In fact, this is the case. In the study in question,8 of the 332 patients who received UFH, pDVT, venous limb ischemia, and/or PE developed in 20 patients (6.0%; pDVT alone, 17 patients; distal DVT plus PE, 1 patient; PE without venographic DVT, 2 patients). Notably, 9 of these 20 patients (45.0%) had HIT. In contrast, of the 333 patients who received LMWH, pDVT, venous limb ischemia, and/or PE developed in 17 patients (5.1%; pDVT alone, 15 patients; venous limb ischemia, 1 patient; PE without DVT, 1 patient).8–9 Only 1 of these 17 patients (5.9%) had HIT. Thus, the risks of VTE being associated with HIT after UFH and LMWH therapy based on this surrogate marker for symptomatic VTE (45.0% and 5.9%, respectively) were greater than the corresponding values reported by Levine and colleagues (17.5% and 0.6%, respectively).6 The implication is that the probability of HIT suggested by Levine and colleagues6 among heparin-treated patients might have been even higher had the data been available to them indicating the frequency of symptomatic VTE. After all, only symptomatic thrombi are detected in the “real world” in which routine imaging studies for VTE are rarely employed. Similar to the main findings of Levine and colleagues,6 symptomatic VTE complicating heparin thromboprophylaxis was more likely to represent HIT when it occurred in association with UFH prophylaxis rather than LMWH prophylaxis (odds ratio, 13.1; 95% confidence interval, 1.37 to 608.7; p = 0.0102).