Intensive Lipid-lowering Therapy Research Articles

Comparison of Effects of Pitavastatin Versus Pravastatin on Serum Proprotein Convertase Subtilisin/Kexin Type 9 Levels in Statin-Naive Patients With Coronary Artery Disease

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of serum low-density lipoprotein cholesterol levels. Although statins increase serum PCSK9 levels, the effects of different types of statins on the serum PCSK9 levels have not been examined in detail. The purpose of the present study was to compare the effects of pitavastatin versus pravastatin on the serum PCSK9 levels. A total of 164 patients with coronary artery disease who were not receiving lipid-lowering therapy were randomly assigned to receive either 4mg/day of pitavastatin (intensive lipid-lowering therapy) or 20 mg/day of pravastatin (moderate lipid-lowering therapy). The serum PCSK9 levels were measured before statin treatment and 8 months after therapy. A significantly greater reduction in low-density lipoprotein cholesterol was observed in the pitavastatin group (-41% vs-28%, p= 0.0001). The serum levels of total PCSK9 and heterodimer PCSK9 significantly increased from 192 to 249 ng/ml (37%, p <0.0001) and 147 to 206 ng/ml (78%, p <0.0001) in the pitavastatin group and from 192 to 249 ng/ml (39%, p <0.0001) and 143 to 201 ng/ml (65%, p <0.0001) in the pravastatin group, respectively. The increase in total and heterodimer PSCK9 did not differ between the 2 groups. No significant correlations were found between the percentage of changes in heterodimer PCSK9 and changes in the various lipid parameters in either group. In conclusion, significant increases in the total and heterodimer PSCK9 levels were observed at 8 months after treatment with pitavastatin and pravastatin; however, these increases did not differ between the 2 statins.

Abstract 148: Intensive Lipid Lowering Therapy Using Rosuvastatin Associates with Greater Atherosclerotic Aortic Plaques Regression - A Magnetic Resonance Imaging Study

Whether intensive lipid-lowering therapy yields greater regression of atherosclerotic plaques remains inconclusive. We therefore performed a prospective, randomized trial comparing standard (achieving LDL-C levels recommended by the Japanese guideline) and intensive (achieving further 30% lower levels than the former) rosuvastatin therapy for 1 year with primary outcome of aortic plaques evaluated by MRI. Sixty dyslipidemic patients, who were eligible for statins therapy, were randomized to standard or intensive group, and dose of rosuvastatin were titrated to achieve the respective target LDL-C. Average doses of rosuvastatin throughout the study were 2.9±3.1 and 6.5±5.1 mg/day in standard and intensive group, respectively. Although both treatments significantly reduced serum LDL-C and hsCRP levels, reduction of LDL-C levels was greater in intensive group than in standard group (-46 vs. -34%). Intensive therapy improved endothelial function as evaluated by FMD in brachial artery compared to standard therapy (95 vs. 22%). MRI study revealed that both thoracic and abdominal plaques were significantly regressed in both groups with greater regression in thoracic plaques in intensive group compared to standard group (-9.1 vs. -3.2%) (Figure A). Correlation analysis revealed no significant association of plaque regression with the doses of rosuvastatin and the changes in serum lipids/FMD. In contrast, thoracic plaque regression correlated with hsCRP reduction (Figure B). Multivariate analysis demonstrated that this association still remain significant even after adjustment of the doses at flow-up, serum lipids and FMD. In conclusions, the present study demonstrated that intensive lipid-lowering using rosuvastatin led to additive plaques regression compared to standard therapy. Therefore, rosuvastatin may provide long term benefit in patients with increased risk through its LDL-C lowering and anti-inflammatory effects.

