To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 + 0.5 years), and late (8.1 + 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 + 73 to 105 + 35 ml/m2, p < .01), a fall in left heart filling pressure (19 + 9 to 12 + 5 mm Hg, p < .01), and maintenance of the cardiac index (3.3 + 0.8 to 3.5 ± 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 ± 13% to 64 ± 10%, NS). By the late study the cardiac index (4.0 ± 0.6 liters/min/m2, p < .01) and left ventricular ejection fraction (66 ± 15%, p < .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 ± 38 vs 120 ± 29 g/m2, p < .01), and a further 13% from the intermediate to the late study (105 ± 32 g/m2, p < .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 ± 36 g/m2), and greater in those with aortic stenosis (158 ± 33 g/m2) than in control subjects (85 ± 9 g/m2, p < .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 ± 29 g/m2) and those with stenosis (114 ± 27 g/m2) than in the control subjects (p < .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium. Circulation 77, No. 6, 1345No. 6, -1355No. 6, , 1988 LEFT VENTRICULAR pressure and volume overloads in response to aortic valve stenosis and aortic valve insufficiency lead to a marked hypertrophic response of the myocardium, likely as an adaptative response to normalize the increased wall stress accompanying these states.' While this allows for maintenance
Two short-term memory experiments examined the nature of the stimulus suffix effect on auditory linguistic and nonlinguistic stimulus lists. In Experiment 1, where subjects recalled eight-item digit lists, it was found that a silently articulated digit suffix had the same effect on recall for the last list item as a spoken digit suffix. In Experiment 2, subjects recalled lists of sounds made by inanimate objects either by listing the names of the objects or by ordering a set of drawings of the objects. Auditory suffixes, either another object sound or the spoken name of an object, produced a suffix effect under both recall conditions, but a visually presented picture also produced a suffix effect when subjects recalled using pictures. The results were most adequately explained by a levels-of-processing memory coding hypothesis.When subjects are asked to recall items from a list that exceeds the capacity of short-term memory, they typically show a bowed serial position function. That is, recall is better on the first few (the primacy effect) and on the last one or two (the recency effect) list items than on intermediate items. However, under auditory presentation conditions, the addition of one extra item at the end of the list impairs recall for the terminal items, even when subjects are instructed to ignore this suffix and omit it from their recall of the list. This elimination of the recency effect is known as the stimulus suffix effect (Crowder, 1967;Crowder & Morton, 1969). Crowder and Morton (1969;Morton, Crowder, & Prussin, 1971) have suggested a theoretical explanation of the suffix and recency effects based on the precategorical acoustic store (PAS). PAS is a sensory storage system that may last for as long as 2 sec, and that contains auditory information in a relatively unprocessed form. Under normal list presentation conditions, the last one or two elements of the list remain in PAS at the time of recall, giving the subject an added source of information upon which to base his recall of these items. However, a stimulus suffix eliminates most, if not all, of the sensory information about the last list elements from PAS, making recall of them equal to intermediate list items whose traces have also been eliminated from PAS.This research was supported by National Science Foundation Grant BNS76-82337 to the first author and a National Science Foundation Undergraduate Research Participation fellowship to the second author. The authors wish to acknowledge Peter D. Eimas both for providing assistance in the production of the stimuli for Experiment 2 and for giving helpful comments on many phases of this research, and Ann Lee, who collected the data for Experiment 2. Reprint requests should be addressed to Kathryn T. Spoehr, Psychology Department, Brown University, Providence, Rhode Island 02912.The PAS explanation of the suffix effect has been supported by much empirical data. Consonant with this theory, for example, are the findings that nonlinguistic auditory suffixes fail to cause a suffix effect (Crowder, ...
Left ventricular function in volume overload hypertrophy is controversial. In humans, chronic severe volume overload eventually results in left ventricular dysfunction; paradoxically, experimental volume overload hypertrophy has nearly always been associated with normal left ventricular function. However, in most cases, experimental volume overload hypertrophy has either been mild or only present for a short duration. To help resolve the issue of contractile function in volume overload hypertrophy, we examined ventricular function in a recently described model of severe chronic experimental mitral regurgitation. Left ventricular function was measured before and 3 mo after the creation of severe mitral regurgitation (averaged regurgitant fraction 0.64 +/- 0.04). At 3 mo end-diastolic volume had increased from 78 +/- 5 to 114 +/- 7 ml (P less than 0.01). Significant left ventricular hypertrophy had occurred with an increase in the left ventricular weight-to-body weight ratio from 3.84 +/- 0.2 to 5.22 +/- 0.2 (P less than 0.01). All indicators of left ventricular function (ejection fraction, the end ejection stress-volume relationship, this relationship corrected for eccentric hypertrophy, and mean velocity of circumferential fiber shortening at a common stress) were reduced at 3 mo. Our study produced 64% volume overload which was maintained for 3 mo at which time there was a 36% increase in left ventricular mass. This amount of volume overload of this duration produced significant left ventricular dysfunction.
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