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1.
Artigo em Inglês | MEDLINE | ID: mdl-32561917

RESUMO

AIMS: Concomitant secondary atrioventricular regurgitation is frequent in patients with severe aortic stenosis scheduled for transcatheter aortic valve replacement (TAVR). The future implications of leaving associated valve lesions untreated after TAVR remain unknown. Aim of the present study was to characterize the evolution of concomitant secondary atrioventricular regurgitations and to evaluate their impact on long-term prognosis. METHODS AND RESULTS: We prospectively enrolled 429 consecutive TAVR patients. All patients underwent comprehensive clinical, laboratory, and echocardiographic assessments prior to TAVR, at discharge, and yearly thereafter. All-cause mortality was chosen as primary study endpoint. At baseline, severe concomitant secondary mitral regurgitation (sMR) was present in 54 (13%) and severe concomitant secondary tricuspid regurgitation (sTR) in 75 patients (17%). After TAVR 59% of patients with severe sMR at baseline experienced sMR regression, whereas analogously sTR regressed in 43% of patients with severe sTR. Persistence of sTR and sMR were associated with excess mortality after adjustment for our bootstrap-selected confounder model with an adjusted HR of 2.44 (95% CI 1.15-5.20, P = 0.021) for sMR and of 2.09 (95% CI 1.20-3.66, P = 0.01) for sTR. Patients showing regression of atrioventricular regurgitation exhibited survival rates indistinguishable to those seen in patients without concomitant atrioventricular regurgitation (sMR: P = 0.83; sTR: P = 0.74). CONCLUSION: Concomitant secondary atrioventricular regurgitation in patients with severe AS is a highly dynamic process with up to half of all patients showing regression of associated valvular regurgitation after TAVR and subsequent favourable post-interventional outcome. Persistent atrioventricular regurgitation is a major determinant of unfavourable outcome after TAVR and proposes a window of early sequel intervention.

4.
Br J Clin Pharmacol ; 2020 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-32598074

RESUMO

AIMS: The clinically investigated rationale for neprilysin (NEP)-inhibition by ARNi-therapy is to induce elevations in endogenous natriuretic peptides. NEP, however, cleaves a broad spectrum of substrates, which partially hold significant implications in HFrEF. The effect of NEP-inhibition on these peptides has not been investigated thoroughly. This study explored the response of adrenomedullin (ADM) regulation to the initiation of ARNi. METHODS: Seventy-four patients with stable HFrEF and initiation of ARNi were prospectively enrolled, sixty-seven patients on continuous ACEi/ARB therapy served as control. Plasma bioactive-ADM (bio-ADM), mid-regional-pro-ADM (MR-proADM), B-type-NP (BNP) and N-terminal-pro-BNP (NT-proBNP) were determined at baseline, short-term, and 1-year and 2-years follow-up (FUP). RESULTS: Following ARNi initiation both bio-ADM and MR-proADM concentrations were significantly increased at early and long-term FUP [bio-ADM (pg/ml): 26.0 (interquartile range (IQR):17.7-37.5) vs 50.8 (IQR:36.5-78.1) vs 54.6 (IQR:42.0-97.1) vs 57.4 (IQR:48.5-161.6); MR-proADM (nmol/l): 0.87 (IQR:0.64-1.12) vs 1.25 (IQR:0.93-1.79) vs 1.42 (IQR:0.95-1.90) vs 1.60 (IQR:1.12-2.46), p<0.0001 for all]. The ratios bio-ADM/MR-proADM and BNP/NT-proBNP increased during ARNi-therapy proving improved availability of bioactive peptides. The proportional increase of bio-ADM markedly exceeded BNP increase. Patients converted to ARNi showed similar biomarker patterns irrespective of baseline RAS-blocker therapy, i.e. ACEi or ARB (p>0.05 for all), indicating that activation of the ADM-axis arises particularly from NEP-inhibition. CONCLUSION: The significant increase of MR-proADM and bio-ADM together with an elevated bioADM/MR-proADM ratio suggest both enhanced formation and reduced breakdown of bioactive ADM following the initiation of ARNi. Activation of the ADM-axis represents a so far unrecognized effect of ARNi.

