Danielson, Gordon

Edwards, William D.

Oh, Jae

Talreia, Deepak R.

Tazelaar, Henry

Elsevier - Publisher Connector 

Constrictive pericarditis with normal pericardial thickness on examination of histopathology 

JACC March 6, 2002 
11:30 a.m. 
813-3 Constrictive PericardiUs With Normal Pericardial 
Thickness on Examination of Hiatopathology 
Deeeak R. Talreia, William D. Edwards, Jae Oh, Henry Tazelaar, Gordon Danielson, 
Mayo Clinic, Rochester, Minnesota. 
Background: Increased pericardial thickness (PT) has been viewed as an essential diag- 
nostic feature for constrictive pericarditls (CP). While there are reports of clinically-dem- 
onstrated CP with normal PT by non-invasive imaging, the evaluation of PT by 
histopathology in CP has not been described. 
Methods: Among 143 pericardial specimens from patients who underwent pedcardiec- 
tomy for clinically- and/or surgically-proven CP at Mayo Clinic Rochester, 26 (18%) had 
normal thickness (that is, <= 2 mm). For these 26 patients, surgical pathology and the 
corresponding microscopic slides were examined for the presence of inflammation, calci- 
fication, and fibrosis. Medical records were reviewed to characterize preoperative fea- 
tures including clinical findings, computed tomography (CT) and radiographic imaging, 
echocardiography and cardiac catheterization. 
Results: The 26 patients ranged from 42 to 81 years old (mean, 58) with a striking male 
preponderance (73%). 
No patient had an entirely normal pericardium. Histopathologic abnormalities included 
fibrosis (85%), inflammation (54%), gross and/or microscopic calcification (35%), fibrin 
deposition (19%) and focal non-caseating granulomas (7%). 
Etiologies for CP included previous cardiac surgery (42%), chest irradiation (19%), 
postinfarctlon (7%), idiopathic (7%) and sarcoidosis, chest trauma, and acute viral peri- 
carditis in the remainder (25%). latrogenic disease was the most common cause of con- 
striction (61%). The most prevalent symptoms were lower extremity edema (88%), 
dyspnea (85%), and abdominal distention (77%). The most common physical findings 
were peripheral edema (85%), increased jugular venous distention (81%) with rapid Y 
descent (54%), hepatomegaly (54%), ascites (54%), and pericardial knock (38%). This 
was essentially no different for patients with CP and increased PT. 
Conclusions: PT is normal in 18% of patients with surgically-proven constrictive peri- 
carditis although histopathology is abnormal. When clinical or hemodynamic features 
indicate CP in patients with heart failure, pericardiectomy should not be denied because 
of normal PT demonstrated by noninvasive imaging. 
11:45 a.m. 
813-4 The Long-Term Follow-Up Results of Alcohol Septal 
Ablation for Symptomatic Hypertrophic ObstrucUve 
Cardiomyopathy: The Baylor Experience (1996-2001) 
Valerian L. Fernandes. Sherif F. Nagueh, Nasser M. Lakkis, Jennifer Franklin, Robed 
Roberts, William H. Spencer, III, Bay/or College of Medicine, Houston, Texas. 
Background: Alcohol Septal Ablation (ASA) is an accepted procedure for relief of outflow 
obstruction and symptoms of Hypertrophic Obstructive Cardiomyopathy (HOCM). How- 
ever, there is still a paucity of data on the long term outcome. Herein we report the long 
term follow-up from the Baylor College of Medicine HOCM Registry. 
Methods: 213 consecutive symptomatic pts (51.2 -+ 16.7 yrs, 122 men) who underwent 
ASA were followed up over 4 years. A mean of 1.35 ± 0.56 septals were injected with 3.0 
± 1.33 cc ethanol per patient. The peak CK post procedure was 1463 _+ 884 Units. 33 
patients (15%) needed a permanent pacemaker post procedure. 
