**7. Inhalent abuse**

arteries may also be very thrombotic with or without atherosclerotic plaque rupture. Finally, a no-flow or slow-flow with normal appearing epicardial vessels was reported as well [48]. Ventricular tachycardia and sudden cardiac death were reported as a complication of canna-

A Brugada-like effect was reported to be associated to cannabis intoxication as described with cocaine abuse [50–52]. This ECG pattern is believed to be related to a partial sodium channel antagonist activity. The ST segment normalizes once the acute intoxication is resolved.

These synthetic drugs are used for their psychostimulant effects. They had been first used by German army during the Second World War for these sought effects. Later, their cardiovas-

The main mechanism of action is an indirect sympathomimetic effect by releasing norepinephrine, dopamine, and serotonin from central and autonomic nervous system terminals, leading, as in cocaine intoxication, to an increase in the central and peripheral catecholamine

High catecholamine levels are known to be cardiotoxic, causing vasospasm, tachycardia, and hypertension, leading to increased myocardial oxygen demand and myocyte necrosis and

The association of these stimulants and sudden cardiac death is well established. A recent histopathological study showed that among 100 methamphetamine poisoning-related deaths, 68% had cardiac lesions [55]. In this context, death can result either from lethal aortic dissection or from ventricular arrhythmia. This latter may complicate either type 1 and type 2 myocardial infarctions or methamphetamine-induced cardiomyopathy and is triggered by catecholamine excess [56]. Furthermore, according to an interesting recent study, among 230 amphetamine abuser patients, 43% presented with sinus tachycardia and 3.5% presented with cardiac arrhythmias: ventricular tachycardia, premature atrial beats, paroxysmal supra-

Morphine and its semisynthetic analogue heroin are the most commonly used recreational narcotic drugs. Narcotic agents act centrally on the vasomotor center to increase parasympathetic and reduce sympathetic activity [48, 53]. These autonomic changes, combined with histamine release from mast cell degranulation, can result in bradycardia and hypotension [53]. Sinus bradycardia, benign atrioventricular block, and resulting atrial or ventricular automatic

ventricular tachycardia, and premature ventricular beats [57].

**4. Amphetamines and derivatives: ecstasy and methamphetamines**

bis-induced MI [49].

184 Cardiac Arrhythmias

**3.4. Sodium channel blockade**

cular dangers were revealed.

concentrations [53].

fibrosis [54].

**5. Heroine**

Inhalant abuse is the intentional inhalation of chemical vapors by sniffing, snorting, bagging, or huffing the substance to attain a euphoric effect. Spray paints, shoe polish, dust-off spray, glue, and lighter fluids are some products commonly abused by people. Glue sniffing has become a widespread form of inhalant abuse, usually among in adolescents and young adults.

Studies have indicated that about 20% of children in middle and high schools have experimented with inhalant substances [63]. These products are cheap, easily accessible at home, school, and workplace, and they are legal for all age groups (e.g., glue). Many common household products containing halogenated hydrocarbon like 1,1-difluoroethane (DFE) (known as Freon 152A used in refrigeration, dust-off spray, and airbrush painting) and toluene (used in glues) are abused by inhalation for euphoric effects [64].

Halogenated hydrocarbon abuse can cause a fatal malignant arrhythmia, termed "sudden sniffing death." Cardiotoxic effects have been described in human and in animal models [64].

Avella et al. [65] have demonstrated different levels in DFE tissues in the brain and heart, but the DFE level in the heart remained higher than the brain tissue after approximately 60-second post-DFE withdrawal. This may further result in abuser inhaling more DFE to sustain euphoric effect because central nervous system effects are reduced and thus lead to accumulation in the heart.

Recently, Joshi et al. [66] have showed that after multiple DFE doses in rats, severe arrhythmias such as ventricular fibrillation and ventricular tachycardia can be triggered. Exposure causes significant higher amount of epinephrine release than the control group [66] and an increased sensitivity of the myocardium to epinephrine [64, 67]. Furthermore, electrolyte imbalance, cardiac biomarkers, and oxidative stress markers were significantly affected and can cause damage to cardiomyocytes [66].

Alper et al. have demonstrated increase in QT duration, QT, and QTc dispersion in toluene users [68]. Toluene can cause inhibition of cardiac sodium currents like class I antiarrhythmics which can cause prolonged QT interval and have proarrhythmic effects [69].

Although the electrical function of the heart can be altered with acute exposure to hydrocarbons, prolonged use can cause structural damage that may also impede normal function [64].

Samples of cardiac muscle taken from inhalant abusers have shown interstitial edema, intramyocardial hemorrhages, contraction band necrosis, [70] edema, swollen and ruptured myofibrils, [71] and myocarditis and interstitial fibrosis [72].

In addition to arrhythmias, halogenated hydrocarbons have negative inotropic, dromotropic, and chronotropic effects on cardiac tissue [73]. Cases of atrioventricular conduction abnormality have been described in toluene intoxication [74].
