Circulatory encephalopathy in patients with arterial hypertension

More accurate definition of the leading factors of development of discirculatory encephalopathy (DE) in patients with arterial hypertension was the aim of this investigation. The analysis of correlations between clinical and computer tomographical symptoms of DE on the one hand and the indices of central hemodynamics, head blood circulation and presence of atherosclerosis of head arteria on the other hand was performed. It was found that congestion in head venous system was the main factor in DE development. The conclusion was made that both atherosclerosis of head arteria and arterial hypertension promoted venous congestion in head by means of decreasing the amplitude of arterial pulsation and in turn the development of DE. Meanwhile, the increase of minute blood flow prevents it.     

Long-term antihypertensive therapy with isradipine. Improvement of coronary flow reserve in patients with arterial hypertension and microvascular angina

Antihypertensive Long-term Therapy with Isradipine/Improvement of coronary flow reserve in patients with arterial and microvascular angina In patients with arterial hypertension coronary flow reserve is often impaired due to left ventricular (LV) hypertrophy and alterations of the coronary microcirculation. Experimental and clinical studies have shown that calcium channel blockers can induce regression of myocardial hypertrophy. Objective of the present study was to see whether chronic antihypertensive treatment with calcium channel blockers can improve the diminished coronary reserve in patients with arterial hypertension and microvascular angina pectoris. Fifteen hypertensive patients with microvascular angina (61 +/- 7 years, normal coronary angiogram, mild LV-hypertrophy) were treated with isradipine (CAS 75695-93-1) (5.3 +/- 0.9 mg/d) for 12 +/- 2 months. Before and after therapy (after a washout period of 1 week) coronary flow was quantitatively measured by the gas chromatographic Argon method. Coronary reserve was calculated as the quotient of coronary resistance under baseline conditions and after dipyridamole (0.5 mg/kg i.v.). Under isradipine therapy systolic blood pressure was lowered from 165 +/- 20 to 140 +/- 13 mmHg (p < 0.01) and diastolic blood pressure from 98 +/- 8 to 88 +/- 6 mmHg (p < 0.01). The LV muscle mass index decreased by 10% from 154 +/- 33 to 139 +/- 28 g/m2 (p < 0.05). Baseline coronary blood flow (81 +/- 13 versus 83 +/- 16 ml/min x 100 g, n.s.) was identical before and after therapy. There were also no differences in coronary perfusion pressure, heart rate, myocardial oxygen consumption and arterio-coronary venous oxygen difference before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular hypertrophy in patients with nephrogenic arterial hypertension

Incidence and geometric peculiarities of hypertrophy of the left ventricle of the heart (HLVH) were studied on the basis of findings from the echocardiographic investigation done in 86 patients with chronic glomerulonephritis (ChGN) with arterial hypertension (AH), with the renal function being preserved and at the early stages of renal insufficiency. HLVH was detected in 30.2% of the patients, in 80.8% of whom it was concentric, and in 19.2% eccentric, in 76%--symmetric and in 23.1%--asymmetric. Incidence of HLVH did not correlate with sex, clinical variant of ChGN, renal function status, and increased with the degree and duration of AH. There was no difference in geometric peculiarities between sexes, clinical variants of ChGN, and no association with degree and duration of AH as well as with functional state of the kidneys.     

Clinical profile of arterial hypertension in patients with cerebrovascular diseases

The aim this work was to assess retrospectively the history of hypertension in patients admitted for cerebrovascular diseases. Two hundred and forty eight patients were studied (69% with ischemic strokes, 24% with hemorrhagic strokes and 7% with transient ischemic attacks. 76% of cases had a history hypertension with an evolution of ten years or more in 81% of cases. No differences in the prevalence of hypertension was observed among the different types of strokes. Of the 139 patients in whom the severity of hypertension was registered, 37% had mild, 45% moderate, 15% severe and 3% systolic hypertension. Those with severe hypertension had a higher incidence of hemorrhagic stroke. Fundoscopic examination was abnormal in 81% of the 64 patients in whom it was performed, left ventricular hypertrophy was found in 62% of the 146 patients in whom it was investigated. 51% of patients were receiving anti hypertensive treatment and it was effective in 26% of them. Thirty one percent of subjects had old lesions in the CAT scan; these subjects had a similar prevalence of hypertension and effectiveness of treatment than patients without old lesions. It is concluded that a history of more than ten years of hypertension is a risk factor for cerebrovascular disease, that severe hypertension is mostly associated to hemorrhagic strokes and that only 26% of patients with stroke had and adequate anti hypertensive treatment.     

