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Juan RussoGeorge A. WellsYeong ChongDerek SoChris GloverMichael FroeschlJung‐Min AhnSung‐Han YoonJae‐Hyung RohHyung LeeMineok ChangHyun ParkJong-Young LeeSoo-Jin KangDuk‐Woo ParkSeung‐Whan LeeYoung‐Hak KimMassimo NapodanoAhmed Al MamaryFilippo ZilioGilberto DariolAnna Chiara FrigoGiuseppe TarantiniGiuseppe SantarpinoVito Giovanni RuggieriGiovanni MariscalcoKarl BounaderCesare BeghiTheodor FischleinFrancesco OnoratiGiuseppe FaggianGiuseppe GattiAniello PappalardoMarisa De FeoCiro BanconeAndrea PerrottiSidney ChocronMagnus DalénPeter SvenarudA RubinoCarmelo MignosaRiccardo GherliFrancesco MusumeciUlas OzgurYusuf OzcanHuseyin AtmacaRangadham NagarakantiLars WallentinHerbert NoackMartina BrueckmannPaul ReillyAndreas ClemensStuart J. ConnollySalim YusufMichael D. EzekowitzVikas SinghApurva BadhekaSamir N. PatelNileshkumar PatelBadal ThakkarNilay PatelShilpkumar AroraNish PatelAchint PatelChirag SavaniAbhijit GhatakSidakpal PanaichSunny JhamnaniAbhishek DeshmukhAnkit ChothaniRajesh SonaniAashay PatelParth BhattAbhishek DaveRonak BhimaniTamam MohamadCindy L. GrinesMichael ClemanConcetta ZitoRoberta ManganaroBijoy K. KhandheriaGiuseppe OretoMaurizio Cusmà PiccioneMaria Chiara TodaroAlessandra CaprinoPietro PugliattiGianluca Di BellaScipione CarerjAlessandra LorenzonKalliopi PilichouIlaria RigatoGiovanni VazzaMarzia De BortoliMartina CaloreGianluca OcchiElisa CarturanElisabetta LazzariniMarco CasonElisa MazzottiGiulia PoloniMaria Luisa MostacciuoloLuciano DalientoGaetano ThieneDomenico CorradoCristina BassoBarbara BauceAlessandra RampazzoJosé M. OliverAna GonzálezJosé Ruiz-CantadorÁngel Sánchez‐RecaldeMaría Luz PoloÁngel Serrano‐Aroca
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Background Right ventricular systolic dysfunction is associated with worsened outcomes and poor survival in patients with heart failure. However, it is unclear what mechanisms, other than the presence of RV infarction, contribute to the development of RV dysfunction in patients with severe ischemic cardiomyopathy. We sought to determine the impact of baseline demographic variables, CAD severity, LV diastolic function assessed by echocardiography, ventriculovascular coupling, LV remodeling, aortic biomechanical properties, and RV infarction, assessed by CMR, on RV ejection fraction. Methods Patients were selected if they had undergone TTE and CMR studies within 7 days (median=1 day). 354 patients with LVEF ≤ 40% and ≥ 70% stenosis in ≥1 coronary artery but without prior mitral valve surgery, fused E/A waves, atrial fibrillation or > moderate mitral regurgitation were included. Of those, 30 patients were excluded due to suboptimal CMR image quality for adequate RV volume tracings. A total 324 charts were reviewed for demographic and laboratorial data. Diastolic function assessment was performed as per guidelines. Aortic biomechanics were measured using previously validated software (ARTFUN, INSERM U678, Paris, France) using semi-automated tracing of aortic contours with phasecontrast images and through-plane velocity encoding of the ascending and descending aorta. CMR evaluation also included long and short axis assessment of LV/RV function respectively on balanced steady state free precession images along with assessment of LV/RV myocardial scar (on phase-sensitive inversion recovery DHE-CMR sequence ~ 10-20 minutes). Multivariate linear regression analysis performed to identify the independent predictors of RVEF. Results
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Patients with permanent pacemaker or automatic implantable cardioverter-defibrillator (AICD) leads have an increased prevalence of tricuspid regurgitation. However, the roles of cardiac rhythm and lead-placement duration in the development of severe tricuspid regurgitation are unclear. We reviewed echocardiographic data on 26 consecutive patients who had severe tricuspid regurgitation after permanent pacemaker or AICD placement; before treatment, they had no organic tricuspid valve disease, pulmonary hypertension, left ventricular dysfunction, or severe tricuspid regurgitation. We compared the results to those of 26 control subjects who had these same devices but no more than mild tricuspid regurgitation. The patients and control subjects were similar in age (mean, 81 ±6 vs 81 ±8 yr; P = 0.83), sex (male, 42% vs 46%; P = 0.78), and left ventricular ejection fraction (0.60 ±0.06 vs 0.58 ± 0.05; P = 0.4). The patients had a higher prevalence of atrial fibrillation (92% vs 65%; P=0.01) and longer median duration of pacemaker or AICD lead placement (49.5 vs 5 mo; P < 0.001). After adjusting for age, sex, and right ventricular systolic pressure by multivariate logistic regression analysis, we found that atrial fibrillation (odds ratio=6.4; P = 0.03) and duration of lead placement (odds ratio=1.5/yr; P = 0.001) were independently associated with severe tricuspid regurgitation. Out study shows that atrial fibrillation and longer durations of lead placement might increase the risk of severe tricuspid regurgitation in patients with permanent pacemakers or AICDs.
