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K Hackney

Publications and source records attributed to K Hackney.

5 recordsLinked to original sources

Echo/Doppler and hemodynamic correlates of vasodilator responsiveness in primary pulmonary hypertension.

To determine correlates of acute vasodilator responsiveness in primary pulmonary hypertension, we retrospectively studied 25 patients, comparing 41 resting echo/Doppler and nine resting catheterization variables with the maximal reduction in pulmonary vascular resistance achieved during vasodilator trials. Twelve vasodilators were tested (mean, 5.6 drugs per patient; range, three to eight). Eight patients were vasodilator responsive, as defined by a reduction in pulmonary vascular resistance greater than or equal to 30 percent in response to at least one agent. Univariate and multivariate analyses revealed only Doppler pulmonic peak flow velocity to be an independent correlate of responsiveness (p less than 0.05). Responders differed from nonresponders in having a higher Doppler pulmonic peak flow velocity (PV) (SD 81 +/- 24 vs 64 +/- 15 cm/s; p = 0.05), lower mean right atrial pressure (RAP) (6 +/- 4 vs 13 +/- 7 mm Hg; p = 0.04), and longer median survival (37 vs 5 months; p = 0.03). Seven of eight responders had RAP less than or equal to 10 mm Hg, and all responders had PV greater than 60 cm/s. Seven of ten patients with both RAP less than or equal to 10 and PV greater than 60 and one of the 15 remaining patients were vasodilator responsive (p less than 0.001). Thus, echo/Doppler and invasive hemodynamic parameters correlate with acute vasodilator responsiveness in primary pulmonary hypertension. Patients with low PV and high RAP values were almost never vasodilator responsive. Doppler pulmonic peak velocity and mean RAP may be useful in identifying patients most likely to respond to acute vasodilator trials and those in whom testing is unlikely to yield positive results.

Adult↗

Two-dimensional and Doppler-echocardiographic and cardiac catheterization correlates of survival in primary pulmonary hypertension.

To determine correlates of survival in primary pulmonary hypertension, we compared 41 echocardiography-Doppler and nine catheterization parameters with outcome in 26 patients. Mean follow-up was 19.7 months in survivors; mean survival was 4.8 months in 16 nonsurvivors. Cox life-table univariate analysis correlated two echocardiographic, three Doppler, and three catheterization variables with poor survival (p less than or equal to 0.05), and chi 2 analysis ensured the best critical values: severity of pericardial effusion, heart rate of more than 87 beats/min, pulmonic flow acceleration time of less than 62 msec, tricuspid early flow deceleration (T-DEC) equal to or less than -300 cm2/sec, mitral early flow-to-atrial flow velocity ratio (M-E/A) equal to or less than 1.0, catheterization cardiac index (CI) equal to or less than 2.3 l/min/m2, mean pulmonary artery pressure of more than 61 mm Hg, and diastolic pulmonary artery pressure of more than 43 mm Hg. Multivariate life-table analysis of noninvasive variables revealed the severity of pericardial effusion to be independently significant (p = 0.006), whereas analysis of catheterization variables revealed cardiac index to be independently significant (p = 0.014). Combined multivariate analysis did not differ from the noninvasive results alone. Categorical modeling of the eight significant variables split at their critical values (present or absent) revealed M-E/A, T-DEC, and CI to be independently significant by multivariate analysis (p = 0.0014). Analysis of the five echocardiography-Doppler variables alone revealed M-E/A, T-DEC, and heart rate to be independently significant (p = 0.0016). In both cases, mortality increased with the number of critical values reached.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

Electrocardiographic diagnosis of exercise-induced left ventricular hypertrophy.

