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)

In a cohort of 417 patients admitted consecutively to the Coronary Care Unit for acute myocardial ischemia (unstable angina pectoris in 121, acute myocardial infarction in 296 patients) 21 cases of non arrhythmogenic sudden death occurred within 24 hours after admission. 16 of these patients suffered from acute myocardial infarction and 5 from unstable angina pectoris. Cause of death was cardiac rupture in 12 and pump failure in 4 patients with acute myocardial infarction, whereas all patients with unstable angina pectoris died from pump failure. Patients with cardiac rupture within 24 hours after admission, had significantly higher systolic and diastolic blood pressure in comparison with the other groups and with patients dying from cardiac rupture on the third day, or later. All patients dying from pump failure with unstable angina pectoris and one of the patients dying from pump failure with acute myocardial infarction had beta blocker therapy. Beta blockers were given to 68 of the patients with unstable angina pectoris. Acute pump failure occurred in this group only. The risk of pump failure with beta receptor blocking drugs is indicated by angina decubitus, marked dyspnea during anginal attacks (even in patients free of signs of cardial insufficiency outside their attacks) and a lack of responsiveness to beta blocking therapy. In these patients rapid coronary angiography and bypass surgery seems to be the prefered method of management. Beta blockers should not be given to these patients or discontinued in cases which lack responsiveness.
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PMID:[Non arrhythmogenic sudden death as complication of coronary heart disease]. 4 54

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

Thirty-two patients with large postinfarction left ventricular aneurysms shown at operation to consist of fibrous tissue are reported. All had angina and/or breathlessness, and none had a history of embolism. Thirty were correctly diagnosed by left ventricular cineangiography. Two of the 3 patients with inferior and 1 with an anterior aneurysm had associated ventricular septal defects, and 3 patients with an anterior aneurysm had mitral regurgitation. All had major coronary arterial lesions and 68 per cent had double or triple vessel disease. The aneurysm was excised in all patients; in 15 this was combined with saphenous vein bypass grafting of coronary arteries supplying surviving myocardium, in 3 with closure of a ventricular septal defect, and in 3 with mitral annuloplasty or replacement. Operative mortality was 6-2 per cent, and 79 per cent of the survivors are asymptomatic with average follow-up period of 18 months after operation.
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PMID:Surgical treatment of postinfarction left ventricular aneurysm in 32 patients. 13 29

A patient with moderate aortic stenosis had severe hypertrophy and a typical hourglass appearance of the left ventricle. His effort-induced angina and dyspnea responded to treatment with verapamil. We suggest that the aortic stenosis resulted in secondary hypertrophic cardiomyopathy which may be treated by calcium antagonists.
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PMID:Co-existing aortic stenosis and secondary hypertrophic cardiomyopathy manifested by an hourglass left ventricle. Successful treatment with verapamil. 15 29

Two hundred consecutive catheterized patients with unstable angina pectoris were reviewed to find clinical and noninvasive indicators of left main coronary artery disease (greater than or equal to 50% lesion). Thirty-five patients (17.5% of total) had left main coronary artery disease. There were no differences between patients with and without left main coronary artery disease in age, sex, results of resting electrocardiogram, congestive heart failure, dyspnea during pain, duration of longest pain, arrhythmias, response to medical therapy, or other risk factors. Crescendo angina pectoris (worsening of pre-existing angina), transient ST-segment depression with pain, simultaneous anterior and inferior ST changes during pain, and fluoroscopic calcification of the left main coronary artery were all significantly more common in patients with left main coronary artery disease. However, low sensitivity or low predictive value, or both, limit the usefulness of these clinical predictors. Left main coronary artery disease cannot be reliably predicted in patients with unstable angina pectoris before coronary arteriography.
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PMID:Clinical indicators of left main coronary artery disease in unstable angina. 15 94

Revascularization of the heart is a means of relieving symptoms of coronary artery disease--such as angina, fatigue, and dyspnea. The question of whether revascularization prolongs the life of the patient has been debated. My colleagues and I have reviewed our years of experience with patients treated by implantation of internal mammary arteries into the ventricles. We have compared our series with other groups of patients treated medically. Our conclusion is that revascularization via internal mammary artery implants does increase longevity.
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PMID:Evidence that revascularization by ventricular-internal mammary artery implants increases longevity. Twenty-four year, nine month follow-up. 24 Sep 82

