scispace - formally typeset
R

Robert J. Siegel

Researcher at Cedars-Sinai Medical Center

Publications -  506
Citations -  25581

Robert J. Siegel is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Mitral regurgitation & Mitral valve. The author has an hindex of 75, co-authored 463 publications receiving 22687 citations. Previous affiliations of Robert J. Siegel include Northern General Hospital & University of California, Los Angeles.

Papers
More filters
Journal ArticleDOI

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

TL;DR: The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures as mentioned in this paper, which may reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.
Journal ArticleDOI

Limitations of postmortem assessment of human coronary artery size and luminal narrowing: Differential effects of tissue fixation and processing on vessels with different degrees of atherosclerosis

TL;DR: Using planimetric techniques, the dimensional changes that occurred with fixation and processing were quantitated in 61 coronary artery segments with minimal or moderate to severe atherosclerosis obtained from 12 patients studied at autopsy.
Journal ArticleDOI

Enhancement of thrombolysis by external ultrasound

TL;DR: In this paper, the efficacy of external ultrasound to enhance in vitro thrombolysis with urokinase or streptokinase was evaluated and it was shown that the combination of ultrasound (2.2 W/cm2, 30 min) and Urokinases or Streptokinases (50, 250, and 2000 mu/ml) significantly increased the lysis rate.
Patent

Stent with sustained drug delivery

TL;DR: A mechanical support or stent containing pharmaceutical agents can be placed in the wall of a blood vessel where it releases pharmaceutical agents to prevent arterial thromboses, platelet aggregation and/or excessive endothelial cell proliferation at the placement site as discussed by the authors.