Aortic valve replacement for aortic regurgitation caused by aortitis

Between January 1984 and December 1998, 19 patients (16 with Takayasu's arteritis, 3 with non-Takayasu's aortitis) underwent surgical treatment for aortic regurgitation resulting from the aortitis. Of the 19 patients, 14 had aortic valve replacement (AVR) and 5 had aortic root replacement. One patient (5.3%) died of graft infection during the hospital stay. During the follow-up period, 1 (5.6%) of the 18 postoperative patients died of paravalvular leakage due to valve detachment, which also required redo-operations in 2 patients with non-Takayasu's aortitis. Both patients were operated on during the active phase of the inflammation without perioperative steroid therapy. Although transmural pledgeted sutures were used for replacement of the detached prosthetic valve in 1 of these 2 patients, disruption of the aortic wall resulted in recurrence of valve detachment. In the other patient, aortic root replacement was successfully performed with the Cabrol technique in the second operation. Perioperaitve steroid therapy plays an important role in preventing complications after AVR when the valve replacement is carried out during the active phase of the inflammation, and for patients with non-Takayasu's aortitis, aortic root replacement should be considered to reduce the tension on the suture line and the native aortic valve annulus.     

Comprehensive analysis of intravascular ultrasound and angiographic morphology of culprit lesions between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome

Background

Some plaques lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation acute coronary syndrome (NSTEACS). We used angiography and intravascular ultrasound (IVUS) to investigate the difference of culprit lesion morphologies in ACS.

Methods

Consecutive 158 ACS patients whose culprit lesions were imaged by preintervention IVUS were enrolled (STEMI = 81; NSTEACS = 77). IVUS and angiographic findings of the culprit lesions, and clinical characteristics were compared between the groups.

Results

There were no significant differences in patients' characteristics except for lower rate of statin use in patients with STEMI (20% vs 44%, p = 0.001). Although angiographic complex culprit morphology (Ambrose classification) and thrombus were more common in STEMI than in NSTEACS (84% vs 62%, p = 0.002; 51% vs 5%, p < 0.0001, respectively), SYNTAX score was lower in STEMI (8.6 ± 5.4 vs 11.5 ± 7.1, p = 0.01). In patients with STEMI, culprit echogenicity was more hypoechoic (64% vs 40%, p = 0.01), and the incidence of plaque rupture, attenuation and “microcalcification” were significantly higher (56% vs 17%, p < 0.0001; 85% vs 69%, p = 0.01; 77% vs 61%, p = 0.04, respectively). Furthermore, the maximum area of ruptured cavity, echolucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.80 ± 0.99 mm² vs 1.13 ± 0.86 mm², p = 0.006; 1.52 ± 0.74 mm² vs 1.21 ± 0.81 mm², p = 0.004; 99.9 ± 54.6° vs 77.4 ± 51.2°, p = 0.01, respectively). Quantitative IVUS analysis showed that vessel and plaque area were significantly larger at minimum lumen area site (16.6 ± 5.4 mm² vs 14.2 ± 5.5 mm², p = 0.003; 13.9 ± 5.1 mm² vs 11.6 ± 5.2 mm², p = 0.003, respectively).

Conclusion

Morphological feature (outward vessel remodeling, plaque buildup and IVUS vulnerability of culprit lesions) might relate to clinical presentation in patients with ACS.     

Intravascular ultrasound morphology of culprit lesions and clinical demographics in patients with acute coronary syndrome in relation to low-density lipoprotein cholesterol levels at onset

