First clinical experience with Celt ACD(®) : a femoral arterial puncture closure device.

INTRODUCTION: This prospective nonrandomized study compared the safety and efficacy of a novel arterial closure device (ACD) in common femoral artery procedures to that of the FDA submitted historical manual pressure control group, who underwent either a diagnostic angiogram (DA) or a percutaneous coronary intervention (PCI) procedure. METHODS AND RESULTS: A total of 55 patients were enrolled in this study of the novel ACD. Of the 55 patients, 39 were enrolled in the DA group and 16 were enrolled in the PCI group. Six patients were excluded. A device was deployed in 49 patients. Time to hemostasis (TTH), time to ambulation (TTA), device function, and device-related vascular complications were measured. In the device group, the TTH for the combined DA and PCI patients was 32 seconds (0.54 ± 0.93 minutes), significantly lower when compared with 16.0 ± 12.2 minutes (P<0.0001) for the control group. Overall major vascular complication rate did not differ significantly, device group (1/49) and the historical control group (1/217). TTA in the combined PCI and DA device group was 226.4 ± 231.9 at the German site (site ambulation policy). In the Irish site, the average TTA in the PCI group was 187 minutes (n=8) and 85 minutes (n=14) in the DA group. CONCLUSION: The Celt ACD® device is safe, effective, and significantly decreases the TTH compared to manual pressure and has a low vascular complications rate. The device may be effective in early ambulation and discharge of patients postcoronary intervention procedures.

Diagnostic accuracy of heart-type fatty acid-binding protein for the early diagnosis of acute myocardial infarction.

OBJECTIVE: The aim of this study was to evaluate the diagnostic efficacy of multiple tests-heart-type fatty acid-binding protein (H-FABP), cardiac troponin I (cTnI), creatine kinase-MB, and myoglobin-for the early detection of acute myocardial infarction among patients who present to the emergency department with chest pain. METHODS: A total of 1128 patients provided a total of 2924 venous blood samples. Patients with chest pain were nonselected and treated according to hospital guidelines. Additional cardiac biomarkers were assayed simultaneously at serial time points using the Cardiac Array (Randox Laboratories Ltd, Crumlin, United Kingdom). RESULTS: Heart-type fatty acid-binding protein had the greatest sensitivity at 0 to 3 hours (64.3%) and 3 to 6 hours (85.3%) after chest pain onset. The combination of cTnI measurement with H-FABP increased sensitivity to 71.4% at 3 to 6 hours and 88.2% at 3 to 6 hours. Receiver operating characteristic curves demonstrated that H-FABP had the greatest diagnostic ability with area under the curve at 0 to 3 hours of 0.841 and 3 to 6 hours of 0.894. The specificity was also high for the combination of H-FABP with cTnI at these time points. Heart-type fatty acid-binding protein had the highest negative predictive values of all the individual markers: 0 to 3 hours (93%) and 3 to 6 hours (97%). Again, the combined measurement of cTnI with H-FABP increased the negative predictive values to 94% at 0 to 3 hours, 98% at 3 to 6 hours, and 99% at 6 to 12 hours. CONCLUSION: Testing both H-FABP and cTnI using the Cardiac Array proved to be both a reliable diagnostic tool for the early diagnosis of myocardial infarction/acute coronary syndrome and also a valuable rule-out test for patients presenting at 3 to 6 hours after chest pain onset.

Very late stent thrombosis immediately after recurrent inappropriate shock delivery by an implantable cardioverter defibrillator.

The case of a 49-year-old man who developed an ST segment elevation myocardial infarction because of very late stent thrombosis occurring in the immediate aftermath of a "storm" of recurrent inappropriate implantable cardioverter defibrillator (ICD) shocks caused by a fracture of a Medtronic Sprint Fidelis (Medtronic Inc., Minneapolis, MN) right ventricular lead is described. A causal relationship between recurrent ICD shocks and stent thrombosis is proposed. This deleterious association is an important observation given the increasing population of patients who receive both coronary stents and ICDs.

European consensus statement for intraoperative fluid therapy in children.

