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Biomedical subjects

J Abrams

Publications and source records attributed to J Abrams.

At least 217 records · Page 12Linked to original sources

Echocardiography: pericardial thickening and constrictive pericarditis.

A total of 167 patients with pericardial thickening noted on M node echocardiography were studied retrospectively. After the echocardiogram, 72 patients underwent cardiac surgery, cardiac catheterization or autopsy for various heart diseases; 96 patients had none of these procedures. In 49 patients the pericardium was directly visualized at surgery or autopsy; 76 percent of these had pericardial thickening or adhesions. In another 8 percent, pericardial adhesions were absent, but no comment had been made about the appearance of the pericardium itself. In the remaining 16 percent, no comment had been made about the pericardium or percardial space. Cardiac catheterization in 64 patients revealed 24 with hemodynamic findings of constrictive pericarditis or effusive constrictive disease. Seven echocardiographic patterns consistent with pericardial adhesions or pericardial thickening are described and related when possible to the subsequent findings at heart surgery or autopsy. The clinical diagnoses of 167 patients with pericardial thickening are presented. The hemodynamic diagnosis of constrictive pericardial disease was associated with the echocardiographic finding of pericardial thickening, but there were no consistent echocardiographic patterns of pericardial thickening diagnostic of constriction. However, certain other echocardiographic abnormalities of left ventricular posterior wall motion and interventricular septal motion and a high E-Fo slope were suggestive of constriction.

Echocardiography↗

Pseudo A-V block secondary to concealed junctional extrasystoles. Case report and review of the literature.

A 23 year old woman, convalescing from a motorcycle accident was noted to have a complex arrhythmia. Short bursts of apparent ventricular tachycardia, sudden P-R delays, and Mobitz I and Mobitz II block were observed as well as frequent junctional premature systoles. Careful analysis revealed that the rhythm disturbances were caused entirely by manifest and concealed atrioventricular (A-V) junctional extrasystoles. This case meets the criteria for concealed junctional extrasystoles producing "pseudo A-V block." Pertinent literature is reviewed, and the manifestations of variable antegrade and retrograde conduction of A-V junctional extrasystoles are discussed. Increased awareness of this unusual rhythm disturbance can prevent unnecessary pacemaker therapy for apparent A-V block.

Adult↗

Kayser-Fleischer-like rings in patients without Wilson's disease.

Three patients, one with cryptogenic cirrhosis, one with active chronic hepatitis and one with neonatal hepatitis, were found to have corneal pigmentation rings indistinguishable from early Kayser-Fleischer rings on slit lamp examination. They did not have the clinical features of Wilson's disease and their serum copper and ceruloplasmin concentrations were normal. Urinary copper excretion rates and hepatic concentrations were only slightly raised but were below the range found in symptomatic Wilson's disease. It is concluded that the Kayser-Fleischer ring would no longer be considered as pathognomonic of Wilson's disease.

Adult↗

Prevention by chlorpromazine of ischemic liver cell death.

Ischemic liver tissue was produced by clamping the portal venous and hepatic arterial blood supply to the left lateral and median lobes of rat liver. If, after 2 to 3 hours of ischemia, reflow to the liver was established by removing the clamp, two-thirds or more of the liver cells were histologically dead 24 hours later. Pretreatment with chlorpromazine (20 mg/kg) 30 minutes before inducing ischemia for up to 3 hours virtually completely prevented this ischemic cell death. If the animals were kept alive for an additional 24 hours with no further treatment, the extent of liver cell necrosis at 48 hours was still markedly less than that seen in the untreated ischemic controls. Administration of chlorpromazine after induction of ischemia and immediately prior to the onset of reflow reduced but did not completely prevent ischemic cell death as determined at 24 hours. This protective action of chlorpromazine was confirmed by the ability of the treated animals to regenerate cellular ATP levels after 3 hours of ischemia. In addition, chlorpromazine was shown to significantly reduce the increases in total liver cell and mitochondrial calcium ion contents that accompany the return of blood flow to irreversibly injured liver cells. The protective effect of chlorpromazine could not be attributed to any effect either on the rate or extent to which the liver cells became ischemic or on the perfusion patterns following release of the obstruction, and it is concluded that the action of chlorpromazine must be on some component(s) of the reaction of the cells to the ischemia itself. The possible basis of this action is discussed.

Adenosine Triphosphate↗

Life-threatening ventricular tachyarrhythmias in delirium tremens.

Ventricular irritability and ventricular fibrillation developed in an alcoholic patient who had withdrawal seizures and delirium tremens; he was successfully resuscitated. Potassium and magnesium level were low; therefore replacement of these electrolytes was carried out, as well as intravenous administration of lidocaine hydrochloride; however, ventricular tachycardia developed again and required countershock. No further arrhythmias occurred after additional potassium chloride and procainamide hydrochloride therapy was given. Hypokalemia and possibly hypomagnesemia are implicated as important factors in the development of ventricular ectopy. Delirium tremens is a potential medical emergency, and in the presence of low potassium and/or magnesium levels, or ventricular irritability, patients with this condition should be treated expectantly in an intensive care unit, with close monitoring and aggressive therapy for life-threatening arrhythmias.

Alcohol Withdrawal Delirium↗