Despite current standards of care aimed at achieving targets for low-density lipoprotein cholesterol (LDL-C), many patients remain at high residual risk of cardiovascular events. We sought to assess the LDL-C-dependent differences in culprit intravascular ultrasound (IVUS) morphologies and clinical characteristics in patients with acute coronary syndrome (ACS). Eighty-six consecutive ACS patients whose culprit lesions imaged by preintervention IVUS were divided into two groups based on the fasting LDL-C level on admission: a low-LDL-C group (LDL-C <2.6 mmol/l, n = 45) and a high-LDL-C group (LDL-C ≥2.6 mmol/l, n = 41). Patients with stable angina with LDL-C <2.6 mmol/l (n = 30) were also enrolled as an age- and gender-matched control. The low-LDL-C ACS group was significantly older (72 ± 12 vs 64 ± 14 years, P = 0.007) and more diabetic (47 % vs 15 %, P = 0.001). Importantly, IVUS morphologies were comparable between low- and high-LDL-C ACS groups (all P not significant), whereas culprit plaque was more hypoechoic and less calcified in the low-LDL-C ACS group than in the low-LDL-C stable angina group. Furthermore, compared with the low-LDL-C ACS nondiabetic group, the low-LDL-C ACS diabetic group was more obese, more triglyceride rich (1.3 ± 0.6 vs 0.9 ± 0.4 mmol/l, P = 0.003), and more endothelially injured, but no different for the culprit IVUS morphologies. In multivariate analysis, diabetes was independently associated with a low LDL-C level on admission in patients with ACS. There was no relationship between the LDL-C level at onset and culprit-plaque IVUS morphologies in ACS patients, although culprit plaque in the low-LDL-C ACS group was more vulnerable than in the low-LDL-C stable angina group. In patients with low-LDL-C levels, diabetes with atherogenic dyslipidemia might be the key residual risk.     

Diagnosis of Atlantoaxial Subluxation in Morquio's Syndrome and Spondyloepiphyseal Dysplasia Congenita

Compression of the spinal cord due to atlantoaxial subluxation was diagnosed in a patient with Morquio's syndrome and in another with spondyloepiphyseal dysplasia (SED) congenita by cervical radiography and magnetic resonance imaging (MRI). The patient with Morquio's syndrome, a 15 year old boy, had no neurologic symptoms and his somatosensory evoked potential (SSEP) was normal. However, MRI demonstrated spinal cord compression at C1-C2. In contrast, the patient with SED congenita, an 11 year old girl, had neck pain, hyperreflexia and loss of vibration sense in both legs. These findings were explained by the absence of P3 and later waves in SSEP and by compression of the spinal cord observed on MRI. Both SSEP and MRI should be used for evaluating disorders in which atlantoaxial subluxation might be present.     

Computer-aided three-dimensional reconstruction of the osseous and membranous labyrinths

Summary In order to obtain an adequate knowledge of the stereoscopic anatomy of the temporal bone, it is very useful to make three-dimensional reconstructions of the bone. By using the histological sections of a human temporal bone processed for routine evaluation, we have undertaken computer-aided reconstruction of the osseous and the membranous labyrinths, as well as the inner ear sensory organs. Reconstructions were done either separately or simultaneously. Owing to the semitransparent display function of the computer system, it was possible to observe the reconstructed membranous labyrinth through the simultaneously reconstructed osseous labyrinth, and the sensory organs through the membranous labyrinth. The results were satisfactory for understanding the spatial relationships among these structures. We also attempted computer-aided measurements of the reconstructed sensory organs and calculated the length of the organ of Corti and the angle between the saccular and the utricular maculae.     

Thrombolytic therapy with tissue plasminogen activator for the treatment of nonstructural malfunction of bileaflet cardiac valve prostheses

This study was conducted to determine the effect of thrombolytic therapy with tissue plasminogen activator (t-PA) for nonstructural malfunction of bileaflet cardiac valve prostheses. Twenty-seven patients with bileaflet prosthetic valve malfunction diagnosed by a combination of cineradiography and transthoracic echocardiography were treated with the administration of intravenous t-PA. The treatment resulted in complete success in 55.6% (15 of 27), partial success in 22.2% (6 of 27), and no change in 22.2% (6 of 27). In the complete success and partial success groups, the condition of the patients in 85.7% (18 of 21) of the cases improved within 24 h after the administration of t-PA. Six cases in whom thrombolytic therapy was instituted more than 1 month (ranged from 1 to 38 months, mean 14.7 months) after the diagnosis of prosthetic valve malfunction showed significantly less effectiveness of thrombolytic therapy with t-PA. Only one patient (3.7%) had a major complication (thromboembolism) after t-PA treatment. The results suggest that thrombolytic therapy with t-PA in patients with nonstructural malfunction of bileaflet cardiac valve prostheses is effective with low incidence of complication when the treatment is instituted early after the diagnosis.     

