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

A 79-year-old female was admitted to our hospital because of a malignant pleural effusion following mastectomy 4 years ago. In the patient's history arterial hypertension and previous inferior myocardial infarction have been known. Two doses of 20 mg mitoxantrone were installed intrapleurally at an interval of 4 weeks. Six hours after the second mitoxantrone application and the patient had increasing dyspnea with consecutive left heart failure, pulmonary congestion, and a drop of blood pressure. The white-cell count was 14800/mm3. The levels of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (SGOT) were in the normal range. Transthoracic echocardiography showed concentric left ventricular hypertrophy and a markedly decreased fractional shortening, but no left ventricular dilatation. The electrocardiogram showed newly appeared down-sloping ST-segments and inverted T-waves. Clinical recovery was achieved after 6 days by application of oxygen, dobutamine and furosemide followed by angiotensin converting enzyme inhibition and digitalis. In the echocardiographic control examination 14 days later left ventricular function had normalized. The changes of electrocardiogram normalized 4 weeks later.
 ...
PMID:[Mitoxantrone-induced acute left heart failure after intrapleural administration]. 937 56

In addition to being accepted therapy in hypertension and heart failure, ACE inhibitors may well offer a new dimension in anti-ischaemic therapy. Currently, anti-ischaemic properties have been demonstrated by ACE inhibitors in selected patient groups, including patients with left ventricular dysfunction with or without a direct temporal relationship with myocardial infarction. Anti-ischaemic effects of ACE inhibitors become apparent late after initiation of treatment and suggest a structural rather than a functional effect. Underlying mechanisms may include a reduction in ventricular dilatation and (abnormal) cardiac hypertrophy, leading to less myocardial oxygen demand and, possibly, improved subendocardial blood supply, and vasculoprotective effects, i.e. anti-atherosclerotic and antiremodelling properties, a beneficial effect on the fibrinolytic system and an improvement in abnormal endothelial vasodilator function. The latter aspect is most probably the pivotal mode of action where the anti-ischaemic profile of ACE inhibition is concerned. An improvement in endothelial dysfunction has been shown in patients with mild to moderate coronary artery disease [Trial on Reversing ENdothelial Dysfunction (TREND)]. It is of importance that, in both clinical experiments and human studies, the role of bradykinin appears central in the structural and functional cardiovascular effects of ACE inhibition. This is particularly true for the improvement of impaired endothelial function. Myocardial ischaemia evokes vasoconstrictor neurohormonal activation, which may lead to coronary vasoconstriction in diseased coronary segments. The subsequent abnormal endothelial function leads to diminished coronary flow and also increases systemic vasotone and afterload, thus unfavourably altering the myocardial oxygen supply/demand ratio. Under laboratory conditions, acute ACE inhibition counteracts this activation in humans. However, it is speculated that this anti-ischaemic mechanism may become operative and clinically important during long term oral ACE inhibitor therapy when endothelial function improves, and may subsequently protect against the vasoconstrictor effect of neurohormonal activation. As it is unlikely that the mechanisms mentioned above are only relevant in patients with ventricular dysfunction or heart failure, several large controlled trials are currently examining the long term anti-ischaemic and cardiovascular protective effects of ACE inhibition in patients at risk of a cardiovascular event [Heart Outcomes Prevention Evaluation study (HOPE)], with a normal cardiac function [Prevention of Events with ACE inhibition study (PEACE)] or in all patients with coronary artery disease irrespective of cardiac function [EUropean trial of Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA)].
 ...
PMID:Bradykinin-mediated cardiovascular protective actions of ACE inhibitors. A new dimension in anti-ischaemic therapy? 942 46

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.
 ...
PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

The renin-angiotensin system is activated during myocardial ischemia, and local angiotensin II formation occurs in ischemic hearts. At least two angiotensin II receptor subtypes, the AT1 and AT2 receptor, have been identified. The cardiovascular effects of angiotensin II have been largely attributed to activation of AT1 receptors. In ventricular preparations from normal rat and pig hearts, the density of AT1 receptors is higher than that of AT2 receptors, whereas data on the AT receptor subtype density and its distribution in human hearts remain controversial. AT1 receptor blockade increases coronary blood flow during ischemia in dogs and during reperfusion in rats. It also reduces the incidence of ischemia-related arrhythmias in rats and guinea pigs, limits infarct size in pigs, improves functional and metabolic recovery following myocardial ischemia, and attenuates ventricular remodelling post-myocardial infarction in rats. The potential mechanisms responsible for the cardioprotection by AT1 receptor blockade remain to be elucidated in detail, but appear to involve AT2 receptor activation and the subsequent action of bradykinin, prostaglandins, and/or nitric oxide. Patients under treatment with AT1 receptor antagonists for indications such as hypertension and ventricular dilatation after myocardial infarction are likely to have improved prognosis when suffering an acute myocardial infarction.
 ...
PMID:AT1 receptor blockade in experimental myocardial ischemia/reperfusion. 983 69

