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Richard D Rothman,
Aaron L Baggish,
Caitlin O'Callaghan,
Patricia A Lowry,
Ami B Bhatt,
Calum A Macrae,
Gia Yannekis,
Danita M Sanborn,
Theofanie Mela,
Robert W Yeh,
Igor Palacios, Gus J Vlahakes,
Michael A Fifer
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ABSTRACT: The likelihood of success of conservative management of obstructive hypertrophic cardiomyopathy (HC) and the predictors of failure of conservative therapy are not known. We therefore evaluated the efficacy of an algorithm for the management of symptoms and predictors of failed conservative therapy in 249 consecutive symptomatic patients with obstructive HC referred to a dedicated HC program for management in general or for septal reduction therapy (SRT) in particular. There was considerable practice variation in the extent to which conservative therapy was optimized before referral for SRT. Over 3.7 ± 2.9-year follow-up, symptoms resolved with addition of or increase in dosage of a β blocker, calcium channel blocker, or disopyramide in 16%, 10%, and 10% of patients, respectively. Pacing with short atrioventricular delay controlled symptoms in 4 of 9 patients. In 63% of patients, conservative measures failed to control symptoms. Multivariate predictors of failure of conservative therapy were presence of New York Heart Association class III or IV symptoms (hazard ratio 2.0, 95% confidence interval 1.4 to 2.9, p = 0.001) and greater septal wall thickness (hazard ratio 1.06, 95% confidence interval 1.02 to 1.10, p = 0.003) at presentation. At time of presentation, 93 patients (37%) were already on optimal therapy and were referred for SRT. Of the remaining 156 patients who did not require immediate SRT, 93 (60%) were free from a recommendation for SRT at the end of the follow-up period. In conclusion, in symptomatic patients with obstructive HC, conservative therapy is successful in >1/3 of referred patients at 3.7-year follow-up, obviating SRT in these patients. Clinicians in programs offering SRT should optimize conservative therapy before recommending SRT.
The American journal of cardiology 07/2012; 110(8):1169-74. · 3.58 Impact Factor
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Jorge Solis,
Robert A Levine,
Benjamin Johnson,
J Luis Guerrero,
Mark D Handschumacher,
Suzanne Sullivan,
Kaitlyn Lam,
Jason Berlin,
Gavin J C Braithwaite,
Orhun K Muratoglu, Gus J Vlahakes,
Judy Hung
[show abstract]
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ABSTRACT: Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling.
Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle-to-mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm(2)to 7.6±1.3 cm(2), P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, τ (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01).
PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.
Circulation Cardiovascular Interventions 10/2010; 3(5):499-505. · 6.06 Impact Factor
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Ronen Beeri,
Miguel Chaput,
J Luis Guerrero,
Yoshiaki Kawase,
Chaim Yosefy,
Suzan Abedat,
Ioannis Karakikes,
Charlotte Morel,
Ashley Tisosky,
Suzanne Sullivan,
Mark D Handschumacher,
Dan Gilon, Gus J Vlahakes,
Roger J Hajjar,
Robert A Levine
[show abstract]
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ABSTRACT: Mitral regurgitation (MR) doubles mortality after myocardial infarction (MI). We have demonstrated that MR worsens remodeling after MI and that early correction reverses remodeling. Sarcoplasmic reticulum Ca(+2)-ATPase (SERCA2a) is downregulated in this process. We hypothesized that upregulating SERCA2a might inhibit remodeling in a surgical model of apical MI (no intrinsic MR) with independent MR-type flow.
