Follow-up Low-density Lipoprotein Cholesterol Levels Research Articles

Impact of statin intensity on adverse cardiac and cerebrovascular events in older adult patients with myocardial infarction.

BACKGROUNDThere is insufficient evidence regarding the effect of high-intensity statin therapy in older adults. This study aimed to investigate the effects of high-intensity statin treatment on the clinical outcomes in older adults with myocardial infarction (MI).METHODSConsecutive patients with MI aged at least 75 years were analyzed retrospectively. The primary endpoint was major adverse cardiac and cerebrovascular events (MACCE), defined as a composite of all-cause death, MI, rehospitalization due to unstable angina, repeat revascularization, and ischemic stroke. The high-intensity group was compared to the low-to-moderate intensity group in the propensity score-matched cohort.RESULTSAverage age of total 546 patients was 81 years. Among them, 84% of patients underwent percutaneous coronary intervention. The unadjusted seven-year MACCE rate differed by statin intensity (high-intensity statin group: 38%, moderate-intensity statin group: 42%, low-intensity statin group: 56%, and no-statin group: 61%, P = 0.004). However, among these groups, many baseline characteristics were significantly different. Among the 74 propensity score-matched pairs, which lacked any significant differences in all baseline characteristics, the high-intensity group had a significantly lower rate of MACCE than the low-to-moderate intensity group (37% vs. 53%, P = 0.047). Follow-up low-density lipoprotein cholesterol levels were significantly lower in the high-intensity group than that in the low-to-moderate intensity group (69.4 ± 16.0 mg/dL vs. 77.9 ± 25.9 mg/dL, P = 0.026). CONCLUSIONSIn older adult patients with MI, the use of high-intensity statin caused significantly less occurrence of MACCE in comparison to that in low-to-moderate intensity for up to seven years of follow-up.

Incidence and Predictors of Neoatherosclerosis in Patients with Early In-Stent Restenosis Determined Using Optical Coherence Tomography

In-stent restenosis (ISR) still exists after drug-eluting stent (DES) implantation, even up to one year. The incidence and risk factors for neoatherosclerosis in patients with early ISR have not yet been elucidated. Here, we used optical coherence tomography (OCT) to evaluate the incidence and predictors of neoatherosclerosis in patients with early ISRs.OCT was performed on ISR lesions in 185 patients in order to detect neoatherosclerosis. The median follow-up was 180 days, and neoatherosclerosis was detected in 37% of early ISR lesions. According to the presence of neoatherosclerosis, patients with ISR were divided into two groups: neoatherosclerosis (group A, n = 69) and non-neoatherosclerosis (group B, n = 116) groups.The risk factors were similar, except for hypercholesterolemia. Moreover, the tissue characteristics were not significantly different between patients with and without neoatherosclerosis. Follow-up low-density lipoprotein-cholesterol (LDL-C) levels were divided into three grades (LDL < 70 mg/dL, 70 mg/dL≤ LDL < 100 mg/dL, and LDL ≥ 100 mg/dL). The incidence of neoatherosclerosis was significantly lower (23% versus 57%, P < 0.0001) in the LDL < 70 mg/dL group. There was no significant difference in the incidence of neoatherosclerosis in patients with lipid levels between 70 and 100 mg/dL (P = 0.53). However, neoatherosclerosis was significantly more common in patients with a follow-up LDL-C level > 100 mg/dL (45% versus 15%, P < 0.0001).In patients with early ISR lesions, the LDL-C levels may be related to the formation and progression of early neoatherosclerosis, and poor LDL-C control may be a risk factor for the occurrence of early-stage neoatherosclerosis following DES implantation.

