2003 ACC Abstract submissions.
IDIOPATHIC HYPEREOSINOPHILIC SYNDROME OF THE HEART.
F Omar MD, D Obeid
MD, G Krishnamorthy MD.
Presented by: Fazal Omar, MD - Sinai-Grace Hospital/Wayne State University
Idiopathic Hypereosinophilic
Syndrome (Loeffler’s syndrome) is a rare disease characterized by eosinophilia associated
with signs and symptoms of end organ dysfunction. Most commonly it affects the heart, skin,
nervous system, lung and spleen.
Here we present a case of
Loeffler’s syndrome with a cardiac presentation.
The patient is a 30 year old
male presented with atypical chest pain.
He had normal physical exam but stress test showed a partially
reversible apical defect. He had high
eosinophil count unexplained by any other etiologies. Cardiac catheterization showed normal
coronaries; 2-D echo showed increased endomyocardial echodensity at the apex
which suggested Loffler’s syndrome.
Biopsy of the Myocardium revealed eosinophilic infiltrates thus
confirming the diagnosis of Loeffler’s syndrome of the heart. The patient was started on Steroids and
experienced significant clinical improvement.
It is very important to
diagnose Loeffler’s syndrome as early as possible because starting treatment
early will decrease mortality and morbidity especially in younger male
patients.
Submitted for ACC Oral Case Presentation
ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY/
DYSPLASIA: PRESENTING AS SHOCK, ACUTE RENAL FAILURE AND TRANSIENT MESENTERIC
ISCHEMIA.
Manesh Kottapuram, M.D.,
Barry Lesser, M.D., F.C.C.P.,
Department of Medicine, Sinai-Grace Hospital, Wayne State University, Detroit,
Michigan.
Presented by: Manesh Kottapuram, MD - Sinai-Grace Hospital/Wayne State University
Arrhythmogenic right
ventricular (RV) Cardiomyopathy/Dysplasia (ARVC/D) is a rare myocardial disease
affecting primarily the RV and characterized histologically by the gradual
replacement of cardiomyocytes by fibro-fatty tissue. It can diffusely involve the whole myocardium
and culminate in biventricular heart failure, arrhythmias and sudden death in young
patients.
We present a forty-five year
old African-American man brought to the emergency room (ER) with complaints of
fever, abdominal pain, vomiting and bloody diarrhea of four days duration. He was a smoker and there was no significant
past or family medical history. At
admission, he was hypothermic (93oF), tachycardic (130/minute),
tachypneic (40/minute) and hypotensive (50/palpable). He appeared drowsy, dehydrated and had
diffusely tender abdomen with decreased bowel sounds. His stool was positive for occult blood. Initial labs were significant for Na+
127, Cl- 82, HCO3- 12 (mmol/L); BUN 70,
Creatinine 8.7 (mg/dL); WBC 10.6 (bands 3.8) K/mm3; ALT 162, AST 257
(U/L), and lactic acid 4.9 mmol/L.
Electrocardiogram was significant for sinus tachycardia and abdominal x-ray
showed small bowel wall edema with ileus.
He remained hypotensive despite intravenous fluids, vasopressors and
broad spectrum antibiotics.
ARVC/D is typically seen in
young men as an autosomal dominant trait with multiple factors facilitating
gene expression. Physicians should
consider this condition in young subjects with cardiac arrhythmias or
unexplained cardiomyopathy. Treatment includes class I antiarrhytmic drugs,
beta blockers, amiodarone, radiofrequency ablation and patients with high risk
of sudden death should receive an implantable cardioverter/defibrillator.
Submitted for ACC Oral Case Presentation
Expression of B2 subunit mutants alters localization of L-type calcium channels in
rat adult cardiomyocytes
Sinoj K John MD, Sabine
Telemaque-Potts MD, Terrie Grain MD, Jeffrey T Potts MD, James D Marsh MD. Sinai-Grace Hospital,
Wayne-State University, Detroit, Michigan, Internal Medicine - Cardiology,
Wayne-State University, Detroit, Michigan.
Presented by: Sinoj k. John, MD - Sinai-Grace Hospital/Wayne State University
Introduction:
The a1C subunit of the L-type calcium
channel is the pore-forming subunit of the channel, allowing calcium entry into
cardiomyocytes and other cells. The intracellular b2a subunit acts as a chaperone
and interacts with the intracellular loop of the a1C subunit. We tested the
hypothesis that overexpession of mutated b subunits could alter membrane
localization and ultimately channel function.
