Corresponding Author
Key words: catheterization, echocardiography, exercise, emitral stenosis
Rheumatic mitral stenosis (MS) is a prominent sequela of rheumatic heart disease, with a global prevalence that has been on the rise in recent years.1 This pathologic condition is characterized by significant narrowing of the mitral valve orifice, which restricts blood flow from the left atrium to the left ventricle (LV). Consequently, patients frequently experience symptoms such as dyspnea on exertion and marked exercise intolerance. However, it is noteworthy that clinical practice often reveals a discordance between findings obtained from resting echocardiography and the symptomatic manifestations reported by patients, particularly concerning their exercise capacity. This discrepancy underscores the complexities involved in the assessment and management of rheumatic MS.
A prior study indicated that exercise intolerance is primarily attributable to constraints in stroke volume reserve, the presence of chronotropic incompetence, and restrictive pulmonary function. In contrast, conventional parameters acquired from stress echocardiography, such as transmitral gradient and systolic pulmonary artery pressure, exhibited no significant correlation with exercise intolerance.2 This highlights the need to focus on intrinsic cardiovascular and pulmonary mechanisms to understand the limitations in exercise capacity.
In this issue of JACC: Asia, Kim et al3 provide mechanistic insights into exercise intolerance in patients with isolated severe rheumatic MS through invasive hemodynamic assessment. The cohort comprised 30 patients exhibiting severe rheumatic MS (mitral valve area <1.5 cm2) alongside 17 control subjects presenting with noncardiac dyspnea. Both groups underwent supine bicycle exercise during right heart catheterization to measure hemodynamic responses. Findings indicated no significant difference in resting cardiac index between the 2 groups. However, during exercise, patients with severe MS demonstrated an inability to sufficiently augment stroke volume in contrast to controls, with a notable peak cardiac index of 5.7 ± 1.7 L/min/m2, compared with 9.4 ± 3.3 L/min/m2 in the control group (P < 0.001). This impaired hemodynamic response was correlated with diminished exercise capacity, as evidenced by peak oxygen consumption (peak VO2) values of 14.2 mL/kg/min vs 16.5 mL/kg/min in controls (P = 0.027). Furthermore, minute ventilation and arterial oxygen content did not exhibit significant differences between the 2 groups, highlighting specific exercise-related hemodynamic limitations in patients with severe rheumatic MS.
In patients with severe MS, the data indicated that LV global longitudinal strain (LV-GLS) and stroke volume index served as significant predictors of exercise intolerance within this population. Among the myriad parameters assessed, LV-GLS has emerged as an important determinant of exercise capacity. However, interpretation of impaired LV-GLS in this population requires caution, as a reduced LV-GLS may also indicate subclinical LV dysfunction,4 which can contribute to exercise intolerance through the mechanism of heart failure with preserved ejection fraction.5 Previous research has demonstrated that LV-GLS is diminished in patients with severe mitral stenosis, with the suggestion that it may improve after percutaneous balloon mitral valvotomy. This finding implies the potential reversibility of LV-GLS through an increase in LV preload postprocedure,6 highlighting the need for careful monitoring and therapeutic strategies in this patient demographic.
These findings further support the concept of impaired exercise capacity in MS that extends beyond traditional resting or exercise hemodynamic evaluations. They align with the hypothesis that certain patients with advanced mitral stenosis may exhibit concurrent myocardial or diastolic dysfunction, resembling a heart failure with preserved ejection fraction phenotype. In clinical practice, distinguishing between pure valvular limitations and myocardial involvement is notoriously challenging. Nevertheless, as illustrated by Kim et al, objective functional parameters, such as LV-GLS, are capable of effectively detecting this subclinical impairment and predicting true exercise tolerance, regardless of the underlying pathophysiological mechanisms.
A significant strength of this study lies in its rigorous methodological approach. By integrating simultaneous right heart catheterization with the direct Fick method, the authors effectively circumvented the prevalent image-quality limitations associated with supine stress echocardiography, thereby ensuring highly accurate measurements of stroke volume. Their findings compellingly illustrate that patients with MS depend heavily on peripheral compensatory mechanisms, particularly a markedly elevated arteriovenous oxygen difference, to adapt to their fixed cardiac output reserve during instances of exertion. Furthermore, the authors discovered that subjective symptom scales, such as the NYHA functional classification, as well as conventional markers of disease severity, did not exhibit a correlation with objective measures of exercise capacity. This underscores a critical clinical concern: the reliance on symptom-based decision-making alone may not yield an adequate representation of patient status.
In conclusion, this study signifies a crucial evolution in the assessment of severe rheumatic MS. It advocates for a departure from the traditional reliance on the 2-dimensional valve area and emphasizes the importance of incorporating functional echocardiographic parameters into routine clinical evaluations. Notably, the use of LV-GLS and resting stroke volume emerges as a critical component in this enhanced assessment framework. Given the widespread availability of speckle-tracking echocardiography in contemporary clinical practice, the implementation of LV-GLS serves as an accessible and noninvasive methodology to elucidate impaired cardiac output reserve. This paradigm shift holds the potential to refine risk stratification processes, align objective diagnostic findings more closely with patient-reported symptoms, and ultimately optimize the timing and selection criteria for percutaneous or surgical interventions in this patient population.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
References
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