Biomedical subjects
Publications and source records attributed to S W Rosenbush.
We describe 2 cases with positive antiphospholipid antibodies (aPL); one with limited scleroderma associated with aortic valve vegetation, the 2nd with systemic lupus erythematosus/scleroderma overlap with recurrent venous thrombosis, pulmonary emboli, hemolytic anemia, and severe mitral regurgitation requiring valve replacement.
One hundred three patients with ischemic heart disease (IHD) were compared with 29 patients with organic heart disease and normal coronary arteries (OHD) and with a control group of 101 patients free of heart disease and matched for age and sex. Twelve patients in the control group, 4 in the OHD group, and 34 patients in the IHD group were found to have hearing loss (HL) of different degrees, cause, and duration (P = 0.0003). Of the HL-IHD group, 19 of the 34 patients had no underlying etiologic factor compared with 4 of the 12 patients in the control group (P = 0.0005); age was not an important factor. Multiple logistic regression analysis suggests that the probability of a patient with HL of unknown etiology to have IHD is eight times greater than in individuals with normal hearing. In the HL groups (12 controls and 34 with IHD), there were no significant differences in sex, hypertension, obesity, or smoking, but there was a lower incidence of diabetes and a higher incidence of family history in the HL-IHD group than in the HL-control group. Two patients in the HL-IHD group had families with many members affected by both deafness and IHD, suggesting a heredofamilial disease. HL always preceded the clinical manifestation of IHD and appears to be an important "early marker" of a vascular or generalized arteriosclerotic process.
The symptoms, signs, and pathophysiology of two major forms of shock are discussed. Newer modalities of pharmacologic and supportive therapy for stabilization and reversal of these states are presented, including the use of the intra-aortic balloon pump and early surgical therapy for cardiogenic shock.
The value of programmable pulse generators for correcting pacing system malfunction without surgical revision was assessed in 293 patients. Twenty-five patients (8.5%) developed malfunctions from one day to 38 months after implant. Of these, 16 or 64% were successfully managed by programming alone, while nine patients required lead repositioning or a new lead. The majority (75%) of isolated pacing and sensing malfunctions were corrected by programming, but programming restored normal pacing function in only one of five patients who had combined sensing and pacing malfunctions which appeared early after pacemaker insertion. We conclude that programmable pulse generators are particularly useful for managing isolated pacing or sensing malfunctions. However, programmability is not a substitute for careful lead placement.
We determined the sequence and timing of inward ventricular wall motion by least-square phase analysis of radionuclide cineangiograms in 10 patients with left bundle branch block (LBBB), five patients with right bundle branch block (RBBB) and 11 patients with normal conduction. All LBBB and RBBB patients had normal coronary arteries and no segmental wall motion abnormalities. The left ventricle (LV) was divided into eight segments and the right ventricle (RV) into three; sequence and timing were scored by three observers. In normal subjects, wall motion begins in either or both ventricles and ends in the LV or both ventricles. In patients with LBBB it begins in the RV and ends in the LV; in patients with RBBB is begins in the LV and ends in the RV or both ventricles. The intraventricular wall motion is also altered in the ventricle ipsilateral to a bundle branch block. In LBBB, the mean time of onset of LV wall motion is delayed 1.9 frames (38 msec), whereas RV wall motion is normal. In RBBB, the onset of RV wall motion is delayed 1.3 frames (26 msec), whereas LV wall motion is not delayed.
Intense, diffuse localization of Tc-99m-pyrophosphate was demonstrated in the right and left ventricles of a patient with biopsy-proved amyloidosis and severe congestive heart failure. This finding is strong presumptive evidence of myocardial infiltration by amyloid in the presence of biopsy-proven amyloidosis elsewhere in the body.
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