Results: A successful procedure resulted in a significant improvement in symptoms, 
exercise tolerance and reduction of outflow gradient (table). The initial benefits were 
maintained at 1,2, 3 and 4 years post procedure. 24 patients needed a repeat procedure 
and 5 patients had a myotomy-myomectomy forpersistence of symptoms following ASA. 
9 deaths (2 procedural, 2 SCD, 5 noncardiac) were recorded during the follow-up. 
Conclusion: Alcohol Septal Ablation is an effective procedure with an acceptable risk for 
patients with symptomatic HOCM. The initial benefits are maintained long term over a 4 
year period. 
Alcohol Septal Ablation - Follow-up Indices 
Indices Baseline 3 month 1 year 2 year 3 year 4 year 
NYHAangina 2.1+0.7" 1.2_+0.4 1.2_+0.4 1.1_+0.4 1,1_+0.3 1.1_+0.3 
NYHA Heart Failure 2.8_+0.6* 1.5_+0.5 1.3_+0.5 1.2_+0.4 1.3+0.5 1.1_+0.3 
SeptalThickness(cm) 2.1±0.5" 1.6_+0.4 1.3_+0.3 1.2±0.3 1.2_+0.4 1.2+0.4 
Resting Gradient (mm Hg) 60± 38* 18± 28 ~ 19 3± 7 5+ 10 8-+ 14 
Provoked Gradient (mm 95-+ 56* 54-+ 66 42_+ 38 28_+ 36 21_+ 20 11_+ 19 
Hg) 
Treadmill duration (sec) 304_+ 199" 425_+202 451_+210 413_+223 403±216 405_+ 161 
Ejection Fraction (%) 75_+ 7* 72_+ 9 69_+ 10 67+ t0 64± 11 63-+ 14 
* p value < 0.001 by ANOVA 
Noon 
813-5 Triphasic Response to Alcohol Septal Ablation 
Danita M. Yeeroer, Michael H. Picard, Igor F. Palacios, Gus J. Vlahakes, Michael A. Fifer, 
Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 
Background: Alcohol (EtOH) septal ablation (SA) is an alternative therapy in selected 
patients with hypertrophic obstructive cardiomyopathy. Acute septal wall motion abnor- 
mality followed by later left ventdcular outflow tract (LVOT) remodeling are described as 
mechanisms for early and late relief of LVOT gradient. We have observed that, despite 
ABSTRACTS - Cardiac Function and Heart Failure 157A 
acute reduction in gradient in the cath lab, it may increase in the days after septal abla- 
tion. This study characterizes the course of LVOT gradient after SA. Methods: 17 
patients were assessed by echo at referral ('nine 1), immediate pre-ablation (Time 2), 
immediate post-ablation (Time 3), pre-discharge (Time 4) and at 3 months (Time 5). 
Results: Patients were grouped according to their pattern of LVOT gradient response: 
monophasic success (n=7), triphasic success (n=7) and failure (n=3). There was no dif- 
ference in LVOT gradient between the 2 success groups at post-procedure Time 3, but 
the LVOT gradient in the triphasic success group was significantly increased at time 4, 
and was not different from that of the failure group at this time point. Groups did not differ 
in age, baseline upper septal thickness, EtOH amount, percent of upper septum perfused 
by EtOH or peak CK. Conclusions: When a significant decrease in gradient is achieved 
during SA, predischarge elevation in gradient does not predict failure. This finding sup- 
ports the mechanisms of acute reversible stunning followed by later long-term LVOT 
remodeling in relief of gradient after SA. 
j 
~ --B-- m0n.phasic success| 
1 zO = tri phasic success 
lOO 
1 z 3 4 f 
Time 
POSTER SESSION 
1110 Heart Failure: Genes Cytokines 
Monday, March 18, 2002, Noon-2:00 p,m, 
Georgia World Congress Center, Hall G 
Presentation Hour: Noon-l:00 p,m, 
1110-141 Clusters of Differential Gene Expression of Structural 
Proteins Between Failing and Nonfailing Hearts: 
Preliminary Insights From OIIgonucleotide Microarrays 
W.H. Wilson Tang, Fen-Lai Tan. Gary S. Francis, Christine S. Moraveo, Jianbo Li, 
Carolyn Apperson-Hansen, Patrick M. McCarthy, James B. Young, Meredith Bond, 