Methods:
Isolated rat adult
cardiomyocytes were infected with adenovirus constructs. The GFP-fusion
constructs encoded either the full-length b2a subunit (GFP-Full) or
putative dominant-negative mutants of the beta interaction domain (BID) portion
of the subunit (GFP-BID: BID only; GFP-N-BID: N-terminal + BID), under CMV
promoter control. After 24 hr, cells were fixed and visualized by
epifluorescence microscopy using standard methods.
Results:
Analysis of 5 independent
cell isolations showed that GFP or GFP-BID are localized to the cytosol of the
myocyte. In GFP-N-BID-infected myocytes, a distinct punctate pattern of protein
expression was observed in all infected cells, without cell membrane
localization. In cells infected with the full-length b2a subunit adenovirus
(GFP-Full), the fluorescence was exclusively visible at the cell membrane.
Conclusion:
These results suggest that
beta subunit decoys can alter localization of the L-type calcium channel to the
sarcolemma, which could result in reduced contractile performance.
Submitted for ACC Poster Research Presentation
CORONARY ARTERY DISEASE RISK FACTORS AMONG PATIENTS WITH
UNRECOGNIZED DEPRESSION. Mehrdad Ghaffari, MD, Haleh Haerian, MD,
Mohamed Karim, MD, Rajika Munasinghe, MD, Sinai-Grace Hospital, Wayne State
University, Detroit, Michigan.
Presented by: Mehrdad Ghafffari, MD - Sinai-Grace Hospital/Wayne State University
Introduction:
Depression is associated with increased morbidity and mortality in patients
with established coronary artery disease (CAD) but the association between
depression and CAD risk factors has been found to be variable. The objective of
this study was to determine the extent of unrecognized depression in an inner
city, primary care internal medicine practice and to evaluate the CAD risk
among patients with unrecognized depression.
Methods: Patients
without a prior diagnosis of depression were screened using the Prime MD
questionnaire, a validated screening tool developed to evaluate for depression.
Information on CAD risk factors was obtained from chart review. The prevalence
of individual CAD risk factors and the composite 10 year CAD risk based on the
Results: Out
of a total of 215 patients evaluated, 53 (24.6%) screened positive for
unrecognized depression. A total of 103 patients without depression and 39
patients with depression had complete information for a comprehensive
assessment of 10 year risk of CAD. Patients with depression were younger (Mean
age 51 vs 56 years P<.035) and had higher diastolic blood pressures
(DBP 86 vs 76 mmHg, P<.01) compared to patients without depression.
The 10 year CAD risk among patients with depression was 9% and comparable to
patients without depression (11%, P=.15). Other CAD risk factors were
similar between the two groups.
Discussion:
Unrecognized depression among patients surveyed in our practice was comparable
to previous estimates reported in the literature. We did not find unrecognized
depression to be associated with a higher risk for CAD.
Submitted for ACC Poster Research Presentation
DO PATIENTS WITH UNRECOGNIZED DEPRESSION RESPOND DIFFERENTLY TO CAD RISK MODIFICATION IN THE PRIMARY CARE SETTING? Mehrdad Ghaffari, MD, Haleh Haerian, MD, Mohamed Karim, MD, Rajika Munasinghe, MD, Sinai-Grace Hospital, Wayne State University, Detroit, Michigan.
Presented by: Mehrdad Ghafffari, MD - Sinai-Grace Hospital/Wayne State University
Introduction:
Depression is known to adversely affect compliance with medical therapy and
rehabilitation after myocardial infarction. The impact of unrecognized
depression on the response of modifiable CAD risk factors to intervention in
the primary care setting is less well known.
Methods:
Established patients in a primary care internal medicine practice were screened
for unrecognized depression using the Prime MD questionnaire, a validated tool
used to screen for depression. Information on the most recent CAD risk assessment
and the predicted 10 risk of CAD based on the
Results: The
systolic and diastolic blood pressures, the LDL cholesterol level and the
Hemoglobin A1c of diabetic patients decreased significantly with treatment. The
mean 10 year risk of CAD declined from 13.7% to 11.9% (p<.001). There were
no significant differences in the magnitude of change in CAD risk factors and
the 10 year CAD risk between patients with unrecognized depression and
controls. The power of this study to detect a 5% or greater difference in each
of the CAD risk factors was greater than 80%.
