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Abstracts Submitted:Oral Presentation (Medical Residents and Biomedical Post-docs only)
Oral session schedule posted at:http://www.etsu.edu.studentresearch/2004schedule.aspx
COMPARISON OF CT-SCAN, SPECT AND BIOPSY RESULTS IN EVALUATION OF PULMONARY NODULES
Michael Puruckherr MD, Payam Pooyan MD, Ryland P Byrd MD FCCP, Jay Metha MD FCCP, Mirle R Girish MD FCCP, Thomas M Roy MD FCCP, Veterans Affairs Medical Center, Mountain Home, TN 37684 and theDivision of Pulmonary Diseases and Critical Care Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN37614
Lung cancer is the leading cause of death secondary to a malignancy in many industrialized nations including the US. Newer non-invasive, less expensive techniques like SPECT-scan can be used to differentiate malignant versus benign lesion. This technique can also be used to determine lymph node involvement and metastatic spread of cancer.
The results of 23 patients who underwent a lung biopsy were retrospectively analyzed and compared to their prior obtained Tc 99m-depreotide-SPECT and CT scan. Also patient demographics including age, sex, body mass index (BMI) and symptoms (cough, hemoptysis and weight loss) were noted.
23 patients with lung biopsy: 16 of 23 (69.5%) had cancer (with 15 primary lung cancer and 1 metastatic) and 7/23 (30.5%) benign lesions. All 23 had a positive SPECT scan which gives an overall positive predictive value (PPV) of 69.5%. Altogether there were 17/23 (73.9%) lesions larger or equal 2 cm on CT the SPECT scan with altogether 13 biopsies positive for cancer (PPV of 76.4%). 6 lesions were smaller than 2 cm, 3 were positive for cancer which equals a PPV of 50%.
Depreotide-SPECT scan is an easily available, noninvasive and less expensive (than PET-scan) technique which can be used to diagnose suspicious malignant neoplasms. Our study showed the PPV increases significantly for lesions above 2 cm. The study is ongoing.
Syndrome X: a bit of a mystery
Anil K. Goli MD, Leeper Stephanie MD, Stephen A. Fahrig MD
Coronary artery disease is a leading cause of death worldwide. Over 1 million coronary angiograms are performed in north America annually, and a significant number are interpreted as normal. In the coronary artery surgery study registry of the 1970s, normal angiograms were found in 20% of patients. The prevalence of normal coronary angiograms has not changed in the current era of more sophisticated noninvasive testing, it is these sub-group of patients with positive stress test are classified as having cardiac syndrome X.
The term Cardiac Syndrome X was first used in 1973 to describe a condition that still to this day remains a bit of a mystery. There is still no agreed definition of Cardiac Syndrome X, the diagnosis is generally made when angina-like chest pain, a positive response to stress testing and angiographically normal coronary arteries are present. In the medical literature, the term microvascular angina has been used interchangeably with the term syndrome X. The prevalence of Syndrome X is significantly higher among post-menopausal women than among men.
More than 30 years after the initial publication, little more definitive information is known about this syndrome. It is now accepted as an heterogeneous clinical entity that is the product of genetic, coronary microvascular, metabolic, and clinical factors. Many theories have evolved through the years, including impaired coronary flow reserve, microvascular spasm, patchy prearteriolar vasoconstriction, disease of small arteries, pain due to excessive adenosine effect and estrogen deficiency.
Both short and long-term prognosis of patients with Syndrome X are excellent. Yet, symptoms can be invalidating and refractory to conventional anti-anginal treatment with nitrates, beta-blockers and calcium-antagonists. Additional drugs which might be helpful in symptom control include: estrogens, adenosine antagonists (theophylline) and tricyclic antidepressants.
We present 2 case reports of patients diagnosed with syndrome X treated with ACE inhibitor showed drematical symptomatic and clinical improvement, presumably due to improved coronary flow reserve due to increased nitric oxide bioavialability. And also discuss the role of long-term ACE inhibitor treatment improved coronary microvascular function as well as myocardial ischemia in patients with syndrome X. Further studies are needed to evaluate the effects of long term ACE inhibitor treatment on clinical outcome.