Statins in Variant Angina

REFER TO THE PAGE 58-63 Variant angina pectoris (VAP) is a form of angina pectoris that shows transient ST-segment elevation on electrocardiogram during an attack of chest pain and is caused by coronary artery spasm.1),2) Although the pathogenesis of coronary artery spasm has not been fully elucidated, endothelial dysfunction and enhanced vascular smooth muscle contractility play major roles in the pathogenesis of coronary artery spasm. Other contributing factors of coronary artery spasm include increased oxidative stress, inflammation, magnesium deficiency, genetic susceptibility, and imbalance in autonomic nervous activity.1-3) Statins have been demonstrated to significantly improve the prognosis and outcome of patients with atherosclerosis mainly because statins can lower low density lipoprotein (LDL)-cholesterol concentration.4),5) However, recent studies suggested that statins may affect the cardiovascular system beyond their effect on the lipid profile (called pleiotropic effects).6) Pleiotropic effects of statins include improvement of endothelial dysfunction, increased nitric oxide bioavailability, antioxidant properties, inhibition of inflammatory responses, and stabilization of atherosclerotic plaques, which may provide a cardiovascular benefit beyond that expected from LDL-cholesterol lowering alone.7),8) These effects of modulated endothelial function and reduced inflammatory processes have been pointed out as one of the possible mechanisms of reducing coronary artery vasospasm in VAP.8) Recent clinical evidences also showed that combined therapy with a statin and a calcium channel blocker may attenuate coronary vasoconstriction as well as systemic endothelial dysfunction in patients with VAP.9),10) In this issue of Journal of Cardiovascular Ultrasound, Kim et al.11) also support the evidence that the use of atorvastatin, regardless of dosage, could improve systemic endothelial function as measured by flow mediated dilation of the brachial artery in patients with VAP. Collectively, statin might modify the underlying pathogenesis of coronary artery spasm and be a novel therapeutic drug for coronary artery spasm in patients with VAP. Kim et al.11) also hypothesized that atorvastatin 40 mg could improve more endothelial function and carotid intima media thickness than those of atorvastatin 10 mg. It has not been demonstrated the dose-dependent effects of statin therapy on vascular function in patients with VAP. Experimental studies support this hypothesis that statins can dose-dependently increase the production of nitric oxide by activation of endothelial nitric oxide synthase and increasing its mRNA half-life, independent of cholesterol levels.12),13) Clinical evidence also suggested that intensive lipid-lowering therapy with statin provides significant clinical benefit beyond lipid-lowering therapy in patients with atherosclerosis, which is suggestive of dose-dependent pleiotropic effects of statin.14) However, Kim et al.11) in this issue of J Cardiovasc Ultrasound concluded that the use of high dose statin (atorvastatin 40 mg) did not show significant additional benefit as compared with the use of low dose statin (atorvastatin 10 mg) with regarding carotid intima media thickness and endothelial function. I have some comments about this study. First, atorvastatin 80 mg as a high dose group rather than atorvastatin 40 mg would be a proper dosage for proving additive beneficial effects of endothelial dysfunction and carotid intima media thickness because no clear evidence exists to support additional beneficial effects of medium-dose statin (atorvastatin 40 mg) on vascular function as well as clinical benefits. Second, the study duration is relatively shorter (6 month) for the detection of changes of carotid intima media thickness and flow mediated dilation. These changes of both flow mediated dilation and carotid intima media thickness with statins correlated with the duration × treatment intensity product.15) It needs more than 2 years for the changes of carotid intima media thickness on the progression of carotid atherosclerosis. Finally, the numbers of the study subjects are relatively small to detect the difference of vascular function between atorvastatin 40 mg and atorvastatin 10 mg. In the study of Kim et al.,11) it seems to be more increase of flow mediated dilation in atorvastatin 40 mg group (7.9 ± 2.7% to 9.5 ± 2.8%) than those in atorvastatin 10 mg group (7.7 ± 2.5% to 8.9 ± 2.2%). But, these results were statistically insignificant due to under-powered sample size. Despite some limitations, the present study of Kim et al.11) showed that an addition of statin to the conventional calcium channel blocker and nitrate for 6 months significantly reduced systemic endothelial dysfunction measured by flow mediated dilation in patient with VAP. Statin might be a promising drug for the treatment of VAP.

