Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six patients in sinus rhythm with congestive heart failure due to either myocardial infarction or cardiomyopathy, were given oral frusemide to eliminate oedema. Symptomatic relief occurred as body weight was reduced, and after a 'dry' basal weight had been achieved, progressive-load exercise testing was done to examine any benefit that derived from adding oral digoxin to the diuretic. Three pairs of sub-maximal exercise tests were done at intervals over three months, and the responses of each patient when using digoxin and diuretics were compared with those when using diuretics alone. One patient did not complete this study, because more frequent premature beats and increased angina followed the withdrawal of digoxin. For the five patients who completed three pairs of tests, there was no significant change in symptoms, in workload achieved, or in heart rate, respiratory rate, ventilation and respiratory quotient, whether digoxin was added or removed. It is concluded that in these patients where salt and water retention was controlled with diuretics, digoxin did not improve the capacity for exercise, and it is suggested that for such patients with myocardial disease in sinus rhythm, treatment should begin with diuretics.
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PMID:The clinical value of digoxin in patients with heart failure and sinus rhythm. 75 Oct 85

Rapid and slow venous infusion of various doses of Verapamil in a mixed series of 185 cases of arrhythmia since 1968 is reported. Results and electrophysiological and ECG changes observed for each type of arrhythmia examined are considered separately: atrial fibrillation-flutter, supraventricular paroxystic tachycardia (atrial and/or junctional), and hyperkinetic ventricular arrhythmia. An association of i.v. Verapamil and a quinidine salt per os is suggested as an alternative to cardioversion in cases of recent atrial fibrillation-flutter. Results obtained in the treatment of arrhythmia due to electrical instability following angina and of angina following arrhythmia are also described. A study of His potentials as the premiss for using Verapamil in subjects with stimulus conductivity changes, including W.P.W. syndrome, is also reported. I.v. Verapamil was used in association with atrial and/or ventricular electrostimulation, and/or with electrical counter-shock in cases of arrhythmia (mostly supraventricular) that were especially refractory. Attention is drawn to the use of Verapamil in the control of arrhythmia after electrical cardioversion.
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PMID:[Anti-arrhythmic therapy with verapamil by intravenous infusion]. 112 29

With the availability of a wide selection of antihypertensive drugs acting by different mechanisms, it should be possible to match the requirement of individual patients with the pharmacological and clinical properties of an appropriate agent. Although the concept of stepped-care therapy is now largely outdated, therapy must be initiated with one agent. Diuretics remain a first-choice option in the elderly and in Black patients, as do calcium antagonists. In patients with ischaemic heart disease or enhanced adrenergic drive, beta-blockers are preferred. Calcium antagonists or ACE inhibitors are finding increasing use as initial therapy when quality of life is important and metabolic neutrality is required. The choice of antihypertensive agent may be limited by adverse effects, e.g. pedal oedema with nifedipine, constipation with verapamil, and cough with ACE inhibitors. Certain advantages are evident for both calcium antagonists and ACE inhibitors. Calcium antagonists are more likely to be effective first-line therapy than ACE inhibitors in Black patients, in those with a high salt intake, in patients with Raynaud's disease, and when angina pectoris is present. ACE inhibitors are preferred for use in combination with diuretic agents, and in the presence of congestive heart failure or low salt intake. Combination therapy between these 2 drug classes is finding increasing acceptance because of its many theoretical advantages, and may provide a means of maximising benefit.
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PMID:Choosing the correct drug for the individual hypertensive patient. 128 79

Nicorandil, a potent coronary vasorelaxant used in the treatment of angina, has differential effects on arteries and veins in vivo. To explain this phenomenon, experiments were designed to characterize the relaxant and inhibitory actions of this compound on canine isolated arteries and veins. Paired rings of canine coronary, femoral, and saphenous arteries and saphenous veins were suspended at optimal length for isometric tension recording in organ chambers containing physiologic salt solution at 37 degrees C and gassed with 95% O2-5% CO2. In certain experiments, one ring of each pair was denuded of the endothelium. Removal of the endothelium did not affect nicorandil-induced relaxations of contracted blood vessels. Nicorandil exerted a differential relaxant effect on arteries and veins contracted with KCl (order of potency: saphenous vein greater than coronary artery greater than femoral artery). No difference in sensitivity to nicorandil was observed in arteries and veins contracted with prostaglandin F2 alpha. Contractions of saphenous arteries and veins to norepinephrine (NE) were equally sensitive to the inhibitory action of nicorandil. However, contractions of saphenous veins induced by sympathetic nerve stimulation were more sensitive to nicorandil than were contractions of saphenous arteries. Furthermore, nicorandil did not affect contractions to phenylephrine in saphenous veins, although contractions to B-HT 920 were virtually abolished by the compound. Saphenous veins contracted with St 587 were more sensitive to the relaxant action of nicorandil than when contracted with phenylephrine. These results suggest that nicorandil inhibits preferentially contractions of canine arteries and veins mediated by alpha 2- rather than alpha 1-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of the antianginal drug nicorandil on canine arteries and veins. 169 40