Prevalence, treatment, and control of severe hyperlipidemia

ObjectiveTo identify the prevalence, treatment, and low-density lipoprotein cholesterol (LDL-C) control of individuals with LDL-C ≥190 ​mg/dL in contemporary clinical practice. MethodsWe included adults (age ≥18 years) with LDL-C ≥190 ​mg/dL, at least one LDL-C level drawn from 255 health systems participating in Cerner HealthFacts database (2000–2017, n ​= ​4,623,851), and a detailed examination within Duke University Health System (DUHS, 2015–2017, n ​= ​267,710). Factors associated with LDL-C control were evaluated using multivariable logistic regression modeling. ResultsThe cross-sectional prevalence of LDL-C ≥190 ​mg/dL was 3.0% in Cerner (n ​= ​139,539/4,623,851) and 2.9% at DUHS (n ​= ​7728/267,710); among these, rates of repeat LDL-C measurement within 13 months were low: 27.9% (n ​= ​38,960) in Cerner, 54.5% (n ​= ​4211) at DUHS. Of patients with follow-up LDL-C levels, 23.6% in Cerner had a 50% of greater reduction in LDL-C, 18.3% achieved an LDL-C <100 ​mg/dL and 2.7% ​< ​70 ​mg/dL. At DUHS, 28.4% had a 50% or greater reduction in LDL-C, 28.4% achieved an LDL-C ≤100 ​mg/dL and 4.4% achieved <70 ​mg/dL. Within DUHS, 71.6% with LDL-C ≥190 ​mg/dL were on any statin during follow-up, but only 28.5% were on a high-intensity statin. In multivariable modeling, seeing a cardiologist (Cerner odds ratio [OR] 1.56, confidence interval [CI] 1.33–1.83; DUHS OR 1.89, 95% CI 1.18–3.01) and having diabetes (Cerner OR 1.34 CI 1.23–1.46; DUHS OR 2.07, CI 1.62–2.65) increased odds of LDL-C control, defined as a ≥50% reduction in LDL-C (at Cerner) or initiation of high intensity statin (at DUHS). Prior atherosclerotic cardiovascular disease (OR 1.19, CI 1.07–1.33), hypertension (OR 1.10, CI 1.03–1.18), African American race (OR 0.79, CI 0.71–0.89), and government (vs. private) insurance (OR 0.90, CI 0.83–0.98) were associated with LDL-C control at Cerner. Female sex was associated with lower odds of appropriate therapy (OR 0.69, CI 0.59–0.81) at DUHS. ConclusionsApproximately 3% of United States adults have LDL-C ≥190 ​mg/dL. Among those with very high LDL-C, rates of repeat measurement within one year were low; of those retested, only about one-fourth met guideline-recommended LDL-C treatment goals.

Preliminary Pilot Study of Combined Effects of Physical Activity and Achievement of LDL-Cholesterol Target on Coronary Plaque Volume Changes in Patients with Acute Coronary Syndrome.

Background: We investigated the combined effects of physical activity (PA) and aggressive low-density lipoprotein cholesterol (LDL-C) reduction on the changes in coronary plaque volume (PV) in patients with acute coronary syndrome (ACS) using volumetric intravascular ultrasound (IVUS) analysis. Methods: We retrospectively analyzed data from two different prospective clinical trials that involved 101 ACS patients who underwent percutaneous coronary intervention (PCI) and assessed the non-culprit sites of PCI lesions using IVUS at baseline and at the follow-up. After PCI, all the patients participated in early phase II comprehensive cardiac rehabilitation. Patients were divided into four groups based on whether the average daily step count, measured using a pedometer, was 7000 steps of more and whether the follow-up LDL-C level was <70 mg/dL. At the time of follow-up, we examined the correlation of changes in the PV with LDL-C and PA. Results: The baseline characteristics of the four study groups were comparable. At the follow-up, plaque regression in both the achievement group (PA and LDL-C reduction) was higher than that in the other three groups. In addition, plaque reduction independently correlated with increased PA and reduction in LDL-C level. Conclusions: Combined therapy of intensive PA and achievement of LDL-C target retarded coronary PV in patients with ACS.

Comparing Primary Prevention Recommendations: A Focused Look at United States and European Guidelines on Dyslipidemia.

Comparing Primary Prevention Recommendations: A Focused Look at United States and European Guidelines on Dyslipidemia.

P824The clinical impact of polyunsaturated fatty acid on clinical outcomes in acute coronary syndrome with dyslipidemia: HIJ-PROPER sub-analysis