Association Between Serum Levels of n-3 Polyunsaturated Fatty Acids and Coronary Plaque Detected by Coronary Computed Tomography Angiography in Patients Receiving Statin Therapy

Intensive lipid-lowering therapy with statins reduces cardiovascular events, but residual cardiovascular risks remain. Intake of n-3 polyunsaturated fatty acids (PUFAs) has been associated with cardiovascular events. We examined the relationships between serum n-3 PUFAs and coronary atherosclerotic findings on computed tomography angiography (CTA) in patients undergoing statin treatment. We enrolled 172 subjects (mean age: 68.2 years; 64% men) prior to statin treatment for 6 months. Serum PUFAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid, were measured. When the patients were divided into 2 groups according to the median EPA level (61.3 μg/ml), the low-EPA group showed higher incidences of 3-vessel plaque involvement (62% vs. 43%, P=0.015), noncalcified plaques (NCPs) (74% vs. 52%, P=0.0016), extensive NCPs (≥ 2 segments) (56% vs. 34%, P=0.0036), and high-risk plaques (minimum CT density <39 HU and remodeling index >1.05) (43% vs. 22%, P=0.0034). Multivariate analyses revealed that low EPA levels were an independent factor for these coronary plaque findings. The DHA levels were not independently associated with these findings. Low serum EPA level, but not serum DHA, is associated with the presence and extent of NCPs and high-risk plaques detected by coronary CTA in patients undergoing lipid-lowering therapy with statins.

Intensive Lipid-Lowering Therapy for Slowing Progression as Well as Inducing Regression of Atherosclerosis in Japanese Patients

This paper describes a subanalysis of the JART Study comparing rosuvastatin and pravastatin treatment. A total of 314 subjects were analyzed in this subanalysis, 282 of whom were eligible for evaluation of the relationship between LDL-C and carotid mean-IMT change. In the subanalysis, we evaluated the extent to which intensive lipid-lowering therapy slowed the mean-IMT progression by a correlation analysis between LDL-C and mean-IMT change after 12 months of statin treatment. Nearly half were male (49.4%) and elderly (49.7%). The majority (84.4%) were treated for primary prevention. Patients with hypertension and diabetes mellitus accounted for 65.3% and 44.0%, respectively. At the 12-month measurement point, mean-IMT change was correlated with LDL-C (R = 0.187; P = 0.0016), LDL-C/ HDL-C ratio (R = 0.152; P = 0.0105), and non-HDL-C (R = 0.132; P = 0.0259). Mean-IMT after 12 months was divided into 4 subgroups by LDL-C at 12 months; < 80, ≥ 80 to < 100, ≥ 100 to < 120, and ≥ 120 mg/dL. A trend analysis using the Jonckheere-Terpstra test showed statistical signifi cance (P = 0.0002). Even for prevention in Japanese patients who have lower risk of atherosclerotic disease than Western patients, lowering the LDL-C level to below the therapeutic target prevented mean-IMT progression after 12 months more strongly. These findings suggest that more intensive control of LDL-C to levels lower than those in current JAS guidelines should be required to achieve slowing of progression as well as induction of regression of atherosclerosis.

Errata: Intensive Lipid-Lowering Therapy for Slowing Progression as Well as Inducing Regression of Atherosclerosis in Japanese Patients [International Heart Journal Vol. 54 (2013) No. 1 p. 33-39

Errata: Intensive Lipid-Lowering Therapy for Slowing Progression as Well as Inducing Regression of Atherosclerosis in Japanese Patients [International Heart Journal Vol. 54 (2013) No. 1 p. 33-39

Abstract 9621: Intensive Lipid Lowering Therapy Using Rosuvastatin Associates with Greater Atherosclerotic Aortic Plaques Regression - A Magnetic Resonance Imaging Study -

