Local arterial hypertension in the pathogenesis of chronic pancreatitis]

Based on the rheographic studies of the postprandial transformation of the splanchnic blood flow and morphological study of the resected parts of the pancreas in patients with chronic fibrosing pancreatitis, the authors revealed functional and morphological attributes of local arterial hypertension and, at the stage of exacerbation of disease--manifestations of a vascular crisis. Local arterial hypertension with vascular crises originating on its basis is an important pathogenetic factor of the progression of chronic pancreatitis. It is assumed that local arterial hypertension develops against the background of depression of cholinergic effects and domination of sympathetic effects.     

Pathophysiology and classification of pulmonary hypertension

Pulmonary hypertension is present when the mean pulmonary pressure is increased above 25 mm Hg in a rest or above 30 mm Hg during exercise. It is possible to divide it from different point of view. Well known is pathophysiologic classification and Venice classification suggested by WHO symposium 2003. The rise of arterial pulmonary pressure is caused by three essential abnormalities, these are elevated pulmonary vascular resistance, blood flow and pulmonary artery wedge pressure. Vasoconstriction, remodeling of vessels and in situ trombosis are pathogenetic mechanism which contribute to rise of pulmonary hypertension.     

中心动脉压与高血压靶器官损害的相关关系研究进展

中心动脉压与高血压靶器官损害之间存在许多联系,中心动脉压是评价动脉结构和功能的重要标志.有研究认为高血压靶器官损害的病理机制和中心动脉压相关,现将二者之间的关系作一综述.     

Arterial hypertension and unilateral small kidney

Within a 10 years period, 612 patients underwent an autopsy, in a geriatric hospital. Seventeen p. 100 were discovered to have a high blood pressure. Twenty-nine patients (that is about 4 p. 100) presented with a small unilateral kidney. The pathogenetic factors of these unilateral nephropathies were various, many causes of which were unilateral pielonephritis. Out of the patients exhibiting a small unilateral kidney, 62 p. 100 had a high blood pressure. Hypertension due to a unilateral nephropathy, when studied on a statistic level, does not induce any atheromatous lesion nor heart ponderal hypertrophy more acute than essential high blood pressure. The unilateral nephropathies hypertension would thus be compared to an hypertension "depending on sodium or volume" and not as an hypertension "depending on renin".     

Pulmonary veno-occlusive disease caused by an inherited mutation in bone morphogenetic protein receptor II

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension in which the vascular changes originate in the small pulmonary veins and venules. The pathogenesis is unknown and any link with primary pulmonary hypertension (PPH) has been speculative. Mutations in the bone morphogenetic protein receptor II (BMPR2) gene have been identified in at least 50% of familial cases and in 25% of sporadic cases of PPH. We report a patient with documented PVOD whose mother had severe pulmonary hypertension. Sequencing of the patient's BMPR2 coding region revealed a del44C mutation in Exon 1 that is predicted to encode for a truncated protein. Analysis of DNA from family members suggests that this mutation was transmitted by the proband's mother to two of her four children. The finding of PVOD associated with a BMPR2 mutation reveals a possible pathogenetic connection with PPH.     

Uric acid: Its relationship to renal hemodynamics and the renal renin-angiotensin system

Reports relating hyperuricemia and hypertension have been fieled for many decades. Nevertheless, controversy remains concerning serum uric acid concentration as an independent risk factor underlying coronary heart disease (CHD) and essential hypertension or as an indirect marker of renovascular involvement. Earlier studies in normotensive subjects and hypertensive patients demonstrated that serum uric acid concentration was closely related to intrarenal hemodynamic alterations, suggesting that it is an excellent marker of vascular involvement. Our data from clinical studies and in an animal model of severe hypertensive nephrosclerosis have strengthened this concept. Conversely, other reports have suggested that uric acid may be a pathogenetic factor. Supporting arguments for this theory maintain that experimental hyperuricemia induces hypertension and renal damage. Epidemiologically, hyperuricemia is associated with hypertension, CHD, renal disease, toxemia of pregnancy, and other outcomes, although mechanisms remain unclear. Additionally, there are no available data on the effects of lowering uric acid on pressure control and organ protection.     

