Norske abstracts preseNtert i stockholm P425 : Asymptomatic arrhyth- Reduced RV and LV strains indicate subclini- cal cardiac dysfunction in asymptomatic ARVC mogenic right ventricular mutation carriers and that strain echocardiog- cardio myopathy mutation car- raphy may be helpful in decisions regarding riers have impaired biventri- preventive treatment. cular function by myocardial strain P431 : Type of fibrosis predicts serious events in patients K.H. Haugaa (Dept of Cardiology, Oslo with obstructive hypertrophic University Hospital, Rikshospitalet, Oslo / Norway), S.I. Sarvari (Dept of Cardiology, cardiomyopathy Oslo University Hospital, Rikshospitalet, Oslo V.M. Almaas (Dept. og Cardiology, Oslo Uni- /Norway), O.G. Anfinsen (Dept of Cardiology, versity Hospital, Rikshospitalet, University Oslo University Hospital, Rikshospitalet, Oslo of Oslo, Oslo /Norway), E. Heyerdahl Strom /Norway), T.P. Leren (Dept of Medical Gene- (Dept. of Pathology, Oslo University Hospi- tics, Oslo University Hospital, Rikshospitalet, tal, Rikshospitalet, Oslo /Norway), H. Scott Oslo /Norway), O.A. Smiseth (Dept of Cardio- (Dept. of Pathology, Oslo University Hospital, logy, Oslo University Hospital, Rikshospitalet, Rikshospitalet, Oslo /Norway), C.P. Dahl Oslo /Norway), J.P. Amlie (Dept of Cardiology, (Research Institute for Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo Oslo University Hospital, Rikshospitalet, Oslo /Norway), T. Edvardsen (Dept of Cardiology, /Norway), T. Edvardsen (Dept. of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo Oslo University Hospital, Rikshospitalet, Oslo /Norway) /Norway), S. Aakhus (Dept. of Cardiology, Purpose: Life threatening arrhythmias can occur Oslo University Hospital, Rikshospitalet, Oslo prior to apparent ventricular dysfunction in /Norway), O.R. Geiran (Dept. of Thoracic arrhythmogenic right ventricular cardiomyopathy and Cardiovascular Surgery, Oslo University (ARVC) mutation carriers. Myocardial strain by Hospital, Rikshospitalet, Oslo /Norway), J.P. echocardiography is a sensitive tool for assessing Amlie (Dept. of Cardiology, Oslo University ventricular function. The purpose of this study Hospital, Rikshospitalet, Oslo /Norway) was to investigate right (RV) and left ventricular Purpose: Myocardial scarring (fibrosis) is an (LV) function by strain in asymptomatic ARVC established pathophysiological feature associ- mutation carriers not fulfilling current ARVC ated with markers of sudden cardiac death (SCD) criteria. in patients with hypertrophic cardiomyopathy Methods: We included 21 individuals (age 39±20 (HCM). The aim of this study was to describe years) positive for an ARVC related mutation the associations between pericellular and (18 Plakophilin2 and 3 Desmoplakin) diagnosed replacement-type fibrosis, serious events and by family genetic screening. 20 age matched risk factors for SCD in HCM-patients undergoing healthy individuals served as control group. septal myectomy. Strain measurements were assessed by speckle Methods: Twenty-four HCM-patients (54.2% tracking echocardiography. RV strain was calcu- men; mean age 58.0±10.4 years) underwent risk lated in a 6 segment model and LV global strain stratification for SCD followed by septal myec- in a 16 segment model. tomy. Risk factors for SCD: prior cardiac arrest; Results: ARVC mutation carriers had signifi- family history of SCD; unexplained syncope; cantly reduced strain in RV compared to healthy non-sustained ventricular tachycardia (nsVT); individuals (-21.8±3.5% vs. -24.5±3.3%, p=0.01). abnormal blood pressure response; hypertrophy In addition, LV strain was significantly reduced in ≥ 30 mm. Degree of pericellular and replacement mutation carriers compared to healthy individu- fibrosis was determined (percentage of total als (-20.4±1.6% vs. -22.4±2.6%, p<0.01). LVEF specimen) on histopathology of surgical speci- did not differ between ARVC mutation carriers men. Patients with earlier myocardial infarction and healthy (63±4% vs. 65±5%, p=0.21). were excluded. Conclusions: Asymptomatic ARVC mutation Results: Maximal interventricular septal thick- carriers with no signs of the disease by cur- ness was 1.9±0.3 cm, intraventricular gradient rent diagnostic guidelines had significantly was 57±23 mmHg, NYHA classification was reduced biventricular function assessed by strain 2.9±0.4 and CCS classification was 1.7±1.1. echocardiography although LVEF was normal. Patients with events (prior cardiac arrest, nsVT, hjerteforum N° 4 / 2010 / vol 23 54 unexplained syncope) had significantly higher ized epicardial ultrasonic transducer for detection median percentage area of pericellular fibrosis of graded myocardial ischaemia. than patients without events (30.0, range 17-62 Methods: Coronary bypass from left inter- v. 