Transient ischemic attack (TIA) is an important predictor of future ischemic events, including stroke. Due to the typically brief period of neurologic dysfunction, patients often overlook the importance of reporting a TIA. We have recently shown that platelet activation plays an important role in TIA pathology. In a similar vein, smoking is associated with a hypercoagulable state and is also one of the important risk factors for stroke. Here we present an interesting case where a 61-year-old male, with hypercholesterolemia, and a previous heart valve replacement, developed a TIA 5 months after he started smoking. Subsequent to the event, Warfarin dosage was monitored monthly using the international normalized ratio (INR). We compared erythrocyte and platelet morphology of healthy individuals, that of smokers, individuals who had a diagnosed TIA (without smoking), and the patient. The erythrocytes from the case study are ultrastructurally similar to that of a smoker, while his platelets are similar to that of smokers and TIA patients who do not smoke. We conclude that smoking exacerbated the chronic inflammation induced by hypercholesterolemia, causing changes in his erythrocyte morphology and platelet activation, and suggest that ultrastructure here explains the clinical manifestations of the thrombotic state of this patient.