Table 1. Models of acute right ventricular failure.

Method	Strengths	Limitations	Mouse	Rat	Rabbit	Dog	Sheep	Pig
Pulmonary embolism
Pharmacological coagulation vasoconstriction	Feasible	Often fatal	(5-9)	(10)
	Minimal instrumentation	Difficult to control thrombus load
	Large clot burden	Unlike human physiology
Exogenous clot Artificial	Feasible	Unlike human physiology		(11-13)	(14,15)	(16)	(17,18)	(19,20)
	Controllable thrombus burden	Only distal thrombus
	Stable and lasting thrombus	Not able to remove thrombus
Exogenous clot Autologous	Comparable to human physiology	Thrombus created ex vivo—Homogenous and fresh			(21-24)	(25-30)	(18,31)	(32-37)
	Thrombus resolution possible	Difficult to administer en block—Risk of fragmentation.
	Controllable thrombus load.
Deep venous thrombosis	Thrombus created in vivo—Heterogeneous and chronic	Challenging setup		(38)				(39)
	Comparable to human physiology	Time needed for thrombus formation
	Central thrombus	Difficult to control thrombus load.
Pulmonary artery occlusion
Pulmonary artery banding	Precise afterload increase	Need for open chest		(40)	(41)	(42)	(43-45)	(46,47)
	Stable afterload	Not suited for pulmonary interventions
	Adjustable	Unlike human physiology
	Wide range of RV strain
Pulmonary artery balloon	Precise afterload increase	Not suited for pulmonary interventions						(48)
	Stable afterload	Unlike human physiology
	Adjustable
	Wide range of RV strain

An overview of models of RV failure stratified to method of afterload increase and animal species.