The purpose of this study was to compare the angiotensin II type 1 receptor antagonist candesartan cilexitil (candesartan) and the angiotensin-converting enzyme inhibitor cilazapril on cardiac function, assessed by Doppler echocardiography and cardiac gene expression associated with cardiac remodeling, in rats with myocardial infarction. Candesartan or cilazapril was administered after myocardial infarction. At 1 and 4 weeks after myocardial infarction, cardiac function and mRNA expression in noninfarcted myocardium were analyzed. Candesartan and cilazapril equally prevented increases in hypertrophy in noninfarcted myocardium, left ventricular dilatation, and ejection fraction at 4 weeks. The E-wave/A-wave velocity ratio and the rate of E-wave deceleration, measures of diastolic function, increased to 9.2+/-0.6 and 26.3+/-2. 6 m/s2 at 1 week after myocardial infarction. Candesartan and cilazapril, administered at a dose of 1 mg/kg per day, prevented increases in E-wave/A-wave velocity ratio and E-wave deceleration at 1 and 4 weeks. Candesartan and cilazapril significantly suppressed increased mRNA expression of beta-myosin heavy chain, alpha-skeletal actin, and atrial natriuretic peptide in noninfarcted ventricle at 1 and 4 weeks and expression of collagen I and III at 4 weeks to a similar extent. When given at a dose of 10 mg/kg per day, both candesartan and cilazapril prevented cardiac dysfunction and gene expression to the same extent as when given at 1 mg/kg per day. In conclusion, Doppler echocardiography showed that candesartan and cilazapril equally improved systolic and diastolic function and that ventricular remodeling accompanied modulation of cardiac gene expression.
Hypertension 1999 Apr
PMID:Effects of candesartan and cilazapril on rats with myocardial infarction assessed by echocardiography. 1020 31

To clarify the relationship between long-term prognosis of patients with stroke and their MRI findings, 103 patients with initial cerebral thrombosis, who survived more than three months after the ictus, were studied for five years. The mean age of 98 patients (T group), who were followed up completely, was 73.1 years-old and 65 were men. The age-matched controls consisted of two groups: 65 subjects, who had hypertension and/or diabetes without a history of stroke (R group), and 85 subjects, who had any hypertension, diabetes and stroke (N group). MRI findings were divided into six categories: 1) types of causative lesion, 2) grades of periventricular hyperintensity (none, rims/caps, patchy, diffuse PVH), 3) number of spotty lesions, 4) presence of silent infarction. 5) ventricular dilatation, and 6) extents of brain atrophy. Types of causative lesion were subdivided into 3 subtypes; infarction of the perforating artery territory (P type), infarction of the cortical artery territory (C type), and brainstem infarction (B type). The presence of vascular risks and dementia, and the extent of activity of daily living (ADL) were assessed. The P, C, and B types were identified by MRI in 46, 36, and 16 of the T group, respectively. Motor impairment, dementia, and an ADL status of complete dependence at discharge were also seen in 84, 44, and 22, respectively. In the T group, 33 patients died during five years, which resulted in a cumulative mortality rate of 33.7% and an annual mortality rate of 8.2%. Based on log-rank analysis, the survival rate of the T group revealed was significantly lower than those of the R and N groups. The recurrent rate in the T group (annual stroke recurrence rate was 4.0%) was higher than in the R and N groups, but stroke recurrence was not the cause of death and two thirds of deaths were due to aspiration pneumonia and/or asphyxia. Cox hazard regression analysis for death due to respiratory diseases showed that the hazard ratios of infarction, patchy PVH, and more than 4 spotty lesions were 8.87 (p < .001), 0.31 (p = .058), and 0.44 (p = .098), respectively. Compared to the survival group, rates of complete dependence in ADL, dementia, and brain atrophy were significantly higher in the death group with low incidences of the P type and patchy PVH, which indicated small vessel disease. These findings suggested that in patients with cerebral thrombosis, even in the chronic phase, care should be taken to prevent pneumonia and/or asphyxia due to bulbar palsy. Furthermore, no MRI findings were distinct predictors of long-term prognosis, although infarction based on the small vessel disease had rather good outcome in terms of respiratory disease.
 ...
PMID:[Long-term prognosis of patients with initial cerebral thrombosis and the MRI findings]. 1036 31

