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Chiung-Jen Wu

Publications and source records attributed to Chiung-Jen Wu.

At least 37 records · Page 2Linked to original sources

Level of high-sensitivity C-reactive protein is predictive of 30-day outcomes in patients with acute myocardial infarction undergoing primary coronary intervention.

BACKGROUND: C-reactive protein (CRP) has been well recognized as a strong independent predictor of short-term and long-term mortality after non-ST-segment elevation acute coronary syndromes. However, limited studies have been conducted correlating CRP levels within 6 h following the onset of ST-segment elevation (ST-se) acute myocardial infarction (AMI) to mortality. The purpose of this study was to evaluate the predictive value of CRP measured by high-sensitivity CRP assay (hsCRP) on 30-day clinical outcomes in patients with ST-se AMI of onset < 6 h undergoing primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: We conducted a prospective cohort study in 146 consecutive patients with ST-se AMI of onset < 6 h who were undergoing primary PCI. Blood samples for hsCRP were obtained in the catheterization laboratory before coronary angiography. Patients were classified into high (group 1: hsCRP > 2.37 mg/L, n = 73) and low (group 2: hsCRP </= 2.37 mg/L, n = 73) hsCRP groups according to the median value of hsCRP after AMI. Univariate analysis demonstrated that the 30-day composite major adverse cardiac events (MACE) [death, recurrent ischemia, and re-occlusion] were significantly higher in group 1 than in group 2 (23.3% vs 4.1%, p = 0.0008). Multiple stepwise logistic regression analysis demonstrated that high hsCRP (p = 0.001), cardiogenic shock (p = 0.0003), and low left ventricular ejection fraction (p = 0.032) were independent predictors of 30-day MACE. CONCLUSIONS: Prospective evaluation of the hsCRP in ST-se AMI of onset < 6 h allows accurate risk stratification of individuals at risk of 30-day MACE after primary PCI.

Angina Pectoris↗

Prognostic value of circulating levels of endothelin-1 in patients after acute myocardial infarction undergoing primary coronary angioplasty.

BACKGROUND: The link between increased circulating level of endothelin (ET)-1 and adverse clinical outcomes after acute myocardial infarction (AMI) has been established. Current studies demonstrate that reperfusion therapy by either thrombolysis or primary percutaneous coronary intervention (PCI) can salvage myocardium, improving survival of AMI patients. However, whether reperfusion therapy by primary PCI can prevent the adverse effect of ET-1 on clinical outcomes in patients after AMI remains unclear. Therefore, this study examined the predictive value of circulating ET-1 levels on 30-day outcomes in ST-segment elevated AMI treated with primary PCI. METHODS AND RESULTS: We conducted a prospective cohort study of 186 consecutive patients with ST-segment elevated AMI of onset < 12 h who underwent primary PCI. Blood samples for plasma concentration of ET-1 were collected in the catheterization laboratory following vascular puncture. Patients were classified into a high group (group 1, ET-1 level >or= 0.632 pg/mL, n = 93) and a low group (group 2, ET-1 level < 0.632 pg/mL, n = 93) according to the median value of ET-1 after AMI. Univariate analysis demonstrated that the 30-day composite major adverse clinical outcomes (MACO) [advanced Killip score >or= 3], severe congestive heart failure (CHF) [New York Heart Association functional class 4], and 30-day mortality were strongly associated with high ET-1 level (>or= 0.632 pg/mL; p < 0.0001), unsuccessful reperfusion (final Thrombolysis in Myocardial Infarction flow <or= 2; p < 0.0001), low left ventricular ejection fraction (< 50%; p = 0.0002), multivessel disease (p = 0.005), and female gender (p = 0.007). Multiple stepwise logistic regression analysis demonstrated that only high ET-1 level (p < 0.0001) and unsuccessful reperfusion (p < 0.0001) were independent predictors of 30-day MACO. Additionally, high ET-1 level (p = 0.0021) along with unsuccessful reperfusion (p = 0.008) and severe CHF (p < 0.0001) were significant independent predictors of increased 30-day mortality. CONCLUSIONS: A high circulating level of ET-1 is a strong independent predictor of 30-day MACO after ST-segment elevated AMI treated with primary PCI.

Aged↗

Percutaneous transluminal mitral valvuloplasty reduces circulating soluble CD40 ligand in rheumatic mitral stenosis.

