Long-term Clinical Outcomes Following Elective Stent Implantation for Unprotected Left Main Coronary Artery Disease

Background/PurposePercutaneous coronary intervention (PCI) has been increasingly adopted for unprotected left main coronary artery (LMCA) disease. The aim of this study was to evaluate the predictors of long-term clinical outcomes in patients after elective stent implantation for unprotected LMCA disease.MethodsA total of 122 patients with medically refractory angina who received coronary stenting for unprotected LMCA disease between August 1997 and December 2008 were included.ResultsDuring the follow-up period of 45 ± 35 months (range: 1–137 months), the incidence of repeated PCI and/or coronary artery bypass grafting (CABG), and cardiovascular and total mortality were 28% (34 patients), 20% (24 patients), and 25% (31 patients), respectively. Multivariate analysis revealed that young age [p = 0.02; hazard ratio (HR): 2.19, 95% confidence interval (CI): 1.11–4.30] and bare-metal stent (BMS) use (p = 0.02; HR: 5.35, 95% CI: 1.27–22.57) were the independent predictors of repeated PCI and/or CABG. Only lower left ventricular ejection fraction (LVEF) could predict both cardiovascular mortality (p = 0.003; HR: 4.25, 95% CI: 1.63–11.08) and total mortality (p = 0.002; HR: 3.95, 95% CI: 1.65–9.45). Lower LVEF (p = 0.001; HR: 0.31, 95% CI: 0.16–0.61) and small stent size (p = 0.01; HR: 5.95, 95% CI: 1.43–24.80) could predict the composite endpoint, including target vessel revascularization and total mortality.ConclusionWe showed that young age and BMS implantation could predict repeated PCI and/or CABG after stent implantation for unprotected LMCA disease. Only lower LVEF could predict both cardiovascular and total mortality. Lower LVEF and small stent size but not BMS implantation could predict composite target vessel revascularization/total mortality

Pericardial Fluid and Serum Levels of Vascular Endothelial Growth Factor and Endostatin in Patients With or Without Coronary Artery Disease

Vascular endothelial growth factor (VEGF) and endostatin are related to ischemic heart disease. This study investigated pericardial fluid and serum levels of VEGF and endostatin in patients with or without ischemic heart disease. Methods: A total of 39 patients (24 patients in the CAD group with significant coronary artery disease; 15 patients in the non-CAD group without coronary artery disease) undergoing open heart surgery were enrolled. In the CAD group, patients were classified according to good coronary collateralization (Group A; n = 11) or poor coronary collateralization (Group B; n = 13). Pericardial fluid and serum samples were obtained at the time of surgery. VEGF and endostatin were measured by enzyme-linked immunosorbent assay. Results: The levels of endostatin in both serum and pericardial fluid were significantly lower in the CAD group than in the non-CAD group (130.5 ± 37.3 ng/mL vs. 172.4 ± 37.8 ng/mL and 119.0 ± 25.0 ng/mL vs. 143.0 ± 23.5 ng/mL). The concentration of serum VEGF in the CAD group (92.6 ± 18.2 pg/mL) was significantly higher than that in the non-CAD group (75.2 ± 22.3 pg/mL). The concentration of serum VEGF in Group A (100.1 ± 20.7 pg/mL) was significantly higher than that in Group B (84.3 ± 12.4 pg/mL). The levels of pericardial fluid VEGF, serum and pericardial fluid endostatin were not significantly different between Groups A and B. Conclusion: Patients with coronary artery disease have lower serum and pericardial fluid levels of endostatin and higher serum levels of VEGF. Serum level VEGF, but not endostatin, is associated with good or poor collateralization in patients with coronary artery disease

Magnolol Depresses Urotensin-Ii-Induced Cell Proliferation in Rat Cardiac Fibroblasts

