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)

The Systolic Hypertension in the Elderly Program (SHEP) was a double-blind placebo-controlled outcome trial on the treatment of isolated systolic hypertension (systolic pressure: 160-219 mmHg and diastolic pressure less than 90 mmHg). From 447, 921 screenes (age greater than or equal to 60 years) 4,736 patients were randomised. A significant reduction of non-fatal stroke (37%), non-fatal myocardial infarction (33%) and left ventricular failure (54%) was observed in the active treatment group. By contrast, the reduction in transient ischaemic attacks (25%), and in total (13%), cardiovascular (20%), cerebrovascular (29%) and coronary (20%) mortality did not reach a level of statistical significance. SHEP is a landmark trial on the treatment of isolated systolic hypertension (ISH) in the elderly. However, the question to what extent the SHEP results can be extrapolated to clinical practice remains open for debate. Indeed, it is possible that due to selection, the SHEP patients were not entirely representative of the elderly with ISH in the population at large. By contrast with previous intervention studies in elderly patients with combined systolic and diastolic hypertension, the SHEP trail did not demonstrate a significant beneficial effect of antihypertensive treatment on any of the cardiovascular mortality endpoints. Confirmation or rejection of the SHEP results in other trials, including the Syst-Eur study, conducted by the rejection of the SHEP results in other trials, including the Syst-Eur study, conducted by the European Working Party on High Blood Pressure in the Elderly and the Chinese trial in elderly ISH patients, is now awaited.
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PMID:Isolated systolic hypertension in the elderly: implications of Systolic Hypertension in the Elderly Program (SHEP) for clinical practice and for the ongoing trials. 179 5

Selected parameters of the pulmonary circulation and right ventricular performance were studied in 30 patients with primary arterial hypertension. Four patients belonged to the WHO class I, four to class I/II, 18 to class II and the remaining four to class III. Patients were eligible, if they were in sinus rhythm, without symptoms of left ventricular failure and diseases that night influence pulmonary pressures, and if drugs affecting cardiac performance could be withdrawn safely for 3 days. Ten healthy subjects served as control group. The mean pulmonary capillary wedge pressure and mean pulmonary artery pressure were similar in both groups. In contrast, the systolic pulmonary arterial pressure exceeded 30 mm Hg in 6 patients. Mean pulmonary vascular resistance was higher in examined patients than in the control group. Right ventricular end-diastolic pressure was above 5 mm Hg in as much as 50% of patients. Mean systolic ejection rate showed a tendency to decrease. The results indicate that part of patients with primary arterial hypertension exhibits disorders in the pulmonary circulation and right ventricular performance.
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PMID:[Pulmonary circulation and right ventricular function in primary arterial hypertension]. 184 61

Small and large airways narrow in LVF and the term cardiac asthma is often used. However, current usage of this term is inconsistent and its meaning is therefore ambiguous. The term is better avoided despite several emerging similarities with bronchial asthma. Airway narrowing may be precipitated by acute elevation of pulmonary or bronchial vascular pressures. This appears to be mainly due to reflex bronchoconstriction. The afferents of this reflex are C-fibers with their endings in the lung parenchyma, bronchi, and pulmonary blood vessels and RAR in the larger airways, and they run in the vagus nerves, as do the efferent bronchoconstrictor fibers. Chronic elevation of pulmonary vascular pressures, as in mitral stenosis, are also associated with airway narrowing. Pulmonary edema (in the absence of vascular hypertension) also causes reflex bronchoconstriction. Bronchial responsiveness to bronchoconstrictor drugs is increased in LVF, partly, at least, due to reflex mechanisms. Bronchial mucosal swelling may also contribute. Narrowing by nonreflex mechanisms definitely occurs and there is direct evidence that decreased lung volume caused by pulmonary edema may cause this. There is little evidence for bronchial narrowing due to the mechanical effect of peribronchial edema, or by swelling of the bronchial mucosa. However, edema foam may terminally cause grave obstruction. Patients with LVF are commonly treated with bronchodilator drugs, but the basis for this approach needs further clarification.
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PMID:Airway obstruction and bronchial hyperresponsiveness in left ventricular failure and mitral stenosis. 192 73

