Biomedical subjects

W C Sternbergh

Publications and source records attributed to W C Sternbergh.

34 records · Page 2Linked to original sources

PubMed1997

Cost savings associated with the nonroutine use of carotid angiography.

BACKGROUND: To evaluate the economic impact of performing carotid endarterectomy based only on a diagnosis of duplex scanning, we evaluated a cohort of patients treated at our institution during 1 calendar year. METHODS: Ninety-seven patients were evaluated and divided into two groups: those with and without arteriogram prior to their operation. Duplex scan and arteriogram results were reviewed to determine their effect on the operative plan. Hospital charges and physician fees were assessed for each patient admission. Operative results, complications, and total charges were compared between the two groups. RESULTS: There was one operative stroke in each group for a stroke rate of 2%. Angiographic complications included one stroke and one femoral artery thrombosis. Two arteriograms led to a change in the operative plan. The hospital charges for patients without an arteriogram was $10,292 verses $13,906 for patients with an arteriogram (P < 0.01). Physician charges for patients without an arteriogram were $3,882, with angiograms and $6,297. The total charges related to the endarterectomy were $14,174 and $20,203, respectively. Arteriograms accounted for an increase of 43% in total charges. CONCLUSION: Nonroutine use of angiography does not increase operative risk or postoperative length of stay, and preoperative angiography increases total charges by 43% ($6,029) per patient.

Aged↗

PubMed1997

Implications for the vascular surgeon with prolonged (3 to 89 days) intraaortic balloon pump counterpulsation.

PURPOSE: The intraaortic balloon pump (IABP) is useful in the treatment of failing hearts. Although most experience with IABPs has been with acute short-term use, the safe duration of therapy and possible complications of long-term IABP use are uncertain. We evaluated the feasibility, management, and complications associated with long-term IABP therapy. METHODS: Fifty consecutive patients with 87 IABPs were evaluated retrospectively. All patients had IABP support for greater than 72 hours. Results and complications were evaluated. RESULTS: The mean duration of IABP support was 23.2 days. There were 21 IABP-related complications in 16 patients: (16 ischemic, three infections, two hemorrhage). The rate of complications was 0.13 per patient-week of support. Significant predictors of complications were total days of IABP support (p < 0.0001), use of multiple IABPs (p < 0.0001), and attempted but unsuccessful percutaneous insertions (p < 0.001). Complications led to 14 vascular procedures (five patch angioplasties, four bypass procedures, two major amputations, one fasciotomy, one groin exploration for hemorrhage, and one removal of an infected Dacron patch). Percutaneous removals had a 14% complication rate compared with none after operative removal (p = 0.02). Thirty-two patients survived (64%). Of the survivors, 27 underwent transplant. CONCLUSIONS: Prolonged IABP therapy is feasible and is associated with an acceptable rate of complications. Operative removal is superior to percutaneous removal. Percutaneous removal should be limited to short-term therapy. There is no need for mandatory removal or site rotation based solely on indwelling time.

Adult↗

PubMed1997

Endovascular treatment of abdominal aortic aneurysms: case report and review of literature.

A case of endovascular treatment of abdominal aortic aneurysm is discussed along with a review of the literature. This recently introduced Food and Drug Administration Phase II treatment modality may have a significant impact on the approach to the treatment of aneurysmal disease. This discussion details the treatment of one typical patient and reviews the current status of endovascular therapy as it applies to infrarenal abdominal aortic aneurysms.

Aged↗

PubMed1995

Heparinoids with low anticoagulant potency attenuate postischemic endothelial cell dysfunction.

PURPOSE: Although standard heparin has been demonstrated to reduce endothelial cell dysfunction in acute ischemia-reperfusion injury, its mechanism of action remains unknown. We hypothesized that heparin's salutary endothelial effects are independent of its conventional anticoagulant activity and are not caused by nonspecific polyanion effects. METHODS: Isolated rat hindlimbs were perfused at constant pressure with an albumin-enriched crystalloid buffer. After 60 minutes of normothermic ischemia, endothelial function was assessed by measurement of endothelial-dependent vasodilation by log increment infusion of acetylcholine. Endothelial-independent vasodilation was measured by exposure to nitroprusside. Some groups were pretreated with heparinoids possessing minimal or intermediate anticoagulant activity. RESULTS: Treatment with heparinoids with low anticoagulant activity significantly increased endothelial-dependent vasodilation when compared with the nontreated ischemic group and were statistically indistinguishable from the nonischemic control. Treatment with dextran sulfate, a randomly sulfated polymer with size and charge characteristics similar to heparin, did not change postischemic vasodilation. Endothelial-independent vasodilation was largely unaffected by ischemia-reperfusion or drug treatment. CONCLUSIONS: A heparinoid with negligible antithrombin-binding activity (Astenose) attenuated postischemic endothelial dysfunction, suggesting that its mechanism of action was independent of anticoagulant activity. Failure of dextran sulfate to be protective implied that the effect was not caused by nonspecific polyanion action.

