The short answer is: none!
The better answer is:
Neuromuscular blocking drugs like atracurium, rocuronium, mivacurium etc act on the neuromuscular junction. They antagonise nicotinic acetylcholine receptors and this cause an inability to pass inputs from nerve to muscle cells (as opposed to suxamethonium which agonises the nictotinic receptors hence people twitch briefly after sux before paralysis sets in).
Cardiac tissues do utilise acetylcholine but they have muscarinic receptors and as such the neuromuscular blockers have no effect. Cardiac tissue also has an intrinsic automaticity which organises cardiac impulses/beating.
It is interesting that when you 'reverse' neuromuscular blockers with neostigmine (an acetylcholineesterase inhibitor) you get more acetylcholine available but not just at the neuromuscular junction, also in cardiac tissue. This means that neostigmine alone would cause a bradycardia (potentially significantly) and so we (almost) always give it with glycopyrrolate which causes a relative tachycardia.
Source: Doctor in critical care/anaesthesia.
Edit: please excuse any mistakes, just finished a long busy night shift!
Edit 2: if you want some real detail here is a like to some stuff I used for my exams (sorry I don't know how to do pretty links!)