Abstract Background Polyunsaturated fatty acids, especially omega-3 and -6 series, are key essential nutrients that play an important role in humans to maintain cell membranes and function. A recent randomized trial reported that adding eicosapentaenoic acid (EPA) to statins was beneficial to cardiovascular disease patients who had a residual risk factor. Further, several studies have reported that the low baseline value for EPA to arachidonic acid (AA) ratio is related to worse clinical outcome and plaque vulnerability in coronary artery disease patients. However, effects of baseline EPA/AA ratio on clinical outcomes in ACS patients have not been thoroughly evaluated. Objectives This study aimed to examine the impact of baseline eicosapentaenoic acid to arachidonic acid (EPA/AA) ratio on clinical outcomes of acute coronary syndrome (ACS) patients and how lipid-lowering therapy affects serum EPA/AA levels in these patients. Methods This is a sub-analysis of HIJ-PROPER assessing the effect of aggressive low-density lipoprotein cholesterol (LDL-C)-lowering treatment with pitavastatin+ezetimibe in 1,734 ACS patients with dyslipidemia. Patients were divided into two groups based on EPA/AA level on admission (cut-off: 0.34 μg/mL; median of baseline EPA/AA level) and clinical outcomes were examined. Results Percent reduction of LDL-C from baseline to follow-up and mean LDL-C level during follow-up were similar regardless of baseline EPA/AA ratio. In the low EPA/AA group, the Kaplan–Meier estimate for the primary endpoint at 3 years was 27.2% in the pitavastatin+ezetimibe group, compared with 36.6% in the pitavastatin-monotherapy group [hazard ratio (HR), 0.69; 95% confidence interval (CI), 0.52–0.93; P=0.015). However, in the high EPA/AA group, there was no significant reduction in the primary endpoint by pitavastatin+ezetimibe therapy (HR, 0.92; 95% CI, 0.70–1.20; P=0.52). Conclusions Aggressive lipid-lowering therapy with ezetimibe had a positive effect on clinical outcomes in the low EPA/AA group of ACS patients with dyslipidemia, but not in the high EPA/AA group. This effect was independent of LDL-C reduction and suggests that EPA/AA measurement on admission in ACS patients contributes to a “personalized” lipid-lowering approach.

Characteristics Detected on Computed Tomography Angiography Predict Coronary Artery Plaque Progression in Non-Culprit Lesions.

ObjectiveThis study sought to determine whether variables detected on coronary computed tomography angiography (CCTA) would predict plaque progression in non-culprit lesions (NCL).Materials and MethodsIn this single-center trial, we analyzed 103 consecutive patients who were undergoing CCTA and percutaneous coronary intervention (PCI) for culprit lesions. Follow-up CCTA was scheduled 12 months after the PCI, and all patients were followed for 3 years after their second CCTA examination. High-risk plaque features and epicardial adipose tissue (EAT) volume were assessed by CCTA. Each NCL stenosis grade was compared visually between two CCTA scans to detect plaque progression, and patients were stratified into two groups based on this. Logistic regression analysis was used to evaluate the factors that were independently associated with plaque progression in NCLs. Time-to-event curves were compared using the log-rank statistic.ResultsOverall, 34 of 103 patients exhibited NCL plaque progression (33%). Logistic regression analyses showed that the NCL progression was associated with a history of ST-elevated myocardial infarction (odds ratio [OR] = 5.855, 95% confidence interval [CI] = 1.391–24.635, p = 0.016), follow-up low-density lipoprotein cholesterol level (OR = 6.832, 95% CI = 2.103–22.200, p = 0.001), baseline low-attenuation plaque (OR = 7.311, 95% CI = 1.242–43.028, p = 0.028) and EAT (OR = 1.015, 95% CI = 1.000–1.029, p = 0.044). Following the second CCTA examination, major adverse cardiac events (MACEs) were observed in 12 patients, and NCL plaque progression was significantly associated with future MACEs (log rank p = 0.006).ConclusionNoninvasive assessment of NCLs by CCTA has potential prognostic value.

Impact of Intensive LDL Cholesterol Lowering on Coronary Artery Atherosclerosis Progression: A Serial CT Angiography Study

