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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in the dynamics of brain serotonin biosynthesis can lead to changes in cardiovascular function. It appears that the activation of cerebral serotonin receptors produces a pressor effect in normotensive rats but produces a depressor effect in normotensive cats or dogs. On the other hand, reductions in the levels of serotonin can prevent the onset of hypertension in some experimental hypertensive models and lower the blood pressure of organisms with established hypertension. The ability of brain serotonin to modulate arterial blood pressure may be mediated by the influences of the serotonergic neuronal systems on efferent sympathetic activity. Finally, the reduction in sympathetic outflow produced by increasing brain serotonin levels in dogs protects the heart against ventricular fibrillation and may, therefore, constitute a reasonable adjunct in the management of high-risk, cardiac-arrest patients.
Hypertension
PMID:Review of the role of the central serotonergic neuronal system in blood pressure regulation. 644 22

The chronotropic effects of digoxin and deslanoside were studied in canine atria cross-perfused with heparinized arterial blood from donor dogs. Intravenous injections of either drug (100 micrograms/Kg) into the donor dog produced bradycardia followed by ventricular tachyarrhythmia, with or without hypertension, in the donor dog. A significant increase in the developed tension was observed in the isolated atria, with or without slight sinus acceleration. These effects continued over 150 min after the injection. Digoxin (200 micrograms/Kg, i.v.) caused an immediate bradycardia followed by ventricular tachycardia. In addition, ventricular fibrillation occurred in 3 out of 5 donor dogs within 20 min of the drug administration. In isolated atria, there was a marked increase in the developed tension, usually with a little sinus tachycardia. Deslanoside (200 micrograms/Kg, i.v.) caused almost the same response patterns as digoxin. However, this dose of deslanoside caused ventricular fibrillation in all 6 experiments. Drug concentrations in the donor's arterial blood decreased rapidly for 15-20 min and then decreased slowly in all experiments. It is concluded that digoxin and deslanoside have no significant direct accelerating action on the SA node in doses which produced marked increases in the developed tension; only extremely high doses cause a direct, slight sinus acceleration.
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PMID:Cardiovascular effects of digitalis on intact dogs and isolated cross-perfused atria. 667 65

1158 patients with acute myocardial infarction hospitalized in 6 clinics at Hamburg were analyzed retrospectively with special regard to older patients. 46% of all patients were older than 70 years. In contrast to former investigations the rate of myocardial infarction of women over 70 is arised. The reason of admission was reinfarction in 39%. The most frequent risk factors were hypertension and diabetes mellitus; but hypertension is not more frequent than in this age-group of the whole population. A so-called "silent" myocardial infarction occurred in 10-15% of patients over 70 years. The clinical course of acute myocardial infarction was injured by hemodynamic complications in 66%. Ventricular fibrillation was more frequent in younger than in older patients. The reanimation of older patients was successful in 25% primary, but the inhospital mortality was unchanged high (50%). In contrast to younger patients 40% of cases of death occurred after the acute phase in the 2.-4. week of hospital treatment.
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PMID:[Heart infarction in persons over 70. Epidemiologic studies of the clinical course]. 685 25

The authors suggest that the males under 60 with myocardial infarction who have no chronic circulatory insufficiency in their case history should be divided into the groups of high and low risk of the development of ventricular fibrillation, thromboembolic complications and acute cardiac aneurysm. The group of risk is determined on the basis of 5 clinical characteristics: the character of myocardial infarction, the stage of arterial hypertension, evaluation of the general state, heart failure and the heart rate.
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PMID:[Prognosis of ventricular arrhythmias in myocardial infarct patients]. 687 59

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.
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PMID:Natural history and prognosis of ischemic heart disease. 688 95

Theoretically, it should be possible to match the requirements of individual patients with the pharmacological and clinical properties of the large number of antihypertensive drugs now available. The concept of automatic sequential stepped-care therapy is now largely outdated, but therapy of clinically important hypertension must be initiated with one agent. Diuretics remain a first-line option in the elderly and in Black patients, as do calcium antagonists. Outcome trials are available only for the elderly, and in these the benefits of initial diuretic therapy are well documented. Nonetheless, diuretics may often need to be co-prescribed with a beta-blocker or an adrenergic modifier such as methyldopa. beta-Blockers are preferred in patients with ischaemic heart disease or enhanced adrenergic drive, while alpha-blockers are preferred in patients with blood lipid abnormalities or prostatic problems. Calcium antagonists or angiotensin converting enzyme (ACE) inhibitors are being increasingly used as initial therapy when quality of life is important and metabolic neutrality is required. Calcium antagonists are more likely to be effective first-line therapy than ACE inhibitors in patients with a high salt intake, in patients with Raynaud's disease, when angina pectoris is present, and in Black patients. ACE inhibitors are preferred for combination with diuretic agents, and in the presence of congestive heart failure or low salt intake. Experimentally, both calcium antagonists and ACE inhibitors can prevent ischaemic ventricular fibrillation and atheroma. Combination therapy between these 2 drug classes is gaining increasing acceptance because of these theoretical advantages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Individualised selection of antihypertensive therapy. 751 67