Diabetic cardiomyopathy: possible pathogenetic role of coronary microcirculation]

The hypothesis that diabetes mellitus provokes a specific cardiomyopathy is supported by numerous clinical, epidemiological and anatomopathological studies. However, the frequent association of diabetes mellitus with other conditions, such as hypertension and coronary atherosclerosis, both capable of causing the dysfunction of the cardiac muscle, makes it difficult to interpret many of the data reported in the literature and contributes to the continuing debate regarding the effective existence of diabetic cardiomyopathy and its possible pathogenetic mechanisms. In clinical terms, diabetic cardiomyopathy is manifested both as an altered diastolic and/or systolic phase, assessed using various non-invasive techniques, or as congested cardiac decompensation. The pathogenesis of diabetic cardiomyopathy is still not altogether clear. The alteration of the smallest coronary vessels might be responsible for the increased interstitial fibrosis found in the heart of diabetic patients. In this paper numerous data from the literature on this argument are reported and the authors advance the hypothesis that endothelial dysfunction may play a pathogenetic role in the development of cardiopathy.     

Association between essential hypertension and immunology]

Using the immunofluorescence method, autoantibodies of serum IgG was investigated in 100 consecutive patients of essential hypertension with or without family history of hypertension. 30 healthy normotensive subjects with family history of hypertension and 40 healthy normotensive subjects of the same age range were also studied. The results showed that in the treated patients, the frequency of smooth muscle antibodies (SMA), antimitochondrial antibodies (AMA), antinuclear antibodies (ANA) and heart reactive antibodies (HRA) was higher than that in healthy normotensive subjects. The frequency of these antibodies was not associated with difference in mean arterial blood pressure, sex, and clinical stage and a possible genetic predisposition is suggested. The autoantibodies may even appear before the elevation of blood pressure in patients with essential hypertension. The above-mentioned results show that lack of autoimmunity may be one of the pathogenetic factors of essential hypertension.     

Long-term favourable effect of nifedipine in primary pulmonary hypertension. Report of a case with hemodynamic evaluation after 3 and after 16 months and with clinical follow-up during 36 months

The favourable effect of long-term (36 months) treatment with nifedipine in a case of primary pulmonary hypertension is described. While clinical improvement was quick, pulmonary hemodynamic data were unchanged after 3 months of treatment, when acute administration of the drug showed a significant fall in pulmonary resistances. After 16 months of treatment a consistent decrease of pulmonary artery pressure was found, suggesting a selective favourable effect of the drug on the pulmonary circulation. The association with systemic arterial hypertension, whose onset was near contemporaneous with pulmonary hypertension, might indicate a common vasoconstrictive pathogenetic mechanism.     

Results of nonmedical interventions in multicenter randomized open study of efficacy of lifestyle modification and therapy with quinapril in patients with obesity and hypertension

There is a pathogenetic interrelationship between obesity and hypertension. Moreover it has become evident that the use of most modern and active antihypertensive drugs can not be effective without concomitant treatment of obesity. This study was conducted in 18 cities of Russian Federation in order to demonstrate influences of lifestyle changes on hypertension and levels of cardiovascular risk factors. The objective was to attract attention of physicians and patients to the problem of obesity and hypertension and to their inherent dangers.     

Primary pulmonary hypertension in a patient with HIV infection

Several case-reports and small series suggest a causal relationship between human immunodeficiency virus (HIV) infection and pulmonary hypertension. We report on a HIV seropositive man with a high and stable CD4 lymphocyte count (+/- 600/mm3) who developed severe pulmonary hypertension, not attributable to other known causes. This case report underscores the fact that the degree of immunosuppression secondary to the HIV-infection seems to be of little relevance in the pathophysiology of the syndrome. HIV-infected patients with dyspnoea, not related to pulmonary infection, with exercise intolerance, syncope or precordial pain should receive an electrocardiogram and echocardiographic assessment. The exact pathogenetic mechanism of this rapidly progressive disease and whether anti-viral therapy should be promoted is still under investigation.     