Whether intensive lipid-lowering therapy yields greater regression of atherosclerotic plaques remains inconclusive. We therefore performed a prospective, randomized trial comparing standard (achieving LDL-C levels recommended by the Japanese guideline) and intensive (achieving further 30% lower levels than the former) rosuvastatin therapy for 1 year with primary outcome of aortic plaques evaluated by magnetic resonance imaging (MRI).Sixty patients, who were eligible for statins therapy (51 primary, 9 secondary prevention), were randomized to standard or intensive group, and dose of rosuvastatin were titrated to achieve the respective target LDL-C. Average doses of rosuvastatin throughout the study were 2.9±3.1 and 6.5±5.1 mg/day in standard and intensive group, respectively. Although both treatments significantly reduced LDL-C and high sensitive CRP(hsCRP) levels, reduction of LDL-C levels was greater in intensive group than in standard group (-46 vs. -34%). MRI study revealed that both thoracic and abdominal plaques were significantly regressed in both groups with greater regression in thoracic plaques in intensive group compared to standard group (-9.1 vs. -3.2%) (Figure A). Moreover, thoracic plaques regression correlated with reductions in hsCRP (FigureB).In conclusions, the present study demonstrated that intensive lipid-lowering using rosuvastatin led to additive plaques regression compared to standard therapy. Therefore, rosuvastatin may provide long term benefit in patients with increased risk through its potent LDL-C lowering and anti-inflammatory effects.

Ang-2 upregulation correlates with increased levels of MMP-9, VEGF, EPO and TGFβ1 in diabetic eyes undergoing vitrectomy

Angiogenesis in diabetic retinopathy (DR) is a multifactorial process regulated by hypoxia-induced growth factors and inflammatory cytokines. In addition to the angiogenic switch, the proteolytic processing and altered synthesis of the extracellular matrix are critical steps in this disease. This study was performed to evaluate the levels of matrix metalloproteinase-2 and matrix metalloproteinase-9 (MMP-2 and MMP-9), angiopoietin-1 and angiopoietin-2 (Ang-1 and Ang-2), vascular endothelial growth factor (VEGF), erythropoietin (EPO) and transforming growth factor-β1 (totalTGFβ1) in the vitreous of diabetic eyes undergoing vitrectomy compared with control eyes operated because of macular hole or pucker. Prospective consecutive controlled observational study performed in the unit of vitreoretinal surgery in Finland during the years 2006-2008. Vitreous samples were collected before the start of the conventional 3-ppp vitrectomy. Vitreous MMP-2 and MMP-9, Ang-1 and Ang-2, VEGF, EPO and TGFβ1 concentrations were measured from 69 patients with Type 1 or 2 diabetes and 40 controls. Comparison of eyes with DR with controls revealed that the mean vitreous concentrations of proMMP-2 (p = 0.0015), totalMMP-2 (p = 0.0011), proMMP-9 (p = 0.00001), totalMMP-9 (p < 0.00001), Ang-2 (p < 0.00001), VEGF (p < 0.00001), EPO (p < 0.00001) and totalTGFβ1 (p = 0.000026) were significantly higher in the former group. A multivariate logistic regression analysis suggested intravitreal Ang-2 concentration being the key marker of PDR (p = 0.00025) (OR = 1507.9). The main new finding is that the intravitreal concentrations of Ang-2 correlated significantly with MMP-9, VEGF, EPO and TGFβ1 levels in diabetic eyes undergoing vitrectomy. Thus, these factors could promote retinal angiogenesis synergistically.

