Seiki Nagata

Plaque Gruel of Atheromatous Coronary Lesion May Contribute to the No-Reflow Phenomenon in Patients With Acute Coronary Syndrome

Background—No-reflow associated with direct angioplasty (PCI) of patients with acute coronary syndromes (ACS) is associated with unfavorable results. Methods and Results—We used a new thrombectomy device to treat 51 lesions in 48 consecutive ACS patients (40 male and 8 female; mean age 63 years) and conducted a microscopic analysis of aspirates and blood samples retrieved from the culprit coronary artery. The first aspirate was collected before PCI and the second was collected separately after percutaneous transluminal coronary angioplasty or stenting, including samples from the no-reflow lumen. Light microscopy showed that the materials obtained from the pre-PCI aspiration consisted of thrombus in 37.5%, thrombus and atheroma in 35.0%, and atheromatous plaque in 27.5%. The materials collected from the post-PCI aspiration were thrombus in 8.3%, thrombus and atheroma in 41.7%, and atheromatous plaque in 50.0%. We then compared the 9 lesions (19.1%) with no-reflow to those without no-reflow. There was no difference in the pre-PCI aspirates. However, after PCI, there was more atheromatous plaque retrieved from patients with no-reflow (P <0.001) as well as significantly more platelet and fibrin complex, macrophages, and cholesterol crystals in the blood aspirated from no-reflow cases. Aspiration of these elements improved the no-reflow in 7 of 9 lesions to TIMI-3 flow. Conclusions—No-reflow after angioplasty may be caused by gruel that formed from an atheroma attributable to mechanical plaque disruption during intervention.

Smoke-like echo in the left atrial cavity in mitral valve disease : its features and significance

In some patients with mitral stenosis, a smoke-like echo is observed in the left atrial cavity. The present study in 116 consecutive patients with rheumatic mitral valve disease investigated the echocardiographic features and clinical significance of this echo. The smoke-like echo is characterized by the following echocardiographic features: 1) it is composed of numerous microechoes; 2) it curls up slowly in the enlarged left atrial cavity; and 3) it vanishes as soon as it pours into the ventricular cavity. Hemostasis in the left atrial cavity was considered to be an important underlying condition for development of the echo. Hemorheologic conditions indicated that the shear rate of blood flow in the left atrial cavity was calculated to be low enough for the development of red blood cell aggregation. These conditions suggest that the source of the smoke-like echo might be aggregated cells due to hemostasis in the left atrial cavity. Left atrial thrombi were detected in many patients who had this echo in the left atrial cavity. Although it has not been conclusively determined that the presence of the smoke-like echo is a necessary condition for thrombus formation, this echo appears to be closely related to thrombus formation in the left atrial cavity. It is concluded that the presence of this echo indicates severe left atrial hemostasis and is a warning for thrombus formation.

Serial Angioscopic Evidence of Incomplete Neointimal Coverage After Sirolimus-Eluting Stent Implantation Comparison With Bare-Metal Stents

