What is the clinical evidence from this study?

Study design: Observational. Population: Hypertrophic cardiomyopathy without left ventricular outflow tract obstruction (n=121). Intervention: Supine incremental exercise vs. Healthy controls. Primary outcome: Pulmonary capillary wedge pressure at peak exercise (p=<0.001).

April 1, 2026Open Access

Haemodynamic response to exercise in patients with hypertrophic cardiomyopathy without left ventricular outflow tract obstruction

Q: What are the key findings of this study?

Patients with HCM without LVOT obstruction had significantly higher pulmonary capillary wedge pressure at peak exercise compared to healthy controls (32 vs 18 mm Hg, p<0.001).

Q: What question did this study set out to answer?

To characterize the haemodynamic response to exercise in patients with hypertrophic cardiomyopathy without left ventricular outflow tract obstruction.

Key Result

Patients with HCM without LVOT obstruction had significantly higher pulmonary capillary wedge pressure at peak exercise compared to healthy controls (32 vs 18 mm Hg, p<0.001).

Key Points

To characterize the haemodynamic response to exercise in patients with hypertrophic cardiomyopathy without left ventricular outflow tract obstruction.
Observed right heart catheterisation
Measured haemodynamic parameters at rest and during incremental exercise
Compared results between patients and healthy controls
Analyzed correlations between pulmonary capillary wedge pressure and exercise capacity
Patients showed higher pulmonary capillary wedge pressure (PCWP) at rest and mild exercise compared to controls
At peak exercise, patients had significantly lower cardiac index and peak oxygen consumption
Abnormal PCWP was observed in 68% of patients at mild exercise and 85% at peak
Significant inverse correlation between PCWP at mild exercise and peak oxygen consumption in patients

Study Design

Type

Observational (n=121)

Structured PICO

Do patients with HCM without LVOT obstruction have abnormal haemodynamic responses to exercise compared to healthy controls?

Population

121 subjects, including 59 patients with hypertrophic cardiomyopathy (HCM) without left ventricular outflow tract (LVOT) obstruction (mean age 58±12 years) and 62 healthy controls (mean age 49±17 years).

Intervention

Right heart catheterisation with haemodynamic measurements during rest and supine incremental exercise.

Comparator

Healthy controls undergoing the same exercise protocol.

Outcome

Left ventricular filling pressure assessed as pulmonary capillary wedge pressure (PCWP) at rest and during exercise.surrogate

Patients with non-obstructive HCM exhibit significantly elevated left ventricular filling pressures even at low exercise workloads, which correlates with reduced exercise capacity.

Main Result

Absolute Event Rate: 32% vs 18%

p-value: p=<0.001

Abstract

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.