Conclusion: Unrecognized depression does not appear to
influence the treatment of CAD risk factors in the primary care setting.
Independent of this finding both CAD prevention and screening and treatment of
depression should be pursed aggressively to improve patient outcomes.
Submitted for ACC Poster Research Presentation
IMPLANTABLE-DEFIBRILLATOR
THERAPY IN COXSACKIE VIRUS-INDUCED CARDIOMYOPATHY
Lourin Chahin, MD, Apurva Motivala, MD, Atul Singh, MD, Marc Meissner, MD, FACC, Dept. of Medicine, Sinai-Grace Hospital, Wayne State University - Detroit, Michigan.
Presented by: Lourin Chahin,
MD - Sinai-Grace Hospital/Wayne State University
Case Report
We
describe a 20-year-old African-American male presenting with severe symptoms of
congestive heart failure (CHF) following an upper respiratory infection. Physical examination revealed respiratory
distress, bilateral rales, summation gallop and mitral regurgitation
murmer. 2D-echocardiography revealed
left ventricular ejection fraction of 20%, global hypokinesis, mitral and
tricuspid regurgitation. He was
discharged after good response to pharmacologic therapy.
Hypertension,
alcohol, toxins, illicit drugs were excluded as etiologies. His presentation
was felt to be due to post-viral myocarditis/cardiomyopathy. Thus, we requested Coxsackie blood titers. B5
titers returned as 1:320.
The
patient returned 2 weeks later with CHF exacerbation. Telemetry tracings variously revealed unsustained
atrial tachycardia, AV- block (Wenckebach, high-grade, 4-second ventricular
asystole), and rapid unsustained ventricular tachycardia (VT).
A
dual-chamber implantable defibrillator (ICD) system was placed, to allow safe
optimization of medical therapy (eg. use of beta blockers in face of
above-noted AV-block), and to protect against sudden death, to which such
patients are very vulnerable. Subsequent
ICD testing revealed elevated defibrillation thresholds (DFTs), and the system
was modified: generator change and
addition of defibrillation-pacing lead placed in a posterolateral coronary vein
via the coronary sinus. This resulted in
successful biventricular pacing and good DFTs.
Conclusion
This
case highlights several interesting points:
wide range of brady- and tachy-arrhythmias in a young man with Coxsackie
cardiomyopathy; technical feasibility and potential therapeutic value of
biventricular 3-lead ICD system capable of improving CHF symptoms and
protecting against sudden death.
Submitted for ACC Oral Case Presentation
MASSIVE RIGHT VENTRICULAR THROMBUS PRESENTING AS ACUTE
ABDOMEN
Manesh Kottapuram, MD,
Shazia Essani, MD, Department
of Internal Medicine, Sinai-Grace Hospital, Wayne State University, Detroit,
Michigan.
Presented by: Manesh Kottapuram, MD - Sinai-Grace Hospital/Wayne State University
Acute
cor pulmonale due to massive right ventricular thrombus presenting as acute
abdomen is a rare event.
We
present a 21 year old caucasian woman who presented to the emergency room with
sudden onset of abdominal pain and shortness of breath. Pain was continuous and generalized but
mainly in the left upper and lower quadrant.
She had three episodes of vomiting.
Past medical history was significant for asthma. She was actively using cocaine and heroin at
the time of hospital admission. Her
initial blood pressure was 100/60 mm of Hg, pulse rate of 112/minute,
respiration of 36/minute and was afebrile.
Her oxygen saturation was 92% on 50% oxygen. She had diffusely tender abdomen with rebound
and guarding but no rigidity. Bowel
sounds were sluggish. She had 2 cm
jugular venous distention and a 2/6 pansystolic murmur in left lower sternal
border. Her labs were significant for
ALT 143, AST 214 (U/L), and PT 13.6.
Electrocardiogram was significant for sinus tachycardia, right atrial
enlargement and incomplete right bundle branch block. Her CT scan of abdomen and pelvis showed
hepatomegaly, large ascites, and cardiomegaly with dense opacification of
cardiac chambers suggestive of delayed circulation. 2D echo showed dilated right atrium and 80%
of right ventricle cavity occupied by a heterogeneous echoic mass suggestive of
tumor. She also developed DVT involving
left brachial, axillary, internal jugular and subclavian vein during hospitalization. She underwent open heart surgery and the mass
was removed. Histology of the lesion
demonstrated a chronic organized thrombus.