In 12 sheep, percutaneous gene delivery was performed by using a validated protocol to perfuse both the left anterior descending and circumflex coronary arteries with occlusion of venous drainage. We administered adeno-associated virus 6 (AAV6) carrying SERCA2a under a Cytomegalovirus promoter control in 6 sheep and a reporter gene in 6 controls. After 2 weeks, a standardized apical MI was created, and a shunt was implanted between the left ventricle and left atrium, producing regurgitant fractions of ≈30%. Animals were compared at baseline and 1 and 3 months by 3D echocardiography, Millar hemodynamics, and biopsies. The SERCA2a group had a well-maintained preload-recruitable stroke work at 3 months (decrease by 8±10% vs 42±12% with reporter gene controls; P<0.001). Left ventricular dP/dt followed the same pattern (no change vs 55% decrease; P<0.001). Left ventricular end-systolic volume was lower with SERCA2a (82.6±9.6 vs 99.4±9.7 mL; P=0.03); left ventricular end-diastolic volume, reflecting volume overload, was not significantly different (127.8±6.2 vs 134.3±9.4 mL). SERCA2a sheep showed a 15% rise in antiapoptotic pAkt versus a 30% reduction with the reporter gene (P<0.001). Prohypertrophic activated STAT3 was also 41% higher with SERCA2a than in controls (P<0.001). Proapoptotic activated caspase-3 rose >5-fold during 1 month in both SERCA2a and control animals (P=NS) and decreased by 19% at 3 months, remaining elevated in both groups.
In this controlled model, upregulating SERCA2a induced better function and lesser remodeling, with improved contractility, smaller volume, and activation of prohypertrophic/antiapoptotic pathways. Although caspase-3 remained activated in both groups, SERCA2a sheep had increased molecular antiremodeling "tone." We therefore conclude that upregulating SERCA2a inhibits MR-induced post-MI remodeling in this model and thus may constitute a useful approach to reduce the vicious circle of remodeling in ischemic MR.
Circulation Heart Failure 09/2010; 3(5):627-34. · 6.29 Impact Factor
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Gus J Vlahakes
The Annals of thoracic surgery 08/2010; 90(2):572. · 3.74 Impact Factor
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ABSTRACT: Ischemic mitral regurgitation is caused by systolic traction on the mitral leaflets related to ventricular distortion. Little is known about how chronic tethering affects leaflet area, in part because it cannot be measured repeatedly in situ. Recently, a new method for 3D echocardiographic measurement of mitral leaflet area was developed and validated in vivo against sheep valves, later excised. Clinical studies (n=80) showed that mitral leaflet area increased by >30% in patients with inferior myocardial infarction and dilated cardiomyopathy versus normal; greater adaptation independently predicted less mitral regurgitation. This study explored whether mitral valve area changes over time within the same heart with ischemic mitral regurgitation.
Twelve sheep were studied at baseline and 3 months after inferior myocardial infarction by 3D echocardiography; 6 were untreated and 6 were treated initially with an epicardial patch to limit left ventricular dilation and mitral regurgitation. Untreated sheep developed left ventricular dilation at 3 months, with global dysfunction (mean+/-SD ejection fraction, 24+/-10% versus 44+/-10% with patching, P=0.02) and moderate mitral regurgitation (vena contracta, 5.0+/-1.0 versus 0.8+/-1.0 mm, P<0.0002). In untreated sheep, total diastolic leaflet area increased from 13.1+/-1.3 to 18.1+/-2.5 cm(2) (P=0.0001). In patched sheep, leaflet area at 3 months was not significantly different from baseline sheep values (13.0+/-1.1 versus baseline, 12.1+/-1.8 cm(2), P=0.31).
Mitral valve area, independent of systolic stretch, increases over time as the left ventricular remodels after inferior myocardial infarction. This increase, however, fails to compensate adequately for tethering to prevent mitral regurgitation. Understanding the mechanism of valve adaptation can potentially suggest new biological and surgical therapeutic targets.
