Physiologie hypertrophy: Effects on left ventricular ...

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JACC Vol. 9. NO.4 April 19~7:776-~3

Physiologic Hypertrophy: Effects on Left Ventricular Systolic Mechanics in Athletes

STEVEN D. COLAN, MD,* STEPHEN P. SANDERS, MD,* KENNETH M. BOROW, MOt

Boston. Massachusetts and Chicago, l/linois

Physiologic hypertrophy resulting from intense athletic participation has been reported to result in normal, reduced and augmented overall left ventricular performance. Rather than representing true differences in left ventricular contractility, these data may reflect the variable degree of ventricular dilation and increased wall thickness that occur with different types of exercise. As such, the resultant altered loading conditions may diminish the ability of the usual indexes of left ventricular function to accurately assess the left ventricular contractile state. Therefore, three groups of elite athletes with distinct patterns of myocardial hypertrophy were investigated utilizing recently developed load-independent contractility indexes. Age-matched-control subjects

= (n 33) were compared with II swimmers, 11 long-

distance runners and 11 power lifters. Rest echocardiogram, phonocardiogram and calibrated carotid pulse tracing were used to calculate left ventricular dimensions, wall thickness, mass, fractional shortening, velocity of shortening and mean, peak and end-systolic wall stresses and the stress-time and minute stress-time integrals.

Compared with control subjects, all athletes had increased left ventricular mass, even when values were normalized for body surface area. Runners had a dilated left ventricle and normal wall thickness, swimmers had a mildly dilated ventricle with increased wall thickness and power lifters had normal cavity size with markedly increased wall thickness. Peak systolic wall stress was normal in runners and swimmers and reduced in power

lifters, whereas end-systolic stress was low in swimmers and power lifters and normal in runners. The minute stress-time integral, a measure of myocardial oxygen consumption, was normal in runners and swimmers but was significantly reduced in lifters. In runners, fractional shortening was significantly reduced with normal velocity of shortening, whereas swimmers and power lifters had significant augmentation of fractional shortening and velocity of shortening. Examination of the rate-corrected velocity of shortening-end-systolic stress relation revealed normal contractility with augmented systolic performance due to reduced afterload in swimmers and power lifters. Comparison of runners and control subjects revealed normal afterload but reduced preload in runners, which was manifested as reduced fractional shortening with normal afterload and contractile state.

Physiologic hypertrophy results in marked alterations in left ventricular loading conditions with secondary changes in systolic performance. When load-independent indexes are employed, the left ventricular contractile state is found to be normal in young athletes despite markedly increased left ventricular mass. Different types of exercise are associated with distinct patterns of left ventricular hypertrophy and dilation, necessitating individual assessment of preload and afterload in the interpretation of indexes of left ventricular function.

(J Am Coil CardioI1987;9:776-83)

Intense athletic participation results in myocardial hypertrophy that can be disproportionate to the increase in body

From the *Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, Massachusetts, and the tCardiovascular Division. Department of Medicine, University of Chicago, Chicago, Illinois. This study was supported in part by Grant HL07193 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.

Manuscript received April IS, 1986; revised manuscript received October I, 1986, accepted October 10,1986.

Address forreprints: Steven D. Colan, MD, Department of Cardiology. The Children's Hospital, 300 Longwood Avenue, Boston, Massachusetts 02115.

? 19~7 by the American College of Cardiology

surface area. Similar degrees of left ventricular hypertrophy may be present in patients with aortic stenosis, coarctation of the aorta or systemic hypertension (1,2). These pathologic cases have demonstrated complex changes in preload, afterload and contractility that lead to the failure of the loaddependent ejection phase indexes (for example, ejection fraction, percent fractional shortening and velocity of fiber shortening) to accurately reflect intrinsic contractile state (2). In highly trained athletes the left ventricle also undergoes geometric and hemodynamic changes that may influence ventricular loading conditions in a manner that could

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l ACC Vol. 9. No.4 April 19X7:776-l\3

COLAN ET AL.

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LEFf VENTRICULA R SYSTOLIC MECHANICS IN ATHLETES

diminish the reliability of traditional measures of left ventricular performance as indexes of myocardial contractility (3- 12). This may explain the reports of normal, decreased and increased ventricular function in subjects with physiologic hypertrophy. Accordingly, we studied left ventricular performance in young elite swimmers, runners and power lifters using noninvasive load-independent indexes of left ventricular contractility. These indexes, which are based on physiologic events at end-systole, were used to elucidate the effects of distinct patterns of left ventricular hypertrophy on myocardial mechanics.

