The interrelationship of arteriosclerotic heart disease and chronic congestive failure

It was the purpose of this study to determine what factors are responsible for the development of chronic congestive failure in chronic coronary disease and myocardial fibrosis.The clinical and post-mortem records of 100 unselected cases were studied. The overwhelming majority were in, or gave a history of, congestive failure. Varying degrees of vascular and myocardial damage were common to the entire series, but the vast majority of those in congestive failure had definite and in most instances advanced cardiac hypertrophy. There were but three exceptions to this rule. The group not in failure had nonhypertrophied or, in a few cases, slightly hypertrophied hearts.The characteristic feature of the chronic congestive phase of chronic coronary artery disease is the presence of cardiac hypertrophy.The genesis of cardiac hypertrophy in relation to muscle damage is discussed. The view is accepted that increased initial fiber tension rather than increased work is the stimulus for generalized cardiac hypertrophy. Contraction with increased initial tension compensates for inadequate contractility. Myocardial disease by diminishing contractile power calls forth increased initial fiber tension and may, according to the above theory, be the cause of generalized cardiac hypertrophy. Application of this concept to the question of cardiac hypertrophy in coronary artery disease is not sufficiently supported, however, by clinical experience. Since the data in the literature are contradictory on this point, it is necessary to study further the causal relationship of chronic coronary artery disease to generalized cardiac hypertrophy by following patients whose blood pressure figures and heart size are known before and after the onset of the disease. Our present belief is that in the majority of cases generalized and advanced cardiac hypertrophy is caused by hypertension, present or antecedent, and not by vascular and myocardial damage.Diminished blood supply and severe muscle damage produce loss of contractility and may cause failure without leading to fiber hypertrophy. The striking predominance of hypertrophied hearts of the group in failure, however, indicates that it is work under long standing increased fiber tension irrespective of the cause, and the eventual loss of contractile power of the hypertrophied fiber, that leads to chronic congestive failure.Congestive failure in chornic arteriosclerotic heart disease is—like that of other types of heart disease—overwhelmingly the failure of the hypertrophied heart. (Table II.)     

Involvement of the motor cortex in pseudochoreoathetosis.

The pathophysiological background of involuntary movements in pseudochoreoathetosis is unclear. We therefore recorded in four patients with pseudochoreoathetosis and in six age-matched controls cortical activity with a whole-head magnetoencephalography (MEG) system and surface EMGs from hand muscles. Subjects performed the following tasks: 1) rest, and 2) constant finger stretch during forearm elevation; controls additionally simulated pseudochoreoathetotic finger movements. During rest, the patients showed involuntary finger movements associated with excessive MEG-EMG coherence at frequencies between 6 and 20 Hz, whereas coherence in controls simulating pseudochoreoathetotic movements did not exceed noise level (P < 0.02). During finger stretch, MEG-EMG coherence in patients was similar to that of controls. Cortical sources of MEG-EMG coherence in patients were localized in the contralateral motor cortex. We conclude that pseudochoreoathetosis is associated with pathologically increased corticomuscular coherence and thus differs, neurophysiologically, from voluntarily simulated pseudochoreoathetotic movements. The enhanced MEG-EMG coherence in pseudochoreoathetosis probably reflects a pathologically strong motor cortical drive of spinal motorneurons after deafferentation.     

Scintigraphic endocrine mimicry

The control of hormone secretion and substrate uptake by the thyroid and inner adrenal cortex is similar because both glands undergo hypothalamic-pituitary trophic hormone modulation and negative feedback by their respective major secretory products: thyroid hormone and cortisol, respectively. As a result of these parallel mechanisms of endocrine function, thyroidal accumulation of radioiodine or Tc-99m pertechnetate and adrenal cortical accumulation of I-131-6 beta-iodomethylnorcholesterol (NP-59) and other radiocholesterol analogs are strikingly similar. The patterns of imaging of these glands are thus functional maps of the process(es) of substrate accumulation and depict the endocrine pathophysiology of these glands in a variety of dysfunctional states. The well-recognized patterns of thyroid imaging can be shown analogous to those of the adrenal cortex.     

Impact of newly revised sterile medication compounding guidelines USP {797} on allergy vial preparation

OBJECTIVES: To highlight newly revised guidelines on sterile medication compounding released by the United States Pharmacopeia (USP 797) in December 2007, and the implications on immunotherapy vial preparation. STUDY DESIGN AND METHODS: A policy review. RESULTS: The newly revised USP chapter on sterile medication guidelines was released December 2007 and becomes effective June 2008. The revised USP 797 now has specific guidelines addressing immunotherapy vial preparation that are a significant change from the previous version. The revised guidelines should be a useful tool for clinicians who are developing and setting office mixing standards. CONCLUSIONS/SIGNIFICANCE: Offices preparing immunotherapy vials should consider formalizing and implementing vial preparation guidelines. These guidelines should be based on expert opinion, experience, and scientific literature.     

Prevention of cisplatin-induced emesis: a double-blind multicenter randomized crossover study comparing ondansetron and ondansetron plus dexamethasone.

Ondansetron (OND) is a new 5-HT3 receptor antagonist that give complete protection from emesis/nausea in approximately 50% of cisplatin (CDDP)-treated patients. To evaluate if dexamethasone (DEX) added to OND increases antiemetic efficacy, we carried out a double-blind randomized crossover study to compare the antiemetic activity of OND with OND plus DEX. One hundred two chemotherapy-naive patients (44 women and 58 men) scheduled to receive CDDP chemotherapy at doses greater than or equal to 50 mg/m2 entered the study. Eighty-nine patients completed both cycles with the following results: complete protection from emesis/nausea was obtained in 57/59 patients (64.0%/66.3%) with OND and in 81/79 (91.0%/88.8%) with OND plus DEX (P = .0005/P = .0021). At the end of the study, 53% of the patients expressed a treatment preference, and of these, 74% chose OND plus DEX compared with 26% who preferred OND alone, a statistically significant difference (P less than .003). Side effects were very mild and not significantly different between the two treatments. We conclude that OND plus DEX is more efficacious than OND in protecting patients from CDDP-induced emesis and nausea.