  Disturbances in calcium homeostasis in a cardiac myocyte can lead to
calcium-overload conditions and abnormal calcium releases, which occur
primarily in the following two phases of the action potential (AP): (a)
triggered or late calcium release (LCR) during the plateau phase; (b)
spontaneous calcium release (SCR) during the diastolic interval (DI).
Experimental and numerical studies of LCRs and SCRs have suggested that these
abnormal calcium releases can lead to triggered excitations and, thence to
life-threatening ventricular arrhythmias. We explore this suggestion in detail
by building on our work in the previous accompanying Paper I, where we have
studied abnormal calcium releases and delayed afterdepolarizations (DADs) in
two state-of-the-art mathematical models for human ventricular myocytes. Here,
we carry out a detailed \textit{in-silico} study of one of these models,
namely, the ten Tusscher-Panfilov TP06~\cite{ten2006alternans} model. We
increase the L-type Ca-channel current $I_{\rm{CaL}}$ to trigger LCRs, and
calcium leak through the ryanodine receptor (RyR) to trigger SCRs, in the
myocyte. We then perform multiscale simulations of coupled TP06-model myocytes
in tissue in one-, two-, and three-dimensional (1D, 2D, and 3D) domains, with
clumps of DAD-capable myocytes, to demonstrate how these clumps precipitate
premature ventricular complexes (PVCs) that lead, in turn, to fibrillatory
excitations like spiral and scroll waves. We examine possible pharmacological
implications of our study for the class of ventricular arrhythmias that result
from Ca\textsuperscript{2+} overload.
