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Charles Marboe

Publications and source records attributed to Charles Marboe.

6 recordsLinked to original sources
PubMed2006

Myocardial lesion formation using high-intensity focused ultrasound.

BACKGROUND: The potential therapeutic uses of ultrasound energy in cardiac disease have not been extensively studied. We have developed a means to deliver high-intensity focused ultrasound (HIFU) to myocardial tissue. Unlike other therapy modalities such as radiofrequency catheter ablation, this system has the advantages of not requiring direct tissue contact and the ability to focus intense energy within a small volume. METHODS: Sections of left and right ventricles from freshly excised canine hearts were treated in vitro with HIFU pulses. Lesions were created using 1-second HIFU pulses with ultrasonic powers ranging from 19.8 to 45.8 W. RESULTS: There was a dose-response relationship between the applied HIFU energy and lesion size (r = 0.70, P < .001). Myocardial lesion formation with HIFU was also performed in vivo in a canine open-chest beating heart model. With 200-millisecond HIFU pulses gated to the electrocardiogram, focal myocardial lesions were created ranging in length from 2 to 6 mm depending on the dose used. Furthermore, both in vitro and in vivo, focal lesions were successfully formed in the midmyocardial wall that spared both the endocardial and epicardial surfaces. CONCLUSION: HIFU is a novel means to create focal myocardial lesions without direct tissue contact. HIFU energy delivery can be gated to the electrocardiogram in an in vivo model, and lesions can be formed intramyocardially. Further application of this technology may prove to be useful for the ablation of myocardial lesions such as arrhythmogenic foci and the hypertrophic ventricular septum in hypertrophic cardiomyopathy. The potential therapeutic uses of ultrasound energy in cardiac diseases have not been well studied. We tested a novel system to deliver high-intensity focused ultrasound energy in vitro and in vivo to canine myocardial samples without direct contact with the target tissue. Focal myocardial lesions were formed in a dose-dependent manner, and myocardial lesions were created. This technology may prove useful for ablation of focal intramyocardial lesions such as arrhythmogenic foci and the hypertrophic left ventricular septum in hypertrophic cardiomyopathy.

Animals↗
PubMed2005

In vitro ablation of cardiac valves using high-intensity focused ultrasound.

The purpose of this study was to evaluate the possibility of using high-intensity focused ultrasound (US), or HIFU, to create lesions in cardiac valves in vitro. Calf mitral valves and aortic valves were examined. Focused US energy was applied with an operating frequency of 4.67 MHz at a nominal acoustic power of 58 W for 0.2, 0.3 and 0.4 s at 4-s intervals. Mitral valve perforation was achieved with 20.8 +/- 3.7 exposures of 0.2 s, 15.4 +/- 2.1 exposures of 0.3 s or 11.2 +/- 2.3 exposures of 0.4 s. Aortic valve perforation was achieved with 13.3 +/- 2.4 exposures of 0.2 s, 10.3 +/- 2.2 exposures of 0.3 s or 8.4 +/- 1.8 exposures of 0.4 s. The mean diameter of the perforated area was 1.09 +/- 0.11 mm. The lesions were slightly discolored and coagulation of tissue around the perforation was observed. HIFU was successful in perforating cardiac valves. With further refinement, HIFU may prove useful for valvulotomy or valvuloplasty.

Animals↗
PubMed2004

Alloantigen specific CD8+CD28- FOXP3+ T suppressor cells induce ILT3+ ILT4+ tolerogenic endothelial cells, inhibiting alloreactivity.

Endothelial cells have been shown to activate T cell responses to alloantigens, triggering transplant rejection. However, they may also play a role in tolerance induction. Using RT-PCR we show here that alloantigen specific CD8(+)CD28(-) T suppressor cells generated in vitro are FOXP3 positive and interact with human endothelial cells. This interaction results in the induction of inhibitory receptors and down-regulation of costimulatory and adhesion molecules, thus rendering endothelial cells tolerogenic. In turn, tolerized endothelial cells elicit the differentiation of CD8(+)CD28(-) FOXP3(+) T suppressor cells. Taken together our data demonstrate a functional and phenotypic overlap between tolerogenic dendritic cells and endothelial cells. Furthermore, alloantigen specific CD8(+)CD28(-) FOXP3(+) T cells, which trigger the upregulation of inhibitory receptors in endothelial cells, are present in the circulation of heart allograft recipients in quiescence as demonstrated by flow cytometry, RT-PCR and luciferase transcription assays. Their detection facilitates the identification of patients who may benefit from partial or complete cessation of immunosuppressive therapy, a goal of obvious importance given the morbidity and mortality associated with chronic immunosuppression. Modulation of endothelial cells in favor of promoting tolerance may be important for long-term survival of organ allografts.

Adult↗
PubMed2004

Anti-HLA antibodies in heart transplantation.

We have analyzed the relationship between the development of transplant-related coronary artery disease (TRCAD) and the following potential risk factors: (a). number of HLA mismatches between recipient and donor; (b). production of anti-HLA antibodies; (c). growth of lymphocytes infiltrating the graft; and (d). frequency of biopsy proven episodes of acute rejection. The study population consisted of 285 adult heart allograft recipients who were monitored over a period of two years or more. The results demonstrate a significant correlation between TRCAD, generation of anti-HLA class II antibodies and potential of lymphocytes infiltrating the graft to proliferate ex-vivo in medium containing IL-2. Humoral and cellular immune responses to HLA-DR antigens expressed by the graft seem to underlie the development of TRCAD.

Antibodies↗
PubMed2003

Foamy podocytes.

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Diagnosis, Differential↗