ObjectivesThe aim of this study was to explore the relationship between temporal changes in coronary plaque volume and the intensity of lipid-lowering treatments, utilizing coronary computed tomography angiography (CTA). BackgroundCoronary CTA has acceptable accuracy in terms of quantitative measurement of plaque volume. Although, coronary CTA is perhaps capable of identifying the differences in plaque volume progression according to the intensity of lipid lowering treatment, to date, few studies have examined this notion. MethodsIn this multicenter, observational study, the authors reviewed 467 patients who underwent serial coronary CTA with a scan period of more than 2 years (median 3.2 years [2.4 to 4.8]) apart, and whose laboratory data were available within 1 month of both the baseline and follow-up coronary CTA. Among them, 147 patients (comprising 336 vessels) with visible plaque were enrolled in this study. The authors performed quantitative assessment of coronary plaque in both. Patients who achieved a low-density lipoprotein cholesterol (LDL-C) with a cut off value below 70 mg/dl at follow-up were compared with those who did not. ResultsPatients with LDL-C below 70 mg/dl displayed a significant attenuation in plaque progression as compared with those with follow-up LDL-C levels ≥70 mg/dl (12.7 ± 38.2 mm3 vs. 44.2 ± 73.6 mm3, respectively; p = 0.014). In multivariate analysis, factors influencing plaque progression per year was follow-up LDL-C levels ≥70 mg/dl (beta 0.193; p = 0.021). ConclusionsStrict LDL-C control appeared to significantly attenuate plaque volume progression based on noninvasive quantitative assessment by coronary CTA.

Obstructive sleep apnea is associated with visit-to-visit variability in low-density lipoprotein-cholesterol in patients with coronary artery disease.

Visit-to-visit variability in low-density lipoprotein-cholesterol (LDL-C) was found to be a novel predictor of adverse cardiac events. Obstructive sleep apnea (OSA), an emerging cardiovascular risk factor, is characterized by sympathetic activation and increased oxidative stress which are regulators of LDL-C metabolism. We hypothesized that OSA was associated with LDL-C variability. We prospectively recruited 190 patients with coronary artery disease for an overnight sleep study. Statin was prescribed upon discharge for 186 patients. Serum LDL-C levels were measured at clinic every 3 to 6months. Severity of OSA (on the basis of apnea-hypopnea index (AHI)) was correlated with visit-to-visit LDL-C variability (on the basis of variation independent of mean (VIM)) in outpatient clinic. The mean AHI was 21.9 ± 18.9. Using an AHI cut-off of 5-14.9, 15-29.9, and ≥30, the prevalence of mild, moderate, and severe OSA was 26.3, 18.9, and 27.4%, respectively. After 53.2 ± 25.3months, LDL-C was recorded over 8.1 ± 4.2 measurements. VIM positively correlated with AHI (Pearson's r = 0.183, p = 0.016), but not body mass index, baseline and mean follow-up LDL-C levels, and number of LDL-C measurements. In multiple linear regression analysis, AHI remained an independent predictor of VIM after adjusting for diabetes mellitus and hyperlipidemia. A 10-unit rise in AHI led to a 3.8% increase in VIM (95% CI 0.1 to 7.4%; p = 0.044). This is the first study to show the independent correlation between OSA severity and visit-to-visit LDL-C variability. Our finding contributes to the understanding of the vasculopathic effects of OSA.

Relation Between Paradoxical Decrease in High-Density Lipoprotein Cholesterol Levels After Statin Therapy and Adverse Cardiovascular Events in Patients With Acute Myocardial Infarction

Statin therapy moderately increases high-density lipoprotein cholesterol (HDL-C) levels. Contrary to this expectation, a paradoxical decrease in HDL-C levels after statin therapy is seen in some patients. We evaluated 724 patients who newly started treatment with statins after acute myocardial infarction (AMI). These patients were divided into 2 groups according to change in HDL-C levels between baseline and 6 to 9 months after initial AMI (ΔHDL). In total, 620 patients had increased HDL-C levels and 104 patients had decreased HDL-C levels. Both groups achieved follow-up low-density lipoprotein cholesterol levels <100 mg/dl. Adverse cardiovascular events (a composite of all-cause death, myocardial infarction, and stroke) have more frequently occurred in the decreased HDL group compared with the increased HDL group (15.4% vs 7.1%, p = 0.01). Multivariate analysis showed that decreased HDL, onset to balloon time, and multivessel disease were the independent predictors of adverse cardiovascular events (hazard ratio [HR] 1.95, 95% confidence interval [CI] 1.08 to 3.52; HR 1.05, 95% CI 1.01 to 1.09; and HR 2.08, 95% CI 1.22 to 3.56, respectively). In conclusion, a paradoxical decrease in serum HDL-C levels after statin therapy might be an independent predictor of long-term adverse cardiovascular events in patients with AMI.

Impact of statin treatment on strut coverage after drug-eluting stent implantation.