Methods

Study subjects. The study group comprised 33 athletes and 33 age-matched normal control subjects (age 16 to 29 years). There were II swimmers, II long-distance runners and II power lifters in the athlete group. Swimmers were recruited from a swim team with a training program of 25 to 30 h/week; all had more than 5 years' experience in competitive participation . Runners were members of a college track team participating in long-distance events; all ran more than 60 miles/week (average 90). Power lifters had all been participants in national competition within the prior 6 months and had more than 4 years of serious lifting experience. Control subjects were healthy, nonsedentary individuals who did not engage in a regular training program. All participants were free of known cardiovascular disease, were taking no cardioactive medications and had a normal physical examination.

Data recording. Data were collected using previously described methods (13-17 ). Echocardiograms were obtained using either a Hewlett-Packard 77020A two-dimensional ultrasound system with two-dimensionally directed M-mode capabilities or an Irex System II ultrasound module. High speed (100 mm/s) hard copy M-mode echocardiograms were obtained of the left ventricular minor axis with simultaneous phonocardiogram, electrocardiogram and indirect carotid pulse tracing. The phonocardiogram was recorded from the right upper sternal border. A Dinamap 845 or 1846P vital signs monitor (Critikon, Inc.) was used to obtain peak systolic and diastolic blood pressure measurements. Long- and short-axis views of the left ventricle were obtained with two-dimensional echocardiography for evaluation of regional wall motion in all participants except swimmers.

Data analysis. High quality tracings from each subject were selected for computer analysis on a Franklin Quantic 1200 echocardiographic review station (Bruce Franklin, Inc. ). This device has a digitizing pad with a sampling rate of 80/cm, giving a net digitizing rate of 800 points/so The carotid pulse tracing and the left ventricular echocardiogram, including the endocardial and epicardial borders of the posterior wall, were digitized. The carotid pulse tracing

was corrected for time delay by aligning the dicrotic notch with the first high frequency component of the aortic component of the second heart sound.

From the digitized data, the foll owing instantaneous measurements were derived by averaging three to jive cardiac cycles: I) left ventricular pressure throughoutejection, determined by linear interpolation using a calibratedcarotid pulse tracing as previously described (13- 17) (this method has been validated against an intraarterial standard in our laboratory! 18]); 2) left ventricular internal diameter; 3) left ventricular posterior wall thickness; and 4) the left ventricular wall stress calculated from the angiographically validated formula (19):

ws =:

(P)(D) 1.35 ,

(h) [I + (hID)] (4)

where WS is wall stress (g/crrr' ), P is pressure (mm Hg), D is dimension, h is posterior wall thickness (ern) and 1.35 is the conversion factor from mm Hg to g/cnr'. Mean ejection wallstress was calculatedfrom instantaneous wall stress values averaged over the period from the onset of ejection to aortic valve closure. The integral of the instantaneous stress-time relation was calculated for the ejection period to obtain the left ventricular stress-time integral, and the latter was multiplied by heart rate to obtain the left ventricular stress-time/min ( 17).

End-diastolic dimension and wall thickness were measured at the Q wave of the electrocardiogram, and endsystolic measurements were taken at the time of the first high frequency component of the second heart sound. The left ventricular percent fractional shortening was calculated as the difference between dimensions at end-diastole and end-systole, divided by the end-diastolic dimension (13). Left ventricular ejection time was measured from the simultaneous carotidpulsetracingand rate-corrected to a heart rate of 60 beats/min by dividing by the square root of the RR interval. The rate-corrected mean velocity of shortening was calculated by dividing fractional shortening by the ratecorrected ejection time (14).

Left ventricular mass was calculated using the modified for mula (~l Devereux and Reichek (20):

Mass =: 1.04 [(0 + 2hj' - D"] - 14g,

where D and h represent end-diastolic dimension and wall thickness, respectively. Because left ventricular mass is directly proportional to body surface area and left ventricular dimension is linearly related to thecubic rootof body surface area (21 ), left ventricular mass index and end-diastolic dimension index were calculated by dividing the nonindexed variables by body surface area and by the cube root of body surface area, respectively.

The relation offra ctional shortening and rate-corrected velocity of shortening to end-systolic wall stress was determinedforeach individual and the meanvalues wereobtained

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COLAN ET AL.

LEFf VENTRICULAR SYSTOLIC MECH ANICS IN ATHLETES

lACC Vol. 9. No.4 April 1987:776- 83

for each of the fourgroups. These were then compared with the previously reported normal values for these indexes

(13, 14).

Statistical analysis. Data are reported as mean ? SD unless otherwise noted. Comparisons amongthefourgroups were performed with one-way analysis of variance using the Tukey method for multiple comparison testing (22). A probability (p) value of ................
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