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Background Cardiac rupture (CR) is a catastrophic complication of acute myocardial infarction. Primary percutaneous coronary intervention (pPCI) reduces the incidence of CR. This study aimed to investigate the clinical risk factors and characteristics of CR after pPCI. Methods This was a retrospective, case-control, multicenter study. We enrolled 2444 consecutive patients with ST-elevation myocardial infarction (STEMI) who had undergone pPCI between 2009 and 2015; 33 patients experienced CR (1.35%): 19 were assigned as early CR (≤72 h) and 14 as late CR (>72 h). The 132 controls were randomly selected from the 2411 STEMI patients without CR, by matching institutions at a 1:4 ratio. Results : Multivariate logistic regression revealed that female sex, acute hyperglycemia, thrombocytopenia (platelets 1, and post-PCI TIMI 1 and thrombocytopenia were strongly associated with late CR. Early CR occurred more frequently between 12:00 and 21:00 h, whereas the peak incidence of late CR was bimodal between 6:00–12:00 and 21:00–24:00 h. Conclusions In STEMI patients after pPCI, acute hyperglycemia and thrombocytopenia are new risk factors for early and late CR, respectively. Clinical risk factors and time of occurrence of early and late CR may differ in the PCI era.

SummaryBackgroundData regarding the relationship between systolic blood pressure (SBP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking in Japan.Methods and resultsA total of 1475 primary PCI-treated AMI patients were classified into quintiles based on admission SBP (

SummaryBackgroundSeveral clinical studies have demonstrated an inverse relationship between systolic blood pressure (SBP) at admission and in-hospital mortality in patients hospitalized for acute myocardial infarction (AMI). However, data on the relation between admission SBP and in-hospital prognosis in AMI patients are still lacking in Japan.Methods and resultsA total of 1211 AMI patients were classified into quintiles based on SBP at hospital admission (

Summary Background Prolonged pre-hospital time for acute myocardial infarction (AMI) is associated with decreased indication for primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI in AMI patients with prolonged pre-hospital time has not been fully investigated in Japan. Methods and results A total of 3010 consecutive AMI patients admitted to AMI-Kyoto Multi-Center Risk Study Group hospitals were retrospectively analyzed, and the clinical characteristics and in-hospital prognosis of these patients were reviewed. Patients with pre-hospital delay [elapsed time (ET) > 12 h] had a lower frequency of Killip ≥ 3 (9.3%) and less frequently received primary PCI (77.7%) compared with patients with ET ≤ 12 h. In the ET > 12 h group, older patients or patients with MI history tended to be complicated by heart failure. Primary PCI was performed for patients with ET > 12 h, irrespective of the severity of heart failure [Killip 1 (78.7%) vs Killip ≥ 2 (74.0%); p = 0.3827]. On multivariate logistic regression analysis, age [odds ratio (OR) 1.053], MI history (OR 2.860), Killip ≥ 2 (OR 10.235), and multi-vessels or left main coronary artery as culprit (OR 11.712) were significant independent positive predictors of in-hospital mortality for patients with ET > 12 h. Practice of primary PCI was not a significant negative predictor for patients with ET > 12 h (OR 0.812), but it was for patients with ET ≤ 12 h (OR 0.425). Conclusions These findings indicate that patients with ET > 12 h have a less severe condition and less frequently receive primary PCI compared with patients with ET ≤ 12 h. Although primary PCI is often performed for these patients irrespective of the severity of heart failure, no preferable effect of primary PCI on the in-hospital mortality is demonstrated. In contrary, practice of primary PCI is a significant negative predictor of in-hospital mortality for patients with ET ≤ 12 h.

Single-strand elbow medial collateral ligament reconstruction strength was evaluated by use of double-docking and interference screw methods with either a palmaris longus tendon or GraftJacket as the reconstruction material. Thirteen upper extremities were mounted in 90 degrees of valgus orientation and subjected to cyclic valgus loading that increased progressively until failure occurred. The double-docking reconstructions outperformed the interference screw reconstructions (P.05), whereas the palmaris longus and GraftJacket performed comparably (P.05). The favorable initial strength of the GraftJacket make it a potentially viable alternative to the use of autogenous palmaris longus tendons; however, further studies are required to evaluate graft strength during healing. The clinical use of the double-docking technique of single-strand medial collateral ligament reconstruction should be considered because of its simplicity and initial strength.

We describe a case of neuro-Behcet's disease (NBD) characterized by recurrent attacks of neurologic deficit. T2-weighted images showed a high signal intensity lesion with extensive edema in the right thalamolenticular region, midbrain, and pons as well as the cerebral white matter. After a relapse of the disease, MRI demonstrated a high signal intensity in the left thalamus, internal capsule, and midbrain. These MRI abnormalities showed marked resolution with steroid treatment. We observed sequential MRI findings in a patient with a relapsing–remitting form of NBD who had parenchymal CNS involvement, and we examined the correlation among the MRI findings and clinical features during the clinical course.

