Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage

Bulsara, Ketan R.; McGirt, Matthew J.; Liao, Lawrence; Villavicencio, Alan T.; Borel, Cecil O.; Alexander, Michael J.; Friedman, Allan H.

doi:10.3171/jns.2003.98.3.0524

Cited by 116 publications

(63 citation statements)

References 67 publications

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“…[3][4][5][6][7] However, to the best of our knowledge, there have only been a handful of reports of true transient LVAB in patients with SAH. [12][13][14][15] Also called Takotsubo cardiomyopathy, this syndrome was first described in 1991 in Japan 16 and named Takotsubo-like LV dysfunction in reference to the associated LV morphological features consisting of akinesia predominately of the apex and midventricle with relative sparing of the basal segment, creating a highly characteristic configuration during systole 8 -11 (Figure 2a; Takotsubo is a pot with a round bottom and narrow neck used for trapping octopuses in Japan).…”

Section: Discussionmentioning

confidence: 99%

“…4 -7 The extent of troponin I elevation and RWMA have been strongly associated with poor outcomes. [3][4][5][6][7] Moreover, the degree of neurological injury has been independently associated with myocardial necrosis. 5,7 Pathologically, this form of myocardial injury is characterized by subendocardial contraction band necrosis, which is thought to result from excessive release of norepinephrine from the cardiac sympathetic nerves.…”

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confidence: 99%

“…T he neurocardiogenic spectrum of subarachnoid hemorrhage (SAH) spans from ECG abnormalities in almost 50% to 100% patients 1,2 (deep T-wave inversions, QT prolongation, and torsades de pointes) to myocardial enzyme release in 20% to 40% [3][4][5] and regional wall motion abnormalities (RWMA) in 10% of patients. 6,7 These cardiac phenotypes have been attributed largely to the catecholamine surge accompanying SAH.…”

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When the Worst Headache Becomes the Worst Heartache!

Hakeem

Marks

Bhatti

et al. 2007

Stroke

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Background and Purpose-Although a great deal of literature has been generated regarding left ventricular wall abnormalities, ECG changes and cardiac enzyme leaks associated with subarachnoid hemorrhage (SAH), there have been only a few reports of true transient left ventricular apical ballooning syndrome in patients with SAH. Several pathophysiological mechanisms have been proposed to explain the unusual features of this syndrome, such as multivessel coronary vasospasm, abnormalities in coronary microvascular function, and catecholamine-mediated cardiotoxicity. Summary of Case-A previously healthy 64-year-old woman with no history of vascular disease was found unresponsive at home. She was taken to the emergency room where a CT head revealed an SAH due to a ruptured aneurysm of the posterior communicating artery. On admission, an ECG showed deeply inverted T-waves and QT prolongation, typical of SAH. Cardiac troponin was measured at 1.2 ng/mL, and later increased to 3.7 ng/mL. A transthoracic echocardiogram on the next day revealed a large left ventricular wall abnormality, characteristic of apical ballooning with an ejection fraction of 25% to 30%. The patient remained hemodynamically stable and was started on low dose ␤-blocker and angiotensin-converting enzyme inhibitor. She had an uneventful cardiac recovery within 5 days at which time a repeat transthoracic echocardiogram revealed a normal ejection fraction with no wall motion abnormality. Conclusions-This report adds to the growing list of "stressors" for Takotsubo cardiomyopathy. Clinicians should be aware of the existence and the typical clinical manifestations of this syndrome, which is increasingly recognized in various populations. In particular, neurologists should consider this syndrome in the differential diagnosis of ECG changes and apical wall motion abnormalities in patients with SAH. Prognosis is generally very good with full recovery in most patients; however, there may be increased morbidity associated in patients with SAH. (Stroke. 2007;38:3292-3295.)

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When the Worst Headache Becomes the Worst Heartache!

Hakeem

Marks

Bhatti

et al. 2007

Stroke

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“…Badania echokardiograficzne ujawniające znaczną niezgodność z badaniami EKG wskazują na dysfunkcję lewej komory związaną z SAH (SM, stunned myocardium). Stężenia cTn < 2,8 µg l -1 u chorych z frakcją wyrzutową poniżej 40% są charakterystyczne dla SM [13]. Kolejną cenną wskazówką diagnostyczną może być mechanizm CA oraz obecność bólu głowy bądź inne objawy neurologiczne w wywiadzie sprzed NZK.…”

Section: Dyskusjaunclassified

Krwawienie podpajęczynówkowe imitujące ostry zespół wieńcowy jako przyczyna pozaszpitalnego zatrzymania krążenia