Diastolic function parameters and atrial arrhythmias in patients with arterial hypertension

OBJECTIVE: To investigate in patients with arterial hypertension (HT) the extent of left ventricular (LV) hypertrophy and diastolic function in relation to atrial arrhythmias. PATIENTS AND METHODS: In 112 hypertensive patients (40 women, 72 men; mean age 50 +/- 6.6 years) with a mean systolic blood pressure for the cohort of 170 +/- 5 mmHg, their first invasive coronary angiography was performed between July 1995 and October 1997 because of angina pectoris and/or an abnormal stress electrocardiogram. After excluding coronary heart disease LV dimensions and diastolic function were measured by echocardiography; in 59 of the 112 patients LV hypertrophy was demonstrated. In addition, long-term blood pressure monitoring, exercise and long-term electrocardiography, late-potential analysis and measurement of heart rate variability were undertaken. The control group consisted of 51 patients without arterial hypertension after exclusion of coronary heart disease. RESULTS: Even in the hypertensive patients without LV hypertrophy diastolic LV function and ergometric exercise capacity were reduced. The risk of LV arrhythmias was significantly higher in patients with LV hypertrophy than those without and in the control group, as measured by the complexity of atrial arrhythmias (P < 0.001), the incidence of abnormal late potentials (P < 0.001) and reduction in heart rate variability (29.3 +/- 5.3 ms vs 47.8 +/- 12.1 ms vs 60.7 +/- 6.6 ms; P < 0.001). There were similar results regarding severe complex atrial arrhythmias (38.5 vs 15.0 vs 0%; P < 0.001). The incidence of atrial arrhythmias correlated with the LV diameter (r = 0.68, P < 0.001), LV morphological dimensions and diastolic function (isovolumetric relaxation time r = 0.44, P < 0.001) and the ratio of early to late diastolic inflow (r = 0.46; P < 0.001). CONCLUSIONS: Hypertensive patients have a higher risk of atrial and ventricular arrhythmias, depending on the degree of LV hypertrophy. But atrial arrhythmias, in contrary to ventricular arrhythmias, are also closely related to abnormalities in LV diastolic function.     

Consequences of intramyocardial arterial lesions in aortic valvular stenosis

Proliferative lesions, which included collagen deposition, developed with age in intramyocardial arteries of 27 patients with aortic stenosis and matched controls. Those with the most extensive intramyocardial artery lesions developed massive subendocardial infarcts during surgery. Using histologic quantitation, the percent of intramyocardial arteries with lesions in a patient was correlated with decreases in the amount of muscle in arterioles between the subepicardial and subendocardial zones of the left ventricle. The mean decrease in arteriolar muscle was 43% in patients with aortic stenosis and 19% in controls. Blood pressures correlate with the amount of muscle in arterioles, so subendocardial perfusing pressures were presumably low in those with aortic stenosis. Patients with the greatest decrease in arteriolar muscle across the myocardium had the most impaired left ventricular function, i.e., highest end diastolic pressures, lowest ejection fractions, and lowest mean fiber shortening rates.     

Increased occurrence of esophageal hypermotility disorders in patients with arterial hypertension

BACKGROUND AND OBJECTIVE: It has been noted in previous manometric examinations of the oesophagus in patients with chest pain that abnormal motility was often associated with arterial hypertension. A systematic study of this relationship was therefore undertaken. PATIENTS AND METHODS: In 40 patients with chest pain (18 women and 22 men, mean age 54.7 [24-70] years) and in 20 healthy volunteers (12 men, 8 women, mean age 50.8 [22-63] years) standardized oesophageal manometry and arterial blood pressure monitoring were performed over 24 hours. Coronary heart disease and gastrointestinal lesions had been excluded by angiography and endoscopy, respectively. RESULTS: 20 patients (group H) had hypertension (median 24-hour blood pressure > 135/85 mmHg), while 20 patients (group N) and the normal controls (group K) were normotensive. Oesophageal manometry data differed significantly between the three groups regarding distal pressure amplitude (in hPa [hectopascals]; group H: 62 hPa*,**, group N 44 hPa* and group K 36 hPa**; [*P < 0.0005]) and the proportion of simultaneous contractions (group H 23%, group N 22%**, group K 10%***; ***P < 0.001). The hypertensive patients had significantly more frequent motility abnormalities than normal controls (13/20 vs 4/20, P < 0.001); while normotensive patients had more frequent episodes of abnormal propulsion in the oesophagus (proportion of propulsive contractions in group H: 53%, in N: 44%, in K: 59%; P < 0.01). CONCLUSION: Oesophageal motility differed significantly in patients with chest pain from that in healthy controls. Patients with chest pain and hypertension more frequently had oesophageal hypermotility. This suggests a generalized abnormality of smooth muscle.     