The intraoperative infusion of isotonic solutions with 1-2.5% glucose in children is considered well established use in Europe and other countries. Unfortunately, a European marketing authorisation of such a solution is currently missing and as a consequence paediatric anaesthetists tend to use suboptimal intravenous fluid strategies that may lead to serious morbidity and even mortality because of iatrogenic hyponatraemia, hyperglycaemia or medical errors. To address this issue, the German Scientific Working Group for Paediatric Anaesthesia suggests a European consensus statement on the composition of an appropriate intraoperative solution for infusion in children, which was discussed during a working session at the 2nd Congress of the European Society for Paediatric Anaesthesiology in Berlin in September 2010. As a result, it was recommended that an intraoperative fluid should have an osmolarity close to the physiologic range in children in order to avoid hyponatraemia, an addition of 1-2.5% instead of 5% glucose in order to avoid hypoglycaemia, lipolysis or hyperglycaemia and should also include metabolic anions (i.e. acetate, lactate or malate) as bicarbonate precursors to prevent hyperchloraemic acidosis. Thus, the underlying intention of this consensus statement is to facilitate the granting of a European marketing authorisation for such a solution with the ultimate goal of improving the safety and effectiveness of intraoperative fluid therapy in children.

Unintentional Extraction of a Deployed Coronary Stent Due to Microcatheter Fracture.

To our knowledge, this is the first reported case of unintentional removal of a deployed stent due to the fracture of a microcatheter tip.

Comparison of echocardiographic measures of left ventricular diastolic function in early hypertension.

Left ventricular (LV) diastolic dysfunction identifies patients at risk of developing heart failure and may be common in patients with hypertension. The prevalence of LV diastolic dysfunction in patients with newly diagnosed hypertension was compared using criteria provided by the Canadian Consensus, European Study Group, and American Medical Association guidelines. One hundred twenty patients with newly diagnosed untreated hypertension (mean age 46.9 +/- 2.1 years; 62 men, 58 women) with increased blood pressure (clinic >140/90 mm Hg, daytime ambulatory >135/85 mm Hg) underwent comprehensive 2-dimensional echocardiography. Transmitral inflow velocities were measured using pulse-wave Doppler with and without Valsalva's maneuver, and a comprehensive assessment of tissue Doppler velocities was performed. The prevalence of LV diastolic dysfunction varied according to criteria used. There was a high prevalence of LV diastolic dysfunction (59%; n = 71) using Canadian Consensus guidelines; 27% of patients (n = 32) had a pseudonormal pattern unmasked using Valsalva's maneuver and 32% (n = 39) had impaired relaxation at rest. Significantly fewer patients (10%; n = 12) had this diagnosis using European or American Medical Association guidelines (23%; n = 27). Using tissue Doppler imaging (early-late diastolic velocity ratio <1), the prevalence of LV diastolic dysfunction was 59% (n = 71), identical to findings using the Canadian Consensus guidelines. In conclusion, current national consensus guidelines defining LV diastolic dysfunction varied widely and underdiagnosed LV diastolic dysfunction in patients with newly diagnosed hypertension. Tissue Doppler imaging assessment is a rapidly and widely available tool that is as sensitive as the most stringent national guidelines and should be systematically incorporated into a more comprehensive assessment of LV diastolic dysfunction in this population.

Inflammatory markers are not associated with outcomes following elective external cardioversion.

BACKGROUND: Electrical cardioversion is a common modality of therapy for persistent atrial fibrillation. Unfortunately even if the cardioversion is initially successful many patients revert to atrial fibrillation. It has been proposed that there may be an inflammatory component to this arrhythmia. It is interesting to speculate that this may have a role in determining the outcome following elective cardioversion. METHODS: The study group consisted of 81 patients with persistent atrial fibrillation undergoing elective external cardioversion. Blood samples were taken immediately prior to the procedure. Soluble E-Selectin, P-Selectin, intra-cellular adhesion molecule and vascular cell adhesion molecule were assayed using a commercially available enzyme linked immunosorbent assay technique (R&D systems) and high sensitivity C reactive protein was measured by rate nephelometry. Patients were reviewed at 8 weeks and bloods were taken at this time. RESULTS: At baseline patients who had an unsuccessful cardioversion (n=15) were compared to those who had a successful cardioversion (n=66). Thirty-two patients of the 66 initially successful patients reverted to atrial fibrillation during the follow-up period. There was no difference in the levels of baseline serum inflammatory markers measured between those with an unsuccessful cardioversion and those who were successful. When the group who reverted to atrial fibrillation were compared to those who remained in sinus rhythm again there was no difference in the levels of serum markers measured at baseline. CONCLUSION: There was no association between maintenance of sinus rhythm following cardioversion and serum inflammatory markers.

Out-of-hours exercise treadmill testing reduces length of hospital stay for chest pain admissions.