高血压脑出血术后D-二聚体动态变化的临床研究

目的研究高血压脑出血术后患者血液中D-二聚体的动态变化与病情程度及预后的关系。方法采用磁珠法对89例高血压性脑出血术后患者的血浆D-二聚体水平进行检测,与36例健康体检者进行对照,并分析其与病情、预后的关系。结果各型脑出血患者血浆D-二聚体含量间差异有统计学意义（P〈0.01）。好转组与无好转组D-二聚体异常率间差异有统计学意义（P〈0.01）。结论动态观察D-二聚体的变化对高血压性脑出血术后的病程、病情判定及评价预后有重要意义,是判断高血压脑出血术后患者病情程度及预后情况的有效指标之一。     

Pulmonary hypertension and systemic lupus erythematosus

Various pleuropulmonary manifestations are reported to occur in the course of systemic lupus erythematosus (SLE). Among these, pulmonary hypertension is one of the most uncommonly observed. The natural course of this involvement can be independent of the primary disease, and resembles primitive pulmonary hypertension. Various pathogenetic mechanisms might be responsible for this picture. In the case here reported, the pathological data were strongly suggestive of pulmonary vasculitis, emphasizing that SLE, like other connective tissue diseases, can be responsible for fatal pulmonary hypertension.     

Hypertension in Cushing's syndrome

Cushing's syndrome can be exogenous, resulting from the administration of glucocorticoids or adrenocorticotrophic hormone (ACTH), or endogenous, secondary to increased secretion of cortisol or ACTH. Hypertension is one of the most distinguishing features of endogenous Cushing's syndrome, as it is present in about 80% of adult patients and in almost half of children and adolescents patients. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. The therapeutic goal is to find and remove the cause of excess glucocorticoids, which, in most cases of endogenous Cushing's syndrome, is achieved surgically. Treatment of Cushing's syndrome usually results in resolution or amelioration of hypertension. However, some patients may not achieve normotension or may require a prolonged period of time for the correction of hypercortisolism. Therefore, therapeutic strategies for Cushing's-specific hypertension (to normalise blood pressure and decrease the duration of hypertension) are necessary to decrease the morbidity and mortality associated with this disorder. The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed.     

The renin-angiotensin-aldosterone system in children and adolescents with nephrogenic hypertension

Renin-angiotensin-aldosterone (RAA) function was studied in children with secondary hypertension of 2 varieties: vasorenal hypertension (VRH) and arterial hypertension (AH) associated with chronic pyelonephritis. Children with VRH showed RAA activation that depended on the duration of the disease for its markedness. A direct correlation found between ABP, on the one hand, and plasma renin activity and blood aldosterone level, on the other, is evidence of the latter's involvement in VRH pathogenesis. In AH that is due to chronic pyelonephritis, RAA activation was also demonstrated, however, its pathogenetic involvement was only documented in children with urinary passage disorders (vesico-renal reflux), whereas in the rest RAA activation was not a primary cause of BP elevation.     