The prevalence of hypertension increases with age. The majority of the hypertensive population is over age 55. Although the treatment of systolic hypertension remains incompletely understood, the reduction of diastolic hypertension with pharmacotherapy has been shown to reduce complications from hypertension in persons over age 55. The older hypertensive patient is at risk for the same complications as the younger patient: angina, myocardial infarction, arteriosclerosis obliterans, stroke, myocardial hypertrophy, congestive heart failure, and renal failure; the risk of sudden death and multi-infarct dementia in the older patient may be somewhat higher. The older hypertensive individual may have reduced plasma volume and defective salt and water conservation, reduced renal function, impairment of baroreceptor reflexes and sympathetic reactivity, and altered drug pharmacokinetics, or may have arteriosclerosis leading to pseudohypertension. Many circumstances interfere with adequate compliance with therapeutic regimens among the elderly. Concomitant medical conditions increase the possibility of drug interactions and require that the practitioner be able to adjust the antihypertensive program to the patient.
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PMID:Treatment considerations for the hypertensive patient over age 55. 189 46

Echocardiographic measurement of left ventricular mass has provided a way of evaluating the undesirable effects of high blood pressure on the heart in the same way as for obesity, excess salt intake and blood hyperviscosity. Recently, the left ventricular mass was shown to correlate (r = 0.81) with the hemodynamic stimuli of blood pressure, stroke volume and left ventricular contractility. Prospective trials at Cornell and Framingham indicate that left ventricular mass is a powerful predictive factor of the risk of complications in hypertension. In the first of these trials, we demonstrated in a 5 year follow-up study of 140 men with uncomplicated hypertension that the incidence of death, myocardial infarction or angina requiring myocardial revascularisation, was four times greater in patients with increased left ventricular mass and that this association was independent of the blood pressure levels. Then, in a 10 year follow-up study of hypertensive patients of both sexes, we established that the left ventricular mass was the most powerful predictive factor of mortality and morbidity and that this was so marked (15% death rate in subjects with LVH vs 1% in subjects with normal left ventricular mass--p less than 0.00001--, cardiovascular accidents in 26% of subjects with LVH compared with 12% in subjects with normal left ventricular mass--p less than 0.0001) that only left ventricular mass and age were independant predictive factors of morbid events in multiple variable analysis. In the Framingham study, the frequency of coronary events in a 4 year follow-up period of healthy subjects from the original cohort (average age 69 years) was significantly related to the left ventricular mass and independent of other risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relationship between left ventricular mass and prognosis of arterial hypertension]. 208 Aug 92

The specific competitive alpha 1-postsynaptic blocking action and haemodynamic effects of prazosin (Minipress) have been summarized. Prazosin causes dilatation of arterioles and veins, reduces total peripheral resistance as well as preload and afterload. Cardiac output does not change at rest, stroke volume and subsequent cardiac output increase during exercise. The changes in heart rate have non-significant. It does not cause sympathetic counter-regulation, plasma renin activity does not increase, aldosterone level decreases, salt- and fluid retention may rarely be observed. It does not provoke angina. The authors report on the results of their examinations with the first dose of prazosin in 61 patients (in 33 cases by the double-blind cross-over method by placebo control), and summarize the observations made with the drug in long-term treatment in Hungary. The authors and other teams used prazosin as a long-term treatment (of approximately 3 months) in combination with other drugs in a total of 344 patients, and as monotherapy in 159 patients. In the course of combination treatment side-effects were observed in 15% of the patients (dizziness, headache, weakness, occasionally palpitation). During monotherapy, side-effects occurred in 12% of the patients (tachycardia, headache, weakness, dizziness). Hungarian results confirm the usefulness of prazosin in all stages of hypertension. It is effective in 30-35% of the cases as a monotherapy (this rate is congruent with the efficacy of beta-blockers, calcium antagonists and antihypertensive drugs of central action). Earlier prazosin had been used as a third agent in combination treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the action of Minipress. Examinations in hypertension. 257 64

