Sang Jae Rhee

The beneficial effect of high loading dose of rosuvastatin before percutaneous coronary intervention in patients with acute coronary syndrome

BACKGROUND Statin therapy prior to percutaneous coronary intervention (PCI) is associated with reduced mortality and periprocedural myocardial injury after PCI. We studied whether single high dose statin loading is beneficial on the outcome of patients with acute coronary syndrome (ACS) underwent PCI. METHODS Consecutive 445 patients with ACS who underwent PCI were randomly assigned to either the group of no statin treatment before PCI (Control group: n=220, 63+/-11 years, male 62%) or the group of 40 mg rosuvastatin loading before PCI (Rosuvastatin group: n=225, 64+/-10 years, male 60%). Incidence of periprocedural myocardial injury was assessed by analysis of creatinine kinase-MB (CK-MB) and cardiac troponin T before PCI, at 6 h and the next morning after PCI. RESULT There were no significant differences in clinical characteristics between the two groups. After PCI, incidence of periprocedural myocardial injury was higher in control than in rosuvastatin group (11.4% versus 5.8%, p=0.035). Mean preprocedural CK-MB and high sensitivity C-reactive protein were similar between the two groups, whereas after PCI, peak values of both markers were elevated significantly higher in control than in rosuvastatin group. Multivariate analysis revealed that no prior use of statin (OR=2.2; 95% CI=1.1-4.6; p=0.029), procedural complication (OR=3.1; 95% CI=1.4-6.9; p=0.007) and multi-vessel disease (OR=2.6; 95% CI=1.0-6.6; p=0.039) were the independent predictors for periprocedural myocardial infarction. CONCLUSION Single high dose of rosuvastatin prior to PCI reduces periprocedural myocardial injury in patients with ACS.

12-month follow-up results of high dose rosuvastatin loading before percutaneous coronary intervention in patients with acute coronary syndrome

BACKGROUND Statin pretreatment before percutaneous coronary intervention (PCI) is associated with a reduced incidence of short-term adverse events and periprocedural myocardial infarction (MI). However, the long-term effects of statin pretreatment have not been evaluated. METHODS Consecutive 445 patients with acute coronary syndrome (ACS) who underwent PCI were randomly assigned to receive no statin treatment before PCI (control group, n=220) or to receive 40 mg rosuvastatin loading before PCI (rosuvastatin group, n=225). The incidence of major adverse cardiac events (MACE), including cardiac death, non-fatal MI, non-fatal stroke, and any ischemia-driven revascularization, was assessed after 12 months. RESULTS During 11±3 months of follow-up, MACE occurred in 20.5% of patients in the control group and 9.8% of patients in the rosuvastatin group (p=0.002). The Kaplan-Meier curves showed that the incidence of death and non-fatal MI was significantly greater in the control group than in the rosuvastatin group (hazard ratio, 3.71; p=0.021). High-sensitivity C-reactive protein levels were less elevated in the rosuvastatin group than in the control group at 24 h after PCI. Multivariate analysis revealed that rosuvastatin loading was an independent predictor of a reduction in the risk of MACE at 12 months (odds ratio, 0.5; p=0.006). CONCLUSIONS High dose rosuvastatin loading before PCI significantly improved 12-month clinical outcomes in patients with ACS who underwent an early invasive strategy.

Relationship between the Echocardiographic Epicardial Adipose Tissue Thickness and Serum Adiponectin in Patients with Angina.

