Poyee P. Tung

Predictors of Neurocardiogenic Injury After Subarachnoid Hemorrhage

Background and Purpose— Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury. Methods— Consecutive patients admitted with SAH were enrolled prospectively. Predictor variables reflecting demographic (age, sex, body surface area), hemodynamic (heart rate, systolic blood pressure), treatment (phenylephrine dose), and neurological (Hunt-Hess score) factors were recorded. Serial cardiac troponin I measurements and echocardiography were performed on days 1, 3, and 6 after enrollment. Troponin level was treated as a dichotomous outcome variable. We performed univariate and multivariate analyses on the relationships between the predictor variables and troponin level. Results— The study included 223 patients with an average age of 54 years. Twenty percent of the subjects had troponin I levels >1.0 &mgr;g/L (range, 0.3 to 50 &mgr;g/L). By multivariate logistic regression, a Hunt-Hess score >2, female sex, larger body surface area and left ventricular mass, lower systolic blood pressure, and higher heart rate and phenylephrine dose were independent predictors of troponin elevation. Conclusions— The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.

Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage

Background— Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals. Methods and Results— For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[123I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake. Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels >1 &mgr;g/L (58% versus 21%, P=0.029). Conclusions— LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.

Prevalence and implications of diastolic dysfunction after subarachnoid hemorrhage

Introduction: Electrocardiographic changes, troponin release, and reduced left ventricular ejection fraction have been described after subarachnoid hemorrhage (SAH). Little is known about the occurrence of diastolic dysfunction in this setting. The purpose of this study was to determine the prevalence of diastolic dysfunction and its association with cardiac outcomes after SAH.Methods: SAH patients were prospectively enrolled into the study, and echocardiographic, clinical, chest X-ray, and cardiac troponin I data were obtained on days 1, 3, and 6 after enrollment. Each echocardiogram included Doppler recordings of mitral inflow and pulmonary venous flow. For each study, diastolic function was categorized as normal, impaired relaxation, pseudonormal, or restrictive. The relationships between diastolic dysfunction and pulmonary edema-elevated cardiac troponin I and left ventricular contractile dysfunction were quantified using both univariate and multivariate statistical methods. Clinical predictors of diastolic dysfunction were defined by multivariate logistic regression.Results: Of 223 enrolled subjects, 207 had technically adequate Doppler data. Diastolic dysfunction was observed in 71% of subjects. The prevalence of diastolic versus systeolic dysfunction in 44 patients with pulmonary edema was 91 versus 37%, respectively (p=0.001). After multivariate statistical adjustment, diastolic dysfunction remained a significant predictor of pulmonary edema (odds ratio [OR] 3.34, 95% CI=1.05−10.59). Diastolic dysfunction also was associated with troponin release (p=0.02). A history of hypertension and increasing age were predictive of diastolic dysfunction.Conclusion: Diastolic dysfunction is common after SAH. It is associated with history of hypertension and older age and may explain the development of pulmonary edema in many SAH patients.

Cardiac injury after subarachnoid hemorrhage is independent of the type of aneurysm therapy.

OBJECTIVE:Subarachnoid hemorrhage (SAH) is associated with cardiac injury and dysfunction. Whether aneurysm clipping versus coiling has a differential effect on the risk of troponin release and left ventricular (LV) dysfunction after SAH is unknown. It is hypothesized that aneurysm treatment does not affect the risk of developing cardiac injury and dysfunction. METHODS:The study included 172 consecutive SAH patients who underwent clipping (n = 109) or coiling (n = 63) aneurysm therapy. Hemodynamic data were collected, cardiac troponin I was measured, and echocardiography was performed on the 1st, 3rd, and 6th days after enrollment. A cardiac troponin I measurement of more than 1.0 &mgr;g/L was considered abnormal. For each echocardiographic examination, a blinded observer measured LV ejection fraction (abnormal if <50%) and quantified LV regional wall motion abnormalities. The incidence of cardiac outcomes in the treatment groups was compared using odds ratios (ORs). RESULTS:The coiled patients were older than the clipped patients (mean age, 59 ± 13 yr versus 53 ± 12 yr; t test, P < 0.001) and were more likely to have posterior aneurysms (33% versus 18%; &khgr;2 test, P = 0.019). There were no significant between-group differences in the risk of cardiac troponin I release (coil 21% versus clip 19%; OR = 0.89, P = 0.789), regional wall motion abnormalities (33% versus 28%; OR = 0.76, P = 0.422), or LV ejection fraction lower than 50% (16% versus 17%; OR = 1.06, P = 0.892). No patient died of cardiac causes (heart failure, myocardial infarction, or arrhythmia). CONCLUSION:Surgical and endovascular aneurysm therapies were associated with similar risks of cardiac injury and dysfunction after SAH. The presence of neurocardiogenic injury should not affect aneurysm treatment decisions.

Floating, Non-Occlusive, Mobile Aortic Thrombus and Splenic Infarction Associated With Protein C Deficiency

The authors report the case of a patient with isolated protein C deficiency detected later in life, presenting with a mobile aortic thrombus and splenic infarction. Only one such case has been previously described. This case emphasizes the importance of including the aorta in the search for a cause of systemic embolization and highlights the diagnostic options and management dilemmas. Although anticoagulation with subsequent reassessment of thrombus size can be considered for layered thrombi, mobile thrombi warrant early surgical intervention to minimize the risk for systemic embolization. This patient was treated surgically with encouraging results.

Nodular Pericardial Metastases

A 50 year-old male with a 60 pack-year smoking history presented with worsening left upper back pain. He also complained of increasing shortness of breath, difficulty in swallowing, and unintentional 40-pound weight loss over the past four months. Chest computed tomography revealed a large left lower lobe mass (asterisk in Fig. 1A) and numerous soft tissue nodules along the pericardium (arrows in Fig. 1A and B). Echocardiogram also revealed echogenic pericardial nodules (Fig. 1C). Findings were most suggestive of primary bronchogenic malignancy with pericardial metastases. Subsequent biopsy of the left lower lobe mass revealed invasive squamous cell carcinoma. Abdominal magnetic resonance imaging done later for other reasons also demonstrated the enhancing nodules along the pericardium (Fig. 1D). Metastases to the heart are far more common than primary cardiac tumours. The pericardium is the most common

Response to Letter Regarding Article by Banki et al, “Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage”

We were very interested to read Dr Gnecchi-Ruscone’s comments regarding our article.1 Similar to stress cardiomyopathy (SC), elevated catecholamine levels are frequently observed after subarachnoid hemorrhage (SAH).2 In our series, the mean plasma epinephrine and norepinephrine levels were 129±102 pg/mL and 372±494 pg/mL, respectively.3 The majority of the levels are lower than those reported for SC, …