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

Chronic aortic valve disease involving stenosis, regurgitation or both is insidious and progressive. Severe valvular dysfunction may be present for years without symptoms, but functional deterioration is often rapid once congestive heart failure, angina or syncope with effort is present. As the severity of aortic stenosis may not be easy to assess clinically, the relative usefulness of various tests is considered in this paper. The difficulty with chronic aortic regurgitation lies not in diagnosing the problem but in detecting early left ventricular dysfunction in time to perform the surgery that can prevent further functional deterioration. Patients with significant aortic valve disease should undergo surgery when the important symptoms of dyspnea, angina or syncope with effort first appear. Surgery should also be considered in selected patients with aortic regurgitation in whom left ventricular function has diminished even without symptoms.
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PMID:Natural history and management of chronic aortic valve disease. 703 96

A 48-year-old man had angina pectoris and symptoms of heart failure. Cardiac catheterization showed severe aortic stenosis and regurgitation, and he underwent aortic valve replacement in 1976 with a 23-mm Carpentier-Edwards aortic porcine heterograft. Initially there was symptomatic improvement, but one year later the patient had the onset of dyspnea and exertional chest pain that became progressively more severe over the next three years. Repeat cardiac catheterization was performed 45 months after valve implantation, and a 76 mm Hg peak to peak and a 44 mm Hg mean systolic gradient across the aortic bioprosthesis were recorded. The porcine heterograft was surgically explanted and found to be obstructed by a subvalvular thrombus that appeared to arise from the junction of the aortic and mitral valve annuli.
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PMID:Subvalvular thrombotic obstruction of an aortic porcine heterograft. 707 13

In 46 patients with aortic valve disease, coronary sinus blood flow was measured using a continuous thermodilution method both at rest and during isometric handgrip exercise. All patients had normal coronary angiograms. The patients were separated into three groups: Group I, 12 patients with aortic stenosis (systolic gradient 72 +/- 12 mm Hg); Group II, 15 patients with both aortic stenosis and regurgitation; Group III, 19 patients with aortic regurgitation. At rest, the coronary sinus blood flow was two to three times normal. However, when corrected for left ventricular mass (ml/100 g), flow was within normal limits. The ratio diastolic pressure-time index/systolic pressure-time index (DPTI/SPTI) was decreased in all three groups at rest. During isometric exercise, coronary sinus blood flow increased significantly: by 60 percent in Group I, by 88 percent in Group II and by 118 percent in Group III. There was a significant reduction of the DPTI/SPTI ratio. Of the 18 patients with angina on effort during the test, 7 were in Group I, 6 in Group II and 5 in Group III. There were no differences in the coronary sinus blood flow between the patients with angina and those who were pain-free, either at rest or during exercise. Angina pectoris does not appear to be caused by a failure of coronary blood flow to increase. There was no discrepancy between myocardial demand, as measured by the pressure-time index and coronary blood flow. However, the DPTI/SPTI ratio was significantly lower during exercise in the patients with angina than in those who were pain-free. Underperfusion of the subendocardial muscle seems to be a causative factor in the patients with angina.
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PMID:Coronary sinus blood flow at rest and during isometric exercise in patients with aortic valve disease. Mechanism of angina pectoris in presence of normal coronary arteries. 746 66

