32 research outputs found

    One-year clinical outcomes in patients with renal insufficiency after contemporary PCI: data from a multicenter registry

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    Chronic kidney disease (CKD) is highly prevalent in patients with coronary artery disease (CAD).Methods e-Ultimaster is a prospective, single-arm, multi-center registry with clinical follow-up at 3 months and 1 year.Objective The outcome following revascularization using contemporary technologies (new-generation abluminal sirolimus-eluting stents with thin struts) in patients with CKD (i.e., glomerular filtration rate of < 60 mL/min/1.73m2) and in patients with hemodialysis (HD) is unknown.Results A total of 19,475 patients were enrolled, including 1466 patients with CKD, with 167 undergoing HD. Patients with CKD had a higher prevalence of overall comorbidities, multiple/small vessel disease (≤ 2.75 mm), bifurcation lesions, and more often left main artery treatments (all p < 0.0001) when compared with patients with normal renal function (reference). CKD patients had a higher risk of target lesion failure (unadjusted OR, 2.51 [95% CI 2.04–3.08]), target vessel failure (OR, 2.44 [95% CI 2.01–2.96]), patient-oriented composite end point (OR, 2.19 [95% CI 1.87–2.56]), and major adverse cardiovascular events (OR, 2.34 [95% CI 1.93–2.83, p for all < 0.0001]) as reference. The rates of target lesion revascularization (OR, 1.17 [95% CI 0.79–1.73], p = 0.44) were not different. Bleeding complications were more frequently observed in CKD than in the reference (all p < 0.0001).Conclusion In this worldwide registry, CKD patients presented with more comorbidities and more complex lesions when compared with the reference population. They experienced higher rate of adverse events at 1-year follow-up

    Correction to: One‑year clinical outcomes in patients with renal insuffciency after contemporary PCI: data from a multicenter registry

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    The original version of this article unfortunately contained a mistake. The given name and family name of the fourth author Saaraaken Kulenthiran were switched in the original publication

    Rotation, Velocity and Deformation Imaging in Hypertrophic Cardiomyopathy

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    Hypertrophic cardiomyopathy (HCM) is regarded as one of the most common inherited cardiac diseases. In a number of population studies the prevalence of HCM is estimated in the general population to be at least 1 in 500. HCM is inherited with an autosomal dominant Mendelian pattern, variable expressivity, and age-related (and incomplete) penetrance. Clinical diagnosis of HCM requires confirmation of phenotypic expression, that is an unexplained increase in left ventricular (LV) wall thickness (≥15 mm in adults) associated with a nondilated LV chamber with cardiac imaging (usually echocardiography). Phenotype positive patients may show different patterns of LV hypertrophy: reverse septal curvature, sigmoidal and apical forms have been described. Relatives identified with pathogenic mutations (gene carriers) but without evidence of the disease phenotype comprise a new HCM subgroup, designated as genotype positive-phenotype negative individuals. The risk of eventually developing LV hypertrophy in this group is currently uncertain. In this thesis we investigated the value of speckle tracking echocardiographically (STE)-derived global and regional LV rotation and strain in HCM mutation gene carriers and patients, both in systole and diastole. In the first part of this thesis STE analysis of myocardial velocity, rotation and strain in systole and diastole is introduced. In Chapter 2 a literature review of LV twist mechanics in cardiomyopathies is presented. Analysis of LV twist mechanics may provide substantial pathophysiological understanding in a variety of cardiomyopathies. In the second part of this thesis the feasibility of STE is studied. In Chapter 3 it is shown with a moving phantom model that mitral annular velocities can be accurately determined by STE in an angle independent way. In Chapter 4 the feasibility, observer variability and test-retest variability of LV twist measurements by STE is described. The method appeared to be feasible in approximately two thirds of the subjects with good observer variability and temporal reproducibility, potentially allowing to study changes in LV twist over time in an individual patient. The third part of this thesis is dedicated to the value of STE in HCM carriers and patients. In Chapter 5 it is shown that in HCM patients, LV basal rotation is increased, whereas apical rotation was normal, resulting in increased LV twist. The increased basal rotation may be explained by loss of counteraction of the subendocardial fibre helix, caused by endocardial ischemia due to microvascular dysfunction. LV apical rotation and twist were dependent on the pattern of LV hypertrophy. In patients with a sigmoidal septal curvature, LV apical rotation and twist are increased as compared to patients with a reverse septal curvature. This may be partly explained by the degree of subendocardial ischemia since patients with a sigmoidal septal curvature more often had LV outflow tract obstruction. The extravascular compressive forces caused by gradients due to the outflow obstruction may lead to more extensive microvascular dysfunction and subendocardial ischemia. In Chapter 6 differences in regional basal rotation in HCM patient with a typical reverse septal curvature are described. Basal septal and anterior segments, the segments mostly involved in the hypertrophic process, showed increased rotation compared to other segments where re-rotation rate, the diastolic LV back rotation velocity, is decreased in the septal segment of the basal LV. In Chapter 7 it is shown that although systolic twist is increased in HCM patients LV untwist is delayed, impairing diastolic filling. In a pilot study described in Chapter 8 we tried to investigate the feasibility and value of LV systolic and diastolic strain and rotation (twist) parameters during exercise in patients with HCM, with emphasize on the reserve as clinical exercise-related symptoms in patients with HCM but without LV outflow-tract obstruction are presumed to be related to diastolic dysfunction. Although in this study a blunted diastolic longitudinal functional reserve as assessed by tissue Doppler and STE analysis in HCM patients during exercise is shown, the principal finding of this study is that the feasibility of STE during upright bicycle testing is very limited. In Chapter 9 the relation between resting diastolic deformation indices and subjective (NYHA Class) and objective (ergometry) exercise tolerance in HCM patients is studied. Although the conventional early diastolic myocardial lengthening velocity parameter (e’) is the strongest predictor for exercise workload in HCM patients also STE deformation parameters like strain, unstrain and untwist showed independent correlations to exercise workload. In the final two chapters we investigated the possibilities of STE in detecting preclinical HCM in family members of HCM patients as an alternative for genetic testing, comparable to prior studies using TDI in which conflicting results were reported, potentially caused by the angle-dependency of TDI. In Chapter 10 increased peak late diastolic annular velocities in HCM genetically affected subjects without LV hypertrophy were shown with STE analysis. In contrast, peak early diastolic values could not differentiate genotype (+) from genotype (-) individuals. Finally, in Chapter 11 it is shown that in HCM mutation carriers untwist and unstrain rates are also decreased and delayed indicating early diastolic abnormalities