Lewandowski

2014

Anaesthesiol Intensive Ther

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Należy cytować anglojęzyczną wersję artykułu z: Lewandowski P: Subarachnoid haemorrhage imitating acute coronary syndrome as a cause of out-of-hospital cardiac arrest -case report. Anaesthesiol Intensive Ther 2014; 46: 289-292 Case report: A 47-year-old man presented with a history of out-of-hospital cardiac arrest due to asystole. He had a medical history of hypertension, smoking, and a diffuse, severe headache for one week. The ECG showed atrial fibrillation, 0,2 mV ST-segment elevation in leads aVR and V1-V3 and 0.2 mV ST-segment depression in leads I, II, aVL and V4-V6. Echocardiography revealed left ventricular function impairment (ejection fraction < 20%). The CK-MB activity was 98 U L -1 and the troponin I concentration was 0.59 µg L -1 . ACS was suspected. Coronarography did not reveal any changes in the coronary arteries. An urgent CT of the head was arranged and showed an extensive SAH.Conclusions: It appears that an urgent CT of the head is the most effective method for the early identification of SAH-induced OHCA, especially in patients with prodromal headache, no history of the symptoms of ACS and CA due to asystole/pulseless electrical activity (PEA). Out-of-hospital cardiac arrest (OHCA) predominantly develops due to acute coronary syndrome (ACS). Extra-cardiac causes, e.g., subarachnoid haemorrhage (SAH), are less common. The purpose of the present case report was to describe a patient with OHCA due to subarachnoid haemorrhage imitating acute coronary syndrome.

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“…1 Troponin T release has been demonstrated in 20 to 40% of SAH patients and was positively correlated with the severity of neurological symptoms. 2,3 ECG abnormalities have been shown in 50 to 100% of SAH patients and mostly consisted of ST-T changes, QT prolongation and U wave abnormalities, whereas rhythm and conductance disturbances were less frequent. [4][5][6] It is thought that improvement in LVEF parallels normalisation of the ECG.…”

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Traumatic subdural haematoma with electrocardiographic abnormalities simulating myocardial infarction

Oostrom

Mauser²,

Wever³

2009

NHJL

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A 58-year-old man with a history of alcohol abuse and smoking presented with a subdural haematoma due to head trauma after alcohol intoxication. He was disorientated; general and specific cardiological and neurological examinationswere unremarkable. Cardiac troponin T (0.053 µg/l), N-terminal pro-B type natriuretic peptide (768 pg/ml) and serum ethanol (3316 mg/l) were elevated. Creatinine kinase (21 U/l) and lactate dehydrogenase (214 U/l) were normal. Other liver function tests and mean erythrocyte cellular volume suggested chronic alcohol abuse. CT scan of the head demonstrated a right-sided subdural haematoma and contusional lesions in the right frontal lobe. At day 2, the haematoma and contusional lesions had slightly increased, without further deterioration at follow-up. His ECG showed a sinus tachycardia with a left axis, left anterior fascicular block and Q waves in the right precordial leads. Follow-up showed reversible diffuse repolarisation abnormalities, suggesting evolving myocardial infarction. Echocardiography at day 16 showed normal dimensions without regional wall motion disturbances or significant valve abnormalities. Myocardial perfusion imaging after three months showed normal left ventricular (LV) function without ischaemic changes. Therefore, the described Q waves were most likely secondary to the axis deviation and the repolarisation changes were ascribed to the traumatic intracranial lesions and not to coronary artery disease or alcoholic cardiomyopathy. Neurogenic cardiac dysfunction due to subdural haematoma has not been extensively investigated, but it is likely to be similar to that seen in subarachnoid haemorrhage (SAH). In the latter, reversible left ventricular dysfunction, troponin release and ECG abnormalities have been observed. In 8 to 15% of these patients a diminished LV ejection fraction (LVEF <50%) was shown; however, cardiogenic shock rarely occurred. 1,2 Wall motion disorders usually occurred in the first days after SAH, did not match coronary artery distribution and generally showed spontaneous improvement. 1 Troponin T release has been demonstrated in 20 to 40% of SAH patients and was positively correlated with the severity of neurological symptoms. 2,3 ECG abnormalities have been shown in 50 to 100% of SAH patients and mostly consisted of ST-T changes, QT prolongation and U wave abnormalities, whereas rhythm and conductance

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Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage

Cited by 116 publications

References 67 publications

When the Worst Headache Becomes the Worst Heartache!

When the Worst Headache Becomes the Worst Heartache!

Krwawienie podpajęczynówkowe imitujące ostry zespół wieńcowy jako przyczyna pozaszpitalnego zatrzymania krążenia

Traumatic subdural haematoma with electrocardiographic abnormalities simulating myocardial infarction

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