Douglas Stoller

Reversing the Cardiac Effects of Sedentary Aging in Middle Age—A Randomized Controlled Trial: Implications For Heart Failure Prevention

Background: Poor fitness in middle age is a risk factor for heart failure, particularly heart failure with a preserved ejection fraction. The development of heart failure with a preserved ejection fraction is likely mediated through increased left ventricular (LV) stiffness, a consequence of sedentary aging. In a prospective, parallel group, randomized controlled trial, we examined the effect of 2 years of supervised high-intensity exercise training on LV stiffness. Methods: Sixty-one (48% male) healthy, sedentary, middle-aged participants (53±5 years) were randomly assigned to either 2 years of exercise training (n=34) or attention control (control; n=27). Right heart catheterization and 3-dimensional echocardiography were performed with preload manipulations to define LV end-diastolic pressure-volume relationships and Frank-Starling curves. LV stiffness was calculated by curve fit of the diastolic pressure-volume curve. Maximal oxygen uptake (Vo2max) was measured to quantify changes in fitness. Results: Fifty-three participants completed the study. Adherence to prescribed exercise sessions was 88±11%. Vo2max increased by 18% (exercise training: pre 29.0±4.8 to post 34.4±6.4; control: pre 29.5±5.3 to post 28.7±5.4, group×time P<0.001) and LV stiffness was reduced (right/downward shift in the end-diastolic pressure-volume relationships; preexercise training stiffness constant 0.072±0.037 to postexercise training 0.051±0.0268, P=0.0018), whereas there was no change in controls (group×time P<0.001; pre stiffness constant 0.0635±0.026 to post 0.062±0.031, P=0.83). Exercise increased LV end-diastolic volume (group×time P<0.001), whereas pulmonary capillary wedge pressure was unchanged, providing greater stroke volume for any given filling pressure (loading×group×time P=0.007). Conclusions: In previously sedentary healthy middle-aged adults, 2 years of exercise training improved maximal oxygen uptake and decreased cardiac stiffness. Regular exercise training may provide protection against the future risk of heart failure with a preserved ejection fraction by preventing the increase in cardiac stiffness attributable to sedentary aging. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02039154.

Healthy aging does not compromise the augmentation of cardiac function during heat stress

During heat stress, stroke volume is maintained in young adults despite reductions in cardiac filling pressures. This is achieved by a general augmentation of cardiac function, highlighted by a left and upward shift of the Frank-Starling relation. In contrast, healthy aged adults are unable to maintain stroke volume during heat stress. We hypothesized that this would be associated with a lack of shift in the Frank-Starling relation. Frank-Starling relations were examined in 11 aged [69 ± 4 (SD) yr, 4 men/7 women] and 12 young (26 ± 5 yr, 6 men/6 women) adults during normothermic and heat stress (1.5°C increase in core temperature) conditions. During heat stress, increases in cardiac output were attenuated in aged adults (+2.5 ± 0.3 (95% CI) vs. young: +4.5 ± 0.5 l/min, P < 0.01) because of an attenuated chronotropic response (+30 ± 4 vs. young: +42 ± 5 beats/min, P < 0.01). In contrast to our hypothesis, a leftward shift of the Frank-Starling relation maintained stroke volume during heat stress in aged adults (76 ± 8 vs. normothermic: 74 ± 8 ml, P = 0.38) despite reductions in cardiac filling pressure (6.6 ± 1.0 vs. normothermic: 8.9 ± 1.1 mmHg, P < 0.01). In a subset of participants, volume loading was used to return cardiac filling pressure during heat stress to normothermic values, which resulted in a greater stroke volume for a given cardiac filling pressure in both groups. These results demonstrate that the Frank-Starling relation shifts during heat stress in healthy young and aged adults, thereby preserving stroke volume despite reductions in cardiac filling pressures.

Implantation of a left ventricular assist device to provide long-term support for end-stage Duchenne muscular dystrophy-associated cardiomyopathy

A young man with Duchenne muscular dystrophy presented to the UT Southwestern Neuromuscular Cardiomyopathy Clinic with advanced heart failure. Despite maximal medical therapy, his cardiac function continued to decline requiring initiation of inotrope therapy. Given the patients clinical deterioration, a left ventricular assist device (LVAD) was implanted as destination therapy after undergoing a multidisciplinary assessment. The patient tolerated the surgical implantation of the LVAD without any significant complications, and he has had a relatively unremarkable course 38 months post‐LVAD implantation. A critical factor contributing to the long‐term success of this patient was the decision to select an LVAD that would not disrupt the diaphragm and thus preserve the respiratory muscle strength. This case demonstrates that permanent mechanical LVADs should be considered for appropriately selected Duchenne muscular dystrophy patients with medically refractory end‐stage cardiomyopathy.

