Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a haemodynamic and angiographic study at rest conducted in 25 men aged from 22 to 68 years who had no more than another risk factor for arterial disease and showed no evidence of cardiac or arterial disease several parameters were measured or calculated. Firstly, a global index of arterial system function (Ea) and its various factors: Ea = ESP/SV [ESP: left ventricular end-systolic pressure; SV: systolic volume]; Ea = (HR x TSR)+Ea' [HR: heart rate/min; TSR: total systemic resistance] where Ea' = (ESP - AoP/SV) [AoP: mean aortic pressure]. Secondly, the parameters concerning the left ventricle were the mass (m) and the m/EDV ratio [EDV: end-diastolic volume] and indices of the left ventricular systolic and diastolic functions, such as ELV = ESP/ESV [ESV: end-systolic volume], kp: the volumic distensibility module of the left ventricular chamber; relations EF - o ES [EF: ejection fraction; o ES: end-systolic constraint], and kp - m/EDV as indice of left ventricular muscle distensibility. In parallel with the subjects' age, Ea increased by joint augmentation of TSR and Ea' while m, m/EDV, ELV and kp also significantly increased. The inotropic quality of the left ventricular muscle and its intrinsic distensibility were found to be decreased in a few subjects aged over 45. Ea/ELV (reverse of ejection fraction -1) tended to increase (ELV relatively less than Ea), but this increase was not significant (P = 0.10). These results show that in the ageing man the improvement observed in the ejection fraction of the left ventricular pump corresponds roughly to the degradation of the arterial system transfer function, and the arterial system-left ventricle coupling, evaluated by the Ea/ELV ratio, is maintained (better in fact than in arterial hypertension and heart failure). This improvement is achieved by increases of m and, chiefly, m/EDV which compensate for both the increase of Ea and the relative decline of left ventricular muscle contractile quality. There is a disorder of the left ventricular pump diastolic function which is due to geometric changes in the chamber and to changes in the intrinsic distensibility of the left ventricular muscle.
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PMID:[Functional coupling of the left ventriculo-arterial system and aging in man]. 140 76

Enalapril (E) was used to treat 16 patients with pulmonary arterial hypertension, 6 primary and 10 secondary, 5 of the latter with congenital heart disease and 5 with chronic obstructive pulmonary disease. The average dose of E was 20 mg/day. All patients underwent pre and post-treatment cardiac catheterization with determination of pressures at: right atrial (RA), main pulmonary artery (MPA), pulmonary capillary wedge pressure ( VCP) and systemic arterial (SA). Resistances forces were also measured as; total pulmonary (TPR), pulmonary arteriolar (PAR) and total systemic (TSR) as well as cardiac output (CO), and echo and electrocardiograms, chest x ray, stress test and respiratory function test. The functional class (NYHA) improved in all (p less than 0.001). The initial mean pressures were: RA 12.24 +/- 4.35; MPA 73.81 +/- 25.16; VCP 12 +/- 2.73 and SA 89 +/- 14; TPR 1477 +/- 761; PAR 1243 +/- 730 and TSR 1684 +/- 505.5; CO 4.5 +/- 1.29. The final values were: RA 9.66 +/- 2.46 (p less than 0.001); MPA 63.26 +/- 24.45 (p less than 0.001); VCP 11.33 +/- 2.38 (p = NS); SA 81 +/- 10 (p less than 0.001); TPR 1009.5 +/- 536.7 (p less than 0.001); PAR 829 +/- 511.5 (p less than 0.001); TSR 1309.6 +/- 296.3 (p less than 0.001); CO 5.2 +/- 1.44 (p less than 0.001). The average of minutes on treadmill was initially 8.2 +/- 2.45 and final 12.46 +/- 3.0 (p less than 0.001). It is concluded that enalapril is a useful drug in the treatment of pulmonary arterial hypertension of any etiology.
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PMID:[Use of enalapril, an angiotensin-converting enzyme inhibitor, in pulmonary artery hypertension]. 303 21

We studied the relationships between blood pressure, anthropometric characteristics and blood lipids in 72 low altitude (LA) Uighurs (600 m), 91 LA-Kirghizs (900 m), 117 medium altitude (MA) Kazakhs (2100 m) and 94 high altitude (HA) Kirghizs (3200 m). All subjects were male and had a similar age (p = ns, ANOVA; range for all 374 subjects: 18-66 yr). Body weight (Wt), body mass index (BM1) and the sum of four skinfolds (4SF) were significantly lower in HA-Kirghizs than the remaining groups (p < 0.0005, p < 0.0005 and p < 0.05 respectively, ANOVA). However, no difference was found in body fat distribution as detected by waist:hip circumference (WHR) and triceps:subscapular skinfold ratios (TSR; p = ns, ANOVA). Stage 1 hypertension was detected in 18% of LA-Uighurs, 2% of LA-Kirghizs, 4% of MA-Kazakhs and 1% of HA-Kirghizs; stage 2 hypertension was detected in 2% of LA-Uighurs and none of the remaining groups; no subject had stage 3 hypertension (The Joint National Committee on Prevention. Detection, Evaluation and Treatment of High Blood Pressure 1997). Blood cholesterol (CH) and triglycerides (TG) did not differ between groups (p = ns, ANOVA). The relationships between systolic (SBP) or diastolic (DBP) blood pressure and age, Wt, BMI, 4SF, WHR, TSR, CH and TG were independent from altitude (p = ns, ANCOVA). In the pooled sample (n = 374), age explained 1 and 3% of SBP (p < 0.05) and DBP (p < 0.005) variance respectively, Wt was the best predictor of SBP and DBP explaining 11 and 10% of their variance respectively (p < 0.0001) and CH explained 5% of DBP variance (p < 0.0001). In conclusion, hypertension is more frequent in LA- than MA- and HA-subjects from Central Asia. However, anthropometric characteristics and blood lipids do similarly contribute to explain blood pressure in these subjects.
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PMID:Relationships between blood pressure, anthropometric characteristics and blood lipids in high- and low-altitude populations from Central Asia. 1067 37

With aging, structural and functional changes occur in the myocardium without obvious impairment of systolic left ventricular (LV) function. Transmural differences in myocardial vulnerability for these changes may result in increase of transmural inhomogeneity in contractile myofiber function. Subendocardial fibrosis and impairment of subendocardial perfusion due to hypertension might change the transmural distribution of contractile myofiber function. The ratio of LV torsion to endocardial circumferential shortening (torsion-to-shortening ratio; TSR) during systole reflects the transmural distribution of contractile myofiber function. We investigated whether the transmural distribution of systolic contractile myofiber function changes with age. Magnetic resonance tissue tagging was performed to derive LV torsion and endocardial circumferential shortening. TSR was quantified in asymptomatic young [age 23.2 (SD 2.6) yr, n = 15] and aged volunteers [age 68.8 (SD 4.4) yr, n = 16]. TSR and its standard deviation were significantly elevated in the aged group [0.47 (SD 0.12) aged vs. 0.34 (SD 0.05) young; P = 0.0004]. In the aged group, blood pressure and the ratio of LV wall mass to end-diastolic volume were mildly elevated but could not be correlated to the increase in TSR. There were no significant differences in other indexes of systolic LV function such as end-systolic volume and ejection fraction. The elevated systolic TSR in the asymptomatic aged subjects suggests that aging is associated with local loss of contractile myofiber function in the subendocardium relative to the subepicardium potentially caused by subclinical pathological incidents.
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PMID:Impaired subendocardial contractile myofiber function in asymptomatic aged humans, as detected using MRI. 1667 4