Cardiac Complications After Subarachnoid Hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome.

Acute cardiac complications frequently occur after subarachnoid hemorrhage (SAH). These complications include electrocardiogram (ECG) abnormalities, the release of cardiac biomarkers, and the development of acute stress-induced heart failure resembling Takotsubo cardiomyopathy 1) 2) 3) 4) 5) 6)

non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.



Lång et al. assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH in a prospective observational multicenter study. They included 192 patients treated for non traumatic subarachnoid hemorrhage. They performed ECG recordings, echocardiogram, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0-64.0) years, 44.3% were male and the median World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage score was 2 (IQR 1-4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak e’ velocity (E/e’) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. They found no demographic or SAH-related factors associated with 90 days cardiac dysfunction 7).


Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).


1)

Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999;44:34–39. doi: 10.1097/00006123-199901000-00013.
2)

Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35:548–551. doi: 10.1161/01.STR.0000114874.96688.54.
3)

Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15–20. doi: 10.3171/jns.2006.105.1.15.
4)

Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown JRD, Wijdicks EFM. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. doi: 10.3171/jns.2006.105.2.264.
5)

Oras J, Grivans C, Bartley A, Rydenhag B, Ricksten SE, Seeman-Lodding H. Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. Crit Care (Lond, Engl) 2016;20:11. doi: 10.1186/s13054-015-1181-5.
6)

van der Bilt IA, Hasan D, Vandertop WP, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72:635–642. doi: 10.1212/01.wnl.0000342471.07290.07.
7)

Lång M, Jakob SM, Takala R, Lyngbakken MN, Turpeinen A, Omland T, Merz TM, Wiegand J, Grönlund J, Rahi M, Valtonen M, Koivisto T, Røsjø H, Bendel S. The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022 Nov 22;12(1):20109. doi: 10.1038/s41598-022-24675-8. PMID: 36418906.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.

Update: Adenosine-induced cardiac standstill with hypotension

Several flow-arrest techniques have been introduced for the treatment of complex aneurysms that cannot be treated with conventional clipping or endovascular coil embolization. Adenosine-induced transient asystole is an alternative method of flow arrest.

Adenosine-induced flow arrest briefly reduces cerebral perfusion pressure and reduces the turgor of the aneurysm, thereby facilitating the clip ligation in complex aneurysms. Periods of flow arrest have to be carefully coordinated with the surgeon such that necessary working time is available for aneurysm dissection and clip placement. Adenosine-induced transient asystole is safe and efficacious when administered at an average of 0.3 to 0.4 mg/kg IBW in combination with remifentanil/low-dose volatile anesthetic with propofol. The adenosine dose will achieve approximately 45 seconds of controlled systemic hypotension and a bloodless surgical field. Adenosine offers the advantage of easy applicability in different situations without advanced preparation or complex logistical coordination with anesthesiology and cardiovascular surgery. This technique also allows the surgeon to have the maximum amount of space available to manipulate the aneurysm and place the clips, as no temporary clips are in the field of view. Also, temporary clips only decrease flow from the clipped inflow, whereas adenosine produces a more global hypotension and therefore often a better collapse of the aneurysm 1).
Adenosine-induced asystole for cerebral aneurysms surgery was first described by Groff et al. 2) in 1999 in posterior circulation aneurysms.
It is an easily applied technique in a variety of clinical situations. Its use requires minimal advanced preparation and no complex logistical coordination with other subspecialties. However, patient-specific dose-response relationships must be determined by exposure, so the relationship may not be known in an emergent situation. Persistent hypotension is a potentially major complication. Rapid ventricular pacing (RVP) has recently been reintroduced into cerebrovascular surgery. It is more predictable than adenosine in response time and, thus, can be used during unanticipated complications, such as aneurysmal rupture. It also induces a shorter period of hypotension compared with adenosine. However, RVP is more invasive and more complex from an anesthesia standpoint. Vascular neurosurgeons should be familiar with these techniques and know their applications and limitations 3).

Case series

2017

The aim of a study is to report the experience in the use of adenosine in aneurysm clipping and arteriovenous malformation (AVM) resection and review the literature. The records of all patients who had adenosine-assisted clipping of intracranial aneurysms and AVM resections between November 2015 and December 2016 were extracted from prospectively maintained database. The following data were collected: patient demographics, comorbidities, size and location of the aneurysms or AVM, number of boluses and total dose of adenosine administered, duration of cardiac standstill and hypotension (systolic blood pressure < 60 mmHg), intraoperative and postoperative complications and outcome scores at discharge. Literature search on Embase and PubMed for the terms “adenosine and clipping”, “adenosine and aneurysm” and “adenosine and AVM” was performed. Eight aneurysms and two AVMs were identified. While both AVMs were elective procedures, half of the aneurysm clippings were on urgent basis.
Al-Mousa et al. used adenosine safely with spontaneous return of rhythm in all cases. Temporary clips to the parent artery were applied for brief periods in 2 patients who had pre-adenosine intraoperative rupture. They did not observe any immediate or late adverse events related to administration of adenosine.
In a review, a total of ten case series and four case reports were identified. There were no reports on the use of adenosine in AVM resection. Transient adenosine-induced asystole is a safe and effective technique in facilitating surgical treatment of complex aneurysms and AVMs. In addition, adenosine use reduces the need, duration, and associated complications of temporary clip applications to parent arteries 4).

