Effects of isometric exercise and increased arterial impedance on left ventricular function in severe aortic valvular stenosis

Abstract

Since critical aortic stenosis imposes severe obstruction to cardiac outflow, the peripheral vascular determinants of left ventricular impedance in this condition remain uncertain. Thus, the systemic arterial and left ventricular haemodynamic responses to acute circulatory interventions were evaluated during cardiac catheterisation in 10 patients with severe aortic stenosis (valve area 0.40 cm2/m2). Sustained isometric handgrip exercise increased systemic vascular resistance to 1278 dynes s cm-5 and arterial blood pressure to peak systolic 143 mmHg( mean 94), which were significantly (P<0.01) greater than control (systemic vascular resistance 1110; BP peak systolic 122; BP mean 80). Isometric handgrip exercise was also accompanied by concordant changes in left ventricular pressures (P<0.01) of peak systolic from 191 to 213 mmHg and end-diastolic from 16 to 23 mmHg; cardiac output (5.62 l/min) and peak systolic left ventricular aortic gradient (69 mmHg) were unchanged (P>0.05). In 7 of these patients intravenous phenylephrine infusion (2.7 to 6.0 μg/min) produced the following responses similar (P>0.05) to isometric handgrip exercise: increases (P<0.01) in systemic vascular resistance to 1549, BP to peak systolic 150 and mean 97, and left ventricular pressures to peak systolic 211 and end-diastolic 22 (P<0.02) without alterations in cardiac output or peak systolic LV-aortic gradient; isometric handgrip exercise was accompanied by an increase (P<0.01) in contractile state indices (peak dp/dt 1882 to 2580 mm/Hg/s; Vmax 4.28 to 6.43 circ/s) and rise in heart rate (72 to 82 bpm) while these variables remained constant (P>0.05) with phenylephrine. Therefore, augmentation of arterial resistance increased left ventricular impedance resulting in abnormalities of cardiac haemodynamics despite the presence of pronounced valvular obstruction. These observations are of potential importance in the pathogenesis of sudden death in severe aortic stenosis and provide therapeutic insight in emergency medical management of ventricular dysfunction in this condition.