Harley, MD, Dushawn

English

eCommons at Roseman University

A Review of Neurogenic Cardiomyopathy in Subarachnoid Hemorrhage and the Prognostic Implications of Cardiac BiomarkersDushawn Harley, MD; Tyler Heldreth, MD; Cory Nichols, DO; Matthew Hanewich, DO; My Huyen Le, DO; Worawith Techathaveewat, DO; Anthony Nguyen, DO; Hoa Coa, DO; Sai Guda, DO; Velliyur Viswesh, PharmD, BCIDP, BCCCP; Scott Silver, DO; Mark Mckenzie, MD; Paul Janda, DO,JD; Paul Stewart, MD; Syed Akbarullah, MDRESULTSThis search yielded thirty-eight articles for review, including case reports, prospective and retrospective studies, and prior literature reviews. The parameters reported included EKG changes, BNP and troponin elevations over time, pulmonary artery catheter pressures, echocardiographic findings, and their relation to morbidity and mortality. These publications and their key findings were summarized in a collected table. Their results and findings are compared within related measured outcomes. Of the articles, 12 of the 38 focused on the relation between cardiac biomarkers, morbidity, and mortality. Of the 12, 10 articles showed elevated cardiac biomarkers to correlate with increased morbidity and mortality CONCLUSIONThe relevance of elevated cardiac biomarkers following an aneurysmal SAH impact on morbidity and mortality is an under-researched topic, and warrants further investigation and development of standardized guidelines. A trend exists between the amount of cardiac biomarker elevation and poor outcomes, however there exist no guidelines aimed at monitoring and managing cardiac complications. REFERENCES1) Ingall, T., Asplund, K., Mähönen, M., & Bonita, R. (2000). A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke, 31(5), 1054–1061. https://doi.org/10.1161/01.str.31.5.10542) Naidech AM, Kreiter KT, Janjua N, Ostapkovich ND, Parra A, Commichau C, Fitzsimmons BF, Connolly ES, Mayer SA. Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage. Circulation. 2005 Nov 1;112(18):2851-6. doi: 10.1161/CIRCULATIONAHA.105.533620. PMID: 16267258.3) Van der Bilt IA, Hasan D, Vandertop WP, Wilde AA, Algra A, Visser FC, Rinkel GJ. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009 Feb 17;72(7):635-42. doi: 10.1212/01.wnl.0000342471.07290.07. PMID: 19221297.4) Tung P, Kopelnik A, Banki N, Ong K, Ko N, Lawton MT, Gress D, Drew B, Foster E, Parmley W, Zaroff J. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004 Feb;35(2):548-51. doi: 10.1161/01.STR.0000114874.96688.54. Epub 2004 Jan 22. PMID: 14739408.5) Banki NM, Kopelnik A, Dae MW, Miss J, Tung P, Lawton MT, Drew BJ, Foster E, Smith W, Parmley WW, Zaroff JG. Acute neurocardiogenic injury after subarachnoid hemorrhage. Circulation. 2005 Nov 22;112(21):3314-9. doi: 10.1161/CIRCULATIONAHA.105.558239. Epub 2005 Nov 14. PMID: 162865836) Sommargren CE, Zaroff JG, Banki N, Drew BJ. Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. J Electrocardiol. 2002;35 Suppl:257-62. doi: 10.1054/jelc.2002.37187. PMID: 12539136.7) Parekh N, Venkatesh B, Cross D, Leditschke A, Atherton J, Miles W, Winning A, Clague A, Rickard C. Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage. J Am Coll Cardiol. 2000 Oct;36(4):1328-35. doi: 10.1016/s0735-1097(00)00857-3. PMID: 11028491.8)  Zahid T, Eskander N, Emamy M, Ryad R, Jahan N. Cardiac Troponin Elevation and Outcome in Subarachnoid Hemorrhage. Cureus. 2020 Aug 16;12(8):e9792. doi: 10.7759/cureus.9792. PMID: 32821636; PMCID: PMC7431985.9)  de Chazal I, Parham WM 3rd, Liopyris P, Wijdicks EF. Delayed cardiogenic shock and acute lung injury after aneurysmal subarachnoid hemorrhage. Anesth Analg. 2005 Apr;100(4):1147-9. doi: 10.1213/01.ANE.0000147704.90285.2A. PMID: 15781536.10)  Hop JW, Rinkel GJ, Algra A, van Gijn J. Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review. Stroke. 1997 Mar;28(3):660-4. doi: 10.1161/01.str.28.3.660. PMID: 9056628.     INTRODUCTIONThe incidence of subarachnoid hemorrhage (SAH) is approximately 2 to 22 per 100,000, with incidence being about twice as high in women than men [1]. Neurogenic cardiomyopathy has become a well known sequelae of SAH, occurring in approximately 20-40% of patients [2,4,6,7]. It is generally believed that sympathetic stimulation of the myocardium causes contraction band necrosis leading to the cardiomyopathy. ECG changes observable in 50-100% of patients, and detectable cardiac troponins observed in 20-40% of patients [2,4,6,7]. Left ventricle wall motion abnormalities (WMA) are detectable on echocardiograms in 20% of patients [2,3,5,7]. These cardiac changes have been associated pulmonary edema, hypotension requiring vasopressor support as well as delayed cerebral ischemia (DCI), a known cause of death in SAH, and longer ICU stay [2,3,5,8,9,10]. It is not well understood how the severity of cardiac