[Cardiac contractility modulation for treatment of chronic heart failure]. / Kardiale Kontraktilitätsmodulation zur Behandlung der chronischen Herzinsuffizienz.

The worldwide prevalence of heart failure is 1-2% with a portion of >10% in patients older than 70 years. In addition to treatment of causal determined factors and lifestyle modification, basic treatment consists of guideline-directed medical therapy with angiotensin-converting enzyme inhibitors (ACE), ß­blockers (BB), mineralocorticoid receptor antagonists (MRA), diuretics, digitalis (class IIb recommendation), angiotensin receptor blockers (ARB), Iƒ-channel blockers plus recently recommended in the guidelines angiotensin receptor neprilysin inhibitor (ARNI) to substitute the ACE inhibitor (class I b). Cardiac contractility modulation (CCM) is a device-based electrical therapy for the treatment of refractory heart failure symptoms. CCM signals are relatively high intensity, nonexcitatory signals applied during the absolute refractory period that have been shown to enhance the strength of left ventricular (LV) contraction and improve exercise tolerance and quality of life. The mechanisms of action appear to involve effects on myocardial gene expression and normalization of myocardial key-proteins. So far, more than 3500 CCM devices have been implanted worldwide. For patients with symptomatic heart failure and narrow QRS complex, CCM is together with baroreceptor activation the only additive electrical therapy which had been approved in Germany. Actually, for the first time, CCM has been referenced in the current Heart Failure Guidelines. Prognostic data with regard to mortality are currently being evaluated in case series; some of which have since been published. Approval by the US Food and Drug Administration (FDA) is expected within the next months.

[Cardiac contractility modulation]. / Kardiale Kontraktilitätsmodulation.

Cardiac contractility modulation (CCM) is a device-based electrical therapy for the additive treatment of chronic drug-refractory heart insufficiency. High-amplitude signals are applied during the absolute refractory period and have been shown to enhance the strength of left ventricular (LV) contraction and improve exercise tolerance and quality of life. The mechanisms of action appear to involve effects on myocardial gene expression and on normalization of key myocardial proteins. So far, more than 3500 CCM devices have been implanted worldwide. For patients with therapy refractory heart insufficiency and narrow QRS complex, CCM is together with baroreceptor activation the only additive electrical therapy which had been approved in Germany. For the first time CCM has been referenced in the current guidelines on cardiac insufficiency. Prognostic data with respect to mortality have been evaluated in case series. Ongoing randomized trials and registries will address these specific endpoints and have to a significant extent already been recently published. A Food and Drug Administration (FDA) approval is expected within the next few months.

[Current impact of cardiac implantable electronic devices]. / Aktueller Stellenwert der Device-Therapie.

Sudden cardiac death and chronic heart failure are among the main contributors to persisting high mortality rates in Germany. In addition to removal of causal factors and guideline-conform pharmacological therapy, therapy with cardiac implantable electronic devices (CIED) is of undisputed importance. Subcutaneous defibrillators have the advantage that they do not have intracardiac electrodes but still have the same efficacy and safety. For patients with a wide QRS complex and reduced ejection fraction, cardiac resynchronization has led to a reduction of morbidity and mortality. For patients with a normal QRS complex, cardiac contractility modulation had been shown to improve the quality of life, exercise capacity and left ventricular function. As a procedure for autonomic modulation in patients with reduced cardiac strength, the data for baroreceptor stimulation are the most convincing.

[Sudden cardiac death : Epidemiology, pathophysiology and risk stratification]. / Plötzlicher Herztod : Epidemiologie, Pathophysiologie und Risikostratifizierung.

Sudden cardiac death (SCD) remains a major public health burden despite revolutionary progress in the last three decades in the treatment of ventricular tachyarrhythmia with the use of implantable cardioverter defibrillator (ICD) therapy. Survivors of sudden cardiac arrest are at high risk for recurrent tachyarrhythmia events. Early recognition of low left ventricular ejection fractions (≤35%) as a strong predictor of mortality and the causal association between ventricular tachyarrhythmia and SCD has led to a significant development of not only pharmacological antiarrhythmic therapy but also device-based prevention of SCD. The ICD therapy is nowadays routinely used for primary prevention of SCD in patients with significant structural cardiomyopathy and primary electrical arrhythmia syndromes, which are associated with high a risk and secondary prevention in survivors of sudden cardiac arrest. Additionally, effective approaches exist to significantly reduce the recurrence rate of ventricular tachyarrhythmia of various origins by complex electrophysiological endocardial and epicardial catheter ablation procedures.