Vocal fold motion impairment in patients with multiple system atrophy: evaluation of its relationship with swallowing function

BACKGROUND: Vocal fold motion impairment (VFMI), especially vocal fold abductor paralysis, is frequently seen in multiple system atrophy (MSA). Since the regulation system of laryngeal function is closely related to swallowing function, swallowing function is considered to be more involved in MSA patients with VFMI than in patients that do not have VFMI. However, the relationship between dysphagia and VFMI in MSA patients has not been systematically explored. OBJECTIVE: To elucidate the relationship between VFMI and dysphagia in MSA. METHODS: We evaluated swallowing function of 36 MSA patients with and without VFMI, by videofluoroscopy, and investigated the relationship between VFMI and pharyngeal swallowing function. RESULTS: VFMI was found in 17 patients (47.2%). Patients with VFMI had advanced severity of the disease. Although there was a tendency for bolus stasis at the pyriform sinus and the upper oesophageal sphincter opening to be more involved in patients with VFMI, statistical analysis did not show significant differences in swallowing function of MSA patients between with and without VFMI. In contrast, patients who underwent a tracheotomy ultimately required tube feeding or a laryngectomy. CONCLUSIONS: Appearance of VFMI is a sign of disease progression but does not necessary mean patients should change their way of taking nutrition. However, MSA patients who need a tracheotomy might have advanced to a high-risk group for dysphagia. Appropriate evaluation and treatment for VFMI and dysphagia are required to maintain patients' quality of life in MSA.     

A case of colon metastasis to the lung treated successfully with combined chemotherapy of CPT-11 and 5'-DFUR

We administered pharmacokinetic modulating chemotherapy (PMC, oral tegafur/uracil [UFT] plus fluorouracil infusion) together with irinotecan hydrochloride (CPT-11) in a patient with rectal cancer, who had multiple lung metastases at 2 years and 7 months after surgery. However, because the patient showed resistance, we attempted combination therapy with CPT-11 and doxifluridine (5'-DFUR) on an outpatient basis, which resulted in NC after 9 months. During this period, the therapy was performed safely without any observable adverse reactions such as diarrhea or myelosuppression. This case suggests the efficacy of combination therapy with CPT-11 and 5'-DFUR, which was expected since this is an established treatment for progressive recurrent colon cancer.     

Primate neurons show different vulnerability to transient ischemia and response to cathepsin inhibition

Previously, we reported "calpain-induced leakage of lysosomal enzyme cathepsin" as a mechanism of ischemic neuronal death specific for primates. Cathepsin inhibitors such as CA-074 and E-64c were demonstrated to significantly inhibit hippocampal neuronal death. Pyramidal neurons of the hippocampus, Purkinje cells in the cerebellum, and neurons in the caudate nucleus, outer putamen and cortical III, V layers, are known to be vulnerable to ischemia. However, regional differences of the vulnerability and response to neuroprotectants, have not been studied in detail. Here, the monkey brains undergoing transient ischemia were studied to clarify such regional differences by the microscopic counting of surviving neurons. The dead neurons were characterized by eosinophilic coagulation necrosis without apoptotic bodies. The control postischemic brain without treatment showed surviving neurons in caudate nucleus (55.8%), outer putamen (44.4%), cortical III layer (37.8%), CA4 (35.3%), cortical V layer (34.1%), cerebellum (28.2%), CA3 (24.3%), CA2 (16.2%), and CA1 (2.0%). Only the CA1 showed an almost total neuronal loss. In contrast, a single postictal injection of CA-074 or E-64c led to significant inhibition of postischemic neuronal death in all brain regions studied. Overall, more surviving neurons were seen after E-64c treatment than with CA-074: cerebellum, 91.6% vs 85.6%; CA4, 88.6% vs 77.3%; caudate nucleus, 86.1% vs 89.8%; CA2, 83.6% vs 53.0%; outer putamen, 81.3% vs 87.7%; CA1, 80.1% vs 47.4%; CA3, 79.6% vs 60.3%; cortical layer III, 75.5% vs 67.7%; and cortical layer V, 75.0% vs 65.9%, for E-64c and CA-074, respectively. Cathepsin plays a critical role in ischemic neuronal death, and its inhibitors may protect neurons throughout the brain.