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1.
J Am Coll Cardiol ; 78(10): 1068-1077, 2021 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-34474740

RESUMO

Ischemic cardiomyopathy results from the combination of scar with fibrosis replacement and areas of dysfunctional but viable myocardium that may improve contractile function with revascularization. Observational studies reported that only patients with substantial amounts of myocardial viability had better outcomes following surgical revascularization. Accordingly, dedicated noninvasive techniques have evolved to quantify viable myocardium with the objective of selecting patients for this form of therapeutic intervention. However, prospective trials have not confirmed the interaction between myocardial viability and the treatment effect of revascularization. Furthermore, recent observations indicate that recovery of left ventricular function is not the principal mechanism by which surgical revascularization improves prognosis. In this paper, the authors describe a more contemporary application of viability testing that is founded on the alternative concept that the main goal of surgical revascularization is to prevent further damage by protecting the residual viable myocardium from subsequent acute coronary events.

2.
Artigo em Inglês | MEDLINE | ID: mdl-34419402

RESUMO

OBJECTIVES: The aim of this study was to evaluate the role of wall shear stress (WSS) as a predictor of ascending aorta (AAo) growth at 5 years or greater follow-up. BACKGROUND: Aortic 4-dimensional flow cardiac magnetic resonance (CMR) can quantify regions exposed to high WSS, a known stimulus for arterial wall dysfunction. However, its association with longitudinal changes in aortic dilation in patients with bicuspid aortic valve (BAV) is unknown. METHODS: This retrospective study identified 72 patients with BAV (45 ± 12 years) who underwent CMR for surveillance of aortic dilation at baseline and ≥5 years of follow-up. Four-dimensional flow CMR analysis included the calculation of WSS heat maps to compare regional WSS in individual patients with population averages of healthy age- and sex-matched subjects (database of 136 controls). The relative areas of the AAo and aorta (in %) exposed to elevated WSS (outside the 95% CI of healthy population averages) were quantified. RESULTS: At a median follow-up duration of 6.0 years, the mean AAo growth rate was 0.24 ± 0.20 mm/y. The fraction of the AAo exposed to elevated WSS at baseline was increased for patients with higher growth rates (>0.24 mm/y, n = 32) compared with those with growth rates <0.24 mm/y (19.9% [interquartile range (IQR): 10.2-25.5] vs 5.7% [IQR: 1.5-21.3]; P = 0.008). Larger areas of elevated WSS in the AAo and entire aorta were associated with higher rates of AAo dilation >0.24 mm/y (odds ratio: 1.51; 95% CI: 1.05-2.17; P = 0.026 and odds ratio: 1.70; 95% CI: 1.01-3.15; P = 0.046, respectively). CONCLUSIONS: The area of elevated AAo WSS as assessed by 4-dimensional flow CMR identified BAV patients with higher rates of aortic dilation and thus might determine which patients require closer follow-up.

3.
J Am Coll Cardiol ; 78(2): 180-188, 2021 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-34238439

RESUMO

Coronary artery disease (CAD) is treated with medical therapy with or without percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). The latter 2 options are commonly referred to as "myocardial revascularization" procedures. We reason that this term is inappropriate because it is suggestive of a single treatment effect of PCI and CABG (ie, the reestablishment of blood flow to ischemic myocardium) and obscures key mechanisms, such as the improvement in coronary flow capability in the absence of ongoing ischemia, the reperfusion in the presence of ischemia, and the prevention of myocardial infarction from CAD progression. We review the current evidence on the topic and suggest the use of a purely descriptive terminology ("invasive treatment by PCI or CABG") which has the potential to improve clinical decision making and guide future trial design.

18.
J Thorac Cardiovasc Surg ; 162(2): e183-e353, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-33972115
19.
Heart Lung Circ ; 30(10): 1496-1501, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34023176

RESUMO

BACKGROUND: Patients with hypertrophic cardiomyopathy (HCM) and an identified sarcomere mutation have worse outcomes than those without though the underlying mechanism is incompletely understood. The presence of replacement fibrosis measured by late gadolinium enhancement (LGE) and diffuse fibrosis measured by extracellular volume (ECV) using cardiac magnetic resonance imaging (CMR) are associated with ventricular arrhythmias and cardiac mortality. We aimed to associate these two forms of fibrosis with identified sarcomere mutations. METHODS AND RESULTS: Three hundred and thirty-six (336) patients with HCM underwent CMR at a single quaternary referral centre between January 2012 and February 2017. Genetic testing was performed in 73 of these patients, yielding an identified sarcomeric mutation in 29 (G+), no mutation in 39 (G-), and a variant of unknown significance (VUS) in five. LGE was more prevalent in G+ compared to G- patients (86 vs. 56%, OR 4.3, p=0.01) and was more extensive (7.5±5.5% of left ventricular [LV] mass vs. 3.0±3.0%, p<0.001). Global ECV from myocardial segments excluding LGE was similar among both groups (26.9±2.9 vs. 25.6±2.8%, p=0.46). However, in G+ patients ECV was greater in the hypertrophied regions of the basal anteroseptum (30.2±7.0 vs. 26.8±3.6%, p=0.004) and basal inferoseptum (28.1±4.3 vs. 26.2±2.9%, p=0.005). CONCLUSIONS: Genotyped HCM patients with an identified sarcomere mutation have greater LGE and greater regional, but not global, ECV than HCM patients without an identified mutation. This difference in fibrosis may contribute to worse outcomes in patients with an identified HCM mutation.


Assuntos
Cardiomiopatia Hipertrófica , Sarcômeros , Cardiomiopatia Hipertrófica/diagnóstico , Cardiomiopatia Hipertrófica/diagnóstico por imagem , Meios de Contraste , Fibrose , Gadolínio , Humanos , Imagem Cinética por Ressonância Magnética , Mutação , Miocárdio/patologia , Sarcômeros/genética
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