Background— The time course of neointimal formation after stent implantation has not been studied extensively by angioscopy in the drug-eluting stent era. Methods and Results— Serial angioscopic findings at first follow-up (3.6±1.1 months), second follow-up (10.5±1.6 months), and third follow-up (21.2±2.2 months) after stent implantation were compared between sirolimus-eluting stents (SES, n=17) and bare-metal stents (BMS, n=11). Neointimal coverage, thrombus, and presence of yellow plaques underneath the stents were assessed. Neointimal coverage was graded as follows: grade 0, stent struts were fully visible; grade 1, struts bulged into the lumen, although they were covered; grade 2, struts were embedded by the neointima but were seen translucently; or grade 3, struts were fully embedded and invisible. Neointimal coverage was remarkably different between SES and BMS at each follow-up point. Neointimal coverage grade was 1.1±0.5 in SES versus 2.9±0.3 in BMS at the first follow-up (P<0.0001), 1.1±0.5 in SES versus 3.0±0.0 in BMS (P<0.0001) at the second follow-up, and 1.3±0.5 in SES versus 3.0±0.0 in BMS at the third follow-up (P=0.0009). No significant serial changes in coverage grade were noted in the BMS group, whereas coverage grade slightly but significantly increased at the third follow-up in the SES group (P<0.05). Thrombi were detected in 4 SES: a red thrombus was seen from the first to the third follow-up in 2; another was detected only at the third follow-up; and the fourth was seen at the first follow-up but disappeared at the second follow-up, associated with a new white thrombus despite dual antiplatelet therapy. Yellow plaques had disappeared by the time of the second follow-up in BMS. In contrast, yellow plaques were exposed in 71% of SES at the first follow-up and remained exposed until the third follow-up. Neointimal coverage grades correlated with thrombi (P=0.002) and with yellow plaques (P<0.0001). Conclusions— Serial angioscopic findings up to 2 years after SES implantation were markedly different from those after BMS. Neointimal coverage was completed by 3 to 6 months in BMS. In contrast, SES demonstrated the presence of thrombi and yellow plaques even as much as 2 years after implantation.

Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves

The rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves, and its relation to aging and valve anatomy are not well known. To elucidate these aspects, 75 patients aged 15 to 76 years were examined by echocardiography. Aortic valve sclerosis began from the second decade, the sclerotic index progressing with age (r = 0.72; p < 0.0001). Aortic valve calcium was noted from the fourth decade. Aortic valve pressure gradient increased approximately 18 mm Hg each decade, concomitant with progression of valve sclerosis (r = 0.78; p < 0.0001). Progression of cusp sclerosis was faster in patients with anteroposteriorly located cusps than in those with right-left-located cusps (p < 0.005), and was faster in those with eccentric cusps (width ratio of major and minor cusps > or = 1.2) than in those with symmetric cusps (p < 0.05). In patients with eccentric and anteroposteriorly located cusps, aortic valve pressure gradient increased 27 mm Hg per decade. In patients with congenital bicuspid aortic valves, the progression of aortic stenosis is rapid, and the rapidity depends to some extent on the position and eccentricity of the cusps.

High prevalence of atrial fibrosis in patients with dilated cardiomyopathy

OBJECTIVES We examined the extent of fibrotic changes in the left atrium of cardiomyopathic human hearts and investigated the relation of mechanical overload caused by left ventricular dysfunction to fibrosis of the left atrium. BACKGROUND Left atrial dysfunction in dilated cardiomyopathy may contribute to progression of heart failure. In contrast to fibrosis of the left ventricle, atrial fibrosis has not been extensively studied in cardiomyopathic hearts. METHODS The extent of fibrosis in the left atrium and left ventricle was determined by an automatic image analyzer in 38 autopsied hearts obtained from 9 patients who died of noncardiac illness (control group), 16 patients with dilated cardiomyopathy, 6 patients with hypertrophic cardiomyopathy with features mimicking dilated cardiomyopathy and 7 patients with a previous myocardial infarction. Transverse sections were obtained at the upper margins of the foramen ovale and left auricle in the left atrium and the median level of the left ventricle. RESULTS There were no significant differences in extent of left atrial dilation, left ventricular dysfunction or duration of illness among the three groups with cardiac disease. Percent area of left atrial fibrosis (mean +/- SD) was significantly greater in the specimens from patients with dilated cardiomyopathy (13.1 +/- 6.1%, p < 0.01) and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (26.5 +/- 9.5%, p < 0.01) than in those from patients with an old myocardial infarction (3.8 +/- 1.1%). Percent area of left ventricular fibrosis in hearts from patients with dilated cardiomyopathy (12.9 +/- 8.6%) was significantly smaller than that in hearts from patients with hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (35.8 +/- 11.9%, p < 0.01) and a previous myocardial infarction (38.4 +/- 8.0%, p < 0.01). Percent area of atrial fibrosis was significantly correlated with left ventricular ejection fraction in the group with a previous myocardial infarction but not in the other groups. CONCLUSIONS There was a high degree of fibrotic change in the left atrium in the groups with dilated cardiomyopathy and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy. Our findings suggest that atrial fibrosis in these patients may not have been related to mechanical overload of the left atrium but to some other, still unknown mechanisms.

