Opioid withdrawal triggered cardiogenic shock and Takotsubo cardiomyopathy in a 64-year-old male, which resolved with supportive care leading to full recovery of ejection fraction to 55-60% by day 7.
Case Report (n=1)
Opioid withdrawal can precipitate a severe hyperadrenergic state leading to Takotsubo cardiomyopathy and cardiogenic shock, which is reversible with early recognition and supportive care.
Abstract Introduction Takotsubo/stress-induced cardiomyopathy is a rare syndrome characterized by a transient LV dysfunction and apical hypokinesis due to a catecholamine surge with rapid recovery of cardiac function with resolution of the stressor. Common triggers include psychological stress and sepsis. While opioid withdrawal is a known hyperadrenergic state, its role in precipitating TCM is rarely reported, and to our knowledge cardiogenic shock requiring inotrope support and multiple pressors in this setting has not been reported thus far. Description A 64-year-old patient presented to the ER after a witnessed opioid overdose prompted EMS activation due to failed response to an unknown amount of narcan. On EMS evaluation, patient was stuporous and hypoxic to the 70s with bilateral rales; saturations improved with CPAP en route and mentation improved on BiPAP in the ER. Labs and vitals were unremarkable; patient was weaned to 4L/min and admitted for persistent hypoxia. An echo showed EF 15-20% with hypokinesis of the anterior, anterolateral, and anteroseptal walls. Over the next day, worsening withdrawal symptoms refractory to methadone and suboxone prompted ICU transfer for Precedex. A steep rise in HS-Troponin from 14 to 2100 led to coronary angiogram which showed no obstruction. A simultaneous RHC revealed elevated PCWP, low PAPi, and borderline cardiac output, so milrinone was started. Ongoing respiratory failure and hemodynamic instability necessitated intubation and vasopressors. By Day 5, patient was weaned off pressors extubated and with intermittent norepinephrine needed briefly. By day 7, hypotension resolved and repeat echo confirmed EF recovery (55-60%), supporting a diagnosis of Takotsubo cardiomyopathy. He was discharged with referral to an outpatient opioid program. Discussion Older studies have demonstrated that chronic opioid exposure causes a tonic inhibition of noradrenergic receptors and abrupt cessation or reversal, as in the case of Narcan administration, causes disinhibition of these receptors leading to sympathetic activation. It is hypothesized that this catecholamine surge leads to myocardial stunning and microvascular vasospasms causing the apical hypokinesis typical of TCM. Early recognition and supportive care allows full recovery. References: 1. Khreshi S, Suleiman M, et al. A Case of Opioid Withdrawal-Induced Takotsubo Cardiomyopathy. Chest. 2024; 2. Olson PC, Agarwal V, Lafferty JC, Bekheit S. Takotsubo Cardiomyopathy precipitated by opiate withdrawal. Heart Lung. 2018 Jan-Feb;47(1):73-75. doi: 10.1016/j.hrtlng.2017.10.001. Epub 2017 Nov 2. PMID: 29103663. 3. Substance Withdrawal as a Trigger for Takotsubo Cardiomyopathy: A Review of Reported Cases. J Addict Med. 2020;14(5):389-395. This abstract is funded by: none
Pandharpurkar et al. (Fri,) conducted a case report in Takotsubo Syndrome triggered by Opioid Withdrawal (n=1). Opioid withdrawal triggered cardiogenic shock and Takotsubo cardiomyopathy in a 64-year-old male, which resolved with supportive care leading to full recovery of ejection fraction to 55-60% by day 7.