A comparison of digital subtraction angiography and noninvasive testing in the diagnosis of cerebrovascular disease

Among the 1,892 patients who underwent cerebrovascular digital subtraction angiography at our hospital over the past 18 months, there was a subgroup of 34 patients (65 carotid arteries) for whom noninvasive cerebrovascular test results and standard cerebral arteriograms were also available. These patients were reviewed retrospectively and the ability of both methods to detect hemodynamically significant lesions, defined as a greater than 50 percent reduction in the diameter of the carotid artery, was determined using the arteriograms as the "gold standard." Noninvasive cerebrovascular tests had a sensitivity of 81 percent, a specificity of 95 percent, a positive predictive value of 92 percent, a negative prediction value of 88 percent, and an overall accuracy of 89 percent. Digital subtraction angiography had a sensitivity of 84 percent, a specificity of 92 percent, a positive predictive value of 88 percent, a negative predictive value of 89 percent, and an overall accuracy of 89 percent. If the four cases of hemodynamically significant stenosis of the carotid siphon not detected by digital subtraction angiography had been considered as false-negatives, its sensitivity would have been reduced to 72 percent. In patients with hemispheric cerebral ischemia, we found noninvasive cerebrovascular tests neither necessary nor cost-effective. Digital subtraction angiography, on the other hand, often provided definitive diagnostic information in such patients if the intracranial circulation was well defined and the extracranial lesion corresponded to the patients' symptoms. Noninvasive cerebrovascular testing was the safest and most cost-effective technique for screening patients with asymptomatic bruits, atypical, nonhemispheric cerebral symptoms, and those who have undergone carotid endarterectomy. If the noninvasive cerebrovascular test result was positive or equivocal, digital subtraction angiography was performed to localize the responsible lesion and exclude carotid occlusion.     

Echocardiographic criteria for aortic root dissection.

Echocardiographic findings from 10 patients without clinical indications of aortic root dissection or aortic valve disease from 1 patient with angiographic confirmation of aortic root dissection are reported and compared. Previously reported echocardiographic findings were confirmed in the patient with aortic root dissection. These include (1) a widened posterior or anterior aortic wall, or both; (2) parallel motion of the separated margins of the aortic walls; and (3) aortic root dilatation (42 mm or more at end-systole). However, all three findings were also noted in 5 of the 10 patients without clinical indications of aortic root dissection or aortic valve disease, and at least two of the three findings were noted in the remaining 5 patients. Echocardiographic detection of aortic root dissection appears to be most reliable when clinical indications of the anomaly are present.     

Pump dysfunction after myocardial infarction: Importance of location,extent and pattern of abnormal left ventricular segmental contraction

To delineate the relative effects on left ventricular function of the site, extent and nature of abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However, paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression (P < 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed (P < 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial infarction is largely the result of the more extensive area of necrosis rather than of the location of the infarction.     

Morphology of chronic lymphocytic leukemia and its relationship to survival

The morphology of lymphocytes in blood and bone marrow from patients with chronic lymphocytic leukemia was studied; blood lymphocyte morphology was related to survival. Three primary morphologic groups emerged. Group I was characterized by small to medium-sized lymphocytes with narrow rims of cytoplasm and coarsely clumped nuclear chromatin. In group II the predominant lymphocytes were large with abundant cytoplasm. Group III was characterized by a heterogeneous population of lymphocytes with characteristics of both groups I and II. Clinical features of the patients were studied, and B and T typing of the lymphocytes was done. The median survival in group I was 26+ months; In group II 46+ months; and in group III 50+ months. Our data are at variance with previous reports and suggest that survival in patients with large lymphocytes Is longer than in those with small lymphocytes.     

Acquired factor X deficiency with associated defects in platelet aggregation: A response to corticosteroid therapy

A 79 year old white woman presented with a severe bleeding disorder. Evaluation revealed a prothrombin time of 27.6 seconds (control, 11 seconds) and an activated partial thromboplastin time of 61 seconds. Specific clotting factor assays showed an isolated deficiency of factor X ranging from 7 to 12 per cent on three determinations. Platelet aggregation and bleeding time were also abnormal in response to epinephrine and collagen. Factor X levels and platelet aggregation returned to normal and bleeding stopped after institution of corticosteroid therapy.     

Nifedipine: a myocardial protective agent.

The effectiveness of the calcium antagonist nifedipine in preserving postischemic myocardial function and structural integrity was experimentally demonstrated in isolated rabbit hearts, in conscious dogs subjected to myocardial infarction, in open chest anesthetized dogs with normothermic regional ischemia induced for 1 to 2 hours and in dogs undergoing hypothermic global ischemia for 2 hours followed by 2 hours of reperfusion. Nifedipine had a beneficial effect on postischemic myocardial stiffness and mitochondrial calcium accumulation, which were correlated. Administration of nifedipine at the onset of myocardial infarction increased blood flow to ischemic zones of myocardial infarction and resulted in less loss of creatine kinase. It reduced by two- to three-fold the volume of the ischemia-reperfusion injury induced by left anterior descending coronary arterial occlusion and release and preserved indexes of hemodynamic function. Nifedipine was found effective in protecting myocardial performance and structure after 2 hours of global ischemia during hypothermic cardiopulmonary bypass. It is suggested that this agent may be useful as an adjunct to cold cardioplegia in man for enhanced myocardial protection during cardiac surgery.     

Decreased contractility and compliance of the left ventricle as complications of thermal trauma

To test the hypothesis that systemic complications of dermal burns encompass dysfunction of myocardial contractile mechanisms, we studied contraction-relaxation properties of isovolumic left ventricular (LV) preparations isolated from guinea pigs 24 hours after full-thickness burn to approximately 47% total body surface area. Compared to control hearts, hearts from burned subjects consistently generated significantly lower values for LV systolic pressure (94 +/- 2 vs 66 +/- 2 mm Hg; p less than 0.001) and maximal rates of LV pressure rise (+ dP/dtmax; 1296 +/-71 vs 1091 +/- 46 mm Hg X sec-1; p less than 0.05) and fall (-dP/dtmax; 1214 +/- 45 vs 856 +/- 34 mm Hg X sec-1; p less than 0.001). The LV contractile deficit of burn hearts was not correlated with changes in tissue water content, and it was not surmountable by excess glucose, insulin, increased coronary flow, or maximal preload elevation. In addition, end-diastolic pressure-volume relationships in burn hearts were shifted upward and to the left of controls in the direction of decreased compliance (p less than 0.05 to p less than 0.01). Thus, LV sequelae of thermal trauma manifest in isolated hearts as decreased contractility, slowed isovolumic relaxation, and decreased diastolic compliance; in the intact animal this combination would reduce ejection and impede filling of the ventricle, with diastolic pressures reflecting changes in compliance as well as in contractile function.