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Treating Comorbid Posttraumatic Stress Disorder and Cardiovascular Disease

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Treating Comorbid Posttraumatic Stress Disorder and Cardiovascular Disease Savvy Psychopharmacology Treating comorbid posttraumatic stress disorder and cardiovascular disease Melissa C. Palmer, PharmD, Stephen Quillen, PharmD, CACP, PA-C, CAQ Psychiatry, Ken Chin, DO, Jeff Garrett, DO, Jonathan Lazzara, DO, and Christopher Thomas, PharmD, BCPP, BCPS r. S, 64, has a history of post- there any evidence to support concomitant traumatic stress disorder (PTSD), therapy? M which has been well controlled for the past 15 years with cognitive-processing PTSD is characterized by emotional and therapy and fluoxetine, 40 mg/d. However, behavioral symptoms following exposure over the past 6 weeks, Mr. S has experienced to a traumatic event. Its 12-month preva- increased hypervigilance, nightmares, and lence in the United States is estimated at Vicki L. Ellingrod, flashbacks. He states that his primary care 3.5%. Diagnostic criteria necessitate the PharmD, FCCP provider recommended an adjustment in presence of intrusive symptoms, persistent Department Editor pharmacotherapy to address this exacer- effortful avoidance of distressing trauma- bation of symptoms. Previous medication related stimuli, negative cognitions or trials include sertraline, 200 mg/d, discon- mood, and alterations in arousal and reac- tinued due to lack of perceived efficacy, and tivity. PTSD negatively impacts social and venlafaxine, 150 mg/d, discontinued due to occupational functioning.1 increased blood pressure. Cardiovascular disease (CVD) comprises Mr. S’s medical history includes hyperten- a number of conditions, including coronary sion, dyslipidemia, and myocardial infarction artery disease, cerebrovascular disease, (MI) 5 years ago. His family history includes congestive heart failure, and venous throm- sudden cardiac death (mother and father) boembolism. CVD accounted for more than and major depressive disorder (sister). His 17 million deaths worldwide in 2012, which blood pressure is currently uncontrolled on is more than any other cause.2 lisinopril, 5 mg/d, and metoprolol succinate, Studies have revealed a correlation 50 mg/d. Today, serial blood pressure read- between the presence of psychosocial fac- ings measured approximately 180/90 mm Hg, tors, such as depression and anxiety, and with a pulse 50-60 beats per minute. the occurrence of cardiovascular events. What is the next step in treating Mr. S’s hypertension and PTSD symptoms? Is Practice Points • Posttraumatic stress disorder and Dr. Palmer is PGY-2 Pharmacy Practice Resident, Dr. Quillen is Clinical cardiovascular disease often are Savvy Psychopharmacology Pharmacy Specialist in Primary Care, Dr. Chin is PGY-3 Psychiatry comorbid, especially in geriatric patients. is produced in partnership Resident, Dr. Garrett is PGY-4 Psychiatry Resident, Dr. Lazzara is Staff with the College Psychiatrist, and Dr. Thomas is Director, PGY-1 and PGY-2 Residency • Angiotensin-converting enzyme of Psychiatric Programs, Clinical Pharmacy Specialist in Psychiatry, Chillicothe inhibitors and angiotensin receptor and Neurologic Veterans Affairs Medical Center, Chillicothe, Ohio. Pharmacists blockers may provide benefit in cpnp.org Disclosures attenuation of hyperarousal symptoms and mhc.cpnp.org (journal) The contents of this article do not represent the views of the U.S. Department of Veterans Affairs or the United States Government. This intrusive thoughts. material is the result of work supported with resources and the use of facilities at the Chillicothe Veterans Affairs Medical Center in Chillicothe, • Alpha-1 antagonists, particularly Ohio. The authors report no financial relationship with any company prazosin, may be useful in treating sleep Current Psychiatry whose products are mentioned in this article or with manufacturers of disturbances and nightmares. 38 August 2017 competing products. Savvy Psychopharmacology Table 1 Increased CVD risk factors among veterans with PTSD Risk factor Odds ratio, malea Odds ratio, femalea Hypertension 2.88 2.99 Dyslipidemia 2.70 2.68 Type 2 diabetes mellitus 2.57 2.86 Obesity 2.35 3.01 Tobacco use 3.63 3.58 CVD: cardiovascular disease; PTSD: posttraumatic stress disorder aCompared with veterans with no mental health diagnosis or with a mental health diagnosis other than PTSD Source: Reference 3 Clinical Point Patients who The mechanism appears to consist of a Evidence supports the use of the behavioral component (eg, poor diet, centrally acting, beta-adrenergic antag- received propranolol tobacco use) and a direct pathophysiologic onist propranolol for decreasing the within several hours component (eg, excessive sympathetic physiologic reactivity to acute trauma. of a traumatic event nervous system activation) (Table 13).4 Emotional arousal