ECG is not a reliable predictor of sudden cardiac death in the general population

Objectives: To determine the predictive value of the ECG for sudden death in the general population. Design: In the Copenhagen City Heart Study, a randomly selected population sample in Copenhagen, Denmarkhas been followed prospectively since 1976. From this population sample, we analyzed ECGs of individuals who had suffered sudden cardiac death (SCD) before the age of 50 years and compared them with ECGs of a randomly selected control individuals from the same population sample. Specific ECG signs that could point toward a condition associated with a risk of SCD were noted. Results: From a total of 18,974 individuals in the cohort, 207 had died at an age younger than 50 years. Among these, 24 persons with SCD were identified. The most prevalent ECG abnormality was QRS fragmentation. We found no ECGs with long or short QTc, Brugada sign or WPW. The prevalence of signs of left ventricular hyper-trophy, early repolarization, or fragmentation was not different from the prevalence of these signs in the control group. Conclusion: In the Copenhagen City Heart Study, the ECG failed to predict SCD in persons who died before the age of 50 years.

Pacemaker implantation in a patient with brugada and sick sinus syndrome

Brugada syndrome (BrS) is a rare and inherited primary arrhythmic syndrome characterized by ST-segment elevations in the right precordial leads (V1 -V3 ) with an increased risk of sudden cardiac death (SCD). Arrhythmias in BrS are often nocturne, and brady-arrhythmias are often seen in patients with loss-of-function mutations in SCN5A . In this case-report we present a 75-year old woman referred to our outpatient clinic for inherited cardiac diseases for a familial clinical work-up. Since childhood she had suffered from dizziness, absence seizures, and countless Syncope's. In 2004 sick sinus syndrome was suspected and she wastreated with implantation of a pacemaker (PM) at another institution. An inherited cardiac disease was one day suddenly suspected, as the patient had a 61-year old brother who was diagnosed with symptomatic BrS, and treated with an implantable cardioverter defibrillator (ICD) after aborted SCD. A mutation screening revealed a SCN5A [S231CfsX251 (c.692-693delCA )] loss-of-function mutation not previously reported, and as a part of the cascade screening in relatives she was therefore referred to our clinic. In the 7 year period after PM implantation she had experienced no cardiac symptoms, although her electrocardiogram changes now were consistent with a BrS type 1 pattern. A genetic test confirmed that she had the same mutation in SCN5A as her brother. In this case-report we present a loss-of function mutation in SCN5A not previously associated with BrS nor presented in healthy controls. Sinus node dysfunction has previously been documented in patients with symptomatic BrS, which suggests it is not a rare concomitant. The only accepted treatment of BrS is today implantation of an ICD. In the future studies should evaluate if PM in some cases of symptomatic BrS can be used instead of ICDs in patients with a loss-of-function SCN5A

Clinical valve thrombosis and subclinical leaflet thrombosis in transcatheter aortic heart valves:clinical manifestations,diagnosis,and treatment

During the last decade,transcatheter aortic valve replacement(TAVR)has rapidly expanded as an alternative to surgical aortic valve replacement(SAVR)in patients with symptomatic severe aortic valve stenosis(AS)and increased surgical risk.In TAVR,a bioprosthetic valve is positioned within the stenotic native aortic valve.Although favorable short-and medium-term outcomes have been reported,thrombosis of the transcatheter heart valve(THV)has occurred,with two different entities being described:clinical valve thrombosis and subclinical leaflet thrombosis.In clinical valve thrombosis,an increase in transvalvular gradient appears as a result of obstructive thrombus formation,which eventually leads to symptoms of heart failure.Subclinical leaflet thrombosis is an incidental finding,characterized by a thin layer of thrombus covering the aortic site of the leaflet—called hypoattenuating leaflet thickening(HALT)—as described on and defined by 4-dimensional computed tomography(4DCT)imaging.This phenomenon may affect motion of the leaflets and is then classified as hypo-attenuation affecting motion(HAM).Even in the case of HAM,the transvalvular pressure gradient remains within the normal range.Clinical valve thrombosis requires treatment,whereas the clinical impact and need for intervention in subclinical leaflet thrombosis is uncertain.Anticoagulant therapy protects against and resolves both clinical valve thrombosis and subclinical leaflet thrombosis,but studies exploring different antithrombotic strategies after TAVR are ongoing.This review summarizes currently available literature within the field of THV thrombosis and provides recommendations for a patient-tailored approach in TAVR patients,although guidelines are still lacking.

Plasma natriuretic peptides during supraventricular tachycardia: A study in patients with atrioventricular nodal reentry tachycardia

Aims: To characterize the plasma levels of the atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in patients with atrioventricular nodal reentry tachycardia (AVNRT), we measured the plasma levels of these peptides before and during tachycardia. Methods: We included 10 consecutive patients scheduled for ablation of typical AVNRT without structural heart disease. Catheters were inserted in the femoral artery, femoral vein, and coronary sinus (CS) prior to the ablation procedure. Blood samples were drawn before and after 3 min of tachycardia to measure plasma levels of ANP and BNP. Right atrial pressure (RAP) was measured at baseline. Results: Of the 10 patients, in three patients it was not possible to induce tachycardia leaving a total of 7 patients available for analysis. Mean age of the seven included patients was 40 ± 12 years (mean ± SD), five were female. ANP levels increased significantly during tachycardia in the artery (p = 0.0009) and vein (p = 0.003), but only borderline in CS (p = 0.09). BNP levels did not change during tachycardia in any location. Conclusion: ANP levels measured in the peripheral circulation increased acutely during tachycardia due to AVNRT. BNP levels did not increase.