    Role of left ventricular twist mechanics in cardiomyopathies, dance of the helices

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    Left ventricular twist is an essential part of left ventricular function. Nevertheless, knowledge is limited in “the cardiology community” as it comes to twist mechanics. Fortunately the development of speckle tracking echocardiography, allowing accurate, reproducible and rapid bedside assessment of left ventricular twist, has boosted the interest in this important mechanical aspect of left ventricular deformation. Although the fundamental physiological role of left ventricular twist is undisputable, the clinical relevance of assessment of left ventricular twist in cardiomyopathies still needs to be established. The fact remains; analysis of left ventricular twist mechanics has already provided substantial pathophysiological understanding on a comprehensive variety of cardiomyopathies. It has become clear that increased left ventricular twist in for example hypertrophic cardiomyopathy may be an early sign of subendocardial (microvascular) dysfunction. Furthermore, decreased left ventricular twist may be caused by left ventricular dilatation or an extensive myocardial scar. Finally, the detection of left ventricular rigid body rotation in noncompaction cardiomyopathy may provide an indispensible method to objectively confirm this difficult diagnosis. All this endorses the value of left ventricular twist in the field of cardiomyopathies and may further encourage the implementation of left ventricular twist parameters in the “diagnostic toolbox” for cardiomyopathies

    Role of left ventricular twist mechanics in cardiomyopathies, dance of the helices

    No full text
    Left ventricular twist is an essential part of left ventricular function. Nevertheless, knowledge is limited in “the cardiology community” as it comes to twist mechanics. Fortunately the development of speckle tracking echocardiography, allowing accurate, reproducible and rapid bedside assessment of left ventricular twist, has boosted the interest in this important mechanical aspect of left ventricular deformation. Although the fundamental physiological role of left ventricular twist is undisputable, the clinical relevance of assessment of left ventricular twist in cardiomyopathies still needs to be established. The fact remains; analysis of left ventricular twist mechanics has already provided substantial pathophysiological understanding on a comprehensive variety of cardiomyopathies. It has become clear that increased left ventricular twist in for example hypertrophic cardiomyopathy may be an early sign of subendocardial (microvascular) dysfunction. Furthermore, decreased left ventricular twist may be caused by left ventricular dilatation or an extensive myocardial scar. Finally, the detection of left ventricular rigid body rotation in noncompaction cardiomyopathy may provide an indispensible method to objectively confirm this difficult diagnosis. All this endorses the value of left ventricular twist in the field of cardiomyopathies and may further encourage the implementation of left ventricular twist parameters in the “diagnostic toolbox” for cardiomyopathies

    Feasibility and reproducibility of left ventricular rotation parameters measured by speckle tracking echocardiography

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    Aims This study sought to find the most robust method for left ventricular (LV) rotation measurement by speckle tracking echocardiography (STE) with the new QLAB Advanced Quantification Software (version 6.0, Philips, Best, The Netherlands). Methods and results The study population consisted of 40 non-selected patients (mean age 48 +/- 18 year, 20 men) and 50 non-selected healthy volunteers (mean age 34 +/- 12 year, 21 men). Feasibility and intra-observer reproducibility of the measurement of LV rotation parameters by STE were assessed for two different methods (Method A: six tracking points placed mid-myocardial and Method B: six tracking points placed endocardial and epicardial forming six myocardial segments). Subsequently, inter-observer and temporal reproducibility of the most robust method were assessed. Complete LV rotation assessment was more feasible with Method A (60 out of 90 subjects, 67% vs. 50 out of 90 subjects, 56%). In the 49 subjects in whom both Methods A and B were feasible, intra-observer reproducibility of LV rotation parameters was better with Method A (variabilities 2 +/- 3 to 10 +/- 9% vs. 2 +/- 4 to 21 +/- 18%). With this method, inter-observer variability varied from 4 +/- 4 to 13 +/- 9% and temporal variability from 4 +/- 6 to 19 +/- 15%. Conclusion The most robust method to assess LV rotation with QLAB software is from the mid-myocardium. This method is feasible in approximately two-thirds of subjects and has good intra-observer, inter-observer, and temporal reproducibility, allowing to study changes over time in LV rotation in an individual patient
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