To assess clinically whether alterations of autonomic tone precede left ventricular dilatation, heart rate variability and early left ventricular dilatation after a first myocardial infarction were assessed. Low-frequency power (LF), high-frequency power (HF), and total power (TP) were obtained by ambulatory electrocardiogram on day 1 in 53 patients with a first acute myocardial infarction. Left ventricular end-diastolic volume determined by echocardiography was obtained on day 1 and day 14. Stepwise linear regression analysis was used to assess the associations of early left ventricular dilatation with heart rate variability adjusted for clinical variables. Higher LF and TP were significantly associated with early left ventricular dilatation after adjustment for age, sex, site of myocardial infarction, acute revasucularization, peak creatine kinase level, history of hypertension, and use of angiotensin-converting enzyme inhibitors and beta-blockers. Higher LF and TP preceded early left ventricular dilatation after myocardial infarction.
 ...
PMID:Heart rate variability and left ventricular dilatation early after myocardial infarction. 1046 69

As accurate assessment of hypertension in renal patients must be the cornerstone of better prevention of its deleterious effects, ambulatory blood pressure monitoring (ABPM) has become an essential clinical and research procedure in day to day nephrological practice. However, despite numerous studies in the renal literature, a consensus is needed for normal (desirable?!) ambulatory daytime and nighttime BP levels and for defining normal sleep BP dipping. Nevertheless, blunted sleep BP fall appears to be a ubiquitous finding in renal disease (primary renal conditions, chronic renal failure pre-dialysis, peritoneal and hemodialysis, and renal transplantation). Abnormal diurnal variability should be considered as an important contributor to cardiac and general morbidity as it is clearly associated with a faster decline in renal function and also with more cardiac structural and functional abnormalities - especially left ventricular dilatation. Several mechanisms have been proposed to explain the reduced BP circadian rhythm, but the majority of the supporting evidence is still contradictory. A novel, unifying hypothesis to be tested in future studies, is linking the common diurnal rhythm abnormalities with functional disturbances in aortic and carotid baroreflexes caused by uraemia-related large arterial structural changes (arterial intima and media thickening, arterial calcifications and increased arterial stiffness).
 ...
PMID:Ambulatory blood pressure monitoring in nephrology: focus on BP variability. 1049 65

Left ventricular remodeling after myocardial infarction involves activation of the renin-angiotensin-aldosterone system. Recently, the biallelic -344T/C polymorphism of the aldosterone synthase gene was associated with increased aldosterone levels, arterial hypertension, diastolic dysfunction, and left ventricular dilatation. We hypothesized that this polymorphism may also affect left ventricular geometry and function after myocardial infarction. By using a standardized questionnaire, as well as anthropometric and echocardiographic measurements, we thus studied 606 patients (533 men and 73 women) who had a myocardial infarction before the age of 60 years. The aldosterone synthase gene polymorphism was analyzed after polymerase chain reaction amplification and restriction enzyme digestion. The results demonstrated that there was no association of the aldosterone synthase gene polymorphism with echocardiographically determined left ventricular dimensions, wall thicknesses, or indexes of systolic or diastolic function. Furthermore, anthropometric data, including blood pressure levels, were balanced between the different genotypes. Finally, the allele frequency was similar for patients with myocardial infarction and a sample group from the normal population (n=1675). The data indicate that the allele status of the aldosterone synthase gene polymorphism is not useful for the identification of patients with myocardial infarction who have impaired left ventricular function or unfavorable remodeling.
Hypertension 2000 Mar
PMID:Evaluation of the aldosterone synthase (CYP11B2) gene polymorphism in patients with myocardial infarction. 1072 May 82

Hypertension is an important risk factor for cardiovascular morbidity and mortality. Hypertension is associated with the development of congestive heart failure by way of left ventricular hypertrophy, with left ventricular dilatation and through myocardial ischemia and left ventricular damage. Reports on the natural history of untreated hypertension indicate that at least 50% of affected subjects develop congestive heart failure. Hypertension is an important precursor of heart failure, and still the most common risk factor for congestive heart failure in the population. In clinical trials, particularly in elderly patients, a reduction in the incidence of congestive heart failure has been observed. Despite increments in the use of antihypertensive drugs, mortality from congestive heart failure among the elderly is increasing. Moreover, several patients with hypertension are unaware, untreated and uncontrolled for the most important risk factor for congestive heart failure. For the primary prevention of heart failure, improvements in blood pressure control are of vast importance.
 ...
PMID:Hypertension: an important precursor of heart failure. 1080 84


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>