Acute Disease↗

PubMed1994

Postischemic extremities exhibit immediate release of tumor necrosis factor.

PURPOSE: Although reperfusion of acutely ischemic extremities can cause cardiopulmonary collapse and death, the humoral agent(s) released from limbs promoting this distant organ injury are not well characterized. We hypothesized that tumor necrosis factor-alpha (TNF-alpha), a cytokine that causes cardiopulmonary dysfunction in septic shock, may be released from postischemic extremities. METHODS: Isolated rat hindlimbs were perfused at constant pressure with a nonrecirculating crystalloid-based buffer. After 60 or 120 minutes of normothermic ischemia, TNF activity was measured in sequential samples of venous effluent by L929 bioassay. Associated limb injury was assessed by the extent of no-reflow after reperfusion, changes in endothelial permeability to iodine 125-labeled albumin and skeletal muscle injury by uptake of technetium 99 pyrophosphate. RESULTS: After 120 minutes of normothermic ischemia (n = 10), a 15-fold increase in TNF-alpha activity in venous effluent occurred, with peak activity at 1.5 minutes of reperfusion (30.6 +/- 8.7 U/ml) falling to near control levels by 5 minutes. This group had a 3.3-fold increase in vascular permeability, a 2.2-fold increase in the muscle injury index and a 71.2% decline in reperfusion flow (all p < 0.05 vs control). Pretreatment of extremities with an anti-TNF-alpha antibody in a second group of limbs undergoing 120 minutes of ischemia (n = 10) decreased TNF activity to levels not significantly different from the nonischemic control group (n = 12). The extent of no-reflow in limbs treated with antibodies was significantly attenuated (flow 44.9% of control vs 29.8% [untreated], p < 0.05). Antibody treatment affected neither muscle injury nor vascular permeability. CONCLUSIONS: Postischemic extremities exhibited a transient, early burst of TNF release on reperfusion, which likely represented washout of TNF produced during ischemia. Suppression of TNF activity with an antibody to TNF-alpha resulted in a salutary increase in postischemic flow rates, suggesting that TNF may play a role in the no-reflow phenomenon.

Animals↗

PubMed1993

A comparative study of heparin responses in arterial and venous thromboembolism using molecular markers for thrombosis.

BACKGROUND: Compared with the therapy of venous thromboembolism, there is little consensus regarding guidelines for heparin anticoagulation of patients with arterial thrombosis. This study aimed to identify the quantitative differences in the activation of the coagulation cascade and platelets in these two syndromes and to characterize their specific biological responses to heparin therapy. METHODS AND RESULTS: Eighteen patients receiving intravenous heparin to treat venous (n = 9) or arterial (n = 9) thromboembolism were prospectively studied for an average of 4 days each. Clinical responses to treatment, activated partial thromboplastin time (aPTT), and molecular markers for thrombosis were measured regularly. Although both groups received equivalent doses of heparin (approximately 1100 units/h), the resulting aPTTs and plasma heparin activity were significantly lower in the arterial patients (P < .05 and P < .01, respectively). The plasma levels of beta-thromboglobulin (a marker for platelet activation and granule release) were significantly higher in the arterial patients (109 +/- 9.5 versus 79 +/- 7.1 ng/mL, mean +/- SEM, P < .05). In vivo fibrin formation, as evidenced by plasma levels of fibrinopeptide A, was less effectively suppressed in the patients with arterial versus venous thrombosis (18.5 +/- 3.2 versus 10.4 +/- 2 ng/mL, P < .05). Prothrombin fragments 1 + 2, a marker for prothrombinase complex activity, was nearly normal in both heparinized groups. CONCLUSIONS: The anticoagulant response to heparin is blunted in patients with arterial thrombosis, at least in part by the antagonistic actions of increased platelet activation. Comparing arterial with venous thrombosis, higher doses of heparin on the average may be required to achieve comparable aPTTs, plasma heparin activity, and comparable suppression of fibrin formation.

