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SUMMARY Left atrial function was evaluated in patients with and without remote myocardial infarction. The simultaneous left atrial pressure recording and left atrial and left ventricular cineangiograms were obtained with a catheter-tip micromanometer. The pressure-volume curve of the left atrium was composed of an A-loop and a V-loop. The ratio of active atrial emptying to left ventricular stroke volume in patients with myocardial infarction was significantly larger than that in normal subjects (42 + 12% vs 29 + 10%, p < 0.05). The left atrial work was also significantly greater in patients with myocardial infarction (1690 + 717 mm Hgml) than in normal subjects (940 426 mm Hg-ml, p < 0.05). The ratio of active atrial emptying to left ventricular stroke volume and left atrial work were significantly related in both normal subjects and patients with myocardial infarction (y = 0.72, p < 0.01). The left ventricular ejection fraction correlated inversely with left atrial work (y = -0.5, p < 0.05). Left atrial work also showed a significant linear correlation with left atrial volume before active atrial emptying (y = 0.82, p < 0.01).We conclude that the left atrial contribution to left ventricular function is increased in patients with remote myocardial infarction. This left atrial contribution to the left ventricle is attributed to the FrankStarling mechanism in the left atrium.LEFT ATRIAL function and its hemodynamic importance for overall cardiac performance have been discussed.' 1-3 The left atrium may serve as a conduit for the passage of blood from the pulmonary veins to the left ventricle during early left ventricular filling, as a reservoir for storing blood during left ventricular systole, and as a contractile chamber for augmentation of left ventricular filling. Understanding each of these functions and the contribution of the left atrium to left ventricular function in normal and diseased hearts is important.In this report, we analyze left atrial pressure-volume relationships in patients with remote myocardial infarction and discuss the importance of left atrial function. MethodsData were obtained during diagnostic cardiac catheterization in two groups of patients. The normal group consisted of eight patients who had no coronary, valvular or congenital heart disease and were hemodynamically normal. These patients were referred for diagnostic cardiac catheterization to evaluate chest pain. The myocardial infarction group consisted of 10 patients who had a documented remote transmural myocardial infarction, and no other associated heart disease. The clinical data for each patient are listed in medications were discontinued for at least 2 days before the study, except for sublingual nitroglycerin, which was allowed for anginal attack, but withheld 12 hours before the study. A Millar catheter-tip micromanometer (Model PC-484A, pigtail) was used for pressure measurement and cineangiography. The transducer was calibrated electronically against mercury at the beginning of each study. The zero shift during the proc...

BACKGROUNDChromosomal instability (CI) leading to aneuploidy is one form of genetic instability, a characteristic feature of various types of cancers. Recent work has suggested that CI can be induced by a spindle assembly checkpoint defect. The aim of the current study was to determine the frequency of a defect of the checkpoint in hepatocellular carcinoma (HCC) and to establish whether alterations of genes encoding the checkpoint were associated with CI in HCC.METHODSAneuploidy and the function of the spindle assembly checkpoint were examined using DNA flow cytometry and morphologic analysis with microtubule disrupting drugs. To explore the molecular basis, the authors examined the expression and alterations of the mitotic checkpoint gene, BUB1, using Northern hybridization and direct sequencing in 8 HCC cell lines and 50 HCC specimens. Furthermore, the authors examined the alterations of other mitotic checkpoint genes, BUBR1, BUB3, MAD2B, and CDC20, using direct sequencing in HCC cell lines with aneuploidy.RESULTSAn impaired spindle assembly checkpoint was found in five (62.5%) of the eight aneuploid cell lines. Transcriptional expressions of the BUB1 gene appeared in all cell lines. While some polymorphic base changes were noted in BUB1, BUBR1, and CDC20, no mutations responsible for impairment of the mitotic checkpoint were found in either the HCC cell lines or HCC specimens, which suggests that these genes did not seem to be involved in tumor development in HCC.CONCLUSIONSThe loss of spindle assembly checkpoint occurred with a high frequency in HCC with CI. However, other mechanisms might also contribute to CI in HCC. Cancer 2002;94:2047–54. © 2002 American Cancer Society.DOI 10.1002/cncr.10448

SummaryBackground and hypothesis: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization.Methocls: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter-tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle.

We investigated the expression of transforming growth factor β1 (TGF‐β1) mRNA in tumor tissues surgically removed from ten patients with hepatocellular carcinoma (HCC). All HCC tissues expressed TGF‐β1 mRNA at different levels, indicating the presence of activated transcription of TGF‐β1 gene in human HCC tissues in vivo. The level of TGF‐β1 mRNA expression showed no relationship to main tumor size or plasma α‐fetoprotein level. Some HCC tissues presenting a relatively low grade of histological differentiation showed the highest levels of TGF‐β1 mRNA expression.