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Heart failure with preserved ejection fraction (HFpEF) is a major cause of morbidity and mortality. Exercise training is an established adjuvant therapy in heart failure; however, the effects of high-intensity interval training (HIIT) in HFpEF are unknown. We compared the effects of HIIT vs. moderate-intensity aerobic continuous training (MI-ACT) on peak oxygen uptake (V̇o₂peak), left ventricular diastolic dysfunction, and endothelial function in patients with HFpEF. Nineteen patients with HFpEF (age 70 ± 8.3 yr) were randomized to either HIIT (4 × 4 min at 85-90% peak heart rate, with 3 min active recovery) or MI-ACT (30 min at 70% peak heart rate). Fifteen patients completed exercise training (HIIT: n = 9; MI-ACT: n = 6). Patients trained 3 days/wk for 4 wk. Before and after training patients underwent a treadmill test for V̇o₂peak determination, 2D-echocardiography for assessment of left ventricular diastolic dysfunction, and brachial artery flow-mediated dilation (FMD) for assessment of endothelial function. HIIT improved V̇o₂peak (pre = 19.2 ± 5.2 ml·kg(-1)·min(-1); post = 21.0 ± 5.2 ml·kg(-1)·min(-1); P = 0.04) and left ventricular diastolic dysfunction grade (pre = 2.1 ± 0.3; post = 1.3 ± 0.7; P = 0.02), but FMD was unchanged (pre = 6.9 ± 3.7%; post = 7.0 ± 4.2%). No changes were observed following MI-ACT. A trend for reduced left atrial volume index was observed following HIIT compared with MI-ACT (-3.3 ± 6.6 vs. +5.8 ± 10.7 ml/m(2); P = 0.06). In HFpEF patients 4 wk of HIIT significantly improved V̇o₂peak and left ventricular diastolic dysfunction. HIIT may provide a more robust stimulus than MI-ACT for early exercise training adaptations in HFpEF.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is being recognized with increasing frequency. Diagnostic and treatment information is limited. A systematic review is presented, focusing on patient demographics, clinical presentation, diagnosis, treatment options, and outcomes. A systematic electronic literature search was conducted for adult DIPNECH cases reported in the English literature during the past 6 years. Twenty-four DIPNECH cases were identified. Another case from our institution is contributed. Women represent 92% (23 of 25). Mean age at diagnosis was 58 years (range, 36-76 yr). Most were nonsmokers (16 of 24). Symptoms included cough (71%), dyspnea (63%), and wheezing (25%) occurring days to years before diagnosis. Pulmonary function testing showed obstructive ventilatory disease in 54%. Lung nodules were seen in 15 patients (63%), ground-glass attenuation in 7 patients (29%), and bronchiectasis in 5 patients (21%). Histological confirmation required surgical lung biopsy for 88%; however, transbronchial biopsies alone were diagnostic in three patients. Treatments strategies included systemic and inhaled corticosteroids, bronchodilators, and lung resection. Available follow-up data in 17 patients showed 6 clinically improved, 7 who remained stable, and 4 clinically deteriorated. The majority of patients presenting with DIPNECH are middle-aged females with symptoms of cough and dyspnea; obstructive abnormalities on pulmonary function testing; and radiographic imaging showing pulmonary nodules, ground-glass attenuation, and bronchiectasis. In general, the clinical course remains stable; however, progression to respiratory failure does occur. Long-term follow-up and treatment remains incomplete. Establishment of a national multicenter DIPNECH registry would allow formulation of optimal evidence-based guidelines for management of these patients.

Among the commonly understood socioeconomic determinants of health, social change, disorganization, and poverty have been associated with an increased risk of morbidity and mortality. One of the postulated mechanisms through which these determinants have been linked to health and illness is their relationship to social support. The health determinant, social isolation or lack of a social support network (SSN), and its effects on premature mortality after acute myocardial infarction mandate further scrutiny by the cardiovascular community for several reasons. First, as a predictor of 1-year mortality, low SSN is equivalent to many of the classic risk factors, such as elevated cholesterol level, tobacco use, and hypertension. Second, treatment of acute myocardial infarction is costly. Because low social support is associated with an increased 1-year mortality, neglecting the role of the SSN may diminish the possible gains accrued during acute-phase treatment. Therefore, lack of an SSN should be considered a risk factor for subsequent morbidity and mortality after a myocardial infarction. Finally, cardiac rehabilitation programs and other extant prevention strategies can be better used to reduce mortality after myocardial infarction. This article systematically reviews recent evidence related to SSNs to provide an update on the role of social support in cardiovascular disease-related outcomes.