BACKGROUND: Recent data suggest that the pathogenesis of vascular inflammation and thrombosis involves CD40 ligand (CD40L), which is mostly derived from platelets. Previous studies have demonstrated that platelet activation occurs in peripheral blood of patients with rheumatic mitral stenosis (MS). However, in patients with MS, the plasma level of soluble CD40L has never been investigated. METHODS AND RESULTS: Seventeen patients with symptomatic MS undergoing percutaneous transluminal mitral valvuloplasty were studied (group 1, 11 patients in permanent atrial fibrillation and 6 patients in sinus rhythm). Solid-phase, sandwich enzyme-linked immunosorbent assay determined the plasma levels of soluble CD40L in the femoral vein and artery, and right and left atria before valvuloplasty, and those in the peripheral venous blood obtained 10 min after valvuloplasty, and at the 4-week follow-up after valvuloplasty. The Doppler pressure half-time method was used to calculate the mitral valve area. Additionally, plasma concentrations of soluble CD40L in the peripheral venous blood obtained from 17 control patients were measured (including nine healthy volunteers in sinus rhythm [group 2] and eight patients in permanent lone atrial fibrillation [group 3]). Plasma levels of soluble CD40L were significantly elevated in group 1 patients (437.6 +/- 370.2 pg/mL) [mean +/- SD] compared with group 2 (203.8 +/- 218.0 pg/mL) and group 3 patients (173.5 +/- 105.0 pg/mL) [p < 0.05]. The area of mitral valve increased significantly after valvuloplasty (1.10 +/- 0.20 cm(2) vs 1.47 +/- 0.29 cm(2), p < 0.0001). The mean left atrial pressure fell significantly and immediately after valvuloplasty (22.8 +/- 4.9 mm Hg vs 17.6 +/- 5.5 mm Hg, p = 0.0004). The peripheral venous plasma levels of soluble CD40L obtained before valvuloplasty significantly fell after valvuloplasty (before, 437.6 +/- 370.2 pg/mL; vs 10 min after, 215.4 +/- 113.9 pg/mL; vs 4 weeks after, 217.5 +/- 111.9 pg/mL; p < 0.02). CONCLUSIONS: Patients with moderate-to-severe MS had higher venous plasma levels of soluble CD40L than healthy volunteers or patients with lone atrial fibrillation. Additionally, the elevated venous plasma levels of soluble CD40L fell significantly following valvuloplasty.

Adult↗

Early administration of intracoronary verapamil improves myocardial perfusion during percutaneous coronary interventions for acute myocardial infarction.

BACKGROUND: Intracoronary calcium-channel blockers administered in the event of no reflow during percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) have been shown to improve myocardial perfusion. STUDY OBJECTIVE: To evaluate the effects of the administration of intracoronary verapamil before the occurrence of no reflow during direct PCI. DESIGN AND SETTING: Single-center, nonrandomized, prospective study with a retrospective control group. PATIENTS AND METHODS: From September 2001 to December 2003, 50 consecutive patients with AMI were prospectively enrolled for intracoronary verapamil treatment. Intracoronary verapamil was administered immediately prior to balloon inflation and at short intervals during the procedure thereafter. Retrospectively, 50 consecutive AMI patients who had undergone direct PCI and had not received intracoronary calcium-channel blockers were enrolled as control subjects. Patients with cardiogenic shock or platelet glycoprotein IIb/IIIa inhibitor were excluded. Thrombolysis in Myocardial Infarction (TIMI) flow grade, corrected TIMI frame count (CTFC), and TIMI myocardial perfusion grade (TMPG) were assessed prior to and following PCI by two independent cardiologists blinded to the procedures. RESULTS: The two groups had similar baseline and post-procedural angiographic characteristics, although the patients who been administered verapamil received more stent implantations than the control subjects (84% vs 60%, p = 0.008). Post-procedural TIMI flow < 3 (odds ratio [OR], 0.39; 95% confidence interval [CI], 0.12 to 1.30; p = 0.18) and TMPG (OR, 1.24; 95% CI, 0.46 to 3.34; p = 0.68) were not associated with the implantation of the stents. There were no significant difference in post-PCI TIMI flow (p = 0.68) and CTFC (p = 0.36) between patients treated with verapamil and the control subjects. Post-PCI TMPG was significantly better in patients treated with intracoronary verapamil (p = 0.003). Forty-two percent of the patients treated with verapamil were found to have TMPG-3, while only 14% of the control subjects were found to have the same degree of TMPG (p = 0.004). Treatment with intracoronary verapamil (OR, 0.26; 95% CI, 0.12 to 0.58; p = 0.001) and pre-PCI TIMI flow (OR, 0.54; 95% CI, 0.35 to 0.84; p = 0.006) were found by multiple logistic regression to be independent predictors of TMPG. CONCLUSIONS: Early administration of intracoronary verapamil during direct PCI improves post-procedural myocardial perfusion, as evaluated by TMPG.

Aged↗

Impact of elevated plasma total homocysteine concentration on coronary atherosclerosis in Chinese patients with acute myocardial infarction undergoing primary coronary intervention.

Elevated plasma total homocysteine (tHcy) has been considered to be a new risk factor for coronary atherosclerotic disease. However, the association has not been proven indisputably, and the strength of the relationship and the interaction of plasma tHcy with other conventional risk factors remain uncertain in the clinical setting of acute myocardial infarction (AMI). The aim of this study was to investigate whether an elevated plasma level of tHcy is an independent predictor of the late stage of coronary atherosclerotic lesions in Chinese patients with AMI, who are undergoing primary percutaneous coronary intervention (PCI). Plasma levels of tHcy were prospectively measured in 178 consecutive patients with ST-segment elevated AMI undergoing primary PCI. The plasma level of tHcy was also measured in 30 control subjects with normal coronary angiographic findings. The plasma level of tHcy was significantly higher in the patients with AMI than in control subjects (10.5 +/- 3.3 micromol/L versus 8.3 +/- 2.4 micromol/L, P = 0.0004). Multiple stepwise logistic regression analysis of the baseline characteristics demonstrated that smoking (P = 0.004) and creatinine level (P < 0.0001) were independent predictors of an elevated plasma level of tHcy. Moreover, an increased plasma level of tHcy (P = 0.003), female gender (P = 0.008), diabetes mellitus (P = 0.020), and the presence of previous myocardial infarction (P = 0.003) were independent predictors of the late stage of multivessel diffuse atherosclerosis (defined by > or = 2 epicardial vessels with moderate or severe diffuse atherosclerosis). In conclusion, this investigation supports the hypothesis that a raised homocysteine concentration is a strong risk factor for the late stage of diffuse coronary atherosclerosis in Chinese patients with AMI undergoing primary PCI. This result therefore raises the prospect of the need for major therapeutic research in Chinese patients.