Circulation 09/2009; 120(11 Suppl):S99-103. · 14.74 Impact Factor
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Peter A Noseworthy,
Michael A Rosenberg,
Michael A Fifer,
Igor F Palacios,
Patricia A Lowry,
Jeremy N Ruskin,
Danita M Sanborn,
Michael H Picard, Gus J Vlahakes,
Theofanie Mela,
Saumya Das
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ABSTRACT: We sought to assess the risk of sudden cardiac death (SCD) and ventricular arrhythmia after alcohol septal ablation (ASA) for obstructive hypertrophic cardiomyopathy. ASA is a nonsurgical alternative to septal myectomy for treatment of symptomatic, drug-refractory, obstructive hypertrophic cardiomyopathy. The effect of ASA on ventricular arrhythmia risk is not well established. We examined the rates of SCD among 89 patients treated with ASA. The secondary end point was ventricular tachycardia/ventricular fibrillation (VT/VF), appropriate implantable cardioverter defibrillator (ICD) therapy, or cardiac arrest after ASA among those with implanted ICDs or permanent pacemakers (n = 42). Patients were classified as either high-risk or low-risk on the basis of established clinical indications for ICD implantation. No mortality was attributable to SCD at a mean follow-up of 5.0 +/- 2.3 years in the entire cohort. Among the 42 patients with an ICD or permanent pacemaker, 9 had documented VT/VF, cardiac arrest, or appropriate ICD therapy, resulting in an annual event rate of 4.9%/year. The annual event rate for VT/VF, cardiac arrest, or appropriate ICD therapy was 2.8%/year (4 of 29 patients) in low-risk patients and 13.4% in high-risk patients (5 of 13 patients). A 10-mm Hg increase in the immediate post-ASA gradient was associated with a hazard ratio of 2.66 for arrhythmic events (95% confidence interval 1.55 to 4.56, p <0.001). In conclusion, ASA was performed in patients with highly symptomatic, drug-refractory hypertrophic cardiomyopathy with no mortality attributable to SCD and an annual rate of VT/VF, cardiac arrest, or appropriate ICD therapy of 4.9%/year.
The American journal of cardiology 08/2009; 104(1):128-32. · 3.58 Impact Factor
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Judy Hung,
Jorge Solis,
J Luis Guerrero,
Gavin J C Braithwaite,
Orhun K Muratoglu,
Miguel Chaput,
Leticia Fernandez-Friera,
Mark D Handschumacher,
Van J Wedeen,
Stuart Houser, Gus J Vlahakes,
Robert A Levine
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ABSTRACT: Ischemic mitral regurgitation (MR) relates to displacement of the papillary muscles from ischemic ventricular distortion. We tested the hypothesis that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) polymer, a biologically inert biomaterial that has been specially formulated to produce an encapsulated, stable, resilient gel once injected into the myocardium. The purpose is to materially support the infarcted myocardium while at the same time repositioning the papillary muscles that become apically tethered in MR.
Nine sheep underwent ligation of circumflex branches to produce acute ischemic MR. PVA polymer was then injected by echo guidance into the myocardium underlying the infarcted papillary muscle. Hemodynamic data, left ventricular ejection fraction, elastance, tau (relaxation constant), left ventricular stiffness coefficient, and 2-dimensional and 3-dimensional echocardiograms were obtained post-MR and post-PVA injection. One animal died after coronary ligation and 2 did not develop MR. In the remaining 6, moderate MR developed. With PVA injection, the MR decreased significantly from moderate to trace-mild (vena contracta: 5+/-0.4 mm versus 2+/-0.7 mm, post-MR versus post-PVA injection; P<0.0001). This was associated with a decrease in infarcted papillary muscle-to-mitral annulus tethering distance (27+/-4 to 24+/-4 mm, post-MR versus post-PVA, P<0.001). Importantly, PVA injection was not associated with significant decreases in left ventricular ejection fraction (43+/-6% versus 37+/-4%, post-MR versus post-PVA, P=nonsignificant), elastance (3.5+/-1.4 versus 2.9+/-1.3; post-MR versus post-PVA injection, P=nonsignificant). Measures of left ventricular diastolic function, tau (100+/-51 ms to 84+/-37 ms, post-MR versus post-PVA; P=nonsignificant), and left ventricular stiffness coefficient (0.18+/-0.12 versus 0.14+/-0.08, post-MR versus post-PVA; P=nonsignificant) did not increase post-PVA.
PVA polymer injection resulted in acute reverse remodeling of the ventricle with papillary muscle repositioning to decrease MR. This was not associated with an adverse effect on left ventricular systolic and diastolic function. This new approach to alter pathological anatomy after infarction may offer an alternative strategy for relieving ischemic MR by correcting the position of the affected papillary muscle, thus relieving apical tethering.