BACKGROUND It is still unknown whether increased cardiac adiposity is related to the risk factors of coronary artery disease (CAD). We measured epicaridal adopose tissue (EAT) and mediastinal adipose tissue (MAT) using echocardiography and examined their correlations with CAD and serum adiponectin. METHODS One hundred fifty three patients who underwent elective coronary angiography for chest pain were measured cardiac adiposity by transthoracic echocardiography. The correlations of cardiac adipose tissue with the presence and severity of CAD and the serum adiponectin level were examined. RESULTS EAT was thicker in patients with CAD (1.8+/-1.4 vs. 3.8+/-1.9 mm, p<0.001), but MAT was not different according to the presence of CAD (2.9+/-2.8 vs. 3.5+/-2.5 mm, p=0.121). EAT showed a significant positive correlation with age (r=0.225, p=0.005), homocystein (r=0.289, p=0.001), fasting glucose (r=0.167, p=0.042), and fibrinogen (r=0.218, p=0.009), and a significant negative correlation with serum adiponectin (r=-0.194, p=0.016). EAT thickness (OR 11.53, 95% CI; 3.61-36.84, p<0.001) and low serum adiponectin (OR 2.88, 95% CI; 1.02-8.15, p=0.046) were independent predictors of obstructive CAD. However, MAT thickness was not associated with CAD. CONCLUSION EAT was associated with the severity and risk factors of CAD and correlated with serum adiponectin level. In contrast with EAT, MAT was not associated with CAD and adiponectin.

Effect of High Dose Rosuvastatin Loading before Primary Percutaneous Coronary Intervention on Infarct Size in Patients with ST-Segment Elevation Myocardial Infarction

Background and Objectives High dose rosuvastatin loading before percutaneous coronary interventions (PCI) reduces the myocardial damage and the incidence of adverse cardiac events in patients with stable angina and acute coronary syndrome. However, no studies are present yet about rosuvastatin loading in patients with ST-segment elevation myocardial infarction (STEMI) in a primary PCI setting. Subjects and Methods A total of 475 patients who underwent primary PCI for STEMI were studied. The study population was divided into two groups with 208 patients in the statin group=40 mg rosuvastatin loading before primary PCI and 267 patients in the control group=no statin pretreatment. At median 3 days after PCI a single-photon emission computed tomography (SPECT) was performed with technetium 99m tetrofosmin For this study were compared infarct size, corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and the myocardial blush grade (MBG) between the both groups. Results Baseline clinical and procedural characteristics were similar between the groups. Infarct size, as assessed by SPECT, was significantly smaller (19.0±15.9% vs. 22.9±16.5%, p=0.009) in the statin group than in the control group. Patients of the statin group showed a lower corrected TIMI frame count (28.2±19.3 vs. 32.6±21.4, p=0.020), and higher MBG (2.49±0.76 vs. 2.23±0.96, p=0.001) than the patients of the control group. The multivariate analysis revealed that rosuvastatin loading {odds ratio (OR) 0.61}, pain to balloon time (OR 2.05), anterior myocardial infarction (OR 3.89) and final the MBG (OR 2.93) were independent predictors of a large infarct size. Conclusion A high dose rosuvastatin loading before the primary PCI reduced the infarct size by microvascular myocardial perfusion improvement.

Response of high-sensitivity C-reactive protein to percutaneous coronary intervention in patients with acute coronary syndrome

Percutaneous coronary intervention (PCI) provokes an inflammatory reaction, as shown by increased concentrations of plasma C-reactive protein (CRP) after PCI. However, the changes of CRP levels after PCI in patients with acute coronary syndrome (ACS) have not been well evaluated. We evaluated the characteristics of the patients with elevated CRP response after PCI and whether an increase in CRP after PCI predicts long-term prognosis in patients with ACS. We studied consecutive 360 patients with ACS who underwent elective coronary stenting. Inflammatory response to PCI was calculated as the difference between the peak postprocedural hsCRP level and the preprocedural hsCRP level (ΔCRP). Twelve months follow-up data were obtained and clinical outcomes were compared with ΔCRP. In receiver operating characteristics analyses, the cutoff point of ΔCRP for major adverse cardiac events (MACE) was 3.0 mg/l, which yielded sensitivity of 61.7% and specificity of 69.7%. The patients with ΔCRP > 3 mg/l revealed higher incidence of myocardial infarction (37.7 vs 14.6%, P < 0.001), and ACC/AHA type B2/C lesion (81.5 vs 68.7%, P = 0.006) than in patients with low ΔCRP. White blood cell count, low-density lipoprotein cholesterol, peak creatinine kinase-MB, and peak troponin T were significantly elevated in patients with ΔCRP > 3 mg/l than in those with ≤3 mg/l. There was significant correlation between ΔCRP and the changes in troponin T after PCI (r = 0.210, P < 0.001). An increase in hsCRP > 3 mg/l after PCI had a higher predictive value for the occurrence of MACE than low hsCRP elevation (hazard ratio 2.1, P = 0.005). In multivariate analysis, ΔCRP and peak troponin T were independent predictors of MACE (P < 0.001 and P = 0.013, respectively). In conclusion, postprocedural hsCRP elevation >3 mg/l was associated with higher incidence of MACE in patients with ACS. ΔCRP determinations may be of value for risk stratification after PCI.