Cleveland Clinic Foundation, Cleveland, Ohio. 
Backgrounc~ Simultaneous identification of differential gone expression of structural 
proteins in the failing heart using microarrey technique has not been reported. 
Method:. Alterations in gene expression were compared between 7 non-failing and 8 fail- 
ing hearts with idiopathic dilated cardiomyopathy using high-density oligonucleotide 
microarrays (Hu-6800, Affymetrix Inc, CA) according to conservative criteria developed 
by our group (Tan et al). 53 known myocardial structural protein components were identi- 
fied and classified into clusters according to their known functional roles: 1) contractile 
proteins; 2) sarcomeric proteins; 3) cytoskeletai proteins; 4) membrane-associated pro- 
teins (MAP); 5) intercalated disc-associated proteins (IDAP); 6) extracellular matrix 
(ECM) proteins. 
Results: Of the 53 structural protein components identified, gene expression in 20 (38%) 
were found to be significantly different between failing and non-failing heads. We 
observed a consistent trend of altered gene expression in clusters of contractile proteins 
(down 1.5-fold in *x-actin, myosin light polypeptide 2 & 3, c~-tropomyosin, troponin T1), 
clusters of IMAPs (up 1.8-fold in connexin-43) and clusters of ECM proteins (up 1.5- to 5- 
fold in collagen, fibronectin, fibromodullin, lumican). On the other hand, gene expression 
of MAPs, sarcomeric and cytoskeletal proteins varied widely within their clusters, but sig- 
nificant changes were observed in c¢l-actinin (down 3.6-fold), c~l-tubulin (down 1.7-fold), 
~lb-tubulin (up 1.6-fold), ~2-tubulin (down 1.5-fold), pinin (up 1.8-fold) and c~-spectrin (up 
1.5-fold). Discrepancies in gene expression of some MAP/sarcomeric proteins between 
our study and published reports may warrant further investigation. 
Conclusion: Microarray technology provides an alternative strategy whereby numerous 
myocardial genes can be studied in a simultaneous manner. Clusters of gene expression 
of structural proteins can be explored according to their functional domains, with genes 
that control contractile function being consistently downregulated whereas genes associ- 
ated with structural integrity have a more heterogeneous pattern of expression. 
1110-142 Transmyocardial Gradient of Proinflammatory 
Cytokines in Patients With Decompensated Idiopathic 
Dilated Cardiomyopathy 
Hvuk-Jae Chano. Joon-Han Shin, So-Yeon Choi, Gyo-Seung Hwang, Myeong-Ho Yoon, 
Han-Soo Kim, Seung-Jea Tahk, Hae-Sim Park, Byung-il W. Choi, Ajou University School 
of Medicine, Suwon, South Korea. 
Background: Proinflammatory cytokines such as tumor necrosis factor alpha(TNFa) and 
intedeukin-6(IL-6) have been recently identified as contributors to the syndrome of 
chronic heart failure. However, the origin of these cytokines in heart failure remains 
unclear. Therefore, we analyzed concentrations of TNFa, IL-6 and their cognitive recep- 
tors in patients with recently(<1 month) decompensated heart failure in peripheral 
vein(PV) and coronary sinus(CS) simultaneously. 
Method: The study group included 24 patients(18 males) with mean age 59±8 years and 
ejection fraction of 29~16%. NYHA functional class were I: 4, II: 8, II1:2 and IV: 10 during 
the episode of decompensation. Blood sampling for TNFa, IL-6 and TNFa recep- 
tor(TNFaR) 1, 2 was collected from CS and PV to measure the difference as a part of 


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Constrictive pericarditis with normal pericardial thickness on examination of histopathology

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