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 effects of intravenous infusions of glyceryl trinitrate and nifedipine on systemic haemodynamic function, coronary haemodynamic function, and global myocardial metabolism were compared in two groups of eleven patients with unimpaired left ventricular function undergoing elective coronary artery operation who were anaesthetised with high dose fentanyl. Severe post-sternotomy hypertension developed in three patients in the glyceryl trinitrate group who were resistant to the hypotensive effect of this agent. All patients given nifedipine remained haemodynamically stable. Coronary sinus blood flow and myocardial oxygen consumption increased and coronary vascular resistance decreased after sternotomy in the nifedipine group but not in the glyceryl trinitrate group. There is no satisfactory explanation for the apparently paradoxical increase in myocardial oxygen consumption in the patients given nifedipine. This phenomenon did not appear to be associated with any detrimental effect of left ventricular function. Thus nifedipine was better than glyceryl trinitrate for the control of post-sternotomy hypertension in patients with good left ventricular function. Intravenous nifedipine is not recommended, however, for the intraoperative control of blood pressure in patients with unstable angina or impaired left ventricular function.
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PMID:Influence of glyceryl trinitrate and nifedipine on coronary sinus blood flow and global myocardial metabolism during coronary artery operation. 309 47

Increased levels of an endogenous inhibitor of tissue-plasminogen activator (t-PA) have been thought to relate to the genesis of acute myocardial ischemia. To examine the role of the rapid inhibitor of t-PA, plasma samples were analyzed from 75 patients with chest pain syndrome undergoing coronary angiography (mean age 57 years), 24 patients with clinically documented coronary artery disease (unstable angina, positive exercise stress test or previous history of myocardial infarction; mean age 58 years) and 15 young normal subjects (mean age 26 years). Plasma t-PA inhibitor levels were similar in age-matched patients regardless of the absence or presence (and degree) of coronary artery disease. Plasma t-PA inhibitor levels correlated significantly with age (r - 0.46, p less than 0.005), suggesting an age-dependent decrease in fibrinolytic activity. Plasma t-PA inhibitor levels also correlated significantly with serum triglyceride levels (r - 0.60, p less than 0.001), but not with coronary risk factors such as serum cholesterol, diabetes, hypertension, serum uric acid levels or body weight. Association of high levels of inhibitor of t-PA with hypertriglyceridemia may be of importance in the development of coronary thrombosis, especially in elderly patients. Nonetheless, this study does not suggest a pathogenic role of t-PA inhibitor in coronary atherosclerosis.
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PMID:Plasma tissue plasminogen activator inhibitor levels in coronary artery disease: correlation with age and serum triglyceride concentrations. 310 May 98

The ELISA test was performed on sera of normal donors and patients with myocardial infarction (MI) and essential hypertension (EH) to detect autoantibodies against prostaglandin F2 alpha (a-PGF2 alpha). The a-PGF2 alpha level was much higher after immune complexes dissociation. Baseline a-PGF2 alpha was elevated in EH patients with a sudden rise in blood pressure, and in MI patients without hypertension and unstable angina. MI patients with bradyarrhythmias also had elevated a-PGF2 alpha levels. Baseline a-PGF2 alpha was rather low in the sera of donors, chronic EH patients with hypertension and unstable angina, suggesting that a-PGF2 alpha has a physiological role to play.
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PMID:[Comparative analysis of the levels of anti-prostaglandin F2 alpha antibodies in the normal state and in cardiovascular diseases]. 316 90

By analyzing the simultaneous recordings of M-type echocardiogram of the mitral valve, apexcardiogram (ACG) phonocardiogram (PCG) in 49 healthy persons, 30 patients with II stage hypertension and 39 patients with unstable angina pectoris was established that the opening of the mitral valve coincides with the moment in which the discending arm of the ACG deviates from its tangent (determined by two points--the first is the point of intersection of the ACG with the perpendicular raised from the initial highfrequency vibrations of the aortic component of the II tone: the second is 20 ms from the first on the discending arm of the ACG). The method allows the determination of the exact moment of the opening of the mitral valve and the duration of the isovolumetric relaxation and of the period of the active suction by the ACG and the PCG only. This increases the apexcardiographic potentialities in the functional diagnosis of the left ventricle.
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PMID:[An apex cardiographic method of determining the moment of mitral valve opening and duration of its isovolumetric relaxation]. 320 3

