Stress and Stressors: Applied Pathophysiology

• Published in: Stress Echocardiography pp. 26 - 33
• Format: Book Chapter
• Language: English
• Published: CRC Press 2010
• Subjects: Inotropic State; Mitral Stenosis; Transvalvular Flow; Stress Echocardiography; Normal Coronary Arteries; Echo; Pulmonary Artery Systolic Pressure; Systolic Pulmonary Pressure; Coronary Vasospasm; Coronary Artery Stenosis; INO; Low Gradient Aortic Stenosis; Adenosine Receptors; HCM; Supply Demand Mismatch; Valvular Heart Disease; Normal Resting Values; Pulmonary Hypertension; Stress Echo; Myocardial Oxygen Consumption; Coronary Flow Reserve; Transvalvular Gradients
• DOI: 10.3109/9781841847146-5

Stresses have different pathophysiological and clinical targets (Table 1): coronary vasospasm; coronary artery stenosis; coronary flow reserve in high-risk patients with normal coronary arteries and negative wall motion response during stress echocardiography; identification of viable myocardium with resting dysfunction; assessment of severity of valvular heart disease in special subsets, such as low-gradient aortic stenosis and mitral stenosis with discordant symptoms and stenosis severity; identification of vulnerability to development of pulmonary hypertension. Each clinical target has a distinct echocardiographic diagnostic marker and a preferred stress. Tests inducing vasospasm (ergometrine infusion and hyperventilation) explore the functional component of myocardial ischemia. Tests targeting coronary stenosis (exercise, dipyridamole or adenosine, dobutamine, pacing) mostly explore the ceiling of coronary reserve as defined by organic factors. Viability stresses elicit a contractile response in myocardium with resting dysfunction through an inotropic challenge, primarily focused on myocyte (dobutamine or enoximone or low-level exercise) or mediated by an increase in coronary flow (dipyridamole or nitroglycerine). Coronary flow reserve is best studied with selective and powerful coronary vasodilators capable of fully recruiting microcirculatory vasodilatory capacity. Valvular function in aortic or mitral stenoses can be challenged with stresses increasing cardiac output and therefore transvalvular flow, which determines a steep increase in transvalvular gradients in functionally more severe stenosis. Finally, a vasoconstriction of pulmonary vasculature can be elicited only with exercise, leading to the identification of subjects with normal resting values of pulmonary artery systolic pressure, but vulnerable to developing genetically or environmentally mediated pulmonary hypertension.