannon

2000

Circulation

View full text Add to dashboard Cite

Effect of Cholesterol-Lowering Therapy on Coronary Endothelial Vasomotor Function in Patients With Coronary Artery Disease

Cited by 110 publications

References 27 publications

Impact of Atorvastatin Treatment in First‐Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double‐Blind, Randomized, Placebo‐Controlled Crossover Trial

Impact of Atorvastatin Treatment in First‐Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double‐Blind, Randomized, Placebo‐Controlled Crossover Trial

Effect of pravastatin on blood pressure in people with cardiovascular disease

Cardiovascular Benefit of Cholesterol-Lowering Therapy

Contact Info

Product

Resources

About