PurposeTo evaluate the effect of statin treatment on strut coverage after drug-eluting stent (DES) implantation.Materials and MethodsIn this study, 60 patients were randomly assigned to undergo sirolimus-eluting stent (SES) or biolimus-eluting stent (BES) implantation, after which patients were randomly treated with pitavastatin 2 mg or pravastatin 20 mg for 6 months. The degree of strut coverage was assessed by 6-month follow-up optical coherence tomography, which was performed in 52 DES-implanted patients.ResultsThe percentages of uncovered struts were 19.4±14.7% in pitavastatin-treated patients (n=25) and 19.1±15.2% in pravastatin-treated patients (n=27; p=0.927). A lower percentage of uncovered struts was significantly correlated with a lower follow-up low-density lipoprotein (LDL) cholesterol level (r=0.486; p=0.009) and a greater decline of the LDL cholesterol level (r=-0.456; p=0.015) in SES-implanted patients, but not in BES-implanted patients. In SES-implanted patients, the percentage of uncovered struts was significantly lower among those with LDL cholesterol levels of less than 70 mg/dL after 6 months of follow-up (p=0.025), but no significant difference in this variable according to the follow-up LDL cholesterol level was noted among BES-implanted patients (p=0.971).ConclusionLower follow-up LDL cholesterol levels, especially those less than 70 mg/dL, might have a protective effect against delayed strut coverage after DES implantation. This vascular healing effect of lower LDL cholesterol levels could differ according to the DES type.

Association Between Persistence with Statin Therapy and Reduction in Low-Density Lipoprotein Cholesterol Level: Analysis of Real-Life Data from Community Settings

To validate the use of drug dispensing data as a measure of drug exposure and to quantify the association between persistence with statin therapy and low-density lipoprotein cholesterol (LDL) levels using real-life community data. Retrospective, population-based cohort study. Maccabi Healthcare Services (MHS) database, which contains linked prescription drug information, hospitalization records, and laboratory test results of 2million members of the second largest health organization in Israel. A total of 87,219 primary prevention patients and 15,139 secondary prevention patients who were MHS members and who started statin therapy between 1998 and 2008. Baseline and follow-up LDL levels were documented from 3months before the date of first dispensed statin (index date) to 6months afterward. Persistence was assessed by proportion of days covered (PDC) with statins during the follow-up period. Over the follow-up period, significant (p<0.001) reductions in LDL levels of 54, 33, and 13mg/dl were noted among highly persistent (PDC≥80%), moderately persistent (34%≤PDC<79%), and poorly persistent statins users (PDC≤33%), respectively. The reduction was observed as early as 2-3weeks after therapy initiation. In a multivariable model controlling for baseline LDL level and traditional coronary heart disease risk factors (diabetes mellitus, hypertension), high persistence with statin therapy was associated with a 27% and 25% decrement in LDL level among the primary and secondary prevention cohorts, respectively. Similarly, a higher proportion of the persistent statins users reached their target LDL level within the study follow-up period: 80% and 58% among primary and secondary prevention cohorts, respectively, compared with only 28% and 17%, respectively, among poorly persistent patients. In this observational population-based study, calculated PDC with statins during study follow-up was strongly associated with drug effect of LDL level reduction. The results agree with previous estimates of statin efficacy from randomized clinical trials, supporting the validity of using PDC methods as a measure of drug exposure.

Rationale of decreasing low-density lipoprotein cholesterol below 70 mg/dL in patients with coronary artery disease: A retrospective virtual histology-intravascular ultrasound study.

The associations between statin and coronary plaque compositional changes were re-ported according to the use of high dose or not. An evaluation of the impact of low-density lipoprotein cholesterol (LDL-C) < 70 mg/dL by using real world dosages of statin on coronary plaque composition was undertaken. The study subjects consisted of 61 patients (mean 59.9 years old, 45 males) who underwent percutaneous coronary intervention, baseline and follow-up (F/U; mean 8.4 months) virtual histology- -intravascular ultrasound (VH-IVUS) examination. Change of plaque composition at peri-stent area, which was selected in order to measure the identical site at F/U study, was compared according to the F/U LDL-C level. Body mass index, prevalence of dyslipidemia, baseline total cholesterol and baseline LDL-C were significantly lower in F/U LDL-C < 70 mg/dL group (14 segments in 10 patients) than F/U LDL-C ≥ 70 mg/dL group (79 segments in 51 patients). F/U high-density lipoprotein cholesterol (HDL-C, OR 1.06, 95% CI 1.00-1.11, p = 0.054) and F/U LDL-C < 70 mg/dL (OR 3.43, 95% CI 0.97-12.17, p = 0.056) showed strong tendency of regression of necrotic core volume (NCV) ≥ 10%. In multivariable logis-tic regression analysis, F/U HDL-C (OR 1.07, 95% CI 1.01-1.14, p = 0.020) and F/U LDL-C < 70 mg/dL (OR 8.02, 95% CI 1.58-40.68, p = 0.012) were the independent factors for regression of NCV ≥ 10%. Follow-up LDL-C level < 70 mg/dL with any types of statins and increase of HDL-C were associated with regression of NCV ≥ 10% in patients with coronary artery disease.

