Heart (British Cardiac Society) · 2026
Haemodynamic response to exercise in patients with hypertrophic cardiomyopathy without left ventricular outflow tract obstruction.
СтатьяНаблюдательное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gudmundsdottir Helga Lillian, Raja Anna Axelsson, Rossing Kasper, Rasmusen Hanne, Snoer Martin, Andersen Lars Juul, Gottlieb Rikke, Christensen Alex Hørby, Bundgaard Henning, Wolsk Emil, Hassager Christian, Gustafsson Finn, Thune Jens Jakob
Аннотация
BACKGROUND: Dyspnoea and reduced exercise capacity are common features in hypertrophic cardiomyopathy (HCM) without left ventricular outflow tract (LVOT) obstruction, yet the haemodynamic mechanisms contributing to these symptoms are poorly described. This study aimed to characterise the haemodynamic response to exercise in patients with HCM without LVOT obstruction.
METHODS: In this observational study, 121 subjects underwent right heart catheterisation with haemodynamic measurements during rest and supine incremental exercise: 59 patients with HCM without LVOT obstruction (58±12 years) and 62 healthy controls (49±17 years). Left ventricular (LV) filling pressure was assessed as pulmonary capillary wedge pressure (PCWP) and compared with diagnostic thresholds (rest: <15 mm Hg; exercise: <25 mm Hg). Group comparisons were performed using Student's t-tests or Wilcoxon rank-sum tests, as appropriate RESULTS: At rest, patients had higher PCWP than controls (14±6 vs 9±2 mm Hg, p<0.001), while other haemodynamic parameters were similar. Already at mild exercise (25 W), patients showed elevated PCWP (27±7 vs 16±7 mm Hg, p<0.001), mean arterial pressure (100±18 vs 93±13 mm Hg, p=0.02), central venous pressure (12±6 vs 9±4 mm Hg, p<0.001) and mean pulmonary artery pressure (38±11 vs 26±8 mm Hg, p<0.001). At peak exercise, patients exhibited higher PCWP (32±8 vs 18±8 mm Hg, p<0.001), with lower cardiac index (6.4±1.8 vs 8.9±1.4 L/min/m², p<0.001), heart rate (114±21 vs 132±19 bpm, p<0.001) and arteriovenous oxygen difference (58±13 vs 64±6%, p=0.004). Peak exercise capacity (119±50 vs 149±40 W, p<0.001) and peak oxygen consumption (21±7 vs 35±8 mL/kg/min, p<0.001) were lower in patients. Abnormal PCWP was found in 68% of patients at mild exercise and 85% at peak, compared with 6% of controls at mild exercise and 24% at peak. PCWP at mild exercise was inversely correlated with peak oxygen consumption in patients (r=-0.61; 95% CI -0.7 to -0.4; p<0.001).
CONCLUSION: Patients with HCM without LVOT obstruction exhibited significant haemodynamic impairments during exercise. Abnormally elevated LV filling pressures were present even at low workloads and were correlated with reduced exercise capacity.
METHODS: In this observational study, 121 subjects underwent right heart catheterisation with haemodynamic measurements during rest and supine incremental exercise: 59 patients with HCM without LVOT obstruction (58±12 years) and 62 healthy controls (49±17 years). Left ventricular (LV) filling pressure was assessed as pulmonary capillary wedge pressure (PCWP) and compared with diagnostic thresholds (rest: <15 mm Hg; exercise: <25 mm Hg). Group comparisons were performed using Student's t-tests or Wilcoxon rank-sum tests, as appropriate RESULTS: At rest, patients had higher PCWP than controls (14±6 vs 9±2 mm Hg, p<0.001), while other haemodynamic parameters were similar. Already at mild exercise (25 W), patients showed elevated PCWP (27±7 vs 16±7 mm Hg, p<0.001), mean arterial pressure (100±18 vs 93±13 mm Hg, p=0.02), central venous pressure (12±6 vs 9±4 mm Hg, p<0.001) and mean pulmonary artery pressure (38±11 vs 26±8 mm Hg, p<0.001). At peak exercise, patients exhibited higher PCWP (32±8 vs 18±8 mm Hg, p<0.001), with lower cardiac index (6.4±1.8 vs 8.9±1.4 L/min/m², p<0.001), heart rate (114±21 vs 132±19 bpm, p<0.001) and arteriovenous oxygen difference (58±13 vs 64±6%, p=0.004). Peak exercise capacity (119±50 vs 149±40 W, p<0.001) and peak oxygen consumption (21±7 vs 35±8 mL/kg/min, p<0.001) were lower in patients. Abnormal PCWP was found in 68% of patients at mild exercise and 85% at peak, compared with 6% of controls at mild exercise and 24% at peak. PCWP at mild exercise was inversely correlated with peak oxygen consumption in patients (r=-0.61; 95% CI -0.7 to -0.4; p<0.001).
CONCLUSION: Patients with HCM without LVOT obstruction exhibited significant haemodynamic impairments during exercise. Abnormally elevated LV filling pressures were present even at low workloads and were correlated with reduced exercise capacity.