Culture of the thrombus was negative.
Her initial hypercoagulable workup (including antiphospholipid antibody
syndrome) was negative.
Right ventricular thrombus has been described in literature, as they were associated with antiphospholipid antibody syndrome and Behcet’s disease. In our patient none of these were found. Also in our patient right ventricular thrombus simulated a cardiac tumor, which is a rare presentati
Submitted for ACC Oral Case Presentation
MATURATION OF THE
MICROVASCULATURE IN HEALING MYOCARDIAL INFARCTS: A POTENTIAL ROLE FOR PDGF.
1KAMAL
1Department
of Internal Medicine, Sinai-Grace Hospital, Detroit Medical Center/Wayne State
University, Detroit MI, and 2Section of Cardiovascular Sciences,
DeBakey Heart Center, Baylor College of Medicine, Houston TX.
Presented by: Manesh Kottapuram, MD - Sinai-Grace Hospital/Wayne State University
Background: The microvasculature in healing wounds undergoes
dynamic changes leading to formation of mature pericyte-coated vessels.
Platelet Derived Growth Factor (PDGF) is crucial for the formation of a
pericyte coat in the developing embryonic vasculature. We hypothesize an
important role for PDGF in vascular maturation of infarct neovessels,
critically regulating healing.
Aims: To investigate the dynamic changes in the infarct microvasculature
and the phenotypic characteristics of smooth muscle cells and fibroblasts in
canine and murine models of experimental myocardial infarction, and to study
the role of PDGF in maturation of the infarct neovasculature.
Methodology: We used established canine and murine models of
experimental myocardial infarction. Hearts were processed and used for
histological studies. Isolated canine jugular vein endothelial cells were used
for in vitro experiments.
Results: The proliferative stage of infarct healing is
characterized by myofibroblast accumulation and a high number of capillaries
critical for sustaining metabolism. In both canine and murine models, infarct
maturation is associated with a decreasing capillary density and an increasing
number of pericyte coated vessels (p<0.01, 7d reperfusion vs 28 days
reperfusion). The muscular coat of infarct vessels stains for a-Smooth Muscle Actin (a-SMAc) and calponin. Only a
subset of the vessels exhibits expression of desmin and smoothelin, markers of
mature contractile smooth muscle cells. PDGF is highly expressed in infarct
neovessels. In addition, PDGF Receptor b is markedly
upregulated in pericyte-like cells infiltrating the infarcted myocardium. PDGF
receptor a synthesis is found in a subset of myofibroblasts and
endothelial cells. Purified PDGF and recombinant PDGF-AA and –BB significantly
induce mRNA expression of the matrix cross-linking enzyme tissue
transglutaminase (tTG) in canine endothelial cells.
Conclusion: The infarct microvasculature undergoes dynamic
changes leading to formation of mature pericyte-coated vessels. PDGF may play
an important role in maturation of the infarct vasculature through regulation
of vascular pericyte coating and by inducing endothelial expression of the cross-linking
enzyme tTG, promoting endothelial basement membrane maturation. Further
experiments using neutralizing antibodies in mice undergoing infarction
protocols will determine the role of PDGF in healing infarcts.
Submitted for ACC Poster Research Presentation
RIGHT ATRIAL MASS PRESENTING AS SYNCOPE – A CASE REPORT. Siddhartha Annamraju, MD, Vijayalakshmi Sankaranarayanan, MD, Antonio Carrillo, MD, FACC and Frank Baciewicz, MD, Sinai-Grace Hospital, Detroit Medical Center / Wayne State University, Detroit, Michigan
Presented by: Siddhartha Annamraju, MD - Sinai-Grace Hospital/Wayne State University
Right atrial masses, viz.
myxomas and thrombi are not entirely uncommon clinical occurrences. Thrombi
attached to the tip of indwelling intravascular catheters aren’t infrequent
either. However, masses attached to the tips of catheters and extending into
the right atrium and ventricle causing
syncope, to the best of our knowledge, have not been reported in the
literature. We present to you the case of a 45-year old lady who presented to
our Emergency Department with syncope and cyanosis. She had a
Submitted for ACC Oral Case Presentation
NON-OBSTRUCTIVE TRIPLE
VESSEL CORONARY ARTERY ANEURYSMS CAUSING
ST ELEVATION MYOCARDIAL INFARCTION: A CASE REPORT.