8.0, range 0-60, P=0.0094, Mann Whitney nal mammary artery (LIMA) to left anterior (Figure)). Patients with one or two risk factors descending coronary artery (LAD) was per- had significantly higher mean percentage area formed in six pigs to regulate coronary perfusion. of pericellular fibrosis than patients with no risk Intermittent ischaemia was induced by reducing factors (26.9±23.8 v. 9.9±6.2, P=0.034, unpaired LIMA-flow to 75%, 50% and 25% for 5 min. Sub- t-test). Replacement fibrosis was not associated endocardial peak systolic (Vsys) and postsystolic with events or with risk factors. (Vpst) velocities were continuously obtained by Conclusion: There is an association between two miniaturized epicardial ultrasonic transduc- increased area of pericellular fibrosis and serious ers (Ø=5mm) in the LAD and circumflex (Cx) events and risk factors for SCD in patients with area. In addition, radial strain was calculated as obstructive HCM. 2D strain by echocardiography. Left ventricular peak (LVP) and end-diastolic pressure (LVEDP) were measured with a micro- manometer. Values are given as median (interquartile range). Results: During all levels of flow reduction Vsys decreased significantly (p<0.05) from baseline, while Vpst increased at 50% and 25% flow (p<0.05) (fig.1A). These findings FIG Pericellular and replacement fibrosis correlate with systolic (R=0.89, p<0.01) and postsystolic (R=0.64, p<0.01) radial strain. No P473 : Systolic and postsystolic changes were seen in the Cx area. Moderate flow reduction (75% and 50%) did not affect hemo- velocities quantify low grade dynamic parameters, but a small decrease in LVP myocardial ischaemia by a (p<0.05) was seen when flow was reduced to miniaturized epicardial ultraso- 25% (fig.1B). nic sensor Conclusion: Mild and moderate myocardial ischaemia can be quantified by tissue velocity S. Hyler (University of Oslo, Faculty Division measurements from epicardial ultrasonic sen- Rikshospitalet University Hospital, Inter- sors. The findings are promising for continuously ventional Centre, Oslo /Norway), S. Pischke real-time monitoring of myocardial function dur- (University of Oslo, Faculty Division Rikshos- ing heart surgery, and with further miniaturizing pitalet University Hospital, Interventional of the sensor, also in the postoperative period. Centre, Oslo /Norway), P.S. Halv- orsen (University of Oslo, Faculty Division Rikshospitalet University Hospital, Interventional Centre, Oslo /Norway), A. Espinoza (University of Oslo, Faculty Division Rikshospitalet University Hospital, Interventional Centre, Oslo /Norway), S. Hestenes (University of Oslo, Faculty Division Rikshospitalet University Hospital, Interventional Centre, Oslo /Nor- way), J. Bergsland (University of Oslo, Faculty Division Rikshospitalet University Hospital, Interventional Centre, Oslo /Norway), E. Fosse (University of Oslo, Faculty Division Rikshospitalet Uni- P631 : Phosphorylation of versity Hospital, Interventional Centre, Oslo syndecan-4 acts as a molecular /Norway), H. Skulstad (University of Oslo, switch of the pro-hypertrophic Faculty Division Rikshospitalet University Hospital, Department of Cardiology, Oslo / calcineurin-NFAT signalling Norway) pathway in the myocardium Background: Early detection of myocardial I.G. Lunde (Institute for Experimental Medical ischaemia during heart surgery is essential to Research, Ullevaal University Hospital, Oslo preserve ventricular function. More sensitive /Norway), A.V. Finsen (University of Oslo, methods for continuous assessment of myocar- Faculty Division Rikshospitalet University dial function are required. We tested a miniatur- 55 hjerteforum N° 4/ 2010 / vol 23 Hospital, Department of Cardiology, Oslo / ing minimally phosphorylated S179 (S179A) Norway), H. Jarstadmarken (Institute for whereas S179D/E mutations did not. Finally, we Experimental Medical Research, Ullevaal recently found that overexpression of calcineurin University Hospital, Oslo /Norway), H. Kvaloy in HEK293 reduces pS179, indicating that calci- (Institute for Experimental Medical Research, neurin regulates its own binding and activation. Ullevaal University Hospital, Oslo /Norway), Conclusions: Our results indicate that in a pres- A. Hasic (Institute for Experimental Medical sure-overloaded heart, serine 179 in syndecan-4 Research, Ullevaal University Hospital, Oslo is dephosphorylated by calcineurin, and calci- /Norway), I. Sjaastad (University of Oslo, neurin binds to the intracellular V-region through Faculty Division Ulleval University Hospital, its autoinhibitory domain. Increased binding of Department of Cardiology, Oslo /Norway), calcineurin to syndecan-4 results in activation T. Tonnesen (Department of Cardiothoracic of NFATc4, a well-known pro-hypertrophic tran- Surgery,