Non-thoracotomy implantable defibrillator (ICD) systems have been shown to have lower costs and fewer complications than thoracotomy systems. Recent interpretation of Health Care Financing ...Administration regulations has challenged reimbursement for investigational devices or combinations of components not approved by the Food and Drug Administration (“off-label”). We compared the costs and complications associated with approved pulse generator/lead systems (CPI 1600/Endotak, CPl 1705/Endotak and Medtronic 7217/Transvene, n=136) with investigational and “off-label” systems (CPI 1625/Endotak, CPI 1715/Endotak, Medtronic 7219/Transvene and Ventritex V100 or V110/TVL and Vl00/Endotak, n=79). Age 63±12 years versus 63±11 years (mean±SD) and ejection fraction (31±15% versus 31±11%) were similar for patients with approved and investigational systems, respectively. However, total hospital charges including preoperative care and evaluation, implant procedure and hardware, postoperative testing and revisions were $64±19,000 for approved devices versus $57±16,000 for non-approved devices (p=0.02) despite higher overall costs of newer pulse generators and leads. Total length of stay was 17±10 days versus 14±8 days (p=0.03) and complications including lead dislodgement, increased defibrillation threshold, hematoma and infection were 25/136 versus 4/77 (p<0.005) for approved and investigational or “off-label” systems, respectively. Based on data provided by the manufacturers, anticipated average battery longevity is 3.8 years for approved systems and 5.5 years for investigational or “off-label” systems.
The prudent use of current investigational or “off-label” nonthoracotomy ICD systems is more cost-effective and is associated with fewer complications than approved ICD systems. When increased battery longevity is considered, long term costs of non-thoracotomy ICD therapy may be improved dramatically with the use of investigational or “off-label” systems. Review of reimbursement regulations may be warranted.
The objective of this study was to compare the in vivo effects of sodium bicarbonate (NaHCO3) and Carbicarb infusion on regional contractile performance and acid-base status in the setting of ...hypercarbic acidosis. Animals (N = 9) were anesthetized and paralyzed using sodium pentothal, halothane, and pancuronium bromide, and mechanically ventilated with an air-O2 mixture so that arterial PO2 was > or = 300 mm Hg. Following beta-adrenergic blockade, alveolar ventilation was gradually reduced over a 50-minute period to increase arterial PCO2 to 60 to 80 mm Hg. Each of the following solutions was then infused in consecutive order directly into the left anterior descending artery coronary artery for 15 minutes: (1) 8.4% NaHCO3 at 2 mL/min; (2) 5% sodium chloride at 2 mL/min, equivalent to NaHCO3 in osmolality; (3) 6.3% Carbicarb at 0.5 mL/min, equivalent to NaHCO3 in buffer capacity; and (4) 6.3% Carbicarb at 2 mL/min, equivalent to NaHCO3 in volume. Regional stroke work analog (ultrasonic dimension transducers), interstitial myocardial pH (Khuri electrode), coronary blood flow (doppler flow probe), and hemodynamic/metabolic variables (heart rate, blood pressure, arterial and coronary venous blood gases) were measured at 1, 5, 10, and 15 minutes during each infusion and 10 minutes after the infusion was discontinued, ie, at 25 minutes. Animals were allowed to recover for 45 minutes between interventions. Values at each time point were compared with baseline for statistical significance. Small reductions in interstitial myocardial pH (P < .05) and stroke work (P > .05) were observed within 1 minute of NaHCO3 administration. Both parameters increased significantly from baseline levels thereafter, ie, interstitial myocardial pH at 5 minutes and stroke work at 15 minutes. Infusion of Carbicarb invariably was associated with an increase (P < .05) in interstitial myocardial pH. Stroke work increased (P < .05) during low-dose Carbicarb administration, but infusion of the higher dose was accompanied by a biphasic response, ie, an increase (P < .05) from 0 to 5 minutes, followed by a gradual decrease that achieved statistical significance 10 minutes after termination of the infusion. End-diastolic length was inversely proportional to changes in stroke work, and coronary blood flow varied directly with changes in coronary venous Pco2. Myocardial O2 consumption decreased (P < .05) during Carbicarb infusion, but changes during NaHCO3 did not reach statistical significance. Our findings lend support to the hypothesis that intramyocardial pH determines myocardial function independent of CO2 production by buffer therapy.
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