scholarly journals Cardiac Arrest and Inverted Takotsubo Cardiomyopathy Following Intramyometrial Vasopressin Injection During Myomectomy

Author(s):  
Alenka Golicnik ◽  
Eda Vrtacnik Bokal ◽  
Vojka Gorjup

Vasopressin is involved in cardiovascular homeostasis that can influence coronary perfusion. It is commonly used as a local vasoconstricting agent during gynaecological procedures. We present a case of cardiac arrest and inverse Takotsubo features following intramyometrial vasopressin administration during myomectomy. The patient was successfully resuscitated and recovered completely. Cardiac presentation was compatible with inverse Takotsubo cardiomyopathy that could have been triggered by high-dose vasopressin-induced coronary vasoconstriction. The patient’s cardiac function resolved with no long-term sequelae. Takotsubo cardiomyopathy usually results from an excessive catecholaminergic surge. High-dose vasopressin-induced coronary vasospasm could have been the mechanism underlying the clinical presentation in our patient.

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.


Author(s):  
Elvira Forte ◽  
Bryant Perkins ◽  
Amalia Sintou ◽  
Harkaran S. Kalkat ◽  
Angelos Papanikolaou ◽  
...  

Background: Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options, morbidity and mortality rates remain high. Although acute inflammation in response to myocardial cell death has been extensively studied, subsequent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of HF. After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells and potentially initiate a persistent autoimmune response against the heart. Cross-priming DC have the ability to activate both CD4+ helper and CD8 + cytotoxic T cells in response to necrotic cells and may thus be crucial players in exacerbating autoimmunity targeting the heart. This study investigates a role for cross-priming DC in post-MI myocardial impairment through presentation of self-antigen from necrotic cardiomyocytes to cytotoxic CD8 + T cells. Methods: We induced type-2 myocardial infarction (MI)-like ischemic injury in the heart by treatment with a single high dose of the beta-adrenergic agonist isoproterenol. We characterized the DC population in the heart and mediastinal lymph nodes and analyzed long-term cardiac immunopathology and functional decline in wild type and Clec9a -depleted mice lacking DC cross-priming function. Results: A diverse DC population, including cross-priming DC, is present in the heart and activated after ischemic injury. Clec9a -/- mice deficient in DC cross-priming are protected from long-term immune-mediated myocardial damage and decline of cardiac function, likely due to dampened activation of cytotoxic CD8 + T cells. Conclusions: Activation of cytotoxic CD8 + T cells by cross-priming DC contributes to exacerbation of post-ischemic inflammatory damage of the myocardium and corresponding decline in cardiac function. Importantly, this provides novel therapeutic targets to prevent immune-mediated worsening of post-ischemic HF.


Author(s):  
Parminder Kaur ◽  
Melvin Santana ◽  
Balraj Singh ◽  
Anuraag Sah ◽  
Raja Pullatt ◽  
...  

Misoprostol is a synthetic E1 prostaglandin commonly used to induce abortion in the United States and elsewhere. There is limited literature on the cardiovascular adverse effects of misoprostol, and, to the best of our knowledge, very few such events have been reported. We describe the case of 52-year-old woman who was given misoprostol for cervical softening before endometrial ablation and experienced a cardiac arrest due to coronary vasospasm. She was successfully resuscitated and echocardiography showed features consistent with Takotsubo cardiomyopathy. Coronary angiography revealed coronary artery spasm which responded to nitroglycerin. Our case adds to the limited literature on this life-threatening adverse event of misoprostol.


1989 ◽  
Vol 18 (4) ◽  
pp. 478 ◽  
Author(s):  
NA Paradis ◽  
GB Martin ◽  
EP Rivers ◽  
J Rosenberg ◽  
TJ Appleton ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Niels Secher ◽  
Leif Østergaard ◽  
Else Tønnesen ◽  
Asger Granfeldt