Nitroglycerin and the long-acting nitrates are beneficial in stable and unstable angina pectoris and acute myocardial infarction and as adjunctive therapy in congestive heart failure. Nitroglycerin compounds relax vascular smooth muscle, producing venous, arterial, and arteriolar dilatation. These actions are modulated by stimulation of intracellular cyclic guanosine monophosphate. Nitrate efficacy in ischemic heart disease is due to peripheral venous and arterial vasodilatation that results in decreased myocardial oxygen consumption. Nitrates also dilate coronary arteries and collaterals, reverse coronary vasoconstriction, and enlarge some coronary atherosclerotic lesions. Nitrates improve exercise performance in stable angina pectoris. Intravenous nitroglycerin should be used in the initial treatment of unstable angina. Nitrates may be beneficial in myocardial infarction for control of ischemic pain, acute hypertension, and left ventricular failure. In subjects with congestive heart failure, nitrates reduce symptoms and improve exercise tolerance. Nitrate tolerance is a problem with continuous nitrate therapy. Tolerance is most likely to occur with frequent dosing or the use of long-acting nitrates, particularly transdermal nitroglycerin disks, and can be prevented or reversed with intermittent-dosing regimens.
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PMID:A reappraisal of nitrate therapy. 327 14

Esmolol is the first intravenous, short-acting, titratable beta-blocker available for use in critical care and surgical settings. The predominant pharmacodynamic actions of the drug include a reduction in HR, BP, rate-pressure product, LVEF, and cardiac index. A desirable pharmacokinetic feature of esmolol is its esterase-induced rapid metabolic inactivation, which results in a return of all hemodynamic parameters to pretreatment levels within 30 minutes after discontinuation of the infusion. Control over the magnitude and duration of beta-blockade and the relative cardioselectivity of esmolol make it an ideal agent for use in critically ill patients, including those who, because of other conditions, are at risk if treated with beta-blockers. The clinical indications for esmolol therapy include SVT and perioperative tachycardia and hypertension. In patients with myocardial ischemic conditions (acute myocardial infarction and unstable angina), esmolol was safe and produced clinically significant reductions in HR and rate-pressure product. In general, untoward reactions to esmolol have been minimal, mild, and transient. Although attention must be given to the possibility of systolic hypotension during esmolol administration, this complication often occurs at doses beyond those which provide optimal therapeutic response and may be avoided by titrating to the minimal effective dose. If systolic hypotension occurs, it is reversible by either reducing the dose or discontinuing the esmolol infusion. A nursing plan of care should be developed for patients receiving esmolol therapy. Dosage and administration must be individualized. Careful titration of the esmolol infusion and monitoring of therapeutic and safety parameters by nursing professionals will promote the achievement of maximum beta-blocker effect while avoiding persistent and unnecessary adverse reactions.
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PMID:Esmolol, the first ultra-short-acting intravenous beta blocker for use in critically ill patients. 327 51

Hypertension and ischaemic heart disease often co-exist. Recent studies, using ambulatory ST-segment and haemodynamic monitoring, have shown that myocardial ischaemia may not necessarily be accompanied by angina pectoris. Unless transient myocardial ischaemia is actively sought it may, therefore, be missed and this may have important prognostic and therapeutic implications. Studies investigating the use of beta-blockers, calcium antagonists and nitrates in angina pectoris have shown that these agents have an equal effect on painless as opposed to painful myocardial ischaemia. While there are no currently completed studies demonstrating the prognostic implication of silent ischaemia in stable angina, it is well known that approximately one-quarter of all myocardial infarctions occur without chest pain. Recent investigation in unstable angina showed that silent ischaemia was an important predictor of future coronary events.
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PMID:Hypertension and the ischaemic myocardium. 331 24