Left Ventricular Thrombus Associated with Takotsubo Cardiomyopathy: A Cardioembolic Cause of Cerebral Infarction.

Takotsubo cardiomyopathy, also called stress-induced cardiomyopathy, usually occurs in patients with severe emotional or physiologic stress. The prognosis is favorable, and the wall motion abnormlities normalize within weeks. However, stress-induced cardiomyopathy is rarely assosicated with left ventricular thrombus and thromboembolic complications. Here, we report a case of stress-induced cardiomyopathy with left ventricular thrombus that embolized to cause cerebral infarction.

Effect of High Dose Rosuvastatin Loading before Percutaneous Coronary Intervention on Contrast-Induced Nephropathy

Background and Objectives Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality. This observational, non-randomized study evaluated the effect of rosuvastatin loading before percutaneous coronary intervention (PCI) on the incidence of CIN in patients with acute coronary syndrome (ACS). Subjects and Methods A total of 824 patients who underwent PCI for ACS were studied (408 patients in the statin group=40 mg rosuvastatin loading before PCI; 416 patients of control group=no statin pretreatment). Serum creatinine concentrations were measured before and 24 and 48 hours after PCI. The primary endpoint was development of CIN defined as an increase in serum creatinine concentration of ≥0.5 mg/dL or ≥25% above baseline within 72 hours after PCI. Results The incidence of CIN was significantly lower in the statin group than that in the control group (18.8% vs. 13.5%, p=0.040). The maximum percent changes in serum creatinine and estimated glomerular filtration rate in the statin group within 48 hours were significantly lower than those in the control group (5.84±22.59% vs. 2.43±24.49%, p=0.038; -11.44±14.00 vs. -9.51±13.89, p=0.048, respectively). The effect of rosuvastatin on preventing CIN was greater in the subgroups of patients with diabetes, high-dose contrast medium, multivessel stents, high baseline C-reactive protein, and myocardial infarction. A multivariate analysis revealed that rosuvastatin loading was independently associated with a decreased risk for CIN (odds ratio, 0.64; 95% confidence interval, 0.43-0.95, p=0.026). Conclusion High-dose rosuvastatin loading before PCI was associated with a significantly lower incidence of CIN in patients with ACS.

An Increased Monocyte Count Predicts Coronary Artery Spasm in Patients with Resting Chest Pain and Insignificant Coronary Artery Stenosis

Background Coronary atherosclerosis with inflammation gives rise to coronary vasospasm in the patients with coronary vasospastic angina. We have postulated that the peripheral leukocyte count and the differential count are associated with vasospastic angina. Methods 144 patients who underwent intracoronary ergonovine provocation testing between January 2002 and December 2004 were divided into two groups: Group I (72 patients with provoked spasm, mean age: 54.8±10.7 years, males: 75%) and Group II (72 without spasm, mean age: 55.3±10.2 years, males: 35%). Blood sampling was done to measure the lipid profiles and inflammatory markers, including the high sensitive C-reactive protein (hsCRP) levels and the monocyte counts. We compared the angiographic findings and laboratory data between the two groups. Results There were no significant differences in the levels of serum lipid and hsCRP between the two groups. The white blood cell count and the monocyte count were higher in Group I than with Group II (7496.4±2622.28 vs. 6703.2±1768.37/mm3, respectively, p=0.035; 627.5±270.70 vs. 426.9±205.76/mm3, respectively, p<0.001). Gensinis score was higher in Group I than in Group II (2.2±2.88 vs. 0.5±1.03, respectively, p<0.001). Multivariate analysis showed that the monocyte count and Gensinis score were independent factors affecting coronary spasm (p=0.047 and p=0.018, respectively). According to a receiver operating characteristics curve analysis, the area under the curve of the monocyte count was 0.738, that of the neutrophil count was 0.577 and that of the WBC count was 0.572. The cut-off value of the monocyte count was 530/mm3; the sensitivity and specificity of this cut-off value were 64% and 76%, respectively. Conclusions The peripheral monocyte count is an independent marker for predicting vasospastic angina in the patients with resting chest pain and insignificant coronary artery stenosis.