AIMS: The objective was to examine the impact of out-of-hours exercise treadmill tests (ETTs) on length of hospital stay (LOS) for patients admitted to a chest pain assessment unit with symptoms suggestive of acute coronary syndrome. METHODS: Prospective observational study with 30-day follow-up of low-to-intermediate-risk chest pain patients undergoing out-of-hours ETT. Eligible patients had a nonischemic ECG, normal 6-12-h ST-segment monitoring, a negative 12-h troponin T assay, and no contraindications to exercise. Observed LOS was compared to expected LOS in the absence of out-of-hours ETT, using Wilcoxon rank-sum test. Estimated bed day savings and major adverse events at 30 days after discharge were examined. RESULTS: Four hundred and twenty-two patients with a mean age of 52 years (SD 13 years, 25-83 years) were evaluated. Fifty-two per cent (n = 221) were men; 66% (n = 279) had one or less cardiovascular risk factors; and 79% (n = 334) of the patients presented on a Friday or Saturday. ETT was performed on a weekend day in 86% (n = 363) of the patients, facilitating same-day discharges in 71% (n =  300). The median LOS (interquartile range) was 1 day (1, 2 days) for patients assessed with out-of-hours ETT. The expected median LOS (IQR) was 3 days (2, 4 days) (P < 0.05) in the absence of out-of-hours ETT. Each out-of-hours ETT was estimated to save a mean (SD, range) of 1.6 (0.6, 1-4) bed days. Thirty-day mortality and readmission rates were 0 and 0.2% (1 of 422), respectively. CONCLUSION: The availability of out-of-hours ETT facilitates safe early discharge and reduced LOS for low-to-moderate-risk patients admitted with symptoms of acute coronary syndrome.

Long-term cardiac monitoring in older adults with unexplained falls and syncope.

AIMS: Unexplained falls account for 20% of falls in older cohorts. The role of the implantable loop recorder (ILR) in the detection of arrhythmias in patients with unexplained falls is unknown. We aimed to examine the diagnostic utility of the ILR in detection of arrhythmogenic causes of unexplained falls in older patients. METHODS: A single centre, prospective, observational cohort study of recurrent fallers over the age of 50 years with two or more unexplained falls presenting to an emergency department. Insertion of an ILR (Reveal, Medtronic, Minnesota, USA) was used to detect arrhythmia. The primary outcome was detection of cardiac arrhythmia associated with a fall or syncope. The secondary outcome was detection of cardiac arrhythmia independent of falls or syncope, and falls or syncope without associated arrhythmia. RESULTS: Seventy patients, mean age 70 years (51-85 years) received an ILR. In 70% of patients cardiac arrhythmias were detected at a mean time of 47.3 days (SD 48.25). In 20%, falls were attributable to a modifiable cardiac arrhythmia; 10 (14%) received a cardiac pacemaker, 4 (6%) had treatment for supraventricular tachycardia. Patients who had a cardiac arrhythmia detected were more likely to experience a further fall. CONCLUSIONS: 14 (20%) patients demonstrated an arrhythmia which was attributable as the cause of their fall. Patients who have cardiac arrhythmia are significantly more likely to experience future falls. Further research is important to investigate if early detection of arrhythmogenic causes of falls using the ILR prevents future falls in older patients.

Optimal suppression of thromboxane A(2) formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor.

OBJECTIVES: We examined the contribution of cyclooxygenase (COX)-1 and -2 to the generation of prostacyclin, thromboxane (Tx) A(2), and 8-epi prostaglandin (PG) F(2alpha) during percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Both TxA(2) and 8-epi PGF(2alpha) activate platelets and are mitogenic, whereas prostacyclin is a platelet inhibitor, and therefore may influence the outcome of PTCA. METHODS: Twenty-one patients undergoing PTCA while receiving aspirin 300 mg daily or aspirin plus the selective COX-2 inhibitor nimesulide were compared with 13 patients treated only with fradafiban, a glycoprotein IIb/IIIa antagonist. Urine was analyzed for the metabolites of TxA(2) (Tx-M) and prostacyclin (PGI-M) and for the isoprostane, 8-epi PGF(2alpha). RESULTS: In the fradafiban group, there was a marked increase in Tx-M during PTCA (mean, 1973; 95% confidence interval [CI] 112 to 3834 rising to mean 7645; 95% CI 2,009 to 13281 pg/mg creatinine, p = 0.018). The Tx-M excretion was similarly reduced by aspirin and the combination of aspirin and nimesulide. In contrast, the combination of nimesulide and aspirin inhibited PGI-M excretion to a greater extent than aspirin (p = 0.001). Urinary 8-epi PGF(2alpha) excretion was elevated following PTCA compared with normal subjects (p = 0.002) and appeared to be unaffected by any of the treatments. CONCLUSIONS: The increase in TxA(2) during PTCA is primarily COX-1 dependent, and aspirin alone is effective in suppressing its formation. In contrast, prostacyclin generation is both COX-1 and COX-2 dependent. The inhibition of COX-1 and COX-2 did not prevent the production of 8-epi PGF(2alpha), suggesting that this is not enzymatically derived. The persistent generation of 8-epi PGF(2alpha) may contribute to the thrombosis and restenosis that complicate PTCA.

Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial.

BACKGROUND: An inflammatory component has been identified in degenerative aortic stenosis (AS). The combination of vitamins E and C has been shown to have anti-inflammatory properties. The aim of this study was to determine the impact of the combination of vitamins C and E or vitamin C only on serum levels of cell adhesion molecules and C-reactive protein in patients with chronic degenerative AS, with or without concomitant coronary artery disease. METHODS AND RESULTS: One hundred patients with asymptomatic or mildly symptomatic moderate AS were randomized in 2:2:1 format in an open-label trial. Forty-one patients received vitamin E (400 IU) and vitamin C (1000 mg) daily, 39 patients received vitamin C (1000 mg) only, and 20 patients were followed as controls. Serum intracellular adhesion molecule (ICAM-1), E selectin, P selectin, vascular-cellular adhesion molecule (VCAM-1), C-reactive protein, and alpha-tocopherol (vitamin E) were measured by enzyme-linked immunosorbent assay at baseline and 6 months postsupplementation. Half of the patients from each of the 2 active groups were followed for further 6 months to determine any changes after cessation of therapy. In the vitamin E and C, group there was reduction in serum ICAM-1 (298 +/- 12 to 272 +/- 12 ng/mL at 6 months, P = .0015) with a return to base line 6 months after cessation of therapy. In the vitamin C only group, there was a reduction in serum P selectin (134 +/- 10 to 118 +/- 10 ng/mL at 6 months, P = .033). All the inflammatory markers were unchanged in control group over 6 months of follow-up. CONCLUSION: Vitamin E and C supplementation had modest anti-inflammatory effect in chronic degenerative AS. The clinical relevance of this would require further clarification.

Vitamin E modulation of C-reactive protein in smokers with acute coronary syndromes.

Acute coronary syndromes are characterized by the expression of proinflammatory cytokines such as C-reactive protein (CRP). Sustained upregulation of inflammatory markers is associated with an adverse prognosis. Vitamin E is known to have significant anti-inflammatory properties and has been associated with a reduction in cardiovascular events in some studies of high-risk patients. The mechanism of benefit remains controversial. We conducted a randomized, double-blind placebo controlled trial of vitamin E 400 IU daily for 6 months in 110 patients with acute coronary syndromes. Serum samples were collected at enrollment and at 2, 4, and 6 months. CRP, interleukin-6 and the soluble cell adhesion molecules were measured. Vitamin E levels increased significantly in the treatment group (from 31 micromol/l at baseline to 51 micromol/l, p <.0001) and were unchanged in the placebo group (32 micromol/l at baseline to 34 micromol/l, p = NS). CRP levels fell in both the vitamin E group and the placebo group over the treatment period (from 17.2 +/- 2.9 to 6.1 +/- 0.8 mg/l and from 21.5 +/- 4.9 to 5.9 +/- 0.9 mg/l, p = NS for the difference between active and placebo groups). However, vitamin E treatment was associated with significantly lower 6 month CRP levels in smokers versus smokers on placebo (4.7 +/- 0.71 mg/l vs. 8.26 +/- 1.5 mg/l, p =.02). Vitamin E reduces CRP levels in smokers with acute coronary syndromes for up to 6 months after hospitalization.

Reciprocal activation of leukocyte-endothelial adhesion molecules in acute coronary syndromes.