Cardiovascular Event Reduction and Adverse Events Among Subjects Attaining Low-Density Lipoprotein Cholesterol

The purpose of this study was to assess the impact on cardiovascular and adverse events of attaining low-density lipoprotein cholesterol (LDL-C) levels <50 mg/dl with rosuvastatin in apparently healthy adults in the JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) trial.The safety and magnitude of cardiovascular risk reduction conferred by treatment to LDL-C levels below current recommended targets remain uncertain.A cohort of 17,802 apparently healthy men and women with high-sensitivity C-reactive protein ≥2 mg/l and LDL-C <130 mg/dl were randomly allocated to rosuvastatin 20 mg daily or placebo, and followed up for all-cause mortality, major cardiovascular events, and adverse events. In a post-hoc analysis, participants allocated to rosuvastatin were categorized as to whether or not they had a follow-up LDL-C level <50 mg/dl.During a median follow-up of 2 years (range up to 5 years), rates of the primary trial endpoint were 1.18, 0.86, and 0.44 per 100 person-years in the placebo group (n = 8,150) and rosuvastatin groups without LDL-C <50 mg/dl (n = 4,000) or with LDL-C <50 mg/dl (n = 4,154), respectively (fully-adjusted hazard ratio: 0.76; 95% confidence interval: 0.57 to 1.00 for subjects with no LDL-C <50 mg/dl vs. placebo and 0.35, 95% confidence interval: 0.25 to 0.49 for subjects attaining LDL-C <50 mg/dl; p for trend <0.0001). For all-cause mortality, corresponding event rates were 0.67, 0.65, and 0.39 (p for trend = 0.004). Rates of myalgia, muscle weakness, neuropsychiatric conditions, cancer, and diabetes mellitus were not significantly different among rosuvastatin-allocated participants with and without LDL-C <50 mg/dl.Among adults with LDL-C <130 mg/dl and high-sensitivity C-reactive protein ≥2 mg/l, rosuvastatin-allocated participants attaining LDL-C <50 mg/dl had a lower risk of cardiovascular events without a systematic increase in reported adverse events.

Clinical predictors for progression of nonintervened nonculprit coronary lesions despite low-density lipoprotein cholesterol less than 1.8 mmol/l after successful stent implantation

Despite achieving very low levels of low-density lipoprotein cholesterol (LDL-C), many patients continue to show disease progression. We sought to characterize the clinical factors that correlate with nonculprit lesion plaque progression in patients with LDL-C level less than 1.8 mmol/l. Between May 2006 and December 2009, 653 patients met the following criteria: (i) underwent coronary angiograms again with a time interval from 6 months to 2 years after successful stent implantation, (ii) less than 50% stenoses of nonintervened nonculprit coronary lesions (NCLs), (iii) follow-up LDL-C levels less than 1.8 mmol/l. Patients were classified as progressors [NCL-percutaneous coronary intervention (PCI)] or nonprogressors (non-NCL-PCI). Five patients with de novo NCL and 87 patients with preexisting NCL developed progression. Progressors had higher percentage of acute coronary syndrome (ACS), multivessel diseases and triglycerides (TGs) at baseline PCI. At follow-up, a significant difference was observed between progressors and nonprogressors in TG (1.73 vs. 1.32 mmol/l, P<0.001), change in TG (-0.18±1.01 vs. -0.42±1.02 mmol/l, P=0.032), high-density lipoprotein cholesterol (HDL-C) (0.98±0.22 vs. 1.08±0.25 mmol/l, P=0.001) and change in HDL-C (0.11±0.17 vs. 0.19±0.27 mmol/l, P<0.001). Multivariate logistic regression analysis revealed that ACS, multivessel diseases, on-treatment TG and HDL-C and smaller increases in HDL-C were independent predictors for progression. Despite attainment of LDL-C level less than 1.8 mmol/l, NCL had still progressed, mainly in preexisting NCL rather than de novo NCL. ACS, multivessel diseases, on-treatment TG, HDL-C and smaller increases in HDL-C were associated with the NCL progression. This finding highlights the need for intensive modification of global risk in patients with coronary artery disease.

