Arrhythmias, especially supraventricular arrhythmias, often complicate the clinical course during autologous hematopoietic cell transplantation (AHCT). We undertook this study to determine the incidence and risk factors for cardiac arrhythmias during AHCT. The study included 983 patients who underwent AHCT between August 2006 and December 2010 at a single institution, and in whom all the relevant medical records were available for review. The median age was 58 years (range; 19–77); 61% were male. AHCT was done for plasma cell disorders in 58% patients and for lymphoma or leukemia in the remaining. Overall, 92 (9.4%) patients developed a supraventricular tachyarrhythmia at a median of 9 days post transplant (range; 0, 18) and with a median duration of <1 day (range; <1 to 17 days). Atrial fibrillation (AF) was the most common and seen in 71 (7%) patients, followed by atrial flutter and supraventricular tachycardia in 12 (1%) and 8 (1%) patients respectively. In multivariate analysis, age > 63 years, presence of premature supraventricular complexes or Atrio-ventricular conduction delay on pre-transplant ECG, and history of any prior arrhythmia increased the risk of arrhythmia. Development of arrhythmia resulted in longer outpatient follow up after AHCT, with the median follow-up for those developing an arrhythmia of 22 days compared with 19 days for the rest; P < 0.001. In conclusion, 9% of patients undergoing ASCT develop supraventricular arrhythmias post transplant and this risk is elevated among the older patients, those with a prior history of arrhythmias, and those with pre-transplant ECG abnormalities.

Proton pump inhibitors (PPIs) are not widely recognized as a cause of drug-induced thrombocytopenia. Literature is mainly confined to case reports and has been insufficient to explore the possibility that this adverse event may be attributed to a class effect of PPI therapy. We present a case where platelet counts dropped from 177 (×10(3) per mm(3)) to 47 (×10(3) per mm(3)) within 6 days after the patient was switched from omeprazole to pantoprazole. There have been case reports of thrombocytopenia caused by PPIs; however, this is noted to be extremely rare. In our case, the patient developed thrombocytopenia on two separate occasions of exposure to pantoprazole, which resolved after stopping the medicine, thus providing definite proof of pantoprazole causing thrombocytopenia. Moreover, the patient did not have thrombocytopenia with omeprazole, thus suggesting that thrombocytopenia with PPIs might be an individual drug effect rather than a class effect. This occurrence has been reported in three other case reports as well. From the nine case reports that we have reviewed, direct causal relationship was found in a few reports only. It has been hypothesized that this adverse effect may be immune mediated, but further investigations are still needed to identify the exact pathogenesis.

It is important to weigh both the risk of CVD and that of breast cancer recurrence in a breast cancer survivor. Certain interventions for the primary prevention of CVD, including diet, physical activity, smoking cessation and aspirin, can reduce breast cancer risk as well. The management of CVD risk factors is of increasing importance in the management of breast cancer survivors.

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