Malignant hypertension (MH) is a severe complication of untreated arterial hypertension that damages the vascular system. It is often accompanied by disturbances in lipid metabolism that could contribute to its pathophysiology. We examined chylomicron metabolism in MH patients using a triglyceride-rich emulsion known to mimic natural chylomicrons when injected into the bloodstream. The emulsion was labeled with [3H]triolein and [14C]cholesteryl oleate and injected intravenously into 15 normolipidemic MH patients aged 29 to 56 years (8 men) for comparison with 17 healthy control subjects. Consecutive plasma samples were taken at regular intervals during 1 hour for determination of the disappearance curves of the labels. The fractional clearance rate of the [3H]triolein emulsion in MH patients was twice as small as that of control subjects (0.061 +/- 0.012 and 0.141 +/- 0.074 min-1, respectively). On the other hand, [14C]cholesteryl oleate fractional clearance rate was not statistically different in MH patients and control subjects (0.032 +/- 0.004 and 0.056 +/- 0.014 min-1, respectively). These results indicate that in MH, lipolysis (measured by the fractional clearance rate of [3H]triolein) is pronounced diminished, whereas the removal of the remnant particles (measured by the fractional clearance rate of [14C]cholesteryl oleate) is not importantly affected. In conclusion, there is an alteration in the circulatory transport of dietary lipids that may be an important component in the vascular disease associated with MH.
Study of pressor response to graded, increased doses of infused norepinephrine in patients with essential hypertension, their normotensive siblings, and normotensive control subjects unrelated to the patients and without a family history of hypertension indicated an increased response in the two former groups. Comparison of the dose-response curves in the three groups showed that the difference in response was due to a reduced threshold to norepinephrine in patients and their siblings and not to differences in the slopes of the dose-response curves. These alterations were not paralleled by differences in heart rate responses. (Hypertension 1990;15(suppl I):I-137-I-139)
To assess the role of arterial hypertension in left ventricle (LV) hypertrophy among hemodialysis patients, echocardiographic evaluation was performed in 10 hypertensive and 13 normotensive hemodialysis subjects matched for age, sex, race, duration of dialysis treatment and degree of interdialytic volume expansion. We excluded from the latter group patients with previous hypertension since hypertensive heart disease may persist after adequate blood pressure control. We also studied 17 normal controls and 10 non-uremic patients with essential hypertension. Comparisons between the two uremic groups showed that the hypertensive patients had a higher mass index(222 ± 74 × 108 ± 26, p = 0.0001)andposteriorwallthickness(12 ± 2 X 9 ± 2, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 ± 0.7 X 5.8 ± 1, p = 0.0001). There were no significant echocardiographic differences between normal controls and normotensive uremics. In contrast, compared to controls, hypertensive uremic patients showed an increased LV mass index (222 ± 74 X 83 ± 21, p = 0.0001) and posterior wall thickness (12 ± 2 X 7 ± 1, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 ± 0.7 X 6.5 ± 1.1, p = 0.001), characterizing concentric hypertrophy. They also had ventricular dilation with larger LV dimensions than in controls (53 ± 5 X 47 ± 4, p = 0.004). In patients with essential hypertension, the mass index (135 ± 22), wall thickness (11 ± 1) and LV radius/wall thickness ratio (4.3 ± 0.7) significantly differed (p = 0.0001) from those in the controls. Hypertensive uremic patients and patients with essential hypertension had similar LV wall and interventricular septum thickness and LV radius/wall thickness ratio, suggesting that arterial hypertension was equally important in the genesis of hypertrophy in both groups. Systolic function was preserved in the three patient groups but hypertensive dialysis individuals had lower ejection fraction and fractional LV shortening than essential hypertensives. LV hypertrophy was found only in patients with arterial hypertension, whereas normotensive dialysis patients showed few echocardiographic abnormalities despite prolonged exposure to hyper-volemia and to the other hemodynamic and metabolic derangements of chronic uremia. It is concluded that arterial hypertension plays a central role in LV hypertrophy in hemodialysis patients.
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