Terumasa Koyama

Influence of chronic tethering of the mitral valve on mitral leaflet size and coaptation in functional mitral regurgitation.

OBJECTIVES The purposes of this study were to examine whether tethering of the mitral leaflets affects coaptation in patients with functional mitral regurgitation (FMR) and to assess the interaction between the mitral coaptation and mitral regurgitation severity. BACKGROUND Functional mitral regurgitation causes restriction of leaflet closure as a result of enhanced tethering of the mitral leaflets and papillary muscle (PM) displacement. METHODS Three-dimensional transesophageal echocardiography was performed in 44 patients with FMR related to the bilateral PM displacement and in 56 controls. The distance between the tip of the anterior or posterior PM and the intervalvular fibrosa were measured as the lateral or medial tethering length (TL) in midsystole. To evaluate the degree of coaptation, coaptation length (CL) at medial, middle, and lateral sites of mitral valve and an estimate of coaptation area (CA) were measured. RESULTS The FMR group showed the significantly decreased CA (1.3 ± 0.4 cm(2) vs. 1.6 ± 0.4 cm(2), p = 0.005) and CL (medial 3.2 ± 0.9 mm vs. 4.8 ± 0.6 mm, middle 3.8 ± 1.3 mm vs. 5.8 ± 0.7 mm, lateral 3.3 ± 0.9 mm vs. 4.8 ± 0.6 mm; all p < 0.0001) compared with the controls. Each CL correlated negatively and significantly with both medial and lateral TL (all p < 0.0001). Annular area (p = 0.004) was significantly smaller and leaflet-to-annular area ratio (p < 0.0001) was significantly larger in patients with nonsignificant FMR than in the patients with significant (moderate to severe) FMR. Significant correlations were found between effective regurgitant orifice area and CA or each CL (all p < 0.0001). CONCLUSIONS Coaptation decreased significantly in patients with FMR. The CL at each region was related to PM displacement and the indexes of coaptation were associated with mitral regurgitation severity.

Systemic inflammation and left atrial thrombus in patients with non-rheumatic atrial fibrillation

BACKGROUND There is an apparent link between thrombogenesis and inflammation. We hypothesized that systemic inflammation [as indicated by C-reactive protein (CRP)] would be related to the presence of left atrial (LA) thrombus in patients with atrial fibrillation (AF). To test this hypothesis, we evaluated the relationship between CRP and LA thrombus in patients with non-rheumatic AF. METHODS AND RESULTS Between October 2004 and December 2008, 190 patients with non-rheumatic AF (122 males, age 71+/-10 years) who underwent transesophageal echocardiography (TEE) were enrolled and analyzed. All patients were examined for presence or absence of LA thrombus by TEE. CRP was measured within 1 week before the TEE examination. LA thrombus was detected in 19 patients (10%). Hypertension, hypertensive heart disease (HHD), valvular heart disease, ticlopidine, and CRP were univariate correlates of LA thrombus. By multivariate analysis, HHD (p<0.01), ticlopidine (p=0.01), and CRP (p=0.03) were independently associated with LA thrombus. A cut-off CRP value for identifying LA thrombus was 0.21mg/dl (sensitivity: 84%, specificity: 60%, positive predictive value: 19%, and negative predictive value: 97%). CONCLUSION A high CRP is related to LA thrombus in patients with non-rheumatic AF.

In vivo assessment of vasa vasorum neovascularization using intravascular ultrasound: A comparison between acute coronary syndrome and stable angina pectoris

BACKGROUND Previous studies have suggested that vasa vasorum (VV) neovascularization plays an important role in the progression and vulnerability of coronary atherosclerotic plaque. METHODS A total of 130 patients with coronary artery disease including 75 acute coronary syndrome (ACS) cases and 55 stable angina pectoris (SAP) cases were studied. By using intravascular ultrasound (IVUS), VV was defined as a small (<1mm) tubular or vesicular, low-echoic structure observed exterior to the media. Prevalence and maximal number of VV were compared between patients with ACS versus SAP. RESULTS The prevalence of VV at the culprit lesion was similar between the 2 groups (97% vs. 93%, p=0.216). On the other hand, it was significantly higher in ACS than SAP at both reference sites (proximal: 93% vs. 81%, p=0.047 and distal: 88% vs. 60%, p<0.001, respectively). The maximum number of VV was significantly higher in ACS than in SAP (at the culprit lesion: 2.8±1.3 vs. 1.8±1.0, p<0.001, at the proximal reference: 1.9±1.1 vs. 1.3±0.9, p=0.003 and distal reference: 1.7±1.1 vs. 1.1±1.1, p=0.003, respectively). CONCLUSIONS VV neovascularization of coronary arteries was more enhanced in patients with ACS than in those with SAP, supporting its relation to plaque vulnerability. VV detected by widely used IVUS could be an adequate surrogate marker for plaque vulnerability in vivo.