SIMULTANEOUS CAROTID ENDARTECTOMY AND CORONARY ARTERY BYPASS GRAFTING; RESULTS IN SPECIFIC PATIENT GROUPS
Panos Kougias MD, Jeffrey R Kappa MD, David H Sewell MD, Richard A Feit MD, Richard E Michalik MD, Mohamed Imam MD, East Tennessee State University, Department of Surgery, Johnson City, TN; Holston Valley Medical Center, Kingsport, TN
We examined the safety of performing synchronous carotid endarterectomy (CEA) and coronary revascularization (CABG) in specific groups of patients with coexistent cerebral and coronary vascular disease.Between 1981 and 2003 8277 patients that underwent CABG in our institution had routine noninvasive screening for carotid disease. Positive results were subsequently confirmed by arteriography or magnetic resonance angiography (MRA). Two hundred seventy seven (3.34%) patients were found to have severe (>70%) carotid stenosis. This patient population was divided in three subgroups. Group A: unilateral carotid disease (n=200). Group B: bilateral carotid disease (n=55). Group C: contralateral carotid occlusion (n=22). In 29 patients (10.4%) the carotid disease was symptomatic. A simultaneous CABG and CEA were performed in all three subgroups. Patients in group B underwent initially repair of the most dominant lesion, soon followed by contralateral CEA. Patients that underwent only CABG (n=8000) served as controls. Overall combined hospital mortality regardless of etiology for the combined group was 3.61% vs. 1.7% for the patients that had CABG only (p > 0.1). The stroke and/or myocardial infarction associated mortality for the simultaneous CEA CABG group was 2.45%. There were 6 deaths in group A (3%), 2 deaths in group B (3.6%) and 2 deaths in group C (9.09%). Early stroke complicated the course of 4 (2%) patients in group A, 1 (1.8%) patient in group B and 3 (13.64%) patients in group C, compared to a stroke rate of 1.28% in the controls (p > 0.1 for the groups A and B, the sample size was too small to make statistical significance results meaningful for the group C of patients with contralateral occlusion). Overall stroke rate in the combined group was 2.8%. History of previous stroke, the presence of contralateral occlusion (p < 0.001) and age > 60 (p < 0.05) were the most important predictors of postoperative stroke and death. In the combined surgery group the postoperative myocardial infarction rate was 0.72
STAPHYLOCOCCUS EPIDERMIDIS--A POTENTIAL RESERVOIR FOR ANTIBIOTIC RESISTANCE IN S. AUREUS
Mustafa Saad, Elaine Walker, Foster Levy, Scott Reynolds and Felix Sarubbi, James H. Quillen VA Medical Center, Mountain Home, TN 37684, and Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614.
Staphylococcus aureus is one of the most common pathogens associated with human disease. Pathogenicity is complicated by a notorious capacity for S. aureus to develop antibiotic resistance. For example, acquisition of resistance to methicillin (methicillin-resistant S. aureus or MRSA) is a widespread problem. Consequently, hospitalized patients have been treated with mupirocin ointment to eliminate nasal carriage of MRSA. Unfortunately, mupirocin use led to mupirocin-resistant MRSA at the James H. Quillen Veterans Affairs Medical Center (VAMC) and the trend towards increasing resistance was only reversed after mupirocin use declined. In a recent survey of staphylococcal colonization of nares in patients at the VAMC, the incidence of mupirocin resistance in S. aureus was low (3%) but resistance was relatively high (33%) in S. epidermidis. Gene exchange is known to occur between these two related species and we have demonstrated interspecific transfer of mupirocin resistance using local isolates. We hypothesized that mupirocin resistance in S. epidermidis was a consequence of high antibiotic usage and that mupirocin resistance would be absent in S. epidermidis recovered from a hospital with a history of lower mupirocin usage. A test of the hypothesis was conducted using samples of S. epidermidis recovered from the Johnson City Medical Center (JCMC). Fifty coagulase-negative staphylococci, a majority of which were S. epidermidis, were isolated from patients at the JCMC, speciated using api Staph (Biomerieux) and tested for mupirocin susceptibility using Etest (AB BioDisk). Interestingly, mupirocin resistance was noted in approximately 40% of these isolates, a frequency similar at the VAMC. A retrospective analysis of archived isolates (1997-8) from the JCMC revealed mupirocin resistance was common (29%) in MRSA at the JCMC at the time when mupirocin-resistant MRSA was widespread at the VAMC. A current (2004) collection of JCMC MRSA is now undergoing mupirocin susceptibility testing. We hypothesize that MRSA from the JCMC will show a parallel pattern of mupirocin resistance frequencies similar to those at the VAMC with a high frequency of resistance in the 1990s and a current low frequency. Regardless of the results, the current prevalence of mupirocin resistance at both facilities and the demonstration of interspecific transfer of resistance in vitro raise concern that S. epidermidis may be functioning as a regional reservoir for antibiotic resistance in S. aureus.