Impact of the attainment of current recommended low-density lipoprotein cholesterol goal of less than 70 mg/dl on clinical outcomes in very high-risk patients treated with drug-eluting stents

We sought to evaluate whether the attainment of low-density lipoprotein cholesterol (LDL-C) goal of less than 70 mg/dl would affect clinical outcomes in Korean patients treated with drug-eluting stents (DES). The current cholesterol guideline has strongly recommended reducing LDL-C to less than 70 mg/dl as the goal of therapy for very high-risk patients. From 2003 to 2006, a total of 1347 very high-risk patients were treated with DES. Among them, we identified 578 eligible patients with follow-up LDL-C within 6-8 months after DES and divided these patients into two groups based on the level of follow-up LDL-C: group A, follow-up LDL less than 70 mg/dl (n=234) and group B, LDL of at least 70 mg/dl (n=344). Then we analyzed the incidence of major adverse cardiac and cerebrovascular events [MACCE: death, myocardial infarction, target-vessel revascularization (TVR), non-TVR, cerebrovascular accidents] of both the groups. During the follow-up (mean duration=30+/-10 months), group A showed a significantly lower TVR (6%) and MACCE rate (14%), compared with group B (TVR: 12%, P=0.032; MACCE: 24%, P=0.002). However, there was no difference in the rate of death, myocardial infarction, or cerebrovascular accidents between the two groups. By multivariate analysis, follow-up LDL-C level of less than 70 mg/dl was one of the significant predictors for the occurrence of MACCE (odds ratio=0.39, 95% confidence interval: 0.21-0.72, P=0.003) or TVR (odds ratio=0.39, 95% confidence interval: 0.20-0.76, P=0.005). This study showed that the attainment of LDL-C goal of less than 70 mg/dl was significantly associated with a lower MACCE or TVR rate in very high-risk Korean patients treated with DES.

Effect of Statin on the Reference Segments after Bare-Metal Stent Implantation

Effect of Statin on the Reference Segments after Bare-Metal Stent Implantation

Impact of Lipid-Lowering Therapy With Pitavastatin, a New HMG-CoA Reductase Inhibitor, on Regression of Coronary Atherosclerotic Plaque A 3-Dimensional Intravascular Ultrasound Study

Recent lipid-lowering trials have reported that statin therapy may retard progression or stimulate regression of human coronary plaque. In the present study volumetric intravascular ultrasound (IVUS) analyses were performed to investigate the effect of pitavastatin, a newly developed statin, on regression of human coronary plaque. Eighty-two patients matched for age and gender from 870 consecutive patients undergoing IVUS guided percutaneous coronary intervention were retrospectively assigned to either lipid-lowering therapy (n=41; pitavastatin 2 mg/day) or control group (n=41; diet only). Serial volumetric IVUS analyses of a matched left main coronary arterial site were performed. A significant reduction in low-density lipoprotein-cholesterol (LDL-C) level of 33.2% (p<0.001) was observed in the pitavastatin group. Plaque volume index (PVI) was significantly reduced in the pitavastatin group (10.6+/-9.4% decrease) compared with the control group (8.1+/-14.0% increase, p<0.001). There were positive correlations between the percent change in the PVI and follow-up LDL-C level (r=0.500, p<0.001) and the percent change in LDL-C level (r=0.479, p<0.001). Lipid-lowering therapy with pitavastatin induced significant coronary plaque regression, associated with a significant reduction in the LDL-C level. The percent change in the PVI showed a significant positive correlation with the percent change in LDL-C level.