Acute Coronary Syndrome Demonstrating Plaque Rupture in Calcified Lesions Visualized by Optical Frequency Domain Imaging

A 68-year-old female with acute coronary syndrome was transferred to our hospital. Emergency coronary angiography showed 90% stenosis with severe calcification in the proximal right coronary artery (RCA). Intravascular ultrasound (IVUS) images were obtained and showed circumferential heavy calcification without any evidence of plaque rupture. Optical frequency domain imaging (OFDI) images were obtained in the RCA lesion 3 days after the initial coronary angiography. A cavity of plaque rupture in the calcified plaque by using OFDI was observed in the lesion, which could not be recognized by IVUS. Necrotic tissue was observed frequently in heavy calcified lesions and was usually hidden behind calcification. Judging from the OFDI images in this case, the thin fibrous cap over the necrotic tissue even if surrounded by calcification was disrupted and might have caused the acute coronary syndrome. However, necrotic tissue surrounded by calcification is generally recognized as calcified plaque in OFDI images because discrimination between necrotic tissue and calcification is based on the border characteristics (low intensity with diffuse border: necrotic tissue, low intensity with sharp border: calcification). Superficial residual necrotic tissue not yet replaced completely by calcification might cause plaque rupture and thus, result in acute coronary syndrome. In fact, there is a variety of OFDI and optical coherence tomography (OCT) characteristics in calcified plaque, such as relatively high intensity without attenuation or very low intensity with attenuation. Residual necrotic tissue within calcification could pose a problem in OCT/OFDI plaque evaluation.

Coronary bifurcation bench test using multimodality imaging: Impact of stent strut link location on stent deformity and jailed side-branch orifices during re-proximal optimizing technique

The purpose of this study was to compare the stent deformation, obstruction of stent struts at a jailed side branch (SB) ostium, and stent strut malapposition after a repetitive proximal optimizing technique (re‐POT) sequence between bifurcation lesions with and without stent links at SB ostia in ex vivo experimental setting.

VASA VASORUM NEOVASCULARIZATION PREDICTS PERI-PROCEDURAL MYOCARDIAL INJURY AFTER SUCCESSFUL CORONARY STENTING IN PATIENTS WITH STABLE ANGINA

Previous studies have suggested that vasa vasorum (VV) neovascularization is related to coronary plaque vulnerability. Vulnerable plaque may have higher risk for peri-procedural myocardial injury during coronary stenting. The purpose of this study was to assess impact of VV on peri-procedural

TCT-601 Serial Optical coherence tomography assessment of natural history of silent plaque rupture

Plaque rupture is one of the characteristics of vulnerable plaque responsible for acute coronary syndrome (ACS). Multiple plaque rupture of the non-culprit lesion could be occasionally detected by intravascular ultrasound or optical coherence tomography (OCT). However, the natural course of non-

FREQUENCY AND NATURAL COURSE OF SILENT PLAQUE RUPTURE

Plaque rupture is one of the characteristics of vulnerable plaque responsible for acute coronary syndrome (ACS). Multiple plaque rupture of the non-culprit lesion could be occasionally detected by intravascular ultrasound or optical coherence tomography (OCT). However, the natural course of non-

Erratum to: Impact of energy loss index on left ventricular mass regression after aortic valve replacement

The original version of this article unfortunately contained errors. In the Methods section under the subheading ‘‘Echocardiography,’’ in the first paragraph, the 13th sentence, ‘‘The ELCo was calculated as [EOA AA]/(AA EOA) [12, 13, 18].’’ should be ‘‘The ELCo was calculated as [EOA 9 AA]/(AA EOA) [12, 13, 18].’’ In the Discussion section, in the fourth paragraph, the last sentence, ‘‘Theoretically, ELI the reflects LV pressure overload better than the EOAI.’’ should be ‘‘Theoretically, the ELI reflects LV pressure overload better than the EOAI.’’ In Table 4, ‘‘Atrial fibrillation (%)’’ should be ‘‘Atrial fibrillation [n (%)].’’ The authors apologize for the errors.

Hinge Motion and Excessive Negative Remodeling as a Cause of Early Saphenous Vein Graft Failure

A 56-year-old male patient underwent a coronary artery bypass graft operation (CABG) using the left internal thoracic artery and saphenous vein graft (SVG) for severe coronary artery disease. Fourteen months later, he was admitted to our hospital because of recurrent angina. A coronary angiogram