Fadi A. Saab, MD,
Presented by: Fadi Saab, MD - Sinai-Grace Hospital/Wayne State University
Multiple Coronary Artery Aneurysms are rarely seen in adults. In association with Myocardial Infarction, there are less than ten cases reported since 1967.
A 55 year-old African- American male presented to the emergency department with classical features of myocardial infaction. Risk factors for coronary artery disease included cigarette smoking and strong family history. EKG displayed ST-elevations in the inferolateral leads. He was treated with Reteplase, intravenous heparin, intravenous nitroglycerin, beta-blocker, and aspirin. He continued to have angina and underwent emergency cardiac catheterization which revealed diffuse aneurysmal dilatation of the Right Coronary, Left Anterior Descending and Left Circumflex Arteries with slow flow. Dilatations ranged from 6 to 8 millimeters. No occlusions were seen. Our patient was discharged two days later with standard medical management and Cardiac Rehabilitation Phase II.
In adults, in addition to congenital aneurysms the etiology of Multiple Coronary Aneurysms includes Systemic Lupus Erythematosis, Neurofibromatosis, Atherosclerosis and Chest Trauma. Treatment options include lifelong anticoagulation, stenting, and surgery although not all authors agree that any treatment is required. Our patient had no evidence of any of the above etiologies for Coronary Aneurysm outside of possibly a Congenital cause.
Coronary Aneurysms are rare in adults and even more rarely lead to ST-Elevation Myocardial Infarction. A consensus on any treatment in addition to the standard Myocardial Infarction medical management has yet to be reached.
Submitted for ACC Oral Case Presentation
Protection of Cardiomyocytes against Metabolic Stress by 17b-Estrogen in Culture
Manesh Thomas Kottapuram, M.D., Department of Internal Medicine, Sinai-Grace Hospital; Dr.Kuo TH, Department of Cell Pathology, Wayne State University School of Medicine, Detroit, Michigan.
Presented by: Manesh Thomas Kottapuram, MD - Sinai-Grace Hospital/Wayne State University
Objectives:
To understand the mechanism in which estrogen protects cardiomyocytes in culture against metabolic stress injury.
Background:
Recent clinical studies indicate that females are protected from a variety of cardiac events including ischemic injury comparable to the male counterparts (ref.1). The beneficial effects of estrogen on the cardiovascular system have been traditionally ascribed to decrease in peripheral vascular resistance and antiatherogenic action (ref.2, 3). However the molecular mechanism for this protection is still poorly understood.
Hypothesis:
Estrogen may protect cardiomyocytes by upregulating the Akt kinase signal transduction pathway and by accomplishing Ca2+ homeostasis at cellular level against different metabolic stresses.
Methods:
Ventricular cardiomyocytes isolated from female Sprague- Dawley rats (ref.4) were incubated in serum free culture medium with and without 17 b- estradiol. Then cells were either lysed to isolate proteins for detection of (a) activation of Akt signal transduction pathway or (b) treated with various agents (2-3 DNP, Thapsigargin, and Ionomycin) to induce chemical hypoxia and Ca2+ loading in cardiomyocytes. Activation of Akt kinase determined by Western Blot assay (ref.5) using specific anti-phospho-Akt antibody. Ca2+ loading and its subsequent homeostasis assessed by Fura-2 dye and dual excitation fluorometer (ref.6).
Results:
Estrogen may upregulate Akt signal transduction pathway in cardiomyocytes. Pre-treatment with estrogen significantly affects Ca2+ loading in cardiomyocytes either by decreased rate of loading or by facilitating efflux of cytoplasmic Ca2+.
Conclusion:
The preliminary reports may support the hypothesis of “protective effect of
estrogen on cardiovascular system can be attributed either to the upregulation
of Akt kinase signal, which is a well-known ‘antiapoptotic’ cell survival
signal or to the efficient cytoplasmic Ca2+ homeostasis in
cardiomyocytes”.
