Measurement of speckle tracking strain during DSE is feasible and similar in accuracy to TVI-strain in the anterior, but not in the posterior circulation.
Exercise training improves functional capacity in patients with exercise limitation attributed to systolic dysfunction (SD), but exercise training effects in patients with diastolic dysfunction is unclear. The authors determined the functional capacity, quality of life, and echocardiography responses of heart failure with preserved ejection fraction (HFpEF) patients to 16 weeks exercise training. Thirty patients with HFpEF were randomized to an exercise training or non-exercising control group. The patients had a baseline mean age of 64AE8 years, left ventricular ejection fraction 57%AE10%, and peak oxygen consumption (peak VO 2 ) of 13.3AE3.8 mL O 2 ⁄ kg ⁄ min. Minnesota Living With Heart Failure and Hare-Davis scores and echocardiographic measures (ejection fraction, systolic and diastolic tissue velocity and filling pressure [E ⁄ E 0 ]) were performed at baseline and after 16 weeks of exercise training. The exercise training and non-exercising control groups showed similar baseline VO 2 (12.2AE3.6 mL ⁄ kg ⁄ min vs 14.1AE4.1 mL ⁄ kg ⁄ min), ejection fraction (58%AE13% vs 57%AE8%), and systolic and diastolic function. After exercise training the increment in peak VO 2 in the exercise training group was (24.6%, P=.02), and the non-exercising control group (5.1%, P=.19). V E ⁄ VCO 2 slope was reduced by 12.7% in the exercise training group (P=.02) but was unchanged in the non-exercising control group (P=.03). No significant changes in diastolic or systolic function were noted in either group. Quality-of-life and depression scores were unchanged with exercise training. Changes in peak VO 2 and V E ⁄ VCO 2 slope were unrelated to measures of diastolic and systolic function. In patients with exercise limitation attributed to HFpEF, the improvement in peak VO 2 with exercise training was not clearly related to changes in cardiac function. Ó2012 Wiley Periodicals, Inc.
Combination of TVI or STE methods with DbE can predict viability, with TVI strain and SR at LDD being the most accurate. TVI measures can predict viability in both anterior and posterior circulations, but STE measurements predict viability only in the anterior circulation.
The mechanisms of reduced cardiorespiratory fitness (CF) in renal transplant recipients (RTR) have not been studied closely. This study evaluated the relationships between CF and specific cardiovascular risk factors (metabolic syndrome [MS], physical inactivity, myocardial ischemia, and atherosclerotic burden) in glucose-intolerant RTR. Data were recorded on 71 glucose-intolerant RTR (mean age 55 yr; 55% male; median transplant duration 5.7 yr). MS was defined using National Cholesterol Education Programme Adult Treatment Panel III criteria. Resting and exercise stress echocardiography were performed, and myocardial ischemia was identified by new or worsening wall motion abnormalities. Cardiorespiratory fitness was determined using peak oxygen uptake (VO 2 ) by expired gas analysis. Atherosclerotic burden was assessed by carotid intima-media thickness (IMT). Mean peak VO 2 was 19 ؎ 7 ml/kg per min and was significantly lower than predicted peak VO 2 (29 ؎ 6 ml/kg per min; P < 0.001). Patients with MS (63%) had reduced CF (17 ؎ 6 versus 22 ؎ 8 ml/kg per min; P ؍ 0.001) and were more likely to be physically inactive (76 versus 48%; P ؍ 0.02). CF was reduced in 14 patients with myocardial ischemia (15 ؎ 3 versus 20 ؎ 7 ml/kg per min; P ؍ 0.05). CF was positively correlated with male gender, height, and physical activity and inversely correlated with number of MS risk factors and IMT (adjusted R 2 ؍ 0.66). Carotid IMT added incremental value to clinical variables in determining VO 2 (adjusted R 2 ؍ 0.65 versus 0.63; P ؍ 0.04). Reduced CF is associated with physical inactivity, MS, and atherosclerotic burden in glucose-intolerant RTR. Further studies should address whether increasing exercise and modifying MS risk factors improve CF in RTR.
Spironolactone-induced changes in myocardial structure and diastolic properties in DCM are small, and are unassociated with changes in collagen biomarkers or T1 values.
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