This prospective clinical study evaluates the possible beneficial effects of increased phenoxybenzamine dosage in the preoperative treatment of patients with pheochromocytoma. For this purpose total blood volume (TBV) prior to and after treatment with phenoxybenzamine and hemodynamic changes during surgery were determined in two groups of patients: group I (n = 12) received a mean dosage of 140 mg, group II (n = 12) 270 mg/day. The mean TBV in group I showed no changes after treatment with phenoxybenzamine, while the TBV in group II increased by 5.6 ml/kg body weight, corresponding to an increase in plasma volume (PV) of 10.2%. These changes were not significant, however. The intraoperative vasodilator requirement for the treatment of catecholamine induced hypertension during tumor manipulation was significantly less for group II: total nitroprusside administration averaged 8.7 mg in group I and 0.8 mg in group II (P less than 0.0005). Patients in group I received a total of 2.6 mg nitroglycerin compared with only 0.5 mg for patients in group II (P less than 0.005). In conclusion, preoperative treatment of patients with pheochromocytoma with increased dosages of phenoxybenzamine is beneficial to intraoperative management by decreasing hemodynamic instability due to tumor manipulation and following resection. This treatment was effective for preventing complications such as excessive tachycardia, cardiac arrhythmias, hypertensive crises, or left ventricular failure.
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PMID:[The importance of high-dose alpha-receptor blockade for blood volume and hemodynamics in pheochromocytoma]. 197 79

The Captopril Prevention Project (CAPPP) is a prospective, randomized, multi-centre intervention trial designed to investigate whether antihypertensive treatment with the angiotensin converting enzyme (ACE) inhibitor captopril may reduce cardiovascular mortality and morbidity more than a therapeutic regimen which does not include an ACE inhibitor. Secondary objectives are to compare total mortality, the development or deterioration of ischaemic heart disease, left ventricular failure, atrial fibrillation, diabetes mellitus and possible differences in renal function in the two groups. Male and female patients with essential hypertension, aged 25-66 years, will be randomly allocated to antihypertensive treatment which will comprise either the use of the ACE inhibitor captopril or will exclude all types of ACE inhibitors. Some 275 hypertension centres and health care centres in Sweden and Finland will take part in this multi-centre trial. A total of 7000 patients will be recruited and studied for an average period of 5 years, the assumption being that a 20% difference in cardiovascular mortality between the two groups can be detected with a power of 80% at the 5% significance level (two-sided test).
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PMID:The Captopril Prevention Project: a prospective intervention trial of angiotensin converting enzyme inhibition in the treatment of hypertension. The CAPPP Group. 198 Dec 18

The authors report two cases of cardiac rupture during acute myocardial infarction successfully treated surgically. In the first case, rupture occurred 7 days after hospital admission for anteroseptal myocardial infarction. The patient developed sudden cardiogenic shock with signs of venous hypertension without left ventricular failure. The second patient was admitted for syncopal chest pain with transient hypotension which regressed after volume repletion and pressor amine therapy. On admission, the patient had signs of cardiac tamponade. The ECG showed recent inferolaterobasal myocardial infarction. In both cases the diagnosis was made by 2D echocardiography which showed voluminous circumferential pericardial effusions probably due to haemorrage, with an image very suggestive of a blood clot in the effusion of the second patient. The two patients underwent emergency cardiac surgery and both survived with a 4 and 1.5 month follow-up respectively. These two cases confirm the value of 2D echocardiography as an emergency bedside procedure for the diagnosis of cardiac rupture, especially when images of intrapericardial thrombosis are observed, as in our second patient. In addition, the first case raises once again the question of the role of late thrombolysis as a predisposing factor of cardiac rupture at a time when this technique is proposed up to 24 hours after the onset of symptoms.
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PMID:[Free-wall rupture during the acute phase of myocardial infarction. Apropos of 2 cases surgically treated with success]. 206 16