P>Accumulating evidence suggests that oxidative stress plays a key role in the development of cardiac fibrosis. Urotensin-II (U-II) has been reported to play an important role in cardiac remodelling and fibrosis. Recently, we demonstrated the involvement of reactive oxygen species (ROS ) production in U-II-induced cardiac fibroblast proliferation. Magnolol is an anti-oxidant compound extracted from the cortices of Magnolia officinalis. Thus, it is feasible that magnolol may attenuate cardiac fibroblast proliferation by inhibiting ROS production. Therefore, the aims of the present study were to determine whether magnolol alters U-II- induced cell proliferation and to identify the putative underlying signalling pathways in rat cardiac fibroblasts. Cultured rat cardiac fibroblasts were pretreated with magnolol (1, 3 and 10 mu mol/L) for 30 min, followed by exposure to U-II (30 nmol/L) for 24 h, after which cell proliferation and endothelin-1 (ET-1) protein secretion was examined. The effects of magnolol on U -II-induced ROS formation and extracellular signal-regulated kinase (ERK) phosphorylation were examined to elucidate the intracellular mechanisms by which magnolol affects cell proliferation and ET-1 expression. Urotensin-II (30 nmol/L) stimulated cell proliferation, ET-1 protein secretion and ERK phosphorylation, all of which were inhibited by magnolol (10 mu mol/L). Pretreatment of cardiac fibroblasts with N- acetylcysteine (5 mmol/L) for 30 min prior to exposure to U- II resulted in inhibition of U-II increased ROS formation. Similar effects were observed with 10 mu mol/L magnolol. In conclusion, the results suggest that magnolol inhibits cardiac fibroblast proliferation by interfering with ROS generation. Thus, the present study provides important new insights into the molecular pathways involved, which may contribute to our understanding of the effects of magnolol on the cardiovascular system

Hypertension Due to Co-existing Paraganglioma and Unilateral Adrenal Cortical Hyperplasia

A rare case of combined unilateral adrenal hyperplasia and paraganglioma is reported. A 27-year-old woman presented with hypertension, palpitation, dizziness, and headache for about 3 months. Elevated plasma aldosterone with low renin and a high level of urine vanillylmandelic acid (VMA) were found. Computed tomography showed a microadenoma of the left adrenal gland and a well demarcated left retroperitoneal para-aortic mass. Adrenal vein sampling for aldosterone and renin levels suggested left adrenal lesion. Surgical removal of the left adrenal gland and para-aortic mass was performed. Pathologic examination of the resected left adrenal gland showed adrenal cortical hyperplasia and the left retroperitoneal para-aortic mass showed a paraganglioma. Postoperatively, blood pressure, plasma renin, aldosterone and urine VMA all returned to within normal ranges. The possible relationship of these two diseases is discussed

Incidence, Predictors and Outcomes of Subacute Stent Thrombosis following Primary Stenting for ST-elevation Myocardial Infarction

Knowledge concerning subacute stent thrombosis (SST) following primary stenting for ST-elevation myocardial infarction (STEMI) is not widely available. We studied the incidence, predictors, and clinical outcomes of SST following STEMI. Methods: We analyzed data from 455 consecutive patients who underwent primary stenting for STEMI. Baseline clinical characteristics, coronary angiographic features, medication and outcome were compared in patients with and without SST. Results: SST occurred in 17 patients, and the incidence was 3.7%. Univariate predictors of SST were being a current smoker (53.0% vs. 82.4%, p = 0.01), Killip class ≥ II (38.4% vs. 58.8%, p = 0.05), no coronary re-flow after stenting (6.2% vs. 17.6%, p = 0.05) and lack of coprescription with a statin (39.5% vs. 5.9%, p<0.01). After multivariate analysis, being a current smoker (odds ratio = 4.76; 95% confidence interval 1.20–18.95) and using statin therapy (odds ratio = 0.09; 95% confidence interval = 0.01–0.75) were independent correlates of SST. Patients with SST were associated with higher 30-day mortality (37.5% vs. 3.1%, p<0.01) and all-cause mortality (23.5% vs. 5.3%, p = 0.01) at long-term follow-up. Conclusion: Although SST is rare in patients with STEMI treated by primary stenting, it imparts a significantly higher mortality at short-term and long-term follow-up. Being a current smoker and the lack of co-prescription with a statin were associated with higher incidence of SST. Our results suggest initiation of statin therapy in patients with STEMI should be considered before discharge