Background <p>Significant tricuspid regurgitation (TR) encompasses a wide range of etiologies, complicating a comprehensive understanding of disease progression and prognostic factors. This study aimed to assess mortality associated with significant TR, focusing on the role of valvular disease etiology and other predictive factors.</p> Methods <p>This is a retrospective, multicenter, cohort observational study, including all consecutive patients with moderate-to-severe or greater TR. The patients were classified into five etiological groups: organic TR, TR secondary to left valvulopathy, TR secondary to left or right ventricular dysfunction, TR secondary to pulmonary hypertension, and atrial TR. The long-term mortality was assessed (median follow-up: 39.8&#xa0;months).</p> Results <p>757 patients were included. The overall mortality incidence rate was 162.5 deaths per 1000 patient-years. Compared to atrial TR, all other etiologies presented a higher mortality risk: organic TR adjusted hazard ratio (aHR) = 2.344 (95% confidence interval [CI]: 1.138–4.829), left valvulopathy-related TR aHR = 1.901 (95% CI: 1.011–3.574), ventricular dysfunction-related TR aHR = 3.683 (95% CI: 1.627–8.338), and pulmonary hypertension-related TR aHR = 2.446 (95% CI: 1.215–4.927). In addition to known factors, male sex was associated with a higher mortality risk (aHR = 1.608, 1.175–2.201), while beta-blocker use was linked to a lower risk (aHR = 0.674, 0.502–0.904).</p> Conclusions <p>In a large cohort of patients with significant TR, and after adjusting for clinical and echocardiographic variables, all etiological groups exhibited a higher mortality risk compared to atrial TR. Additionally, male patients with TR had a higher mortality risk, while beta-blocker therapy emerged as a protective factor.</p>

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Etiology of tricuspid regurgitation and mortality: a multicenter cohort study

  • Jorge Rodríguez-Capitán,
  • Paloma Márquez-Camas,
  • Jesús Carmona-Carmona,
  • Diego Félix Arroyo Moñino,
  • Marinela Chaparro-Muñoz,
  • Matías Soler-González,
  • Manuel García del Río,
  • Teodora Egido de la Iglesia,
  • Jorge Segovia-Reyes,
  • Mora Murri,
  • José Raúl López Salguero,
  • David Couto-Mallón,
  • Miguel Romero-Cuevas,
  • Francisco Javier Pavón-Morón,
  • Mario Gutiérrez-Bedmar,
  • Manuel Jiménez-Navarro

摘要

Background

Significant tricuspid regurgitation (TR) encompasses a wide range of etiologies, complicating a comprehensive understanding of disease progression and prognostic factors. This study aimed to assess mortality associated with significant TR, focusing on the role of valvular disease etiology and other predictive factors.

Methods

This is a retrospective, multicenter, cohort observational study, including all consecutive patients with moderate-to-severe or greater TR. The patients were classified into five etiological groups: organic TR, TR secondary to left valvulopathy, TR secondary to left or right ventricular dysfunction, TR secondary to pulmonary hypertension, and atrial TR. The long-term mortality was assessed (median follow-up: 39.8 months).

Results

757 patients were included. The overall mortality incidence rate was 162.5 deaths per 1000 patient-years. Compared to atrial TR, all other etiologies presented a higher mortality risk: organic TR adjusted hazard ratio (aHR) = 2.344 (95% confidence interval [CI]: 1.138–4.829), left valvulopathy-related TR aHR = 1.901 (95% CI: 1.011–3.574), ventricular dysfunction-related TR aHR = 3.683 (95% CI: 1.627–8.338), and pulmonary hypertension-related TR aHR = 2.446 (95% CI: 1.215–4.927). In addition to known factors, male sex was associated with a higher mortality risk (aHR = 1.608, 1.175–2.201), while beta-blocker use was linked to a lower risk (aHR = 0.674, 0.502–0.904).

Conclusions

In a large cohort of patients with significant TR, and after adjusting for clinical and echocardiographic variables, all etiological groups exhibited a higher mortality risk compared to atrial TR. Additionally, male patients with TR had a higher mortality risk, while beta-blocker therapy emerged as a protective factor.