Aged↗

Utilization of a double-wire technique to treat long extended spiral dissection of the right coronary artery. Evaluation of incidence and mechanisms.

While coronary artery dissection caused by a guiding catheter, which is one of the most commonly occurring complications during diagnostic cardiac catheterization or coronary intervention, has various forms, extensive antegrade and retrograde dissections of the right coronary artery (RCA) are rarely observed during these procedures. Within the last three years, we retrospectively reviewed our experience with 12,600 consecutive patients who underwent either diagnostic cardiac catheterization or coronary angioplasty, and found that 17 (0.14%) of the patients displayed extensive antegrade and retrograde RCA dissection. The antegrade dissection always propagated to the distal RCA either on bifurcation of the posterior descending artery and posterolateral artery (PLA) or to the proximal PLA. The retrograde dissection was always observed close to the ostium of the RCA or extending to the ostium of the RCA. TIMI-0 flow in the RCA was immediately observed in all the patients. Chest pain associated with an electrocardiogram showing ST-segment elevation was soon observed in most of the patients. The true lumen could be entered successfully using a single wire in 8 of 17 patients. However, a double-wire technique was required for 7 patients. This technique involved first advancing a wire along to the false lumen and then pulling back the guiding catheter away from the ostium of the RCA for a few millimeters followed by anchoring with the wire. Another wire was then gently inserted into the true lumen from the dissection entrance point, which was located near or at the ostium of RCA, and carefully advanced to the distal RCA. Coronary stenting was successfully deployed in 15 patients. However, the procedure failed in 2 patients. Furthermore, this complication caused 7 patients to have acute myocardial infarctions, 2 patients to develop atrial fibrillation, and I to die from ischemic enterocolitis due to cardiac embolism after 7 months of follow-up. In conclusion, with an increase in experience, we now better understand this complication. However, this complication, which is a formidable challenge for coronary intervention, may be a life-threatening complication, and patients with this complication may face the potential risk of a nonfatal myocardial infarction, or even a long-term fatal outcome in the long-term. Accordingly, it is important to learn how to promptly manage this complication.

Aortic Dissection↗

Levels and values of inflammatory markers in patients with angina pectoris.

Inflammation plays an important pathogenic role in the initiation and progression of atherosclerotic plaque lesions. C-reactive protein (CRP), which directly participates in plaque inflammation, induces vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. However, the levels and values of high-sensitivity (hs)-CRP, white blood cell (WBC) count, and VCAM-1 in both stable and unstable angina pectoris (AP) have not been fully investigated. This study examines the levels and values of these inflammatory markers in patients with stable or unstable AP. From March 2003 to December 2003, a prospective cohort study was conducted in 128 consecutive patients, including unstable AP patients (class I: n = 59; combined class II and III: n = 16) and stable AP patients (n = 53) undergoing elective coronary stenting. Blood samples for hs-CRP, WBC count, and VCAM-1 were obtained in the catheterization laboratory before coronary angiography. The circulating levels of hs-CRP and VCAM-1 were also evaluated in 40 healthy volunteers. The circulating levels of these three inflammatory markers were substantially higher in patients than in healthy volunteers (all P values < 0.0001). Additionally, circulating levels of hs-CRP and the WBC count were significantly higher in patients with unstable AP than in patients with stable AP (all P value < 0.0001). However, only those patients with class II and III unstable AP had significantly higher circulating levels of VCAM-1 than patients with stable AP (P < 0.0001). On the other hand, the circulating levels of VCAM-1 did not differ between patients with class I unstable AP and patients with stable AP (P = 0.782). Multiple stepwise logistic regression analysis showed that only hs-CRP level was independently associated with unstable AP (P = 0.0002). In conclusion, circulating levels of hs-CRP, WBC count, and VCAM-1 were significantly increased in patients with AP. The circulating level of hs-CRP was strongly associated with the clinical setting of unstable AP.

Aged↗

Circulating levels of soluble P-selectin in patients in the early and recent phases of myocardial infarction.