2015

A total of 22 aneurysms in 22 different patients that underwent adenosine-induced transient asystole during aneurismal neck clipping within the past 4 years were retrospectively reviewed. Adenosine was administrated intravenously in a test-incremental manner (starting with 6-12 mg and then giving additional doses as needed) in 11 patients and in an estimated manner (pre-calculated as 0.3-0.4 mg/kg) in 11 patients.
Overall, the study consisted of 18 unruptured saccular aneurysms, three ruptured saccular aneurysms, and a ruptured pseudoaneurysm. Adenosine-induced transient asystole was used in cases of temporary clipping inability, wide necked aneurysm, deep-seated aneurysm, or a thin aneurysm wall. The number of administrations, dose (mg/kg in ideal body weight) and duration of asystole were 1-4 (mean, 2.3) times, 0.08-1.27 (mean, 0.36) mg/kg and 0-30 (mean 13) seconds in the test-incremental manner and 1-2 (mean, 1.09) times, 0.24-0.42 (mean, 0.34) mg/kg and 13-41 (mean, 24) seconds in the estimated manner, respectively. There was a linear relationship between the dose and the duration of asystole. Twenty out of 22 aneurysms were clipped successfully with adenosine-induced transient asystole. However, in the other two cases, additional suction decompression was required for the final clipping. Adenosine-related cardiologic complications occurred in two cases of self-limited atrial fibrillation during restoration of the cardiac rhythm.
In our experience, adenosine-induced transient asystole was safe and helpful for satisfactory clipping of a complicated aneurysm. An estimated dose injection of adenosine was more convenient than the test-incremental method and did not result in serious cardiologic problems 5).

2009

A report describes three children, aged eight to 11 years, with high-flow cerebral arteriovenous malformations who underwent interventional neuroradiological procedures involving glue (N-butyl cyanoacrylate) embolisation under general anaesthesia. The procedure was facilitated by relative hypotension induced by esmolol infusion and intravenous adenosine boluses. To allow controlled deposition of N-butyl cyanoacrylate into the arteriovenous malformations, glue injection was synchronised with the onset of adenosine-induced brief cardiac standstill. This resulted in satisfactory obliteration of the arteriovenous malformations nidus in all cases. The haemodynamic modulations, including the adenosine-induced brief cardiac standstill, was noted to not affect the BIS values in our patients. All patients had satisfactory obliteration of their arteriovenous malformations and had good neurological outcomes at one-year follow-up 6).
1)

Britz GW. Adenosine-induced transient asystole. Methodist Debakey Cardiovasc J. 2014 Oct-Dec;10(4):220-3. doi: 10.14797/mdcj-10-4-220. Review. PubMed PMID: 25624976; PubMed Central PMCID: PMC4300060.
2)

Groff MW, Adams DC, Kahn RA, Kumbar UM, Yang BY, Bederson JB. Adenosine-induced transient asystole for management of a basilar artery aneurysm. Case report. J Neurosurg. 1999 Oct;91(4):687-90. PubMed PMID: 10507394.
3)

Rangel-Castilla L, Russin JJ, Britz GW, Spetzler RF. Update on transient cardiac standstill in cerebrovascular surgery. Neurosurg Rev. 2015 Oct;38(4):595-602. doi: 10.1007/s10143-015-0637-z. Epub 2015 May 1. PubMed PMID: 25931209.
4)

Al-Mousa A, Bose G, Hunt K, Toma AK. Adenosine-assisted neurovascular surgery: initial case series and review of literature. Neurosurg Rev. 2017 Jul 22. doi: 10.1007/s10143-017-0883-3. [Epub ahead of print] Review. PubMed PMID: 28735438.
5)

Lee SH, Kwun BD, Kim JU, Choi JH, Ahn JS, Park W, Yun JH. Adenosine-induced transient asystole during intracranial aneurysm surgery: indications, dosing, efficacy, and risks. Acta Neurochir (Wien). 2015 Nov;157(11):1879-86; discussion 1886. doi: 10.1007/s00701-015-2581-7. Epub 2015 Sep 18. PubMed PMID: 26385113.
6)

Puri GD, Sen I, Bapuraj JR. Adenosine-induced cardiac standstill to facilitate endovascular embolisation of cerebral arteriovenous malformations in children. Anaesth Intensive Care. 2009 Jul;37(4):619-23. PubMed PMID: 19681422.
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