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Dive into the research topics where Andrew Farb is active.

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Featured researches published by Andrew Farb.


American Journal of Cardiology | 1994

The contribution of tissue removal to lumen improvement after directional coronary atherectomy

Fadi Matar; Gary S. Mintz; Andrew Farb; Phillipe Douek; Augusto D. Pichard; Kenneth M. Kent; Lowell F. Satler; J.J. Popma; Michael B. Keller; Ellen Pinnow; Alan J. Merritt; Joseph Lindsay; Martin B. Leon

The contribution of tissue removal to lumen improvement after directional coronary atherectomy remains controversial. The purpose of this study was to validate the intravascular ultrasound measurement of plaque volume and use it to study the contribution of tissue removal to lumen improvement after directional coronary atherectomy. With use of intravascular ultrasound, 12 human coronary vessels were imaged in vitro. With use of computer-assisted planimetry, the external elastic membrane and lumen cross-sectional areas were manually traced and the plaque+media area was calculated at 1 mm axial intervals. Then, plaque+media volume was calculated by Simpsons rule. After imaging, ultrasound measurements of plaque+media volume were compared with histologic measurements. Similarly, volumetric intravascular ultrasound imaging was performed before and after directional atherectomy in 47 patients. In vitro, the mean plaque+media volume measured by intravascular ultrasound was 134.0 +/- 94.8 mm3 and compared well with that derived by histology (187.4 +/- 128.8 mm3, r = 0.96, p < 0.001). In vivo, the lumen volume increased from 27.2 +/- 12.3 to 58.7 +/- 30.3 mm3, and the mean plaque+media volume decreased from 122.0 +/- 74.0 to 97.5 +/- 63.5 mm3. The mean intravascular ultrasound atherectomy index was 76 +/- 23%. In 11 of the 47 patients (23.4%), tissue removal alone accounted for lumen improvement. Volumetric intravascular ultrasound image analysis indicates that the mechanism of directional coronary atherectomy primarily is tissue removal. As a result, the contribution of arterial remodeling (expansion and dissection) probably is less important.


American Heart Journal | 1995

Coronary artery morphologic features after coronary rotational atherectomy: Insights into mechanisms of lumen enlargement and embolization

Andrew Farb; David K. Roberts; Augusto D. Pichard; Kenneth M. Kent; Renu Virmani

The coronary arteries and myocardium from two patients who died after coronary rotational atherectomy were analyzed to gain insights into the mechanisms of lumen enlargement and to document embolization of calcified plaque. Rotational atherectomy resulted in sharp cuts in plaque, producing a relatively smooth luminal surface. When extensive nodular calcific atherosclerosis was present, the luminal surface was focally uneven with exposure of jagged calcified plaque to blood flow. Deep plaque fissures and medial dissections were also seen. These fissures may have been created by the rotoblator or by adjunctive balloon angioplasty. Multiple calcific atheroemboli were present after rotoblator use in plaques containing extensive nodular calcification; in moderately calcified plaque only one small atheroembolus was found. Thus embolization of calcified plaque can occur after rotational atherectomy and may correlate with the severity of plaque calcification. Rotational atherectomy produces a focally smooth, sharp-edged, luminal surface, a lumen enlargement mechanism different from balloon angioplasty.


Coronary Artery Disease | 1995

A modified directional atherectomy catheter for resection of calcified atherosclerotic plaques

Mun K. Hong; Wong Sc; Gary S. Mintz; Andrew Farb; Kenneth M. Kent; A.D. Pichard; Lowell F. Satler; Jeffrey J. Popma; Sidawy A; Renu Virmani

