ABSTRACT
BACKGROUND: As part of conducting a randomized control trial (RCT) to treat chronically high utilizing patients with medically unexplained symptoms (MUS), we developed the chart rating method reported here to identify and classify MUS subjects. METHOD: Intended at this point only as a research tool, the method is comprehensive, uses explicit guidelines, and requires clinician raters. It distinguishes primary organic disease patients from those with primary MUS, quantifies medical comorbidities in primary MUS patients, and also distinguishes subgroups among MUS patients that we call somatization (resembles DSM-IV somatoform disorders) and minor acute illness (MAI) which differs from DSM-IV somatoform definitions. Scoring rules are used to generate the diagnoses above. The rules may be set according to the investigator's needs, from highly sensitive to highly specific. RESULTS: We found high levels of agreement with the gold standard for MUS vs. organic disease (97.6%) and among raters for the key individual chart elements rated (92-96%). The method identified 206 MUS subjects and the extent of their medical comorbidities for entry into a RCT. It also identified somatization and MAI; the latter supports the validity of this newly reported MAI syndrome. CONCLUSION: We concluded that this method offered research potential for identifying MUS patients, for quantifying their medical comorbidities, and for classifying MUS subgroups.
Subject(s)
Practice Guidelines as Topic , Psychiatric Status Rating Scales , Psychophysiologic Disorders/classification , Psychophysiologic Disorders/diagnosis , Comorbidity , Diagnosis, Differential , Diagnostic and Statistical Manual of Mental Disorders , False Positive Reactions , Health Status , Humans , Medical History Taking , Medical Records , Observer Variation , Physician-Patient RelationsABSTRACT
Distal coronary artery perforation with a coronary guidewire is a relatively rare but potentially fatal complication during PTCA. Historically, these types of perforations have been easy to control with reversal of heparin anticoagulation combined with prolonged distal balloon inflation. In the modern era, with widespread use of potent glycoprotein IIb/IIIa inhibitors, this type of distal wire perforation has become more difficult to manage and potentially lethal. In this article, we report two cases of guidewire-related distal coronary artery perforation, successfully treated using a new technique using localized, distal intracoronary thrombin injection. During prolonged low-pressure balloon inflation, a small dose of thrombin was injected just proximal to the wire perforation site via the lumen of a coronary balloon catheter. This approach appears to be a relatively rapid and effective way to control this troublesome complication.
Subject(s)
Angioplasty, Balloon, Coronary/adverse effects , Catheterization/methods , Coronary Vessels/injuries , Heart Injuries/etiology , Heart Injuries/therapy , Hemostatics/administration & dosage , Hemostatics/therapeutic use , Injections, Intralesional/methods , Intraoperative Complications , Thrombin/administration & dosage , Thrombin/therapeutic use , Aged , Aged, 80 and over , Coronary Angiography , Female , Heart Injuries/diagnostic imaging , Humans , MaleABSTRACT
OBJECTIVE: Thrombin activates platelets and contributes to the occlusion of arteries following thrombolytic therapy or angioplasty. Thrombostatin (RPPGF), the angiotensin converting enzyme degradation product of bradykinin, inhibits alpha-thrombin induced platelet activation. We hypothesized that thrombostatin prevents platelet aggregation and adhesion after balloon angioplasty (BA). METHODS: Platelet-rich plasma (PRP) was obtained from 22 Beagle dogs before sacrifice and 10% of the PRP was labeled with 111In. Carotid arteries were then removed from each dog and mounted in a dual perfusion chamber and intimal injury was performed with BA. 111In-PRP with or without thrombostatin or aspirin alone was perfused through the arteries for 60 min. During perfusion, platelet volume was measured using a Coulter counter and a laser-light scattering technique. Platelet adhesion to arteries was measured by radioactivity count. RESULTS: Arterial injury alone compared to non-injury increased platelet volume in the circuit by 1.4 times (x) (P<0.05) using a Coulter counter or 1.8x (P<0.05) using laser-light scattering and increased platelet adhesion by 2.3x (P<0.01). When compared to BA injury alone, the addition of thrombostatin reduced platelet volume by 1.8x (P<0.03) as measured by Coulter counter or 1.9x (P<0.01) by laser-light scattering and platelet adhesion by 4.2x (P<0.05). Compared to BA injury alone, aspirin reduced platelet volume by 1.2x (P<0.01) as assessed by Coulter counter or 1.5x (P<0.03) using laser-light scattering and platelet adhesion by 1.8x (P<0.02). CONCLUSION: Thrombostatin or aspirin independently decreases evidence of platelet activation in the canine carotid artery model of BA injury.