5.
J Am Heart Assoc ; 9(11): e015071, 2020 Jun 02.
Artigo em Inglês | MEDLINE | ID: mdl-32427034

RESUMO

Background Neprilysin is a transmembrane endopeptidase involved in the breakdown of a variety of vasoactive peptides and serves as a therapeutic target in heart failure with reduced ejection fraction (HFrEF). This study aimed to investigate the relationship of circulating neprilysin with neurohumoral activation and the impact of plasma neprilysin activity on prognosis in HFrEF. Methods and Results A total of 369 chronic HFrEF patients were enrolled prospectively. Plasma neprilysin concentration and activity were determined by a specific ELISA and a fluorometric method. The association between plasma neprilysin and heart failure (HF) severity, neurohumoral activation, ie norepinephrine and absolute renin concentration, as well as all-cause mortality was assessed. Median plasma neprilysin concentrations and activity levels were 413 pg/mL (interquartile range 0-4111) and 2.36 nmol/mL per minute (interquartile range 1.16-4.59). No correlation could be shown between plasma neprilysin concentrations and activity (rs=0.09, P=0.088). Plasma neprilysin activity correlated with HF severity reflected by New York Heart Association stage (P=0.003) and tertiles of N-terminal pro-B-type natriuretic peptide (P<0.001), whereas neprilysin concentrations did not (P=0.220; P=0.849). There was no relevant relationship between plasma neprilysin concentrations and activity, with neurohumoral activation reflected by absolute renin concentration (rs=-0.02, P=0.648; rs=0.03, P=0.574) or norepinephrine levels (rs=-0.06, P=0.248; rs=0.20, P<0.001). Neither circulating neprilysin concentrations nor activity were associated with outcome. Conclusions Plasma neprilysin concentrations and activity are not directly related to neurohumoral activation, indicating that neprilysin regulation is either more complex or not correctly mirrored by circulating neprilysin as a biomarker. Circulating neprilysin concentrations and activity were not associated with overall survival, implicating limited prognostic value of plasma neprilysin measurements in HFrEF patients.

7.
Eur Heart J ; 2020 Apr 29.
Artigo em Inglês | MEDLINE | ID: mdl-32350503

RESUMO

Secondary mitral regurgitation and secondary tricuspid regurgitation due to heart failure (HF) remain challenging in almost every aspect: increasing prevalence, poor prognosis, notoriously elusive in diagnosis, and complexity of therapeutic management. Recently, defined HF subgroups according to three ejection fraction (EF) ranges (reduced, mid-range, and preserved) have stimulated a structured understanding of the HF syndrome but the role of secondary valve regurgitation (SVR) across the spectrum of EF remains undefined. This review expands this structured understanding by consolidating the underlying phenotype of myocardial impairment with each type of SVR. Specifically, the current understanding, epidemiological considerations, impact, public health burden, mechanisms, and treatment options of SVR are discussed separately for each lesion across the HF spectrum. Furthermore, this review identifies important gaps in knowledge, future directions for research, and provides potential solutions for diagnosis and treatment. Mastering the challenge of SVR requires a multidisciplinary collaborative effort, both, in clinical practice and scientific approach to optimize patient outcomes.

8.
JACC Cardiovasc Imaging ; 13(3): 891, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32139037
9.
Eur J Heart Fail ; 2020 Mar 23.
Artigo em Inglês | MEDLINE | ID: mdl-32202022

RESUMO

AIMS: Cancer patients suffer from impaired cardiovascular function. Elevated resting heart rate (RHR) has been identified as a marker for increased long-term mortality in cancer patients prior to the receipt of anticancer treatment. We aimed to establish whether RHR is associated with survival in treatment-naïve cancer patients. METHODS AND RESULTS: This prospective study enrolled 548 unselected treatment-naïve cancer patients between 2011 and 2013. The median age of the cohort was 62 years; 40.9% were male and 32.7% had metastatic disease. Median RHR was 72 b.p.m. Most patients were in sinus rhythm (n = 507, 92.5%). Clinical heart failure was noted in 37 (6.8%) patients. RHR was not related to cancer stage (P = 0.504). Patients in the highest RHR tertile had higher levels of high-sensitivity troponin (P = 0.003) and N-terminal pro-B-type natriuretic peptide (P = 0.039). During a median follow-up of 25 months (interquartile range: 16-32 months; range: 0-40 months), 185 (33.8%) patients died from any cause [1-year-mortality: 17%, 95% confidence interval (CI) 13-20%]. In univariate survival analysis, RHR predicted all-cause mortality [crude hazard ratio (HR) for a 5 b.p.m. increase in RHR: 1.09, 95% CI 1.04-1.15; P < 0.001], and remained significantly associated with outcome after adjustment for age, gender, tumour entity, tumour stage, cardiac status and haemoglobin (adjusted HR for a 5 b.p.m. increase in RHR: 1.10, 95% CI 1.04-1.16; P < 0.001). There was no significant impact of metastatic/non-metastatic disease state on the predictive value of RHR (P = 0.433 for interaction). In subgroup analyses, the strongest associations for RHR with mortality were observed in lung (crude HR 1.14; P = 0.007) and gastrointestinal (crude HR 1.31; P < 0.001) cancer. CONCLUSIONS: Treatment-naïve cancer patients with higher RHRs display higher levels of cardiovascular biomarkers. RHR was independently associated with all-cause mortality, especially in lung and gastrointestinal cancers. Elevated RHR and cardiovascular biomarkers may represent early signs of incipient cardiac dysfunction.

10.
ESC Heart Fail ; 7(2): 654-662, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32096921

RESUMO

AIMS: The progression of heart failure is presumably dependent on the individual inflammatory host response. The combination of the inflammatory markers, albumin, and C-reactive protein, termed modified Glasgow prognostic score (mGPS), has been derived from cancer patients and validated in multiple cohorts. This study aimed to investigate the impact of the easily available mGPS on survival of stable patients with heart failure with reduced ejection fraction (HFrEF). METHODS AND RESULTS: Patients with stable HFrEF undergoing routine ambulatory care between January 2011 and November 2017 have been identified from a prospective registry at the Medical University of Vienna. Comorbidities, laboratory data as well as the nutritional risk index at baseline were assessed. All-cause mortality was defined as the primary study end point. The mGPS was calculated, and its association with heart failure severity and impact on overall survival were determined. Data were analysed for a total of 443 patients. The mGPS was 0 for 352 (80%), 1 for 76 (17%), and 2 for 14 (3%) patients, respectively. Elevation of mGPS was associated with worsening of routine laboratory parameters linked to prognosis, especially NT-proBNP [median 1830 pg/mL (IQR 764-3455) vs. 4484 pg/mL (IQR 1565-8003) vs. 6343 pg/mL (IQR 3750-15401) for mGPS 0, 1, and 2, respectively; P < 0.001] and nutritional risk index. In the Cox regression analysis, the increase of mGPS was associated with adverse outcome in the univariate analysis [crude hazard ratio 3.00 (95% CI 2.14-4.21), P < 0.001] and after adjustment for multiple covariates as age, gender, body mass index, and glomerular filtration rate as well as heart failure severity reflected by NT-proBNP and New York Heart Association class [adj. hazard ratio 1.87 (95% CI 1.19-2.93), P = 0.006]. CONCLUSIONS: Enhanced inflammation and nutritional depletion are more common in advanced heart failure. The inflammation-based score mGPS predicts survival in HFrEF patients independently of NT-proBNP emphasizing the significance of the individual pro-inflammatory response on prognosis.

11.
Eur Heart J Cardiovasc Imaging ; 21(2): 168-174, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31257452

RESUMO

AIMS: Recent progress in the diagnosis of functional valve regurgitation forms a coherent perception of severity thresholds by quantitative assessment. However, thresholds focused on either valve in isolation-not accounting for the global haemodynamic burden arising from concomitant functional regurgitation of the mitral and tricuspid valves. We sought to determine whether the global regurgitant volume is associated with adverse cardiac remodelling and mortality. METHODS AND RESULTS: This long-term observational study included 414 patients on guideline-directed medical therapy. Baseline global regurgitant load defined as the sum of mitral and tricuspid regurgitant volume was assessed by the proximal flow convergence method. All-cause mortality during 5 years follow-up served as the primary endpoint. The median global regurgitant load was 30 mL (interquartile range 15-49) with 67% accounting for mitral and 33% accounting for tricuspid regurgitant volume. The global regurgitant load had significant impact on outcome with a crude hazard ratio of 1.46 (1.28-1.66; P < 0.001) for a 1-SD increase in global regurgitant volume, results that remained virtually unchanged after bootstrap or clinical confounder-based adjustment (P < 0.001 for adjusted models). Spline curve analysis showed a linearly increasing risk with a threshold of 50 mL and sustained increasing risk thereafter. CONCLUSIONS: The present study demonstrates the detrimental effect of the global regurgitant load in patients with heart failure with reduced ejection fraction. The threshold where heart failure is driven by the valve lesions is a global regurgitant volume of 50 mL with continuously increasing risk beyond that threshold. Future studies need to address whether an attempt to reduce the global regurgitant volume can improve outcome.

