When should Doppler-determined valve area be better than the Gorlin formula?: Variation in hydraulic constants in low flow states.

In low flow states, underestimation errors occur when the Gorlin formula is used to calculate valve area. A model of valvular stenosis designed to examine changes in the hydraulic discharge coefficient (Cd) and coefficient of orifice contraction (Cc) may explain these errors. Unsteady flow was examined in a pulsatile pump model and in a dog model. Valve areas were calculated from pressure and flow data using: a modified form of the Gorlin formula (assuming constant values for Cd and Cc) and a corrected formula (with values of Cd and Cc obtained from steady state data). Valve area was also calculated using the continuity equation with velocity and flow data (constant Cc). Flow velocities were measured using a newly designed ultrasound Doppler catheter capable of resolving flow velocities of up to 5.5 m/s. Both the corrected formula and continuity equation were highly predictive of actual valve area (r = 0.99, slope or M = 0.96 and r = 0.99, M = 1.06, respectively). The modified Gorlin equation was less accurate and tended to underestimate valve areas (r = 0.87, M = 0.83). This underestimation was most notable at low rates of flow (Gorlin: r = 0.94, M = 0.53; continuity: r = 0.93, M = 0.81 and r = 0.94, M = 0.89, respectively) more accurately than the modified Gorlin formula (r = 0.69, M = 0.49). In patients with low cardiac output, hemodynamic formulas, such as the Gorlin formula, which assume a constant value for the hydraulic discharge coefficient (Cd), may be less accurate than formulas using either a corrected value of Cd or Doppler-determined flow velocity and mean systolic flow.

Cardiovascular responses to handgrip isometric exercise in patients following cardiac transplantation.

The effects of cardiac denervation on the hemodynamic responses to isometric handgrip contraction were studied in patients 1--5 years after allograft cardiac transplantation. The objective of these studies was to determine the role of cardioacceleration and myocardial contractility on the increase in systemic arterial pressure during isometric exercise. Initially, noninvasive measurement of brachial artery pressure and heart rate during 60 seconds of isometric exercise at 50% of maximal voluntary contraction (50% MVC) were recorded in 23 cardiac transplant patients, 18 ischemic heart disease patients, and 15 healthy controls. While the increases in arterial pressure were not significantly different among the three groups and the heart rate response for the healthy controls and ischemic heart disease patients were similar, the transplant patient's heart rate remained essentially unchanged. In an attempt to determine the mechanisms for the increase in arterial pressure, despite any increase in heart rate in transplant patients, we recorded left ventricular volumes before and at the end of 50% MVC using fluoroscopy of tantalum midwall myocardial markers in seven cardiac transplant recipients and seven nontransplant cardiac surgery patients. The rise in arterial pressure during isometric exercise in both groups of patients resulted from a significant increase in peripheral vascular resistance but not in stroke volume or cardiac output. These data demonstrate that the rise in arterial pressure observed during isometric exercise can be achieved by increased peripheral vascular resistance alone in patients who lack the capacity to increase heart rate or stroke volume.

Effects of relaxation therapy on cardiac performance and sympathetic activity in patients with organic heart disease.

Six patients, with surgically implanted tantalum myocardial markers, were trained in deep muscle relaxation therapy. Analysis of individual responses and group means of blood pressure and ventricular dimensions during relaxation showed a decrease in plasma norepinephrine levels and indices of myocardial contractility compared to the control state. Heart rate changes in individuals during relaxation were directly correlated with changes in plasma norepinephrine levels, although group means for heart rate did not change significantly between control and relaxation periods. Base-line plasma norepinephrine levels were directly correlated with systolic blood pressure and were inveresly correlated with a measure of myocardial contractility. These data suggest that physiological changes during relaxation may be mediated through the sympathetic nervous system.