Naima Carter-Monroe

CVPath Institute, Maryland, United States

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Publications (10)56.45 Total impact

  • Elena Ladich · Masataka Nakano · Naima Carter-Monroe · Renu Virmani
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    ABSTRACT: With the aging of the general population in industrialized nations, calcific aortic stenosis (CAS) is becoming an increasingly important medical problem. The etiology is for the most part, dependent on the age at presentation; the two predominant causes in the western world are calcific aortic valve disease arising in a tricuspid aortic valve and bicuspid aortic valve (BAV). CAS is a progressive disease, exhibiting a spectrum of pathologic findings, ranging from valvular sclerosis to severe nodular calcification. Aortic valve replacement is the recommended treatment for severe disease but tissue valves may also calcify over time. Various atherosclerotic risk factors have been linked to aortic stenosis and there are mechanistic similarities between atherosclerosis and CAS. The precise pathologic mechanisms underlying aortic stenosis are poorly understood.
    Future Cardiology 09/2011; 7(5):629-42. DOI:10.2217/fca.11.53
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    ABSTRACT: Author Summary Family studies have clearly demonstrated a role for genes in modifying risk for sudden cardiac death (SCD), however genetic studies have been limited by available samples. Here we have assembled over 4,400 SCD cases with >30,000 controls, all of European ancestry, and utilize a two-stage study design. In the first stage, we conducted an unbiased genome-wide scan in 1,283 SCD cases and >20,000 controls, and then performed follow-up genotyping in the remainder of the samples. We demonstrate strong association to a region of the genome not previously implicated in SCD, the BAZ2B locus, which contains 3 genes not previously known to play a role in cardiac biology. In addition, we used the genome-wide scan data to test a focused hypothesis that genetic variants that modulate ECG traits associated with SCD (QT, QRS, and RR intervals) also modify risk for SCD, and we demonstrate that QT- and QRS-prolonging alleles are, as a group, associated with increased risk of SCD. Taken together, these findings begin to elucidate the genetic contribution to SCD susceptibility and provide important targets for functional studies to investigate the etiology and pathogenesis of SCD.
    PLoS Genetics 06/2011; 7(6):e1002158. DOI:10.1371/journal.pgen.1002158 · 7.53 Impact Factor
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    Journal of the American College of Cardiology 04/2011; 57(14). DOI:10.1016/S0735-1097(11)61664-1 · 16.50 Impact Factor
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    Naima Carter-Monroe · Renu Virmani
    Revista Espa de Cardiologia 01/2011; 64(1):10-2. DOI:10.1016/j.rec.2010.09.004 · 3.79 Impact Factor
  • Naima Carter-Monroe · Renu Virmani
    Revista Espa de Cardiologia 01/2011; 64(1):10-12. DOI:10.1016/j.recesp.2010.09.004 · 3.79 Impact Factor
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    ABSTRACT: Understanding the natural history of carotid atherosclerosis is essential in the management of patients at risk for stroke. Atherosclerotic plaque at the carotid bifurcation is the underlying cause of the majority of ischemic strokes and the degree of carotid stenosis is strongly associated with stroke risk in symptomatic patients. Pathologic studies comparing symptomatic and asymptomatic carotid plaques have demonstrated that specific plaque characteristics are associated with ischemic brain injury and the mechanisms underlying plaque instability in the carotid circulation are similar to those in the coronary circulation. This chapter will focus on the morphologic classification of carotid atherosclerosis based on a modification of the AHA classification system (with a comparison to atherosclerosis in the coronary vasculature) and will consider morphologic differences between carotid plaques in asymptomatic vs. symptomatic patients. In addition, we provide brief overview of the burgeoning number of imaging modalities used in the characterization of carotid plaques, as they compare to histologic studies. KeywordsAtherosclerosis-Fibroatheroma-Thin-cap fibroatheroma-Plaque rupture-Plaque erosion-Carotid-Endarterectomy-Plaque morphology-Inflammation-Magnetic resonance imaging-Angiography-Doppler ultrasound
    Atherosclerosis Disease Management, 12/2010: pages 3-35;