12.
JACC Cardiovasc Interv ; 12(19): 1915-1923, 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31601387

RESUMO

OBJECTIVES: The aim of this study was to assess the prognostic impact of post-procedural troponin T increase and mortality in patients undergoing percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) to define the threshold at which procedure-related myocardial injury drives mortality. BACKGROUND: Coronary CTO recanalization represents the most technically challenging PCI. The complexity harbors a significant increased risk for complications with CTO PCI with compared with non-CTO PCI. However, there are evidenced biomarker cutoff levels that help identify those patients at risk for unfavorable clinical outcomes. METHODS: A total of 3,712 consecutive patients undergoing PCI for at least 1 CTO lesion were enrolled, and comprehensive troponin T measurements were performed 6, 8, and 24 h after the procedure. All-cause mortality was defined as the primary study endpoint. RESULTS: Using spline curve analysis, a more than 18-fold increase of troponin above the upper reference limit was significantly associated with mortality. In a Cox regression analysis, the crude hazard ratio was 2.32 (95% confidence interval: 1.83 to 2.93; p < 0.001) for a ≥18-fold increase compared with patients with post-procedural troponin increase <18-fold of the upper reference limit. Results remained virtually unchanged after bootstrap- or clinical confounder-based adjustment. CONCLUSIONS: This large-scale outcome study demonstrates for the first time the prognostic value of post-procedural troponin T elevation after PCI in patients with CTOs. A threshold was defined for procedure-related myocardial injury in patients with CTOs to differentiate them from those without CTOs that may help guide post-procedural clinical care in this high-risk patient population.

14.
Eur J Clin Invest ; 49(11): e13168, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31463975

RESUMO

AIM: GDF-15 is an established cardiovascular risk marker but is equally implicated in tumour biology. Elevated levels of GDF-15 have indeed been observed in distinct tumour entities. This study aimed to explore the relation of GDF-15 to other cardiac biomarkers and the general association of GDF-15 on prognosis in an unselected cohort of treatment-naïve cancer patients. METHODS: We prospectively enrolled 555 consecutive patients at time of diagnosis of malignant disease prior receiving anticancer therapy. Plasma GDF-15 concentrations were determined alongside other cardiac and routine laboratory markers. All-cause mortality was defined as primary endpoint. RESULTS: GDF-15 levels were 338 ng/L (IQR:205-534) for the total cohort, and values were comparable for different tumour entities except breast cancer. Metastatic disease was characterized by higher plasma GDF-15 [435 ng/L (IQR:279-614) vs 266 ng/L (IQR:175-427), P < .001]. GDF-15 correlated positively with inflammatory status reflected by CRP, SAA and IL-6 [r = .31, P < .001, r = .23, P < .001 and r = .14, P = .002] and cardiac biomarkers as NT-proBNP, hsTnT, MR-proADM and CT-proET-1 [r = .46; r = .46; r = .59 and r = .50; P < .001 for all]. GDF-15 was significantly associated with all-cause mortality after multivariate adjustment [adj.HR for ln(GDF-15) 1.78, 95%CI:1.47-2.16, P < .001]. There was a significant interaction between solid and haematological malignancies with loss of association of GDF-15 with outcome in myelodysplastic and myeloproliferative disease. CONCLUSIONS: Elevated plasma GDF-15 is associated with progressing disease severity and poor prognosis in solid tumours of treatment-naïve cancer patients. GDF-15 increase is accompanied by worsening systemic inflammation and a subclinical functional impairment of different organs including the heart. GDF-15 represents a promising target for our pathophysiologic understanding in cardio-oncology linking conditions of both cardiac and neoplastic disease.

