Real-time myocardial perfusion contrast echocardiography and regional wall motion abnormalities after aneurysmal subarachnoid hemorrhage. Clinical article.

OBJECT: 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.