Importance of the angiosome concept for endovascular therapy in patients with critical limb ischemia

Objective: We investigated the role of the angiosome concept in endovascular therapy (EVT) for limb salvage. Background: The angiosome concept is clinically useful in bypass surgery for critical limbs ischemia (CLI). However, comparison with direct and indirect flow to the site of ulceration based on angiosome concept regarding freedom from amputation has not been systematically studied for the patient with CLI undergoing EVT. Methods: We analyzed 203 limbs in 177 consecutive patients (male = 127, age = 70 ± 11 years) with ischemic ulceration that was Rutherford 5 or 6 (5 in 145 limbs and 6 in 58 limbs; pretreatment ankle‐brachial index = 0.74 ± 0.27), who underwent EVT alone without bypass surgery. We classified these patients into direct and indirect groups depending on whether feeding artery flow to the site of ulceration was successfully acquired or not acquired based on the angiosome concept. Freedom from amputation was compared between the direct and the indirect groups by Kaplan‐Meier analysis. Results: The overall limb salvage rate was 82% (167/203). Skin perfusion pressure was significantly higher in the direct group (67 ± 25 mm Hg) than in the indirect group (41 ± 20 mm Hg, P = 0.002). The limb salvage rate was also significantly (P = 0.03) higher in the direct group (86%) than in the indirect group (69%) for up to 4 years after the procedure. The number of vessels with run‐off flow did not influence the limb salvage rate in either the direct group (P = 0.84) or the indirect group (P = 0.90). Conclusion: Acquiring direct flow based on the angiosome concept is important for limb salvage by EVT in patients with CLI.© 2010 Wiley‐Liss, Inc.

Cilostazol reduces restenosis after endovascular therapy in patients with femoropopliteal lesions

BACKGROUND Despite the recent development of endovascular therapy (EVT), a high incidence of restenosis remains as an unsolved issue in patients presenting with femoropopliteal lesions. We investigated whether cilostazol reduces restenosis after successful EVT for de novo femoropopliteal lesions. METHODS This study was designed as a prospective, randomized, open-label, blinded end point study in a single institution. Between March 2004 and June 2005, we randomized 127 patients who were successfully treated with EVT for de novo femoropopliteal lesions to receive cilostazol (200 mg/d, n = 63) or ticlopidine (200 mg/d, n = 64) in addition to aspirin (100 mg/d). Antiplatelet medications were started at least 1 week before EVT and were continued until the end of follow-up. Patency was defined by duplex ultrasound imaging with peak systolic velocity ratio >2.4. RESULTS There were no significant differences in the patients and lesion characteristics. Sixteen patients dropped out of the study protocol, six of whom were withdrawn due to adverse drug effects (cilostazol, n = 5; ticlopidine, n = 1; P = .09). Ten patients died (cilostazol, n = 4; ticlopidine, n = 6; P = .53) during the follow-up period. Patency rates at 12, 24, and 36 months were 87%, 82%, and 73% in the cilostazol group and 65%, 60%, and 51% in ticlopidine group by intention-to-treat analysis (P = .013) and were 87%, 82%, and 73% in the cilostazol group and 64%, 57%, and 48% in the ticlopidine group (P = .0088) by as-treated analysis. Freedom from target lesion revascularization and all adverse events (restenosis, amputation, and death) was significantly higher in cilostazol group than in ticlopidine group (P = .036, P = .031). No acute, subacute, or chronic thrombotic occlusion was encountered, and bleeding complication rates were similar between the two groups. CONCLUSIONS Cilostazol significantly reduces restenosis after EVT in femoropopliteal lesions.