In recent years, coronary artery bypass grafting has been extended to include patients with very low left ventricular ejection fractions. Should concomitant mitral valve regurgitation be corrected simultaneously? Between January 1990 and July 1994, 43 patients with preoperative left ventricular ejection fractions < or = 25% and echocardiographic evidence of concomitant mitral valve regurgitation (grade I, 18 patients; II, 19 patients; and III, 6 patients) underwent primary coronary artery bypass grafting. None of these patients underwent simultaneous mitral valve surgery. Twenty-four patients (56%) had pulmonary artery pressures > or = 40 mmHg (pulmonary hypertension). The mean preoperative left ventricular ejection fraction was 18.7% +/- 4.4% (range, 10% to 25%), and the mean pulmonary artery pressure was 45.6 +/- 15.8 mmHg. The average of number of grafts per patient was 4.5 +/- 1.5. Five patients underwent simultaneous repair of a left ventricular aneurysm. The hospital mortality rate was 4.7% (2/43). Transient low cardiac output occurred postoperatively in 13 patients (30%). Sixteen patients (37%) had no postoperative complications. The average follow-up of the 41 hospital survivors was 6 months (range, 1 to 32 months). One patient died 8 months after surgery for an overall mortality rate of 7%. Another 2 patients had graft occlusions that did not require reoperation. In the 40 surviving patients, follow-up echocardiography revealed that 37 patients (93%) had either no mitral valve regurgitation or only very mild mitral valve regurgitation (grade I). Three patients had grade II mitral valve regurgitation, but none required mitral valve surgery. The New York Heart Association functional class improved significantly in all hospital survivors (from 3.4 +/- 0.6 to 1.7 +/- 0.7; p > 0.001), and left ventricular ejection fractions rose from 19.0% +/- 4.6% to 42.0% +/- 8.3%. Coronary artery bypass grafting is possible in patients with very low left ventricular ejection fractions who present with 2- or 3-vessel disease, significant coronary artery stenoses (less than or equal 70%), and angina. The mortality rate is acceptable and morbidity is low. If there is no rupture of papillary muscle or chordae, concomitant ischemic mitral regurgitation (grades I through III) seems to return to normal after coronary artery bypass grafting and, therefore, does not need to be corrected surgically during the primary operation.
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PMID:Mitral regurgitation in patients with coronary artery disease and low left ventricular ejection fractions. How should it be treated? 758 Mar 62

Occult or overt but delayed cardiac disease after thoracic radiotherapy for Hodgkin's disease may be common. Detailed cardiac evaluation was performed in 108 patients, mean age 46 +/- 6.2 years, with Hodgkin's disease at 175 +/- 43 months after irradiation. The study protocol included clinical examination, graded treadmill exercise test and echocardiography. Some patients with angina pectoris, previous myocardial infarction and an abnormal ECG were studied by thallium-201 scintigraphy, cardiac catheterization and coronary angiography. Cardiac disease was found in 12 patients (11%). Three patients had angina pectoris, one patient had myocardial infarction, two complained of dyspnea on effort and two had congestive heart failure. At catheterization, constrictive pericarditis was diagnosed in four patients; in two additional patients an occult constrictive pericarditis was found. One patient had both mitral and tricuspidal regurgitation and one had mitral regurgitation alone. Eight patients (7.4%) had severe coronary artery disease; four of these had associated constrictive pericarditis. Four patients had a pericardiectomy and another four had undergone coronary artery by-pass graft. Two patients died after operation from persistent pericardial constriction. It is concluded that the incidence of delayed cardiac disease after radiotherapy is relatively high; chronic pericardial disorders and coronary artery disease are the most frequent manifestations of this disease. Standard surgical treatment may be beneficial because of the relative youth of these patients.
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PMID:Cardiac disease after chest irradiation for Hodgkin's disease: incidence in 108 patients with long follow-up. 760 65

Chronic Esophageal reflux induces reflux esophagitis, which is a common finding in gastroenterological practice. Reflux esophagitis produce symptoms like pirosis, regurgitation and in some cases respiratory complains resembling asthma or angina-like chest pain. The pathophysiology of this disease is based on a multifactorial origin, which usually results in the chronic evolution of the disease. In recent years, there have appeared new evidences pointing out to alterations in the relaxing mechanisms of the lower esophageal sphincter; however, some patients having reflux esophagitis show normal shincteric pressure. The sweep action of esophageal smooth muscle is a key point for sending back to stomach the eventually refluxed material; it has been demonstrated that this sweeping action is impaired in many patients having reflux esophagitis. Incompetence of lower esophageal sphincter seems to be related a local to neural alteration rather than to smooth muscle functional disturbance. Recent findings stablis a link between local nitric oxide release and relaxation of the lower esophageal sphincter. Esophageal mucosaldisplay an intrinsic resistance to HCL, pepsin, bilis and enzymes deleterious action by a blockade of back-defusion of hydrogen ions contained in the refluxed material. Nevertheless, some other luminal and non-luminal factors are involved in this mucosalprotection. When these intrinsic resistance factors are abated, tisular lesions like ersion, ulcer and Barret's mucosal changes can occur; is of particular interest because its potential malignant evolution. Esophageal reflux usually resolves with medical treatmen, but in some particular cases surgical correction is indicated for improving the antireflux barrier.
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PMID:[Reflux esophagitis]. 776 23