Perspectives on the renin-angiotensin-aldosterone system in hypertension

In the syndrome of hyperaldosteronism, the abnormal electrolyte metabolism, secondary to mineralocorticoid excess, seems to play a predominant pathogenetic role in causing elevation of the blood pressure, since the renin-angiotensin system is depressed and unresponsive. The available evidence (results of treatment, consistent failure to cause high blood pressure by administration of excessive salt-remaining steroids to normotensive volunteers, the salt-hypertension model in experimental animals, the higher incidence of adrenal adenomas in hypertensive patients, etc.), however, suggests that other factors participate in the mechanism of hypertension. Angiotensin II stimulates aldosterone secretion, thereby affecting electrolyte balance; in addition, this polypeptide is the most powerful vasoconstrictor known today, the effectiveness of which is greater in a Na-replete condition. In some hypertensive states (renovascular hypertension, end-stage renal disease, malignant phase hypertension, hypertension related to oral-contraceptive medication, and primary reninism) both the renin-angiotensin system and aldosterone production may be elevated. In this group, however, correlation between the latter two variables and hypertension is not sufficiently consistent to implicate them as the sole pathogenetic factors. In the larger group of patients with essential hypertension, the renin-angiotensin-aldosterone system and electrolyte metabolism range from normal to subtle changes (depressed plasma renin, incomplete aldosterone suppression by salt load, decrease in aldosterone metabolism, exaggerated natriuresis, reversal of electrolyte circadian cycle) of difficult interpretation. We suggest that the same factors, clearly abnormal in hypertensive states of more defined etiology, are also at play in causing essential hypertension, perhaps through some as yet undefined abnormal interrelationship.     

Indices of the body's neurohumoral activity and hemodynamic types in hypertension

A study of neurohumoral parameters in patients with essential hypertension and different hemodynamic types demonstrated different patterns of hormonal change in patients with hyperkinetic, eukinetic and hypokinetic hypertension. Elevated blood tri-iodothyronine and thyroxine, seen in patients with hyperkinetic hemodynamic type, and increased catecholamine excretion in patients with hypokinetic hemodynamics may be indicative of the pathogenetic significance of the hormones in question for the formation of respective variants of essential hypertension.     

The emerging role of gut microbiota in cardiovascular diseases

There is mounting evidence which suggests the involvement of gut microbiota dysbiosis in the pathogenesis of various cardiovascular diseases (CVD) and associated risk states such as hypertension, type 2 diabetes, obesity and dyslipidaemia, atherosclerosis, heart failure and atrial fibrillation. The current review comprehensively summarizes the various pathogenetic mechanisms of dysbiosis in these conditions and discusses the key therapeutic implications. Further deeper understanding of the pathogenetic links between CVD and gut microbiota dysbiosis can aid in the development of novel microbiota-based targets for the management of CVDs.     

Residual hypertension after removal of a pheochromocytoma (morphologic study of the kidneys)

Renal parenchyma, and the juxtaglomerular apparatus in particular, was studied in 23 patients with verified diagnosis of pheochromocytoma. Intraoperative renal biopsy was performed in 21 cases, and kidneys obtained at nephrectomy or autopsy were examined in 2 cases. Twenty-one patients were examined following the removal of pheochromocytoma (2 patients died). Arterial BP returned to normal in 86.4%, and residual hypertension due to continuous hyperfunction of the juxtaglomerular apparatus in the presence of hypertensive angiosclerosis was recorded in 13.6%. Tubular epithelial atrophy of varying markedness, associated with renal ischemia, was detected in all cases. The pathogenetic contribution of the renin-angiotensin system to pre- and postoperative hypertension in pheochromocytoma patients is discussed.     

Noncirrhotic portal hypertension

Noncirrhotic portal hypertension represents a heterogeneous group of conditions that have distinct clinical and hemodynamic features that often help distinguish them from cirrhosis. [figure: see text] The sites of portal flow resistance may not be precisely localized to one area of the hepatic lobule and may extend beyond the site where the pathogenetic process began. Even in patients with portal hypertension caused by an increased flow, there may be subsequent development of increased resistance. The prognosis is variable; outcomes are better in patients with presinusoidal portal hypertension. A good understanding of the presentation of the various noncirrhotic conditions that cause portal hypertension will help determine the cause, the site of resistance, and the therapeutic plan. Ascites is not a feature of presinusoidal portal hypertension, whereas it may be the predominant feature in postsinusoidal portal hypertension.