Percutaneous aortic valve replacement: valvuloplasty studies in vitro

Haberthür, David; Lutter, Georg; Appel, Marie; Attmann, Tim; Schramm, René; Schmitz, Christoph; Quaden, René

doi:10.1016/j.ejcts.2010.07.045

Cited by 16 publications

(3 citation statements)

References 17 publications

(14 reference statements)

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“…First, direct myocardial damage is induced by mechanical compression of the left ventricular outflow tract during balloon dilatation and valve implantation and-to a greater extent-by myocardial puncture during transapical interventions. Second, some, 23 but not all, mechanistic studies employing magnetic resonance imaging 24 pointed to the primary role of distal embolization of calcium microparticles into the coronaries during valvuloplasty and prosthesis implantation-a mechanism that is consistent with preclinical evidence 25 as well as evidence of cerebrovascular microemboli post-TAVI. 26 Third, temporary hypotension during rapid pacing or balloon predilatation, excessive bradycardia because of conduction abnormalities, or, conversely, tachycardia in the setting of inotropic hemodynamic support can result in myocardial ischemia attributed to hypoperfusion of the typically hypertrophic myocardium.…”

Section: Discussionmentioning

confidence: 99%

Post‐Procedural Troponin Elevation and Clinical Outcomes Following Transcatheter Aortic Valve Implantation

Koskinas

Stortecky

Franzone

et al. 2016

JAHA

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BackgroundBiomarkers of myocardial injury increase frequently during transcatheter aortic valve implantation (TAVI). The impact of postprocedural cardiac troponin (cTn) elevation on short‐term outcomes remains controversial, and the association with long‐term prognosis is unknown.Methods and ResultsWe evaluated 577 consecutive patients with severe aortic stenosis treated with TAVI between 2007 and 2012. Myocardial injury, defined according to the Valve Academic Research Consortium (VARC)‐2 as post‐TAVI cardiac troponin T (cTnT) >15× the upper limit of normal, occurred in 338 patients (58.1%). In multivariate analyses, myocardial injury was associated with higher risk of all‐cause mortality at 30 days (adjusted hazard ratio [HR], 8.77; 95% CI, 2.07–37.12; P=0.003) and remained a significant predictor at 2 years (adjusted HR, 1.98; 95% CI, 1.36–2.88; P<0.001). Higher cTnT cutoffs did not add incremental predictive value compared with the VARC‐2–defined cutoff. Whereas myocardial injury occurred more frequently in patients with versus without coronary artery disease (CAD), the relative impact of cTnT elevation on 2‐year mortality did not differ between patients without CAD (adjusted HR, 2.59; 95% CI, 1.27–5.26; P=0.009) and those with CAD (adjusted HR, 1.71; 95% CI, 1.10–2.65; P=0.018; P for interaction=0.24). Mortality rates at 2 years were lowest in patients without CAD and no myocardial injury (11.6%) and highest in patients with complex CAD (SYNTAX score >22) and myocardial injury (41.1%).Conclusions VARC‐2–defined cTnT elevation emerged as a strong, independent predictor of 30‐day mortality and remained a modest, but significant, predictor throughout 2 years post‐TAVI. The prognostic value of cTnT elevation was modified by the presence and complexity of underlying CAD with highest mortality risk observed in patients combining SYNTAX score >22 and evidence of myocardial injury.

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Section: Discussionmentioning

confidence: 99%

Post‐Procedural Troponin Elevation and Clinical Outcomes Following Transcatheter Aortic Valve Implantation

Koskinas

Stortecky

Franzone

et al. 2016

JAHA

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“…[4][5][6][7] Myocardial injury after TAVI is caused by many factors such as acute aortic regurgitation, elevation of left ventricular ejection fraction, temporary mitral valve regression, hypotension of coronary artery flow during rapid ventricular pacing, coronary ostia occlusion following valve deployment, direct myocardial injury by wire, suicide left ventricle, and particle embolization into the coronary arteries. 5,[8][9][10][11][12][13][14][15] (Figure 1) Elevated troponin level is an index of myocardial injury. Previous studies show that myocardial injury is significantly associated with a high rate of mortality.…”

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confidence: 99%

Incidence, Predictors, and Midterm Clinical Outcomes of Myocardial Injury After Transcatheter Aortic-Valve Implantation

et al. 2018

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Our aim was to assess the clinical effects of myocardial injury after transcatheter aortic-valve implantation (TAVI). Between October 2013 and July 2016, 157 patients underwent TAVI with Sapien XT, Sapien 3, or Cor-eValve prostheses at our institute. Of these, 130 patients for whom the transapical approach was not used were included in this study. Myocardial injury was defined as a peak troponin I level of ! 1.5 ng/mL within 48 hours after TAVI. We evaluated the predictors of myocardial injury and compared the clinical outcomes of 82 patients classified as the myocardial injury group and 44 patients classified as the non-myocardial injury group. The patients were aged 85 6 years. Myocardial injury occurred in 82 patients (65.1%). Age (per 1 increase) (odds ratio [

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“…In the same study, an inverse relationship was found between the aortic annulus-coronary ostium distance and MI ratios, similar to our results; however, unlike our results, the correlation was not statistically significant. 19 In an experimental study in porcine hearts, 22 multiple embolic particles were detected in all coronary arteries after in vitro balloon valvuloplasty of calcified AVs.…”

Section: Discussionmentioning

confidence: 99%

Predictors and Prognostic Implications of Myocardial Injury After Transcatheter Aortic Valve Replacement

Güney

Keleş

Karaduman

et al. 2022

Texas Heart Institute Journal

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Myocardial injury (MI) is not unusual after transcatheter aortic valve replacement (TAVR). To determine precipitating factors and prognostic outcomes of MI after TAVR, we retrospectively investigated relationships between MI after TAVR and aortic root dimensions, baseline patient characteristics, echocardiographic findings, and procedural features. Of 474 patients who underwent transfemoral TAVR for severe aortic stenosis in our tertiary center from June 2011 through June 2018, 188 (mean age, 77.7 ± 7.7 yr; 96 women [51%]) met the study inclusion criteria. Patients were divided into postprocedural MI (PMI) (n=74) and no-PMI (n=114) groups, in accordance with high-sensitivity troponin T levels. We found that MI risk was associated with older age (odds ratio [OR]=1.054; 95% CI, 1.013–1.098; P=0.01), transcatheter heart valve type (OR=10.207; 95% CI, 2.861–36.463; P=0.001), distances from the aortic annulus to the right coronary artery ostium (OR=0.853; 95% CI, 0.731–0.995; P=0.04) and the left main coronary artery ostium (OR=0.747; 95% CI, 0.616–0.906; P=0.003), and baseline glomerular filtration rate (OR=0.985; 95% CI, 0.970–1.000; P=0.04). Moreover, the PMI group had a longer time to hospital discharge (P=0.001) and a higher permanent pacemaker implantation rate (P=0.04) than did the no-PMI group. Our findings may enable better estimation of which patients are at higher risk of MI after TAVR and thus improve the planning and course of clinical care.

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Percutaneous aortic valve replacement: valvuloplasty studies in vitro

Cited by 16 publications

References 17 publications

Post‐Procedural Troponin Elevation and Clinical Outcomes Following Transcatheter Aortic Valve Implantation

Post‐Procedural Troponin Elevation and Clinical Outcomes Following Transcatheter Aortic Valve Implantation

Incidence, Predictors, and Midterm Clinical Outcomes of Myocardial Injury After Transcatheter Aortic-Valve Implantation

Predictors and Prognostic Implications of Myocardial Injury After Transcatheter Aortic Valve Replacement

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