biomarkers elevation correlates with clinical outcomes, however. The purpose of this review is to identify and summarize the incidence and prognostic implications of elevated cardiac biomarkers on SAH outcomes.METHODSA search was performed on Pubmed database for the keywords ‘aneurysmal subarachnoid hemorrhage’ AND ‘cardiomyopathy’ OR ‘troponin’ OR ‘BNP’ OR ‘ECG’ OR ‘echocardiography’ for the time period of  2001 to 2021. Studies among references in articles identified by this search were also screened for inclusion in the systematic review. A study was considered eligible if it was an English language article and reported quantitative data cardiac biomarkers (troponin, BNP, pro-BNP), ECG, or echocardiogram with ejection fraction and wall motion abnormalities. Data were extracted about the incidence of cardiac complications following subarachnoid hemorrhage, qualitative measurement of severity of the cardiac complications (cardiac biomarkers, ECG, echocardiogram), clinical interventions, inpatient complications, and clinical outcomes.Summary of clinical studies and reviews evaluating the prevalence of cardiac biomarkers and prognostic impact in aneurysmal SAHNaidech, A. M., et. al.  (2005). Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage. Circulation, 112(18), 2851–2856. ● cTnI reached peak around day 3 from SAH onset● Peak cTnI was significantly associated w/ a significantly increased risk of abnormal LV wall motion on echo, pulmonary edema, hypotension treated with pressors, Delayed cerebral ischemia (DCI) from vasospasm, and cerebral infarction from any cause ● Peak cTnI lvl:○  >0.5 mcg/L → 50% risk for DCI○  >2.0 mcg/L → 30% risk for Pulm Edema○  >10.0 mcg/L → 40% risk for developing hypotension● cTnI elevation was significantly associated w/ an increased likelihood of death or severe disability at discharge ● cTnI elevation was associated w/ increased hospital stay (mean: 22.9d)Schuiling, W. J. et. al.  (2006). ECG abnormalities in predicting secondary cerebral ischemia after subarachnoid haemorrhage. Acta neurochirurgica, 148(8), 853–858.● Only ST segment depression predicted the occurrence of DCI● ST depression and ischemic ECG abnormalities (presence of ST depression or TWI, or both in at least 2 leads) appeared independent predictors of poor outcomevan der Bilt, I. A. et. al. (2009). Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology, 72(7), 635–642. ● Wall motion abnormalities (WMAs), elevated troponin, and proBNP lvls, tachycardia, and Q aves, ST depression, and T wave abnormalities were significantly associated w/ an increased risk of death● WMAs, elevated troponin/CK-MB/proBNP lvls, ST-segment depression were significantly associated w/ an increase risk of the development of DCI● Elevated troponin and CK-MB lvls, ST-depression were significantly associated w/ poor outcome Murthy, S. B. et. al.. (2015). Neurogenic Stunned Myocardium Following Acute Subarachnoid Hemorrhage: Pathophysiology and Practical Considerations. Journal of intensive care medicine, 30(6), 318–325. ● Recent studies have shown that ST-T changes and QTc prolongation have no correlation with the development of delayed cerebral ischemia, raised intracranial pressure, or mortality● A small retrospective study observed that cTI elevation was significant associated with vasospasm and mortality, after adjusting for admission Hunt-Hess grade, age, and aneurysm size● Patients having elevated cTI are more likely to have severe vasospasmAkkermans, A. et. al. (2019). Cardiac events within one year after a subarachnoid haemorrhage: The predictive value of troponin elevation after aneurysm occlusion. European journal of preventive cardiology, 26(4), 420–428. ● Troponin I elevation after occlusion of a ruptured intracranial aneurysm predicts the occurrence of a major adverse cardiac event within one year after ASAH, as measured by MACE.Zahid, T. et. al. (2020). Cardiac Troponin Elevation and Outcome in Subarachnoid Hemorrhage. Cureus, 12(8), e9792. ● Cardiac troponin elevation post-SAH is associated w/ many systemic complications, poor outcomes and increase mortality  ● Elevated troponin and BNP predict worse outcomes after SAH● Cardiac dysfunction defined by myocardial WMAs or positive troponin after SAH is also linked to decreased focal and global cerebral perfusion ● WMAs are risk factor for poor clinical outcome after SAH

C34: A Review of Neurogenic Cardiomyopathy in Subarachnoid Hemorrhage and the Prognostic Implications of Cardiac Biomarkers

https://ecommons.roseman.edu/cgi/viewcontent.cgi?article=1064&amp;context=researchsymposium

C34: A Review of Neurogenic Cardiomyopathy in Subarachnoid Hemorrhage and the Prognostic Implications of Cardiac Biomarkers

Abstract

Similar works

Full text

Available Versions

eCommons at Roseman University