Summary:A total of 51 patients with hypertrophic cardiomyopathy (HCM) were followed for at least 3 years (mean follow-up period 6.5 years) by serial M-mode and two-dimensional echocardiography. An increase of the left ventricular diastolic dimension (LVDd) to 2 55 mm with a decrease in the left ventricular ejection fraction (LVEF) to < 55% was observed in eight (15.7%) patients (progressive disease group). In five of these eight patients, the LVDd was 2 60 mm and the LVEF was c 40%. Ventricular enlargement was closely related to mortality and death due to congestive heart failure occurred in t h m of these patients. No deaths occurred among the 37 patients without significant progression of ventricular enlargement (nonprogressive group). The annual changes of LVEF and LVDd in the progressive disease goup were larger than in the nonprogressive group (LVEF -0. I8 k 1.45 vs. -2.46 f 1.47 %/year; LVDd 0.22 f 0.81 vs. 1.43 f 0.77 mdyear). An increment in LVDs occurred earlier than the enlargement of the LVDd. Therefore, close attention to the LVDs seems to be important to detect early left ventricular morphological changes in HCM. In summary, this study indicates that HCM patients include a subgroup with symptoms resembling dilated cardiomyopathy, in whom the left ventricle enlarges with hypofunction and in whom there is high mortality due to congestive heart failure.

Ongoing basic molecular analyses are being performed in mice, and a simple long-surviving murine model of myocardial infarction (MI) would be very useful in this regard. Although a few studies have induced MI in mice by coronary artery ligation, the induction involves a complex technique and has a relatively high mortality rate. In addition, the identification of the basic pathological sequence is essential to the interpretation of experimental results. We developed a simple technique for the induction of MI in mice and examined qualitative and quantitative conventional microscopic findings during the pathological evolution over a 28-day observation period. Male BALB/c mice weighing approximately 25-30 g were anesthetized and then ventilated with a positive pressure ventilator. The heart was exposed by thoracotomy. Left coronary artery occlusion was performed by thermocoagulation using a thermocoagulation knife at the level of the tip of the left atrium. After establishing this surgical method, we used it to induce MI in 71 mice. The operative and postoperative mortality rates of this model were 5.6% (4/71) and 12.6% (9/71), respectively. In 3 (5.2%) of the 58 surviving mice, the area of infarct was not sufficient. The infarct area in the remaining 55 mice was 40 +/- 9% of the entire perimeter of the left ventricle. Conventional microscopic examinations with hematoxylin-eosin and Masson-trichrome staining disclosed that all of the characteristic histopathological features of MI occurred 1-2 days earlier than those in rats. Our surgical technique provides a sufficient infarct area, with an acceptable mortality rate. The present study clarified the histopathological sequence in this long surviving murine MI model.

We successfully revascularized the acutely occluded superior mesenteric artery (SMA), caused by a thromboembolus, with a combination of thrombolysis and percutaneous transluminal angioplasty (PTA) in 2 patients. Considerable percent luminal reduction (>90%) was still observed after thrombolysis in both patients. Subsequent adjunctive balloon angioplasty produced sufficient luminal diameter of the SMA (<20% luminal reduction). No serious acute procedural complication occurred. The time from onset to partial reperfusion by thrombolysis was approximately 4.5 and 5.5 hours. Approximately 1 week after the combination therapy, colonoscopy and a small bowel radiocontrast series showed localized mucosal ischemia with mild erosions and ulcerations in the terminal ileum and ascending colon in 1 patient. Subsequent bowel resection was required but the resection was short (<20 cm). The other patient's bowel condition was good and did not require any surgical treatment. The present cases suggest that combination therapy is useful for achieving rapid and sufficient revascularization of acute proximal thromboembolic SMA occlusion, and prevents the considerably broad bowel necrosis that requires surgical bowel resection, resulting in short bowel syndrome.

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SUMMARYThe type X\'II collagen al chain has been identified as a component of the type I hemidesmosome, and is thus thought to play a role in extracellular matrix ECM maintenance and signal transduction between the cell and the EC\I. We examined the expression of type XVII collagen al chain mRNA in the mouse heart by Northern blot analysis and determined the sequential changes of its expression in different developmental stages of the heart using the reverse transcriptase-polymerase chain reaction (RT-PCR) method..Vorthem blotting: Total RNA was extracted from 10 adult mouse hearts by the guanidine/cesium method. Hybridization was performed with mouse cDNA for a1 XVIL collagen. RT-PCP,• Total RNA was extracted from 7 embryos . 4 neonates and 8 adult mice. Reverse transcription was performed using oligo-dT primer and \I\ILV. Amplification was carried out in a1 XVIIi collagen and glyceraldehyde 3-phosphate dehvdrogenase (GAPDH). GAPDH served as an internal control. Northern blotting revealed a 5.6 kb signal that was identical to that of the a1 XVII) of skin and transformed keratinocyte reported previously. The sequences of the PCR products were also identical to those reported. The normalized expression ratios of al XVII) were 0.91 ± 0.20 in the embryonic heart, 0.36 ± 0.20 in the neonatal heart and 0.96 ± 0.21 in the adult heart. In conclusion, we identified the expression of type XVII collagen al chain mRNA in the mouse heart, suggesting that the type I hemidesmosome is located in the heart. The results of the RT-PCR at different developmental stages of the heart suggest that type XVII collagen contributes not only to cardiogenesis in the embryonic stage but also to maintenance of architecture and function in the adult heart. (Jpn Heart J 1998; 39: 211-220)