With the inception of continuous ECG monitoring with high-fidelity reproduction of the ST-segment, silent myocardial ischemia has been regarded with increasing importance in the detection and management of coronary artery disease. With the aid of a variety of invasive and noninvasive methods, the validity of ST-segment depression as indicative of myocardial ischemia, even in the absence of symptoms, has been adequately documented. In completely asymptomatic subjects with positive evidence of silent ischemia in the exercise ECG or Holter monitoring, the risk of developing a future manifestation of coronary artery disease may be up to ten-fold higher than in individuals with negative tests In patients with established coronary artery disease, concomitant use of continuous ECG monitoring and exercise testing, methods which complement each other rather than being mutually exclusive, a substantial number of patients with otherwise typical angina pectoris may be found to have silent ischemic episodes. An adequate differentiation between those with symptomatic and those who are asymptomatic based on characterization with respect to age, sex, hypertension, coronary anatomy, etc., has not been successful. Patients with silent ischemia during exercise may also exhibit more episodes of silent ischemia during daily activities and up to 75% of ischemic episodes may be asymptomatic. In general, however, silent ischemia during exercise appears more common than silent ischemia only during daily activities. In the latter case, since there is usually no increase in heart rate, the pathophysiology is regarded as dissimilar from that associated with exercise-induced ischemia. While the presence of silent ischemia appears quite common in patients after acute myocardial infarction, its occurrence, to date, has not been confirmed to carry additional risk, whereas in unstable angina, the association of silent ischemia is indicative of a higher probability of subsequent cardiac events.
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PMID:Silent myocardial ischemia: diagnosis, clinical significance and management. 331 17

This study examines the risk factor profile, in-hospital course and outcome of 337 women and 643 men admitted with a first episode of acute coronary insufficiency or myocardial infarction. The women were older than the men and had a risk factor profile dominated by hypertension and hypercholesterolemia rather than smoking. Women had a higher rate of unstable angina than did men after adjustment for age distribution. Women with acute infarction showed a higher rate of complications, which was associated with their greater age. They had a higher in-hospital mortality rate (12.6%) than did men (6.6%, p = 0.002). A logistic regression was used to adjust mortality and complication rates for differences in age between the sexes. When this was done, women and men had similar in-hospital prognoses. It is concluded that differences in risk factor profile may result in differences between the sexes in the expression of acute coronary heart disease, but that gender as such does not exert an independent influence on short-term prognosis in this disease.
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PMID:Risk factors and in-hospital course of first episode of myocardial infarction or acute coronary insufficiency in women. 335 38

Although lipids have received most attention in relation to atherosclerosis, vessel injury also has a role in the development of atherosclerotic lesions. Thrombi that form at sites of injury can be incorporated into the wall, causing thickening, and platelets that adhere to damaged vessel walls release a growth factor (PDGF) that stimulates smooth muscle cell proliferation. The early lesions of atherosclerosis are focal and develop around vessel orifices and branches in relation to the patterns of blood flow and areas of increased permeability and endothelial cell damage. Platelets also contribute to the complications of advanced atherosclerosis caused by occlusive thrombi, thromboembolism, and spasm. The causes of vessel wall injury are not established, although there is evidence pointing to disturbed blood flow, hypertension, antigen--antibody complexes, complement, materials originating from platelets and white blood cells, bacteria, endotoxin, viruses, smoking, dietary lipids, homocystinemia, diabetes, other metabolic disorders, and stress. Platelets do not adhere to intact endothelium, but they adhere to the constituents of the subendothelium, release the contents of their granules (including PDGF), and form thromboxanes. If blood flow is disturbed, platelet--fibrin thrombi can form at sites of injury. Platelet adherence to a damaged wall does not require von Willebrand factor except under conditions of high wall shear. Repeated injury of a vessel wall leads to the development of lipid-rich atherosclerotic lesions, even in normocholesterolemic animals, but these lesions do not form if the experimental animals are made thrombocytopenic before injury is induced. Measurable changes in platelets that are associated with the clinical complications of atherosclerosis include shortened survival, release of granule contents (platelet factor 4, beta-thromboglobulin, thrombospondin), formation of thromboxanes, and decreased buoyant density. "Antiplatelet drugs" such as aspirin are proving to be beneficial in selected groups of patients, such as those with unstable angina. Thromboxane synthetase inhibitors and agents that block the thromboxane receptor on platelets are under investigation. Long term administration of "antiplatelet drugs" to affect the rate of development of atherosclerosis seems neither feasible nor desirable. Modification of dietary and smoking habits and control of hypertension are more likely to be beneficial for most individuals.
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PMID:The role of platelets in the development and complications of atherosclerosis. 351 36


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