BACKGROUND: Circulating soluble P-selectin (sP-selectin), a biomarker of platelet activation is substantially increased in patients with acute myocardial infarction (AMI). However, the circulating level of sP-selectin in patients in the early (onset of AMI > 12 h but < 7 d) or recent (onset of AMI > 8 d but < 21 d) phase after AMI remains unclear. The purpose of this study was to prospectively evaluate whether the circulating level of sP-selectin remains elevated in these two consecutive phases after an AMI. METHODS: Blood samples were collected in the catherization room before coronary angiography to assess the circulating level of sP-selectin. A total of 53 consecutive patients, 34 with early MI (group 1) and 19 with recent MI (group 2), who had had no prior thrombolytic therapy were included. Circulating levels of sP-selectin were also measured in 30 risk control (stable angina) subjects undergoing elective percutaneous coronary intervention and in 20 healthy subjects who comprised the healthy control group. RESULTS: The circulating level of sP-selectin did not differ between patients with early AMI and those with recent MI (p = 0.632). However, the plasma level of sP-selectin was significantly higher in group 1 and 2 patients than in the risk control and healthy control subjects (all p values < 0.0001). CONCLUSIONS: Circulating sP-selectin was elevated in patients 12 hours to 7 days after AMI and the elevation was maintained until 21 days after AMI. Therefore, investigation of longer utilization of anti-platelet and anti-inflammatory agents for patients following AMI might be worthwhile.

Adult↗

Levels and value of soluble P-selectin following acute myocardial infarction: evaluating the link between soluble P-selectin levels and recruitment of circulating white blood cells and the marker for the rapid diagnosis of chest pain.

BACKGROUND: Platelet activation that results from coronary plaque rupture is important in the pathogenesis of acute myocardial infarction (AMI). Soluble p-selectin (sP-selectin) is crucial in modulating leukocyte adhesion to both platelets and endothelial cells during inflammatory response and thrombus formation. We hypothesized that sP-selectin, an index of both platelet activation and acute inflammation, rapidly increases and modulates the recruitment of circulating white blood cells (WBC) in patients following AMI. METHODS: We conducted a prospective cohort study of 142 consecutive patients with ST-segment elevated AMI of onset < 12 h who were undergoing primary percutaneous coronary intervention. Blood samples for plasma levels of sP-selectin were obtained in the catheterization laboratory before coronary angiography was performed. The plasma levels of sP-selectin were also measured in 30 risk control subjects and 20 healthy control subjects. RESULTS: The plasma level of sP-selectin and the circulating WBC count were significantly higher in patients with AMI than in either the risk control or healthy subjects (all of p values < 0.0001). Additionally, repeated measures of ANOVA demonstrated that there were no significant differences in plasma levels of sP-selectin (p > 0.10) in three intervals from the start of chest pain to blood sample collection (< 180 min, > or = 180 < 360, and > or = 360 < 720) following AMI. Correlation analysis demonstrated that the increase in the plasma level of sP-selectin was significantly related to the circulating WBC count (r = 0.248, p = 0.003). CONCLUSIONS: sP-selectin was markedly elevated in an early phase of AMI. sP-selectin may be involved in modulating the recruitment of circulating WBC during AMI. These findings raise the need for a prospective investigation of sP-selectin as a potential reliable clinical tool for rapidly diagnosing AMI.

Adult↗

Effects and safety of intracoronary thrombectomy using transradial application of the PercuSurge distal balloon protection system in patients with early or recent myocardial infarction.

BACKGROUND: Distal embolization and no reflow are likely during primary percutaneous coronary intervention (PCI) on the large infarct-related artery (IRA), which mostly contains high-burden thrombus formation (HBTF) and plaque burden. Mechanical devices to prevent distal atheroembolism may be of importance for preserving reperfusion and microvascular integrity in IRA. METHODS AND RESULTS: Between May 2002 and December 2002, transradial application (TRA) of the PercuSurge GuardWire device with 7-french arterial sheath was performed in 39 consecutive patients who experienced early (>12 h and </=7 days) or recent (>7 days and <14 days) myocardial infarction (MI) associated with large IRA (vessel size >/=3.5 mm with HBTF; group 1). Between January 2001 and April 2002, 64 consecutive patients who had early or recent MI associated with HBTF in IRA of a vessel size >/=3.5 mm received TRA of PCI with adjunctive tirofiban therapy but without using the adjunctive PercuSurge GuardWire device (group 2). The angiographic and clinical outcomes of both groups were compared in a chronologically consecutive manner. The procedural success rate and post-PCI myocardial blush grades were significantly higher in group 1 than in group 2 patients (all p values <0.05), whereas a combined incidence of vascular and bleeding complications and 30-day major adverse cardiac events (defined as death, reinfarction and repeated PCI of IRA) were significantly higher in group 2 than in group 1 patients (all p values <0.05). CONCLUSIONS: Our data suggested that TRA using the PercuSurge GuardWire device during PCI for patients with early or recent MI and HBTF in IRA was safe and feasible. This mechanical device provided more additional benefit to patients in this clinical setting than a combination of conventional PCI and tirofiban therapy.

Aged↗

Transradial application of PercuSurge GuardWire device during primary percutaneous intervention of infarct-related artery with high-burden thrombus formation.