enhances the con- experienced fewer Management of concomitant PTSD and solidation of emotional experiences into physiologic signs of CVD presents a challenge to clinicians. long-term memories via the adrenal This article summarizes the evidence stress hormones epinephrine and corti- PTSD at follow-up for the use of CVD medications in treating costerone. The amygdala mediates these PTSD (Table 2, page 40) and how to apply stress hormones and releases norepi- these principles in patient care (Table 3,5-14 nephrine, which subsequently activates page 41). noradrenergic receptors essential for memory enhancement. Several studies ACEIs, ARBs, beta blockers, and have reported that patients who received calcium channel blockers propranolol within several hours of a trau- Angiotensin-converting enzyme inhibitors matic event experienced fewer physiologic (ACEIs) and angiotensin receptor block- signs of PTSD at follow-up 1 month later.16 ers (ARBs) inhibit the renin-angiotensin Moreover, researchers have hypothesized system: ACEIs prevent formation of that chronic treatment with proprano- angiotensin II, a potent vasoconstrictor, lol may be effective in decreasing hyper- and ARBs prevent interaction between arousal symptoms in patients with chronic angiotensin II and its receptor. In one PTSD by reducing tonically elevated nor- study, patients were recruited from a epinephrine signaling.6 large public hospital serving primarily a Chronic elevation of noradrenergic highly traumatized, low-income popu- activity may induce lipoprotein lipase lation. Patients taking an ACEI or ARB and suppress low-density lipoprotein who had experienced at least 1 traumatic (LDL) receptor activity, which in turn event exhibited significantly decreased elevates serum cholesterol levels. The Discuss this article at hyperarousal symptoms and decreased results of one study suggested that vera- www.facebook.com/ CurrentPsychiatry intrusive thoughts on the PTSD Symptom pamil, a non-dihydropyridine calcium Scale and Clinician Administered PTSD channel blocker, significantly improves Scale.5 Other studies have reported that serum cholesterol levels in patients blockade of angiotensin II AT1 receptors with PTSD by increasing LDL receptor may result in decreased stress, anxiety, activity and decreasing norepinephrine Current Psychiatry and inflammation.15 release.7 Vol. 16, No. 8 39 continued Savvy Psychopharmacology Table 2 Safety and efficacy of CVD medications in PTSD Medication class Safety Efficacy ACEIs/ARBs Hyperkalemia, renal ACEIs and ARBs may decrease hyperarousal impairment, hypotension symptoms Beta-blockers Sleep disturbances, Propranolol may decrease signs and symptoms bradycardia, hypotension of PTSD, both acutely and chronically Calcium-channel Constipation, hypotension Verapamil may improve serum cholesterol in blockers patients with PTSD Alpha-1 Dizziness, headache, Prazosin is well studied and shown to reduce antagonists orthostatic hypotension frequency of PTSD nightmares. Doxazosin and terazosin may be considered second-line Clinical Point Alpha-2 agonists Dizziness, headache, Clonidine may reduce agitation. Guanfacine may Prazosin reduces orthostatic hypotension reduce frequency of PTSD nightmares in children but not adults the fight-or-flight Antihistamines Drowsiness, confusion, Cyproheptadine and hydroxyzine may reduce and hyperarousal increased appetite the frequency of PTSD nightmares and improve sleep quality reactions related to Serotonin Drowsiness, orthostatic Trazodone and nefazodone may reduce the nightmares caused antagonists hypotension. Priapism frequency of PTSD nightmares and improve by PTSD relatively rare sleep quality TCAs Conduction abnormalities. TCAs may be as effective as SSRIs in treating Not safe for use in patients anxiety and depression associated with PTSD with CVD ACEI: Angiotensin-converting enzyme inhibitor; ARB: angiotensin receptor blocker; CVD: cardiovascular disease; PTSD: posttraumatic stress disorder; TCA: tricyclic antidepressant Alpha-1 and alpha-2 antagonists with weekly adjustments and blood pres- Alpha-1 antagonists relax vascular smooth sure monitoring. muscle by blocking norepinephrine stimu- Other α-1 antagonists have shown effi- lation at postsynaptic α-1-adrenergic recep- cacy in a limited number of trials and may tors. They frequently are prescribed for be considered second-line treatment of hypertension and benign prostatic hyper- PTSD hyperarousal symptoms. Doxazosin trophy. One α-1 antagonist in particular, has a longer half-life compared with prazo- prazosin, appears especially useful in treat- sin (22 hours vs 3 hours) and may be useful ing sleep disturbances, which occur in up in treating daytime hyperarousal with once- to 90% of patients with PTSD.17 Because of daily dosing. However, its hydrophilicity its relatively greater lipophilicity, prazosin prevents it from crossing
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