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Left ventricular outflow tract gradient provoked by upright position or exercise in hypertrophic cardiomyopathy without obstruction at rest

Dear Editor,

In a recent study published in the Heart, Shah et al. [1] assess the inducibility of left ventricular outflow tract gradient by upright exercise (bicycle ergometer) in patients with hypertrophic cardiomyopathy (HCM) without obstruction at rest. Similarly to Maron et al. [2] they [1] documented frequent provocation of the gradient by exercise. Interestingly, in HCM the obstruction may increase also due to load reduction after change of position from supine to upright [1,3] or amyl nitrate. [4] Previous studies [1,2] were performed after drug discontinuation. To assess the efficacy of current pharmacotherapy we studied 37 HCM treated patients with left ventricular outflow tract (LVOT) gradient < 30 mmHg at rest in supine position. The patients were then placed in upright position and the gradient was re-examined. Since 8 patients developed LVOT gradient > 30 mmHg during this maneuver (values ranged from 32 to 141 mmHg), the remaining nonobstructive 29 patients performed moderate-intensity exercise on a treadmill (modified Bruce protocol) with continuous monitoring of LVOT gradient. The exercise was stopped at 8 minutes or earlier if patients were unable to continue exercise (dyspnea in 11 patients), 10 patients developed a significant gradient. For comparison with rest values we measured LVOT gradients at peak exercise, and as soon as possible after exercise (within the first 60 seconds of the recovery period in left lateral decubitus). The resting minimal distance between mitral valve and ventricular septum at systole was used to assess the degree of narrowing of LVOT and this parameter differentiated between provocable and non-provocable subgroups. Patients with provocable gradient (either by changing position or exercise) presented with lower values of this parameter than non-provacable subgroup (table 1). At recovery in supine position, this significant gradient disappeared in 6 of 10 patients despite only a short delay of measurement. Similarly to Cotrim et al. [3] we demonstrated that LVOT gradient assessed in the immediate recovery period (in re-supine position) does not accurately reflect what happens during effort.

The simultaneous evaluation of the gradient with exercise can help us to better understand the pathophysiology of patients with HCM and to optimize treatment (currently several methods are available). Like in the study of Cotrim et al. [3] our patients exercised moderately in upright position on a treadmill which was selected as a more physiological (reflects physical exercise during everyday activity) assessment of dynamic changes of the gradient. A substantial proportion of our patients had limiting exercise symptoms; therefore, identification of latent, exercise-triggered obstruction not only defined the probable mechanism for such symptoms but in many cases also created important options for their relief. The intensification of pharmacotherapy or use of nonpharmacological methods may be needed to consider for a significant portion of patients regarded as nonobstructive but only at rest.

The moderate workload exercise on a treadmill was well tolerated in almost all patients (only 2 patients – one with suboptimal echo image and one with orthopaedic disease were excluded from the study). Table 2 summarizes the methodological considerations. We agree with previous studies [1-3] that exercise is the only provocative manoeuvre that is truly physiologically based. Without exercise echocardiography, the capability of HCM patients to develop elevated LVOT gradient during normal physical activity would have remained undefined.

References

1. Shah JS, Tome Esteban MT, Thaman R, et al.
Prevalence of Exercise Induced Left Ventricular Outflow Tract Obstruction in Symptomatic Patients with Non-obstructive Hypertrophic Cardiomyopathy.
Heart. 2007 Nov 21; [Epub ahead of print]

2. Maron MS, Olivotto I, Zenovich AG, et al.
Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction.
Circulation. 2006;114:2232-9.

3. Cotrim C, Loureiro MJ, Simoes O, et al.
Evaluation of hypertrophic obstructive cardiomyopathy by exercise stress echocardiography. New methodology.
Rev Port Cardiol. 2005;24:1319-27.