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

Abnormalities in the diastolic function of the left ventricular pump are the common determinant and, above all, the earliest manifestation of all forms of chronic left ventricular failure, whether or not the left ventricular systolic function is abnormal. Congestive signs, in particular, are directly related to abnormalities of ventricular filling. Primary diastolic dysfunction is the cause of left ventricular failure in about 40 p. 100 of the cases, but it may also be observed in almost all cardiopathies. In myocardial ischaemia the pressure-volume relation is displaced upwards owing to a slowed down, inhomogeneous and incomplete relaxation. Left ventricular hypertrophy, whether it is due to excessive pressure (arterial hypertension, aortic stenosis) or reflects a primary hypertrophic cardiomyopathy, is associated with a slowing down of ventricular relaxation and a reduction of left ventricular diastolic distensibility, even though the ventricular pump systolic function remains normal for a long time. Outside alterations in the distensibility of the ventricular muscle, ventricular dilatation alters ventricular filling by forcing the ventricle to function on the vertical part of its diastolic pressure-volume relation. Nowadays, the aged hearts is the most frequent cause of heart failure with normal systolic function. In all cases dysrhythmias and atrioventricular desynchronization act as aggravating factors. Treatment is often difficult since positively inotropic drugs or arterial vasodilators frequently have a modest or even deleterious effect.
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PMID:[Disorders of diastolic function in chronic left ventricular insufficiency]. 214 34

Quinapril hydrochloride, a new, orally active, nonpeptide, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor, has been studied extensively in a variety of in vitro and in vivo animal models. Quinapril inhibits the contractile and pressor effects of angiotensin I in rabbit aorta and in rats, respectively, and lowers blood pressure in both high- and normal-renin rodent and diuretic-treated dog models of hypertension. No tolerance to the antihypertensive effects of quinapril was noted in spontaneously hypertensive rats treated with quinapril for up to 14 consecutive days. As with other ACE inhibitors, quinapril had virtually no effect on the development of hypertension in the renin-independent one-kidney deoxycorticosterone (DOCA)-salt hypertensive rat. Antihypertensive activity best correlates with the inhibition of tissue (vascular) ACE, and thus the reduction in peripheral vascular resistance associated with plasma and tissue ACE most likely accounts for the therapeutic benefit of quinapril. Preliminary data from a trial of quinapril in cardiomyopathic hamsters show that the drug prevents the anticipated decline in left ventricular contractile function and retards the temporal progression of left ventricular failure. ACE inhibitors have been found to have a lipid-neutral profile, unlike some other classes of antihypertensives. Quinapril is rapidly absorbed and extensively distributed to all tissues except brain. It is rapidly hydrolyzed to quinaprilat, its pharmacologically active diacid form. Metabolism to other compounds is not extensive. Quinapril's preclinical toxicologic profile is similar to that of other ACE inhibitors. Long-term toxicology studies show that quinapril is not teratogenic, carcinogenic, or mutagenic.
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PMID:Quinapril: overview of preclinical data. 218 23

The usual presentation of phaeochromocytoma is well known. It is a catecholamine producing tumor of the sympathochromaffin system that typically cause sustained hypertension or hypertensive crisis. Rarely it has an uncommon clinical presentation with or without arterial hypertension and so the most significant symptoms are episodes of left ventricular failure, arrhythmias, ischemic ECG changes, angina pectoris, myocardial infarction, hypertrophic or dilated cardiomyopathy. On report two cases of uncommon presentation of phaeochromocytoma and a few cases of myocardial damage from the literature are reviewed.
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PMID:[Myocardial damage and pheochromocytoma. Description of 2 cases and review of the literature]. 223 73


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