Correlation between echocardiographic changes and parameters of pulmonary function in patients with arterial hypertension

This study comprised 30 patients with mild or moderate arterial hypertension (according to classification of the World Health Organization) in whom some echocardiogram and parameters of the lung function were studied in order to establish correlation between them. A good correlation exists between LV (left ventricle) mass index and vital capacity (r = 0.562, p < 0.01), ejection fraction and forced mid expiratory flow (r = 0.717, p < 0.01), LV mass index and Tiffenau index (r = 0.620, p < 0.01), shortening fraction and forced mid expiratory flow (r = 0.591, p < 0.01), airways resistance and posterior wall thickness (r = 0.591), p < 0.01) and between LV mass index and total lung capacity (r = 0.821, p < 0.01). There was not a good correlation or it was not significant (p > 0.05) between other echocardiographic changes and lung function tests.     

Serum angiotensin converting enzyme activity in patients with untreated essential arterial hypertension

The serum angiotensin converting enzyme (ACE) in 30 patients with untreated essential arterial hypertension, 30 patients with chronic renal failure accompanied with arterial hypertension and 30 healthy individuals was measured. The subjects of both sexes have been old 35-60 years. The serum ACE activity was determined by the spectrophotometric method, using Hip-Gly-Gly as a substrate. The serum ACE activity significantly increased in patients with arterial hypertension (32.48 +/- 2.02; X +/- SEM) and patients with chronical renal failure accompanied with arterial hypertension (37.10 +/- 1.45) when compared to the healthy individuals (20.83 +/- 1.33). Possible mechanisms of increasing ACE activity with the patients suffering of arterial hypertension are discussed.     

Structural and functional responses of mammalian thick filaments to alterations in myosin regulatory light chains

The ordered array of myosin heads, characteristic of relaxed striated muscle thick filaments, is reversibly disordered by phosphorylating myosin regulatory light chains, decreasing temperature and/or ionic strength, increasing pH, and depleting nucleotide. In the case of light chain phosphorylation, disorder, most likely due to a change in charge affecting the light chain amino-terminus, reflects increased myosin head mobility, thus increased accessibility to actin, and results in increased calcium sensitivity of tension development. Thus, interactions between the unphosphorylated regulatory light chain and the filament backbone may help maintain the overall order of the relaxed filament. To define this relationship, we have examined the structural and functional effects of such manipulations as exchanging wild-type smooth and skeletal myosin light chains into permeabilized rabbit psoas fibers and removing regulatory light chains (without exchange) from such fibers. We have also compared the structural and functional parameters of biopsied fibers from patients with severe familial hypertrophic cardiomyopathy due to a single amino acid substitution in the regulatory light chains to those exhibited by fibers from normal relatives. Our results support a role for regulatory light chains in reversible ordering of myosin heads and suggest that economy of energy utilization may provide for evolutionary preservation of this function in vertebrate striated muscle.     

Normalization of abnormal coronary vasomotion by calcium antagonists in patients with hypertension

