The possible role of cardiovascular reactivity in coronary heart disease was supported by evidence from both basic and clinical studies. The hemodynamic forces resulting from turbulence and shear stress at curves and bifurcations of the coronary arteries had been cited as responsible for the greater degree of atherosclerosis in high heart rate, as opposed to low heart rate animals. Monkeys with large elevations of heart rate in response to psychological arousal developed significantly more atherosclerosis. Although the above findings had not been confirmed in humans as of 1988, a substantial majority of studies reported greater reactivity of Type A subjects during stress.