We investigated the osteogenic potential of skin fibroblasts that overexpressed BMP-2 or Runx2 by using adenoviral vectors. In in vitro experiments, skin fibroblasts infected with adenovirus vector encoding BMP-2 (AdBMP-2) released substantial levels of BMP-2 proteins into culture media, and those infected with adenovirus vector encoding Runx2 (AdRunx2) produced its protein. Transduction of BMP-2 or Runx2, respectively, increased alkaline phosphatase (ALP) activity and induced expression of mRNAs of ALP, osteocalcin, and osterix in skin fibroblasts. In in vivo experiments, we investigated the bone induction activity by transplantation of a complex composed of carrier [poly-D,L-lactic-co-glycolic acid/gelatin sponge (PGS)] and skin fibroblasts (PGS/SF complex). Transplantation of PGS/SF complexes composed of skin fibroblasts transduced with AdBMP-2-induced ectopic bone formation when transplanted into the subfascia of back muscle, unlike those infected with AdRunx2. Transplantation of PGS/SF complexes composed of skin fibroblasts transduced with AdBMP-2 into craniotomy defects induced bone formation from 2 weeks after transplantation, and almost all PGS was replaced by newly synthesized bone at 6 weeks. To investigate the fate of the transplanted cells, we transplanted skin fibroblasts isolated from green fluorescence protein transgenic mice into craniotomy defects. Transplantation of these skin fibroblasts transfected with AdBMP-2 generated green fluorescence protein-positive osteoblasts and osteocytes, indicating that the transplanted skin fibroblasts differentiated into osteoblastic lineage cells during bone repair. In contrast, transplantation of PGS/SF complexes composed of skin fibroblasts transduced with AdRunx2 induced a few ALP-positive cells at 1 week after transplantation, but their number decreased depending on time after transplantation. In addition, transplantation of these complexes was insufficient to induce bone repair. Taken together, our results suggest that skin fibroblasts expressing BMP-2 are more suitable for cell-mediated therapy of bone repair than those expressing Runx2.

We investigated the independent change in pulmonary diffusing capacity (DLCO) as one manifestation of pulmonary microangiopathy and to analyze the correlation between DLCO and serum ACE. We also examined the association between DLCO and the ACE genes. We examined pulmonary functions, especially %DLCO/VA (DLCO corrected by alveolar volume, percent predicted) in 54 NIDDM patients and 34 age-matched normal control subjects. Subjects were subdivided according to the degree of retinopathy. Serum ACE level was assayed by a colorimetric method in 54 patients and an insertion/deletion polymorphism in the ACE gene was amplified using the polymerase chain reaction in 52 of the 54 patients. There was a significant reduction of %DLCO/VA (percent predicted P0.05) in diabetic patients. In the proliferative retinopathy (PDR) group. %DLCO/VA was significantly (P0.05) lower than in the no diabetic retinopathy (NDR) and simple diabetic retinopathy (SDR) groups. Although the levels of serum ACE were within normal ranges in all diabetic groups, %DLCO/VA was negatively correlated with serum ACE values (r = 0.49, P0.0002, y = -1.4x + 109.3). Differences among DD, ID and II type of the ACE gene, with respect to the incidence of abnormal values of each clinical parameter, were not significant. DLCO was significantly reduced in patients with PDR and the serum ACE was significantly related to impaired DLCO. Our study suggests the existence of microangiopathic involvement of pulmonary vessels in NIDDM patients.

Mutation in the mitochondrial gene at position 3243 was recently identified in a large pedigree of diabetes mellitus and deafness. As the mitochondria play an important role in glucose-stimulated insulin secretion in pancreatic beta-cells, we therefore searched for such mutations to detect a candidate gene for diabetes. We screened 10 diabetic subjects with clinical features suggesting mitochondrial DNA mutations. An adenine to guanine point mutation in tRNA(Lys) in at position 8296 (the 8296 mutation) was newly identified. Subsequently, we screened 1216 diabetic subjects, 44 patients with sensorineural deafness subjects and 300 non-diabetic control subjects for this mutation. We identified the mutation in 11 (0.90%) unrelated diabetic subjects, one (2.3%) patient with deafness and no non-diabetic control subject. Seven of these 12 subjects showed maternal inheritance. Deafness was seen in 7 of 12 probands. Four family pedigrees showed maternal inheritance of diabetes over two or three generations. Subjects carrying the 8296 mutation may develop diabetes and the mutation can explain as high as ca. 1% of the causes of diabetes.

A huge saccular idiopathic dilatation of the right atrium was detected with angiography and echocardiography in a 75 year old man. Cardiac catheterization data were compared with data obtained 4 years earlier. Idiopathic right atrial enlargement is not usually accompanied by tricuspid valve disease, but in this case tricuspid insufficiency did occur over a period of 4 years, possibly as a complication in the late stage of idiopathic right atrial enlargement.

A case of traumatic tricuspid insufficiency is presented. In the diagnosis of raptured chordae tendineae of the tricuspid valve, two-dimensional echocardiography was an essential diagnostic procedure, while M-mode echocardiography showed no specific findings. Ruptured chordae tendineae of the tricuspid valve were confirmed at operation.

A patient with click and late systolic murmur syndrome originating in the right side of the heart is described. Prolapse of the anterior tricuspid leaflet was demonstrated by subxiphoid two-dimensional echocardiography alone. Neither of the mitral leaflets showed any evidence of prolapse on the echocardiogram. The prolapsed anterior tricuspid leaflet and mild regurgitation were confirmed by right heart cineangiogram.