A neural network to predict the knee adduction moment in patients with osteoarthritis using anatomical landmarks obtainable from 2D video analysis.

OBJECTIVE: The knee adduction moment (KAM) can inform treatment of medial knee osteoarthritis; however, measuring the KAM requires an expensive gait analysis laboratory. We evaluated the feasibility of predicting the peak KAM during natural and modified walking patterns using the positions of anatomical landmarks that could be identified from video analysis. METHOD: Using inverse dynamics, we calculated the KAM for 86 individuals (64 with knee osteoarthritis, 22 without) walking naturally and with foot progression angle modifications. We trained a neural network to predict the peak KAM using the 3-dimensional positions of 13 anatomical landmarks measured with motion capture (3D neural network). We also trained models to predict the peak KAM using 2-dimensional subsets of the dataset to simulate 2-dimensional video analysis (frontal and sagittal plane neural networks). Model performance was evaluated on a held-out, 8-person test set that included steps from all trials. RESULTS: The 3D neural network predicted the peak KAM for all test steps with r2( Murray et al., 2012) 2 = 0.78. This model predicted individuals' average peak KAM during natural walking with r2( Murray et al., 2012) 2 = 0.86 and classified which 15° foot progression angle modifications reduced the peak KAM with accuracy = 0.85. The frontal plane neural network predicted peak KAM with similar accuracy (r2( Murray et al., 2012) 2 = 0.85) to the 3D neural network, but the sagittal plane neural network did not (r2( Murray et al., 2012) 2 = 0.14). CONCLUSION: Using the positions of anatomical landmarks from motion capture, a neural network accurately predicted the peak KAM during natural and modified walking. This study demonstrates the feasibility of measuring the peak KAM using positions obtainable from 2D video analysis.

Control of atrial natriuretic peptide secretion in patients with severe congestive heart failure.

Congestive heart failure (CHF) is marked by activation of multiple hormone systems that increased peripheral vasoconstriction and produce sodium and water retention. Plasma atrial natriuretic peptide (ANP) levels are frequently elevated in patients with severe CHF and may act to counterbalance these hormonal actions. To determine whether CHF patients maintain a physiological response to the presumed major stimulus to ANP secretion, atrial stretch, 22 CHF patients and 8 normal volunteers were studied. Atrial distention was produced in 10 CHF patients with a mannitol infusion and in 12 with lower body positive pressure. Eight normal volunteers also underwent a mannitol infusion. Both stimuli provoked increases in plasma ANP levels in the CHF patients, and the relative increase in plasma ANP after mannitol was similar in the CHF patients and the normal volunteers. We conclude that ANP secretion responds to atrial stretch in CHF patients, suggesting maintenance of the physiological release of this peptide.

Acute hemodynamic and hormonal effects of CI-930, a new phosphodiesterase inhibitor, in severe congestive heart failure.

The phosphodiesterase inhibitor CI-930 hydrochloride exerts a positive inotropic and vasodilator effect in experimental animals. The acute hemodynamic and hormonal effects of intravenous CI-930 were studied in 9 patients with severe congestive heart failure. At 60 minutes of drug infusion, there was an increase in cardiac index (2.7 +/- 0.9 vs 2.0 +/- 0.7 liters/min/m2, p less than 0.01) and positive dP/dt (1,390 +/- 470 vs 1,100 +/- 300 mm Hg/s, p less than 0.02). Additionally, there were decreases in mean systemic arterial (78 +/- 16 vs 86 +/- 15 mm Hg, p less than 0.01), mean right atrial (5 +/- 3 vs 9 +/- 4 mm Hg, p less than 0.02), mean pulmonary arterial (27 +/- 11 vs 37 +/- 9 mm Hg, p less than 0.01) and LV end-diastolic (19 +/- 8 vs 28 +/- 6 mm Hg, p less than 0.01) pressures. Heart rate did not change (97 +/- 17 vs 97 +/- 22 beats/min). The inotropic response correlated significantly (r = 0.70, p less than 0.05) with the dose of CI-930. Plasma renin activity did not change significantly (from 16 +/- 9 to 23 +/- 15 ng/ml/hour), nor did plasma norepinephrine or arginine vasopressin levels. The plasma atrial natriuretic peptide level decreased (from 153 +/- 97 to 83 +/- 35 pg/ml, p less than 0.02). These findings suggest that intravenous CI-930 hydrochloride is a useful therapeutic agent in congestive heart failure and that its use does not appear to further activate potentially deleterious hormonal systems.

The acute effect of an oral "inotropic" placebo on the exercise capacity of patients with chronic cardiac failure.

Uncontrolled studies have suggested that the newer oral phosphodiesterase inhibitors milrinone and enoximone acutely improve exercise performance in patients with severe chronic cardiac failure. To determine whether an oral placebo presented as an inotropic agent could acutely enhance exercise capacity, two separate groups of stable heart failure patients were studied by serial exercise testing and respiratory gas exchange analysis. Group 1 had nine patients studied four hours after a single oral dose of placebo, and group 2 had ten patients retested after one to two weeks of placebo therapy. No significant change was seen in the mean exercise time, mean peak oxygen consumption, and the mean oxygen consumption at anaerobic threshold after placebo administration in both group 1 and group 2 patients. Improvements in exercise time, peak oxygen consumption, and oxygen consumption at anaerobic threshold occurred in five patients in group 1 and seven patients in group 2. The improvements exceeded the baseline variability of 10 percent in three group 1 patients. Among group 2 patients, the increase in exercise time, peak oxygen consumption, and oxygen consumption at anaerobic threshold exceeded 10 percent in six, four, and four patients, respectively. Thus, stable chronic heart failure patients can achieve a true baseline exercise capacity. Small improvements in exercise performance seen acutely after oral inotropic drug therapy in individual heart failure patients must be interpreted with caution, as they may be due to a placebo effect.

Combined therapy with dobutamine and amrinone in severe heart failure. Improved hemodynamics and increased activation of the renin-angiotensin system with combined intravenous therapy.

The hemodynamic and hormonal responses to dobutamine alone and with the addition of amrinone were studied in ten patients with severe heart failure. Dobutamine significantly increased heart rate, cardiac index, and stroke volume index and significantly decreased mean right atrial and systemic arterial pressures and systemic and pulmonary vascular resistance. The addition of amrinone further decreased significantly mean right atrial, pulmonary arterial, and pulmonary arterial wedge pressures and systemic vascular resistance, while heart rate rose. The response of the cardiac index was variable, increasing in seven and decreasing in three patients. Plasma renin activity rose significantly with dobutamine and further increased with amrinone. We conclude that in most patients with severe heart failure, amrinone, when combined with dobutamine, improves hemodynamics. The further increase in heart rate, variable effects on the cardiac index, and marked activation of the renin-angiotensin system suggest caution and potential limitations in the use of this combination.