TCT-244 Impact of Intensive Statin Therapy on Plaque Characteristics as Assessed by Serial Optical Coherence Tomography

Recent clinical trials have demonstrated that intensive lipid-lowering therapy by statins could prevent recurrent cardiac events after acute coronary syndrome (ACS). Optical coherence tomography (OCT) is capable of estimating fibrous cap thickness (FCT) of coronary atherosclerotic plaques, which

Effect of intensive lipid‐lowering therapy on cardiovascular outcome in patients with and those without inflammatory joint disease

To examine the effect of intensive lipid-lowering therapy on a composite cardiovascular outcome (cardiovascular disease [CVD]), consisting of mortality and morbidity end points, in patients with inflammatory joint disease (rheumatoid arthritis [RA], ankylosing spondylitis [AS], or psoriatic arthritis [PsA]) by post hoc analysis of 2 prospective trials of statins with a secondary end point of CVD outcome (the Treating to New Targets [TNT] and Incremental Decrease in End Points Through Aggressive Lipid Lowering [IDEAL] studies). Of the 18,889 patients participating in the 2 trials, 199 had RA, 46 had AS, and 35 had PsA. Lipid-lowering therapy consisted of an intensive regimen of atorvastatin 80 mg or a conventional/low-dose regimen of atorvastatin 10 mg or simvastatin 20-40 mg. The median duration of followup was nearly 5 years. Changes in lipid levels were examined by analyses of covariance. The effect on CVD was examined by Cox regression analyses, and heterogeneity tests were performed. Patients with RA and those with AS had lower baseline cholesterol levels than patients without inflammatory joint disease (least squares mean ± SEM 180.7 ± 2.3 mg/dl and 176.5 ± 4.7 mg/dl, respectively, versus 185.6 ± 0.2 mg/dl; P = 0.03 and P = 0.05, respectively). Statin treatment led to a comparable decrease in lipid levels and a 20% reduction in overall risk of CVD in both patients with and those without inflammatory joint disease. Our findings indicate that patients with and those without inflammatory joint disease experience comparable lipid-lowering effects and CVD risk reduction after intensive treatment with statins.

Search and rescue for hypotheses surviving AIM-HIGH, the niacin therapy earthquake: Still problematic after the primary publication

Search and rescue for hypotheses surviving AIM-HIGH, the niacin therapy earthquake: Still problematic after the primary publication

Time to consider an Asian guideline for management of dyslipidemia?

Time to consider an Asian guideline for management of dyslipidemia?

Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis

Systemic therapy with statin has been shown to lower the risk of coronary events; however, the in vivo effects of statin therapy on plaque volume and composition are less understood. We conducted a prospective, open-labeled, randomized, multicenter study in 11 centers in Japan. A total of 164 patients were randomized to receive either 4 mg/d of pitavastatin (intensive lipid-lowering therapy) or 20 mg/d of pravastatin (moderate lipid-lowering therapy). Analyzable intravascular ultrasound data were obtained for 119 patients at baseline and at 8-month follow-up. The primary end point was the difference of volume changes in each of the 4 main plaque components (fibrosis, fibrofatty, calcium, and necrosis), assessed by virtual histology intravascular ultrasound, between the 2 groups. The mean low-density lipoprotein cholesterol level at follow-up was significantly lower in the pitavastatin than in the pravastatin group (74 vs 95 mg/dL, P < .0001). During the 8-month follow-up period, statin therapy reduced the absolute and relative amount of fibrofatty component (pitavastatin: from 1.09 to 0.81 mm(3)/mm, P = .001; pravastatin: from 1.05 to 0.83 mm(3)/mm, P = .0008) and increased in the amount of calcium (pitavastatin: from 0.42 to 0.55 mm(3)/mm, P < .0001; pravastatin: from 0.44 to 0.55 mm(3)/mm, P = .005), whereas volume changes in both plaque components were not statistically different between the 2 groups. Both pitavastatin and pravastatin altered coronary artery plaque composition by significantly decreasing the fibrofatty plaque component and increasing the calcified plaque component.

