Association between the G protein beta3 subunit 825t allele and radial artery hypertrophy

The GNB3 C825T gene polymorphism has recently been identified and associated with hypertension, obesity and left ventricular hypertrophy. The aim of the study was to determine the relationship between the C825T polymorphism of the gene encoding for the G protein beta3 subunit (GNB3 C825T) and vascular hypertrophy. We studied a cohort of 306 subjects (age 49 +/- 12 years) without evidence of cardiovascular disease and never treated with cardiovascular drugs. Vascular phenotypes were evaluated for the common carotid and radial arteries using high-resolution echo-tracking devices. Genotype frequencies were in agreement with the Hardy-Weinberg equilibrium. For the radial artery, mean wall thickness was significantly higher in subjects carrying the 825T allele than in CC genotype subjects (240 +/- 54 microm for CT genotype and 241 +/- 53 microm for TT genotype vs. 222 +/- 52 microm for CC genotype, p = 0.01). The frequency of the 825T allele was significantly different in subjects with (52%) and without (35%) radial artery hypertrophy (chi(2) = 10.88, p < 0.001). The relative risk of radial artery hypertrophy in subjects carrying the 825T allele compared with those with the CC genotype was 3.02 (95% CI 1.53- 5.95). A logistic regression analysis indicated that the positive and significant association between the 825T allele and radial artery hypertrophy was independent of age, blood pressure, gender and BMI. In contrast, no association between genotypes and carotid artery wall thickening was observed. These results suggest that some genetic characteristics determine in part the patterns of radial artery geometrical changes. As the 825T allele is associated with vascular hypertrophy of a muscular artery but not with structural changes of an elastic artery, we hypothesize that the 825T allele may be a genetic marker of arteriolosclerosis.     

Systolic Blood Pressure Revisited

The clinical importance of systolic blood pressure (SBP) needs no emphasis. Its determinants are well known, but recent studies of one of these determinants, arterial distensibility, have led to results that now have clinical relevance. This review summarizes the role of arterial stiffness in ventricular-vascular coupling in the normal circulation and that disordered by aging and hypertension. The discussion defines the unfamiliar terms of compliance, distensibility and modulus and indicates how they are measured. Such measurements have increased our understanding of the parts played by the inhomogeneity of the arterial tree and reflected pressure waves in governing SBP. Elevated SBP is a recognized risk factor for cardiovascular complications among older patients, but when this elevation is due to a stiffened arterial tree, diastolic blood pressure (DBP) is necessarily reduced. Early epidemiologic studies in hypertension required a DBP ≥90 mm Hg for hospital admission. They therefore excluded persons with high SBP, low DBP and very wide pulse pressure (PP). More recent inclusion of such patients has shown that elevation of SBP and PP is a strong predictor of cardiovascular risk. These considerations point to a possible redefinition of hypertension to include patients with lower DBP and to the inaccuracy but indispensability of the brachial artery pressure as a surrogate for aortic pressure—the pressure the heart sees. Finally, we review the known effects of available antihypertensive drugs on the arterial wall and indicate possible future directions of research stemming from wider understanding of the role of arterial distensibility in hypertension.

(J Am Coll Cardiol 1997;29:1407–13)     

Brain lactate and alanine-glutamate ratios during and after asphyxia in rats

Recently, Conger, Garcia, Kauffman, Lust, Murakami and Passonneau, (1981) proposed the use of brain alanine-glutamate ratios (A:G) for the prediction of outcome after brain ischemia. This study evaluates this parameter and brain lactate concentration during and after asphyxial insults in rats. During the first 15 min of asphyxial death in rats (n = 37), lactate increased sharply from mean values of 1.48 to 18.06 mumol g-1 wet brain, and thereafter to 19.44 mumol g-1 wet brain at 180 min. During total body asphyxia (n = 38) and recovery after resuscitation, brain lactates increased to mean values of 15 and 17.5 mumol g-1 wet brain at 5 and 10 min, respectively, to recover after 30-60 min to baseline. The alanine-glutamate ratios did not rise during the insult; however, after restoration of circulation, the ratios rose to peak at about 15 min post-restoration of circulation and recovered slowly during the next 165 min to still slightly increased levels. During intermittent asphyxia (n = 15), lactate and alanine-glutamate ratios followed the same patterns as found before except at lower levels. The conclusions of this study are: (1) brain lactate concentrations had no value in predicting the potential of recovery; (2) increased lactate concentrations during recovery indicated secondary insult; (3) brain A:G's did not increase during asphyxiation; (4) brain alanine-glutamate ratios increased after restoration of circulation and may have reflected the quality of reflow; (5) increased ratios during recovery beyond 20 min indicated secondary insult. Brain alanine-glutamate ratios could not be used for prediction of outcome in asphyxial insults in rats.     

