Kaitlyn Lam

The Impact of Exercise Training on Conduit Artery Wall Thickness and Remodeling in Chronic Heart Failure Patients

Exercise training is an important adjunct to medical therapy in chronic heart failure, but the extent to which exercise impacts on conduit artery remodeling is unknown. The aim of this study was to evaluate the impact of aerobic and resistance exercise training modalities on arterial remodeling in patients with chronic heart failure. We randomized 36 untrained subjects with chronic heart failure to resistance training (58.8±3.5 years), aerobic training (61.3±2.8 years), or an untrained control group (64.4±2.4 years). Peak oxygen consumption during cycle ergometry increased after 12 weeks in both the resistance and aerobic training (P<0.001) groups, but not in controls, whereas leg strength only increased after resistance training (P<0.05). Brachial artery wall thickness decreased in the resistance training group (475±10 versus 443±13 &mgr;m; P<0.01), whereas no changes were apparent in the aerobic or control groups. Brachial diameter increased by ≈6% and ≈5% in the aerobic training and resistance training groups (P<0.01), with no change evident in the control group. The wall:lumen ratio consequently declined in the resistance training group at 12 weeks (0.121±0.004 versus 0.107±0.004; P<0.01) and increased in the control group (0.111±0.006 versus 0.121±0.009; P<0.05). No wall:lumen change was evident in the aerobic training group. Our findings suggest that exercise has a systemic impact on remodeling of conduit arteries in humans and that resistance exercise training may be advantageous in subjects with chronic heart failure in this regard.

Observations From Non-Invasive Measures of Right Heart Hemodynamics in Left Ventricular Assist Device Patients

BACKGROUND Left ventricular assist devices (LVADs) reduce pulmonary vascular resistance (PVR) in patients with severe heart failure. The aim of this study was to noninvasively assess the effect of LVAD implantation on PVR and right-heart function. METHODS In 21 patients with HeartMate II LVADs, serial echocardiograms were reviewed prior to implantation and 1 and 6 months after implantation. Echocardiographic and Doppler indices of right-heart structure and function were measured along with LVAD settings, hemodynamics, and biochemistry, and the Minnesota Living With Heart Failure Questionnaire (MLHFQ) and 6-minute walk test were administered. RESULTS Comparing values before and 1 month after implantation, there were reductions in PVR (3.51 +/- 0.9 vs 2.0 +/- 0.5 Wood units, P < .0001), right ventricular (RV) systolic pressure (49 +/- 11 vs 34 +/- 7 mm Hg, P < .0001), and tricuspid regurgitation severity, with no change in RV size, RV fractional area change, or tricuspid annular plane systolic excursion. Patients with larger PVR reductions had better clinical status (MLHFQ score, 28 +/- 12 vs 60 +/- 29, P = .04; 6-minute walking distance, 1706 +/- 71 vs 1141 +/- 387 ft, P = .04). Patients with significant deteriorations in RV function had poorer clinical status (MLHFQ score, 79 +/- 13 vs 51 +/- 27, P = .04; 6-minute walking distance, 480 +/- 275 vs 1030 +/- 437 ft, P = .04). CONCLUSIONS Echocardiographically detected changes in right-heart hemodynamics were associated with symptomatic status after LVAD implantation.

Polymer Injection Therapy to Reverse Remodel the Papillary Muscles Efficacy in Reducing Mitral Regurgitation in a Chronic Ischemic Model

Background— Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results— Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P =0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P =0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P =0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P =0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P =NS), end-systolic elastance, τ (82±36 ms to 72±26, P =NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions— PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.Background—Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results—Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, &tgr; (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions—PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.

Polymer Injection Therapy to Reverse Remodel the Papillary MusclesClinical Perspective

Background— Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results— Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P =0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P =0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P =0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P =0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P =NS), end-systolic elastance, τ (82±36 ms to 72±26, P =NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions— PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.Background—Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results—Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, &tgr; (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions—PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.

The use of exercise echocardiography in the evaluation of mitral regurgitation.

Mitral regurgitation (MR) is the second most common valvular disease in western countries after aortic stenosis. Optimal management of patients with MR depends on the etiology of the regurgitation and is based predominantly on left ventricular function and functional status. Recent outcome studies report high risk subsets of asymptomatic patients with MR, and practice guidelines underscore the importance of a well-established estimation of exercise tolerance and recommend exercise testing to objectively assess functional status and hemodynamic factors.

Polymer Injection Therapy to Reverse Remodel the Papillary MusclesClinical Perspective: Efficacy in Reducing Mitral Regurgitation in a Chronic Ischemic Model

Background— Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results— Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P =0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P =0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P =0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P =0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P =NS), end-systolic elastance, τ (82±36 ms to 72±26, P =NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions— PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.Background—Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results—Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, &tgr; (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions—PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.

Polymer Injection Therapy to Reverse Remodel the Papillary Muscles

Background— Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results— Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P =0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P =0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P =0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P =0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P =NS), end-systolic elastance, τ (82±36 ms to 72±26, P =NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions— PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.Background—Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling. Methods and Results—Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, &tgr; (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01). Conclusions—PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.