Lipemia retinalis – an unusual cause of visual acuity deterioration

SummaryBackgroundHyperlipidemia is an identified factor of premature vessel atherosclerosis. Lipemia retinalis is an unusual retinal manifestation of hyperlipidemia and is thought to be directly correlated with the serum triglyceride level.Case ReportThis paper discusses the case of a 55-year-old patient with lipemia retinalis, which deteriorated his visual acuity. The patient had an extremely high serum cholesterol level (1053 mg/dl) and a very high level of triglycerides (1513 mg/dl). The normalization of serum lipids, reversion of retinal vessels alterations and visual acuity improvement was achieved after an intensive statin lipid-lowering therapy. Pathological changes of the patient’s retina, connected with lipemia retinalis, disappeared completely.ConclusionsHyperlipidemia can cause lipemia retinalis, which is characterized by the hyperlipidemic vascular lesions-whitish color of vessels, lipid infiltration into the retina and decrease of visual acuity. The lipid-lowering therapy may lead to the normalization of the appearance of the fundus and restore the visual acuity.

Effect of Intensive Lipid-Lowering Therapy With Rosuvastatin on Progression of Carotid Intima-Media Thickness in Japanese Patients

(Circ J 2012; 76: 221-229)

Unstable Angina and Non–ST Elevation Myocardial Infarction

Non-ST elevation acute coronary syndromes are responsible for approximately 1 million admissions to U.S. hospitals and twice as many to European hospitals each year. Thus, they are among the most common serious illnesses in adults, and are associated with an in-hospital mortality of approximately 5%. The most common cause is rupture of an atherosclerotic coronary plaque, resulting in subtotal coronary occlusion. Diagnosis is based on the clinical picture of retrosternal chest pain, aided by electrocardiographic findings of ST segment deviations and biomarker abnormalities (elevation of troponin and natriuretic peptides) and cardiac imaging (myocardial scans showing perfusion defects). Treatment involves antiischemic agents (nitrates and β blockers), antiplatelet drugs (aspirin, P2Y(12), and glycoprotein IIb/IIIa receptor blockers), and anticoagulants (unfractionated and low-molecular-weight heparins). Patients should undergo risk stratification, and those with high-risk factors should undergo coronary arteriography promptly with the intent to carry out coronary revascularization. Those at low risk should continue to receive intensive antiischemic and antithrombotic therapy. At discharge, patients should receive intensive lipid-lowering therapy with high doses of a statin, as tolerated.

Effect of Intensive Lipid-Lowering Therapy With Rosuvastatin on Progression of Carotid Intima-Media Thickness in Japanese Patients

A recent trial in Western countries has shown that rosuvastatin slows progression of carotid intima-media thickness (IMT) in patients with modest carotid IMT thickening and elevated levels of low-density lipoprotein cholesterol (LDL-C). We conducted a prospective, randomized, open-label, blinded-endpoint trial to determine whether rosuvastatin is more effective than pravastatin in slowing progression of carotid IMT in Japanese patients. Adult patients with hypercholesterolemia who had a maximum IMT ≥1.1mm were randomly assigned to receive rosuvastatin or pravastatin. The primary endpoint was the percent change in the mean-IMT, which was measured by a single observer who was blinded to the treatment assignments. The trial was stopped on April 2011 according to the recommendation by the data and safety monitoring committee. A total of 348 patients (173 rosuvastatin; 175 pravastatin) were enrolled and 314 (159 rosuvastatin; 155 pravastatin) were included in the primary analysis. Mean (SD) percentage changes in the mean-IMT at 12 months were 1.91% (10.9) in the rosuvastatin group and 5.8% (12.0) in the pravastatin group, with a difference of 3.89% (11.5) between the groups (P=0.004). At 12 months, 85 patients (59.4%) in the rosuvastatin group achieved a LDL-C/high-density lipoprotein cholesterol ratio ≤1.5 compared with 24 patients (16.4%) in the pravastatin group (P<0.0001). Rosuvastatin significantly slowed progression of carotid IMT at 12 months compared with pravastatin.

