Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography.
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The clinical relevance of reciprocal changes in the ST segment occurring at the time of acute myocardial infarction was studied prospectively in 85 consecutive uncomplicated cases. Reciprocal depression of the ST segment was defined as depression of 1 mm or more in electrocardiogram leads other than those reflecting the infarct. All patients underwent maximal, symptom limited treadmill stress testing two weeks after the infarct and coronary angiography six weeks after infarction. Forty six patients had inferior, 34 anterior, and five true posterior infarction. Of the 51 patients with reciprocal changes, 45 (88%) developed exercise induced ST segment depression in areas remote from the infarction zone. At angiography all 45 patients were shown to have stenoses greater than 70% in at least two major vessels. Four patients had negative exercise electrocardiograms and were sequently shown to have single vessel disease subtending their infarct, and the remaining two patients had a false negative treadmill test result. Of the 27 patients without reciprocal changes, 21 (78%) had negative treadmill stress test results associated with single vessel coronary disease. Five had positive stress test results and multivessel coronary disease, and one had a false negative stress test result. The remaining seven patients had ST segment elevation without Q wave formation in the reciprocal areas and were assessed separately. Of these, six had positive stress test results and multivessel coronary disease and one had a negative stress test result and single vessel coronary disease to the infarct area. Twenty one patients with anterior infarcts (62%) and 27 with inferior infarcts (59%) had reciprocal changes. No differences emerged in the relation between infarct site, reciprocal change, and presence of additional coronary disease. At follow up of the 51 patients with reciprocal changes in the ST segment 36 had become symptomatic, of whom 29 had undergone coronary artery bypass surgery. By contrast, only four of the 27 patients without reciprocal changes in the ST segment had developed symptoms, and two of these had undergone coronary revascularisation. Reciprocal ST segment depression at the time of acute myocardial infarction may identify patients with severe coronary disease who are at risk of subsequent cardiac events and appears to be as reliable as results of early postinfarction treadmill stress testing in predicting the underlying coronary anatomy. When the electrocardiogram does not show reciprocal changes treadmill testing provides valuable additional information. (+info)
Is there an indication for coronary angiography in patients under 60 years of age with no or minimal angina pectoris after a first myocardial infarction?
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Coronary angiography and exercise stress tests were performed in 91 consecutive patients under 60 years of age having either no or only mild angina pectoris with or without medication after a first myocardial infarction. Nine (10%) patients had angiographic high risk coronary artery disease defined as three vessel disease, left main stenosis, or proximal stenosis of the left anterior descending artery. Eighteen patients had a positive electrocardiographic exercise stress test including eight of the nine patients with angiographic high risk coronary artery disease. It may be concluded therefore that coronary angiography to detect high risk coronary artery disease in this group can be restricted to patients with a positive exercise stress test. This policy would obviate the need for about 80% of coronary angiograms performed in this age group. (+info)
Comparative recognition of left ventricular thrombi by echocardiography and cineangiography.
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Studies performed in 47 patients, 11 of whom underwent surgery for aneurysmectomy and 36 of whom underwent cardiac transplantation, were reviewed to assess the diagnostic accuracies of cross sectional echocardiography and cineangiography in detecting left ventricular mural thrombi and the effect of anticoagulation treatment on the incidence of such thrombi. Cross sectional echocardiography in 37 patients and cineangiography in 26 (16 patients were examined by both methods) were analysed independently by sets of two observers experienced in the respective methods. All four observers were blinded to the pathological or surgical findings regarding mural thrombus. Mural thrombus was confirmed by pathological investigation in 14 of 47 (30%) cases; 11 of these 14 patients had intra-aneurysmal thrombi. The negative predictive value was quite good for both methods, but cross sectional echocardiography had a superior positive predictive value. This was due both to detailed soft tissue resolution by cross sectional echocardiography and to overdetection of mural thrombi by cineangiography in cases of aneurysms without mural thrombi. Mural thrombi were present in three of 20 patients with preceding anticoagulation and in 10 of 19 patients without anticoagulation. The results emphasise that cross sectional echocardiography is more reliable than cineangiography in recognising thrombi. (+info)
Transposition of the great arteries and narrowing of the aortic arch. Emphasis on right ventricular characteristics.
