Takotsubo Cardiomyopathy as a Sequela of Elective Direct-Current Cardioversion for Atrial Fibrillation

Siegfried, Jonathan S.; Bhusri, Satjit; Guttenplan, Nils; Coplan, Neil L.

doi:10.14503/thij-12-3063

Cited by 15 publications

(12 citation statements)

References 16 publications

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“…All patients had a full clinical and echocardiographic recovery in one week on average. SCM has been reported consequent to various forms of electrical stimulation including DCCV 3,4,5 ,electroconvulsive therapy, 6,7 and electrocution caused by lightning strike8.The pathophysiology of SCM remains unclear. Several mechanisms have been proposed including catecholamine induced myocardial stunning with an apical preference because of a natural increasing gradient of catecholamine receptors from base to apex, ischemia mediated stunning due to epicardial coronary artery disease or spasm of the microvascular coronary bed 10,12,21 .…”

Section: Discussion and Literature Reviewmentioning

confidence: 99%

Recurrent Direct Current Cardioversion Induced Takotsubo Cardiomyopathy

Smyrlis

Yaranov²,

Galin

et al. 2015

ICFJ

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A 61-year-old female with past medical history significant only for hypertension on treatment with an ACE-I presented with palpitations and was found to have new onset Afib. Initial workup including an echocardiogram and TSH were unremarkable. Beta blocker therapy and rivaroxaban were initiated and outpatient DCCV was scheduled for one month later. She underwent successful DCCV with one 120J shock. Within 6 hours of DCCV she experienced severe shortness of breath at rest for which she did not seek medical attention as it was short lived (less than 12hours). On follow up office visit one week later she was found to have recurrent Afib. She was started on flecanide and was scheduled for repeat DCCV. Within 4 hours of repeat DCCV she experienced severe shortness of breath. In the emergency room she was noted to be in severe respiratory distress with a respiratory rate of 40, hypoxic saturating 82% on room air. She denied chest pain and review of systems was otherwise negative. Her heart rate was 130 while and blood pressure 110/70. She had elevated JVP and bilateral crackles on lung exam as well as an S3 gallop. Her EKG revealed sinus tachycardia at 129 beats per minute with new Q waves in V1-V4 and non-specific ST changes (Fig. 1). Laboratory tests, including initial cardiac troponin-I levels, were within normal limits. An urgent echocardiogram revealed severe LV dysfunction with apical ballooning, hypercontractile basal segments and an ejection fraction of 20-25% (Figs. 2, 3). After 4 hours of positive pressure ventilation and adequate diuresis with 160mg of IV lasix her symptoms significantly improved. She was admitted to the intensive care unit for monitoring. Repeat ECG revealed A-fib with rapid ventricular response and new anterior T wave inversions. (Fig. 4) Troponin I level peaked at 0.95 ng/mL. Coronary angiogram on day two of hospitalization revealed minimal coronary artery disease. LVEDP was 8mmHg. (Figs. 5,6.7)The final diagnosis of DCCV induced stress cardiomyopathy was made. Upon hospital discharge on day three, her medications included carvedilol, an angiotensin receptor blocker and rivaroxaban. Echocardiogram 2 weeks later on follow up office visit revealed complete resolution of her LV dysfunction while her ECG returned to baseline (Figs. 8,9 AbstractStress cardiomyopathy (SCM), also called broken heart syndrome and Takotsubo cardiomyopathy is an increasingly reported syndrome generally characterized by transient systolic dysfunction of the apical and or mid segments of the left ventricle that mimics myocardial infarction, in the absence of obstructive coronary artery disease. Typically patients present within a few hours of exposure to physical or emotional stress. However, the mechanism by which these stressors result in myocardial dysfunction is unclear. Proposed factors include catecholamine excess and coronary vasospasm1. We present the case of a 61-year-old female who experienced acute pulmonary edema secondary to stress cardiomyopathy, on two occasions immediately after undergoing elective ...

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Section: Discussion and Literature Reviewmentioning

confidence: 99%

Recurrent Direct Current Cardioversion Induced Takotsubo Cardiomyopathy

Smyrlis

Yaranov²,

Galin

et al. 2015

ICFJ

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“…DC cardioversion can stun the myocardium and could probably increase myocardial insult. 40 Similarly, digoxin should be avoided as it can worsen the LVOT obstruction and instead, beta-blocker should be the first line of treatment for rate control.…”

Section: B) the Acute Phasementioning

confidence: 99%

Takotsubo Syndrome Therapy: Current Status and Future Directions

Singh¹,

Akashi²,

Horowitz³

2016

ICFJ

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<p>Tako-Tsubo Cardiomyopathy (TTC), which is now known as Tako-Tsubo Syndrome (TTS) is a transient left ventricular (LV) systolic dysfunction of uncertain pathogenesis, which occurs predominantly in ageing women. There is considerable uncertainty regarding the management of TTS related acute and chronic issues and most of the evidence regarding therapy comes from retrospective data and case studies. In this review we have tried to concise the available information on the TTS therapeutics to help clinicians make treatment decisions in patients diagnosed with TTS. At the same time we have highlighted some of the uncertainties regarding TTS therapy, in particular the inability of b-blocker therapy to improve survival or prevent recurrence. We have also emphasized the issue of incomplete recovery in some cases of TTS where there is ongoing inflammation and evidence of impaired myocardial energetics despite normalization of LV ejection fraction. Although there is no scientific evidence on how to improve or fasten the recovery of TTS, we believe therapy improving energy efficiency may play some role in future. Lastly, we would like to reiterate that in the absence of randomized studies evaluating medical therapy in TTS, the treatment for this syndrome remains entirely empirical and should be individualized according to the patient characteristics at the time of presentation.</p>

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“…We present a case of an elderly woman who developed pulmonary oedema due to TS after elective electrical cardioversion for atrial fibrillation (AF). To our knowledge this is only the fourth reported case of electrical cardioversion-related TS [2][3][4] and suggests that elderly patients, especially women, should be carefully counselled about the risk of acute heart failure and other potential complications related to the stress of electrical cardioversion.An 87-year old woman with a history of asthma, hypertension, hypercholesterolemia, chronic kidney disease, mitral valve prolapse and persistent AF (CHADSVASc = 5) was admitted in left heart failure (HF) due to AF with a rapid ventricular response. Her transthoracic echocardiogram (TTE) showed normal left ventricular (LV) systolic function with an ejection fraction (EF) of N60% and no regional wall motion abnormality.…”

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confidence: 99%

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confidence: 99%