We experienced a rare case of Marfan's syndrome with annulo-aortic ectasia, aortic regurgitation and Prinzmetal's variant angina. In a modified Bentall's operation (button technique), perioperative severe coronary artery spasm occurred in spite of the preventive use of nitroglycerin infusion, which resulted in profound ventricular fibrillation and subsequent chordal rupture of the mitral valve with Sellers IV regurgitation. Use of nicardipine contained in cardioplegia, continuous infusion of nicardipine and nitroglycerin after aortic declamping completely prevented coronary spasm throughout the course of a second surgery for mitral valve replacement. It is worthy to report this case because of rarities such as Marfan's syndrome accompanied by Prinzmetal's variant angina, perioperative coronary artery spasm in modified Bentall's operation, and perioperative chordal rupture of the mitral valve and progression of mitral valve regurgitation. We also stress the efficacy of a new calcium antagonist, nicardipine, to prevent coronary artery spasm during open heart surgery.
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PMID:Perioperative coronary artery spasm in modified Bentall's operation for annulo-aortic ectasia in Marfan's syndrome. A case report of perioperative chordal rupture of the mitral valve. 779 Mar 34

Left ventricular wall perforation after acute myocardial infarction, without immediate rupture to fatal haemopericardium, is a rare complication that may result in a pseudoaneurysm. Transoesophageal echocardiography demonstrated a posterior wall perforation and the unique blood flow pattern at the neck of a pseudoaneurysm 6 days after acute myocardial infarction. In a second patient with angina and congestive heart failure 7 years after an acute myocardial infarction echocardiography demonstrated a huge pseudoaneurysm. Surgical repair was successful in both patients. Turbulence of blood at the neck of a pseudoaneurysm generates a murmur, and systolic regurgitation into a large aneurysm may cause symptoms of heart failure. Exact diagnosis, anatomical relations and size can be assessed with echocardiography. Angiography is required before surgery only to rule out coronary artery pathology. Occasionally a pseudoaneurysm may persist for many years but because of a high risk of rupture, prophylactic repair is indicated soon after diagnosis.
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PMID:Postinfarction left ventricular pseudoaneurysm--echocardiographic diagnosis and surgical repair. 795 49

In patients with aortic valve regurgitation anginal pain without coronary artery disease is a consequence of both impairment of coronary flow (CF) reserve and reduction of diastolic CF (D) due to a diminished coronary perfusion pressure (CPP). Aim of this study was to evaluate with transesophageal multiplane echocardiography CF pattern in 15 patients with severe aortic regurgitation (AR) in the operative room before and after aortic valve replacement and to correlate it with hemodynamic parameters of left ventricular systolic (echocardiographic fractional shortening area) and diastolic (Doppler E/A ratio of mitral flow and X/Y ratio of pulmonary venous flow; pulmonary wedge pressure) function. Patients were compared to a control group (C) of 10 subjects. Coronary flow was divided into systolic (S), protodiastolic (PD) and end-diastolic (ED) components. In AR we observed a reduction in D/S ratio (2.6 +/- 1.3 versus 3.5 +/- 0.8, NS) and an increase in PD/ED ratio (2.24 +/- 2.8 versus 1.05 +/- 0.15, p < 0.001). A positive correlation was observed between PD/ED ratio and left ventricular diastolic impairment (E/A ratio: r = 0.71, p < 0.001; wedge pressure: r = 0.70, p < 0.001) and a negative correlation with CPP (r = -0.6, p < 0.02). Forty-five min after aortic valve replacement diastolic function improvement and CPP increase were associated with a normalization of CF pattern (D/S = 4.35 +/- 1.9/PD/ED = 1.06 +/- 0.16). In conclusion in AR diastolic dysfunction and abnormal CPP are strictly related to the reduction in diastolic CF; valve replacement normalizes the former two parameters and redistributes CF in late diastole.
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PMID:[Transesophageal coronary flowmetry and ventricular diastolic properties in surgically treated aortic insufficiency]. 802 52

Heartburn and epigastric pain are the leading symptoms of reflux disease. Next to other symptoms like pharyngeal burning, regurgitation and retrosternal pain, chronic hoarseness and coughing as well as angina pectoris symptoms may point towards a pathological reflux. In endoscopically verified reflux esophagitis proton pump inhibitors are the treatment of first choice. Aim of therapy is loss of symptoms, healing of epithelial defects and prevention of Barrett's esophagus. If a columnar epithelium-lined esophagus is seen, surveillance is recommended in one- or two-year intervals.
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PMID:[Reflux disease and Barrett esophagus--monitoring and therapy]. 802 95


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