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6
CARDIAC TOXICITY
RALF KETTENHOFEN AND SILKE SCHWENGBERG
6.1 INTRODUCTION
In the past 30 years, 28% of all approved drugs had to be withdrawn from the market
due to cardiac toxicity. These compounds are categorized into two major groups
depending on the mechanisms of their toxic action: ion channel-related and nonion
channel-related cardiac toxicity. The former group of compounds interferes with the
cardiac electrophysiology and are proarrhythmic or induce arrhythmias and sudden
cardiac death (SCD). The latter group consists of compounds exhibiting cardiac
cytotoxic properties such as induction apoptosis, necrosis, or metabolic disruption.
6.2 ION CHANNEL-RELATED CARDIAC TOX ICITY
Functional and regular rhythmic beating of the heart is a prerequisite for the
preservation of vital functions of the body and requires a well-defined and subtle
interplay between a subset of cardiac ion channels, ion exchangers, and ion pumps.
Interference with and perturbation of these intricate processes may cause cardiac
toxicity by rising the proarrhythmic risk, inducing atrial and ventricular arrhythmias
and fibrillation, and SCD.
The occurrence of life-threatening Torsades de Pointes (TdP) ventricular tachyarrhythmia and SCD in patients treated with approved drugs (e.g., cisapride,
terolidine, and terfenadine) lead to the withdrawal of the drugs from the market.
Additionally, the incidence rendered the necessity to evolve a generally accepted and
harmonized guidance to assess torsadogenic potentials of drug candidates in clinical
ADMET for Medicinal Chemists: A Practical Guide, Edited by Katya Tsaioun and Steven A. Kates
Copyright 2011 John Wiley & Sons, Inc.
287
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trials as well as in preclinical studies. The International Conference on Harmonization
(ICH) of technical requirements for registration of pharmaceuticals for human use
elaborated and filed the guidelines E14 (clinical) and S7B (preclinical) to address the
issues of cardiac safety [1, 2].
The scientific basis for the guidelines benefited from the discovery that patients
with congenital long QT syndrome (LQTS) have a higher probability to suffer from
TdP tachyarrhythmia. To date, mutations in 12 different genes have been identified,
including 8 ion channel a- and b-subunits that are able to cause LQTS. The potential
to delay ventricular repolarization has become an accepted surrogate biomarker
linked to an enhanced proarrhythmic risk of drug candidates although it is not a
necessary condition to provoke life-threatening arrhythmias because other mechanisms are also reported to be proarrhythmic (see 6.2.3 and 6.2.4).
It is discussed that an increase in transmural dispersion of the repolarization (TDR,
differential repolarization in the endo-, epi-, and myocard) rather than a delayed
ventricular repolarization is predictive and responsible for torsadogenic risk [3]. To
date, effects on TDR can be approximated only by in vivo or ex vivo preparation of
perfused ventricular wedges or Langendorff-perfused hearts. These studies are costly
and time-consuming that cause early cardiac safety studies to rely on simplified
models that are discussed in Section 6.2.5.
In addition to delayed ventricular repolarization, evidence was recently provided
and discussed that shortening of ventricular repolarization is a risk factor for
ventricular arrhythmias [4–6]. Only a few patients with congenital short QT syndrome
(SQTS) have been described to date, but all suffer from an increased vulnerability to
atrial and ventricular fibrillation and sudden cardiac death [7]. Mutations in four
cardiac ion channels have been identified to have implications in SQTS.
6.2.1 Cardiac Electrophysiology
A short introduction to cardiac electrophysiology is provided to understand the
mechanism of ion channel-related cardiac toxicity.
The electrical activity of the heart can be recorded with electrodes from the surface
of the body as an electrocardiogram (ECG) (Figure 6.1). The occurring pattern in the
ECG is mainly characterized by the P wave, the Q, R, and S spikes (QRS complex),
and the T wave.
The QT interval of the ECG describes the time frame starting with the excitation of
the ventricle (Q spike) to its relaxation (end of the T wave). The duration of the QT
interval has an inverse relationship to the heart rate and has to be normalized to judge
drug-induced effects on the heart rate corrected QTc interval. Commonly used
correction formulas are described by Fridericia and Bazett although they appear to
have some limitations in the correct assessment of drug-induced QTc prolongation [8]. On a single cell level, the QT interval has its counterpart in the action potential
duration of a ventricular cardiomyocyte (Figure 6.1).
At rest, the myocyte exhibits an electrochemical gradient across the plasma
membrane of the main cardiac ions sodium (Na
þ
), calcium (Ca
2 þ
), and potassium
(K
þ
) with low intracellular Naþand Ca
2 þ
concentrations ([Naþ]i, [Ca
2 þ
]i) and
288 CARDIAC TOXICITY
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