Methods of cult-building and cult-dismantling in communist Hungary : the case of Mátyás Rákosi, 1945-1956

Defence date: 29 September 2006Examining board: Prof. Arfon Rees (Supervisor) ; Prof. László Bruszt ; Prof. Robert Service ; Prof. Árpád von KlimoPDF of thesis uploaded from the Library digitised archive of EUI PhD theses completed between 2013 and 201

Interview with Balazs Apor, March 23, 2012

How Apor came to the study of communist leader cults (1:00) How Apor's view of Rakosi and the leader cult has changed since starting work on it (2:20)How the assessment of Rakosi’s legacy has changed (or not) since 1956 (4:00) On the inadequacy of the term "cult of personality" versus "leader cult" (7:45) On the challenges of doing research on Rakosi's leader cult and what Apor found in his research that surprised him (11:15) The extent to which people were willing participants in leader cults and why (18:30) Comparison of Rakosi to other leaders like Miklos Horthy and Imre Nagy in terms of leader cults (29:25) On whether writing about the leader cult speaks to how Hungarians come to terms with their own history (45:15) On teaching East-Central European history in Ireland and where the field is headed (49:05)Interview with Balazs Apor, Director of the MPhil program in European Studies at Trinity College Dublin. Interviewed conducted in Dublin, Ireland on March 23, 2012. Balazs Apor specializes in the history of East-Central Europe under communism, especially on the leader cult. He has co-edited two volumes, including The Leader Cult in Communist Dictatorships: Stalin and the Eastern Bloc (2004), and The Sovietization of Eastern Europe: New Perspectives on the Postwar Period (2008). He is currently at work on a monograph on the leader cult of the Hungarian Stalinist Matyas Rakosi.1_3vv35pz

Diagnostic Performance of On-Site Computed Tomography Derived Fractional Flow Reserve on Non-Culprit Coronary Lesions in Patients with Acute Coronary Syndrome

The role of coronary computed tomography angiography (CCTA) derived fractional flow reserve (CT-FFR) in the assessment of non-culprit lesions (NCL) in patients with acute coronary syndrome (ACS) is debated. In this prospective clinical study, a total of 68 ACS patients with 89 moderate (30–70% diameter stenosis) NCLs were enrolled to evaluate the diagnostic accuracy of on-site CT-FFR compared to invasive fractional flow reserve (FFRi) and dobutamine stress echocardiography (DSE) as reference standards. CT-FFR and FFRi values ≤0.80, as well as new or worsening wall motion abnormality in ≥2 contiguous segments on the supplying area of an NCL on DSE, were considered positive for ischemia. Sensitivity, specificity, positive, and negative predictive value of CT-FFR relative to FFRi and DSE were 51%, 89%, 75%, and 74% and 37%, 77%, 42%, and 74%, respectively. CT-FFR value (β = 0.334, p < 0.001) and CT-FFR drop from proximal to distal measuring point [(CT-FFR drop), β = −0.289, p = 0.002)] were independent predictors of FFRi value in multivariate linear regression analysis. Based on comparing their receiver operating characteristics area under the curve (AUC) values, CT-FFR value and CT-FFR drop provided better discriminatory power than CCTA-based minimal lumen diameter stenosis to distinguish between an NCL with positive and negative FFRi [0.77 (95% Confidence Intervals, CI: 0.67–0.86) and 0.77 (CI: 0.67–0.86) vs. 0.63 (CI: 0.52–0.73), p = 0.029 and p = 0.043, respectively]. Neither CT-FFR value nor CT-FFR drop was predictive of regional wall motion score index at peak stress (β = −0.440, p = 0.441 and β = 0.403, p = 0.494) or was able to confirm ischemia on the territory of an NCL revealed by DSE (AUC = 0.54, CI: 0.43–0.64 and AUC = 0.55, CI: 0.44–0.65, respectively). In conclusion, on-site CT-FFR is superior to conventional CCTA-based anatomical analysis in the assessment of moderate NCLs; however, its diagnostic capacity is not sufficient to make it a gatekeeper to invasive functional evaluation. Moreover, based on its comparison with DSE, CT-FFR might not yield any information on the microvascular dysfunction in the territory of an NCL