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      Dobutamine Stress Echocardiography in Hypertrophic Cardiomyopathy


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          Aims: Myocardial ischemia in the absence of coronary artery disease is common in patients with hypertrophic cardiomyopathy (HCM). Dobutamine stress echocardiography (DSE) induces left ventricular (LV) new wall motion abnormalities (NWMA) in some patients with HCM. We evaluated the effects of dobutamine on LV performance and hemodynamics in HCM. Methods and Results: Eighteen patients with non-obstructive HCM underwent DSE. Dobutamine was administered at dosages of 5, 10, 20, 30 and 40 µg/kg/min with increments at intervals of 3 min. Seven patients developed NWMA, whereas the other 11 did not. During DSE, heart rate increased significantly more in NWMA patients,whereas LV outflow tract gradient (OTG) increased significantly and similarly in both groups. At peak dobutamine dose, NWMA patients had a significant increase in LV end-systolic diameter and volume and a significant decrease in LV fractional shortening and ejection fraction. Posterior wall thickening increased significantly, whereas septal thickening did not increase throughout DSE in both groups. Conclusions: In a subgroup of patients with HCM, DSE induces NWMA, associated with a greater increase in heart rate, irrespective of LVOTG. NWMA induce a depression of global LV systolic performance. The septum shows no contractile reserve, regardless of NWMA. These phenomena may be the result of induction of ischemia and/or impaired LV systolic function due to fast heart rate.

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          Hemodynamic determinants of exercise-induced abnormal blood pressure response in hypertrophic cardiomyopathy.

          We sought to assess the hemodynamics of exercise in patients with hypertrophic cardiomyopathy (HCM), with and without an exercise-induced abnormal blood pressure (BP) response, by ambulatory radionuclide monitoring of left ventricular (LV) function with the VEST device (Capintec Inc., Ramsey, New Jersey). Blood pressure fails to increase >20 mm Hg during exercise in about one-third of patients with HCM. This carries a high risk of sudden death. Forty-three patients with HCM and 14 control subjects underwent maximal symptom-limited exercise on a treadmill during VEST. The VEST data were averaged for 1 min and analyzed at baseline, 3 min and peak exercise. The LV end-diastolic, end-systolic and stroke volumes, cardiac output and systemic vascular resistance were expressed as the percentage of baseline. Ejection fraction and stroke volume fell in patients with HCM, although they increased in control subjects (p < 0.001 and p = 0.002, respectively). Cardiac output increased significantly more in control subjects than in patients with HCM (p = 0.001). In 17 patients with HCM (39%) with an abnormal BP response, ejection fraction and stroke volume fell more (p = 0.032 and p = 0.009, respectively) and cardiac output increased less (p = 0.001) than they did in patients with HCM with a normal BP response. Systemic vascular resistance decreased similarly in patients with HCM, irrespective of the BP response. In patients with HCM with and without an abnormal BP response, abnormal hemodynamic adaptation to exercise was qualitatively similar but quantitatively different. An abnormal BP response was associated with exercise-induced LV systolic dysfunction. This causes hemodynamic instability, associated with a high risk of sudden cardiac death.
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            Left ventricular systolic dysfunction during exercise and dobutamine stress in patients with hypertrophic cardiomyopathy.

            We sought to characterize stress-induced left ventricular systolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). Myocardial ischemia and diastolic dysfunction occur in patients with HCM. We hypothesized that, in the setting of transient myocardial ischemia, left ventricular systolic dysfunction occurs during exercise and dobutamine stress. We studied 39 patients with HCM but without obstructive symptoms at rest or coronary artery disease. A continuous ventricular function monitor equipped with cadmium telluride detectors (VEST) was used to evaluate left ventricular function during supine bicycle ergometer exercise. Dobutamine stress echocardiography (DSE) was also performed. The left ventricular ejection fraction (LVEF) and regional wall motion were determined from echocardiographic images. Changes in the LVEF correlated between exercise and dobutamine stress (r = 0.643, p < 0.0001). The LVEF decreased more than 5% at peak exercise in 17 of patients (group II), while the other patients had normal responses (group I). New regional wall motion abnormalities during dobutamine infusion were detected in 18 of 110 (16.4%) segments in group I and 42 of 85 (49.4%) segments in group II. Decreased or unchanged regional wall motion occurred more frequently in hypertrophied segments than in nonhypertrophied segments (p < 0.0001). There were significant inverse correlations between the LVEF responses during both stresses and the number of abnormal segments noted during dobutamine stress in all patients (VEST: p < 0.005; DSE: p < 0.0005). Signs of left ventricular obstruction were observed in 11 of 39 patients during DSE. However, there was no significant correlation between the LVEF response and the dobutamine-induced left ventricular pressure gradient. Exercise-induced systolic dysfunction occurred in 50% of patients with HCM. In these patients, regional wall motion abnormalities were present in hypertrophied segments.
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              Exercise-induced abnormal blood pressure responses are related to subendocardial ischemia in hypertrophic cardiomyopathy


                Author and article information

                S. Karger AG
                October 2003
                17 October 2003
                : 100
                : 2
                : 93-100
                Department of Clinical Medicine, Cardiovascular and Immunological Sciences, ‘Federico II’ University of Naples, Naples, Italy
                73045 Cardiology 2003;100:93–100
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 34, Pages: 8
                Noninvasive and Diagnostic Cardiology


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