Chronotropic incompetence in patients with an implantable cardioverter defibrillator: prevalence and predicting factors.

Chronotropic incompetence (CI), which has not been systematically examined in the ICD patient population, may have implications for device programming. A total of 123 ICD patients were classified into three groups: single-chamber ICD with sinus rhythm, dual-chamber ICD with sinus rhythm, and single-chamber ICD with permanent atrial fibrillation. Heart rate response, maximum oxygen uptake, and oxygen uptake at the anaerobic threshold were measured during treadmill exercise testing. In addition, clinical variables such as antiarrhythmic drug therapy, underlying heart disease, and left-ventricular (LV) ejection fraction were recorded. Of the patients studied, 38% were chronotropically incompetent (47/123). Significant predictors of CI were as follows: presence of a coronary disease (P = 0.036), prior cardiac surgery (P = 0.037), chronic drug therapy with beta-blockers (P = 0.032), administration of amiodarone (P = 0.025), and a combination of these two forms of treatment (P = 0.01). Spiroergometry revealed reduced exercise capacity (P = 0.041) and lessened VO2max (P = 0.034) among chronotropically incompetent patients. A large percentage of ICD patients demonstrates CI with subsequently reduced physical stress tolerance. In light of the DAVID study, we believe that a closer examination of rate-adaptive modes for ICD patients is warranted under enhanced conditions: (1) optimized AV interval programming; (2) utilization of new algorithms to reduce ventricular pacing in combination with rate-adaptive atrial pacing, with the goal of addressing CI while minimizing ventricular pacing; and (3) an optimized upper heart-rate limit.

Reduction of morbidity by immunoadsorption therapy in patients with dilated cardiomyopathy.

BACKGROUND: In patients with dilated cardiomyopathy (DCM) and severe congestive heart failure, immunoadsorption (IA) and subsequent IgG substitution leads to an acute and prolonged hemodynamic improvement. Goal of this study was to investigate the long-term effect of immunoadsorption on morbidity. METHODS: In a retrospective analysis of 34 patients (17 patients who have received immunoadsorption therapy and 17 control patients) were included. Inclusion criteria were DCM, left ventricular ejection fraction less than 35%, NYHA classes II-III. The average time after immunoadsorption was 3.0 years (median 2.3 years). Both groups did not differ concerning sex, age, duration of disease, medication, baseline ejection fraction and NYHA class. RESULTS: In patients who have received immunoadsorption (IA) the days of hospitalisation for congestive heart failure per year could be significantly reduced in contrast to the control patients (17.2 days prior to IA, 4.3 days after IA). Even if the procedural days for immunoadsorption were included there was still a significant reduction of hospitalisation if IA therapy was longer than 2.5 years ago. The days of hospitalisation increased gradually with time during the follow up period. IA induced an acute increase in EF (19.8-25.7%, p<0.01 vs. baseline). CONCLUSION: IA not only leads to an acute hemodynamic improvement in patients with DCM but may also reduce morbidity in these patients during the next 3 years.

Potential role of humoral immunity in cardiac dysfunction of patients suffering from dilated cardiomyopathy.

OBJECTIVES: This research was conducted to evaluate the role played by the humoral immune system in cardiac dysfunction among dilated cardiomyopathy (DCM) patients, as enabled by immunoadsorption therapy (IA) that effectively removes functionally active cardiac autoantibodies from plasma. BACKGROUND: Various circulating autoantibodies have been detected among patients suffering from DCM. METHODS: Before IA, antibodies were purified from plasma of 45 DCM patients (left ventricular ejection fraction [LVEF] <30%). We analyzed the functional effects of antibodies (300 mg/l) on calcium transients and on systolic cell shortening in adult rat cardiomyocytes. After this in vitro analysis, IA was performed in four courses at one-month intervals until month 3. RESULTS: Antibodies from 29 patients induced a reduction (>10%) in calcium transients (mean reduction: -16.5 +/- 1.9%) and a simultaneous reduction (>10%) of cell shortening (mean reduction: -21.2 +/- 1.8%) on cardiomyocytes (p < 0.001) (cardiodepressant group). Antibodies from 16 patients did not significantly influence calcium transients and cell shortening (<10%) (non-cardiodepressant group). During the first IA course, the cardiodepressant group demonstrated an acute increase in cardiac index (CI) from 2.2 +/- 0.1 l/min/m(2) to 2.9 +/- 0.1 l/min/m(2) (p < 0.001). In the non-cardiodepressant group, hemodynamics did not significantly change throughout three months. After three months before the final IA course (prolonged effects), the CI was 2.1 +/- 0.1 l/min/m(2) in the non-cardiodepressant group and 2.9 +/- 0.1 l/min/m(2) in the cardiodepressant group (p < 0.001). After three months LVEF increased only in the cardiodepressant group: from 20.8 +/- 1% to 30.5 +/- 1% (p < 0.01). CONCLUSIONS: In the majority of DCM patients, disturbances of humoral immunity with production of cardiodepressant antibodies may play a functional role in cardiac dysfunction. Evidence of cardiodepressant antibodies predicts hemodynamic benefits during IA.