Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

The levels of plasma arginine-vasopressin (AVP) in 80 patients with essential hypertension were measured, and its impact on the disease and its clinical significance were studied. The results showed that: (1) The levels of plasma AVP in patients with essential hypertension were significantly higher than that in normotensive subjects (P < 0.001). It dropped to normal level after antihypertensive drugs. (2) The concentrations of plasma AVP in both hypertensive subjects and normotensive subjects were not correlated with age and sex (P < 0.05). (3) The concentration of plasma AVP in patients with essential hypertension was the highest in stage III, the lowest in stage I, and middle in stage II. (4) The levels of plasma AVP in patients with malignant hypertension were significantly higher than that in patients with benign hypertension (P < 0.05). A positive correlation was found between the levels of plasma AVP and blood pressure (r = 0.3398, P < 0.01). (5) The concentrations of plasma AVP in hypertensive subjects with ventricular hypertrophy were higher than that in hypertensive subjects with out ventricular hypertrophy (P < 0.05). (6) The concentrations of plasma AVP in hypertensive subjects with heart failure were significantly higher than that in hypertensive subjects with out heart failure (P < 0.001). The results suggest that AVP has a role in the pathogenesis of hypertension, hypertension complicated with ventricular hypertrophy and hypertension complicated with heart failure. The levels of plasma AVP may be viewed as an index of the patient's condition in hypertensive subjects.
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PMID:[The changes in plasma arginine-vasopressin in patients with essential hypertension and the correlation with patient's condition]. 824 27