COVID-19 is associated with cardiac dysfunction. This study tested the relative prognostic role of left (LV), right and bi- (BiV) ventricular dysfunction on mortality in a large multicenter cohort of ...patients during and after acute COVID-19 hospitalization.
All hospitalized COVID-19 patients who underwent clinically indicated transthoracic echocardiography within 30 days of admission at four NYC hospitals between March 2020 and January 2021 were studied. Images were re-analyzed by a central core lab blinded to clinical data. Nine hundred patients were studied (28% Hispanic, 16% African-American), and LV, RV and BiV dysfunction were observed in 50%, 38% and 17%, respectively. Within the overall cohort, 194 patients had TTEs prior to COVID-19 diagnosis, among whom LV, RV, BiV dysfunction prevalence increased following acute infection (p<0.001). Cardiac dysfunction was linked to biomarker-evidenced myocardial injury, with higher prevalence of troponin elevation in patients with LV (14%), RV (16%) and BiV (21%) dysfunction compared to those with normal BiV function (8%, all p<0.05). During in- and out-patient follow-up, 290 patients died (32%), among whom 230 died in the hospital and 60 post-discharge. Unadjusted mortality risk was greatest among patients with BiV (41%), followed by RV (39%) and LV dysfunction (37%), compared to patients without dysfunction (27%, all p<0.01). In multivariable analysis, any RV dysfunction, but not LV dysfunction, was independently associated with increased mortality risk (p<0.01).
LV, RV and BiV function declines during acute COVID-19 infection with each contributing to increased in- and out-patient mortality risk. RV dysfunction independently increases mortality risk.
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Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Right ventricular hypertrophy (RVH) provides a key remodeling index alterable by pulmonary hypertension. Although echocardiography commonly integrates linear wall thickness and chamber dimensions to ...quantify left ventricular remodeling, the utility of an equivalent right ventricular (RV)-based approach is unknown.
This was a retrospective analysis of 200 patients undergoing transthoracic echocardiography and cardiac magnetic resonance (CMR) within 30 days (median = 3 days; interquartile range, 15 days), stratified by echocardiography-quantified pulmonary artery systolic pressure (<35, 35 to <55, 55 to <75, or ≥75 mm Hg). Echocardiographic assessment included RV linear dimensions in parasternal long-axis and apical four-chamber views and wall thicknesses in parasternal long-axis, four-chamber, and subcostal views. Subcostal wall thickness was integrated with chamber diameters to calculate RV mass, which was tested in relation to CMR-quantified RV mass and all-cause mortality.
Echocardiography-based quantification of all linear dimensions was feasible in 95% of patients (190 of 200). RV wall thicknesses in all orientations increased in relation to pulmonary artery systolic pressure (P < .001) and was greater among patients with, versus those without, CMR-evidenced RVH (P < .001 for all). Correlations between echocardiography and CMR were greatest for RV basal diameter (r = 0.73), RV subcostal wall thickness (r = 0.71), and global RV mass (r = 0.82; P < .001 for all). Echocardiography-derived global RV mass cutoffs were established in a derivation cohort and tested in a validation cohort. Results demonstrated good sensitivity and specificity (75.5% and 74.0%, respectively) in relation to CMR-quantified RVH. During follow-up (median, 4.2 years), 18% of patients (n = 36) died. Echocardiography-evidenced RVH (hazard ratio, 1.98; 95% CI, 1.09-3.88; P = .048) conferred similar mortality risk compared with RVH on CMR (hazard ratio, 2.41; 95% CI, 1.22-4.78; P = .01).
Echocardiography-quantified RV parameters provide a robust index of RV afterload. Global RV mass calculated using a novel echocardiographic formula based on readily available linear indices yields good diagnostic performance for CMR-evidenced RVH and confers increased mortality risk.
McCorquodale DS III, Ozomaro U, Huang J, Montenegro G, Kushman A, Citrigno L, Price J, Speziani F, Pericak‐Vance MA, Züchner S. Mutation screening of spastin, atlastin, and REEP1 in hereditary ...spastic paraplegia.
Hereditary spastic paraplegia (HSP) comprises a group of clinically and genetically heterogeneous diseases that affect the upper motor neurons and their axonal projections. Over 40 chromosomal loci have been identified for autosomal dominant, recessive, and X‐linked HSP. Mutations in the genes atlastin, spastin and REEP1 are estimated to account for up to 50% of autosomal‐dominant HSP and currently guide the molecular diagnosis of HSP. Here, we report the mutation screening results of 120 HSP patients from North America for spastin, atlastin, and REEP1, with the latter one partially reported previously. We identified mutations in 36.7% of all tested HSP patients and describe 20 novel changes in spastin and atlastin. Our results add to a growing number of HSP disease‐associated variants and confirm the high prevalence of atlastin, spastin, and REEP1 mutations in the HSP patient population.
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