Anabolic androgenic steroids produce dose-dependant increase in left ventricular mass in power atheletes, and this effect is potentiated by concomitant use of growth hormone.

Power athletes abuse anabolic androgenic steroids (AASs) and growth hormone (GH) to gain their muscular mass and strength. We wanted to determine how massive, self-administered doses of AASs with or without GH affect the left ventricular (LV) dimensions in power athletes. These substances are assumed to increase LVmass mainly by thickening the ventricular walls. Anecdotal evidence suggests a higher risk of cardiovascular events in AAS abusers. We were interested to see if LV dimensions and function in AAS abusers would indicate this increased risk. Twenty healthy male power athletes using massive doses of AAS without (n = 16) or with (n = 4) GH volunteered for the study. The controls were 15 sedentary male non-users of hormones. LV mass, geometry and filling were studied using standard echocardiographic methods. We found a significant association between LV mass and AAS dose (r = 0.54, p < 0.015). In contrast to the controls, LV mass (274 g in the athletes, 167 g in the controls) among the AAS abusers did not correlate with body weight or height. Concomitant use of AAS and GH further increased LV mass and associated with concentric remodelling of LV. Multiple regression analysis indicated that the mean AAS dose accounted for 29 %, age for 14 % and systolic blood pressure for 17 % of the variance in LV mass. We concluded that AAS abuse associates dose-dependently with myocardial hypertrophy and that concomitant use of GH associates with concentric remodelling of the LV. Our findings suggest that AASs and GH have a direct effect on the myocardium.

Chronic exertional compartment syndrome: MR imaging at 0.1 T compared with tissue pressure measurement.

PURPOSE: To compare low-field-strength magnetic resonance (MR) imaging with intracompartmental tissue pressure measurement for the diagnosis of chronic exertional compartment syndrome. MATERIALS AND METHODS: Thirteen patients suspected clinically of having chronic exertional compartment syndrome in the anterior tibial compartment were studied. MR imaging at 0.1-T and intracompartmental tissue pressure measurements of the anterior tibial compartment were performed before and immediately after standard treadmill exercise. The MR measurements were also obtained in eight anterior tibial compartments of four control subjects without the syndrome. Intracompartmental signal intensity was normalized with the signal intensity from lower leg tissues not affected by the compartment syndrome (subcutaneous fat, tibial bone marrow, or superficial posterior compartment). RESULTS: In the patient group, the relative change from rest to the postexercise state in the normalized MR signal intensity parameter correlated significantly (P < .001) with the respective change in intracompartmental pressure and with the absolute postexercise pressure. In the patients with elevated postexercise intracompartmental pressure, the increase in normalized MR signal intensity from rest to the postexercise state was significantly greater (P < .01) than that in the control subjects or the patients with normal or borderline postexercise intracompartmental pressure. In the latter two groups, the MR results were comparable. CONCLUSION: MR imaging performed at rest and immediately after muscular exercise is a promising method for diagnosing chronic exertional compartment syndrome and assessing its severity.

Do high proinsulin and C-peptide levels play a role in autonomic nervous dysfunction?: Power spectral analysis in patients with non-insulin-dependent diabetes and nondiabetic subjects.

BACKGROUND: Immunoreactive insulin has been shown to predict the development of parasympathetic autonomic neuropathy. It is possible that constituents of immunoreactive insulin could explain this association. In this cross-sectional study, the relationship of specific insulin, C-peptide, and proinsulin with autonomic nervous dysfunction was evaluated in 57 NIDDM patients and 108 control subjects. METHODS AND RESULTS: The frequency-domain analysis of heart rate variability was determined by using spectral analysis from stationary regions of registrations while the subjects breathed spontaneously in a supine position. Total power was divided into three frequency bands: low (0 to 0.07 Hz), medium (MFP, 0.07 to 0.15 Hz), and high (HFP, 0.15 Hz to 0.50 multiplied by the frequency equal to the mean RR interval). In NIDDM patients, total power, the three frequency bands (P<.001 for each), and the MFP/HFP ratio (P=.016), which expresses sympathovagal balance, were reduced compared with control subjects. Fasting proinsulin (r(s)=-.324, P=.014 for diabetics and r(s)=-.286, P=.003 for control subjects), C-peptide (r(s)=-.492, P<.001 for diabetics and r(s)=-.304, P=.001 for control subjects), and total immunoreactive insulin (r(s)=-.291, P=.028 for diabetics and r(s)=-.228, P=.017 for control subjects) were inversely related to MFP/HFP. For proinsulin and C-peptide the results did not change after controlling for the effects of age, body mass index, and fasting glucose. CONCLUSIONS: Both proinsulin and C-peptide levels were significantly associated with the sympathovagal balance of autonomic nervous function in NIDDM patients and control subjects, but this study cannot determine whether these compounds are directly involved in autonomic nervous dysfunction.

Occurrence, predictors, and clinical significance of autonomic neuropathy in NIDDM. Ten-year follow-up from the diagnosis.