Usefulness of Follow-Up Low-Density Lipoprotein Cholesterol Level as an Independent Predictor of Changes of Coronary Atherosclerotic Plaque Size as Determined by Intravascular Ultrasound Analysis After Statin ( Atorvastatin or Simvastatin) Therapy

Using serial intravascular ultrasound (IVUS), we identified independent predictors of changes in coronary plaque size in relation to serum lipid levels. One hundred three patients with nonstenotic coronary plaques underwent baseline and 12-month follow-up IVUS studies; 54 patients (52%) were treated with statins. Standard IVUS analyses were performed. Baseline IVUS study showed no statistical differences in mean external elastic membrane, lumen, and plaque/media (P&M) area between statin-treated and nonstatin-treated patients. Although there was an increase in mean P&M cross-sectional area in nonstatin-treated patients, mean P&M cross-sectional area decreased in statin-treated patients (0.11 +/- 0.24 vs -0.20 +/- 0.30 mm(2), p <0.001). There was a positive relation between changes in mean P&M area and follow-up low-density lipoprotein (LDL) cholesterol level (r = 0.430, p <0.001), follow-up total cholesterol level (r = 0.365, p <0.001), changes in LDL cholesterol level (r = 0.312, p = 0.002), and changes in total cholesterol level (r = 0.252, p = 0.012). In multivariate linear regression analysis, the only independent predictor of changes in mean P&M area was follow-up LDL cholesterol level (r = 0.469, p <0.001, 95% confidence interval 0.003 to 0.006). The cut-off value of follow-up LDL cholesterol for no change or a decrease in mean P&M area was <100 mg/dl at regression analysis. In conclusion, the present 12-month follow-up IVUS study showed that follow-up LDL cholesterol level was the only independent predictor of changes in coronary plaque size. When patients achieved a follow-up LDL cholesterol level <100 mg/dl, regression or no progression of coronary plaque was expected. Aggressive lipid-lowering treatments with statins to decrease the follow-up LDL cholesterol level to <100 mg/dl are recommended.

Statin Initiation Following Coronary Artery Bypass Grafting: Outcome of a Hospital Discharge Protocol

<h3>Study objectives</h3> To evaluate the outcome of a hospital discharge statin drug therapy initiation protocol following coronary artery bypass graft (CABG) surgery. Our goal was to measure the percentage of patients receiving statin drugs at hospital discharge and at a post-hospital discharge assessment following the implementation of the statin drug therapy initiation protocol. We also evaluated low-density lipoprotein cholesterol (LDL-C) goal attainment (<i>ie</i>, < 100 mg/dL), safety monitoring, and tolerability of the statin drug. <h3>Design</h3> Single-center, observational study with a historical control group. <h3>Setting</h3> University-affiliated health system with a comprehensive heart care program that included a 14-bed cardiac surgery ICU. Approximately 400 CABG procedures are performed annually. <h3>Patients</h3> Patients who underwent CABG surgery were eligible for inclusion in the study. The exclusion criteria were as follows: contraindications to statin therapy; refusal to take a statin drug; refusal to give informed consent; and age < 18 years. <h3>Intervention</h3> A protocol was implemented to recommend treatment with a statin drug at hospital discharge in all post-CABG surgery patients if the presurgical LDL-C level was > 100 mg/dL or the patient was receiving a statin prior to hospital admission. The protocol also included a presurgical assessment of lipoprotein levels and hepatic function. All cardiac surgery staff were educated regarding the specifics of the protocol. <h3>Results</h3> A total of 403 patients were included in the study. The historical control group (202 subjects) and the intervention group (201 subjects) were similar with respect to gender, age, and baseline lipoprotein levels. The follow-up assessment interval was approximately 6 months in both groups. Overall, patients were more likely to receive a statin at hospital discharge in the intervention group compared to the control group (relative risk [RR], 1.6; 95% confidence interval [CI], 1.3 to 2.0). Attainment of the goal for LDL-C level was similar between the intervention and control groups in the overall sample. Patients who were not at their LDL-C goal at baseline were more likely to have a follow-up LDL-C level of < 100 mg/dL in the intervention group (RR, 1.9; 95% CI, 1.0 to 3.5). The rate of liver function assessment was similar in the control and intervention groups. No patients in either group experienced elevations of alanine aminotransferase levels that were more than three times the upper limit of normal, and no cases of muscle toxicity were noted. <h3>Conclusion</h3> The initiation of therapy with a statin drug at hospital discharge following CABG surgery was associated with increased utilization rates. The LDL-C goal attainment improved in patients who were not at their goal prior to surgery. However, the persistence of medication use declined within 6 months. Statin therapy initiation was well-tolerated in this cohort of patients.