Reversible left ventricular dysfunction after subarachnoid hemorrhage

Handlin, Larry R.; Kindred, Lynn H.; Beauchamp, Gary D.; Vacek, James L.; Rowe, Steven K.

doi:10.1016/s0002-8703(07)80039-1

Cited by 33 publications

(13 citation statements)

References 15 publications

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“…5,[23][24][25][26][27][28][29] Furthermore, it was reported that myocardial necrosis occurred in these patients, as evidenced by elevated serum concentrations of CK-MB, troponin T, or myosin light chain above the normal values within 2 to 3 days after the onset of SAH as well as the contraction band, myocardial fragmentation, and focal myocytolysis observed in the myocardium at autopsy. 9,30 -32 We investigated the pathogenesis of cardiopulmonary complications on the basis of the clinical observation of 717 cases in the acute phase of SAH.…”

Section: Discussionmentioning

confidence: 88%

Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

Masuda

Sato

Yamamoto

et al. 2002

Stroke

174

117

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Background and Purpose-Obvious cardiac dysfunction, including ECG abnormalities and left ventricular asynergy, is known to develop after subarachnoid hemorrhage (SAH). To clarify the close relationship between myocardial damage and sympathetic nervous activity immediately after SAH, a novel experimental animal model was used. Methods-SAH was provoked by perforation of the basilar artery with the use of a microcatheter inserted through the femoral artery in 18 beagle dogs. Hemodynamic changes were recorded, and plasma concentrations of noradrenaline, adrenaline, and 3-methoxy-4-hydroxy-phenylethylene glycol (MHPG) and serum levels of creatine kinase-MB (CK-MB) and troponin T were measured at 0, 5, 15, 30, 60, 120, and 180 minutes after SAH. Results-Noradrenaline (pg/mL), adrenaline (pg/mL), and MHPG (ng/mL) increased abruptly from 120Ϯ70, 130Ϯ70, and 1.3Ϯ0.5 before SAH to 1700Ϯ1200, 5600Ϯ3500, and 3.2Ϯ1.2 at 5 minutes after SAH, respectively. Aortic pressure, left ventricular wall motion, and cardiac output increased by 60%, 40%, and 30%, respectively (PϽ0.001) at 5 minutes and then decreased by 50%, 55%, and 40%, respectively (PϽ0.001) Ͼ60 minutes after SAH compared with baseline values. The peak value of CK-MB correlated positively with the peak values of noradrenaline and adrenaline (rϭ0.730 and rϭ0.611, respectively). The peak value of troponin T also correlated positively with the peak values of noradrenaline and adrenaline (rϭ0.828 and rϭ0.792, respectively). Conclusions-These results suggest that the elevated activity of the sympathetic nervous system observed in the acute phase of SAH induced myocardial damage and contributed to the development of cardiac dysfunction.

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Section: Discussionmentioning

confidence: 88%

Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

Masuda

Sato

Yamamoto

et al. 2002

Stroke

174

117

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“…Indeed, in neurosurgical models and clinical studies, 40% to 100% with SAH can have ECG changes or arrhythmias, 16–20 11% to 21% can have myocardial enzyme elevation, 17,19,20 and 2% to 30% may have left ventricular dysfunction manifested by hypokinetic wall-motion abnormalities on echocardiography. 17–20 Compared with AIS, heart–brain interactions in SAH have been more widely investigated, 21–34 with literature describing reversible myocardial stunning, 35 histologic evidence of myocardial necrosis, 36 elevation of natriuretic factors, 37,38 secondary neurogenic pulmonary edema, 39 elevation of systemic plasma catecholamines, 40,41 and impairment of regional myocardial perfusion. 42,43 Additionally, in the neurosurgical literature, hemodynamic manipulations have been more rigorously evaluated, specifically for the management of cerebral vasospasm after SAH 44 …”

