Writing and Publishing Scientific Articles
5-20
Example of a Poorly Written Discussion (Clinical Study)
Before our study, the clinical importance of ventricular ectopy during exercise stress testing was uncertain. There was conflicting evidence about the relationship of exercise-induced ventricular ectopy to coronary artery disease and to cardiovascular risk. 1 – 10 In addition, the prognostic implications of when ventricular ectopy occurs (i.e., during or after exercise) had not been well characterized. A recent study established that vagal reactivation normally occurs early in recovery, immediately after exercise. 11 In the absence of normal vagal reactivation, heart-rate recovery is attenuated and mortality increases. 12 – 15 Therefore, attenuated vagal reactivation during recovery might be associated with ventricular ectopy that is not suppressed. Thus, we prospectively tested the hypothesis that ventricular ectopy during recovery is a stronger predictor of an increased risk of death than ectopy during exercise. Consecutive patients referred for symptom-limited treadmill exercise testing at the Cleveland Clinic Foundation in Cleveland between 1990 and 1999 were eligible for our study. Information regarding ventricular ectopy at rest as well as during each stage of exercise and recovery was systematically recorded according to prespecified definitions. We prospectively defined frequent ventricular ectopy as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation. The primary end point was death from all causes, which is an objective, clinically relevant, and unbiased end point. 20,21 After adjustment for the variables listed in Table 1 and for frequent ventricular ectopy during exercise, frequent ventricular ectopy during recovery was a predictor of an increased risk of death (adjusted hazard ratio, 1.6; 95 percent confidence interval, 1.3 to 1.9; P<0.001). The prognostic importance of frequent ventricular ectopy during recovery in this propensity-matched cohort is shown in Figure 2. Patients with frequent ventricular ectopy during recovery had decreased survival, particularly after three to four years of follow-up. After adjustment for the propensity score, frequent ventricular ectopy during exercise, and the other variables listed in Table 2, frequent ventricular ectopy during recovery predicted an increased risk of death (adjusted hazard ratio, 1.5; 95 percent confidence interval, 1.1 to 1.9; P=0.003). A similar analysis was performed regarding frequent ventricular ectopy during exercise. Frequent ventricular ectopy during exercise was not associated with decreased survival in this propensity-matched cohort (adjusted hazard ratio, 1.1; 95 percent confidence interval, 0.9 to 1.3; P=0.53). In conclusion, frequent ventricular ectopy during recovery from exercise was found to be an important, independent predictor of an increased risk of death in a large clinical cohort. Frequent ventricular ectopy that occurred only during exercise did not independently predict an increased risk. In accordance with previous findings of a strong relationship between attenuated recovery of the heart rate after exercise and an elevated risk of death, these results support the central importance of vagal mediation in cardiac function. They also underscore the value of the exercise stress test as a tool for prognosis and risk stratification.
Adapted from the well-written Discussion in Frolkis JP et al. Frequent ventricular ectopy after exercise as a predictor of death. N Engl J Med 348:781 – 790, 2003.
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