Impact of coronary plaque burden and composition on periprocedural myocardial infarction and coronary flow reserve after percutaneous coronary intervention.

Periprocedural myocardial infarction (PMI) is one of the major complications of percutaneous coronary intervention (PCI). We investigated the influence of coronary plaque burden and characteristics on PMI using intravascular ultrasound (IVUS) with radiofrequency-based tissue characterization technology (iMAP). The study population consisted of 33 consecutive patients with stable angina pectoris who underwent PCI. IVUS images were recorded before and after PCI for offline analysis, and coronary flow reserve (CFR) was measured after PCI. PMI was defined as a post-PCI cardiac troponin T elevation > 5 × 99(th) percentile of the upper reference limit (0.014 ng/mL). Plaque volume in patients with PMI (n = 12) was significantly greater than that in patients without PMI (n = 21) (240.4 ± 106.0 mm(3) versus 152.1 ± 76.9 mm(3), P = 0.0096). The iMAP-IVUS analysis demonstrated that the fibrotic, lipidic, and necrotic tissue volume within culprit lesions were also greater in patients with PMI than in patients without PMI (129.4 ± 52.2 mm(3) versus 94.6 ± 40.8 mm(3), P = 0.041; 26.8 ± 10.5 mm(3) versus 15.8 ± 11.5 mm(3), P = 0.011; and 81.3 ± 48.4 mm(3) versus 40.2 ± 33.6 mm(3), P = 0.0071, respectively). Multivariate logistic analysis demonstrated that necrotic tissue volume was the only independent predictor of PMI. Multiple regression analysis demonstrated that the post-PCI CFR values signifi cantly correlated with percent plaque burden, and there were no correlations with the percent tissue burden of each plaque component. In conclusion, the iMAP-IVUS analyses demonstrate that necrotic tissue volume is a potent predictor of PMI. Microcirculatory disturbance after PCI is significantly influenced by percent plaque burden, regardless of plaque compositions.

[Anesthesia and perioperative management in a patient with acquired angioedema].

We experienced anesthesia and perioperative management for hysterectomy in a patient with acquired angioedema. Angioedema due to C1 esterase inhibitor (C1-INH) deficiency (loss or dysfunction of C1-INH) is one of the rarest diseases, and is characterized by recurrent episodes of regional hard edema and ascites induced by mechanical stimuli or mental stress. Edema spreads to the subcutaneous and submucosal layer, and laryngeal edema may cause the upper airway obstruction. Tranexamic acid and C1-INH concentrates were administered perioperatively for prophylaxis of attacks, and combined spinal and epidural anesthesia was performed for hysterectomy. We could manage perioperative care without causing edema.

Angioscopic differences of coronary intima between diffuse and focal coronary vasospasm: Comparison of optical coherence tomography findings.

BACKGROUND: Coronary artery vasospasm (CS) can be identified as either a diffuse type or focal type; however, the difference in endothelial characteristics between these spasm types remains unclear. The features of coronary intima associated with diffuse spasm and focal spasm using coronary angioscopy (CAS) were evaluated and the optical coherence tomography (OCT) findings were compared. METHODS: CAS and/or OCT observational analysis was performed in 55 patients (mean age: 61.4 years, 31 men) who had acetylcholine-provoked CS (diffuse CS, 31 patients; focal CS, 24 patients). The yellowness of the intima, presence of thrombus in CAS, and intimal characteristics based on the OCT results were evaluated. RESULTS: CAS showed more atherosclerotic yellow plaques at the focal spasm segment than at the diffuse spasm segment (p=0.032). Moreover, there were more thrombi at the focal spasm segment (p=0.039). In addition, OCT results revealed that the intima area, maximum intima thickness, and lipid content in the focal CS group were larger than the diffuse CS group (4.22±1.67mm2 vs. 3.45±2.36mm2; 0.71±0.29mm vs. 0.53±0.30mm; 55.9% vs. 32.0%, p<0.001, respectively). CONCLUSIONS: These results indicate that the presence of atherosclerotic plaques at the spasm site is likely to be related to the occurrence of a focal vasospasm. This may support the difference of features between focal CS and diffuse CS and contribute to precise treatment for each spasm type.

Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats.

Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries.

Tissue characteristics of non-culprit plaque in patients with acute coronary syndrome vs. stable angina: a color-coded intravascular ultrasound study.

Patients with acute coronary syndrome (ACS) are thought to have multiple vulnerable coronary plaques. We analyzed non-culprit plaques in patients with ACS vs. stable angina pectoris (SAP) by means of color-coded intravascular ultrasound (iMap-IVUS). Patients who underwent percutaneous coronary intervention were divided into an ACS group (n = 39) and an SAP group (n = 35). Non-culprit lesions were imaged by 40-MHz iMap-IVUS, and the plaque characteristics were compared between the two groups. Plaque volume was similar between the two groups. The fibrotic volume (%FV) was less in the ACS group than in the SAP group (70.2 ± 10.4 vs. 76.5 ± 7.2 %, respectively, P < 0.01), whereas the lipidic volume and necrotic volume (%NV) were greater in the ACS group (8.2 ± 0.4 vs. 6.3 ± 0.4 %, P < 0.01; 15.1 ± 7.9 vs. 9.9 ± 4.8 %, P < 0.01). An inverse correlation was found between %FV and total plaque volume (ACS group: r = -0.52, P < 0.01; SAP group: r = -0.31, P = 0.01), and a positive correlation was found between %NV and total plaque volume (ACS group: r = 0.56, P < 0.01; SAP group: r = 0.41, P < 0.01). Furthermore, the slope of the regression line showing the relation between plaque volume and necrotic volume was significantly steeper for the ACS group than for the SAP group (P < 0.05). Non-culprit lesions are particularly vulnerable in ACS patients. Non-culprit lesions are particularly vulnerable in ACS patients. Furthermore, the stronger correlation between plaque volume and %NV was observed in ACS patients than in SAP patients.

[Reevaluation of protective effects of alprostadil on hepatic function in patients undergoing hepatectomy].

BACKGROUND: The protective effect of alprostadil (PGE1), used during hepatectomy, on hepatic function has not been clearly proven. We reevaluated this effect by measuring serum alpha-glutathione S-transferase (aGST), which detects liver injury sensitively. METHOD: Thirty hepatocellular carcinoma patients scheduled for hepatectomy were randomly assigned to control (n=12) and PGE1 (n=10) groups. In the latter group, PGE1 was administered intravenously at a rate of 0.05 microg x kg(-1) x min(-1) during surgery. For measuring alphaGST, arterial blood samples were obtained before anesthesia, following laparotomy, and immediately, 2, 4, and 6 hrs after liver resection. RESULTS: The alphaGST concentrations after liver resection were significantly higher, while mean arterial pressures were significantly lower in the PGE1 group. CONCLUSIONS: Our findings suggest that PGE1 medication during hepatectomy cannot protect hepatic function during and after liver resection.

[Anesthetic management for removal of pheochromocytoma in a patient after repair of tetralogy of Fallot].

A 45-year-old woman after repair of tetralogy of Fallot at the age of 19, was admitted to the hospital for treatment of paroxysmal hypertension. She was diagnosed with pheochromocytoma of the left adrenal gland, and was scheduled for removal of pheochromocytoma. She received doxazosin for preoperative preparation. Anesthesia was induced with propofol and vecuronium, and maintained with intermittent fentanyl and sevoflurane in nitrous oxide and oxygen. Before induction of anesthesia, magnesium sulfate 40 mg x kg(-1) was injected, and followed by continuous infusion of 40 mg x kg(-1) x hr(-1) until the removal of pheochromocytoma. Under neuromuscular monitoring, vecuronium was administered prudently. Cardiac output was continuously monitored with pulmonary arterial catheter and transesophageal aortic blood flow monitor. Blood pressure and heart rate were stable even though the tumor was handled, and no additional vasodilator therapy was needed. After surgery, prolonged neuromuscular blockade caused by magnesium sulfate was not observed. We consider that successful management was feasible by administration of magnesium sulfate and preoperative administration of alpha1 blocker, under adequate perioperative monitoring.

