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Bioeffects of myocardial contrast microbubble destruction by echocardiography.

作者信息

Chen Shuyuan, Kroll Martin H, Shohet Ralph V, Frenkel Peter, Mayer Susan A, Grayburn Paul A

机构信息

Departments of Internal Medicine (Cardiology Division) and Pathology, Dallas VA Medical Center, Dallas, Texas 75216, USA.

出版信息

Echocardiography. 2002 Aug;19(6):495-500. doi: 10.1046/j.1540-8175.2002.00495.x.

Abstract

BACKGROUND

Microbubble destruction during contrast echocardiography is known to cause capillary leaks and red blood cell extravasation in skeletal muscle. This study evaluated the biological effects of microbubble destruction on cardiac muscle.

METHODS

Contrast echocardiography was performed in 36 rats randomized to receive either Definity or Optison at a mechanical index (MI) of 1.6, 1.2, or 0.8. Myocardial bioeffects were assessed by measuring left ventricular (LV) size and fractional area shortening and histopathology. In addition, blood samples for troponin T were drawn at baseline, postinfusion (30 minutes), day 1, day 4, and day 7. LV size and function were measured at baseline and immediately prior to euthanasia on day 7, after which the heart was removed and sectioned for histopathology.

RESULTS

There was no statistical difference in LV size or function regardless of the contrast agent or MI, nor was there any histopathological evidence of myocardial damage. However, troponin T increased over time (F = 3.77, P = 0.012), peaking at 30 minutes and returning to normal by day 4. The difference between Definity and Optison was not statistically significant. However, troponin T values were higher at a higher MI (F = 5.01, P = 0.012). Of 12 rats imaged at a MI of 1.6, 9 (75%) had elevated troponin T as compared to 4 (33%) of 12 at a MI of 1.2. None of the 12 rats imaged at a MI of 0.8 had an elevated troponin T at any time point.

CONCLUSIONS

Microbubble destruction at high acoustic power (MI 1.6) can cause mild troponin T elevations that are not associated with LV dysfunction or histopathological evidence of myocardial damage.

摘要

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