Objective: To determine the cost of heart failure–related hospital admissions and to compare the cost of admissions for sodium retention with the cost of admissions for other decompensating factors. ...Design: Retrospective, non-experimental, cost analysis. Setting: Midwestern university-affiliated, tertiary care, medical center. Sample: Two hundred seven heart failure–related admissions, 117 (57%) of which were for sodium retention leading to volume overload. Outcome Measures: Cost of hospitalization. Procedure: Data obtained from the patient and financial records of patients hospitalized for heart failure in 1992 were analyzed using the ratio of cost-to-charge accounting procedure. Results: The total cost was $2,442,720 for the 207 heart failure–related admissions; the average cost was $12,400 per admission. Approximately half of the cost of the hospitalizations was expended in the 4 cost centers comprising routine and critical care services, which incorporate room charges and nursing care. Another one third of the cost was for supplies, medications, and laboratory tests. Admissions as a result of sodium retention had lower costs than admissions as a result of other factors. Conclusion: The cost of hospitalization for heart failure is high. Routine services, supplies, medications, and laboratory tests used by these patients contribute to the high cost of care. Improved outpatient management strategies are necessary to reduce hospital admissions as a result of sodium retention. (Heart Lung® 1999;28:102-9)
Gap junctional proteins (connexins) form aqueous channels that enable direct cell-cell transfer of ions and small molecules. The distribution and conductance of gap junction channels in cardiac ...muscle determine the pattern and synchrony of cellular activation. However, the capacity for smooth muscle to restrict contractile events temporally and spatially suggests that cell-cell coupling or its regulation may be decidedly different in this tissue. We isolated a cDNA from vascular smooth muscle which encodes a connexin (Mr 43,187) structurally homologous to cardiac connexin43. Vascular smooth muscle connexin43 mRNA was expressed prominently in smooth muscle tissues, cultured vascular myocytes, and arterial endothelial cells. A model for functional expression of connexins was developed in two-cell B6D2 mouse embryos. Microinjection of in vitro transcribed vascular smooth muscle connexin43 mRNA was shown to be sufficient to induce intercellular coupling in previously uncoupled blastomeres. Through the construction of two deletion mutants of connexin43, we also show that the formation of cell-to-cell connections does not depend upon a predicted cytoplasmic region within 98 residues of the carboxyl terminus. Finally, the identification of connexin43 in smooth muscle and endothelial cells provides supporting evidence for the existence of heterocellular coupling between cells of the vascular intima.
We assessed the effect of amlodipine on cause-specific mortality in 1,153 patients with advanced heart failure enrolled in a double-blind, randomized, placebo-controlled trial.
The long QT syndrome: A G or not a G? Pressler, Milton L.; Hathaway, David R.
Journal of the American College of Cardiology,
08/1992, Letnik:
20, Številka:
2
Journal Article
Regulation of intracellular pH (pHi) and the relationship between H+ and Ca2+ may vary during activity. Ion-selective microelectrodes were used to record pHi during action potentials of sheep ...Purkinje fibres prolonged by low temperature (21 degrees C) and elevated CO2 content. Intracellular pH also was measured during changes in extracellular calcium concentration, Ca2+o. Cytosolic alkalinization (peak pHi change, 0.03-0.05) was observed during the long action-potential plateau and transient acidification (0.01-0.02 units) upon repolarization. Potassium-induced depolarization to plateau potentials (i.e. to -15 +/- 2 mV) simulated the peak magnitude of the alkalinization. However, compensation for the alkalinization occurred at a faster rate during the action potential (8.9 +/- 4.3 nM/min) than during K+ depolarization (1.2 +/- 0.5 nM/min). In comparison, the cytoplasm acidified in resting fibres (0.06-0.07 log units) during changes of Ca2+o thought to increase intracellular calcium concentration. Alterations of pHi were translated into changes of proton concentration (H+i). Ten- to twenty-fold elevation of Ca2+o evoked a comparable change in H+i (mean increase, 5.7 nM) but oppositely directed from that during the plateau (mean decrease, 8.8 nM). The findings in resting fibres seem consistent with displacement of bound protons by Ca2+. In contrast, the initial change in pHi during the plateau is proposed to be consequent to Ca2+-release from sarcoplasmic reticulum and/or phosphocreatine hydrolysis coupled to ATP regeneration.
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