ANGIOTENSIN CONVERTING ENZYME INHIBITORS MAY DECREASE THE RISK OF DEVELOPING RIGHT VENTRICULAR DYSFUNCTION IN PATIENTS WITH ACUTE PULMONARY EMBOLISM.
Kais Albalbissi, MD, Bahaeddin Shabaneh, MD, Jack Whitaker, MD, FACC, Israel Garcia, MD, Division of Cardiology, Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University
Right ventricular dysfunction is an ominous sign in patients with pulmonary embolism. It is associated with poor short-term and long-term outcomes. Right ventricular dysfunction is diagnosed primarily by echocardiography. Other potentially useful tests are electrocardiography, elevated cardiac enzymes and probably elevated beta type natriuretic peptide. Fibrinolytics could potentially treat this condition but they have limited indications and safety concerns.
Our study is a retrospective analysis of 200 charts of hospitalized patients with a primary diagnosis of pulmonary embolism. Thirty-two charts only qualified for inclusion into the study. All patients were hospitalized with acute pulmonary embolism. Among the 32 patients who were included in the study, 12 patients (37.5%) were on angiotensin converting enzyme inhibitor as outpatient therapy. From these 32 patients, 12 patients (37.5%) had evidence of right ventricular dysfunction by electrocardiographic or echocardiographic criteria with absence of an alternative diagnosis. Among the patients who were on angiotensin converting enzyme inhibitor therapy, only 3 patients (25%) developed right ventricular dysfunction. On the other hand, among the patients who were not on angiotensin converting enzyme inhibitor therapy, 9 patients (45%) developed right ventricular dysfunction.
We conclude that patients admitted to the hospital with the diagnosis of acute pulmonary embolism have less risk of developing right ventricular dysfunction if they were on prior angiotensin converting enzyme inhibitors. Potential explanations include suppression of angiotensin II which is associated with decreased t-PA, increased PAI-1, platelet activation and pulmonary vasoconstriction. This is a retrospective analysis with several limitations but further studying is needed to elucidate this plausible protective role.
DISCOVERY OF A C-REACTIVE PROTEIN MUTANT THAT DOES NOT BIND TO LOW-DENSITY LIPOPROTEIN
Sanjay K. Singh, M. V. Suresh, Antonio E. Rusinol and Alok Agrawal, Department of pharmacology and Department of Biochemistry & Molecular Biology, ETSU, Johnson City, TN - 37614
Human C-reactive protein (CRP) is an acute phase protein whose production by hepatocytes is induced under inflammatory conditions. Elevated serum CRP level indicates the onset or the presence of inflammatory diseases such as atherosclerosis. Immunohistochemistry has shown deposition of CRP in the atherosclerotic lesions and it is felt that CRP may play a role in the development of such lesions. The major binding specificity of CRP is for phosphocholine (PCh)-containing ligands including oxidized low-density lipoprotein (oxLDL). The goal of the present study was to define the binding site on CRP for oxLDL. We hypothesized that the PCh-binding site of CRP might be involved in binding to oxLDL because PCh was found to inhibit CRP-oxLDL interaction. Based on the crystal structure of CRP-PCh complex, we previously employed site-directed mutagenesis to mutate the PCh-binding site and generated a CRP mutant (F66A) incapable of binding to PCh. To test the hypothesis that the PCh-binding site of CRP is also involved in binding to oxLDL, we compared the ox-LDL-binding activity of native and F66A mutant CRP. In an ELISA-based CRP-oxLDL binding assay that we developed for this purpose, native CRP bound to oxLDL in a dose-dependent manner while the F66A mutant did not bind oxLDL at all. We conclude that the PCh-binding site of CRP participates in the interaction with oxLDL and that Phe66 in CRP is critical for binding to both PCh and oxLDL. For our ongoing experiments employing ApoE knockout mice to investigate the functions of passively administered human CRP in atherosclerosis, the F66A CRP incapable of binding to PCh and oxLDL is a precious mutant.
