Aspetti processuali del Regolamento n. 1/2003/Ce

The recent reform in European antitrust enforcement is embodied in Regolation n. 1/2003/ Ce and related Communications. Since 2004 when it came into force, some crytical assessments can already be made. The work starts from some technical analysis of the reform, under a procedural perspective, to assess the proceedings’ real impact on parties’ rights and to criticize its limits. Decentralisation has brought about more complicacies, since community procedural systems are not harmonized, neither in their administrative rules, nor in their civil proceedings, which are all involved in the European antitrust network. Therefore, antitrust proceedings end un as being more jurisdictional in their effects than in their guarentees, which is a flaw to be mended by legislators. National laws shoud be harmonized, community law should be clarified and the system should turn more honestly towards a rationalized jurisdiction-cented mechanism. Otherwise, parties defense rights and the overall efficiency are put into doubt. Italy is a good exemple of how many colmlicacies can outburst from national procedures and national decentralised application. An uncertain pattern of judicial control, together with unclear relationships among the institutions to cooperate in the antitrust network can produce more problems than they aim to solve. As to the private enforcement, Regulation n.1 does not even attempt to give precise regulation to this underdeveloped sector. A continual comparison with U.S. system has brought the Commission to become aware both of the risks and of the advanteges of an increased civil antitrust litigation in fronto of national judges. In order to substain a larger development of this parallel and, presently, difficult way of judicial compensation, it is presently ongoing a consultation among states to find suitable incentives to make private enforcement more appealing and effective. The solution to this lack of private litigation is not to be sought in Regulation n. 1 which calls into action national legislators and proceedures to implement further improvements. As a conclusion, Regulation n. 1 is the outpost of an ambitious community design to create an efficient control mechanism over antitrust violations. It focuses on Commission proceedings, powers and sanctions in order to establish deterrence, then it highlights civil litigation perspectives and it involves directly states into antitrust application. It seems that more could be done to technically shape administrative proceedings in a more jurisdictionally oriented form, then to clarify respective roles and coordination mecanisms in order to prevent difficulties easy to forsee. Some of jurisprudential suggestions have been accepted, but much more is left to be done in the future to improve european antitrust enforcement system.

A simple voltage/mass index increases the suspicion of amyloidotic cardiomyopathy: an electrocardiographic and echocardiographic study of 767 patients with increased left ventricular wall thickness due to different causes

Background-Amyloidotic cardiomyopathy (AC) can mimic true left ventricular hypertrophy (LVH), including hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD). We assessed the diagnostic value of combined electrocardiographic/echocardiographic indexes to identify AC among patients with increased echocardiographic LV wall thickness due to either different etiologies of amyloidosis or HCM or HHD. Method-First, we studied 469 consecutive patients: 262 with biopsy/genetically proven AC (with either AL or transthyretin (TTR)-related amyloidosis); 106 with HCM; 101 with HHD. We compared the diagnostic performance of: low QRS voltage, symmetric LVH, low QRS voltage plus interventricular septal thickness >1.98 cm, Sokolow index divided by the cross-sectional area of LV wall, Sokolow index divided by body surface area indexed LV mass (LVMI), Sokolow index divided by LV wall thickness, Sokolow index divided by (LV wall/height^2.7); peripheral QRS score divided by LVMI, Peripheral QRS score divided by LV wall thickness, Peripheral QRS score divided by LV wall thickness indexed to height^2.7, total QRS score divided by LVMI, total QRS score divided by LV wall thickness; total QRS score divided by (LV wall/height^2.7). We tested each criterion, separately in males and females, in the following settings: AC vs. HCM+HHD; AC vs. HCM; AL vs. HCM+HHD; AL vs. HCM; TTR vs. HCM+HHD; TTR vs. HCM. Results-Low QRS voltage showed high specificity but low sensitivity for the identification of AC. All the combined indexes had a higher diagnostic accuracy, being total QRS score divided by LV wall thickness or by LVMI associated with the best performances and the largest areas under the ROC curve. These results were validated in 298 consecutive patients with AC, HCM or HHD. Conclusions-In patients with increased LV wall thickness, a combined ECG/ echocardiogram analysis provides accurate indexes to non-invasively identify AC. Total QRS score divided by LVMI or LV wall thickness offers the best diagnostic performance.

Relationship between aetiology and left ventricular systolic dysfunction in hypertrophic cardiomyopathy

Background: Hypertrophic cardiomyopathy (HCM) is a common cardiac disease caused by a range of genetic and acquired disorders. The most common cause is genetic variation in sarcomeric proteins genes. Current ESC guidelines suggest that particular clinical features (‘red flags’) assist in differential diagnosis. Aims: To test the hypothesis that left ventricular (LV) systolic dysfunction in the presence of increased wall thickness is an age-specific ‘red flag’ for aetiological diagnosis and to determine long-term outcomes in adult patients with various types of HCM. Methods: A cohort of 1697 adult patients with HCM followed at two European referral centres were studied. Aetiological diagnosis was based on clinical examination, cardiac imaging and targeted genetic and biochemical testing. Main outcomes were: all-cause mortality or heart transplantation (HTx) and heart failure (HF) related-death. All-cause mortality included sudden cardiac death or equivalents, HF and stroke-related death and non-cardiovascular death. Results: Prevalence of different aetiologies was as follows: sarcomeric HCM 1288 (76%); AL amyloidosis 115 (7%), hereditary TTR amyloidosis 86 (5%), Anderson-Fabry disease 85 (5%), wild-type TTR amyloidosis 48 (3%), Noonan syndrome 15 (0.9%), mitochondrial disease 23 (1%), Friedreich’s ataxia 11 (0.6%), glycogen storage disease 16 (0.9%), LEOPARD syndrome 7 (0.4%), FHL1 2 (0.1%) and CPT II deficiency 1 (0.1%). Systolic dysfunction at first evaluation was significantly more frequent in phenocopies than sarcomeric HCM [105/409 (26%) versus 40/1288 (3%), (p<0.0001)]. All-cause mortality/HTx and HF-related death were higher in phenocopies compared to sarcomeric HCM (p<0.001, respectively). When considering specific aetiologies, all-cause mortality and HF-related death were higher in cardiac amyloidosis (p<0.001, respectively). Conclusion: Systolic dysfunction at first evaluation is more common in phenocopies compared to sarcomeric HCM representing an age-specific ‘red flag’ for differential diagnosis. Long-term prognosis was more severe in phenocopies compared to sarcomeric HCM and when comparing specific aetiologies, cardiac amyloidosis showed the worse outcomes.