Monozygotic twins are, as recently described in this journal, subject to many complications 1 including the twin reverse arterial perfusion sequence (TRAP), which has an incidence between 0.3 and 1%. Arrested cardiac development within the abnormal twin and failure of the heart due to reverse perfusion by the co-twin through placental vascular anastomoses, have been proposed as underlying etiologies 2. We describe a case that demonstrates aspects of the evolution of TRAP. A woman presented at 12 weeks of gestation with a monochorionic diamniotic gestation (single placental mass and the “T” sign). One fetus appeared normal with a crown–rump length (CRL) of 63.5 mm and normal nuchal translucency. The second fetus was smaller (CRL 47 mm) with nuchal edema (11.4 mm) and hydrops. The extremities appeared disproportionately small and the intracranial anatomy was abnormal. Umbilical and ductus-venosus Doppler images of the larger twin were normal, whereas a biphasic pattern was identified within the umbilical cord of the second twin; comprising two superimposed unsynchronized arterial waveforms of similar rate (160 bpm), indicating the presence of significant inter-twin transfusion. One week later both twins remained viable; the normal twin had grown appropriately while the other demonstrated minimal growth with worsening hydrops (nuchal edema now 16.4 mm). The bidirectional perfusion of this twin's umbilical cord now demonstrated heart rates that were discordant; the abnormal twin being bradycardic. By 14 weeks, the CRL of the abnormal twin was 65 mm; the other twin demonstrated normal growth. The abnormal fetus continued to demonstrate a bradycardia and bidirectional perfusion in its' cord (Figure 1). Given the increasing overall pregnancy loss rate with delayed co-twin demise, selective termination was performed at this stage. This was achieved using radiofrequency cord occlusion (Radionics Cooltip Probe, Valley Lab, Boulder, CO, USA) combined with amniocentesis (normal karyotype reported). Subsequent to this, the surviving fetus continued to develop normally and the pregnancy, complicated only by gestational diabetes, ended with a healthy infant delivered vaginally at 39 weeks (birthweight 3.2 kg). In TRAP, placental vascular anastamoses allow the torso of the dead twin to be perfused by the surviving “pump” twin. The increased cardiac load faced by this twin is partly dependent upon the size of the “acardiac mass” and accounts for the high mortality (50–70%) observed with TRAP. The etiology of TRAP remains poorly understood. The high rate of aneuploidy observed (30%) 3 has led to speculation that fertilization anomalies produce chromosomally discordant twins that are predisposed to the development of TRAP. Karyotypic discordance in monochorionic twins has been reported, however dizygosity is very rare with the data overwhelmingly supporting monozygosity. Indeed, genetic evaluation of TRAP cases has excluded the presence of fertilization disorders, including fertilization of either the first or second polar body, moreover suggesting that TRAP pregnancies are monozygous 4. Only the abnormal twin was karyotyped here. Although genetic confirmation of monozygosity was therefore not obtained, available data would suggest dizygosity to be very unlikely. Alternative hypotheses suggest that TRAP arises as the result of reversed twin-perfusion through vascular anastomoses 5. Several pathologies might contribute to such a process, including cardiac malformations 2 or severe growth discordance. This case lends support to the theory that in some cases, TRAP evolves as the result of circulatory inequalities that result in co-perfusion of one twin by the other with this progressing to complete reverse perfusion upon fetal demise – the hypothesized “cardiac regression sequence” 6.