Pulsatile diameter and elastic modulus of the aortic arch in essential hypertension: a noninvasive study

A noninvasive evaluation of the aortic arch diameter was performed in 16 subjects with sustained essential hypertension and in 15 normal subjects of similar age, gender and body surface area. In all subjects, measurements were obtained of brachial mean arterial pressure and pulse pressure, cardiac mass (judged on echocardiography) and carotid-femoral pulse wave velocity together with ultrasound determinations of aortic arch diastolic and systolic diameter (suprasternal window). For each subject, pulsatile change in aortic diameter, strain and aortic arch elastic modulus were calculated. Compared with normal subjects, the hypertensive subjects showed an increase in aortic arch diameter (diastolic diameter 29.6 +/- 1.0 versus 25.4 +/- 1.0 mm, p less than 0.01), in elastic modulus (1.071 +/- 0.131 versus 0.526 +/- 0.045 10(5) N.m-2, p less than 0.001) and pulse wave velocity (11.8 +/- 0.5 versus 8.9 +/- 0.3 m/s, p less than 0.001). In the study group, a positive correlation was observed between diastolic aortic arch diameter and mean arterial pressure (r = 0.54, p less than 0.01) and between elastic modulus and cardiac mass (r = 0.60, p less than 0.01). Elastic modulus and age were positively correlated (r = 0.73, p less than 0.01) in hypertensive but not in normal subjects (r = 0.08, NS). This study is the first to demonstrate noninvasively that both the aortic arch diameter and the elastic modulus are increased in patients with sustained uncomplicated essential hypertension. These findings suggest that the increase in elastic modulus could influence the development of cardiac hypertrophy, and that both age and blood pressure act independently as factors that alter the arterial wall of subjects with sustained essential hypertension.     

Emphysema in the renal allograft

Two diabetic patients in whom emphysematous pyelonephritis developed after renal transplantation are described. Clinical recognition of this unusual and serious infection is masked by the effects of immunosuppression. Abdominal radiographic, ultrasound, and computed tomography findings are discussed. The clinical presentation includes urinary tract infection, sepsis, and acute tubular malfunction of the allograft in insulin-dependent diabetics.     

Baroreflex sensitivity and cardiopulmonary blood volume in normotensive and hypertensive patients.

Baroreflex sensitivity and cardiopulmonary blood volume were determined in 95 men, including normotensive and hypertensive subjects with normal renal function and balanced sodium intake and urinary output. Baroreflex sensitivity was estimated by determining the slope of the regression line relating the increase of systolic pressure to the cardiac slowing after transient rises of arterial pressure. A technique of gradual atropinisation was used to evaluate the parasympathetic mediated component of the reflex. With this method, it was possible to calculate the exact atropine dose abolishing the reflex sensitivity. This index was not dependent on age. It was negatively correlated to the diastolic pressure in normotensive patients but not in hypertensive patients. The ratio between the cardiopulmonary and the total blood volume was considered as an index of sympathetic venous tone. This ratio was positively correlated to the diastolic pressure in normotensive patients, but not in hypertensive patients. This study strongly suggests that a precise sympathetic-parasympathetic balance existed in the normotensive patients. This balance was disrupted in the hypertensive patients pointing to abnormalities in the autonomic nervous system of permanently hypertensive patients.