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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the course of coronary heart disease an aneurysmal dilatation of the left ventricle may occur. This may be an additional risk for the patient by changed haemodynamics. Depending on the extent of the aneurysm and the contractile potency of the remaining myocard the cardiac compensation may be sufficient. A reduction of the pump efficiency is not necessarily the consequence. In case there is an increasing cardiac insufficiency by means of a pathologic ventricular filling pressure pulse, the best therapy is digitalis in combination with a reduction of volume by sodium-selective diuretics. Under same haemodynamic conditions the treatment of angina pectoris consists of long acting nitrites in combination with a betablocking agent having some intrinsic activity. Special care for the choic of medicaments has to be taken in relation to the sufficiency of the remaining myocard, if an antiarrhythmic therapy is necessary. If there is no stabilisation of the haemodynamic parameters by conservative therapy, the left ventricular function is meliorated by surgical aneurysmectomy. The data demonstrate, that under resting condition a normalisation and under exercise condition at least a melioration of pulse pressure and circulation is achieved after resection of the aneurysma. A small but measurable decrease in cardiac output under exercise condition is the consequence of a persisting cardiodepressive effect due to the operation.
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PMID:[Ventricular aneurysm and coronary heart disease. Pathophysiology, differential therapy, and postoperative haemodynamics (author's transl)]. 24 99

The effect of the intra-arterial injection of 5 to 10 microng of sodium nitroprusside on the caliber of normal and diseased coronary arteries was evaluated in 21 patients during diagnostic cardiac catheterization. In addition, the effect of intra-graft injection of 5 microng of the same agent on the blood flow in aorta-right coronary artery saphenous vein bypass grafts was also evaluated intra-operatively in two patients. The compound induced an increase in the caliber of both normal and stenosed coronary arteries as well as an increase of flow in the grafts. Consistent with measurements of coronary flow response to sodium nitroprusside, angina pectoris which developed in four patients during cardiac catheterization was immediately relieved and the ischemic ST-segment depression significantly reversed after injection of 5 to 10 microng of the drug into the left main coronary artery. Within the dose range used, the drug caused no significant effect on systemic blood pressure or apparently deleterious electrophysiologic changes. No side effects were observed. We conclude that the primary direct action of sodium nitroprusside in the human coronary artery is vasodilatory.
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PMID:Sodium nitroprusside as a coronary vasodilator in man. I. Effect of intracoronary sodium nitroprusside on coronary arteries, angina pectoris, and coronary blood flow. 30 May 57

The effect of lidoflazine on action potential, membrane currents and contraction of frog atrial fibers was tested using the double sucrose voltage clamp technique. Lidoflazine was found to decrease the sodium conductivity of the heart cell membrane, probably by blocking the sodium channels. The availability of the sodium system at resting potential was slightly enlarged by lidoflazine and the recovery from inactivation was prolonged in most of the preparations tested. A small decrease of the slow inward current and a reduction of phasic and tonic tension was observed. The outward current at higher depolarizations was increased by lidoflazine resulting in a shortened action potential duration. The data suggest that lidoflazine's antifibrillatory properties are less pronounced than those of classical antiarrhythmic agents; but the slight antifibrillatory and negative inotropic effect might be helpful in the treatment of angina pectoris.
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PMID:Effect of lidoflazine on membrane currents and contraction in voltage-clamped frog atrial fibers. 31 39

Hemodynamic monitoring after a single dose (10 mg) of nifedipine in 27 primary hypertensive subjects (diastolic pressure greater than 110 mm Hg) documented that this calcium antagonistic agent exerts a potent arteriolar vasodilating action, which results in prompt (-21% of control at 30 minutes) and persistent (-16% of control at 120 minutes) fall in mean arterial pressure associated with a rise in cardiac output and pulse rate. The same patients received oral treatment for 3 weeks. Hourly pressure readings showed that 1) the antihypertensive response to each dose lasts 8--12 hours; and 2) nifedipine every 6 hours significantly reduced blood pressure throughout the 24 hours, without postural hypotension. Side effect were short-lasting (headache in five patients, palpitation without arrhythmias in eight patients, burning sensation in the face and legs in five patients and sporadic extrasystoles in five patients) and tended to disappear with continued treatment. Development of drug resistance, sodium retention, plasma volume expansion, renin release or angina pectoris were not observed during the study. Although these findings seem to differentiate nifedipine from other vasodilators currently used in the treatment of hypertension, broader experience and more prolonged trials with nifedipine as an antihypertensive agent will be needed before conclusions can be drawn on these particular aspects.
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PMID:Treatment of hypertension with nifedipine, a calcium antagonistic agent. 37 56

1. A quantitative in vitro study has been made of the actions of glyceryl trinitrate and sodium nitrite on vascular smooth muscle (dog femoral artery and saphenous vein; rat portal vein); these have been compared with the actions of papaverine, isoprenaline, salbutamol, pentaerythritol tetranitrate and trimetazidine. 2. Glyceryl trinitrate was more active on the saphenous vein than on the femoral artery in inhibiting noradrenaline and potassium-induced tone. 3. Unlike glyceryl trinitrate, sodium nitrite and isoprenaline, papaverine and diazoxide inhibited noradrenaline-induced contractions of venous and arterial smooth muscle to the same extent. 4. The selective dilator effects of glyceryl trinitrate on venous smooth muscle may explain its action in alleviating the pain of angina pectoris. It is suggested that the use of these three vascular smooth muscle preparations (arterial, and veins with and without spontaneous myogenic activity) is a useful initial screening procedure for prospective antianginal drugs acting by venodilatation.
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PMID:Comparative effects of glyceryl trinitrate on venous and arterial smooth muscle in vitro; relevance to antianginal activity. 40 60