Volume loading augments cutaneous vasodilatation and cardiac output of heat stressed older adults

Age‐related changes in cutaneous microvascular and cardiac functions limit the extent of cutaneous vasodilatation and the increase in cardiac output that healthy older adults can achieve during passive heat stress. However, it is unclear if these age‐related changes in microvascular and cardiac functions maximally restrain the levels of cutaneous vasodilatation and cardiac output that healthy older adults can achieve during heat stress. We observed that rapid volume loading, performed during passive heat stress, augments both cutaneous vasodilatation and cardiac output in healthy older humans. These findings demonstrate that the microcirculation of healthy aged skin can further dilate during passive heat exposure, despite peripheral limitations to vasodilatation. Furthermore, healthy older humans can augment cardiac output when cardiac pre‐load is increased during heat stress.

Stiff Left Atrial Syndrome after Multiple Percutaneous Catheter Ablations: Role for Invasive Hemodynamic Exercise Testing

Refractory atrial arrhythmias often require repeat catheter ablations causing decreased atrial compliance. Overtime, dyspnea may develop from secondary elevated pulmonary pressures because of a noncompliant left atrium (LA), referred to as the stiff LA syndrome. We present a case of a patient with a complicated arrhythmia history refractory to antiarrhythmic medications necessitating multiple ablations presenting with dyspnea on exertion. Cardiopulmonary exercise testing (CPET) with invasive hemodynamic measurement supported the diagnosis of stiff LA syndrome noticeable only during exercise. The patient is a 68-year-old male with a history of atrial arrhythmias refractory to anti-arrhythmic medications and repeat left atrial ablations who presents with exercise intolerance. A transthoracic echocardiogram showed preserved ejection fraction, biatrial enlargement, grade II diastolic dysfunction, and mildly elevated right ventricular systolic pressure, while a nuclear perfusion myocardial scan, cardiac computed tomography angiography, CPET, pulmonary function test, and ventilation-perfusion scan were unremarkable. Diuretics for presumed heart failure with preserved ejection fraction subsequently caused orthostatic symptoms. As such, he was referred for a repeat CPET with the addition …

Electrocardiographic patterns of proximal left anterior descending artery occlusion in ST-elevation myocardial infarction may be modified by 3-vessel coronary artery disease.

BACKGROUND The electrocardiographic (ECG) pattern of ST-segment deviation in myocardial infarction is integral to the proper assessment of the location, extent, and functional significance of the infarct but may be modified by the underlying coronary artery anatomy. METHODS We describe the ECG findings in 2 cases of proximal left anterior descending (LAD) artery occlusion in ST-elevation myocardial infarction (STEMI) associated with 3-vessel coronary artery disease. RESULTS Both patients had atypical ECG patterns of ST-segment elevation in leads V(2), I, and aVL and ST-segment depression with positive T waves suggestive of extensive subendocardial ischemia in leads II, III, aVF, and V(3) through V(6); acute proximal LAD occlusion and concomitant 3-vessel coronary artery disease were observed angiographically. CONCLUSION Electrocardiographic changes in proximal LAD STEMI may be modified by the presence of significant atherosclerotic disease elsewhere in the coronary vasculature. Recognition of this ECG pattern may aid the clinician in the rapid identification of high-risk STEMI.

Electrocardiographic characteristics, antiarrhythmic utilization, and outcomes in patients with left ventricular assist devices

Left ventricular assist devices (LVAD) are an increasingly used therapy for patients with advanced heart failure. Arrhythmias are common complications following LVAD implantation requiring admission, initiation, and escalation of medical therapy. Despite their frequent use in the treatment of arrhythmias, little has been reported regarding electrocardiographic changes, antiarrhythmic utilization, and outcomes post-LVAD.

Does High-Intensity Endurance Training Increase the Risk of Atrial Fibrillation?: A Longitudinal Study of Left Atrial Structure and Function

Background: Exercise mitigates many cardiovascular risk factors associated with atrial fibrillation. Endurance training has been associated with atrial structural changes which can increase the risk for atrial fibrillation. The dose of exercise training required for these changes is uncertain. We sought to evaluate the impact of exercise on left atrial (LA) mechanical and electrical function in healthy, sedentary, middle-aged adults. Methods: Sixty-one adults (52±5 years) were randomized to either 10 months of high-intensity exercise training or yoga. At baseline and post-training, all participants underwent maximal exercise stress testing to assess cardiorespiratory fitness, P-wave signal-averaged electrocardiography for filtered P-wave duration and atrial late potentials (root mean square voltage of the last 20 ms), and echocardiography for LA volume, left ventricular end-diastolic volume, and mitral inflow for assessment of LA active emptying. Post-training data were compared with 14 healthy age-matched Masters athletes. Results: LA volume, Vo2 max, and left ventricular end-diastolic volume increased in the exercise group (15%, 17%, and 16%, respectively) with no change in control (P<0.0001). LA active emptying decreased post-exercise versus controls (5%; P=0.03). No significant changes in filtered P-wave duration or root mean square voltage of the last 20 ms occurred after exercise training. LA and left ventricular volumes remained below Masters athletes. The athletes had longer filtered P-wave duration but no difference in the frequency of atrial arrhythmia. Conclusions: Changes in LA structure, LA mechanical function, and left ventricular remodeling occurred after 10 months of exercise but without significant change in atrial electrical activity. A longer duration of training may be required to induce electrical changes thought to cause atrial fibrillation in middle-aged endurance athletes. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT02039154.