Key result
Severe secondary TR and chronic AF demonstrate low exercise capacity comparable to cardiac amyloidosis.
Why the study?
Less is reported about clinical performance, exercise capacity, and hemodynamics in symptomatic patients with chronic atrial fibrillation and severe functional tricuspid regurgitation.
Does severe secondary tricuspid regurgitation with chronic atrial fibrillation result in similar exercise hemodynamic impairments as cardiac amyloidosis in patients with preserved LVEF?
Cross-Sectional (n=44)
No
Does severe secondary tricuspid regurgitation with chronic atrial fibrillation result in similar exercise hemodynamic impairments as cardiac amyloidosis in patients with preserved LVEF?
Severe secondary tricuspid regurgitation with chronic atrial fibrillation produces profound exercise intolerance and hemodynamic derangements, including reduced cardiac output and elevated filling pressures, comparable to those seen in cardiac amyloidosis.
Answers are grounded in this paper and cite their sources.
Comparable exercise intolerance in severe secondary TR-AF and amyloidosis should not yet change practice; leaves open need for prospective hemodynamic trials.
OBJECTIVE: The study aimed to investigate the functional capacity and hemodynamics at rest and during exercise in patients with chronic atrial fibrillation and severe functional symptomatic tricuspid regurgitation (AF-FTR). BACKGROUND: Symptoms and clinical performance of severe AF-FTR mimic the population of patients with heart failure with preserved ejection fraction (HFpEF). Severe AF-FTR is known to be associated with an adverse prognosis whereas less is reported about the clinical performance including exercise capacity and hemodynamics in patients symptomatic AF-FTR. METHODS: Right heart catheterization (RHC) at rest and during exercise was conducted in a group of patients with stable chronic AF-TR and compared with a group of patients with HFpEF diagnosed with cardiac amyloid cardiomyopathy (CA). All patients had preserved ejection fraction and no significant left-sided disease. RESULTS: Patients with AF-FTR demonstrated a low exercise capacity that was comparable to CA patients (TR 4.9 ± 1.2 METS vs. CA 4. 7 ± 1.5 METS; P = 0.78) with an average peak maximal oxygen consumption of 15 mL/min/kg. Right atrium pressure increased significantly more in the AF-FTR patients as compared to CA patients at peak exercise (25 ± 8 vs 19 ± 9, p < 0.01) whereas PCWP increased significantly to a similar extent in both groups (31 ± 4 vs 31 ± 8 mmHg, p = 0.88). Cardiac output (CO) was significantly lower among AF-FTR at rest as compared to CA patients (3.6 ± 0.9 vs 4.4 ± 1.3 l/min; p < 0.05) whereas both groups demonstrated a poor but comparable CO reserve at peak exercise (7.3 ± 2.9 vs 7.9 ± 3.8 l/min, p = 0.59). CONCLUSIONS: AF-FTR contributes to the development of advanced heart failure symptoms and poor exercise capacity reflected in increased atrial filling pressures, reduced cardiac output at rest and during exercise sharing common features seen in HFpEF patients with other etiologies.
No takes yet. Share an insight, caveat, or question.
Jensen et al. (2021) conducted a cross-sectional in Severe secondary tricuspid regurgitation and chronic atrial fibrillation (n=44). Severe secondary tricuspid regurgitation and chronic atrial fibrillation (AF-FTR) vs. Cardiac amyloid cardiomyopathy (CA) was evaluated on Exercise capacity (METS) (p=0.78). Patients with severe secondary tricuspid regurgitation and chronic atrial fibrillation demonstrated a low exercise capacity (4.9 METS) that was comparable to patients with cardiac amyloidosis.
Synapse has enriched 10 related papers. Consider them for comparative context: