Biomedical subjects
Publications and source records attributed to Gregory J Dehmer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVES: To evaluate the feasibility of an assay for urinary levels of matrix metalloproteinases (MMPs) and the potential usefulness of urinary MMPs as a marker of coronary atherosclerosis or acute coronary syndromes (ACS). METHODS AND RESULTS: We measured urine and plasma MMP-9, MMP-2 and urine tissue inhibitor of metalloproteinase (TIMP-1) in patients with ACS (n=27), patients with coronary artery disease (CAD), but no clinical instability (n=47) and a group of healthy volunteers (n=15) who were <35 years of age, had no risk factors for CAD and did not undergo angiography. Compared with volunteers, patients with ACS and CAD had higher urine MMP-9, urine TIMP-1, plasma MMP-9 and plasma MMP-2 levels, but these did not differ between those with CAD and ACS. Using the volunteers to roughly establish an upper limit of normal, 84% of the urine TIMP-1 values and 95% of the urine MMP-9 values were abnormally elevated among those with CAD and ACS. CONCLUSIONS: Urine MMP-9 and TIMP-1 levels are elevated in patients with CAD and ACS compared with healthy volunteers. A high percent of patients with CAD or ACS had elevated urine values of MMP-9 and TIMP-1 suggesting these variables might be a useful marker of atherosclerotic disease.
Explore the source record for details and available documents.
In the early years of diagnostic cardiac catheterization, strict sterile precautions were required for cutdown procedures. Thirteen years ago, when the original guidelines were written, the brachial arteriotomy was still frequently utilized, femoral closure devices were uncommon, "implantables," such as intracoronary stents and PFO/ASD closure devices, were in their infancy, and percutaneous valve replacement was not a consideration. In 2005, the cardiac catheterization laboratory is a complex interventional suite with percutaneous access routine and device implantation standard. Despite frequent device implantation, strict sterile precautions are often not observed. Reasons for this include a decline in brachial artery cutdown, limited postprocedure follow-up with few reported infections, limited use of hats and masks in televised cases, and lack of current guidelines. Proper sterile technique has the potential to decrease the patient infection rate. Hand washing remains the most important procedure for preventing infections. Caps, masks, gowns, and gloves help to protect the patient by maintaining a sterile field. Protection of personnel may be accomplished by proper gowning, gloving, and eye wear, disposal of contaminated equipment, and prevention and care of puncture wounds and lacerations. With the potential for acquired disease from blood-borne pathogens, the need for protective measures is as essential in the cardiac catheterization laboratory as is the standard Universal Precautions, which are applied throughout the hospital. All personnel should strongly consider vaccination for hepatitis B. Maintenance of the cardiac catheterization laboratory environment includes appropriate cleaning, limitation of traffic, and adequate ventilation. In an SCAI survey, members recommended an update on guidelines for infection control in the cardiac catheterization laboratory. The following revision of the original 1992 guidelines is written specifically to address the increased utilization of the catheterization laboratory as an interventional suite with device implantation. In this update, infection protection is divided into sections on the patient, the laboratory personnel, and the laboratory environment. Additionally, specific CDC recommendation sections highlight recommendations from other published guidelines.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In 29 patients undergoing percutaneous coronary intervention (PCI), we obtained blood samples at baseline, 10 minutes after standard weight-based abciximab (n=15) or double-bolus eptifibatide (n=14) and 5 minutes after unfractionated heparin (UFH; 70 U/kg bolus). The median percent inhibition was significantly higher in the eptifibatide group compared with the abciximab group both before (96.5% [94-100] vs. 85% [77-89.5] [adenosine diphosphate; ADP]; 89.5% [84-95] vs. 59% [37.5-76.5] [thrombin receptor agonist peptide; TRAP], p<0.001 for both) and after UFH (95% [93-100] vs. 79% [68.8-87.5] [ADP]; 82% [77-93] vs. 51% [34.5-71.3] [TRAP], p<0.001 for both). Addition of UFH significantly reduced platelet inhibition in the abciximab group (85% [77-89.5] vs. 79% [68.8-87.5] [ADP]; 59% [37.5-76.5] vs. 51% [34.5-71.3] [TRAP], p<0.05 for both) but not in the eptifibatide group (96.5% [94-100] vs. 95% [93-100] [ADP]; 89.5% [84-95] vs. 82% [77-93] [TRAP], p=ns for both). Eptifibatide achieved superior platelet inhibition before but especially after UFH compared with abciximab.