BACKGROUND: The acute coronary syndromes are associated with an intense inflammatory response and sustained leukocyte activation. This inflammatory state has been correlated with an adverse prognosis, but the source of this inflammation remains controversial, with evidence that it may arise either from the coronary vasculature or from the systemic endothelium. METHODS: Levels of soluble cell adhesion molecules, and of their respective monocyte cell surface ligands, were measured in the peripheral serum of 21 patients presenting with acute coronary syndromes. Soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were measured by enzyme linked immunosorbent assay and expression of the monocyte integrins CD11b (Mac-1) and CD49d (VLA-4) was measured by direct immunofluorescence using flow cytometry. RESULTS: High levels of the monocyte receptor CD11b (531 vs. 345 MFI, P<0.01), and its soluble intercellular adhesion molecule-1 (329 vs. 232 ng/ml, P<0.01), were noted in patients with acute coronary syndromes compared to healthy controls. CONCLUSIONS: Reciprocal activation of monocyte receptor ligands and endothelial adhesion molecules was found in the peripheral blood of patients with acute coronary syndromes. This may indicate a coordinated state of pro-inflammatory upregulation with widespread activation of both leukocytes and endothelium and suggests a systemic rather than local source for inflammation in acute coronary disease.

Endothelial inflammation and thrombolysis resistance in acute myocardial infarction.

BACKGROUND: Despite recent refinements to thrombolysis for acute myocardial infarction, a significant minority of patients still fail to reperfuse. There is no reliable predictor of this state of "thrombolysis resistance", but platelet and endothelial factors are believed to be important. Cell adhesion molecules are expressed by the endothelium when activated and their shed or soluble portion can be quantified in the peripheral serum, where they may be taken as a measure of endothelial activation. We sought to find a link between markers of endothelial inflammation at time of infarction and failure to reperfuse as measured by vessel occlusion at angiography. METHODS: Patients presenting with their first acute myocardial infarction had levels of soluble adhesion molecules, C-reactive protein and monocyte chemotactic protein-1 measured prior to thrombolysis. An angiogram on day five after admission was performed to establish patency of the index vessel. RESULTS: Levels of soluble vascular adhesion molecule-1 (sVCAM-1) taken prethrombolysis were significantly elevated compared to those with a patent vessel (620+/-90 vs. 418+/-28 ng/ml, P<0.03. The positive predictive value of sVCAM-1 for vessel patency was 88%. CONCLUSIONS: We found elevated serum levels of the adhesion molecule soluble vascular adhesion molecule-1 (sVCAM-1) at presentation in patients with acute myocardial infarction who did not respond to thrombolysis. Endothelial activation may be important in thrombolysis resistance.

Early diastolic filling dynamics in diastolic dysfunction.

BACKGROUND: The aim of the study was to determine the relationship between the rate of peak early mitral inflow velocity and the peak early diastolic mitral annular tissue velocities in normal controls and to compare them with subjects with diastolic dysfunction. METHODS: The relationship between early passive diastolic transmitral flow and peak early mitral annular velocity in the normal and in diastolic dysfunction was studied. Two groups comprising 22 normal controls and 25 patients with diastolic dysfunction were studied. RESULTS: Compared with the normal group, those with diastolic dysfunction had a lower E/A ratio (0.7 +/- 0.2 vs. 1.9 +/- 0.5, p < 0.001), a higher time-velocity integral of the atrial component (11.7 +/- 3.2 cm vs. 5.5 +/- 2.1 cm, p < 0.0001), a longer isovolumic relaxation time 73 +/- 12 ms vs. 94 +/- 6 ms, p < 0.01 and a lower rate of acceleration of blood across the mitral valve (549.2 +/- 151.9 cm/sec2 vs. 871 +/- 128.1 cm/sec2, p < 0.001). They also had a lower mitral annular relaxation velocity (Ea) (6.08 +/- 1.6 cm/sec vs 12.8 +/- 0.67 cm/sec, p < 0.001), which was positively correlated to the acceleration of early diastolic filling (R = 0.66), p < 0.05. CONCLUSIONS: This investigation provides information on the acceleration of early diastolic filling and its relationship to mitral annular peak tissue velocity (Ea) recorded by Doppler tissue imaging. It supports not only the premise that recoil is an important mechanism for rapid early diastolic filling but also the existence of an early diastolic mechanism in normal.

Left ventricular structural and functional changes in the metabolic syndrome.

