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.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Coronavirus disease 2019 (COVID-19) is a growing pandemic that confers augmented risk for right ventricular (RV) dysfunction and dilation; the prognostic utility of adverse RV remodeling in COVID-19 ...patients is uncertain.
The purpose of this study was to test whether adverse RV remodeling (dysfunction/dilation) predicts COVID-19 prognosis independent of clinical and biomarker risk stratification.
Consecutive COVID-19 inpatients undergoing clinical transthoracic echocardiography at 3 New York City hospitals were studied; images were analyzed by a central core laboratory blinded to clinical and biomarker data.
In total, 510 patients (age 64 ± 14 years, 66% men) were studied; RV dilation and dysfunction were present in 35% and 15%, respectively. RV dysfunction increased stepwise in relation to RV chamber size (p = 0.007). During inpatient follow-up (median 20 days), 77% of patients had a study-related endpoint (death 32%, discharge 45%). RV dysfunction (hazard ratio HR: 2.57; 95% confidence interval CI: 1.49 to 4.43; p = 0.001) and dilation (HR: 1.43; 95% CI: 1.05 to 1.96; p = 0.02) each independently conferred mortality risk. Patients without adverse RV remodeling were more likely to survive to hospital discharge (HR: 1.39; 95% CI: 1.01 to 1.90; p = 0.041). RV indices provided additional risk stratification beyond biomarker strata; risk for death was greatest among patients with adverse RV remodeling and positive biomarkers and was lesser among patients with isolated biomarker elevations (p ≤ 0.001). In multivariate analysis, adverse RV remodeling conferred a >2-fold increase in mortality risk, which remained significant (p < 0.01) when controlling for age and biomarker elevations; the predictive value of adverse RV remodeling was similar irrespective of whether analyses were performed using troponin, D-dimer, or ferritin.
Adverse RV remodeling predicts mortality in COVID-19 independent of standard clinical and biomarker-based assessment.
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.
Abstract
OBJECTIVES
Among patients with ascending thoracic aortic aneurysms, prosthetic graft replacement yields major benefits but risk for recurrent aortic events persists for which mechanism is ...poorly understood. This pilot study employed cardiac magnetic resonance to test the impact of proximal prosthetic grafts on downstream aortic flow and vascular biomechanics.
METHODS
Cardiac magnetic resonance imaging was prospectively performed in patients with thoracic aortic aneurysms undergoing surgical (Dacron) prosthetic graft implantation. Imaging included time resolved (4-dimensional) phase velocity encoded cardiac magnetic resonance for flow quantification and cine-cardiac magnetic resonance for aortic wall distensibility/strain.
RESULTS
Twenty-nine patients with thoracic aortic aneurysms undergoing proximal aortic graft replacement were studied; cardiac magnetic resonance was performed pre- 12 (4, 21) days and postoperatively 6.4 (6.2, 7.2) months. Postoperatively, flow velocity and wall shear stress increased in the arch and descending aorta (P < 0.05); increases were greatest in hereditary aneurysm patients. Global circumferential strain correlated with wall shear stress (r = 0.60–0.72, P < 0.001); strain increased postoperatively in the native descending and thoraco-abdominal aorta (P < 0.001). Graft-induced changes in biomechanical properties of the distal native ascending aorta were associated with post-surgical changes in descending aortic wall shear stress, as evidenced by correlations (r = −0.39–0.52; P ≤ 0.05) between graft-induced reduction of ascending aortic distensibility and increased distal native aortic wall shear stress following grafting.
CONCLUSIONS
Prosthetic graft replacement of the ascending aorta increases downstream aortic wall shear stress and strain. Postoperative increments in descending aortic wall shear stress correlate with reduced ascending aortic distensibility, suggesting that grafts provide a nidus for high energy flow and adverse distal aortic remodelling.
Prosthetic aortic graft replacement is widely used to treat patients with thoracic aortic aneurysms (TAAs).