Effects of intravenous low-dose recombinant human atrial natriuretic peptide on renal function in the perioperative management for gastrointestinal perforation or ileus: a retrospective single-center study.

PURPOSE: We studied the effectiveness of human atrial natriuretic peptide (hANP) on management of acute kidney injury. METHODS: This retrospective single-center study included 43 patients from January 2007 to February 2010 who had undergone non-elective abdominal surgery for gastrointestinal perforation and ileus. Patients were separated into 2 groups according to whether hANP was administered or not, and 4 subgroups according to whether or not baseline serum creatinine <1.2 mg/dL; normal cre/hANP (-) (n = 22), high cre/hANP (-) (n = 10), normal cre/hANP (+) (n = 4), and high cre/hANP (+) (n = 7). The administration of hANP was started during operation. RESULTS: The administration rate of hANP ranged between 0.02 and 0.05 µg/kg per minute, except for one patient and the average postoperative administration time of hANP was 167 ± 237 h (range, 8-888 h). There were no significant differences in characteristics of patients within four subgroups, except for patient's weight. Serum creatinine in high cre/hANP (+) got to decrease more than high cre/hANP (-). Outcomes such as 28-day mortality were not significantly different among four subgroups. No patients required renal replacement therapy in each subgroup. CONCLUSION: Intravenous low dose of hANP was useful as acute kidney injury management in gastrointestinal perforation and ileus patients undergoing non-elective surgery.

Serial change and its determinants of residual plaque characteristics under sirolimus-eluting stent: a coronary angioscopic study.

OBJECTIVES: To examine serial change in the residual plaque behind the sirolimus-eluting stent (SES) using coronary angioscopy in patients with SES implantation and to identify its baseline determinants. BACKGROUND: Previous coronary angioscopic studies have demonstrated that SES enhances the yellow grade of residual plaque during follow-up period. METHODS: A total of 42 patients with stable angina pectoris or silent ischemic heart disease, who had a successful SES implantation were examined by coronary angioscopy both at the baseline (SES implantation) and the follow-up period (9-14 month follow-up). The patients were divided into three groups as: worsened group (WS: yellow color grade of coronary plaque at the follow-up period was worsened compared to the baseline period, n=15), no change group (NP: no change compared to the baseline, n=16), and improved group (IP: improved compared to the baseline, n=11). Then, the determinants of the nominal change of yellow color grade were examined by multiple regression analysis. RESULTS: The low-density lipoprotein cholesterol (LDL-C) level in IP group at the follow-up was significantly decreased compared to baseline (from 120.0±29.8mg/dl to 74.3±16.7mg/dl, p=0.0005), and was the lowest among three groups (WS: 103.5±16.4mg/dl, NC: 105.7±18.7mg/dl, and IP: 74.3±16.7mg/dl). Multiple regression analysis revealed that family history, statin administration, baseline serum creatinine, baseline 'in-stent' thrombus, and follow-up LDL-C were significant determinants to the nominal change of yellow color grade after the SES implantation (p<0.0001). CONCLUSIONS: Serial change in tissue characteristics within residual plaque under SES is determined by several factors, especially LDL-C level as well as statin administration. Adequate management of LDL-C by statins might be crucial for stabilizing residual plaque after SES implantation.

Three-dimensional visualization of scoring mechanism of 'AngioSculpt' balloon for calcified coronary lesions using optical coherence tomography.