Section: Discussionmentioning

confidence: 99%

Cardiac Complications in Acute Ischemic Stroke

Wira¹,

Rivers²,

Martinez-Capolino³

et al. 2011

WestJEM

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IntroductionTo characterize cardiac complications in acute ischemic stroke (AIS) patients admitted from an urban emergency department (ED).MethodsRetrospective cross-sectional study evaluating AIS patients admitted from the ED within 24 hours of symptom onset who also had an echocardiogram performed within 72 hours of admission.ResultsTwo hundred AIS patients were identified with an overall in-hospital mortality rate of 8% (n = 16). In our cohort, 57 (28.5%) of 200 had an ejection fraction less than 50%, 35 (20.4%) of 171 had ischemic changes on electrocardiogram (ECG), 18 (10.5%) of 171 presented in active atrial fibrillation, 21 (13.0%) of 161 had serum troponin elevation, and 2 (1.1%) of 184 survivors had potentially lethal arrhythmias on telemetry monitoring. Subgroup analysis revealed higher in-hospital mortality rates among those with systolic dysfunction (15.8% versus 4.9%; P = 0.0180), troponin elevation (38.1% versus 3.4%; P < 0.0001), atrial fibrillation on ECG (33.3% versus 3.8%; P = 0.0003), and ischemic changes on ECG (17.1% versus 6.1%; P = 0.0398) compared with those without.ConclusionA proportion of AIS patients may have cardiac complications. Systolic dysfunction, troponin elevation, atrial fibrillation, or ischemic changes on ECG may be associated with higher in-hospital mortality rates. These findings support the adjunctive role of cardiac-monitoring strategies in the acute presentation of AIS.

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“…The association of left ventricular dysfunction with female sex was of borderline significance but is in agreement with reports describing a striking preponderance of females among patients with abnormal wall motion after SAH (28/31 cases), for reasons unknown. [11][12][13][14][15][35][36][37][38] Our main finding is the association of CK-MB release and abnormal left ventricular wall motion with impaired left ventricular hemodynamic performance. Indicators of left ventricular performance (LVSVI, LVSWI, and CI) were abnormally high in patients with no CK-MB release, and these measures fell progressively as the severity of cardiac injury increased (see the Figure).…”

Section: Discussionmentioning

confidence: 99%

“…Normal coronary arteries have been found in the vast majority of SAH patients with left ventricular hypokinesis after SAH studied by angiography or autopsy. [12][13][14][15][35][36][37][38] We identified severity of SAH on the admission CT scan (Fisher grade III or IV) and depressed CI measured on the first postoperative day as independent predictors of clinical deterio- ration related to vasospasm. In addition to the extent of blood on CT, which is the most powerful determinant of symptomatic vasospasm, 29,[42][43][44][45][46] younger age, 42 poor clinical grade, 42,46 angiographic vasospasm, 43 early surgery, 43 treatment with antifibrinolytics, 44,46 preexisting hypertension, 43 and cigarette smoking 45 have been previously identified as risk factors for delayed ischemia after SAH.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Injury and Left Ventricular Performance After Subarachnoid Hemorrhage

Mayer

Lin

Homma

et al. 1999

Stroke

260

149

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Background and Purpose-Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. Methods-We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (nϭ67) or on the day of echocardiography (nϭ5) if surgery was not performed (mean, 3.3Ϯ1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB Ͻ1%, nϭ36), mild (peak CK-MB 1% to 2%, nϭ21), moderate (peak CK-MB Ͼ2%, nϭ6), or severe (abnormal left ventricular wall motion, nϭ9). Results-Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels Ͼ2% (PϽ0.0001), poor neurological grade (Pϭ0.002), and female sex (Pϭ0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels Ͻ1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both PϽ0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (PϽ0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; Pϭ0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; Pϭ0.04) were independent predictors of symptomatic vasospasm. Conclusions-Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm. (Stroke. 1999;30:780-786.)

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Reversible left ventricular dysfunction after subarachnoid hemorrhage

Cited by 33 publications

References 15 publications

Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

Cardiac Complications in Acute Ischemic Stroke

Myocardial Injury and Left Ventricular Performance After Subarachnoid Hemorrhage

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