Impairment of myocardial perfusion and function during painless myocardial ischemia.

Left ventricular (or pulmonary and systemic arterial) hemodynamics were measured for a mean of 13.6 hours during continuous electrocardiographic monitoring in 14 patients admitted to the coronary care unit because of angina at rest. Of 293 episodes of transient ST segment and T wave changes identified, 247 (84%) were completely asymptomatic. Sixty-three percent of asymptomatic episodes were associated with an elevation of the left ventricular end-diastolic or pulmonary artery diastolic pressure of 5 mm Hg or more; in 15% there were smaller elevations (2 to 4 mm Hg) and in 22% there were no changes or less than a 2 mm Hg elevation of pressure. The peak contraction and relaxation dP/dt (first derivative of left ventricular pressure) were reduced to 100 mm Hg/s or more in 84 and 81% of asymptomatic episodes, respectively. Great cardiac vein oxygen saturation measured in three patients showed an increased myocardial oxygen extraction similar to that seen in painful episodes, which preceded and accompanied asymptomatic electrocardiographic changes. These results indicate that asymptomatic electrocardiographic changes represent transient myocardial ischemia. Comparison of asymptomatic and symptomatic episodes revealed that asymptomatic episodes were generally shorter (253 +/- 159 versus 674 +/- 396 seconds, probability [p] less than 0.001) and produced less impairment of left ventricular function: there were smaller elevations of left ventricular end-diastolic or pulmonary artery diastolic pressure (5.9 +/- 5.0 versus 16.5 +/- 6.9 mm Hg, p less than 0.001), and smaller reductions of peak left ventricular contraction dP/dt (252 +/- 156 versus 395 +/- 199 mm Hg/s, p less than 0.001) and relaxation dP/dt (259 +/- 191 versus 413 +/- 209 mm Hg/s, p less than 0.001). In individual patients, however, asymptomatic and symptomatic episodes of similar duration and severity were observed. The duration and severity of ischemia appear important for the genesis of anginal pain, but additional factors must be involved.