[The subcutaneous cardioverter-defibrillator: When less is more]. / Der subkutane Kardioverter-Defibrillator : Weniger ist mehr.

INTRODUCTION: In the last few decades, defibrillator therapy has revolutionized treatment of patients at risk for sudden cardiac death. Multiple clinical trials have shown the benefit of implantable cardioverter-defibrillators (ICD) for primary and secondary prevention of sudden cardiac death. Being an entirely subcutaneous system, the S-ICD® avoids important periprocedural and long-term complications associated with transvenous implantable cardioverter-defibrillator (TV-ICD) systems as well as the need for fluoroscopy during implant surgery. METHODS AND RESULTS: In patients with challenging anatomic conditions or after infection, the S-ICD® might be reasonable. In multicenter studies and registries efficacy and safety of the S-ICD® was equal or better to transvenous implantable defibrillators. The cardiac rhythm is detected by the use of 1 of the 3 potential vectors. The S-ICD® automatically selects the most suitable vector for rhythm detection. If ventricular tachyarrhythmia is detected, the device is able to deliver up to five shocks of 80 J, while postshock pacing is available at 50 bpm for 30 s. The implantation technique is different from that of conventional ICDs, but easily learnable by experienced cardiologists. Initially observed hurdles (e.g., inappropriate shocks or infections) have been overcome by standardized implantation techniques, operator learning curves, and modification of algorithms. CONCLUSIONS: The S-ICD® predominately might be suitable in all patients with ICD indication except patients with pacing or cardiac resynchronization therapy (CRT) indication, ventricular tachycardia < 170 bpm, negative screening, or in the occasional patient whose arrhythmia might be suppressed by overdrive pacing. The system received CE certification in 2009 and was approved by the FDA in 2012. Currently, in Germany the S-ICD® has been integrated into the DRG system and can be reimbursed as a single chamber ICD.

CMR-derived TAPSE measurement: a semi-quantitative method of right ventricular function assessment in patients with hypertrophic cardiomyopathy.

AIM: To compare cardiovascular magnetic resonance (CMR)-derived right ventricular fractional shortening (RVFS), tricuspid annular plane systolic excursion with a reference point within the right ventricular apex (TAPSEin) and with one outside the ventricle (TAPSEout) with the standard volumetric approach in patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: 105 patients with HCM and 20 healthy subjects underwent CMR. In patients with HCM, TAPSEin (r = 0.31, p = 0.001) and RVFS (r = 0.35, p = 0.0002) revealed a significant but weak correlation with right ventricular ejection fraction (RVEF), whereas TAPSEout (r = 0.57, p < 0.0001) showed a moderate correlation with RVEF. The ability to predict RVEF < 45 % in HCM patients was best for TAPSEout. In patients with hypertrophic obstructive cardiomyopathy (HOCM), RVEF showed a significant but weak correlation with TAPSEout (r = 0.36, p = 0.02) and no correlation with TAPSEin (r = 0.05, p = 0.07) and RVFS (r = 0.02, p = 0.2). In patients with hypertrophic non-obstructive cardiomyopathy (HNCM), there was a moderate correlation between RVEF and TAPSEout (r = 0.57, p < 0.0001) and a weak correlation with TAPSEin (r = 0.39, p = 0.001) and RVFS (r = 0.38, p = 0.002). In the 20 healthy controls, there was a strong correlation between RVEF and all semi-quantitative measurements. CONCLUSION: CMR-derived TAPSEin is not suitable to determine right ventricular function in HCM patients. TAPSEout showed a good correlation with RVEF in HNCM patients but only a weak correlation in HOCM patients. TAPSEout might be used for screening but the detection of subtle changes in RV function requires the 3D volumetric approach.