Despite developments in coronary interventional cardiology, plaque calcification is a critical issue of stent expansion. AngioSculpt Scoring Balloon Catheter® (AngioSculpt; AngioScore Inc., Fremont, CA, USA) can produce more 'scoring' marks, which leads to prevention of 'plaque shift' and 'balloon slippage'; moreover, the 'scoring' produces some cutting effect, leading to successful stent implantation even on severe calcified lesions. We have applied AngioSculpt on severe calcified lesions to achieve its adequate expansion, and report the mechanism of the 'scoring' and its efficacy evaluated by three-dimensional stereoscopic reconstruction (3-D) of optical coherence tomography (OCT; LightLab Imaging, Inc., Westford, MA, USA). The patient is a 64-year-old male, who had diffuse stenosis in the left circumflex coronary artery (LCX) with severe calcifications, and was treated using AngioSculpt. AngioSculpt predilatation with a high pressure led to successful stent implantation. The radial scores were clearly imaged by 3-D OCT, demonstrating that radial nitinol wires made spiral indents from the relative weak points at the surface adjacent to calcification, which resulted in a less traumatic and safe dilatation although the scoring mark was not recognized clearly in intravascular ultrasound. This report suggests AngioSculpt might become one of the options for a severe calcified lesion.

Compositional analysis of angioscopic yellow plaques with intravascular ultrasound radiofrequency data.

BACKGROUND: To identify subclinical high-risk plaques is potentially important because those vulnerable plaques may have a greater likelihood of rupture and subsequent thrombosis. The aim of this study is to reveal the histology of angioscopic yellow plaques known as vulnerable plaques by intravascular ultrasound radiofrequency data analysis. METHODS: Thirty-one coronary plaques in 21 patients, which were non-culprit, de novo, angiographically non-obstructive (<50%) lesions, were analyzed with Virtual Histology - intravascular ultrasound (VH-IVUS) and coronary angioscopy. These plaques were prospectively divided into 4 groups (Grade 0 to 3) by the yellow color intensity and we compared plaque morphology, echogenicity and composition among their groups. RESULTS: Morphology and echogenicity evaluated by standard gray-scale IVUS were not significantly different among those groups. On analyzing plaque composition by VH-IVUS, mean percentage of necrotic core was significantly larger in yellow plaque (Grade 2 and 3) than white plaque (Grade 0). CONCLUSIONS: Angioscopic yellow plaque included a larger amount of necrotic core analyzed by VH-IVUS than white plaque.

Stent-based delivery of antisense oligodeoxynucleotides targeted to the PDGF A-chain decreases in-stent restenosis of the coronary artery.

BACKGROUND: Although the use of drug-eluting stents (DESs) has been shown to limit neointima hyperplasia, currently available DESs may adversely affect reendothelialization, possibly precipitating cardiac events. We evaluated the effect of an antisense oligodeoxynucleotide (ODN) targeted to the platelet-derived growth factor (PDGF) A-chain on in-stent restenosis in pig coronary artery. METHODS: A bare metal stent coated with phosphorothioate-linked antisense ODN or nonsense ODN, or a bare metal stent without ODN (control), was implanted in the mid segment of the left anterior descending artery (LAD). Twenty-eight days after implantation, angiography and intravascular ultrasound (IVUS) were performed, the LAD was removed, and stenosis was evaluated pathologically. RESULTS: Volumetric stenosis ratios were 64 +/- 11.9, 44 +/- 3.4, and 26 +/- 3.8% in coronary arteries implanted with control, nonsense ODN-coated, and antisense ODN-coated stents, respectively. In angioscopic findings, the lumen surface was smooth in the stented segments in all groups. Struts of antisense ODN-coated stents were observed embedded in the neointima, whereas embedding was not observed in nonsense ODN-coated stents or control stents, indicating a decrease in hyperplasia in response to antisense ODN treatment. Pathologic findings showed 77 +/- 5.8, 68 +/- 12.2, and 38 +/- 5.3% stenosis in coronary arteries implanted with control stents, nonsense ODN-coated stents, and antisense ODN-coated stents, respectively. A continuous lining of endothelial cells was observed along the lumen of coronary arteries implanted with antisense ODN-coated stents. CONCLUSIONS: Stent-based delivery of an antisense ODN targeted to the PDGF A-chain effectively inhibits neointima formation after stent implantation in pig coronary artery by suppressing VSMC hyperplasia and preserving endothelialization. Antisense-ODNs may provide a therapy for in-stent restenosis of the coronary artery.