Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the possible echocardiographic progression of left ventricular (LV) hypertrophy, in different stages of primary hypertension. Both morphological (LV mass and ratio of interventricular septal thickness to posterior wall thickness-IVST/PWT-, in M-mode) and functional data (parietal stress, duration, degree and velocity of filling in the four phases of diastole, obtained through computerised interpretation of M-mode tracings), were examined. We also tried to assess the morphofunctional differences between LV hypertrophy secondary to primary hypertension and LV hypertrophy secondary to renovascular hypertension, hypertrophic obstructive cardiomyopathy and physical training. Patients with primary hypertension were further subdivided in three groups: A) 14 patients with hypertension of less than one year's duration, B) 28 patients with long-lasting hypertension, and C) 5 patients with cardiomegaly. There was a progressive increase from controls to Group C patients of left ventricular mass (controls 171 +/- 25; Group A 168 +/- 72; Group B 253 +/- 83; Group C 439 +/- 117) and septal hypertrophy (controls IVST/PVT 1 +/- 0.1; Group A 1.2 +/- 0.2; Group B 1.4 +/- 0.3; Group C 1.5 +/- 0.1). The isovolumic relaxation period was prolonged only in Group C (controls 8.6 +/- 3.5 per cent of the diastole; Group C 15 +/- 3.5%) LV dimensions during slow filling and atrial contraction as well as filling velocity during this latter phase of the cardiac cycle were increased in Group A (7.8 +/- 2.3 and 7.3 +/- 2%; 1.2 +/- 0.6 cm/cm X sec respectively) and B (10 +/- 6 and 10.8 +/- 4%; 1.2 +/- 0.6 cm/cm X sec) compared to the controls (5 +/- 2.8 and 3.7 +/- 2%; 0.7 +/- 0.2 cm/cm X sec). The Vcf max was not significantly different in the three groups. The patients with renovascular hypertension (N = 14) could be differentiated from those with primary hypertension of Group B for a greater increase in LV mass, with concentric hypertrophy (IVST/PWT = 1.2 +/- 0.2), for a greater prolongation of IRP (16 +/- 0.6% of diastole), with increased diameter changes in this phase (displacement ratio = 3.3 +/- 2.3%, in Group B; 4.7 +/- 3.8%, in renovascular hypertension), for a normal displacement and velocity of slow and atrial filling, despite the impairment of rapid filling found in this group, too (% displacement and velocity, respectively: 19 +/- 5% and 1.8 +/- 0.6 cm/cm X sec).
 ...
PMID:[Morphologic and functional aspects of left ventricular hypertrophy evaluated by computerized echocardiography]. 668 67

Blood vessels are remodeled in hypertension both structurally and functionally. The changes that occur in their structure, mechanical properties, and function contribute to blood pressure elevation and to complications of hypertension. We studied the remodeling of small arteries in experimental animals and humans. Smooth muscle cells of small arteries are restructured around a smaller lumen, with significant remodeling of the extracellular matrix and collagen and fibronectin deposition. Interestingly, there is no evidence of net growth of the vascular wall (which results in so-called eutrophic remodeling), particularly in the milder forms of human essential hypertension. Hypertrophic remodeling and increased small artery stiffness may be found in more severe forms of hypertension. Almost all hypertensive patients have vascular structural remodeling. However, only some exhibit endothelial dysfunction. This is particularly true in mild hypertension, in which endothelial dysfunction is less common. A 1-year treatment of hypertensive patients with angiotensin converting enzyme inhibitors, angiotensin AT1 receptor antagonists, and long acting calcium channel blockers corrected small artery structure and, to variable degrees depending on the agents used, impaired endothelial function. In contrast, beta blockers did not improve structure, function, or mechanics of vessels. When beta-blocker-treated patients were switched to an AT1 receptor antagonist, small artery structure and impaired endothelial function were corrected. The vascular protective action of some antihypertensive agents may contribute to improve outcome for hypertensive patients, although this is presently unproven.
 ...
PMID:Effect of antihypertensive treatment on small artery remodeling in hypertension. 1271 May 31