The Number of Endothelial Progenitor Cells is Decreased in Patients With Non-Dipper Hypertension

Background and Objectives Circulating endothelial progenitor cells (EPCs) play a key role in the maintenance of endothelial homeostasis and promote vascular repair. A reduced number of EPCs and the functional activity have been associated with several cardiovascular risk factors. However, the relationship between the number of EPCs and circadian rhythm of the blood pressure (BP) remains unclear. The purpose of the present study was to evaluate the relationship between the circadian rhythm of the BP and EPCs in patients with essential hypertension. Subjects and Methods A total of 45 patients with essential hypertension who were newly identified by outpatient BP measurements, underwent 24-hour ambulatory BP monitoring. Among the 45 patients with essential hypertension, 20 were classified as dippers (12 men and 8 women; mean age 48±14 years) and 25 as non-dippers (14 men and 11 women; mean age 52±18 years). The EPC count was isolated from the peripheral bloodstream and quantified by flow cytometry. Results The baseline clinical characteristics were similar between the dipper and non-dipper hypertensive patients. The circulating EPCs were statistically reduced in the non-dipper patients as compared to the dippers (104±60 vs. 66±47 EPCs per 106 mononuclear cells, p=0.027). The circulating EPC level correlated positively with the circadian changes in the systolic and diastolic BP (r=0.435, p=0.003, and r=0.310, p=0.038, respectively). Conclusion The present study demonstrated that the EPC count was reduced in the peripheral bloodstream in non-dipper hypertensive patients.

Rosuvastatin-induced high-density lipoprotein changes in patients who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome

BACKGROUND Clinical significance of statin-induced high-density lipoprotein cholesterol (HDL-C) changes is not well known. We investigated the factors affecting rosuvastatin-induced HDL-C changes and their correlation with 12-month major adverse cardiovascular events (MACE) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and percutaneous coronary intervention (PCI). MATERIALS AND METHODS We analyzed 556 consecutive NSTE-ACS patients who underwent PCI and received rosuvastatin 10mg before discharge. We measured serum lipids, including total cholesterol, triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and HDL-C at baseline and at 4 weeks. The relationship between on-treatment lipid levels, baseline lipid levels, and 12-month MACE was assessed. RESULTS Rosuvastatin treatment increased the mean HDL-C concentration by 1.1 ± 9.8 mg/dl (4.3 ± 23.0%). HDL-C was increased in 312 patients (56.1%), but decreased in 244 patients (43.9%) after statin treatment. Changes in HDL-C during first month were inversely correlated with baseline HDL-C levels (r=-0.379, p<0.001). The patients with increased HDL-C showed higher baseline TG levels but lower on-treatment TG levels. Changes in TG were correlated with changes in HDL-C (r=-0.212, p<0.001). The incidence of 12-month MACE according to changes in HDL-C was similar between the two groups (11.9% vs. 12.3%, p=0.875). Multivariate analysis revealed that baseline HDL-C level was the only significant predictor of rosuvastatin-induced HDL-C changes. CONCLUSION Baseline HDL-C concentration was an independent predictor of rosuvastatin-induced HDL-C changes. Statin-induced HDL-C changes did not predict 12-month MACE in patients with NSTE-ACS.