Aged↗

PubMed1993

Nitric oxide-mediated, endothelium-dependent vasodilation is selectively attenuated in the postischemic extremity.

BACKGROUND: Attenuation of endothelium-dependent relaxing factor (EDRF) release may contribute to adverse sequelae commonly seen after reperfusion of an acutely ischemic extremity. The purpose of this study was to identify the compound responsible for the EDRF activity in the extremity and to evaluate its modulation by ischemia and reperfusion. METHODS: Isolated rat hindlimbs were perfused at constant pressure with an albumin-enriched crystalloid buffer. Increasing log dose infusions of acetylcholine and nitroprusside were used to measure endothelium-dependent (EDRF-mediated) and endothelium-independent vasoreactivity, respectively. RESULTS: Graded reductions in total vascular resistance were seen in response to both agonists in the control group (n = 11). In the postischemic group (n = 7), 60 minutes of normothermic ischemia and 10 minutes of reperfusion reduced endothelium-dependent vasodilation to acetylcholine by approximately 40% (p < 0.01). Endothelium-independent vasodilation to nitroprusside was unaffected. NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide release, attenuated vasodilation to acetylcholine (p < 0.01) but not nitroprusside in both control and postischemic groups. CONCLUSIONS: Endothelium-dependent vasodilation in the rat hindlimb, mediated by nitric oxide, was selectively impaired by injury from ischemia and reperfusion. Strategies designed to minimize postischemic attenuation of nitric oxide release may be beneficial in the management of acute limb ischemia.

Acetylcholine↗

PubMed1993

Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity.

PURPOSE: Heparin may have protective effects on postischemic vascular endothelial cell function that are distinct from its anticoagulant, antiplatelet, or anticomplement activity. We tested this hypothesis in isolated rat hindlimbs. METHODS: Isolated rat hindlimbs underwent 60 minutes of normothermic ischemia and 10 minutes of reperfusion. Potential heparin interaction with plasma-based proteins or cells was eliminated by perfusion of the hindlimbs with a nonrecirculated albumin-enriched crystalloid buffer. Endothelial function was assessed by measurement of endothelium-derived relaxing factor (EDRF) activity. Limbs perfused at constant pressure were subjected to increasing log dose infusions of acetylcholine and nitroprusside to measure endothelial-dependent (EDRF-mediated) and endothelial-independent vasoreactivity, respectively. Fifty limbs were divided into seven groups: two nonischemic groups (one with heparin) and five ischemia/reperfusion groups treated with increasing doses of heparin (0 to 1.0 U/ml perfusate). RESULTS: The nontreated ischemia/reperfusion group (n = 12) had a 46.2% reduction in endothelial-dependent vasodilation of the rat hindlimb when compared with the nonischemic control (n = 7, p < 0.05). Treatment with heparin 0.5 U/ml (n = 6) nearly abolished this attenuation of endothelial-dependent vasodilation (4.3% reduction, p = not significant vs nonischemic control). The endothelial protective effect of heparin was dose-dependent: groups treated with 0.25 U/ml (n = 6) and 0.1 U/ml heparin (n = 7) showed progressive impairment in postischemic EDRF-mediated vasodilation. Endothelial-independent vasodilation induced by nitroprusside was unchanged by ischemia/reperfusion or heparin treatment, which confirmed that the postischemic damage and its protection by heparin were specific to the endothelium. CONCLUSIONS: Heparin prevented postischemic endothelial cell dysfunction by a mechanism independent of its interactions with plasma-based proteins or cells. This nonanticoagulant protective effect may contribute to the salutary effects of heparinization during acute ischemic events.

Animals↗

PubMed1992

Skeletal muscle fiber type does not predict sensitivity to postischemic damage.