A large infarct-related artery (IRA), which mostly contains high-burden thrombus formation (HBTF) and lipid pool-like plaque contents, has been suggested to play a pivotal role in the no-reflow phenomenon during primary percutaneous coronary intervention (p-PCI). To reduce the thrombus burden of the IRA using the PercuSurge GuardWire device before intervention may be of crucial importance to preventing no-reflow. The purposes of this study were to test the transradial application (TRA) of this new mechanical device and to determine its impact on prevention of no-reflow during p-PCI. From May to September 2002, the PercuSurge GuardWire device was utilized in 42 consecutive patients with acute myocardial infarction and large IRA (vessel size >or= 3.5 mm with HBTF; group 1). From January to December 2000, p-PCI was performed in large IRA (vessel size >or= 3.5 mm) with HBTF using tranfemoral arterial approach in 101 consecutive patients (group 2). The angiographic and clinical outcomes of the two groups were compared in a chronologically consecutive manner. Successful reperfusion (final TIMI-3 flow) was significantly higher in group 1 than in group 2 patients (95.2% vs. 79.1%; P = 0.005). Moreover, the combined incidence of vascular complications, post-PCI thromboembolisms (defined as a distal embolism and a post-PCI residual thrombus score of >or= 3), and combined 30-day major adverse cardiac events were significantly lower in group 1 than in group 2 patients (all P values < 0.05). In group 1 patients, post-p-PCI myocardial blush (MB) of >or= 2 grades was found to be more than 88.0%. Furthermore, when compared with preintervention, thrombus scores were significantly reduced after aspiration (P = 0.0001), whereas the minimal lumen diameter (P = 0.0001), TIMI flow grade (P = 0.0001), and MB grade (P = 0.0001) had all significantly increased after aspiration using Export Aspiration Catheter. There were no significant differences in corrected TIMI frame count (P = 0.42), TIMI flow grade (P > 0.5), or MB grade (all P values > 0.5) between postaspiration and post-PCI. The TRA of the PercuSurge GuardWire device during primary intervention of large IRA with HBTF was safe and feasible and provided benefits to patients. The initial successful reduction of the thrombus burden with this mechanical device before intervention can be translated into increased final TIMI-3 flow, a combined MB of >or= 2 grades, and fewer final thromboembolic events.

Adult↗

Increased circulating endothelin-1 in rheumatic mitral stenosis: irrelevance to left atrial and pulmonary artery pressures.

BACKGROUND: Increased plasma endothelin (ET)-1 concentrations have been observed in patients with rheumatic mitral stenosis (MS). However, the mechanisms of increased circulating ET-1 in patients with MS remain unclear. METHODS: We measured plasma concentrations of ET-1 in blood samples from the femoral vein and artery, and right and left atria obtained from 20 patients with moderate-to-severe rheumatic MS before and after percutaneous transluminal mitral valvuloplasty (PTMV) [group 1; 16 patients in chronic atrial fibrillation and 4 patients in sinus rhythm]. In addition, we measured plasma concentrations of ET-1 in the peripheral venous blood samples obtained from 22 control patients (including 14 healthy volunteers in sinus rhythm [group 2] and 8 patients in chronic lone atrial fibrillation [group 3]). Plasma ET-1 concentrations were measured by solid-phase, sandwich enzyme-linked immunosorbent assay. RESULTS: The peripheral venous plasma concentrations of ET-1 were significantly higher in group 1 patients (2.46 +/- 0.90 pg/mL) than in group 2 and group 3 patients (0.74 +/- 0.42 pg/mL and 0.99 +/- 0.41 pg/mL, respectively [mean +/- SD]; p < 0.0001). However, there was no significant difference in the peripheral venous concentrations of ET-1 between group 2 and group 3 patients. In group 1 patients, the plasma ET-1 concentration in the femoral vein (2.46 +/- 0.90 pg/mL) was significantly higher than that in the right atrium (2.02 +/- 0.69 pg/mL), left atrium (2.11 +/- 0.99 pg/mL), and femoral artery (2.05 +/- 0.75 pg/mL) [p = 0.0001]. The plasma ET-1 concentration in the femoral vein was not correlated with the mean left atrial pressure (r = 0.05; p = 0.838) and mean pulmonary artery pressure (r = 0.07; p = 0.757). The plasma ET-1 concentration in the left atrium was also not correlated with the mean left atrial pressure (r = 0.11; p = 0.656), mean pulmonary artery pressure (r = 0.06; p = 0.788), or mitral valve area (r = 0.02; p = 0.936). Although the area of mitral valve increased significantly (1.06 +/- 0.17 cm(2) vs 1.48 +/- 0.32 cm(2); p < 0.0001), and the mean left atrial pressure (23.0 +/- 5.1 mm Hg vs 17.6 +/- 5.9 mm Hg; p < 0.0001) and mean pulmonary arterial pressure (31.0 +/- 7.9 mm Hg vs 25.5 +/- 7.0 mm Hg; p < 0.001) fell significantly and immediately after PTMV, there were no significant changes in the plasma ET-1 concentrations in the femoral vein, right atrium, left atrium, and femoral artery immediately after PTMV. CONCLUSION: Increased production of ET-1 in the pulmonary circulation in response to increased pulmonary artery pressure was not the mechanism of increased circulating ET-1 concentration in patients with MS. We proposed that one of the mechanisms of increased ET-1 concentration in the femoral vein was increased peripheral ET-1 release due to increased systemic venous pressure and mechanical damage of the endothelium.

Adult↗

Percutaneous transluminal mitral valvuloplasty reduces circulating vascular cell adhesion molecule-1 in rheumatic mitral stenosis.