Circulation 10/2008; 118(14 Suppl):S263-9. · 14.74 Impact Factor
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ABSTRACT: Functional mitral regurgitation (MR) is caused by systolic traction on the mitral leaflets related to ventricular distortion. Little is known about whether chronic tethering causes the mitral leaflet area to adapt to the geometric needs imposed by tethering, in part because of inability to reconstruct leaflet area in vivo. Our aim was to explore whether adaptive increases in leaflet area occur in patients with functional MR compared with normal subjects and to test the hypothesis that leaflet area influences MR severity.
A new method for 3-dimensional echocardiographic measurement of mitral leaflet area was developed and validated in vivo against 15 sheep heart valves, later excised. This method was then applied in 80 consecutive patients from 3 groups: patients with normal hearts by echocardiography (n=20), patients with functional MR caused by isolated inferior wall-motion abnormality or dilated cardiomyopathy (n=29), and patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (n=31). Leaflet area was increased by 35+/-20% in patients with LV dysfunction compared with normal subjects. The ratio of leaflet to annular area was 1.95+/-0.40 and was not different among groups, which indicates a surplus leaflet area that adapts to left-heart changes. In contrast, the ratio of total leaflet area to the area required to close the orifice in midsystole was decreased in patients with functional MR compared with those with normal hearts (1.29+/-0.15 versus 1.78+/-0.39, P=0.001) and compared with patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (1.81+/-0.38, P=0.001). After adjustment for measures of LV remodeling and tethering, a leaflet-to-closure area ratio <1.7 was associated with significant MR (odds ratio 23.2, 95% confidence interval 2.0 to 49.1, P=0.02).
Mitral leaflet area increases in response to chronic tethering in patients with inferior wall-motion abnormality and dilated cardiomyopathy, but the development of significant MR is associated with insufficient leaflet area relative to that demanded by tethering geometry. The varying adequacy of leaflet adaptation may explain in part the heterogeneity of this disease among patients. The results suggest the need to understand the mechanisms that underlie leaflet adaptation and whether leaflet area can potentially be modified as part of the therapeutic approach.
Circulation 08/2008; 118(8):845-52. · 14.74 Impact Factor
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ABSTRACT: Concomitant mitral regurgitation (MR) is frequently seen in patients undergoing aortic valve replacement (AVR) for aortic stenosis. This study was undertaken to characterize the magnitude of MR in these patients and identify factors associated with significant postoperative change.
Between 2002 and 2006, 391 patients with stenotic AV disease but no structural mitral valve disease underwent AVR without coronary artery bypass grafting. Excluded were 164 patients with combined aortic and mitral intervention, right heart surgery, or moderate to severe aortic insufficiency, to yield a final study group of 227 patients. Follow-up echographic evaluation of MR was obtained in 87 of 219 patients (40%) discharged alive without mitral valve intervention.
Overall mortality was 3.5%. After AVR, intraoperative MR severity improved in 66% of patients. Independent predictors of lower postoperative MR were small left atrial size (p = 0.03), the presence of aortic insufficiency (p < 0.01), and preoperative congestive heart failure (p = 0.04). Prosthetic valve type or size was not an independent predictor of postoperative MR. After adjustment for intraoperative underestimation of MR grade, there was no difference between the postprocedural MR grade and the early or late follow-up MR grade (p = 0.6 and p = 0.8, respectively).
The results of this study support a conservative, tailored approach to concomitant mitral surgery in patients presenting for correction of aortic stenosis who demonstrate functional mitral regurgitation. Characteristics associated with resolution may allow for identification of patients most likely to benefit from mitral valve repair or replacement.
The Annals of thoracic surgery 08/2008; 86(1):56-62. · 3.74 Impact Factor
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Circulation 02/2008; 117(3):429-39. · 14.74 Impact Factor
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Ronen Beeri,
Chaim Yosefy,
J Luis Guerrero,
Francesca Nesta,
Suzan Abedat,
Miguel Chaput,
Federica del Monte,
Mark D Handschumacher,
Robert Stroud,
Suzanne Sullivan,
Thea Pugatsch,
Dan Gilon, Gus J Vlahakes,
Francis G Spinale,
Roger J Hajjar,
Robert A Levine
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ABSTRACT: We examined whether mitral regurgitation (MR) augments post-myocardial infarction (MI) remodeling.