The relationships between aortic stenosis, coronary artery disease, angina pectoris, and myocardial infarction were examined in 173 patients with isolated calcific aortic stenosis who had coronary arteriography as well as cardiac catheterization. All were over age 40 and had definite cardiac symptoms; 156 later had aortic valve replacement. Coronary lesions narrowing the lumen by 50% or more were present in 37% of patients aged 40 to 59 and 68% of those aged 60 to 82. Coronary disease was present in 64% of patients with angina pectoris and 33% of those without angina. Angina which occurred only in association with dyspnea on exertion was associated with coronary disease in 45% of instances, whereas angina which also occurred on exertion without any dyspnea or which occurred with emotional stress, after meals, during sleep, or at rest unprovoked was associated with coronary disease in 80% of instances. Patients with coronary disease without any chest pain or with atypical pain considered nonanginal were men, usually over age 60, with congestive heart failure as the predominant symptom. Electrocardiograms showing transmural inferior or anterolateral infarction nearly always indicated coronary disease, while QS patterns in Leads V1-2 occurred frequently with normal coronary arteries. Serum cholesterol was elevated in 23% of those with coronary disease and 8% of those without. A group of patients with moderate aortic stenosis could be identified, with aortic valve areas of 0.55 to 0.80 cm. per square meter, in whom coronary disease was the sole or chief cause of symptoms. The operative mortality rate with aortic valve replacement was 9.6% in those with coronary disease and 1.4% in those without significant coronary disease. Coronary disease is frequently present in patients with calcific aortic stenosis, particularly in those over 60, those with angina, and those with symptoms despite only moderate aortic stenosis. The type of anginal syndrome, the ECG evidence of transmural infarction, and the coronary risk factors provide additional clues for clinical diagnosis.
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PMID:Aortic stenosis, angina pectoris, and coronary artery disease. 30 Feb 16

Coronary angiography was performed before and after coronary revascularization in 67 patients. The interval between studies ranged from 1 to 38 months (average 9.9). The patients were separated into four clinical groups on the basis of their symptoms at the time of restudy; Group I, 13 asymptomatic patients; Group II, 19 patients with nonanginal chest pain (18 cases) or dyspnea (1 case); Group III, 12 patients whose angina was relieved but not eliminated; and Group IV, 23 patients whose angina was not alleviated. The graft patency rate was 72 percent in Group I, 78 percent in Group II, 61 percent in Group IIII and 34 percent in Group IV. The sum of diseased, but not bypassed and unsuccessfully bypassed arteries per patient was 1.6 in Groups I and II. 2.9 in Group III and 4.0 in Group IV. The incidence of perioperative myocardial infarction, defined using enzymatic and electrocardiographic criteria, was 8 percent for Group I, 26 percent for Group II, 25 percent for Group III and 52 percent for Group IV. Anginal relief after coronary bypass surgery is achieved by successful and complete revascularization rather than by perioperative myocardial infarction.
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PMID:Mechanism of relief of angina after coronary bypass surgery: an angiographic study. 31 47

Forty patients with persistent or recurrent angina after an aortocoronary bypass procedure underwent a second operation. The cause of recurrent angina, defined by angiography, was thought to be isolated graft failure in 13 patients, progression of disease in ungrafted vessels in 4, incomplete revascularisation in 2, and stenoses distal to patent grafts in 1. More than one factor was responsible in 20 patients. There was 1 early postoperative death and 3 perioperative myocardial infarctions. Thirty-four patients have been followed for more than 3 months (4 to 63 months). Of these, 17 had previously bypassed vessels regrafted and 5 are sympton free, 4 have mild angina, and 8 have severe angina. Ten patients had previously ungrafted vessels grafted and 4 are sympton free, 3 have mild angina, 2 have severe angina, and 1 is limited by breathlessness. Seven patients had a combined procedure and 4 are sympton free, 1 has mild angina, and 2 have severe angina. Reoperation can be carried out safely but the results are less satisfactory than for a primary procedure.
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PMID:Reoperation for recurrent angina. 31 82

Knowledge and due consideration of the natural history of valvular heart disease are prerequisites for their operative therapy. Presumptive mortality and morbidity of the surgical intervention must be weighted against the expected prognosis under medical treatment alone. The timing of the operation depends on these considerations. Mitral stenosis and the chronic forms of mitral and aortic incompetence have similar natural histories and for both signs and symptoms are good indicators for an eventual progression of the condition. The length of the period during which the patient is free of complaints may be quite variable but a critical change in the natural history comes about once the disease causes signs and symptoms. Surgical repair is indicated when the patient reaches stage III according to the NYHA-classification. The prognosis is worst for aortic stenosis, in particular due to the danger of sudden death. Patients with high pressure gradients are at particularly high risk; this holds even true for those patients which are not yet suffering from any complaints. The prognosis becomes even more serious, when signs such as dyspnea, anginal pain, or syncopal attacks occur. Prognosis and indication for surgical intervention cannot be evaluated reliably by considering only the clinical signs without knowledge of hemodynamic parameters. Acute mitral and aortic incompetence, in paricular when they occur during baterial endocarditis, must be observed very closely because of their most serious prognosis; if necessary, emergency surgery must be carried out in these cases.
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PMID:[Natural history in patients with mitral- and aorticvalve-disease (author's transl)]. 32 60


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