Little is known about the occurrence and predictive factors of autonomic neuropathy and its relationship to cardiovascular mortality in NIDDM patients, and no long-term follow-up studies including nondiabetic control subjects are available. A total of 133 patients with newly diagnosed NIDDM (70 men) and 144 control subjects (62 men) were examined at baseline and after 5 and 10 years of follow-up. Deep-breathing tests (baseline, 5-year, and 10-year) and active orthostatic tests (5- and 10-year) were performed. Criteria for autonomic neuropathy were parasympathetic (expiration-to-inspiration ratio /- 30 mmHg in the orthostatic test), and combined autonomic neuropathy (parasympathetic with sympathetic neuropathy). The frequency of parasympathetic neuropathy (NIDDM patients versus control subjects) was 4.9 vs. 2.2% (P = 0.224) at baseline, 19.6 vs. 8.5% (P = 0.017) at 5 years, and 65.0 vs. 28.0% (P < 0.001) at 10 years of follow-up. The frequency of sympathetic neuropathy was 6.8 vs. 5.6% (P = 0.709) at 5 years and 24.4 vs. 9.0% (P = 0.003) at 10 years of follow- up. These figures for combined autonomic neuropathy were 2.1 vs. 1.8% (P = 0.869) at 5 years and 15.2 vs. 4.2% (P = 0.007) at 10 years of follow-up. NIDDM patients with parasympathetic neuropathy at the 10-year examination showed worse glycemic control and higher insulin values than those without parasympathetic neuropathy. Furthermore, in our subjects, women were more prone to have parasympathetic neuropathy than men. Parasympathetic neuropathy at baseline was more frequent in those who died from a cardiovascular cause than those who did not (13 vs. 3%, P = 0.045). Similarly, sympathetic autonomic nervous dysfunction at the 5-year examination predicted the 10-year cardiovascular mortality. In conclusion, the frequency of autonomic neuropathy in NIDDM patients increases sharply with time. The development of autonomic neuropathy is connected with poor glycemic control. Interestingly, a high insulin level seems to have a predictive role in the development of parasympathetic autonomic neuropathy irrespective of obesity and glycemia.

Simultaneous invasive and noninvasive evaluations of baroreflex sensitivity with bolus phenylephrine technique.

Estimation of baroreflex sensitivity (BRS) is receiving increasing attention in clinical and experimental cardiology. Until recently, in most studies BRS has been assessed on the basis of invasive blood pressure measurement, which limits its use in large-scale studies and in clinical practice. The development of continuous noninvasive blood pressure monitoring has made it possible to assess BRS noninvasively. We compared central invasive and peripheral noninvasive techniques in the assessment of BRS during cardiac catheterization in 40 patients with possible coronary artery disease. The correlation between noninvasive and invasive BRS was high (r = 0.92; p < 0.001). However, the noninvasive method resulted in significantly higher BRS values than did the invasive method (7.1 +/- 6.5 msec/mm Hg vs 5.1 +/- 4.3 msec/mm Hg, respectively; p < 0.001) because of the smaller increase in systolic blood pressure after phenylephrine injection by the noninvasive technique than by the invasive technique (18.9 +/- 6.8 mm Hg vs 25.2 +/- 7.8 mm Hg, respectively; p < 0.01). The difference between noninvasive and invasive BRS correlated positively with invasive BRS (r = 0.54; p < 0.001) and inversely with age (r = -0.39; p < 0.01) and resting systolic blood pressure (r = -0.30, p < 0.05). A noninvasive BRS value of < 4.0 ms/mm Hg showed a sensitivity of 94%, a specificity of 91%, and an accuracy of 93% in identifying cases of reduced invasive BRS (< 3.0 msec/mm Hg). Our findings encourage the use of finger-cuff method in the assessment of BRS. However, noninvasive BRS values were slightly but significantly higher than invasive BRS values, a difference that should be taken into account when BRS is measured by the noninvasive approach.

Blood pressure reactivity in patients with neurocirculatory asthenia.

The hemodynamic reactions of 30 young men with neurocirculatory asthenia (NCA) were compared to those of 30 healthy controls in isometric handgrip test, orthostatic test, and cold pressor test in order to study the regulation of the central circulation of NCA patients. The measurements were made using sphygmomanometry, ECG, and impedance cardiography. In the isometric handgrip test the heart rate and the diastolic and mean blood pressure increased slightly more (P less than 0.05) in the NCA group than in the controls. In the NCA group the blood pressure rise was, on average, due to an increase in the peripheral vascular resistance, while in the control group it was caused by an elevation in the cardiac output. In the orthostatic and cold pressor tests the hemodynamic alterations were quite similar in the two groups. It is concluded that the NCA patients have in the orthostatic and cold pressor tests a normal ability to elevate the blood pressure by increasing the peripheral vascular resistance. The lack of rise in the cardiac output during the isometric handgrip test in the NCA group is an abnormal reaction, the reason of which remains to be studied.