MR doubles mortality after MI, but its additive contribution to left ventricular (LV) remodeling is debated and has not been addressed in a controlled fashion.
Apical MIs were created in 12 sheep, and 6 had an LV-to-left atrial shunt implanted, consistently producing regurgitant fractions of approximately 30%. The groups were compared at baseline, 1, and 3 months.
Left ventricular end-systolic volume progressively increased by 190% with MR versus 90% without MR (p < 0.02). Pre-load-recruitable stroke work declined by 82 +/- 13% versus 25 +/- 16% (p < 0.01) with MR, with decreased remote-zone sarcoplasmic reticulum Ca(2+)-ATPase levels (0.56 +/- 0.03 vs. 0.76 +/- 0.02, p < 0.001), and decreased isolated myocyte contractility. In remote zones, pro-hypertrophic Akt and gp130 were upregulated in both groups at 1 month, but significantly lower and below baseline in the MR group at 3 months. Pro-apoptotic caspase 3 remained high in both groups. Matrix metalloproteinase (MMP)-13 and membrane-type MMP-1 were increased in remote zones of MR versus infarct-only animals at 1 month, then fell below baseline. The MMP tissue inhibitors rose from baseline to 3 months in all animals, rising higher in the MI + MR-group border zone.
In this controlled model, moderate MR worsens post-MI remodeling, with reduced contractility. Pro-hypertrophic pathways are initially upregulated but subsequently fall below infarct-only levels and baseline; with sustained caspase 3 elevation, transformation to a failure phenotype occurs. Extracellular matrix turnover increases in MR animals. Therefore, MR can precipitate an earlier onset of dilated heart failure.
Journal of the American College of Cardiology 02/2008; 51(4):476-86. · 14.16 Impact Factor
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ABSTRACT: Relief of obstruction using ventricular septal ablation (VSA) may not eliminate systolic anterior motion (SAM) of the mitral valve and mitral regurgitation (MR) in patients with obstructive hypertrophic cardiomyopathy. The hypothesis was that persistent SAM after VSA was secondary to anterior papillary muscle displacement and malcoaptation of mitral valve leaflets and that these findings could predict persistence of SAM. Echocardiograms were examined from 37 patients with obstructive hypertrophic cardiomyopathy before and 12+/-3 months after VSA. Anterior leaflet malposition (anterior-to-posterior leaflet coaptation position ratio), papillary muscle malposition (septal-to-lateral/left ventricular internal diameter ratio), and anterior position of coaptation relative to the septum (coaptation-to-septal distance) were assessed. MR proximal jet width was also measured. Of 37 patients, 30 underwent successful VSA (left ventricular outflow tract gradient reduction>50%); 22 of 30 and 7 of 7 with <50% reduction (total 29 of 37; 78%) showed persistent SAM at 12+/-3 months. These patients had more anterior malposition of the mitral valve and less MR reduction than those without SAM: anterior-to-posterior leaflet coaptation position ratio 0.42+/-0.06 versus 0.56+/-0.09, septal-to-lateral/left ventricular internal diameter ratio 0.39+/-0.12 versus 0.55+/-0.12, coaptation-to-septal distance 1.8+/-0.42 versus 2.8+/-0.30 cm, and MR reduction by 29+/-22% versus 71+/-12% (p<0.0001). Gradients, both at rest and provokable, were higher (27+/-33 vs 4+/-5 mm Hg, p=0.0004; >45 mm Hg in 9 vs 0, p=0.03, respectively) in patients with persistent SAM. Anterior malposition was present before VSA, with anterior-to-posterior leaflet coaptation position ratio<0.5 predicting SAM after VSA (p<0.0001). In conclusion, SAM and MR were often not eliminated using VSA. Mitral valve malposition was a strong predictor of SAM and MR reduction after VSA and may need to be considered in optimizing results of this procedure.
