Biomedical subjects

Peter Sogaard

Publications and source records attributed to Peter Sogaard.

4 recordsLinked to original sources

PubMed2004

Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? A critical appraisal.

Cardiac resynchronization therapy (CRT) has been proposed as an alternative treatment in patients with severe, drug-refractory heart failure. The clinical results are promising, and improvement in symptoms, exercise capacity, and systolic left ventricular (LV) function have been demonstrated after CRT, accompanied by a reduction in hospitalization and a superior survival as compared with optimized medical therapy alone. However, 20% to 30% of patients do not respond to CRT. Currently, patients are selected mainly on electrocardiogram criteria (wide QRS complex, left bundle branch block configuration). In view of the 20% to 30% of nonresponders, additional selection criteria are needed. Echocardiography (and, in particular, tissue Doppler imaging) may allow further identification of potential responders to CRT, based on assessment of inter- and intraventricular dyssynchrony. In addition, echocardiography may allow optimal LV lead positioning and follow-up after CRT. In the current review, the different echocardiographic approaches to predict response to CRT are discussed. In addition, the use of echocardiography to guide LV lead positioning and follow-up after CRT are addressed.

Clinical Trials as Topic↗

PubMed2004

Delay in right ventricular activation contributes to Brugada syndrome.

BACKGROUND: Although Brugada syndrome revolves around reduced net depolarizing force, the electrophysiological mechanisms of its defining features (right precordial ST-segment elevation and ventricular tachyarrhythmias) remain unresolved. Two proposed mechanisms are (1) right ventricular (RV) conduction delay and (2) selective and significant RV subepicardial action potential shortening. Both mechanisms must cause disparate contractile changes: delay in RV contraction and reduction of contractile force, respectively. We aimed to establish the electrophysiological mechanism of Brugada syndrome by studying the timing and force of RV contraction. METHODS AND RESULTS: Using tissue Doppler echocardiography, we studied how these contractile variables change on induction of the characteristic ST-segment changes of Brugada syndrome by flecainide challenge. Accordingly, we studied patients in whom flecainide induced these changes (inducible) and those in whom these changes were not induced (control). We found that (1) the occurrence of a positive response (coved-type ST elevation) after flecainide coincides with delay in the onset of contraction between the RV and left ventricle (LV); (2) the extent of contraction delay between RV and LV correlates with the magnitude of ST elevation; and (3) RV ejection time (duration of RV ejection phase) shortens as the Brugada ECG pattern emerges. CONCLUSIONS: These results indicate that both proposed mechanisms of Brugada syndrome may be operative.

Action Potentials↗

PubMed2004

Sequential biventricular pacing: evaluation of safety and efficacy.

The study evaluated the clinical safety, performance, and efficacy of sequential biventricular pacing in the InSync III (Model 8042) biventricular stimulator in a multicenter, prospective 3-month study and assessed the proper functioning of features aiming at improving biventricular AV therapy delivery. The system was successfully implanted in 189 (95.9%) of 198 patients with symptomatic systolic heart failure and a prolonged QRS complex duration. Patients significantly improved their 6-minute hall walk distance (baseline 339 +/- 92 vs 3-month 422 +/- 127 meter, P < 0.001) and NYHA class (baseline 3.1 +/- 0.5 vs 3-month 1.9 +/- 0.7, P < 0.001). Echocardiographic optimization of sequential biventricular pacing showed an improvement in stroke volume compared to simultaneous stimulation (sequential 68 +/- 24 mL vs simultaneous 56 +/- 23 mL, P < 0.001) at baseline and at 3 months. In 88% (30/34) of the patients these improvements were seen within a small range of V-V delays of +/-20 ms and in 94% (32/34) within V-V delays of +/-40 ms. In contrast, programming beyond this range reduced stroke volume below that during simultaneous biventricular pacing. The device functioned as expected. LV lead dislodgement was observed in 12 patients and phrenic nerve stimulation required lead repositioning in 2 patients. Eight patients died during the study. Patient survival at 3 and 6 months was 97 +/- 2% and 94 +/- 2%, respectively. Cause of death was cardiac (n = 7), heart failure related (n = 3), arrhythmia related (n = 2), and unknown (n = 2). In conclusion, this sequential biventricular pacemaker was safe and efficacious.

Aged↗

PubMed2002

Sequential versus simultaneous biventricular resynchronization for severe heart failure: evaluation by tissue Doppler imaging.

BACKGROUND: Cardiac resynchronization therapy (CRT) by means of simultaneous biventricular pacing improves left ventricular systolic performance and synchrony in patients with heart failure and bundle-branch block. We used tissue tracking and 3D echocardiography to evaluate the impact of sequential CRT with individualized interventricular delay programming. METHODS AND RESULTS: Twenty consecutive patients with severe heart failure and left bundle-branch block were included. Tissue tracking and 3D echocardiography were carried out before and on the day after pacemaker implantation. Eleven different interventricular delays were examined in each patient. Patients were reexamined after 3 months. Simultaneous CRT immediately reduced the extent of myocardium displaying delayed longitudinal contraction (DLC) from 48.6+/-16% to 23.2+/-13% (P<0.01) and increased left ventricular ejection fraction percentage (LVEF%) from 22.4+/-6% to 29.7+/-5% (P<0.01). However, optimum sequential CRT caused a further reduction in the extent of DLC from 23.2+/-13% to 11.1+/-7.2% (P<0.01), with a simultaneous increase in LVEF% (from 29.7+/-5% to 33.9+/-6%, P<0.01). Three months of optimum sequential CRT further improved LVEF% (from 33.6+/-6% to 38.6+/-7.2%, P<0.01). Tissue tracking detected the segments with DLC, and their location determined optimum interventricular delay programming. Compared with simultaneous CRT, sequential CRT increased diastolic filling time by 7+/-2.5%. CONCLUSIONS: Compared with simultaneous CRT, sequential CRT significantly improves left ventricular systolic and diastolic performance. Tissue tracking can be used to select optimum interventricular delay during CRT.

Aged↗