Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

196 III. SUBSTANCES OF ABUSEand more than one-third have two or more (Haller et al., 1993; Marlowe et al.,1995). Males are more likely to have comorbid alcohol dependence, stimulantdependence, antisocial personality disorder, and narcissistic personality disorder,whereas females are more likely to be diagnosed with mood disorders andBPD. It is important to evaluate patients routinely for Axis II disorders at pointof treatment entry and to design drug treatment programs that provide adequateattention to these comorbid conditions.Unfortunately, psychiatric comorbidity has negative implications for symptomexpression, prognosis, medical compliance, and services utilization (Bartelset al., 1993; Moos, Mertens, & Brennan, 1994; Moos & Moos, 1995; Pristach &Smith, 1990). It is important for substance abuse and mental health cliniciansto become aware of patterns of comorbidity among their patients and todevelop treatment plans that address dual disorders simultaneously. Awarenessof subtypes of cocaine abusers may help to guide treatment in both pharmacologicaland psychological intervention.MEDICAL COMPLICATIONSDirect Results of Cocaine UseMedical consequences of acute and chronic cocaine abuse may be categorizedas those caused directly by cocaine, those due to adulterants, and those relatedto route of administration. The most common direct medical consequences ofcocaine use include cardiovascular and CNS difficulties.Cocaine use may account for up to 25% of cases of acute myocardialinfarction among patients 18–45 years of age (Weber, Hollander, Murphy,Braunwald, & Gibson, 2003). Upon acute administration, cocaine increasesblood pressure and heart rate, primarily through an action on the sympatheticnervous system. Through its pharmacological effect at alpha- and betaadrenergicreceptors, cocaine may increase oxygen demand of the myocardiumby increasing blood pressure and heart rate. Cocaine also suppresses thebaroreflex response and vagal tone, further contributing to its effects on heartrate. At the same time that cocaine is increasing the workload on the heart, itinduces coronary artery vasoconstriction and platelet aggregation, potentiallyleading to coronary spasm and/or cardiac ischemia (Schrank, 1993). In addition,cocaine use is also associated with significantly decreased coronary bloodflow velocity, leading to increased microvascular resistance. Slow coronary fillingmay also suggest the possibility of cocaine use in patients in whom it wasnot otherwise suspected (Kelly, Sompalli, Sattar, & Khankari, 2003). At higherdoses, cocaine can depress ventricular function and slow electrical conductionin the heart. Both these effects appear to be mediated by cocaine’s localanesthetic action. Cocaine may potentiate catecholamine activity, impactingvoltage-dependent sodium ion channels related to local anesthetic properties.