Anatomical atrial septal defect (ASD) diameter measured by transesophageal echocardiography (TEE) underestimates the Amplatzer septal occluder (ASO) size for ASD closure. The aim of this study is to investigate whether a new echocardiographic diameter (procedural ASD diameter) may enable precise measurements of ASO device size. Fifty adult patients with secundum ASD were evaluated by TEE for percutaneous closure. The procedural ASD diameter was measured using the steadier rim borders where thickness was 2.5 mm. Out of the 50 patients, 12 were considered unsuitable for Amplatzer device closure. The other 38 patients underwent percutaneous closure. The mean anatomical ASD diameter was 14.8 +/- 7.0 mm, the mean procedural ASD diameter measured 19.5 +/- 8.1 mm, and the mean stretched balloon diameter (SBD) was 20.0 +/- 8.0 mm. ASO device size was 20.1 +/- 8.0 mm. At linear regression analysis, a high correlation (r = 0.99) was found between procedural ASD diameter and SBD. Procedural ASD diameter correlates with SBD and may allow reliable prediction of Amplatzer device in an adult population undergoing percutaneous ASD closure.

No abstract

We assessed the influence and clinical consequences of different AV delay on ventricular filling in 30 patients (mean age 60 +/- 5 years) who had DDD pacemakers for AV block. All 30 patients presented a normal ejection fraction, but in 18 cases (Group I), an echo-Doppler examination revealed ventricular hypertrophy (mean end-diastolic wall thickness of 1.4 +/- 0.16 cm, LV mass index 155 +/- 17 g/m2), and an abnormal relaxation pattern (isovolumetric relaxation time = 124.72 +/- 11.82; early to late peak velocity = 0.6 +/- 0.03; deceleration time = 296.83 +/- 34.02 ms). Group II included the remaining 12 patients who had a normal filling pattern. In all 30 patients, the pattern was reassessed following modification of the AV delay (200, 150, 100, and 75 ms). Patients at baseline (AV delay of 200 ms) also underwent an exercise test with determination of respiratory gas exchange. In Group I, 13 (72.5%) patients were classified as Weber class B (VO2 Max 16.8 +/- 1.7 mL/min per kg); and 5 (27.5%) were Class A (VO2 Max 22.5 +/- 1.4 mL/min per kg). In Group II, all 12 patients were classified as Weber Class A. In Group II, changes in AV delay caused no consistent variations in filling pattern, and therefore AV delay was not modified. In Group I patients, since reduction to 100 ms resulted in normalization of the filling pattern, the AV delay was programmed to 100 ms. A graded exercise test repeated after 6 months' follow-up showed an improved Weber class in 13 patients (from B to A) and greater VO2 Max in the remaining five already in Class A. We concluded that, in sequential paced patients with normal ejection fraction but abnormal relaxation pattern, modification in AV delay can induce normalization of filling and improvement in cardiac functional capacity.

This report presents a case of left ventricular intramyocardial dissection masquerading as a ventricular pseudoaneurysm. Only serial echocardiograms could lead to the correct diagnosis, and left ventricular angiography could appropriately direct further testing and treatment.

Le malattie cardiovascolari associate all’aterosclerosi sono la prima causa di mortalità e morbilità. Diversi studi evidenziano che il tessuto adiposo viscerale ha un ruolo importante nello sviluppo di uno stato infiammatorio sistemico che contribuisce al rischio cardiovascolare e allo sviluppo della patologia ischemica. I mediatori circolanti dell’infiammazione partecipano ai meccanismi del danno vascolare. Nei pazienti obesi tali sostanze sono secrete direttamente dagli adipociti e dai macrofagi del tessuto viscerale e dagli epatociti e contribuiscono all’insorgere dell’insulino-resistenza. Questa rassegna mostra come lo stato infiammatorio si associa ad insulino-resistenza e come questo agisca nella formazione della placca ateromasica. Inoltre, descrive come l’insulino-resistenza potenzia altri fattori di rischio cardiovascolare associati all’obesità; e suggerisce importanti raccomandazioni nella pratica clinica per i pazienti cardiovascolari con obesità viscerale