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Of 279 patients with transposition of the great arteries, 14(5%) had narrowing of the aorta, including local coarctation (6), isthmus hypoplasia (6), isthmus atresia (1), and kinking of the aorta (1). There were six deaths in 10 surgically treated patients; in addition four patients died before operation. Two of the four survivors had a subpulmonary malalignment ventricular septal defect with angiocardiographic narrowing of the right ventricular outflow tract, two had evidence of redundant muscle tissue obstructing the right ventricular outflow tract. Necropsy showed the presence of anatomical right ventricular outflow tract or inflow tract obstruction or both in all 10 cases. Outflow tract obstruction was represented by anterior displacement of the infundibular septum and ventriculoinfundibular fold (in hearts with a subpulmonary malalignment ventricular septal defect) or by redundant muscle tissue; inflow tract obstruction was represented by hypoplasia of the tricuspid valve. It is concluded that the combination of transposition of the great arteries and narrowing of the aorta is always accompanied by right ventricular outflow or inflow tract obstruction or both; the right ventricular abnormalities are probably responsible for the presence of the aortic arch anomalies by reducing aortic flow during morphogenesis. Successful surgical treatment of this complex anomaly is feasible in selected cases. (+info)
Mustard's operation for patients with ventriculoarterial concordance. Report of two cases and a cautionary tale.
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Three patients with ventriculoarterial concordance and an abnormal atrioventricular connexion were investigated. One patient had total anomalous pulmonary venous connexion to a left vertical vein. In 1972 this was repaired and a ventricular septal defect was closed, but the presence of atrioventricular discordance was missed and the patient died. In the other two patients, Mustard's operation resulted in survival. One patient had situs solitus and atrioventricular discordance with an associated ventricular septal defect, which was closed. The other had left isomerism (quasi solitus) with an ambiguous atrioventricular connexion (quasi discordant). A previously noted ventricular septal defect had spontaneously closed. (+info)
Persistent left sided fifth aortic arch in a neonate.
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A persistent left sided fifth aortic arch with coarctation of the aorta and persistence of the ductus arteriosus was recognised and treated surgically in a newborn infant. The fifth arch was used to repair the coarctation, and five years later the child had normal peripheral pulses and no residual murmurs. (+info)
Cross sectional echocardiographic and angiocardiographic correlation in criss cross hearts.
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Cross sectional echocardiography can provide accurate anatomical diagnosis in congenital heart diseases and therefore should be able reliably to identify criss cross hearts and enable the analysis of their sequential arrangement non-invasively. The cross sectional echocardiographic diagnoses in eight consecutive patients with this condition were compared with those made at cardiac catheterisation and cineangiocardiography (five retrospectively, three prospectively). The mean number of invasive studies required to reach the diagnosis was 1.9 (range 1-4). Complete anatomical diagnosis was achieved with cross sectional echocardiography in all patients, but identification of ventricular morphology was much more straightforward using cineangiocardiography. If the transducer was held steady in either a precordial or subcostal position and rocked anteriorly and posteriorly the characteristic crossing over of the ventricular inflows could easily be seen. In no plane was there normal parallel arrangement of ventricular inflows. A complete diagnosis should be possible in these patients using cross sectional echocardiography in experienced hands and at a single session in the cardiac catheterisation laboratory. (+info)
Ventricular hypertrophy in cardiomyopathy.
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Semantic difficulties arise when hypertrophic obstructive cardiomyopathy is seen without obstruction and with congestive failure, and also when congestive cardiomyopathy is seen with gross hypertrophy but without heart failure. Retention of a small left ventricular cavity and a normal ejection fraction characterizes hypertrophic cardiomyopathy at all stages of the disorder. Congestive cardiomyopathy is recognized by the presence of a dilated left ventricular cavity and reduced ejection fraction regardless of the amount of hypertrophy and the presence or not of heart failure. Longevity in congestive cardiomyopathy seems to be promoted when hypertrophy is great relative to the amount of pump failure as measured by increase in cavity size. Conversely, death in hypertrophic cardiomyopathy is most likely when hypertrophy is greatest at a time when outflow tract obstruction has been replaced by inflow restriction caused by diminishing ventricular distensibility. Hypertrophy is thus beneficial and compensatory in congestive cardiomyopathy, whereas it may be the primary disorder and eventual cause of death in hypertrophic cardiomyopathy. Reasons are given for believing that hypertension may have been the original cause of left ventricular dilatation in some case of congestive cardiomyopathy in which loss of stroke output thenceforward is followed by normotension. Development of severe hypertension in these patients after recovery from a prolonged period of left ventricular failure with normotension lends weight to this hypothesis. No fault has been found in the large or small coronary arteries in either hypertrophic cardiomyopathy or congestive cardiomyopathy when they have been examined in life by selective coronary angiography, or by histological methods in biopsy or post-mortem material. Coronary blood supply may be a limiting factor in the compensatory hypertrophy of congestive cardiomyopathy, and the ability to hypertrophy may explain the better prognosis of some patients. In hypertrophic cardiomyopathy excessive metabolic demand may not be met, and inadequacy of blood flow may contribute both to sudden death and to progressive replacement fibrosis in this disease. Histochemical and ultrastructural methods have failed to show any fundamental differences between hypertrophic cardiomyopathy and congestive cardiomyopathy, whereas conventional histology permits recognition of hypertrophic cardiomyopathy and distinction both from congestive cardiomyopathy and from ;normal' secondary hypertrophy in organic aortic stenosis. (+info)