BackgroundThe purpose of this study was to determine the feasibility of resecting calcified atherosclerotic plaques in human cadaveric vessels by using a modified directional coronary atherectomy catheter and to correlate these results with bench tests using an in-vitro sea coral model. MethodsThe conventional directional coronary atherectomy catheter was modified by changing the cutter blade to a tungsten carbide material and by increasing the torsional strength of the drive cable. The performance of the modified directional coronary atherectomy (DCA) catheter was compared with the conventional catheter using a sea coral model to simulate calcified material. Then, 10 human ex-vivo arteries (eight with calcification) were treated with both conventional and modified catheters, and the results studied with intravascular ultrasound and confirmed by histologie examination. ResultsUsing the modified directional coronary atherectomy catheter it was possible to perform effective and consistent longitudinal cutting, and to resect a significantly larger amount of coral (1.0 ±0.1 mm2 versus 0.2 ± 0.1 mm2 with conventional cutter, P<lt; 0.0001). In heavily calcified ex-vivo arteries, the modified catheter was more effective in removing calcified plaques (13 ± 11 mg versus 3.7 ± 1.4 mg with conventional cutter, P = 0.07). Intravascular ultrasound confirmed the effective atherectomy (residual area stenosis 28 ±16% versus 47 ±10% with the conventional device, P<lt; 0.05), and histologie examination showed calcified nodules in the atherectomy samples obtained with the modified cutter (area of calcium 1.43 ± 0.89 mm2 versus 0.93 ± 0.83 mm2 with the conventional cutter). ConclusionsThe modified directional coronary atherectomy catheter effectively removed both non-calcified and calcified plaques in the ex-vivo human cadaveric arteries, thus demonstrating the feasibility of directional coronary atherectomy of calcified plaques. This modified device shows promise for treating calcified coronary lesions, especially in larger vessels.


Archive | 2003

Coronary Arterial Response to Injury

Robert S. Schwartz; Renu Virmani; Andrew Farb

Both stent implantation and simple balloon angioplasty induce marked injury in the coronary artery or peripheral vessels. The artery’s response to that injury is critical to the long-term success or failure of the procedures [1–3]. The coronary artery responds to injury incurred during revascularization with neointimal hyperplasia, forming neointima of varying thickness, and with thickening of the adventitia. This latter process frequently causes vessel shrinkage, or negative remodeling, and is a principal cause of restenosis when a stent is not present to resist the constriction [4–8]. When a stent is placed, neointimal hyperplasia is the determining factor for in-stent restenosis and is the major target of drug-eluting stents. Presented in this chapter are animal models and human examples of the coronary artery’s response to injury during revascularization procedures.


Catheterization and Cardiovascular Diagnosis | 1994

Coronary artery lumen volume measurement using three‐dimensional intravascular ultrasound: Validation of a new technique

Fadi Matar; Gary S. Mintz; Philippe Douek; Andrew Farb; Renu Virmani; Saturnine P. Javier; Jeffrey J. Popma; Augusto D. Pichard; Kenneth M. Kent; Lowell F. Satler; Michael B. Keller; Martin B. Leon


Archive | 1995

Fibrosing Cardiomyopathy in Captive Western Lowland Gorillas (Gorilla gorilla gorilla) in the United States: A Retrospective Study

F. Yvonne Schulman; Andrew Farb; Renu Virmani; Richard J. Montali


Archive | 1996

Atlas of cardiovascular pathology

Renu Virmani; Allen P. Burke; Andrew Farb


The Vulnerable Atherosclerotic Plaque: Strategies for Diagnosis and Management | 2007

Pathogenesis and Significance of Calcification in Coronary Atherosclerosis

Allen P. Burke; Frank D. Kolodgie; Andrew Farb; Renu Virmani


Circulation 102(18 Supplement) | 2000

Platelet-rich intramyocardial thromboemboli are frequent in acute coronary thrombosis, especially plaque erosions

Andrew Farb; Allen P. Burke; Frank D. Kolodgie; You Hui Liang; Robert Kutys; Renu Virmani


/data/revues/00028703/v137i4/S0002870399702140/ | 2011

Pathology of bailout coronary stenting in human beings

Andrew Farb; Joseph Lindsay; Renu Virmani

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Frank D. Kolodgie

Vanderbilt University Medical Center

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Kenneth M. Kent

MedStar Washington Hospital Center

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Augusto D. Pichard

MedStar Washington Hospital Center

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Gary S. Mintz

MedStar Washington Hospital Center

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Joseph Lindsay

MedStar Washington Hospital Center

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Lowell F. Satler

MedStar Washington Hospital Center

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Fadi Matar

University of South Florida

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