Introduction: Age is an independent predictor of poor outcome after cardiac arrest (CA), and age reduces organ function and increase infarct size, oxidative stress and inflammation in studies of regional ischemia reperfusion injury. Meanwhile, experimental CA studies are mostly performed in young, healthy animals, and our understanding of the CA pathophysiology may therefore fail to address the age-effects inherent to human CA. Objective: To investigate whether high age affects the reduction in cardiac function, increased inflammation, and endothelial activation observed after CA. Method: Aged (26 months, n=12) and young (5 months, n=10) male Sprague Dawley rats were subjected to 8 min of asphyxia induced CA, resuscitated using adrenalin and mechanical CPR, and observed for 360 min. Coronary perfusion pressure (CPP) was measured during CPR, and left ventricular end diastolic pressure, dP/dtmax, and dP/dtmin were determined at baseline and at the end of follow up. Blood samples at baseline, 120min, and 360min after CA were analysed for IL-6, IL-10, elastase, sE-selectin, and sI-CAM1. Results: We found no difference in CPP (aged: 16 [95%CI 13;20] vs young: 23 [95%CI 12;34]) or rate of ROSC (aged: 9/12 vs. young 9/10) between groups. During the first hour after resuscitation, a hyperperfusion phase was seen in the young group but not in the aged group (MAP aged: 50mmHg [95%CI 38;62] vs MAP young 105 [95%CI 88;123]). Left ventricular end diastolic pressure and dP/dtmax was higher in aged animals at baseline (p<0.02). We observed a significant decrease in dP/dtmax and increase in dP/dtmin after CA, with no group difference. Compared to young rats, aged animals showed a significantly higher increase in plasma elastase and sE-selectin levels after CA. In contrast, plasma IL-6 and IL-10 increased from baseline to end of follow up, but with no difference between the groups. sI-CAM1 showed no difference over time or between groups. Conclusion: We found increased endothelial activation and a blunted hyperperfusion in aged compared to young rats after CA. Age did not affect cardiac function and cytokine levels.


Hand Surgery ◽  
2002 ◽  
Vol 07 (02) ◽  
pp. 187-189 ◽  
Author(s):  
John L. Kelly ◽  
Michael O'Shaughnessy ◽  
Thomas P. F. O'Connor

Sarcoidosis of the phalanx is rare and is usually associated with severe systemic disease. We present a patient with recurrent phalangeal sarcoidosis and new evidence of a changing radiological pattern. The clinical presentation and outcome is discussed. High dose steroid treatment and careful long-term follow-up is recommended.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Sune Forsberg ◽  
Lis Abazi ◽  
Pär Forsman

Abstract Background Severe venlafaxine intoxication may cause arrhythmias, cardiac failure, and even cardiac arrest. Case presentation A 48-year-old caucasian male with an extensive psychiatric history ingested a high dose of venlafaxine causing a serum venlafaxine concentration of 12.6 mg/L 24 hours after ingestion. Seven hours post-ingestion, he experienced tonic–clonic seizures, and 8 hours later, takotsubo cardiomyopathy was recognized followed by cardiac arrest. The patient was resuscitated with prolonged cardiopulmonary resuscitation including ongoing automatic external compressions during helicopter transportation to a tertiary hospital for extracorporeal membrane oxygenation treatment. Despite a cardiopulmonary resuscitation duration of 2 hours, 36 hours of extracorporeal membrane oxygenation, and a total of 30 days of intensive care, the patient made a full recovery. Conclusion In cases of intoxication-induced cardiac arrests among otherwise young and healthy patients, prolonged cardiopulmonary resuscitation and extracorporeal circulation can be a life-saving bridge to recovery.


Author(s):  
Gavin D. Perkins

When cardiac arrest occurs, blood flow to the vital organs diminishes rapidly. Chest compressions are an essential element of cardiopulmonary resuscitation (CPR), yet they achieve, at best, one-third of the normal cardiac output. The speed of initiating CPR, as well as its quality is critical to patient outcomes. Optimal chest characteristics of compressions are defined as pushing hard (depth > 5 cm) and fast (compression rate 100–120/min). Pressure should be released fully between sequential chest compressions and interruptions in chest compressions should be minimized. Even short interruptions in CPR around the time of attempted defibrillation can be harmful. CPR feedback and prompt devices can be used to monitor the quality of CPR. Studies have shown these devices can improve the quality of CPR, but do not improve overall survival. Mechanical chest compression devices may be usefully deployed when it is difficult or unsafe to perform manual CPR, but there is no evidence that the routine deployment of these devices improves outcome. Vasoactive drugs improve coronary perfusion pressure and increase the chances of return of spontaneous circulation. However, there is no definitive evidence that they improve long-term survival. Recent data have raised the possibility that adrenaline may worsen long-term outcomes.


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