To assess the prevalence of physiologic left ventricular hypertrophy and the usefulness of ECG criteria for its diagnosis, we compared ECGs and M-mode echocardiograms from 44 ultraendurance athletes and 20 similarly aged sedentary control subjects. Left ventricular mass was elevated in 25 of 44 (57%) athletes including 17 of 29 (59%) men greater than 134 gm/m2 and 8 of 15 (53%) women greater than 110 gm/m2. The sensitivity and specificity of the three ECG criteria used to diagnose left ventricular hypertrophy were: Sokolow-Lyon voltage (S-V1 + R-V5 greater than or equal to 3.5 mV), 65% and 61%; Romhilt-Estes score (greater than or equal to 4), 16% and 84%; and Cornell voltage (R-aVL + S-V3 greater than 2.8 mV in men and greater than 2.0 mV in women), 8% and 95%, respectively. Left ventricular mass, mass index, posterior wall thickness, chamber diameter, and relative wall thickness were not related to any measurement of QRS voltage. Nonvoltage ECG criteria for left ventricular hypertrophy were rare in athletes. Thus hypertrophy is a common but not universal adaptation to exercise. It is only moderately well detected by standard voltage criteria for left ventricular hypertrophy and is not reflected in nonvoltage criteria.

Adult↗

Contribution of afterload, hypertrophy and geometry to left ventricular ejection fraction in aortic valve stenosis, pure aortic regurgitation and idiopathic dilated cardiomyopathy.

To investigate the relation of left ventricular (LV) afterload, hypertrophy, geometry and systolic pump function, 17 normal persons, 24 patients with aortic stenosis (AS), 20 with aortic regurgitation (AR) and 15 with idiopathic dilated cardiomyopathy (DC) were studied. Two-dimensional echograms were used to assess end-systolic meridional and circumferential stresses and their ratio, LV mass, relative wall thickness (h/R ratio) and the ratio of LV minor axis to length, used as an index of shape. Independently obtained ejection fraction (EF) was used to determine which patients had normal (EF greater than or equal to 55%) and which had depressed (EF less than 55%) pump function. Patients with AS and low EF had similar LV mass (228 vs 215 g) but larger LV cavity (5.6 vs 4.5 cm), lower h/R ratio (0.53 vs 0.73, p less than 0.01), and therefore higher circumferential stress (336 vs 268 kdyne/cm2, p less than 0.05). Compared with normal persons, patients with DC had a lower h/R ratio (0.28 vs 0.38, p less than 0.01), higher circumferential stress (362 vs 215 kdyne/cm2, p less than 0.01) and more uniform stress distribution (meridional to circumferential stress ratio 0.57 vs 0.39, p less than 0.01), implying that meridional stress overestimates effective afterload. Afterload excess and LV shape change may be important to pump function in patients with AS or DC. In contrast, in those with AR, no significant shape differences were noted, although LV mass was higher in those with low EF (279 vs 211 g, p less than 0.05). Depressed pump function may result from impaired myocardial performance in AR without afterload excess.

Adult↗

Cardiac fatigue after prolonged exercise.

To determine the effects of prolonged exercise on systolic and diastolic left ventricular function, we studied 21 athletes before, at the finish (within 11 +/- 5 min), and during recovery (28 +/- 9 hr) after the Hawaii Ironman Triathlon (2.4 mile swim, 112 mile bike, 26.2 mile run). Two-dimensionally guided M mode echocardiograms were digitized for wall thickness, cavity dimension, fractional shortening, and peak rates of cavity enlargement and wall thinning. Pulsed Doppler left ventricular inflow recordings were analyzed for peak early and late velocities and their ratio. Left ventricular diastolic dimension was reduced at race finish (5.4 +/- 0.6 to 5.1 +/- 0.6 cm) and remained reduced after 1 day of recovery (5.2 +/- 0.6 cm, p less than .05). Fractional shortening fell at race finish (39 +/- 5% to 35 +/- 5%), although systolic blood pressure was unchanged, and rose to 40 +/- 4% after recovery (p less than .05). The return to prerace shortening values after recovery occurred despite continued reduction in diastolic size. Peak circumferential shortening did not change significantly. Individual reductions in fractional shortening were correlated with increases in systolic cavity size (r = -.64, p less than .01), but not with decreases in diastolic size. The stress-shortening relationship was displaced downward at race finish, but returned toward baseline after 1 day of recovery, despite a persistent reduction in cavity size. This suggests that the decrease in shortening was due to impaired contractility as well as altered preload.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