1. Physiological Basis of MCP It is known that muscle mass of the lower extremities, the abdomen wall and the back, contain high volumes of blood and active, directional displacement of this blood can significantly affect hemodynamics. Moreover, they play an important role for pre-, after-load and total peripheral resistance formation. The ability to manage above-mentioned process, especially facing pathology, represents a very promising strategic issue. Arterial displacement is generated during muscular contraction and squeezing of blood vessels and venous flow towards the heart is accelerated. Correctly timed arterial retrograde flow together with peripheral arterial pulsation propagating pressure pulse waves proximally will contribute to increasing coronary perfusion. During muscular relaxation the arterial discharge contributes to this blood flow increase, as venous valves will ensure the blood flowing in one direction only. Altogether, this unloads the heart via hemodynamic improvement and at the same time increases local perfusion. Muscular Counter Pulsation for Inoperable CAD Patients with Severe CHF L.V. Lapanashvili*, T.G. Lobjanidze, S.T. Matskeplishvili, V.I. Ioshina, G.I. Kassirsky, B.R. Sandukhadze, Y.I. Buziashvili, L.A. Bockeria Bakoulev Scientific Center for Cardio-vascular Surgery, Moscow, Russia *Georgian State Medical University, Tbilisi, Georgia * CardioLa Ltd., Winterthur, Switzerland Introduction Congestive heart failure (CHF) is a major public health problem associated with considerable morbidity and mortality that will grow in importance as the average age of the population increases. The most severe category of end-stage coronary artery disease (CAD) patients with CHF not suitable for interventions (coronary bypass surgery or PTCA) have limited alternatives of pharmacological treatment. An increasing number of such patients either are resistant to medications or suffer from many side and adverse effects. Objective Muscular counter pulsation (MCP) – a completely non-invasive biomechanical way of assisting the heart – could be a solution for an effective non-invasive combined drug & device therapy for end-stage CAD patients with CHF. Patients and methods The study included 35 male CAD patients (66% with Angina Pectoris and an average CCS class 3.3) not suitable for coronary bypass surgery or PTCA and refractory to a maximal drug therapy with CHF (average NYHA class 2.4) and average EF=35.2 % MCP (n=21)Control (n=14) Age, y58.1 ± 7.857.2 ± 9.5 BMI, kg/m 2 29.2 ± 2.529.8 ± 3.9 Ejection fraction, %33.6 ± 5.837.7 ± 3.1 Cardiac output, l/min 3.1 ± 0.7 3.9 ± 1.0 The ECG, resting echocardiography, tetrapolar impedance rheography, peripheral venous blood gases and treadmill test according to the Bruce protocol were registered and recorded pre- and post-MCP therapy. All the hemodynamic assessment was done according to non- invasive tetrapolar impedance rheography. Results The key hemodynamic and stress test parameters changed as follows (Tab. 1): –26% (p < 0.0001) decrease of systemic vascular resistance in the main group versus no significant change in the control group. –34% and 23% (p < 0.0001) increase of cardiac indexes and ejection fraction respectively in the main group versus no significant change in the control group. –Unchanged heart rate and mean arterial pressure in both groups. –63% and 66 % (p < 0.005) increase in stage (Bruce protocol) and exercise capacity respectively with 13% (p < 0.08) improvement of maximal oxygen uptake in the main group versus no changes in the control group. Subjectively all MCP group patients started to feel lighter and more active as from day 2-4 of the MCP treatment onwards. Fig. 1: MCP setup, 1-4 active electrodes, 5-6 passive electrodes stimulation Heart synchronization MCP Off MCP On Baseline Clinical Bakoulev: Patient V., 41 years, IHD, EF 52% Fig. 2: Effect of MCP shown with ECG and aortal pressure (measured invasively) Limitations –Screening of patients in groups was not done blindly, for the MCP group more severe patients were chosen on purpose to give them more benefit –Hemodynamic parameters were measured non-invasively. The Rheography device uses standard constant values for the calculation of central venous and end-diastolic pressures which is OK for healthy people but could give some errors in case of pathology. Unchanged heart rate and mean arterial pressure in both groups. –It was decided to include the stress test during the course of the study. This explains why the stress test was performed only with the last 16 patients in the year 2006. –VO 2 max was assessed theoretically based on the formula of Foster C. et al. (VO 2 max = 14.76 – [1.379 × T] + [0.451 × T 2 ] – [0.012 × T 3 ]). Certainly a direct spirometry would have been preferable. Fig. 4: SVRI development form baseline (BL) to end, MCP Group (n=21) and Control Group (n=14) 0 1000 2000 3000 4000 5000 6000 7000 8000 BLEnd SVRI (dynes*sec*m 2 /cm 5 ) - 26% * 0 1000 2000 3000 4000 5000 6000 7000 8000 BLEnd SVRI (dynes*sec*m 2 /cm 5 ) MCP Group Control - Group Fig. 5: CI development form baseline (BL) to end, MCP Group (n=21) and Control Group (n=14) 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 BLEnd CI (l/min*m 2 ) 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 BLEnd CI (l/min*m 2 ) + 34%* MCP Group Control Group Conclusions MCP treatment is associated with a reliable improvement of the patients’ general performance and myocardial function through marked benefitial hemodynamics. Thus, MCP could be a new promising non-invasive technique for the treatment of low cardiac output heart failure due to systolic dysfunction. In combination with conventional treatment MCP could be considered a destination therapy for end-stage CAD patients with CHF not suitable to surgical intervention. All patients were receiving standard pharmacological treatment including β-blockers, Са2+ antagonists, ACE inhibitors, Diuretics and Glycosides. In addition a MCP device-based treatment of daily 30 minutes for 8 consecutive days was performed in the MCP-group (n=21). MCP treatment was applied with the cardiosynchronized pulse generator (“CardioLa”, Switzerland) in counterpulsation mode on the lower extremities (Fig. 1). In this case the device and the body represent a bio-mechanical system, by which heart assistance (1:1 mode) is being achieved by sequential diastolic work (1:4 mode) on each of the 4 muscle groups chosen. Even slight contraction of one muscle group per heartbeat is enough to achieve the therapeutic effect. Fig. 6: Relation of ejection fraction and duration of the treadmill test, MCP Group (n=8) and Control Group (n=8) 0 50 100 150 200 250 300 350 400 450 500 102030405060 EF (%) Duration (s) BL -End MCP Group 0 50 100 150 200 250 300 350 400 450 500 102030405060 EF (%) Duration (s) Control Group BL -End Fig. 3: Treadmill Test development (Bruce protocol) compared to own BL, MCP (n=8) & Control (n=8) -20% -10% 0% 10% 20% 30% 40% 50% 60% 70% 80% StageDurationVO2 maxHR startHR end % difference MCP Group Control Group p=0.003 p=0.002 p=0.08 p=0.05 p=0.14 BL Tab. 1: Hemodynamic development in MCP and Control group