Objectives: Three-dimensional transesophageal echocardiography (TEE) is widely used to guide decision-making for mitral repair. The relative impact of surgical mitral valve repair (MVr) and MitraClip ...on annular remodeling is unknown. The aim was to determine the impact of both mitral repair strategies on annular geometry, including the primary outcome of annular circumference and area.
Design: This was a retrospective observational study of patients who underwent mitral intervention between 2016 and 2020.
Setting: Weill Cornell Medicine, a single, large, academic medical center.
Participants: The population comprised 50 patients with degenerative mitral regurgitation (MR) undergoing MVr.
Interventions: Elective MVr and TEE.
Measurements and Main Results: Patients undergoing MitraClip or surgical MVr were matched (1:1) for sex and coronary artery disease. Mitral annular geometry indices were quantified on intraprocedural three-dimensional TEE. Mild or less MR on follow-up transthoracic echocardiography defined optimal response. Patients undergoing MitraClip were older (80 ± eight v 66 ± six years; p < 0.001) but were otherwise similar to surgical patients. Patients undergoing MitraClip had larger baseline left atrial and ventricular sizes, increased tenting height, and volume (p < 0.01), with a trend toward increased annular area (p = 0.23). MitraClip and surgery both induced immediate mitral annular remodeling, including decreased area, circumference, and tenting height (p < 0.001), with greater remodeling with surgical repair. At follow-up (4.1 ± 9.0 months) optimal response (≤ mild MR) was ∼twofold more common with surgery than MitraClip (81% v 46%; p = 0.02). The relative reduction in annular circumference (odds ratio OR 1.05 1.00-1.09 per cm; p = 0.04) and area (OR 1.03 1.00-1.05 per cm2; p = 0.049) were both associated with optimal response.
Conclusions: Surgical MVr and MitraClip both reduce annular size, but repair-induced remodeling is greater with surgery and associated with an increased likelihood of optimal response.
Reply Kim, Jiwon; Mitlak, Hannah W.; Weinsaft, Jonathan W.
Journal of the American College of Cardiology,
04/2021, Letnik:
77, Številka:
13
Journal Article
Abstract only Introduction: Functional mitral regurgitation (FMR) alters left ventricular (LV) remodeling, providing a nidus for non-ischemic fibrosis (NIF). Cardiac magnetic resonance (CMR) can ...measure FMR and LV tissue properties. Prevalence, remodeling manifestations, and prognostic implications of NIF in patients with FMR are unknown. Hypothesis: Among post-myocardial infarction (MI) patients with FMR, NIF associates with advanced LV remodeling and predicts adverse prognosis. Methods: The population comprised post-MI patients with FMR undergoing CMR. CMR exams were retrieved from a single-center registry, reviewed for MR etiology (degenerative excluded) and analyzed for FMR severity, LV structure/function, and late gadolinium enhancement (LGE) including ischemic pattern MI and NIF, which was defined via established criteria (mid-myocardial or epicardial LGE). Follow-up was performed for all-cause mortality. Results: 467 consecutive FMR patients (74% male, 63±16 years old) were studied, of whom 14% had NIF. Prevalence of NIF increased stepwise with FMR severity (12% mild, 16% moderate, 21% severe; p=0.33). Patients with NIF had higher LV end-diastolic (241±72ml vs 194±64ml) and end-systolic volumes (174±70ml vs 120±63ml), paralleled by lower EF (31±13% vs 41±15%) and stroke volumes (67±20ml vs 74±24ml); all p<0.001. LV infarct size was similar between patients with and without NIF (13±8.6 vs 15±10, p=0.17). During follow-up (mean 3.0±2.5 years), overall mortality was 14% and was increased in patients with advanced (≥ moderate) FMR (HR 1.65 CI 1.13-2.42, p=0.01) and NIF (HR 2.35 CI 1.32-4.19, p=0.004: Figure). In multivariate analysis, NIF conferred over a 2-fold increase in risk for death (HR 2.15 CI 1.20-3.85, p=0.01) independent of age and FMR severity. Conclusions: Among post-MI patients with FMR, NIF identifies an aggressive phenotype as evidenced by associations with adverse LV remodeling on CMR and increased mortality.
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