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The association between mitral valve disease and atrial fibrillation (AF) is well known, but few data exist regarding the impact of AF after mitral valve replacement (MVR) on NYHA functional class, atrial size and hemodynamic parameters. The present study was conducted to evaluate these issues.Eighty-six patients (26 men, 60 women) who underwent MVR were evaluated by transthoracic echocardiography. Fifty-nine patients had chronic AF (AF group), and 27 were in sinus rhythm (sinus group). Variables analyzed included end-systolic left atrial and right atrial areas, tricuspid regurgitation, and presence and duration of AF. Peak and mean transprosthetic mitral valve gradients and pulmonary pressure were estimated by Doppler echocardiography.Groups were matched for age, sex and time from MVR (mean 6.6 years). Sixty-four patients (77%) had rheumatic heart disease, 18 (21%) had mitral valve disease, and two (2%) had mitral valve prolapse. Mean duration of AF was 11+/-12 years (range: 8-50 years). Preoperatively, AF patients had a worse NYHA class than sinus patients (2.8+/-0.8 versus 1.1+/-0.7, p = 0.001), but both had similar fractional shortening of the left ventricle and preserved prosthetic mitral valve function. Multivariate analysis identified AF as a single predictor of NYHA class after MVR. Although left and right atrial areas were larger in AF patients (47+/-25 versus 27+/-7 cm2, p = 0.0001 and 30+/-12 versus 17+/-5 cm2, p = 0.0001, respectively), the left:right atrial size ratio was not significantly different between groups. Multivariate analysis identified mean transmitral gradient and duration of AF as independent predictors of left atrial size after MVR (p = 0.01 and p = 0.0001, respectively). Tricuspid regurgitation and duration of AF were independent predictors of right atrial size (p = 0.003 and p = 0.0001, respectively).The presence of AF after MVR is associated with a worse NYHA functional class, increased transmitral gradients, and larger areas of both atria, when compared with sinus rhythm. Hence, a special effort should be made to correct arrhythmia during surgery, and in case of paroxysmal arrhythmia, earlier surgery should be considered before the condition becomes chronic.
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To investigate the relationship between brachial-ankle pulse wave velocity (baPWV) and different stage of cardiac dysfunction.253 consecutive patients with coronary atherosclerotic heart disease were enrolled from August 2006 to February 2007. Patients were grouped according to the functional classification of New York Heart Association (NYHA). The baPWV was measured non-invasively with a VP1000 automated PWV/ABI analyzer (PWV/ABI, Colin CO. Ltd., Komaki, Japan). At the same time, BNP, EF, LAEDV and LVESV were measured in all the patients.Brachial-ankle PWV was significantly correlated with cardiac function classification of NYHA (r = 0. 444, P < 0.001), BNP( r = 0.394, < 0.001) and left ventricular end diastolic volume (r = - 0.130, P < 0.05). The under area of receiver operating charachateistic (ROC) curve was 73.9%. The ROC curve demonstrated that when the value of brachial-ankle PWV was equal to or larger than 1717 cm/s (> 1717 cm/s), the sensitivity of diagnosing mild cardiac dysfunction was 72.9% and specifity 61.8%. When its value was equal to or larger than 1900 cm/s (> or = 1900 cm/s), the sensitivity and specificity were 61.5% and 81.9% respectively.Brachial-ankle PWV is significantly correlated to the NYHA classification of heart failure and it may be a prospective index to diagnose early stage of cardiac dysfunction.
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Background: The coronary microvascular vasodilating function is an important determinant of patient outcomes in a number of clinical settings, including coronary artery disease, hypertensive heart disease, or cardiomyopathy. However, the characteristics or the implication of coronary microcirculation in valvular heart disease has not been fully elucidated. The present study was designed to assess coronary vasodilating function and its effects on systolic function in patients with aortic regurgitation (AR) and mitral regurgitation (MR). Methods: Forty-four consecutive patients (66 yrs) with moderate to severe AR and 45 consecutive patients with moderate to severe MR (64 yrs) were enrolled for this study. All patients were free of coronary artery stenosis. Fifty-one age-matched patients without underlying cardiovascular disease served as controls. Endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were assessed by coronary blood flow (CBF) response to acetylcholine and papaverine, respectively. Left ventricular ejection fraction (LVEF) was determined by echocardiography as an indicator of systolic function. Results: In patients with AR, both %change in CBF response to acetylcholine and papaverine were significantly lower than controls (32 ± 61 vs 64 ± 84, 172 ± 87 vs 268 ± 105, p < 0.05, p < 0.01, respectively). Further, %change in CBF response to acetylcholine positively correlated with LVEF (r = 0.45, p < 0.01). In patients with MR, %change in CBF response to papaverine was significantly lower than controls (221 ± 123 vs 268 ± 105, p < 0.05), but %change in CBF response to acetylcholine was comparable with controls. Moreover, neither %change in CBF response to acetylcholine nor CBF response to papaverine had significant correlation with LVEF. Conclusion: In patients with AR, both endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were deteriorated. Further, endothelium-dependent vasodilating function may be associated with left ventricular systolic function. Our findings indicate coronary microvascular endothelial dysfunction as a potential target for prevention of systolic heart failure in patients with AR.
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