The anginal syndrome (AP) typically includes sensations of chest tightness or difficulty in breathing. Left ventricular (LV) dysfunction during myocardial ischemia incident with AP is now well documented. Since secondary alterations in lung mechanics could relate to these symptoms, we examined airway resistance (Raw), lung volume (TGV), lung compliance (CL), and LV pressure-volume relations during pacing-induced AP.LV end-diastolic pressure (EDP) increased suddenly with AP, (mean + 41%,p< 0.01), without change in end-diastolic volume (EDV). LV distensibility (EDV/EDP) decreased abruptly, (−37%,P< 0.01), with reduction in airway conductance (1/Raw/TGV), (−40%,P< 0.05), and CL(−27%,P< 0.05). When AP was relieved, these changes returned toward preangina levels.Ischemia-induced LV dysfunction abruptly increases LVEDP. The resulting increased pulmonary capillary pressure effects an alteration of lung mechanics consisting of increasing Raw and reduced CL. The changes in ventilatory effort which ensue may be interpreted as chest tightness, heaviness, or constriction by the AP patient.