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    ABSTRACT: To evaluate the potential for mitral annular (MA) size reduction using a novel device utilising therapeutic ultrasound (TU). The ReCor device (ReCor Medical, Inc., Ronkonkoma, NY, USA, Investigational device, not for use in human application) was studied in a closed chest canine animal model (35 dogs). Under fluoroscopy, a 12 Fr TU balloon catheter was advanced into the left atrium (transseptal approach). The TU balloon was inflated with contrast-saline, positioned at the MA and energy delivered circumferentially, to heat the tissue locally. Five TU applications were delivered (at least 60W for at least 40 sec). Relative to baseline, mitral valve annular diameter reduction (measured by transthoracic echocardiography) was 8.4% immediately post procedure(p<0.001), 8.6% at one week (p<0.001), 8.8% at two weeks (p<0.001), 9.3% at three weeks (p<0.001), 10.8% at four weeks (p<0.001), 8.6% at three months (p<0.001) and 5.7% at six months (p<0.001). Histology showed an increase in elastin associated with tissue thickening at the annular level. Transmission electron microscopy demonstrated a decrease in diameter of individual collagen fibres in treated regions compared to controls. Therapeutic ultrasound (TU) energy application to the mitral annulus is feasible percutaneously. A reduction in annular dimensions occurs immediately and appears to be durable without peri-annular damage.
    EuroIntervention: journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology 05/2010; 6(1):54-62. DOI:10.4244/EIJV6I1A9 · 3.77 Impact Factor
  • The American Journal of Cardiology 04/2010; 11(4):279-279. DOI:10.1016/j.carrev.2010.03.032 · 3.28 Impact Factor
  • Naima Carter-Monroe · Elena Ladich · Renu Virmani · Frank D Kolodgie
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    ABSTRACT: Cardiac regeneration in the form of cell-based therapy offers hope of becoming the breakthrough technology that transforms the state of cardiac medicine. Before attempting to develop the techniques to assess the effectiveness of myocardial regeneration in humans, researchers must have at least a basic understanding of the human heart in its embryonic, normal, and diseased states. To this end, we provide an overview of the histology of the heart, including the current theories on normal embryogenesis and the histology of normal and ischemic myocardium as visualized by pathologists. Knowledge of the cellular constituents, including the controversial existence of resident cardiac stem and/or progenitor cells, and their actions and interactions in the normal state and under the conditions of myocardial ischemia is also crucial before embarking on the quest for cardiac regeneration. Despite widespread optimism in the success of cell-based therapy, inherent difficulties remain in the identification of effective cell populations proposed for cell-based therapy in the human heart.
    Methods in molecular biology (Clifton, N.J.) 01/2010; 660:125-48. DOI:10.1007/978-1-60761-705-1_9 · 1.29 Impact Factor
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    ABSTRACT: The aim of this study was to assess differences in thrombus healing between ruptured and eroded plaques, given the natural difference in lesion substrate and that thrombi might exist days to weeks before the presentation of sudden coronary death. Although the ability to distinguish ruptures and erosions remains a major clinical challenge, in-hospital patients dying with acute myocardial infarction establish that erosions account for 25% of all deaths, where women experience a higher incidence compared with men. Coronary lesions with thrombi (ruptures, n = 65; erosions, n = 50) received in consultation from the Medical Examiner's Office from 111 sudden death victims were studied. Thrombus healing was classified as early (<1 day) or late stage characterized in phases of lytic (1 to 3 days), infiltrating (4 to 7 days), or healing (>7 days). Morphometric analysis included vessel dimensions, necrotic core size, and macrophage density. Late-stage thrombi were identified in 79 of 115 (69%) culprit plaques. Women more frequently had erosion with a greater prevalence of late-stage thrombi (44 of 50, 88%) than ruptures (35 of 65, 54%, p < 0.0001). The internal elastic lamina area and percent stenosis were significantly smaller in erosions compared with ruptures (p < 0.0001 and p = 0.02), where plaque burden was greater (p = 0.008). Although macrophage infiltration in erosions was significantly less than ruptures (p = 0.03), there was no established relationship with thrombus organization. Other parameters of thrombus length and occlusive versus nonocclusive showed no association with healing. Approximately two-thirds of coronary thrombi in sudden coronary deaths are organizing, particularly in young individuals-especially women, who perhaps might require a different strategy of treatment.
    Journal of the American College of Cardiology 10/2009; 55(2):122-32. DOI:10.1016/j.jacc.2009.09.007 · 16.50 Impact Factor