The American Journal of Cardiology 12/2007; 100(11):1691-5. · 3.37 Impact Factor
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Ronen Beeri,
Chaim Yosefy,
J Luis Guerrero,
Suzan Abedat,
Mark D Handschumacher,
Robert E Stroud,
Suzanne Sullivan,
Miguel Chaput,
Dan Gilon, Gus J Vlahakes,
Francis G Spinale,
Roger J Hajjar,
Robert A Levine
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ABSTRACT: Mitral regurgitation (MR) doubles postmyocardial infarction (MI) mortality. We have shown that moderate MR augments remodeling in an apical MI model (no intrinsic MR) with independent left ventricle-to-left atrial MR-type flow. We hypothesized that repairing moderate MR 1 month after MI reverses this remodeling.
Anteroapical MIs were created in 18 sheep, and a left ventricle-to-left atrial shunt implanted in 12 (regurgitant fraction, 30%). Six sheep had the shunt closed at 1 month (repair group). Sheep were compared at baseline, and at 1 and 3 months. Sheep in the MI+MR (unrepaired) and repaired groups remodeled during the first month (120% increased left ventricular end-systolic volume [ESV; P<0.01]), but shunt closure reversed remodeling at 3 months, with end-diastolic volume (EDV) and ESV 135% and 128% of baseline versus 220% and 280% without repair (P<0.001). At 3 months, dP/dt and preload-recruitable stroke work were relatively maintained in the repaired and MI-only groups versus nearly 50% decreases without repair. Prohypertrophic gp130 and antiapoptotic pAkt increased followed by exhaustion below baseline without repair, but remained elevated at 3 months with repair or MI only. With repair, matrix metalloproteinase-2 decreased to < or = 50% that without repair in remote and border zones at 3 months, and the matrix metalloproteinase inhibitor TIMP-4 increased dramatically.
Early repair of moderate MR in the setting of apical MI substantially reverses the otherwise progressive remodeling process, with reduced left ventricular volumes, relatively maintained contractility, persistently activated intracellular signals promoting hypertrophy and opposing apoptosis, and reduced matrix proteolytic activity. These findings are of interest for the current controversy regarding potential benefits of repair of MR after MI.
Circulation 09/2007; 116(11 Suppl):I288-93. · 14.74 Impact Factor
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ABSTRACT: The need for bileaflet repair in bileaflet mitral valve prolapse (MVP) remains controversial. Will anterior leaflet prolapse resolve with posterior leaflet repair or should both leaflets be addressed? Single-leaflet MVP produces oppositely directed mitral regurgitant jets. Some patients show two crossed jets oppositely directed from the coaptation zone. We hypothesized that these indicate bileaflet lesions requiring complex repair.
Echocardiograms and surgical reports of 52 consecutive patients with MVP undergoing surgery were reviewed.
First, all 14 patients with two oppositely directed jets had prolapse of more than one leaflet. Each jet was related to discrete leaflet distortions causing malcoaptation. Six underwent valve replacement. Seven had both leaflets repaired. One had posterior leaflet repair and annuloplasty, with persistent mitral regurgitation requiring valve replacement. Second, 36 of 38 patients with single jets had single-leaflet MVP. One underwent replacement; all others did well with single-leaflet repair. Two patients with bileaflet MVP but only one jet did well with single-leaflet repair or annuloplasty.
This crossed swords sign is an important clue to bileaflet mechanism of mitral regurgitation in MVP, associated with complex repair procedures. Thus, it provides a clue in the dilemma of bileaflet versus single-leaflet repair.
Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 07/2007; 20(6):698-702. · 2.98 Impact Factor
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ABSTRACT: The aim of this study was to evaluate the impact of either left atrial or aortic spontaneous echocardiographic contrast (SEC), as identified on intraoperative transesophageal echocardiography, on short-term morbidity and mortality in patients with left atrial enlargement undergoing cardiac valvular surgery.
Retrospective and observational.
Single-center, university teaching hospital.
The authors identified 197 patients (105 males and 92 females; mean age, 68 +/- 14 years) with left atrial enlargement who underwent surgical intervention for valvular heart disease from January 1, 2004 to January 1, 2005.
Of the total population, 40 patients (20.3%) showed left atrial SEC, and 10 patients (5.1%) showed aortic SEC. On multivariate analysis, increasing left atrial size and the absence of mitral regurgitation were independent predictors for the presence of left atrial SEC. On multivariate analysis, the presence of atrial fibrillation and a dilated descending aorta were predictive of aortic SEC. Although the identification of left atrial SEC was an echocardiographic marker of an increased risk for thromboembolic events postoperatively, this finding did not hold true for the presence of aortic SEC.