Intensive Lipid-Lowering Therapy With Statins for Primary Prevention

Intensive Lipid-Lowering Therapy With Statins for Primary Prevention

Abstract P268: Telephone Counseling to Activate Peripheral Arterial Disease Patients Toward Improved Low Density Lipoprotein Cholesterol Levels: A Randomized Controlled Clinical Trial

BACKGROUND: Patients with lower extremity peripheral arterial disease (PAD) have high rates of cardiovascular events but are less likely to achieve ideal low density lipoprotein cholesterol (LDL-C) levels than coronary artery disease patients. We determined whether a telephone counseling intervention, designed to activate PAD patients to request more intensive LDL-C lowering therapy from their physician, can help PAD patients achieve lower LDL-C levels compared to two control groups. METHODS: Three hundred fifty-five participants with PAD and baseline LDL-C ≥ 70 mg/dl were randomized to one of three parallel arms: telephone counseling intervention, attention control condition, and usual care. The primary outcome was change in LDL-C level at twelve- month follow-up. The secondary outcome was the percent of PAD participants with an LDL-C &lt; 100 mg/dl at 12 month follow-up. The intervention consisted of eight patient-centered telephone counseling calls that encouraged PAD participants to request more intensive lipid-lowering therapy from their physician. The attention control group consisted of eight telephone calls providing knowledge about PAD. The usual care group participated in baseline and follow-up testing only. RESULTS: At 12-month follow-up, the telephone counseling intervention was associated with lower LDL-C levels as compared to attention control (-18.4 mg/dl vs. -6.8 mg/dl, p= 0.010) but not as compared to usual care (-18.4 mg/dl vs. -11.1 mg/dl, p= 0.208). Both attention control and the usual care condition were less likely to achieve an LDL-C &lt; 100 mg/dl, compared to the intervention (odds ratio = 0.34, 95% Confidence Interval (CI) = 0.17-0.69, p=0.003 and odds ratio = 0.42, 95% CI = 0.20-0.86, p=0.018, respectively). Participants in the intervention were more likely to start a new statin medication than the attention control arm (18.6% vs. 5.5%, p=0.008) and usual care arm (18.6% vs. 5.5%, P=0.005). CONCLUSION: Among patients with PAD, a telephone counseling intervention designed to activate patients to request more intensive LDL-C lowering therapy from their physician resulted in lower LDL-C levels and higher rates of initiating cholesterol-lowering drugs, compared to control groups. 1

Benefit of Early Statin Therapy in Patients With Acute Myocardial Infarction Who Have Extremely Low Low-Density Lipoprotein Cholesterol

We investigated whether statin therapy could be beneficial in patients with acute myocardial infarction (AMI) who have baseline low-density lipoprotein cholesterol (LDL-C) levels below 70 mg/dl. Intensive lipid-lowering therapy with a target LDL-C value <70 mg/dl is recommended in patients with very high cardiovascular risk. However, whether to use statin therapy in patients with baseline LDL-C levels below 70 mg/dl is controversial. We analyzed 1,054 patients with AMI who had baseline LDL-C levels below 70 mg/dl and survived at discharge from the Korean Acute MI Registry between November 2005 and December 2007. They were divided into 2 groups according to the prescribing of statins at discharge (statin group n = 607; nonstatin group n = 447). The primary endpoint was the composite of 1-year major adverse cardiac events, including death, recurrent MI, target vessel revascularization, and coronary artery bypass grafting. Statin therapy significantly reduced the risk of the composite primary endpoint (adjusted hazard ratio [HR]: 0.56; 95% confidence interval [CI]: 0.34 to 0.89; p = 0.015). Statin therapy reduced the risk of cardiac death (HR: 0.47; 95% CI: 0.23 to 0.93; p = 0.031) and coronary revascularization (HR: 0.45, 95% CI: 0.24 to 0.85; p = 0.013). However, there were no differences in the risk of the composite of all-cause death, recurrent MI, and repeated percutaneous coronary intervention rate. Statin therapy in patients with AMI with LDL-C levels below 70 mg/dl was associated with improved clinical outcome.