Cardiomyopathy
Timing and Significance of Exercise-Induced Left Ventricular Outflow Tract Pressure Gradients in Hypertrophic Cardiomyopathy

https://doi.org/10.1016/j.amjcard.2010.06.057Get rights and content

The relation of exercise-induced left ventricular (LV) outflow tract obstruction to functional capacity in hypertrophic cardiomyopathy (HC) is incompletely defined. Thus, we assessed the patterns of onset of physiologically provoked LV outflow gradients and exercise performance in 74 consecutive patients with HC (age 45 ± 16 years; 74% men) without LV outflow obstruction at rest. The subaortic gradients were measured serially using echocardiography in these 74 patients during maximum, symptom-limited, upright bicycle exercise testing. The time course of the provoked gradients and the relation to exercise performance were assessed. Of the 74 patients, 30 (41%) developed a dynamic LV outflow gradient of ≥30 mm Hg (mean 78 ± 37 mm Hg) during upright exercise testing that correlated highly with the gradients measured with the patients supine during the immediate recovery period (R2 = 0.97). The 16 patients in whom outflow obstruction developed rapidly at low exercise levels (≤5 METs) had a significantly reduced exercise capacity (6.1 ± 1.3 vs 8.0 ± 1.6 METs; p <0.01) compared to the other 14 patients in whom obstruction appeared later at greater exercise levels of >5 METs. The timing of the gradient onset was not predictable from the baseline clinical and echocardiographic features, peak exercise LV outflow tract gradient, or symptoms. In conclusion, in patients with HC without outflow obstruction at rest, the earlier onset of LV outflow tract gradients during physiologic exercise was associated with impaired exercise performance. These findings have provided insights into the determinants of functional impairment in HC and support the potential value of exercise echocardiography in the clinical assessment of patients with HC.

Section snippets

Methods

The study group included 74 patients with HC but without LV outflow tract obstruction at rest (basal outflow gradient <30 mm Hg). They were consecutively studied at our institution using exercise echocardiography (Table 1). The mean patient age was 45 ± 16 years, and 53 (72%) were men. Historically, most patients (n = 70, 95%) had no or only mild exertional symptoms (Table 1). The clinical diagnosis of HC was determined by the demonstration on the 2-dimensional echocardiogram of a hypertrophied

Results

Data were obtained for 74 patients with HC with a LV outflow gradient of <30 mm Hg at rest in the supine position and erect on a cycle ergometer (Table 1). Of the 74 patients, 24 (32%) attained >85% of their maximum predicated heart rate, and 50 (68%) achieved submaximum target heart rates and terminated the test because of fatigue (n = 40), and/or dyspnea (n = 26), and/or a systolic blood pressure decrease of >25 mm Hg during exercise (n = 4).

Of the 74 study patients, 30 (40%) developed

Discussion

To achieve an enhanced understanding of the pathophysiology of exercise-induced LV outflow obstruction in patients with HC, we devised the present study protocol according to a serial gradient assessment at each step of a symptom-limited upright bicycle exercise test. We found that this strategy provided important information not available using a single gradient measurement at peak exercise or in the immediate recovery period. With real-time monitoring of the LV outflow tract velocities during

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      This complex mechanism involves an interplay of reduced LV outflow tract cross-sectional area, anterior and/or posterior mitral leaflet elongation, anterior position of mitral valve and papillary muscles, and bulging contour of anterior septum into LV cavity (1–3,36,37). Occasionally, impedance to LV outflow occurs by virtue of muscular mid-cavity apposition, associated either with LV apical aneurysms or by direct insertion of anterolateral papillary muscle into anterior mitral leaflet (1–3,36,37). Posteriorly directed mitral regurgitation (usually mild-to-moderate) is a secondary consequence of SAM.

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    This work was supported by Ministero Istruzione Università e Ricerca (PRin), Rome, Italy, the European Union (STREP Project 241577 “BIG HEART,” Seventh European Framework Program), Brussels, Belgium, and the Hearst Foundations, New York, New York.

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