Submitted for ACC Poster Research Presentation
ICD DEFIBRILLATION THRESHOLD DETRMINATION VIA SINGLE VF INDUCTION
Siddhartha Annamraju, M.D., Randy Lieberman, M.D.,FACC, Marc Meissner, M.D.,FACC, Sinai-Grace Hospital, Wayne State University, Paul DeGroot, Michael RS Hill, Medtronic Research
Presented by: Siddhartha Annamraju, MD - Sinai-Grace Hospital/Wayne State University
Introduction: Determination of defibrillation threshold (DFT) at the time of ICD implant enables programming the ICD to an energy less than full output. This decreases capacitor charge time and episode duration and conserves battery energy. However, accepted DFT protocols such as Binary Search (BS) or Step-Down methods require multiple VF (ventricular fibrillation) inductions. Fewer VF inductions and an appropriate determination of DFT are clinically desirable. We hypothesized that the DFT can be determined by a single VF induction utilizing a Step-Up (SU) protocol.
Methods: After informed consent was obtained, paired DFTs were determined in patients undergoing initial ICD implant for approved indications using an active Can + transvenous RV lead system. In the SU protocol, energies of 3-6-10-12-15-18 joules were delivered sequentially after a single VF induction until VF was terminated. SU DFT was defined as the energy that terminated VF. DFT was also measured using BS protocol starting at 12 J with 6 J and then 3 J steps. VF not terminated by highest protocol energy was shocked externally and a DFT of 24 J assigned.
Results: 25 patients were enrolled. Age – 54 ± 15 years, EF 25 ± 9 % and CAD 65%. SU DFT and BS DFT were identical in 15/25 patients. In 5 patients, SU DFT was 3 J < BS DFT. In 5 patients, SU DFT was 3 J > BS DFT. On a second repeated VF episode, SU DFT was identical to the first in 21/25 patients.
Conclusions: SU DFT highly correlates with BS DFT and is highly reproducible. SU protocol reduces the number of VF inductions needed to determine DFT. SU protocol reduces total time in VF compared to the BS protocol. Further clinical research is required to verify the suitability of determining DFT and programming ICDs based on a single VF induction via SU protocol.
Submitted for ACC Poster Research Presentation
THE
ROLE OF FINE PARTICULATE AIR POLLUTION AND ELEVATION OF CIRCULATING ASYMMETRIC DIMETHYLARGININE (ADMA) LEVELS
Sanjay Rajagopalan, MD1, Robert D. Brook, MD1, Gerald
J. Keeler, PhD1, J. Timothy Dvonch, PhD1, Frank J.
Marsik, PhD1, Masako Morishita, PhD1, Jeff R. Brook, PhD2,
Lou D’Alecy, PhD1, Apurva Motivala, MD3, Edward J. Timm4,
James Wagner4, and Jack R. Harkema, DVM PhD4 – 1The
University of Michigan, Ann Arbor, 2University of Toronto, Canada, 3Sinai-Grace
Hospital/Wayne State University, Detroit, 4Michigan State University,
East Lansing.
Presented by: Apurva Motivala, MD - Sinai-Grace Hospital/Wayne State University
Background and Aim: The health effects of fine ambient particulate matter (PM2.5) and its potential impact on vascular endothelial function have not been thoroughly investigated. As endothelial dysfunction plays an important role in atherosclerosis and cardiovascular disease, we examined the effects of concentrated fine ambient particles (CAPs) on the plasma levels of asymmetric dimethylarginine (ADMA) in a pilot study. ADMA is an endogenous inhibitor of nitric oxide synthase that is associated with impaired vascular function and an increased risk of cardiovascular events.
Methods: A mobile air research laboratory (AirCARE 1), equipped with whole body inhalation chambers and a Harvard type ambient fine particle concentrator, was used in the study. AirCARE 1 was designed and constructed collaboratively by Michigan State University and the University of Michigan. The CAPs exposures for this study were conducted in the urban community of southwest Detroit. Fourteen Brown Norway rats were exposed to filtered air (FA) (n=7) or CAPs (0.1-2.5 µm) (n=7) for 3 consecutive days (8h/day) in July, 2002. Rats were exposed during these periods to average particle mass concentrations of 367 µg/m3. Rat plasma samples were collected 24h post-exposure.
Results: Plasma concentrations of ADMA were significantly elevated in the rats exposed to CAPs versus those exposed to FA (1.49 ± 0.18 vs 1.29 ± 0.26 *M, p*0.05 by 1 tailed t-test).
Conclusion: Fine particulate air pollution exposure at high concentrations triggers an acute increase in circulating ADMA level. This could potentially cause impaired vascular endothelial function and enhance the risk for cardiovascular disease.
Submitted for ACC Poster Research Presentation