To test the hypothesis that the cardiac structural and functional abnormalities of the metabolic syndrome (MS) are independent of body mass index (BMI), 160 untreated patients (aged 47+/-1 years [mean +/- SEM], 53% male) underwent 2-dimensional echocardiography and tissue Doppler imaging and evaluation for MS. Participants with MS and controls were similar in age, BMI, and ejection fraction, but those with MS had greater left ventricular relative wall thickness (RWT) (0.43+/-0.008 vs 0.39+/-0.005, P<.001), reduced midwall fractional shortening (MFS) (13%+/-0.3% vs 14.2%+/-0.3%, P<.05), and reduced peak mitral annular velocity (Em) (9.9+/-0.5 vs 12.3+/-0.5 cm/sec, P<.01) than controls. There was a linear relationship between the number of features of MS and Em velocity (P<.001), RWT (P<.001), and MFS (P<.05). In a stepwise multiple regression analysis adjusting for likely determinants, MS was an independent predictor of Em in addition to age and nonindexed left ventricular mass. MS is associated with left ventricular concentric remodeling and reduced systolic and diastolic function independent of BMI.

Blood pressure control determines improvement in diastolic dysfunction in early hypertension.

BACKGROUND: Diastolic dysfunction is common in early hypertension. We hypothesized that improvement in diastolic dysfunction is blood pressure (BP) dependent and may occur early with treatment in newly diagnosed untreated hypertensive patients. METHODS: Forty untreated hypertensive subjects (age 52 +/- 1.4 years, mean +/- s.e.m.) with diastolic dysfunction based on Canadian Consensus Guidelines, received either bendroflumethiazide 2.5 mg (1.25 mg for the first month), or candesartan 16 mg (8 mg for the first month). Left ventricular (LV) structure and function, early diastolic velocity (E') and systolic velocity, and systolic myocardial velocity (Sm) were assessed echocardiographically using M-mode, 2-dimensional, and tissue Doppler imaging (TDI) before and at 1 and 3 months following treatment. RESULTS: Antihypertensive treatment reduced BP significantly at 3 months (168 +/- 2/97 +/- 1-143 +/- 2/86 +/- 1 mm Hg, P < 0.0001). Both drugs had similar and significant effects on TDI E' which increased from 7.8 +/- 0.2 to 10 +/- 0.3 cm/s (P < 0.001). The improvement in TDI E' was independent of LV mass index (LVMI) regression but was significantly related to the improvement in Sm (r = 0.73, P < 0.0001) and the fall in systolic BP (R = 0.51, P < 0.001). Normalization of diastolic function was associated with better control of BP (130 +/- 4/81 +/- 2 mm Hg vs. 149 +/- 2/88 +/- 1 mm Hg, P < 0.05). In a stepwise regression model, reduction in systolic BP (P < 0.001) and TDI Sm (P < 0.0001) emerged as independent determinants of improvement in TDI E' with no contribution from age, gender or change in relative wall thickness (RWT) (R(2) = 0.68, P < 0.0001). CONCLUSIONS: Achieving good BP control and enhancement in systolic function determines the improvement in diastolic function in early hypertension.

Effects of rosuvastatin and atorvastatin on the apolipoprotein B/apolipoprotein A-1 ratio in patients with an acute coronary syndrome: The CENTAURUS trial design.

BACKGROUND: The mechanism underlying rapid, statin-induced event reduction in patients with an acute coronary syndrome (ACS) remains to be clarified. AIM: The primary objective is to compare the efficacy of rosuvastatin 20 mg/day and atorvastatin 80 mg/day in reducing the apolipoprotein B/apolipoprotein A-1 (apoB/apoA-1) ratio at three months, in ACS patients. Secondary objectives include a comparison of the effects of early-started rosuvastatin and placebo on inflammatory markers. METHODS: This is a randomized, double-blind, parallel-group study. Patients with non-ST-segment elevation ACS, symptom onset less than 48 h before admission, and for whom a percutaneous coronary intervention is planned, are eligible for inclusion and are randomized into three groups (G1, G2 and G3). The study comprises two double-blind periods. Period 1 starts at hospital admission and lasts until Day 0 (discharge or less or equal to 6 days after admission); patients in G1 receive one tablet of rosuvastatin 20 mg/day and patients in G2 and G3 receive one matching placebo tablet per day. Period 2 starts at Day 0 and lasts for three months; patients in G1 continue to receive rosuvastatin 20 mg/day, patients in G2 receive rosuvastatin 20 mg/day and patients in G3 receive atorvastatin 80 mg/day. Recruitment of 1075 patients will ensure an 80 power to detect a 3% difference in percentage change in the apoB/apoA-1 ratio and a 20% difference in percentage change in high-sensitivity C-reactive protein. RESULTS: Inclusion phase is complete; results will be reported at a later date. CONCLUSION: This is the first trial investigating the effect of statins on apolipoproteins in ACS patients.