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OBJECTIVE:This study sought to evaluate the prevalence of human papillomavirus (HPV) types 16 and 18 in women with clinical stage IB cervical cancer treated by radical hysterectomy with pelvic lymphadenectomy as well as to establish a correlation between HPV type and cancer prognosis.METHODS:A single-center cohort study was conducted with 86 patients who had undergone radical hysterectomy for stage I cervical cancer. Prognostic factors and the presence of HPV 16 and 18 were analyzed using a polymerase chain reaction assay. A univariate analysis using Kaplan-Meier curves was conducted to estimate survival.RESULTS:The prevalence of HPV 16 in the study group was 65.3%, and the prevalence of HPV 18 was 33.3%. The prevalence of infection with both viruses was 26.9%. Overall survival at 5 years was 91% among women with HPV 18 and 96% among those without this virus type (p = 0.133). Among the women with HPV 16, the overall survival was 94%, whereas this rate was 96% among those without this virus type (p = 0.663). Disease-free survival was unaffected by the presence of HPV type 16 or 18.CONCLUSION:In the present study, despite the high prevalence of HPV types 16 and 18, the presence of these virus types did not affect the prognosis of patients with stage I cervical cancer who underwent radical hysterectomy.

Left ventricular (LV)' systole can be divided into phases: isovolumic contraction, ejection, end-systole, and isovolumic relaxation (1). Indices have been developed that describe LV performance during each of these four phases. However, it has been difficult to provide a description of the LV that spans all four phases, unifying and relating the various measures of LV performance. One possibility is to consider that LV systolic pumping function can be described as a time-varying elastance (2-5). In this concept, the LV is considered to behave as an elastic structure that stiffens in a predictable manner during systole. The LV pressure, P(t), at any time after the onset of contraction, t, is described by: P(t) = E(t) [V(t) -V0], where E(t) is LV elastance at t, V(t) the LV volume at t, and V0 the minimum volume required for the LV to generate super-atmospheric pressure. LV elastance, E(t), reaches a maximum value, E., at time t.,,, which has been termed end-systole. Ema,31which is the slope of the end-systolic pressure (PEs)-volume (VEs) relation, is a measure ofthe global inotropic state of the LV and is relatively insensitive to changes in loading conditions in isolated canine hearts (2, 3, 5-10), conscious dogs (1 1), and man (12, 13). Inotropic stimulation with catecholamines increases Emax and decreases t., the time from enddiastole to end-systole (2-4).In addition to the PES VEs relation, the time-varying elastance model has other implications that suggest links between the four phases ofsystole. For example, the model suggests that the maximum rate of rise of LV pressure (dP/dt4,), normally occurring during isovolumic contraction, is linearly related to the LV end-diastolic volume (VED) (3,4). The slope of this relation, dE/dtm., is also predicted to be sensitive to inotropic state and proportional to Ema/tm., providing a link between events occurring during isovolumic contraction and at endsystole. Further consideration of the time-varying elastance hypothesis (Appendix) also suggests that the rate of LV pressure fall during isovolumic relaxation should be inversely proportional to tm.. These predictions of the time-varying elastance model linking events occurring during isovolumic contraction (dP/dtm.,-VED relation), at end-systole (the PES-VES relation and tma), and during isovolumic relaxation (T) suggest that this model may provide a unified description of LV performance throughout systole.1. Abbreviations used in this paper: dE/dt., slope of dP/dtm,.-end-diastolic volume relation; dP/dtma, maximum rate of rise of P(t); ED, end-diastolic; Em,,t, slope ofend-systolic pressure-volume relation; ES, end-systolic; LV, left ventricular; P(t), LV pressure; t,,,, time from end-diastole to end-systole.Effect ofDobutamine and Ouabain 613 J. Clin. Invest.

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