Real-time myocardial perfusion contrast echocardiography and regional wall motion abnormalities after aneurysmal subarachnoid hemorrhage. Clinical article.
OBJECTIVE
The pathophysiology of myocardial dysfunction after subarachnoid hemorrhage (SAH) remains unclear. Using myocardial real-time perfusion contrast echocardiography (RTP-CE), the authors evaluated microvascular function in patients with acute SAH.


METHODS
Over a 15-month period, 10 patients with acute SAH and evidence of cardiac dysfunction were prospectively enrolled. The authors performed RTP-CE within 48 hours of SAH diagnosis. Wall motion and myocardial perfusion were evaluated in 16 left ventricle segments. Qualitative and quantitative RTP-CE analyses were conducted to compare patients with and without regional wall motion abnormalities (RWMAs). Follow-up RTP-CE at a mean of 53.7 +/- 43 days was undertaken in patients with baseline RWMAs.


RESULTS
Ten patients with SAH and evidence of cardiac dysfunction were prospectively enrolled. There were 3 men and 7 women whose mean age was 63.5 +/- 10.1 years. The authors documented evidence of RWMAs in 6 patients. Normal perfusion was demonstrated by RTP-CE in all patients at baseline and follow-up, despite the presence of RWMAs. Compared with patients presenting with normal wall motion, in patients with RWMAs there was a trend for higher quantitative RTP-CE parameters, suggesting hyperemia with mean myocardial blood flow velocity (beta, s(-1)) of 1.08 +/- 0.61 (95% CI 0-2.61) compared with 1.62 +/- 0.64 (95% CI 0.94-2.29) and myocardial blood flow (A x beta, dB/s) of 0.99 +/- 0.41 (95% CI 0-2.0) versus 1.63 +/- 0.86 (95% CI 0.72-2.53). Follow-up RTP-CE was feasible in 3 patients with RWMAs. Regional systolic function was restored in those who completed follow-up.


CONCLUSIONS
The authors found that RTP-CE readily evaluates microvascular function in patients with SAH. Wall motion and perfusion dissociation were observed. Quantitative RTP-CE showed a trend for microvascular hyperemia in patients with RWMAs, suggesting that post-SAH myocardial dysfunction could occur in the absence of microvascular dysfunction.
Abdelmoneim
Sahar S
SS
Division of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
Wijdicks
Eelco F M
EF
Lee
Vivien H
VH
Daugherty
Wilson P
WP
Bernier
Mathieu
M
Oh
Jae K
JK
Pellikka
Patricia A
PA
Mulvagh
Sharon L
SL
D000368:Aged; D001013:Aorta, Thoracic / Q000000981:diagnostic imaging; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D004452:Echocardiography / Q000379:methods*; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D015600:Glasgow Coma Scale; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D015588:Observer Variation; D013345:Subarachnoid Hemorrhage / Q000000981:diagnostic imaging* / Q000503:physiopathology*