Initial Assessment and Treatment
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Summary Cancer studies frequently employ clinical endpoints for outcome reporting in order to estimate treatment effect sizes. Most often these outcome assessments use time‐to‐event measures in addition to tumour response, toxicity and quality of life (QOL). The Kaplan‐Meier method is often used to estimate the actuarial rate for time‐to‐event measures. Non‐stratified or stratified log‐rank tests are frequently applied assessing the treatment effect among groups. The Cox proportional hazards regression model is commonly used to estimate the hazard ratio between different treatments. Because cancer outcome is often confounded by multiple other outcomes (e.g. various causes of death), competing risks regression models are used to assess the treatment effect. In addition, intermediary endpoints, such as changes in tumour size, tumour‐related chemical markers and tumour metabolism may also assist in evaluating new treatments. Therefore, the ability to accurately and reliably assess the direct antitumour effect of investigational therapies is critical for the optimal conduct of clinical trials. The goal of this chapter is to summarize general principles of cancer outcome reporting and estimation of treatment effect, and response assessment.
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The assessment of severity of any valvular pathology is based on the development of symptoms or complications as well as the severity at which intervention improves symptoms. Cardiac surgery has favorably altered the course of the natural history of mitral stenosis (MS). However, the natural history studies of MS that predated the arrival of cardiac surgery have been primarily based on symptomatology rather than on an assessment of severity of MS based on mitral valve area (MVA). Whether, the symptoms developed due to progression of disease or due to other secondary sequelae could not be assessed. Some of the complications of MS such as atrial fibrillation (AF) and stroke have been shown not to be consistently related to the severity of MS. Similarly, the exact level of left atrial pressure at which pulmonary edema may develop in an individual varies and is further modified by lymphatic drainage. Paul Wood had noted in his seminal paper on MS "Certainly pulmonary edema was just as likely to occur in a patient with an average or relatively large orifice (provided it was within the critical range) as with extreme stenosis; auricular fibrillation, hemoptysis, and systemic embolism were also indifferent to the size of the orifice". As such, the grading of MS, although intuitive, is to some extent arbitrary. The classification of MS as mild, moderate and severe is based on theoretical thresholds of pulmonary edema at a certain cardiac output, heart rate, and MVA. It should be emphasized that the mitral valve gradient is directly proportional to the square of mitral flow in diastole (cardiac output) and inversely proportional to the time in diastole (heart rate). Thus, even patients with mild MS may develop pulmonary edema. With this background, it is essential to remind ourselves that the management of MS should not be based solely on arbitrary cut-off values of MVA but rather on the hemodynamic and symptomatic status of the individual patient. MS should be viewed as a disease spectrum.
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