Relation of Elevation in Cardiac Troponin I to Clinical Severity, Cardiac Dysfunction, and Pulmonary Congestion in Patients With Subarachnoid Hemorrhage

Abstract

An increase in cardiac troponin I (cTnI) occurs often after aneurysmal subarachnoid hemorrhage (SAH), but its significance is not well understood. One hundred three patients with SAH were prospectively evaluated in the SAHMII Study to determine the relations of cTnI to clinical severity, systolic and diastolic cardiac function, pulmonary congestion, and length of intensive care unit stay. Echocardiographic ejection fraction, wall motion score, mitral inflow early diastolic (E) and mitral annular early (E′) velocities were assessed. Thirty patients (29%) had mildly positive cTnI (0.1 to 1.0 ng/ml), 24 (23%) had highly positive cTnI (>1.0 ng/ml), and 49 (48%) had negative cTnI (<0.1 ng/ml). Highly positive cTnI was associated with worse neurologic disease, longer intensive care unit stay, and slight depression of ejection fraction (51 ± 11% [p <0.05] vs 59 ± 8% and 63 ± 6% in mildly positive or negative cTnI groups, respectively). Highly positive cTnI was also associated with abnormal wall motion acutely (>1.31 ng/ml; 76% sensitivity, 91% specificity), which typically resolved within 5 to 10 days. Both mildly or highly positive cTnI were associated with acute diastolic dysfunction, with E/E′ of 17 ± 6 and 16 ± 6 (both p <0.05) vs 13 ± 4 in patients with negative cTnI. Prevalences of pulmonary congestion were 79% (p <0.05) in patients with highly positive cTnI, 53% (p <0.05) in patients with mildly positive cTnI, and 29% in cTnI-negative patients. In conclusion, highly positive cTnI with SAH was associated with clinical neurologic severity, systolic and diastolic cardiac dysfunction, pulmonary congestion, and longer intensive care unit stay. Even mild increases in cTnI were associated with diastolic dysfunction and pulmonary congestion.

The Role of Norepinephrine and Estradiol in the Pathogenesis of Cardiac Wall Motion Abnormality Associated With Subarachnoid Hemorrhage

“…Interestingly, neither high norepinephrine levels in the presence of high estradiol nor low estradiol levels in the presence of low norepinephrine were associated with elevated incidence of WMA. These results are in concordance with those in the literature [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] and seem to explain why WMA develops most frequently in postmenopausal women with poor-grade SAH. Although this retrospective study does not provide clues to the mechanism of possible cardiac protection by estrogen, there is much circumstantial evidence to support current results.…”

“…5,7,8 It has been hypothesized that massive release of catecholamine into the systemic circulation after SAH results in the nonischemic usually reversible myocardial injury. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] In the cardiology literature, the possible role of estrogen in the pathogenesis of WMA has recently been suggested in patients with takotsubo (stress) cardiomyopathy (TCM). 16 -18 This hypothesis is based on the clinical observation that a majority of patients with TCM are postmenopausal women, whereas only a few young women are diagnosed with TCM.…”

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] WMA occurs in patients with SAH with a reported incidence of 8% to 27%. 5,7,8 It has been hypothesized that massive release of catecholamine into the systemic circulation after SAH results in the nonischemic usually reversible myocardial injury.…”

“…It is probable that decreased estrogen levels are causally associated with WMA in patients with SAH, because SAH-induced WMA also occurs more frequently in postmenopausal women with poor-grade SAH. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] In our institution, plasma catecholamine (epinephrine/norepinephrine) and estradiol levels are measured and transthoracic echocardiogram (TTE) is routinely performed in patients with SAH shortly after admission. This study was conducted to clarify the role of catecholamine and estrogen in the pathogenesis of SAH-induced WMA.…”

Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure

“…Increased cTn values have been associated with intracerebral hemorrhage and independently associated with inhospital mortality (29 ). Both retrospective (30 ) and prospective (31,33 ) stud-ies have demonstrated a relationship between cTn increases and adverse outcomes in subarachnoid hemorrhage. Overall, cTn is increased in approximately 10% of stroke patients and is associated with worse outcomes.…”