Intraoperative identification of left atrial dilatation or aortic dilatation is predictive of SEC in the left atrium or descending aorta, respectively. The identification of left atrial SEC is an echocardiographic marker of an increased risk for thromboembolic events in this high-risk population.
Journal of Cardiothoracic and Vascular Anesthesia 01/2007; 20(6):772-6. · 1.64 Impact Factor
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ABSTRACT: Impaired diastolic function is responsible for many of the clinical features of hypertrophic cardiomyopathy. In patients with hypertrophic obstructive cardiomyopathy (HOCM) whose symptoms are refractory to medical therapy, alcohol septal ablation (ASA) reduces left ventricular (LV) outflow tract gradient, with short-term improvement in LV diastolic function. Little is known about the longer term impact of ASA on diastolic function.
We evaluated LV diastolic function at baseline and 1- and 2-year follow-up after successful ASA. In 30 patients (58+/-15 years, 22 men) who underwent successful ASA, New York Heart Association class was lower at 1-year follow-up compared with baseline (3.0+/-0.5 to 1.5+/-0.7; P<0.0001). LV outflow tract gradient (76+/-37 to 19+/-12; P<0.0001), interventricular septal thickness (19+/-2 to 14+/-2; P<0.0001), and left atrial volume (26+/-5 to 20+/-4; P<0.0001) were decreased. Significant improvement in E-wave deceleration time, isovolumic relaxation time, early diastolic mitral lateral annular velocity (E'), mitral inflow propagation velocity (V(p)), ratio of transmitral early LV filling velocity (E) to early diastolic Doppler tissue imaging of the mitral annulus (E/E'), and E/V(p) were observed at 1 year following successful ASA. These changes persisted in the subset cohort (n=21) for whom 2-year data were available.
Successful ASA for HOCM leads to significant and sustained improvement in echocardiographic measures of diastolic function, which may contribute to improved functional status after successful ASA.
European Heart Journal 08/2006; 27(15):1805-10. · 10.48 Impact Factor
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Emmanuel Messas,
Chaim Yosefy,
Miguel Chaput,
J Luis Guerrero,
Suzanne Sullivan,
Philippe Menasché,
Alain Carpentier,
Michel Desnos,
Albert A Hagege, Gus J Vlahakes,
Robert A Levine
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ABSTRACT: Severing a limited number of second-order chordae to the anterior leaflet can improve ischemic mitral regurgitation (MR). Some concerns have been raised regarding possible influence on regional and global left ventricle (LV) function. We evaluated changes in cardiac function in 5 normal sheep with cutting of pre-instrumented chords in the beating heart to maintain constant load.
Under cardiopulmonary bypass, wires were placed around the 2 central basal chordae and brought outside the heart, which was restarted. Hemodynamic and imaging data were collected before and after chordal cutting by radiofrequency ablation using those wires. Segmental contractility was assessed invasively using sonomicrometers and noninvasively using Doppler tissue velocity and strain rate (with strain rate viewed as less load-dependent than ejection fraction) at 6 sites: base, mid-ventricle, and apex along the anteroseptal and posterolateral walls. We found no changes from before to after chordal cutting in LV end-diastolic volume (47.2+/-3.3 after cutting versus 48.4+/-4.6 mL before cutting, P=0.66), end-systolic volume (21.5+/-1.2 versus 22.3+/-2.8 mL, P=0.68), ejection fraction (54.2+/-1.8 versus 54.2+/-2.7%, P=0.96), systolic ventricular elastance (7.28+/-1.68 versus 7.66+/-2.11 mm Hg/mL, P=0.64), preload-recruitable stroke work (46.6+/-7.7 versus 50.2+/-10.7 mm Hg, P=0.76), and LVdP/dt (1480+/-238 versus 1392+/-250 mm Hg/s, P=0.45). Doppler tissue velocities and longitudinal strain rates surrounding the papillary muscles were unchanged, as were sonomicrometer longitudinal and mediolateral absolute strains. No wall motion abnormalities were visible around the papillary muscles, and no MR developed.