BACKGROUND: Endothelial dysfunction with a loss of endothelium-dependent vasodilation has been reported in patients with arterial hypertension. The purpose of the present study was to evaluate coronary vasomotor response to dynamic exercise in patients with coronary artery disease with and without arterial hypertension and to determine the effect of calcium antagonists on coronary vasomotion. METHODS AND RESULTS: Cross-sectional areas of a normal and a stenotic coronary vessel segment were examined in 79 patients with coronary artery disease at rest and during supine bicycle exercise (Ex). Change in luminal area after acute administration of a calcium antagonist (diltiazem or nicardipine), during exercise, and after sublingual nitroglycerin (percent change compared with rest = 100%) was assessed by biplane quantitative coronary arteriography. Patients were divided into two groups: Group 1 (control) consisted of 48 patients without (normotensive subjects, n = 30; hypertensive subjects, n = 18) and group 2 of 31 patients with (normotensive subjects, n = 15; hypertensive subjects, n = 16) pretreatment with a calcium antagonist immediately before exercise. The groups did not differ with regard to clinical characteristics or hemodynamic data measured during exercise. Mean aortic pressure at rest, however, was significantly increased in hypertensive patients compared with normotensive subjects in group 1 (103 mm Hg versus 92 mm Hg, P < .01) and group 2 (110 mm Hg versus 98 mm Hg, P < .025). In group 1, exercise-induced vasomotor response was significantly different between normotensive and hypertensive patients in normal (+20% versus +1%, P < .003) and stenotic vessels (-5% versus -20%, P < .025). However, in group 2 there was coronary vasodilation in normotensive and hypertensive patients for both normal (delta Ex +23% versus +21%, P = NS) and stenotic vessel segments (+24% versus +26%, P = NS). CONCLUSIONS: Abnormal coronary vasomotion during exercise can be observed in hypertensive patients with reduced vasodilator response in normal arteries and enhanced vasoconstrictor response in stenotic arteries. Calcium antagonists prevent the abnormal response of normal and stenotic coronary arteries to exercise in hypertensive patients and thus may compensate for endothelial dysfunction with reduced vasodilator response to exercise.     

Structural and functional analysis of the cytidine deaminase gene in patients with acute myeloid leukaemia

Gene transfer of the cytidine deaminase (CDD) cDNA has recently been shown to induce cellular resistance to cytarabine (AraC) in vitro. To investigate the role for CDD in acute myeloid leukaemia (AML) we analysed the CDD activity and CDD gene structure in blast material from well-defined patients with untreated and AraC refractory (RF) AML. Median CDD activity in previously untreated AML was significantly lower than in RF-AML blasts (P=0.015) and was significantly lower in patients with complete remission than with blast persistence following induction chemotherapy (P=0.043). Structural investigation of the CDD gene by Southern analyses and RT-PCR showed no detectable aberrations. Sequence analysis of the CDD cDNA from nine RF-AML patients showed inconsistent aberrations in three patients. Semiquantitative assessment of CDD mRNA expression revealed a significant correlation with CDD activity. In conclusion, concordant with another recent study our data suggest a correlation of pretherapeutic CDD activity with induction treatment response. Besides the previously described prognostic impact of mdrl expression, this result could be useful for the development of risk-adapted AML treatment strategies and warrants further studies of CDD activity in well-defined cohorts of AML patients and of the mechanisms involved in the regulation of CDD activity.     

Endosonographic, endoscopic, and histologic evaluation of alterations in the rectal venous system in patients with portal hypertension

BACKGROUND: Colorectal varices and congestive rectopathy or colopathy have been erratically reported in patients with portal hypertension. The clinical importance of these entities has not been described. We assessed the changes in the venous system of the rectum by endoscopy and rectal endosonography (EUS). We also assessed the role of factors such as etiology of portal hypertension, grade of esophageal varices, sclerotherapy, and liver disease severity on the occurrence of these vascular changes. METHODS: We studied changes in the venous system of the rectum using endoscopy and EUS in 60 patients with portal hypertension (cirrhotic 41, noncirrhotic 19). Ten patients with irritable bowel syndrome and 6 patients with hemorrhoids served as controls. Rectal varices were classified as tortuous, nodular, and tumorous. Corresponding appearances on rectal EUS were classified as single or discrete multiple, multiple, and innumerable submucosal veins, respectively. Evidence of congestive rectopathy was also recorded. RESULTS: Prevalence of rectal varices was 43.3% on endoscopy (73% tortuous, 19% nodular, and 8% tumorous) and 75% on EUS (p < 0.0005). The latter showed corresponding appearances of submucosal veins in 25 of 26 patients and detected submucosal veins not identified at endoscopy in 19 other patients. Congestive rectopathy was found in 38.3% of patients. Multiple small dilated vessels in the submucosa were seen in 23.3% patients on rectal EUS. The development of these vascular changes was significantly influenced by sclerotherapy, but not by higher grade of esophageal varices, the etiology of portal hypertension, or severity of liver disease. CONCLUSIONS: Changes in the rectal venous system are common, with rectal EUS being superior to endoscopy in detecting early, as well as florid, changes.