BACKGROUND: The circulating levels of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), have been demonstrated to be elevated in patients with rheumatic mitral stenosis (MS). However, the impact of percutaneous transluminal mitral valvuloplasty (PTMV) on the elevated circulating levels of VCAM-1 and ICAM-1 in patients with MS has never been investigated. METHODS: and results: A total of 19 patients with symptomatic MS undergoing PTMV were studied (group 1) [15 patients in chronic atrial fibrillation, and 4 patients in sinus rhythm]. The plasma levels of soluble VCAM-1 and ICAM-1 in the femoral vein and artery, and right and left atria before PTMV, and those in the peripheral venous blood at the 1-week and 4-week follow-ups after PTMV were determined by solid-phase sandwich enzyme-linked immunosorbent assay. The mitral valve area was calculated by means of the Doppler pressure half-time method. In addition, we measured plasma concentrations of soluble VCAM-1 and ICAM-1 in the peripheral venous blood samples obtained from 22 control patients (including 14 healthy volunteers in sinus rhythm [group 2] and 8 patients in chronic lone atrial fibrillation [group 3]). The plasma level of soluble VCAM-1 was significantly elevated in group 1 patients (1,205.4 +/- 462.4 ng/mL [mean +/- SD]) compared with group 2 (580.9 +/- 208.0 ng/mL) and group 3 patients (716.4 +/- 221.6 ng/mL) [p < 0.0001]. In group 1 patients, the plasma levels of soluble VCAM-1 and ICAM-1 in the left atrium did not differ from those in the right atrium, femoral vein, or femoral artery (p = 0.668 for VCAM-1, and p = 0.232 for ICAM-1). The area of mitral valve increased significantly after PTMV (1.08 +/- 0.14 cm(2) vs 1.48 +/- 0.33 cm(2), p < 0.0001). The mean left atrial pressure fell significantly after PTMV (22.9 +/- 5.2 mm Hg vs 17.7 +/- 6.0 mm Hg, p < 0.0001). The peripheral venous plasma level of soluble VCAM-1 obtained before PTMV fell significantly after PTMV (before, 1,205.4 +/- 462.4 ng/mL; 1 week after PTMV, 915.7 +/- 280.2 ng/mL; 4 weeks after PTMV, 859.0 +/- 298.7 ng/mL; p < 0.0001). CONCLUSIONS: In patients with moderate-to-severe MS, the venous plasma level of soluble VCAM-1 fell significantly after PTMV, and the elevated plasma soluble VCAM-1 concentration was associated with hemodynamic abnormality rather than with rheumatic activity.

Adult↗

The potential impact of primary percutaneous coronary intervention on ventricular septal rupture complicating acute myocardial infarction.

BACKGROUND: Recent data suggest that the risk of acquired ventricular septal defect (VSD), a complication of acute myocardial infarction (AMI), could be reduced using thrombolytic therapy. There are, however, still no available data regarding the potential impact of primary percutaneous coronary intervention (PCI) on AMI-related VSD in a clinical setting. The purposes of this study were to delineate the incidence and the potential risk factors of AMI-related VSD in the Chinese population, and to determine whether primary PCI could reduce such risk. METHODS AND RESULTS: From May 1993 through March 2003, a total of 1,321 patients with AMI (for < 12 h) underwent primary PCI in our hospital. Of these 1,321 patients, 3 patients (0.23%) developed VSD after undergoing a primary PCI, with a mean (+/- SD) time of occurrence of 25.3 +/- 12.2 h. During the same period, a total of 616 consecutive, unselected patients with early AMI [ie, > 12 h and < or = 7 days] or recent myocardial infarction (MI) [ie, > or = 8 days and < 30 days] who had not received thrombolytic therapy underwent elective PCI. Of these 616 patients, 18 (2.9%) had VSD either on presentation or during hospitalization, with a mean time of occurrence of 71.1 +/- 64.2 h. Clinical variables were utilized to statistically analyze the potential risk factors. Univariate analysis demonstrated that the enrollment variables strongly related to this complication were advanced age, hypertension, nonsmokers, anterior infarction, female gender, and lower body mass index (BMI) [all p < 0.005]. Using multiple stepwise logistic regression analysis, the only variables independently related to VSD were advanced age, female gender, anterior infarction, and low BMI (all p < 0.05). The in-hospital mortality rate was significantly higher in patients with this complication than in patients without this complication (47.6% vs 8.0%; p < 0.0001). The incidence of this complication was significantly lower in patients with AMI who underwent primary PCI than in those with early or recent MI who underwent elective PCI (3.0% vs 0.23%, respectively; p = 0.0001). CONCLUSION: Primary PCI had a striking impact on reducing the incidence of VSD after AMI compared to elective PCI in patients who did not receive thrombolytic therapy. Advanced age, female gender, anterior infarction, and low BMI had potentially increased the risk of this catastrophic complication after AMI in this Chinese population.

Aged↗

Mechanism of reducing platelet activity by percutaneous transluminal mitral valvuloplasty in patients with rheumatic mitral stenosis.