We find no evidence for acutely decreased global or segmental LV contractility with chordal cutting. This absence of adverse effects is consistent with long-term clinical experience with cutting these chords in valve repair.
Circulation 08/2006; 114(1 Suppl):I524-8. · 14.74 Impact Factor
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The Journal of thoracic and cardiovascular surgery 06/2006; 131(5):1169-70. · 3.41 Impact Factor
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ABSTRACT: Alcohol septal ablation (ASA) causes remodeling of the upper septum and left ventricular outflow tract (LVOT) and reduction in the LVOT gradient. The time course of gradient reduction early after ASA has not been established. This study characterized the time course of gradient response early after ASA. Patients underwent clinical assessment and transthoracic echocardiography at baseline and immediately, 3 days, 3 months, and 1 year after ASA. Forty-seven patients underwent ASA. The baseline LVOT gradient was 98 +/- 48 mm Hg. Three-month echocardiographic success, defined as > or = 50% gradient reduction from baseline, was achieved in 41 procedures (87%); thus, there were 6 failures. On the basis of percentage reduction in LVOT gradient at 3 days, 2 distinct subgroups of the success group were identified. These were monophasic success (> or = 50% gradient reduction at 3 days and 3 months, n = 25) and triphasic success (< 50% gradient reduction at 3 days but > or = 50% gradient reduction at 3 months, n = 16). LVOT gradient in the triphasic success group was similar to that in the failure group at 3 days (81 +/- 28 vs 99 +/- 31 mm Hg, p = NS) but similar to that of the monophasic success group at 3 months (24 +/- 20 vs 12 +/- 16 mm Hg, p = NS) and at 1 year (27 +/- 24 vs 13 +/- 20 mm Hg, p = NS). In conclusion, many patients who undergo ultimately successful ASA demonstrate triphasic LVOT gradient response patterns, with a large gradient 3 days after the procedure.
The American Journal of Cardiology 05/2006; 97(10):1511-4. · 3.37 Impact Factor
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ABSTRACT: Controversy exists over the short-term results and long-term efficacy of concomitant coronary artery bypass grafting and carotid endarterectomy. Additionally, in this population actual versus actuarial assessment of nonfatal late events has not been previously reported.
Hospital records of 500 consecutive patients having concomitant carotid endarterectomy and coronary artery bypass grafting between 1979 and 2001 were reviewed, allowing at least 1 year of follow-up on all patients. Long-term nonfatal complications were assessed by actual and actuarial methods.
Patient demographics revealed a mean age of 69 years; 74% (370 patients) were male; 75% (377 patients) presented with unstable coronary syndromes; 10% (50 patients) had an intraaortic balloon pump; and 66% (329 patients) were neurologically asymptomatic. Hospital mortality was 3.6% (18 patients). Significant multivariable predictors of hospital death were preoperative transient ischemic attack or myocardial infarction, and nonelective operation. Perioperative strokes were 4.6% (23 patients), of which 2.4% (12 patients) were ipsilateral and 2.2% (11 patients) were contralateral. Significant multivariable predictors of stroke were peripheral vascular disease and use of the right internal mammary artery. Ten-year actuarial survival was 43%. Ten-year actual versus Kaplan-Meier actuarial freedoms with 95% confidence limits from late events were myocardial infarction 87% (78% and 92%) versus 81% (75% and 87%); percutaneous coronary intervention 92% (85% and 96%) versus 89% (84% and 94%); reoperative coronary grafting 96% (89% and 99%) versus 94% (90% and 98%); total stroke 85% (77% and 91%) versus 82% (76% and 87%); ipsilateral stroke 90% (83% and 94%) versus 87% (82% and 92%); carotid endarterectomy 82% (73% and 88%) versus 75% (69% and 82%).
Concomitant carotid and coronary artery surgery is safe and effective, particularly in preventing ipsilateral stroke, and neutralizes the impact of unilateral carotid stenosis on early and late stroke. Actual, not actuarial, methods more accurately represent the true risk of nonfatal late events.
The Annals of thoracic surgery 01/2006; 80(6):2091-7. · 3.74 Impact Factor