From pharmacological investigations and clinical studies, it is known that ACE inhibitors exhibit additional local actions that are not related to hemodynamic changes and that cannot be explained only by interference with the renin-angiotensin system by means of an inhibition of ANG II formation. Because ACE is identical to kininase II, which inactivates the nonapeptide BK and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. ACE inhibition, concentration, and time dependently increased the formation of NO and PGI2 in cultured endothelial cells of different origin and from different species, including humans. The specific B2 kinin receptor antagonist, icatibant, suppressed the ACE inhibitor-induced increase in endothelial cyclic GMP accumulation index for NO-formation and, in parallel, attenuated the increase in PGI2 release. In renovascular models of hypertension associated with a stimulated renin-angiotensin system (two-kidney, one-clip), blood pressure reduction by ACE inhibitors was attenuated by icatibant, whereas in rats with genetic hypertension with normal to low plasma renin, blood pressure reduction through ACE inhibitors was not affected. In experimental atherosclerosis in rabbits, ACE inhibitors were able to preserve endothelial function and vascular reactivity and to reduce surface involvement. In the balloon denudation model of carotid arteries in rats, it was found that ACE inhibition markedly reduced neointima formation. However, when the ACE inhibitor was given together with icatibant, its effect was significantly blunted. Perfusion with ACE inhibitors induced a reduction of the incidence, as well as of the duration, of ventricular fibrillation and improved cardiodynamics and myocardial metabolism. BK perfusion induced comparable cardioprotective effects. In addition, perfusion with ACE inhibitors markedly increased the outflow of BK and related kinins from isolated rat hearts. The antiischemic effect of ACE inhibitors and BK were abolished by the addition of L-NNA (1 x 10(-6) mol/l) or icatibant (1 x 10(-9) mol/l). Similar results were found in dogs and rabbits with myocardial infarction. BK and related kinins also seem to be involved in preconditioning and remodeling. The effect of ACE inhibition in LVH was investigated in rats made hypertensive by aortic banding. ACE inhibition with ramipril, in the antihypertensive dose of 1 mg/kg/day for 6 weeks, prevented the increase in blood pressure and the development of LVH. A lower, nonantihypertensive dose of the ACE inhibitor (10 micrograms/kg/day for 6 weeks) had no effect on the increase in blood pressure or on plasma ACE activity, but also prevented LVH after aortic banding.4+ off
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PMID:Contribution of kinins to the cardiovascular actions of angiotensin-converting enzyme inhibitors. 778 79

A 70-year-old woman with a history of hypertension had been well until 3 years before when she developed atrial fibrillation and subsequently congestive heart failure. The heart failure became worse and she had three fainting spells. Low voltage on electrocardiogram and global hypokinesis on echocardiography were suggestive of cardiac amyloidosis. The patient died suddenly of intractable ventricular fibrillation. Autopsy confirmed heavy infiltration of the myocardium by amyloid.
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PMID:Amyloid disease of the heart. 762 27

Our experience with 18 cases of isolated right ventricular infarction is reported and the literature is reviewed. Chronic lung disease with right ventricular hypertrophy is an important risk factor. Chest pain is the usual symptom at presentation but some cases can have breathlessness, palpitations or syncope. Some cases can have sinus bradycardia, atrial fibrillation or ventricular tachycardia. Atrioventricular block is rare. Cases with pulmonary artery hypertension, extensive right ventricular infarction due to proximal occlusion of the right coronary artery, right atrial infarction or atrial fibrillation can have hypotension and/or systemic venous congestion. A surface electrocardiogram mainly showing changes in leads conventionally considered to represent left ventricle and right-sided chest leads may not show an infarct pattern in some cases. Echocardiography is, therefore, more reliable in diagnosing this condition. The cautious use of small doses of nitrates and diuretics is not hazardous in the absence of hypotension. High doses of steroids and anti-coagulants can be helpful. The prognosis is usually good, although sudden collapse can occur due to ventricular fibrillation, rupture of the right ventricular free wall or a massive pulmonary embolism.
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PMID:Isolated right ventricular infarction. 796 Feb 76

The primary purpose of this study is to examine the influence of the female gender on the early and 1-year post-discharge prognosis after acute myocardial infarction (AMI). Moreover, the therapeutic approaches are compared between the two sexes during the early phase of AMI. We performed a retrospective cohort study of 341 patients, 219 men and 122 women, consecutively admitted to the coronary care unit with AMI. Among the baseline characteristics, the age greater than 70 years, the systemic hypertension and the diabetes mellitus are more represented in women; on the contrary cigarette smoking is prevalent in the male gender. The analysis of laboratory and clinical parameters does not show any statistic differences between the two sexes, except the ejection fraction and the coronary reperfusion. The first turns out to be lower in the females and the second one is more often observed in the males. As for the intra-hospital complications, the cardiogenic shock is prevalent in the female gender, the early mortality gets to 26% in women and 11% in men (p < 0.01). The late mortality during the follow-up does not present any difference between the two sexes. From our data, we conclude that transmural AMI, cardiogenic shock, ventricular fibrillation and 2-3 degree atrio-ventricular blocks are significantly bound to a higher early mortality in women. In them the atrial fibrillation is the only predictor of 1-year mortality. Finally, thrombolysis, beta-blockers and significantly aspirin and heparin (p < 0.05), are less used in the female patients, while diuretics and digoxin are more employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Female gender and acute myocardial infarction: what role does it play in the early and late prognosis]. 799 Nov 58


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