Incidence and clinical characteristics of takotsubo cardiomyopathy post-aneurysmal subarachnoid hemorrhage

Thura, T.; Hayek, Salim S.; Cheng, Jeh Wei; Samuels, Owen; Wittstein, Ilan S.; Lerakis, Stamatios

doi:10.1016/j.ijcard.2014.07.279

Cited by 50 publications

(38 citation statements)

References 9 publications

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“…Nonetheless, the most frequent triggers are brain- In large series of TTS due to SAB, however, NPE has not been described [93,94]. NOP, number of patients; ns, not specified; NPE, neurogenic pulmonary edema; AVM, arterio-venous malformation; SAB, subarachnoid bleeding; TTS, Takotsubo syndrome.…”

Section: Discussionmentioning

confidence: 99%

Neurological Perspectives of Neurogenic Pulmonary Edema

Finsterer¹

2019

Eur Neurol

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Background: Neurogenic pulmonary edema (NPE) is characterized by acute respiratory distress triggered by acute, severe compromise of the central nervous system (CNS). This review aims at summarizing and discussing recent and previous findings about the type and frequency of CNS triggers of NPE, pathogenesis, diagnosis, treatment, and outcome of patients experiencing NPE. Key Messages: NPE is diagnosed in the presence of pink, frothy sputum, pulmonary edema, bilateral opacities on X-ray, PaO2:PiO2 <200 mm Hg, acute CNS compromise with increased intra-cranial pressure, rapid resolution within 48–72 h, and the absence of alternative causes of respiratory distress. The most common cerebral triggers of NPE include enterovirus-71-associated brainstem encephalitis, subarachnoid bleeding, intracerebral bleeding, traumatic brain injury, epilepsy, ischemic stroke, intracranial/spinal surgery, multiple sclerosis, electroconvulsive therapy, subdural/epidural hematoma, intoxication, hypoxia, and hydrocephalus. Simultaneous treatment of CNS and pulmonary compromise is required. Cerebral treatment involves infectiologists, neurologists, and neurosurgeons. Pulmonary treatment is mainly supportive, but if ineffective, extracorporeal membrane oxygenation or thermodilution are alternative options. Applying intensive care measures, the outcome of NPE has improved. Summary: CNS-disease triggering NPE is more variegated than anticipated. Delineation of NPE from other pulmonary or cardiac conditions mimicking NPE is crucial to take appropriate measures and improve the outcome of these patients.

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Section: Discussionmentioning

confidence: 99%

Neurological Perspectives of Neurogenic Pulmonary Edema

Finsterer¹

2019

Eur Neurol

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“…Takotsubo kardiyomiyopatisi, belirgin koroner arter stenozu olmamasına rağmen sol ventrikül duvar hareket bozukluğu, EKG değişiklikleri ve miyokard enzimlerinin salınımı ile karakterize bir sendromdur (11). Genellikle duygusal ya da fiziksel stresör bir tetikleyici sonrası ortaya çıkmaktadır (12).…”

Section: Subaraknoid Kanamanın Kalbe Etkileriunclassified

Relationship Between Neutrophil Gelatinase-associated Lipocalin and Mortality in Acute Kidney Injury

Kayaalti¹,

Kayaalti²,

Aksebzeci³

2018

tybd

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ÖZ Tıbbi ve cerrahi tedavideki gelişmelere rağmen, anevrizmatik subaraknoid kanama (SAK) erken yaştaki mortalitenin ana nedenlerinden biri olmaya devam etmektedir. Kardiyak ve pulmoner komplikasyonlar mortalitenin başlıca nedenlerindendir. En şiddetli kardiyak komplikasyonlardan biri nörojenik stres kardiyomiyopatisidir. Nörojenik stres kardiyomiyopatisinde görülen sol ventrikül disfonksiyonu genellikle birkaç gün içinde geri dönüşümlü olmasına rağmen şiddetli hipotansiyona, pulmoner ödeme ve kardiyojenik şoka neden olabilir. SAK sonrası gelişen kalp yetmezliğinin geleneksel tedavisi, noradrenalin, dobutamin ve yüksek miktarda sıvıların kullanımına dayanmaktadır. Ancak SAK'de azalmış kalp debisinin tedavisi zordur. Çünkü SAK'de artmış adrenerjik stimülasyona bağlı miyokard hücreleri zaten stres altındadır. Ekzojen katekolaminlerin kullanımı miyokard hücrelerinde ilave nörokardiyojenik hasara, aşırı kalsiyum yüküne, serebral kan akımında azalmaya ve gecikmiş serebral iskemi gelişimine neden olabilir. Levosimendan kullanımı ile ekzojen katekolaminlerin kullanımı azaltılarak katekolaminlerin oluşturduğu kardiyotoksisitenin kısır döngüsü kırılabilir. Levosimendan miyokardın oksijen tüketimini artırmadan kalp debisinin hızla eski haline getirilmesini sağlayan ve serebral perfüzyonu optimize eden adrenerjik olmayan bir inotropik kalsiyum sensitizörüdür. Gecikmiş serebral iskemi patogenezinde sol ventrikül sistolik fonksiyonundaki azalmanın yer aldığını düşünürsek bu hastalarda levosimendan uygulaması ile nörolojik komplikasyon gelişme riski azalabilir. Ayrıca deneysel çalışmalarda levosimendanın SAK'de nöroprotektif etkileri olabileceğine dair yeni veriler de mevcuttur. Bu derlemede SAK seyrinde gelişen hemodinamik bozuklukların tedavisinde levosimendan kullanımı güncel bilgiler eşliğinde tartışılmıştır. Anahtar Kelimeler: Subaraknoid kanama, travmatik, anevrizma, intrakraniyal vazospazm, yoğun bakım, levosimendan, nörojenik stres kardiyomiyopatisi ABSTRACT Despite improvements in medical and surgical treatment, aneurysmatic subarachnoid hemorrhage (SAH) remains one of the main causes of early mortality. Cardiac and pulmonary complications are the main causes of mortality. One of the most severe cardiac complications is neurogenic stress cardiomyopathy. Left ventricular dysfunction which is seen in neurogenic stress cardiomyopathy, although it is usually reversible within a few days, can cause severe hypotension, pulmonary edema and cardiogenic shock. Traditional treatment of heart failure after SAH is based on the use of noradrenaline, dobutamine and high volume of fluids. However, it is difficult to treat reduced cardiac output in SAH. Because, myocardial cells are already under stress due to increased adrenergic stimulation. The use of exogenous catecholamines may cause additional neurocardiogenic damage in myocardial cells, excessive calcium burden, decreased cerebral blood flow, and delayed cerebral ischemia. By reducing the use of exogenous catecholamines with levosimendan, the vicious circle of cardiotoxicity i...

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“…TS has also been associated with a wide variety of central neurologic insults that are known to result in hyperadrenergic stimulation, such as subarachnoid hemorrhage, ischemic or hemorrhagic stroke, seizure, encephalitis, traumatic brain injury, acute hydrocephalus, posterior reversible encephalopathy syndrome, and even severe headache. [17][18][19][20][21] Patients with stroke at or near the insular cortex with resulting overflow of sympathetic nerve trafficking seem to be particularly susceptible to TS. 22 TS has also been reported with several other conditions of enhanced sympathetic tone, including postural orthostatic tachycardia syndrome, 23 alcohol and opioid withdrawal, 24,25 and cocaine use.…”

Section: Association With High Catecholamine Statesmentioning

confidence: 99%