Situations requiring immediate lowering of systemic blood pressure are infrequent. Certain clinical syndromes resulting from or complicated by severe hypertension demand vigorous, usually parenteral, antihypertensive therapy. Such syndromes include (1) diastolic hypertension accompanied by sudden disruption of cerebral function, (2) dissecting or leaking aortic aneurysm; (3) accelerated or malignant hypertension, (4) toxemia of pregnancy when either the fetus' or the mother's life is immediately threatened, (5) some instances of diastolic hypertension and acute left ventricular failure, (6) uncontrolled hypertension in the patient who requires emergency surgery, (7) refractory elevation of the diastolic pressure in the kidney transplant patient, and (8) refractory hypertension complicating myocardial infarction or angina. Drugs useful in acutely lowering blood pressure include diazoxide, sodium nitroprusside, methyldopa intravenously, reserpine intramuscularly, and trimethaphan camsylate intravenously. Use of furosemide reinforces the hypotensive effect of these agents. Theoretical advantages and disadvantages of these agents are not always encountered in clinical use.
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PMID:Hypertension crisis. Recognition and management. 57 54

The effects of orthostatic tilting were studied in 12 mongrel dogs anesthetized with sodium pentobarbital. Orthostasis produced significant decreases in cardiac output and left ventricular dimensions. Secondary decreases in coronary flow and myocardial oxygen consumption were also documented. These changes were attenuated when the animals were pretreated with propranolol. The upright posture may be of value in treatment of angina pectoris.
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PMID:Effects of orthostatic postural changes on myocardial oxygen demands. 84 62

In 12 patients with acute myocardial infarction, seven of whom had high and five low blood pressure measurements, sodium nitroprusside infusions were given to reduce the myocardial oxygen consumption. The dosage was between 20 and 300 mug/min. Sodium nitroprusside led to a considerable reduction of the systemic arterial pressure, while the left ventricular filling pressure was less influenced. In normotensive patients the filling pressure could often not be sufficiently lowered as a too severe reduction of arterial pressure occurred beforehand. In hypertensive patients the relationship between left ventricular filling pressure and arterial pressure was better: in all patients the arterial pressure could be lowered to normal values and the filling pressure also became normal in most cases. Angina pectoris improved markedly in all patients. These results show that sodium nitroprusside has a satisfactory effect on the haemodynamics in hypertensive infarct patients, whereas it is less suitable for the treatment of normo- or hypotensive patients.
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PMID:[Treatment of acute myocardial infarction with sodium nitroprusside (author's transl)]. 92 57

Since the inception of mobile coronary care units (MCCU), patients with sudden cardiac death (SCD) saved by advanced emergency medical technicians (EMT-A) can be studied retrospectively and prospectively. Forty-eight cases of SCD found in ventricular fibrillation (VF) were successfully resuscitated. Only 32% had a myocardial infarction. Most survivors were New York Heart Association (NYHA) class I or II. All class IV survivors with severe congestive heart failure died within 45 days. All class II survivors had angina as the limiting factor. Of all patients with VF, 23% survived. Eighty percent of survivors were class I or II and have resumed previous lifestyles. No clear cut symptom complex was identified. Rescue response time was generally less than five minutes. Intracardiac medications were administered without complications. Empirical administration of sodium bicarbonate correlated poorly with arterial blood gas determinations.
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PMID:Sudden cardiac death: a retrospective and prospective study. 93 9

Trapymin (TM) relaxed excised renal, coronary, pulmonary, femoral and mesenteric arteries and this relaxation was not antagonized by propranolol. The dose-response curve of TM was parallel to that of nitroglycerin and papaverine and steeper than that of dipyridamol or adenosine. TM exerted inotropic and chronotropic actions on excised rat atrium. TM was also effective through the oral route and the effectiveness tended to decrease slightly after repeated use for ten days. TM was effective on vasopressin induced angina in rats and electrocoagulation-induced myocardial infarction. TM suppressed adrenaline-induced arrhythmia but not CaCl2-induced arrhythmia. TM reduced catecholamine content in brain, adrenals and heart but had no influence on monoamine oxidase or dopamine-beta-hydroxylase. TM revealed ganglion-blocking and neuron-blocking actions in cervical ganglion in cats. With propranolol, TM-induced hyperglycemia and reduction in glycogen content in liver and heart was antagonized but TM-induced rise in free fatty acid in serum was not antagonized. Na+-K+ dependent ATPase of bovine heart and P/O ratio of mitochondria of rat heart was not influenced by TM. ADP-induced aggregation of platelets was antagonized by TM. These data indicate that TM induced coronary dilation is partly due to a papaverine like action and also to ganglion-blocking, neuron-blocking and anti-adrenergic action. On the other hand, TM possessed catecholamine release and cardiotonic action as related to beta-receptors.
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PMID:[Pharmacology of cornary dilator agent, trapymin. (2) Analysis of its mode of action]. 124 70


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