15.
Eur J Clin Invest ; 49(11): e13159, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31356682

RESUMO

BACKGROUND: Secondary mitral regurgitation (sMR) drives adverse cardiac remodelling in patients with heart failure with reduced ejection fraction (HFrEF). Progression in severity over time contributes to a transition towards more advanced HF stages. Early identification of patients at risk for sMR progression remains challenging. We therefore sought to assess a broad spectrum of neurohumoral biomarkers in patients with HFrEF to explore their ability to predict progression of sMR. METHODS: A total of 249 HFrEF patients were enrolled. Biomarkers encompassing key neurohumoral pathways in heart failure were sampled at baseline, and sMR progression was assessed over 3 years of follow-up. RESULTS: Of 191 patients with nonsevere sMR at baseline, 18% showed progressive sMR within three years after study enrolment. Progression of sMR was associated with higher levels of MR-proADM (adj.OR 2.25, 95% CI 1.29-3.93; P = .004), MR-proANP (adj.OR 1.84, 95% CI 1.14-3.00; P = .012), copeptin (adj.OR 1.66, 95% CI 1.04-2.67; P = .035) and CT-pro-ET1 (adj.OR 1.68, 95% CI 1.06-2.68; P = .027) but not with NT-proBNP (P = .54). CONCLUSION: Increased plasma levels of neurohumoral cardiac biomarkers are predictors of sMR progression in patients with HFrEF and add easily available incremental prognostic information for risk stratification. Importantly, NT-proBNP was not useful to predict progressive sMR in the present analysis. On the contrary, MR-proANP, primarily produced in the atria, copeptin partly triggered by intra-cardiac and intra-arterial pressures and MR-proADM, a marker of forward failure and peripheral released vasoactive CT-proET1, increase based on a progressive loading burden by sMR and may thus serve as better predictors of sMR progression.

17.
J Am Coll Cardiol ; 73(20): 2506-2517, 2019 05 28.
Artigo em Inglês | MEDLINE | ID: mdl-31118144

RESUMO

BACKGROUND: Diverging guideline definitions for the quantitative assessment of severe secondary mitral regurgitation (sMR) reflect the lacking link of the sMR spectrum to mortality and has introduced a source of uncertainty and continuing debate. OBJECTIVES: The current study aimed to define improved risk-thresholds specifically tailored to the complex nature of sMR that provide a unifying solution to the ongoing guideline-controversy. METHODS: This study enrolled 423 heart failure patients under guideline-directed medical therapy and assessed sMR by effective regurgitant orifice area (EROA), regurgitant volume (RegVol), and regurgitant fraction (RegFrac). RESULTS: Measures of sMR severity were consistently associated with 5-year mortality with a hazard ratio of 1.42 for a 1-SD increase (95% confidence interval [CI]: 1.25 to 1.63; p < 0.001) for EROA, 1.37 (95% CI: 1.20 to 1.56; p < 0.001) for RegVol, and 1.50 (95% CI: 1.30 to 1.73; p < 0.001) for RegFrac. Results remained statistically significant after bootstrap- or clinical confounder-based adjustment. Spline-curve analyses showed a linearly increasing risk enabling the ability to stratify into low-risk (EROA <20 mm2 and RegVol <30 ml), intermediate-risk (EROA 20 to 29 mm2 and RegVol 30 to 44 ml), and high-risk (EROA ≥30 mm2 and RegVol ≥45 ml) groups. In the intermediate-risk group, a RegFrac ≥50% as indicator for hemodynamic severe sMR was associated with poor outcome (p = 0.017). A unifying concept based on combined assessment of the EROA, the RegVol, and the RegFrac showed a significantly better discrimination compared with the currently established algorithms. CONCLUSIONS: Risk-based thresholds tailored to the pathophysiological concept of sMR provide a unifying solution to the ongoing guideline controversy. An algorithm based on the combined assessment of the unifying cutoffs for EROA, RegVol, and RegFrac improves risk prediction compared with currently established grading.


Assuntos
Algoritmos , Ecocardiografia Tridimensional/métodos , Insuficiência da Valva Mitral/diagnóstico , Valva Mitral/diagnóstico por imagem , Função Ventricular Esquerda/fisiologia , Idoso , Ecocardiografia Doppler em Cores/métodos , Feminino , Seguimentos , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Insuficiência da Valva Mitral/complicações , Insuficiência da Valva Mitral/fisiopatologia , Fatores de Risco , Índice de Gravidade de Doença , Volume Sistólico
19.
Sci Rep ; 9(1): 2554, 2019 02 22.
Artigo em Inglês | MEDLINE | ID: mdl-30796257

