A recent study investigated the impaired systolic-diastolic (S-D) coupling in patients with HCM and its impact on exercise intolerance.

“With the use of primary prevention implantable cardioverter defibrillators, the mortality is now very low for patients with HCM, but morbidity remains significant,” authors wrote in a study published online in Echcardiography.

“Exercise intolerance, manifesting as dyspnea on exertion, is the most common symptom of patients with HCM and has been attributed to left ventricular outflow tract obstruction, diastolic dysfunction, and sedentary lifestyle. Cardiorespiratory fitness, defined as peak oxygen uptake (peak VO2), is commonly reduced in patients with HCM and is associated with long-term outcomes in patients with HCM.”

The study compared 25 patients with HCM (mean age, 47 ±9 years) with 115 healthy adults (mean age, 49 ±10 years). Both groups underwent cardiopulmonary exercise testing (CPET) and echocardiograms to assess S-D coupling, defined as the ratio of early diastolic excursion (EDexc) to systolic excursion (Sexc) of the mitral annulus. Key exercise metrics, such as peak oxygen uptake (peak VO2), cardiac index, and stroke volume index (SVi), were also measured.

The results of the study indicated that S-D coupling was significantly lower in patients with HCM compared to healthy controls (HCM: 0.56 ±0.10 vs Controls: 0.63 ±0.08; P<0.001). Additionally, HCM patients exhibited lower peak VO2 and stroke volume reserve com – pared to healthy controls (peak VO2: HCM 23.7 ±7.2 vs Controls 28.5 ±5.5 mL/kg/min; P<0.001; stroke volume reserve: HCM 30 ±18 vs Controls 39 ±16 mL; P=0.008). In patients with HCM, S-D coupling showed significant associations with peak VO2 (r=0.47, P=0.018), peak cardiac index (r=0.60, P=0.002), and peak SVi (r=0.63, P<0.001).

“Lower cardiorespiratory fitness is common in patients with HCM and is predictive of long-term morbidity and mortality,” the authors wrote. “This reduction in fitness is primarily driven by the inability to augment stroke volume and cardiac output as required for metabolic demand. While most patients with HCM have a preserved or hyperdynamic left ventricular ejection fraction, their systolic function is likely still impaired.”

The study suggests that impaired S-D coupling, particularly in the septal wall, may contribute to reduced exercise capacity in HCM. This impairment affects the heart’s ability to efficiently augment stroke volume and cardiac output during exercise. These findings highlight the importance of S-D coupling as a potential mechanism linking diastolic dysfunction, insufficient stroke volume generation, and exercise intolerance in HCM. Further research is needed to explore the therapeutic implications of improving S-D coupling to enhance exercise capacity for patients with HCM.