BACKGROUND: Previous studies have demonstrated that platelet activity significantly decreased after optimal percutaneous transluminal mitral valvuloplasty (PTMV) in patients with rheumatic mitral stenosis (MS). However, the mechanism of reducing platelet activity by valvuloplasty remains unclear. METHODS AND RESULTS: We studied 19 patients with symptomatic MS who were undergoing PTMV. The fractions of unstimulated platelets expressing P-selectin in the venous blood obtained before, and at the 1-week and 4-week follow-ups after PTMV were determined by flow cytometry. The mitral valve areas, measured before and at the 1-week follow-up after PTMV, were calculated by means of the Doppler pressure half-time method. The mean (+/- SD) area of the mitral valve increased significantly after PTMV (1.05 +/- 0.17 vs 1.44 +/- 0.27 cm2, respectively; p < 0.0001). The mean left atrial area was reduced in size significantly after PTMV (36.6 +/- 11.4 vs 33.9 +/- 13.4 cm2, respectively; p < 0.05). The mean left atrial pressure (23.3 +/- 5.1 vs 18.0 +/- 5.8 mm Hg, respectively; p < 0.0001) and the mean pulmonary arterial pressure (31.4 +/- 7.8 vs 26.1 +/- 7.7 mm Hg, respectively; p < 0.0001) fell significantly after PTMV. The fraction of platelets expressing P-selectin in the venous blood fell significantly after PTMV (before PTMV, 4.7 +/- 2.4%; 1 week after PTMV, 2.2 +/- 2.1%; 4 weeks after PTMV, 2.0 +/- 1.7%; p < 0.0001). Correlation analysis demonstrated that there was a significantly direct relationship between the magnitude of increase in mitral valve area and the magnitude of decrease in the fraction of platelets expressing P-selectin in the venous blood 4 weeks after PTMV (p = 0.0013; r = 0.682). However, there was no significant correlation between the magnitude of decrease in the fraction of platelets expressing P-selectin in the venous blood and the magnitude of decrease in the left atrial area, the decrease in left atrial pressure, or the decrease in the pulmonary artery pressure after PTMV. CONCLUSIONS: In patients with moderate-to-severe MS, increased platelet activation fell significantly after PTMV. It was the increase in mitral valve area by PTMV, instead of hemodynamic and echocardiographic factors, that accounted for the decrease in the fraction of venous platelets expressing P-selectin after PTMV.

Adult↗

Delayed post-myocardial infarction invasive measures, helpful or harmful? A subgroup analysis.

BACKGROUND: In patients who have experienced acute myocardial infarction (MI), primary percutaneous coronary intervention (PCI) has been shown to be of benefit in terms of clinical outcomes. However, the value of performing routine PCI in patients with early MI (ie, an MI occurring > 12 h to < or = 7 days before patient presentation) or recent MI (ie, an MI occurring > or = 8 days to < 30 days before patient presentation) has not been established. The purposes of this prospective observational study were to evaluate the impact of PCI on outcomes, and to delineate the predictors of lack of response to reperfusion and the prognostic determinants in patients with this clinical condition. METHODS AND RESULTS: A total of 377 consecutive unselected patients who had experienced early or recent MI underwent PCI. Successful reperfusion (ie, Thrombolysis in Myocardial Infarction flow grade 3 of the infarct-related artery [IRA]) was achieved in 90.2% of patients. By multiple stepwise logistic regression analysis, high-burden thrombus formation (odds ratio [OR], 15.53; 95% confidence interval [CI], 6.09 to 39.60; p < 0.0001) in the IRA, early PCI (ie, < or = 3 days) [OR, 4.10; 95% CI, 1.79 to 7.36; p = 0.0008], advanced congestive heart failure (CHF) [OR, 4.10; 95% CI, 1.70 to 9.91; p = 0.002], and diabetes (OR, 3.03; 95% CI, 1.03 to 7.06; p = 0.010) were independent predictors for lack of response to reperfusion. The 30-day mortality rate was 6.8%. The only variables that were independently related to the 30-day mortality rate were advanced CHF (OR, 29.85; 95% CI, 7.84 to 113.7; p < 0.0001), lack of response to reperfusion (OR, 7.57; 95% CI, 2.29 to 25.07; p = 0.0009), early PCI (OR, 4.81; 95% CI, 1.60 to 14.41; p = 0.005), and multivessel disease (OR, 9.22; 95% CI, 1.63 to 52.04; p = 0.0119). The surviving 351 patients were discharged from the hospital and followed-up for a mean (+/- SD) 38.9 +/- 14.2 months. Coronary angiographic follow-up was performed in 285 patients (81.2%). Restenosis of the IRA was found in 101 patients (35.4%). Reinterventions of the IRA were required in 69 patients (24.2%). Follow-up measurements of left ventricular ejection fraction (LVEF) showed significantly more improvement than the initial LVEF (59.3 +/- 13.8% vs 50.4 +/- 13%; p < 0.0001). The total cumulative mortality rate after hospital discharge was 6.5% for the entire group. Only advanced CHF (OR, 3.46; 95% CI, 1.26 to 9.52; p = 0.016) and old age (ie, > or = 70 years of age) [OR, 4.41; 95% CI, 1.59 to 12.24; p = 0.004] were independent predictors of long-term mortality. CONCLUSION: The performance of PCI on > or = day 4 in patients after they had experienced an MI was safe and had a high rate of success. The clinical benefits of a relative low mortality rate associated with successful PCI for patients with early and recent MI was maintained during the long-term follow-up. However, patients with advanced CHF along with old age continued to have a poor prognosis.

