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• Congestive Heart Failure

  Heart Failure

   When you have heart failure, the heart is not able to pump as well as it should. Blood and fluid may back up into the lungs (congestive heart failure), and some parts of the body don’t get enough oxygen-rich blood to work normally.
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• General Cardiology

  Home Page - Cardiovascular Diseases

  Cardiovascular diseases include coronary heart disease, stroke, high blood pressure, and rheumatic heart disease.
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• Heart Valve Disease

  Heart Valve Diseases

  Heart valves can malfunction on one of two ways: They can fail to close completely, allowing blood to flow backward, or they can become damaged, limiting blood flow. Your doctor may think you have heart valve disease if your heart sounds heard through a stethoscope are abnormal. 
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• Transesophageal Echocardiogram (TEE)
• Transthoracic Echocardiography

  Transesophageal Echocardiogram

  A transesophageal echocardiogram (TEE) uses echocardiography to assess how well the heart works. During the procedure, a transducer (like a microphone) is lowered into the esophagus. It sends out ultrasonic sound waves at a frequency too high to be heard. When the transducer is placed at certain locations and angles, the ultrasonic sound waves move through the skin and other body tissues to the heart tissues, where the waves bounce or "echo" off of the heart structures.
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The main research interests of our laboratory are focused on two areas of investigation:

1. Environmental Cardiology: We are dissecting the mechanisms by which exposure to air particulate matter promotes atherosclerosis and ischemic heart disease and studying gene-environment interactions of relevance in the development of cardiovascular disease. We have determined that air pollutant chemicals such as those present in diesel exhaust particles are able to induce inflammatory genes in endothelial cells, in a synergistic fashion with oxidized phospholipids. This synergy was also present in tissues harvested from animals exposed to concentrated ambient ultrafine particles which are the smallest (<0.18 µm) and most abundant particulate pollutants in urban settings, responsible for the largest promotion of atherosclerosis as compared with particles of bigger size. One of the mechanisms how air pollution appears to promote atherosclerosis is via the generation of dysfunctional HDL that either loses its anti-inflammatory capacity or even becomes proinflammatory.
2. Biology of vascular oxidative stress: We are interested in genes and pathways of relevance in the vascular oxidative stress generated in atherosclerosis and cardiac allograft rejection response, such as heme oxygenase-1 (HO-1) and its transcription factor Nrf2. We have shown that HO-1 is an important antioxidant and anti-inflammatory protective gene that may play a central role in orchestrating the antioxidant defense of vascular cells. We are currently studying how is that HO-1 expression modulates various inflammatory pathways via the use of genetic and biochemical approaches. We have established a good complementation in between our two areas of investigation as it appears that the generation of reactive oxygen species in the vasculature and the expression of Nrf2-regulated antioxidant genes represent important elements in the systemic effects of air particulate pollutants.

1. Araujo JA, Meng L, Tward A, Hancock WW, Zhai Y, Lee A, Iyer S, Buelow R, Busuttil RW, Shih DM, Lusis AJ, Kupiec-Weglinski JW. Systemic rather than local heme oxygenase-1 overexpression improves cardiac allograft outcomes in a new transgenic mouse. J Immunol 2003: 171: 1572-80.
2. Tsuchihashi SI, Livhits M, Zhai Y, Bussutil RW, Araujo JA, Kupiec-Weglinski JW. Basal rather than induced HO-1 levels are crucial in the antioxidant cytoprotection. J Immunol 2006, 177: 4749-57.
3. Orozco LD, Kapturczak MH, Barajas B, Wang X, Weinstein MM, Wong J, Deshane J, Bolisetty S, Shaposhnik Z, Shih D, Agarwal A, Lusis AJ, Araujo JA. Heme oxygenase-1 expression in macrophages plays a beneficial role against atherosclerosis. Circ Research 2007; 100: 1703-1711.
4. Gong KW, Zhao W, Li N, Barajas B, Kleinman M, Sioutas C, Horvath S, Lusis AJ, Nel A, Araujo JA. Air pollutant chemicals and oxidized lipids exhibit genome wide synergistic effects on endothelial cells. Genome Biology 2007; 8: R149.
5. Araujo JA, Barajas B, Kleinman M, Wang X, Bennett B, Gong KW, Navab M, Harkema J, Sioutas C, Lusis AJ, Nel A. Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress. Circ Research 2008; 102 (online ahead of print).