Filio (Phyllis) Billia, PhD, MD, FRCPC

Heart failure and cardiac regeneration

Heart failure is the leading cause of morbidity and mortality in North America and has been identified as the second leading cause of extended hospital stays. The quality of life and the prognosis for this group of patients remains poor with one-year survival rates less than 40%. In addition, more than $1B of Canada's annual health budget is being spent for the care of patients with heart failure, rendering this disease an ever increasing socioeconomic burden.

Heart failure occurs when the heart is unable to adequately pump blood to meet the demands of the body. In the adult, cardiomyocytes are post-mitotic terminally differentiated cells that are unable to proliferate. This renders the heart particularly vulnerable to ischemic, toxic or biomechanical injury. In order to compensate for the irreversible damage that ensues, the left ventricle undergoes hypertrophy and dilatation. This process is ultimately detrimental and progressive left ventricular dysfunction develops. Our existing armamentarium of conventional pharmacological therapy can only slow the progression of the disease by alleviating the workload of the heart. Alternatives to medical therapy are limited to transplantation or mechanical assist devices. These approaches are highly invasive and associated with significant morbidity and mortality. Various cell-based therapies have also been described in the treatment of heart failure, however, the clinical significance of these approaches remains unclear. While these cell-based therapies continue to attract considerable interest, they are sufficiently problematic. As such, it is exceedingly important to consider alternative approaches that allow the discovery of novel treatment strategies to effectively maintain tissue homeostasis and restrict cardiomyocyte loss. Providing new therapies for heart failure will not only improve the quality of life for patients but also reduce the costs associated with patient care.

Tumour suppressors and the regulation of normal tissue homeostasis

Our concept of preventing cardiomyocyte loss through the regulation of tumour suppressor genes is aimed at reactivation of transcription factors necessary for maintenance of tissue homeostasis.
Hypertension. 2019 Jan 14;:HYPERTENSIONAHA11811828
Dingwell LS, Shikatani EA, Besla R, Levy AS, Dinh DD, Momen A, Zhang H, Afroze T, Chen MB, Chiu F, Simmons CA, Billia F, Gommerman JL, John R, Heximer S, Scholey JW, Bolz SS, Robbins CS, Husain M
J Card Fail. 2019 Jan 07;:
Grosman-Rimon L, Ajrawat P, Lioe J, Tumiati LC, Rao V, Billia F, Chruscinski A
Heart. 2018 Dec 04;:
Yamamura K, Yuen D, Hickey EJ, He X, Chaturvedi RR, Friedberg MK, Grosse-Wortmann L, Hanneman K, Billia F, Farkouh ME, Wald RM
JACC Clin Electrophysiol. 2018 Nov;4(11):1480-1481
Bokhari MM, Spears DA, Lai PF, Si D, Billia F, Parker JD, Al-Hesayen AO, Azam MA, Riazi S, Nanthakumar K
Cardiovasc Res. 2018 May 25;:
Bugyei-Twum A, Ford C, Civitarese R, Seegobin J, Advani SL, Desjardins JF, Kabir G, Zhang Y, Mitchell M, Switzer J, Thai K, Shen V, Abadeh A, Singh KK, Billia F, Advani AA, Gilbert RE, Connelly KA
Cardiol Rev. 2018 Mar 30;:
Grosman-Rimon L, Billia F, Kobulnik J, Bar-Ziv SP, Cherney DZ, Rao V
PLoS One. 2017;12(12):e0189861
Hauck L, Stanley-Hasnain S, Fung A, Grothe D, Rao V, Mak TW, Billia F
Int J Cardiol. 2017 Oct 31;:
Van De Bruaene A, Hickey EJ, Kovacs AH, Crean AM, Wald RM, Silversides CK, Redington AN, Ross HJ, Alba AC, Billia F, Nair K, Benson L, Horlick E, Osten M, Colman J, Heggie J, Oechslin EN, Roche SL
Circ Heart Fail. 2017 Sep;10(9):
Duero Posada JG, Moayedi Y, Alhussein M, Rodger M, Alvarez J, Wintersperger BJ, Ross HJ, Butany J, Billia F, Rao V
Cell Cycle. 2017 Jul 26;:0
Stanley-Hasnain S, Hauck L, Grothe D, Aschar-Sobbi R, Beca S, Butany J, Backx PH, Mak TW, Billia F



Assistant Professor, Department of Medicine, University of Toronto
Medical Director, Mechanical Circulatory Support Program
Co-Director of the Peter Munk Cardiovascular Biobank