Impedance cardiography: a useful and reliable tool in optimization of cardiac resynchronization devices.

AIMS: Optimizing cardiac resynchronization therapy (CRT) devices has become more complex since modification of both atrioventricular (AV) and interventricular (VV) stimulation intervals has become possible. The current paper presents data from the routine use of impedance cardiography (IC)-based cardiac output (CO) measurements to guide the optimization of AV- and VV-interval timing of CRT devices. METHODS AND RESULTS: Forty-six patients with heart failure (left ventricular ejection fraction <35%, New York Heart Association (NYHA) III-IV) and left bundle branch block (>130 ms) in sinus rhythm were evaluated 3-5 days after implantation of a CRT device by means of IC. CO was measured without pacing and with biventricular pacing using a standard protocol of VV- and AV-interval modification from -60 to +60 ms and 80 to 140 ms, respectively, in 20 ms steps. Mean CO without pacing was 3.66 +/- 0.85 L/min and significantly increased to 4.40 +/- 1.1 L/min (P<0.05) with simultaneous biventricular pacing and an AV interval of 120 ms. 'Optimizing' both VV and AV intervals further increased CO to 4.86 +/- 1.1 L/min (P<0.05). Maximum CO was measured in most patients with left ventricular pre-excitation. The proportion of 'non-responders' to CRT was reduced by 56% following AV- and VV-interval modification using IC guidance. CONCLUSION: Modification of both AV and VV intervals in patients with a CRT device significantly improves CO compared with standard simultaneous biventricular pacing and no pacing. IC is a useful non-invasive technique for guiding this modification. Marked variability of optimal AV and VV intervals between patients requires optimization of these intervals for each patient individually.

Septic cardiomyopathy - A not yet discovered cardiomyopathy?

Myocardial depression in human sepsis was only unequivocally proven in the 1980s by the group of Parrillo, who used nuclear imaging techniques to measure heart volumes and function in intensive care patients. Heart failure in sepsis is frequently masked by a seemingly normal cardiac output. However, relative to the lowered systemic vascular resistance - resulting in a reduced afterload - cardiac outputs and ventricular ejection fractions are often not adequately enhanced. This septic cardiomyopathy (impairment of the heart within the scope of systemic sepsis) involves both the right and the left ventricles, and is potentially reversible. In response to volume substitution, the heart can be considerably enlarged. The cardiomyopathy is not primarily hypoxic in nature, but may be aggravated by ischemia. Autonomic dysfunction, documented by a reduced heart rate variability and impaired baroreflex and chemoreflex sensitivities, forms part of the disease entity. The severity of myocardial depression correlates with a poor prognosis. Noninfectious systemic inflammatory response syndrome can give rise to an analogous disease entity, namely, systemic inflammatory response syndrome cardiomyopathy.The etiology of septic cardiomyopathy is multifactorial. Several candidates with a potential pathogenetic impact on the heart were identified: bacterial toxins; cytokines and mediators including tumour necrosis factor-alpha, interleukin-1 and nitric oxide; cardiodepressant factors; oxygen reactive species; and catecholamines. Symptomatic treatment consists of volume substitution and catecholamine support; causal therapeutic approaches aiming at an interruption of the proinflammatory mediator cascades are being tested.