Cardiac mass and function, carotid artery intima-media thickness, and lipoprotein levels in growth hormone-deficient adolescents

The objective of our study was to evaluate whether cardiac mass and functio n, carotid artery intima-media thickness, and serum lipid and lipoprotein(a ) levels are abnormal in adolescents with GH deficiency. Young adults with childhood-onset and adulthood-onset GH deficiency have be en found to have a higher cardiovascular risk, as manifested among other fa ctors by reduced left ventricular mass, impaired systolic function, signifi cant increase in arterial intima-media thickness, and dyslipidemia. Twelve adolescents (seven males and five females) with GH deficiency (10 id iopathic and 2 organic), with an age of 14.2 +/- 2.8 yr and a height of 140 .6 +/- 17.9 cm (height so score, -2.6 +/- 0.3), were studied. Six children had received GH in the past but were off therapy for several years, whereas six patients had never been treated with GH. Fasting blood samples were ob tained for serum lipids and lipoprotein(a) analysis. Patients underwent tra nsthoracic M-mode and two-dimensional echocardiographic evaluation for meas urement of interventricular septal thickness, left ventricular posterior wa ll thickness, and left ventricular mass, as well as left ventricular ejecti on fraction at rest and pulmonary Venous flow velocities; carotid artery in tima-media thickness was measured using high-resolution mode B ultrasound. Seven GH-deficient (GHD) adolescents on GH at the time of the study and 19 healthy adolescents, all comparable for age, pubertal status, height, weigh t, blood pressure, and pulse, participated in this study as controls. Interventricular septal thickness (6.5 +/- 1.3 vs. 7.0 +/- 1.5 mm), left ve ntricular posterior wall thickness (7.0 +/- 1.8 us. 7.5 +/- 2.0 mm), and le ft ventricular mass after correction for body surface area (71.2 +/- 21.8 v s. 70.7 +/- 18.0 g/m(2)) were similar in untreated GHD patients and healthy controls. Similarly, the left ventricular ejection fraction at rest was si milar in untreated GHD subjects and controls (70.0 +/- 0.7 vs. 70.0 +/- 0.6 %), as were the pulmonary venous flow velocities (0.54 +/- 0.16 vs. 0.55 +/ - 0.10 m/s for diastolic peak velocity; 0.51 +/- 0.16 vs. 0.50 +/- 0.09 m/s for systolic peak velocity; and 0.19 +/- 0.06 vs. 0.19 +/- 0.05 m/s for at rial reversal filling). Carotid artery intima-media thickness (0.60 +/- 0.0 2 mm and 0.59 +/- 0.02 mm for the right and left carotid arteries, respecti vely) was also normal in our untreated GHD patients when compared with heal thy controls. In addition, all echocardiographic measurements were similar in GHD subjects on or off GH at the time of the study. Low-density lipoprotein cholesterol levels were increased in untreated GHD patients when compared with healthy controls (3.17 +/- 0.70 vs. 2.33 +/- 0. 36 mmol/L; P < 0.01), whereas total cholesterol, high-density lipoprotein c holesterol, and triglyceride concentrations were similar to that of control s. Total cholesterol levels were increased in our untreated GHD adolescents when compared with GHD subjects receiving GH therapy at the time of the st udy, while low-density lipoprotein cholesterol and triglyceride levels were also elevated, although not significantly. Lipoprotein(a) levels were elev ated in untreated GHD adolescents when compared with healthy controls, and untreated GHD subjects had higher Lipoprotein(a) concentrations than GH-tre ated patients. GHD adolescents, regardless of whether or not they received GH therapy, do not seem to show alterations in cardiac mass and function or early atherosc lerotic changes. They must, however, be followed carefully because they alr eady present cardiovascular risk factors such as dyslipidemia, which may in crease their cardiovascular morbidity over time.