Hepatitis C and Dilated Cardiomyopathy
Said Iskandar, MD, Stephen D. Loyd, MD, Christopher J. Downs MD, FACC, Thomas M. Roy, MD, FCCP, FCCM, Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University
Hepatitis C virus is the most common blood-borne infection in the United States. It is the leading cause of chronic liver disease with about 35000 new cases diagnosed each year. The prevalence of infection remains high (approximately 2.7 million Americans) as chronic hepatitis C develops in up to 85% of those infected Although the enteroviruses are implicated as the most common pathogens responsible for viral myocarditis, preliminary reports suggest that hepatitis C virus (HCV) infection may also be associated with several myocardial diseases, including dilated cardiomyopathy and myocarditis. A 55-year-old African-American female who was diagnosed with hepatitis C in 1993 presented to the emergency room with a 3-day history of persistent chest discomfort. Her pain was not relieved with sublingual nitroglycerin or antacids. She also complained of dyspnea with exertion, orthopnea and paroxysmal nocturnal dyspnea. Her last echocardiogram 1 month ago showed an ejection fraction (EF) of 40-45% with mild mitral regurgitation. On physical examination her vitals were stable. Distended jugular veins, bilateral crackles, an S3 sound as well as a IV/VI systolic ejection murmur that was best heard over the apex of the heart were noted. A repeated echocardiogram showed an ejection fraction of 20% with severe hypokinesis and akinesis of the anteroseptal region of the left ventricle, and severe mitral and tricuspid regurgitation. Her cardiac catheterization was normal. Acute myocarditis was suspected. Viral serology done for the most common causes was negative.
PCR for hepatitis C virus showed 900,000 copies/mL (360000 IU/mL). An interleukin 1-beta level was 20 pg/ml (<150 pg/ml), interleukin-6 was 44 pg/ml (<5 pg/ml) and interleukin-2 was 2143 pg/ml (190-570 pg/ml). The patient was referred for repair of her mitral valve. She appeared to tolerate her surgery well and was discharged home in a stable condition. Patient had refused muscle biopsy before the procedure. Within 2 weeks, she again developed chest pain and the signs and symptoms of congestive heart failure recurred. She was hospitalized but she eventually succumbed to arrhythmia and multiorgan failure. Her severe and acute cardiomyopathy was related to myocarditis thought to be due to hepatitis C virus infection since no other etiology could be found.
To our knowledge, our patient would be the first reported case in the USA suggesting a possible association between HCV and dilated cardiomyopathy. In the absence of a controlled trials in the United States, we can only offer our observations with the hope that clinicians treating patients with HCV infection become aware of this possible association that has been made in other parts of the world.
COLORECTAL CANCER IN ELDERLY: PATTERN OF CARE STUDY.
O. Aljitawi, T. Ward, and A. Karnad. Division of Hematology/Oncology, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614
Introduction: Cancer is an age-related disease with peak incidence and mortality rates in the segment of population 65 years and older. Thus, it is surprising that so little descriptive information is available about cancer treatment in older persons. Colorectal cancer is second only to lung cancer as a cause of cancer death in the United state, it generally occurs in individuals 50 years. Currently, 60% occurs in patients over 65 years of age. More than one half of these are over 70 years old and one fourth are over eighty years old. Though treatment guidelines are available for younger age groups with colorectal cancer, only limited data are available on the risks and benefits of specific cancer treatment regimens in the elderly, especially in those 80 years old.Methods: In this retrospective study we utilize veteran affair hospitals data base for newly diagnosed cases of colorectal cancer in patients 80 years old across the country during the period 2001-2002. Data regarding age at diagnosis, histology, stage (utilizing TNM staging), and treatment were extracted. Results: Of the patients 80 years old diagnosed with colorectal cancer, 310(83%) were in 80-85 age group, and 60 patients were above 85(17%). Adenocarcinoma was diagnosed in 317 patients. These 317 patients had the following stages: stage 0(in situ) in 26 patients, stage 1 in 66, stage IIa in 85, stage IIb in 7, stage IIIa in 6, IIIb in 37, IIIc in 18, and finally stage IV in 63. Stage was unknown in 51 patients. Eight patients had chemotherapy alone, 8 had radiation therapy alone, 6 received chemotherapy and radiation, and 240 had surgery with no post-op chemotherapy. Only 34 patients received adjuvant chemotherapy following surgery, of these 8 received radiation treatment for rectal cancer. No treatment was offered to 62 patients. Significant number of patients 80 years with colorectal cancer didnt have formal staging (51 out of 317). Of the 153 patients eligible for adjuvant chemotherapy according to stage alone (stage II and III), only 34(approximately one third) patients received chemotherapy. Conclusion: Though elderly represent the peak age group for colorectal cancer they are less likely to receive the standard of care in terms of cancer staging and treatment.