Previous studies have demonstrated variation in vascular events with respect to season and time of day. Changes in barometric pressure display daily and seasonal variations and could modulate the occurrence of vascular events. The objective of this study was to determine whether a relation exists between changes in barometric pressure and occurrence of stroke or acute myocardial infarction (AMI). A retrospective analysis of hospital admissions for AMI and stroke from 1993 to 1996 in central Texas was related to changes in atmospheric pressure that were obtained from the National Climatic Data Center. Patients who had AMI (n = 1,327) or stroke (n = 839) were identified from a computerized hospital database. Mean atmospheric pressure, greatest change in pressure, and rate of change in pressure per 24-hour period were computed. One-, 2-, and 3-day and seasonal groupings of cardiovascular events were related to corresponding changes in barometric pressure. The fall and winter seasons had the highest variability in atmospheric pressure readings. There was a significant correlation (p = 0.0083) between a decrease in atmospheric pressure and the occurrence of AMI the day after a pressure decrease, especially during the fall and winter seasons. No relation between stroke and atmospheric pressure was demonstrated. In conclusion, we conclude that rapid decreases in barometric pressure are associated with the occurrence of AMI but not of stroke.
Mast cells may participate actively in the inflammatory process of atherosclerotic plaques by releasing proteolytic enzymes and various other pro-inflammatory substances. We hypothesized that increased levels of mast cell tryptase, could be an important biomarker in patients with stable coronary artery disease (CAD). We measured tryptase in 102 patients without acute coronary syndromes undergoing cardiac catheterization. Patients with significant CAD [> or =50% stenosis in > or =1 artery (n=66)] had significantly higher serum tryptase than patients with normal angiography (n=13) or non-significant CAD [<50% stenosis (n=23)]. The median, 25th and 75th percentiles for tryptase in these two groups were 8.38 (6.4 and 10.7)mug/L versus 6.78 (5.61 and 9.72) microg/L, p=0.014. Patients in the highest quartile of tryptase levels had a 4.3-fold risk for CAD [Odds ratio (OR): 4.3; 95% confidence interval (CI): 1.08-17.19; p=0.04]. In a multivariate regression analysis, tryptase remained an independent predictor for CAD along with age (OR: 1.178; 95% CI: 1.021-1.359, p=0.025). High circulating tryptase levels may be a result of chronic low-grade inflammatory activity present in atherosclerotic plaques. Tryptase measurements may emerge as a novel way of identifying asymptomatic patients with CAD, and represent a new biomarker of therapeutic efficacy in patients with CAD.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Manual hemostasis facilitated by a SyvekPatch with 1 hour of bedrest after coronary angiography using 6Fr catheters was evaluated in a study of 200 patients. There were no major adverse events and 2% minor adverse events, all of which were managed successfully with additional bedrest of 1 to 2 hours. The findings suggest that the 1-hour bedrest protocol using the SyvekPatch is safe and effective in low-risk patients.
Enoxaparin is being used more frequently in patients undergoing percutaneous coronary intervention (PCI). In this study, we determined the effect of intravenous enoxaparin on activated clotting time (ACT) measurements in the setting of PCI. In 67 consecutive patients, either 1 mg/kg intravenous enoxaparin alone was given for anticoagulation or 0.75 mg/kg given in patients receiving eptifibatide. ACT was measured before and 5 min following enoxaparin administration. After 1 mg/kg enoxaparin (n = 22), mean ACT increased from 122 +/- 22 to 199 +/- 20 sec. After 0.75 mg/kg enoxaparin and eptifibatide (n = 45), mean ACT increased from 125 +/- 22 to 194 +/- 24 sec. The mean increase in ACT was 77 +/- 26 sec in the 1 mg/kg group and 69 +/- 23 sec in the 0.75 mg/kg group (both P values < 0.0001). Moreover, in a subgroup of 26 patients, there was an excellent correlation (r = 0.86) between ACTs and the ENOX test, a new point-of-care test for assessing enoxaparin anticoagulation. None of the patients had transient abrupt closure, thrombus formation, major bleeding, or required urgent revascularization. Intravenous enoxaparin at clinically relevant doses with and without eptifibatide increases ACT levels at 5 min in patients undergoing PCI. These data suggest the ACT may be useful in the assessment of anticoagulation by enoxaparin.
Temporary pacing is occasionally required during percutaneous coronary artery interventions. This can be accomplished by the insertion of a temporary transvenous pacemaker wire into the right ventricle, but there is some risk and inconvenience associated with this approach. Temporary pacing using the coronary artery guidewire was described in 1985 but is used infrequently. Using currently available equipment, we evaluated guidewire pacing in 26 patients. Guidewire pacing was successful in all patients, but not with all coronary guidewires at acceptable ventricular capture thresholds. No complications occurred from guidewire pacing. Bench testing of multiple different wires showed several with very high resistances likely unsuitable for clinical use. Temporary guidewire pacing is easily performed and should be considered as an alternative to the separate placement of a temporary transvenous pacemaker.