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PART II Iatrogenicity of Cardiovascular Drugs and Cardiovascular Toxicity of Noncardiac Drugs Arshad Jahangir Gan-Xin Yan ­ Great deeds are usually wrought at ­ great risks. Herodotus (Ἡρόδοτος), c. 484–­ c. 425 b.c. (Book 7, Chapter 50, The Histories, trans. Robin Waterfield, 1998) INTRODUCTION Medicine is a part of life, and iatrogenicity is a part of medicine. Iatrogenicity in cardiovascular (CV) medicine, a part of general (medical) iatrogenicity, is well known among clinicians, drug developers, regulators, and patients, and caretakers long ago realized that even intended effects of drugs ­ were not always or entirely beneficial. Iatrogenic complications of drugs and interventions culminating in sudden and unexpected cardiac death is of major concern in modern CV medicine. Many ­ factors can be contributed to CV iatrogenicity, among them: • Poor overall medical assessment • Erroneous diagnosis or treatment • Delay of correct diagnosis or treatment • Negligence and malpractice • Insufficient knowledge of pharmacological peculiarities of the drug • Misuse of guidelines • Unnecessary procedures or interventions • Inadequate efforts in identification and mitigation of risk ­ factors • Improper or inadequate follow-­ up. The significance and role of each of ­ these ­ factors (and their combination) in CV iatrogenicity vary significantly among patients and even within the same patient, CHAPTER 6 Clinical Manifestations of Acute and Chronic Drug-­ Induced Iatrogenic Cardiovascular Diseases and Syndromes Ihor B. Gussak, Gan-­ Xin Yan, Arshad Jahangir, Georg Gussak, and John B. Kostis 48 / Acute and Chronic Drug-Induced Iatrogenic Cardiovascular Diseases and Syndromes DRUG-­INDUCED CARDIOVASCULAR TOXICITY AND ITS CLINICAL CONSIDERATIONS Drug Toxicity: Terminology and Definitions Drug toxicity is defined as the degree to which any chemical or biological substance, other than food, used for medicinal (diagnostic, preventive, or therapeutic ) purposes can do the following: (a) produce an appreciably harmful or unpleasant body response impacting the patient’s management or prognosis; (b) predict a hazard from ­ future administration ; and/or (c) warrant prevention or treatment modifications or alteration of the dosage regimen,“black label” warnings or precautions, or withdrawal from the market. Commonly, the term drug toxicity does not include accidental or intentional poisoning and also differs from overdose or combined drug intoxication (known as “multiple drug intake” or polydrug/polypharmacy). Polypharmacy is commonly defined as simultaneous multiple (five or more) prescribed medi­ cations per patient. It is often associated with unintended drug-­ drug interactions that can result in deterioration of health or sudden iatrogenic death, particularly in the el­ derly. The risk of iatrogenic complications is likely to be higher in patients who take over-­ the-­ counter medi­ cations in addition to prescribed drugs. A considerable number of cardiac and non-­ cardiac drugs on the market or in development are known for their toxic effects on the CV system , and many have been withdrawn or severely restricted to specific indications ­ because of an unexpected adverse effects (AEs). Typically, AEs are detected by laboratory tests (e.g., biochemical , hematological, immunological, radiological) or by clinical investigation (e.g., endoscopy, cardiac catheterization, X-­ ray), whereas an adverse drug reaction (ADRs) are recognized by their clinical manifestations (symptoms and/or signs). This distinction suggests several dif­ fer­ ent causal relationships between AE and ADR, for example : (a) ADR can result directly from AE or can occur without preceding AE, whereas AE may not necessarily result in appreciable ADR; (b) AE and ADR may not have a causal relationship; or depending on stage and progression of disease, age, gender, comorbidity, and medi­ cations. While clinical manifestations of cardiac toxicity of a variety of cardiac and non-­ cardiac medi­ cations have been recognized in modern clinical cardiology for many de­ cades, arguably the first clinical study that attracted broad and renewed attention to CV iatrogenicity was the report by the Cardiac Arrhythmia Suppression Trial (CAST) study published in 1989 (1). This study revealed increased mortality in patients with recent myo­ car­ dial infarction and premature ventricular complexes (PVCs) who ­ were on active treatment with a sodium (Na+ ) channel blockers compared with­ those on placebo, thus highlighting the potential hazard of antiarrhythmic drugs that ­ were other­ wise highly effective in suppressing premature ventricular complexes (2). Since then, many examples of life-­ threatening cardiac proarrhythmia have been demonstrated for antiarrhythmic drugs as well as for other cardiac and non-­ cardiac drugs. In another example of drug-­ induced cardiac toxicity that includes proarrhythmia, worsening arrhythmia , and increased cardiac mortality, a link was established between drugs with potassium (K+ ) channel blocking properties and QT-­ prolongation culminating in development of torsade de pointes (TdP). It appears that agents with a potential to shorten the length of ventricular...


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