Angioplasty, Balloon, Coronary↗

Increased plasma levels of soluble P-selectin in rheumatic mitral stenosis.

BACKGROUND: Previous studies have demonstrated that platelet activation occurs in peripheral blood of patients with rheumatic mitral stenosis (MS). However, in patients with MS, the plasma level of soluble P-selectin (a marker of platelet activation) remains unsettled. METHODS AND RESULTS: A total of 20 patients with symptomatic MS undergoing percutaneous transluminal mitral valvuloplasty (PTMV) were studied (group 1; 16 patients in permanent atrial fibrillation, and 4 patients in sinus rhythm). The plasma levels of soluble P-selectin in the femoral vein and artery, and right and left atria before PTMV and those in the peripheral venous blood at the 1-week and 4-week follow-ups after PTMV were determined by solid-phase, sandwich, enzyme-linked immunosorbent assay. The mitral valve area was calculated by means of the Doppler pressure half-time method. In addition, we measured plasma concentrations of soluble P-selectin in the peripheral venous blood samples obtained from 22 control patients (including 14 healthy volunteers in sinus rhythm [group 2] and 8 patients in permanent lone atrial fibrillation [group 3]). The plasma levels of soluble P-selectin were significantly elevated in group 1 patients (49.78 +/- 37.72 ng/mL) [mean +/- SD] compared with group 2 (25.52 +/- 15.38 ng/mL) and group 3 patients (32.17 +/- 14.18 ng/mL) [p < 0.005]. In group 1 patients, the plasma levels of soluble P-selectin in the left atrium did not significantly differ from those in the right atrium, femoral vein, or femoral artery (p = 0.05). The area of mitral valve increased significantly after PTMV (1.06 +/- 0.17 cm(2) vs 1.48 +/- 0.32 cm(2), p < 0.0001). The mean left atrial pressure fell significantly and immediately after PTMV (23.0 +/- 5.1 mm Hg vs 17.6 +/- 5.9 mm Hg, p < 0.0001). The peripheral venous plasma levels of soluble P-selectin obtained before PTMV did not significantly fall after PTMV (before, 49.8 +/- 37.7 ng/mL; 10 min after, 39.8 +/- 19.1 ng/mL; 1 week after, 46.1 +/- 20.8 ng/mL; and 4 weeks after, 41.2 +/- 15.9 ng/mL; p = 0.145). CONCLUSIONS: The venous plasma levels of soluble P-selectin in patients with moderate-to-severe MS were significantly higher than those in healthy volunteers or patients with lone atrial fibrillation. In addition, in patients with MS, there was no difference in the plasma levels of soluble P-selectin between the left and right atrial blood and between peripheral and atrial blood. Moreover, there was no change in soluble P-selectin levels as a result of PTMV.

Adult↗

Levels and values of serum high-sensitivity C-reactive protein within 6 hours after the onset of acute myocardial infarction.

BACKGROUND: C-reactive protein (CRP), which has been suggested to directly enhance inflammation in plaques, is rapidly synthesized and secreted in the liver 6 h after an acute inflammatory stimulus. Therefore, serum levels of CRP within 6 h after the onset of acute myocardial infarction (AMI) merely reflect a chronic and persistent inflammatory process and are not due to acute myocardial damage. We hypothesized that the serum CRP level, which would abnormally elevate thereafter, is followed by a plaque rupture in the clinical setting of AMI. METHODS AND RESULTS: CRP was prospectively measured by high-sensitivity CRP assay (hs-CRP) in 157 consecutive patients (106 patients within 6 h, and 51 patients >/= 6 h but < 12 h after the onset of AMI) with ST-segment elevation AMI undergoing primary percutaneous coronary intervention (PCI). Serum levels of hs-CRP were also measured in 30 patients with stable angina undergoing elective PCI and in 30 healthy control subjects. The serum level of hs-CRP was significantly higher in patients with an onset of AMI < 6 h than in patients with angina pectoris (2.7 +/- 2.3 mg/L vs 1.4 +/- 0.7 mg/L, p < 0.0001 [mean +/- SD]) and in healthy subjects (2.7 +/- 2.3 mg/L vs 1.0 +/- 0.6 mg/L, p < 0.0001). There were no significant differences in serum levels of hs-CRP in patients with an onset of AMI </= 3 h than in those patients with an onset of AMI > 3 h but < 6 h (2.7 +/- 2.5 mg/L vs 2.7 +/- 2.2 mg/L, p = 0.87). However, the serum level of hs-CRP was significantly higher in patients with an onset >/= 6 h than in patients with an onset < 6 h (14.1 +/- 16.5 mg/L vs 2.7 +/- 2.3 mg/L, p < 0.0001). CONCLUSIONS: Serum levels of hs-CRP were significantly higher in patients with an onset of AMI < 6 h than in healthy subjects and in patients with angina pectoris undergoing PCI. The inflammatory process has been proved as one of the mechanisms causing plaque rupture. Elevated serum hs-CRP levels in patients with AMI < 6 h may portend vulnerable plaque rupture.

C-Reactive Protein↗