In patients with subarachnoid hemorrhage, functional denervation was associated with higher rates of LV regional wall-motion abnormalities (92% vs 52%, P=0.030) and cTI >1 microg/L (58% vs 21%).
Observational (n=42)
Blinded observer
Is left ventricular systolic dysfunction in patients with subarachnoid hemorrhage associated with myocardial ischemia or abnormal sympathetic innervation?
Left ventricular systolic dysfunction following subarachnoid hemorrhage is associated with abnormal sympathetic innervation rather than myocardial ischemia, suggesting a catecholamine-mediated mechanism of injury.
Absolute Event Rate: 92% vs 52%
p-value: p=0.030
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-(123)Iiodobenzylguanidine (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 microg/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.
Banki et al. (Tue,) conducted a observational in Subarachnoid hemorrhage (n=42). Abnormal MIBG uptake (functional denervation) vs. Normal MIBG uptake was evaluated on LV regional wall-motion abnormalities (p=0.030). In patients with subarachnoid hemorrhage, functional denervation was associated with higher rates of LV regional wall-motion abnormalities (92% vs 52%, P=0.030) and cTI >1 microg/L (58% vs 21%).
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