Assessment of a New Experimental Model of Isolated Right Ventricular Failure Petronio G. Thomaz, Renato S. Assad, Maria C.D. Abduch, Euclides Marques, Vera D. Aiello, and Noedir A.G. Stolf Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil Abstract: We assessed a new experimental model of iso- lated right ventricular (RV) failure, achieved by means of intramyocardial injection of ethanol. RV dysfunction was induced in 13 mongrel dogs via multiple injections of 96% ethanol (total dose 1 mL/kg), all over the inlet and trabe- cular RV free walls. Hemodynamic and metabolic param- eters were evaluated at baseline, after ethanol injection, and on the 14th postoperative day (POD). Echocardio- graphic parameters were evaluated at baseline, on the sixth POD, and on the 13th POD.The animals were then eutha- nized for histopathological analysis of the hearts.There was a 15.4% mortality rate.We noticed a decrease in pulmonary blood flow right after RV failure (P = 0.0018), as well as during reoperation on the 14th POD (P = 0.002). The induced RV dysfunction caused an increase in venous lactate levels immediately after ethanol injection and on the 14th POD (P < 0.0003). The echocardiogram revealed a decrease in the RV ejection fraction on the sixth and 13th PODs (P = 0.0001). There was an increased RV end- diastolic volume on the sixth (P = 0.0001) and 13th PODs (P = 0.0084). The right ventricle showed a 74%  0.06% transmural infarction area, with necrotic lesions aged 14 days. Intramyocardial ethanol injection has allowed the creation of a reproducible and inexpensive model of RV failure. The hemodynamic, metabolic, and echocardio- graphic parameters assessed at different protocol times are compatible with severe RV failure. This model may be useful in understanding the pathophysiology of isolated right-sided heart failure, as well as in the assessment of ventricular assist devices. Key Words: Heart failure congestive—Ventricular dysfunction right—Myocardial ischemia/chemically induced—Animal model. The cumulative knowledge achieved through experimental models of induced heart failure (HF) has allowed a more accurate characterization and better understanding of the underlying pathophysi- ological mechanisms; this knowledge has also validated new clinical and surgical strategies in the treatment of HF (1). Several experimental models of induced HF in different animal species have been published in which the following diverse methods were used: volume overload, pressure overload, arti- ficial rapid ventricular stimulation, myocardial infarc- tion induction, and cardiotoxic drugs, among others (2). However, most of them promote biventricular HF, and only a few can selectively induce right or left ventricular (LV) failure. In addition, previous models hardly reproduce the natural history of HF, with limi- tations and interests for specific areas. Although rare, isolated right ventricular (RV) failure can complicate an acute myocardial infarction (3–6) or a coronary artery bypass grafting surgery, as a consequence of inadequate myocardial protection (7,8). At present, the ideal clinical and/or surgical treatment of RV failure is not very well established. A better under- standing of RV failure pathophysiology could be achieved by establishing an animal model that more closely resembles the clinical status of the disease. Previous attempts to induce experimental right-sided HF were made by means of RV free wall cauteriza- tion (9). However, the hemodynamic picture of right- sided HF was not completely achieved. Recently, acute RV failure studies emphasize the importance of the right ventricle in the global hemodynamic perfor- mance of the heart, establishing the concept of ven- tricular interdependence. Increased intrapericardial pressure, as a result of marked RV dilation, and doi:10.1111/j.1525-1594.2009.00716.x Received December 2007; revised February 2008. Address correspondence and reprint requests to Dr. Petronio G. Thomaz, Heart Institute University of Sao Paulo, Division of Sur- gical Research,Avenue Dr. Eneas Carvalho Aguiar, 44, Sao Paulo, SP 05403-000 Brazil. E-mail: petronio@sbccv.org.br Artificial Organs 33(3):258–265, Wiley Periodicals, Inc. © 2009, Copyright the Authors Journal compilation © 2009, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc. 258