RESUMO

The transmembrane zink-metalloendopeptidase neprilysin (NEP) is implicated in cardiovascular disease but also tumor biology. The aim of the study was to investigate the relationship of circulating NEP (cNEP) levels with established cardiovascular biomarkers and its effect on overall survival in an unselected cohort of treatment-naïve cancer patients. 555 consecutive cancer patients prior anticancer therapy were enrolled prospectively. NEP levels were determined alongside routine laboratory parameters, established cardiac biomarkers, i.e. NT-proBNP, hsTnT, MR-proANP, MR-proADM, CT-proET-1 and Copeptin, and inflammatory parameters, i.e. CRP, IL-6 and SAA, in venous plasma samples. All-cause mortality was the primary endpoint. cNEP levels of 276 pg/ml (IQR: 0-5981) displayed a weak inverse correlation with age [r = -0.12, p = 0.023] and inflammatory status [r = -0.14, p = 0.007 CRP; r = -0.20, p < 0.001 IL-6 and r = -0.18, p < 0.001 SAA]. cNEP was comparable between different tumor entities and stages and not related to functional parameters of other organ systems as kidney, liver or especially the heart. Moreover, cNEP was not associated with overall survival in the total cohort [adj.HR for ln (cNEP) 1.00, 95% CI: 0.94-1.06, p = 0.887] but in myelodysplatic malignancies [adj.HR for ln (cNEP) 1.27, 95% CI: 1.01-1.61, p = 0.044]. In conclusion, cNEP lacks association with outcome but for myelodysplastic disease. cNEP shows no correlation with established cardiovascular biomarkers related to prognosis, thereby holding a limited potential as a biomarker in cardio-oncology.

20.
JACC Cardiovasc Imaging ; 12(3): 389-397, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30660536

RESUMO

OBJECTIVES: This study sought to define the relationship between functional tricuspid regurgitation (TR) and mortality in patients with heart failure with reduced ejection fraction (HFrEF); and to establish the prognostic value of quantitative measures of TR severity (i.e., effective regurgitant orifice area [EROA] and regurgitant volume). BACKGROUND: The significance of TR in chronic heart failure is controversial. Earlier studies have shown an independent impact of TR on mortality, whereas more recent evidence suggests myocardial impairment to be the driving force of mortality rather than TR itself. Earlier studies have used qualitative measures of TR severity, hence the prognostic value of more quantitative measures of TR severity (i.e., EROA and regurgitant volumes) remains unclear. METHODS: We enrolled 382 patients with HFrEF on guideline-directed medical therapy and assessed TR EROA and regurgitant volume by Doppler/2-dimensional echocardiography. All-cause mortality was defined as the primary study endpoint. RESULTS: TR severity was associated with the HFrEF phenotype with more symptoms (p = 0.004), higher neurohumoral activation (p < 0.001), progressive right-ventricular dilatation (p < 0.001), and impaired function (p < 0.001). Cox regression showed a strong association between quantitative measures of TR with mortality (all p < 0.001). Quantitative metrics of TR severity were consistently associated with mortality with a hazard ratio of 1.009 (95% confidence interval: 1.004 to 1.013; p < 0.001) per 0.01 cm2 increase of the EROA and of 1.013 (95% confidence interval: 1.007 to 1.020; p < 0.001) per 1-ml increase in regurgitant volume. Results remained unchanged after bootstrap- or clinical confounder-based adjustment. A spline curve pattern illustrates the association with mortality with thresholds for the EROA ≥0.2 cm2, and the regurgitant volume ≥20 ml with sustained excess mortality thereafter. CONCLUSIONS: This large-scale outcome study demonstrates the prognostic value of quantitative Doppler-echocardiographic measures of TR severity in HFrEF. The thresholds for EROA and TR regurgitant volume associated with mortality in our study fall within current ranges defining nonsevere TR. This may potentially impact therapeutic decision making, particularly timing of intervention.


Assuntos
Ecocardiografia Doppler , Insuficiência Cardíaca/diagnóstico por imagem , Insuficiência da Valva Tricúspide/diagnóstico por imagem , Valva Tricúspide/diagnóstico por imagem , Idoso , Fármacos Cardiovasculares/uso terapêutico , Causas de Morte , Feminino , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/fisiopatologia , Hemodinâmica , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Prognóstico , Fatores de Risco , Índice de Gravidade de Doença , Volume Sistólico , Fatores de Tempo , Valva Tricúspide/efeitos dos fármacos , Valva Tricúspide/fisiopatologia , Insuficiência da Valva Tricúspide/tratamento farmacológico , Insuficiência da Valva Tricúspide/mortalidade , Insuficiência da Valva Tricúspide/fisiopatologia , Função Ventricular Esquerda
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