Novel missense mutation in α-tropomyosin gene found in Japanese patients with hypertrophic cardiomyopathy

Abstract We have searched for mutations in α-tropomyosin gene in 50 Japanese patients with hypertrophic cardiomyopalhy (HCM) by means of polymerise chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis. Two missense mutations of the α-tropomyosin gene were detected in Japanese patients with familial HCM. Sequencing analysis revealed a C to T transition at codon 63 leading to a replacement of Ala with Vat residue. and a G to A transition with replacement of Asp by Asn at codon 175. These missense mutations were found at residues which were markedly conserved across the species, and have been reported to interact with troponin T. This is the first report on a mutant α-tropomyosin gene in a Japanese Population. Familial HCM is a genetically heterogeneous disease in Japanese patients, similar to that reported in Caucasian kindreds.

Influence of stent fracture on the long-term patency in the femoro-popliteal artery: experience of 4 years.

OBJECTIVES We investigated the time course of stent patency in the femoro-popliteal artery for as long as 4 years. BACKGROUND Stent fracture has been related to poor 2-year patency in the femoro-popliteal artery. METHODS We studied 239 consecutive patients who underwent provisional de novo stenting with nitinol stents for 333 limbs (Luminexx stent [C. R. Bard, Inc., Murray Hill, New Jersey] in 91 limbs; Smart stent [Cordis Corp., Miami Lakes, Florida] in 242 limbs) from April 2004 to December 2007. Stent fracture was determined by X-ray with multiple projections. Patency was assessed by duplex ultrasonography as peak systolic velocity ratio <2.4 or by angiography (% diameter stenosis <50%). Primary patency in those with and without stent fracture at follow-up was assessed along with factors influencing stent fracture. RESULTS Primary patency was 81%, 74%, 68%, and 65% at 1, 2, 3, and 4 years, respectively. Stent fracture occurred in 14% (78 of 544) per stent and 17% (55 of 333) per limbs. Stent fracture was significantly associated with multiple stent deployments (with fracture = 2.3 +/- 0.9 stents vs. without fracture = 1.5 +/- 0.7 stents, p < 0.001) and long lesions (with fracture = 208 +/- 84 mm vs. without fracture = 121 +/- 79 mm, p < 0.001). Primary patency was 68% with fracture versus 83% without fracture at 1 year, p = 0.03; 65% versus 75% at 2 years, p = 0.05; 61% versus 69% at 3 years, p = 0.06; and 61% versus 65% at 4 years, p = 0.07. Neither type 1 nor type 3 fracture affected patency, although type 2 showed the worst patency. CONCLUSIONS Stent fracture worsened the patency during the first 2 years, but it did not apparently affect patency beyond 2 years. In particular, complete stent separation did not affect patency.

Three autopsy cases of progression to left ventricular dilatation in patients with hypertrophic cardiomyopathy

The hearts of three cases of congestive heart failure with dilated left ventricles developing in patients with symptomatic hypertrophic cardiomyopathy (HCM) were morphologically investigated. The results showed that disproportionate hypertrophy and dilatation of the left ventricles, accompanied by massive fibrosis and myocardial disarray, were present in the three patients. The mean percent area of fibrosis of the left ventricle was 34.7% and 47.4% at the upper third and lower third levels, respectively, and was much more frequently associated with disarray (84.4 +/- 12.3%). Moreover, the fibrosis was most extensive in the lateral wall of the left ventricle, followed by the posterior, anterior, and interventricular walls. The fibrosis was also diffuse regardless of the subendocardial or subepicardial region of the heart. The findings in the present study suggest that the disarray in this particular series of HCM might be responsible for the mechanism of the fibrosis leading to dilatation of the left ventricle.