Coronary artery vasomotion may be important in the pathogenesis of angina pectoris. Numerous experimental studies demonstrated accentuated arterial vasomotion in endothelium-damaged vessels. We examined interactions of stenosis, arterial vasoconstriction, and endothelium denudation in a stenosed artery preparation in vitro. Canine carotid arteries and porcine coronary arteries were perfused with a physiological salt solution under constant pressure and a fixed distal resistance. Pressures at the proximal and distal ends of the artery, as well as the flow, were continuously recorded. Hemodynamic responses to serotonin, norepinephrine, and angiotensin II were separately studied. In intact arteries without stenosis, the agonists produced a 30-40% reduction in lumen diameter without altering flow or distal pressure. After a luminal stenosis was created, vasoconstriction produced by the agonists decreased flow and increased the pressure gradient across the stenosis. Flow decreased to (or near) zero, indicating occlusion at the stenotic site. After endothelial loss, this effect was amplified, demonstrating occlusion of the artery and suppression of the flow at significantly (P less than 0.05) lower concentrations of agonist (0.1-0.3) compared with endothelial intact arteries. These studies illustrate 1) the necessity for the presence of stenosis in large arteries for vasoconstriction to impair flow and 2) the protecting effect of intact endothelium in blunting the effects of arterial vasoconstriction in stenosed vessels. Through the reciprocal interaction of arterial stenosis, vasoconstriction, and endothelial damage, ischemic events associated with certain types of vasomotion can be explained.
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PMID:Mutual interaction of vasoconstriction and endothelial damage in stenotic arteries. 292 45

Reduced responsiveness of platelets to prostacyclin, reported in vitro in patients with coronary artery disease, has been thought to be a factor predisposing toward coronary thrombosis and vasospasm as a result of enhanced in vivo release of cyclic endoperoxides and thromboxane A2 by the platelets. In this study, specific binding of prostacyclin to intact platelets was determined in patients with coronary artery disease by direct binding studies using 9-3H-prostacyclin sodium salt. In addition, the inhibitory effect of prostacyclin on primary aggregation induced by adenosine diphosphate and cyclic adenosine monophosphate (cyclic AMP) accumulation stimulated by prostacyclin was examined. Twenty patients with angiographically documented coronary artery disease and stable angina, 8 patients with acute myocardial infarction, 14 healthy volunteers and 10 patients with normal angiograms were studied. In patients with stable angina, binding capacity and affinity of platelet prostacyclin binding sites and prostacyclin-induced cyclic AMP accumulation were not different from those of control subjects. In patients with acute myocardial infarction, however, binding capacity of platelet prostacyclin receptors was significantly reduced (0.69 +/- 0.45 versus 1.35 +/- 0.37 pmol/10(9) platelets, p = 0.001) and the postreceptor response, represented by platelet responsiveness to prostacyclin and prostacyclin-induced cyclic AMP synthesis, was impaired. Because all patients with myocardial infarction were receiving intravenous heparin and nitroglycerin, which might interfere with platelet prostacyclin binding, competition experiments were performed in vitro. Neither heparin (3 to 250 IU/ml) nor nitroglycerin (0.8 to 22 microM) displaced specifically bound 9-3H-prostacyclin. L-Epinephrine in concentrations up to 10 microM also exhibited no competition with specific platelet prostacyclin binding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet prostacyclin binding in coronary artery disease. 301 61

The clinical use of calcium antagonist drugs in coronary artery disease preceded knowledge of the mechanism of their action. Basic research into their pharmacological actions and development of a wide range of compounds which block calcium entry into cells enabled clinicians to greatly expand the indications for their use. Thus the calcium antagonists were rediscovered and found to be potent anti-anginal drugs when used in adequate dosage for effort related angina. Knowledge of their potent relaxing action on vascular smooth muscle led to their use in coronary artery spasm. The exact trigger mechanism/s for spasm and the reason for enhanced vascular reactivity remain unclear, perhaps explaining the failure of specific antagonist therapy. Calcium antagonists acting nonspecifically inhibit both induced and spontaneous attacks of vasospastic angina. They may favourably influence the prognosis and are now drugs of first choice for this condition. The vasodilator action of these drugs has most recently been utilized to treat hypertension, with efficacy confirmed in many controlled trials. Unlike other vasodilators, the calcium antagonists reduce blood pressure without salt and water retention, and with mild or no stimulation of renin, aldosterone, or sympathetic nervous overactivity, and without postural effects. This spectrum of action makes them ideal therapeutic agents, and current guidelines are changing to include calcium antagonists as first or second line therapy.
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PMID:Calcium antagonist drugs in the treatment of coronary spasm, effort angina and hypertension. 330 67


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