Monozentrische echokardiographische Analyse des linksventrikulären „reverse remodeling“ während der ersten 42 Monate kardialer Resynchronisationstherapie bei Patienten mit nicht-ischämisch und ischämisch bedingter linksventrikulärer Dysfunktion

In patients with heart failure, ventricular conduction delays mostly caused by left bundle branch block (LBBB) may have a deleterious effect on pre-existing left ventricular dysfunction. The mechanical consequences of dyssynchrony include reduction of left ventricular (LV) contractile force, a reduction in ejection fraction (EF), functional mitral regurgitation and a shortened left ventricular filling time. Dyssynchronous ventricular contraction can be addressed by electrically activating both ventricles in a synchronized manner using biventricular pacing devices (cardiac resynchronization therapy = CRT) with or without defibrillator backup (CRT-P or CRT-D). Re synchronized activation of the ventricles can improve cardiac function and reduce left ventricular end-systolic and end-diastolic volumes as well as mitral regurgitation. These effects are called “reverse remodeling”. Short-term results of CRT appear to be promising, but there are still only few studies analyzing the long-term results of this therapy. Therefore, further studies are needed to determine, whether reverse LV remodeling leads to better long-term symptomatic and prognostic outcome. The aim of the current study was to evaluate the relation between the extent of left ventricular reverse remodeling after 12 months of cardiac resynchronization therapy and its long-term success evaluated at 42 months of CRT. A total of 42 patients with advanced heart failure were investigated. Echocardiography was performed to measure LV volumes, to calculate left ventricular ejection fraction and to assess the severity of mitral regurgitation before onset of cardiac resynchronization therapy as well as at 12, 24, 30, 36 and 42 months thereafter. The echocardiographic data collected at baseline prior to CRT and after 12 and 24 month of CRT had already been analyzed in two preceding study projects and were kindly provided for the current project. Most of the echocardiographic data collected at the 30, 36 and 42 month follow-ups had already been stored on Magneto Optical Disks. I analyzed the echocardiographic image material and organized and supported the echocardiographic image acquisition of the remaining follow-ups. My results were reviewed and validated by an experienced cardiologist who was unaware of patient identity and therapy information. The underlying cardiac diagnosis was dilated cardiomyopathy in 32 patients (76,2 %) and ischaemic heart disease in 10 patients (23,8 %). Most patients with dilated cardiomyopathy have had an endomyocardial biopsy in the course of their medical history, some patients long before the beginning of CRT. The existing biopsy results were thoroughly analyzed to discriminate whether a patient´s cardiac function and structure had improved because of spontaneous or therapy-associated healing myocarditis or whether cardiac function and structure had improved due to CRT. The analysis showed, that the documented improvement in cardiac function and structure in this study is very unlikely linked to spontaneous or therapy-linked healing of an underlying myocarditis. After 12 months of CRT patients were stratified according to the extent of LV reverse remodeling, as measured by the reduction of patients’ LV endsystolic volume. The magnitude of LV reverse remodeling varied significantly among patients. Patients who showed ≤ 15% reduction in LV endsystolic volume after one year of CRT were classified as nonresponders (12 patients (28,6%)). Patients with a reduction in LV endsystolic volume by 15% to 29% were classified as responders 15 (9 patients (21,4 %)). Patients with a reduction in LV endsystolic volume by ≥ 30 % were classified as responders 30 (21 patients (50 %)). Later than 12 months of CRT only minor changes of LV Volumes were observed. This means that LV reverse remodeling appears to be largely completed after 12 months of CRT and that it is quite stable thereafter. Particularly in responder 30 patients the echocardiographic improvement of LV function persisted over the entire follow-up period of 42 months. Mortality was assessed after a mean follow-up-time of 68 months (5,7 years). During that period of time seven patients (58,3 %) of the nonresponder group and four patients (44,4 %) of the responder 15 group died. During the entire follow-up period of 68 months only one patient (4,8 %) of the responder 30 group died. This group differed obviously from the two other groups with respect to long-term survival. For the responder 30 group the extent of LV reverse remodeling after 12 months of CRT was associated with a favorable long-term survival. The question why some patients showed extensive reverse remodeling, whereas others experienced less or no reverse remodeling, must of course remain unanswered even after this study. Further large controlled clinical trials addressing this interesting issue are needed.