Because the three distinct fiber types of skeletal muscle have significant metabolic differences, the predominant fiber type in a muscle may influence its sensitivity to injury from ischemia and reperfusion. The few studies to address this issue have been conflicting. We explored possible differences in the sensitivity of fiber types to ischemia/reperfusion injury with an isolated rat hindlimb preparation perfused with an albumin-enriched Krebs buffer. Following 120 min of ischemia and 60 min of reperfusion, the tibialis anteriorwhite, tibialis anteriorred, soleus, and plantaris muscles were assessed for injury by examining three parameters: skeletal muscle injury (via 99Tc-pyrophosphate), microvascular injury (via 125I-albumin), and tissue water content. There was no consistent correlation between fiber type and sensitivity to postischemic injury. Both the soleus (slow twitch) and plantaris (fast twitch) muscles sustained similar significant injury: muscle damage was 133 and 167% greater than controls, and microvascular damage 96 and 91% greater than controls, respectively. However, other fast twitch muscles (tibialis anteriorwhite and tibialis anteriorred) exhibited no significant injury. Both injured muscles were in the posterior compartment while the uninjured muscles were in the anterior compartment. Regional flow as measured by microspheres revealed no correlation between postischemic flow and muscle injury, microvascular injury, or compartmental location. Skeletal muscle fiber type was not consistently predictive of its sensitivity to ischemia/reperfusion-induced injury. Compartmental location may have played an as yet unknown role in modulating vulnerability to postischemic damage.

Animals↗

PubMed1992

The temporal relationship between endothelial cell dysfunction and skeletal muscle damage after ischemia and reperfusion.

Reperfusion-induced vascular endothelial cell dysfunction may exacerbate skeletal muscle damage after an ischemic insult. Although concurrent endothelial and skeletal muscle injury has been documented after ischemia and reperfusion, their temporal relationship has not been well characterized. An isolated rat hindlimb model was used to measure the effect of progressive ischemia and reperfusion on both endothelial cell function and skeletal muscle damage. Endothelial cell dysfunction as reflected by changes in permeability was measured by protein clearance techniques with use of albumin labeled with iodine 125 (125I-albumin). Skeletal muscle damage was assessed by tissue uptake of technetium 99m pyrophosphate (99mTc-pyrophosphate). The soleus muscle was used for evaluation of endothelial and skeletal muscle damage throughout the study. Significant increases in vascular permeability preceded skeletal muscle damage. The protein leak index increased after 60 minutes of ischemia and reperfusion (7.5 +/- 1.2 vs 4.1 +/- 0.9 control), whereas the muscle injury index did not change until 120 minutes of ischemia and 60 minutes of reperfusion (10.5 +/- 0.6 vs 4.5 +/- 0.5 control). Significant graded increases in both indexes were noted with longer intervals of ischemia. Electron microscopy revealed ultrastructural evidence of endothelial and skeletal muscle damage after 120 minutes of ischemia and 60 minutes of reperfusion but not after 60 minutes of ischemia and reperfusion. These studies indicate that microvascular injury precedes skeletal muscle damage after ischemia and reperfusion. This temporal relationship may have important implications in designing strategies to minimize ischemia-reperfusion injury.

Analysis of Variance↗

PubMed1989

Basal metabolic energy requirements of polarized and depolarized arrest in rat heart.

Basal energy requirements of polarized [tetrodotoxin (TTX), 25 microns] and depolarized [potassium (K), 20 mM] arrested hearts were studied by continuously measuring myocardial oxygen consumption (MVO2) during 60 min of normothermic arrest in isolated Langendorff-perfused rat hearts. TTX, a fast sodium channel blocker, was used to produce polarized arrest because of its specificity and reversibility. MVO2 was significantly lower in the polarized (TTX) group at all time points, a typical difference occurring 30 min after arrest (0.070 +/- 0.005 vs. 0.109 +/- 0.006 ml O2.min-1.g dry wt-1, P less than 0.001). Coronary flow was lower in the polarized group (14.3 +/- 1.4 vs. 28.4 +/- 2.2 ml.min-1.g dry wt-1, P less than 0.001, data at 30 min of arrest), but flow-restricted studies showed basal MVO2 to be independent of variation in coronary flow within this range. Recovery of function was similar in both groups. Ventricular pressure during cardiac arrest was lower in the polarized group (5.5 +/- 1.2 vs. 10.3 +/- 1.3 mmHg, P less than 0.01, data at 30 min of arrest), implying reduced myocardial wall tension and a lower intracellular calcium concentration. These results suggest that polarized arrest can decrease myocardial metabolic demands below that of depolarized arrest. A plausible mechanism is a reduction in myocardial wall tension caused by decreased calcium influx mediated by the Na-Ca exchanger.

Animals↗

PubMed1972