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Am J Physiol Regul Integr Comp Physiol (October 18, 2001). doi:10.1152/ajpregu.00467.2001
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Articles in PresS, published online ahead of print October 18, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00467.2001
Submitted on August 2, 2001
Accepted on October 15, 2001

Functional Restitution of Cardiac Controlin Heart Transplant Patients

Eran Toledo1, Pinhas Itzhak1, Dan Aravot2, Yael Almog1, and Solange Akselrod1*

1 The Abramson Center of Medical Physics, Sackler Faculty of Exact Sciences, Tel Aviv University, Tel Aviv, Israel
2 Heart-Lung Transplant Unit, Rabin Medical Center, Petach Tikva, Israel

* To whom correspondence should be addressed. E-mail: solange{at}post.tau.ac.il.

Cardiovascular control is fundamentally altered after heart transplantation due to the surgical denervation of the heart. The main goal of this work was the non-invasive characterization of cardiac rate control mechanisms following cardiac transplantation and the understanding of their nature. We obtained 25 recordings from 13 male heart transplant patients (age: 28-68), Time after Transplant (TAT) was 0.5-62.5 months. The control group included 14 healthy male subjects (age: 28-59). ECG, continuous blood pressure (BP) and respiration were recorded for 45 min, first supine, then during active change of posture (CP) to standing. The signals were analyzed, both in time domain (mean and variance of HR, and rise time of HR in response to CP) and frequency domain (LF and HF). Our principal finding was the consistent pattern of evolution of the HR response to standing: from no response, via a slow response (>40 sec, TAT>6 weeks), to a fast increase (<20 sec, TAT>24 months). HR response correlated with TAT (p<0.001). LF correlated with HR response to CP (p<0.0001), yet HF and HR did not. An important finding was the presence of Very High Frequency (VHF) peaks in the power spectrum of HR and BP fluctuations. Extensive arrhythmias tended to appear at the TAT, which corresponds to the transition from slow to fast HR response to CP. Our results indicate the existence of a biphasic evolution in cardiac control mechanisms from lack of control to a first order control loop, followed by partial sympathetic reinnervation and finally, the direct effect of the old SA node on the pacemaker cell of the new SA node. No indication of vagal reinnervation was observed.




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