One drunk-dials me, throwing tinyconstellations of pebbles at my window.Another pounds on the wood planksof my heart until I relent and unlock the latch.The one with the well-water eyes offersto glue all the chipped china back togetherwith his sweat. Then wants to fix the faultydrawbridge with woolly ropes of his hair.
In 2013, jazz composer and alto saxophonist Caroline Davis got some troubling news. Her father had a potentially dangerous condition - arrhythmia, an irregular heartbeat. Her concern for him led to a unique musical response and eventually her new album. Michelle Mercer has this review.
MICHELLE MERCER, BYLINE: Caroline Davis has a Ph.D. in music cognition. So when her father was diagnosed with arrhythmia, she became interested in how inconsistent heart rhythms could affect her father in ways he might not even realize.
MERCER: Then Davis began composing the music that became "Heart Tonic," her new album. On this tune, "Footloose And Fancy Free," a cyclical baseline represents a ventricular rhythm, a rhythm of a human heart.
MERCER: Along with its exploration of the heart's biology, this album uses the heart as a metaphor for bravery and sympathy. We hear that on the waltzing "Fortune," where Davis' saxophone commands a strong melody while also swaying into a familiar harmony and soothing rhythm.
MERCER: The thing is, even if we don't recognize rhythmic effects on "Heart Tonic," we feel them as Caroline Davis explores both symptoms and cures for some physical and emotional challenges. And thanks to Davis' sensitivity and skill, it makes for an album of big-hearted and beautiful music.
Excessive lung function decline is associated with increased risks of respiratory morbidity and mortality outcomes including chronic obstructive pulmonary disease (COPD). COPD is a disease afflicting approximately 80 million people worldwide and as of 2002, the fifth leading cause of death. COPD is an increasing problem, with substantial increases projected in COPD deaths if there is no reduction of the causal risk factors. By 2030, COPD is projected to be the third leading cause of death worldwide, an increase mainly due to extended life expectancies and that COPD deaths occur at older ages. COPD is also largely underdiagnosed, partially due to the gradual development of the disease, and is a very costly illness that reduces labor force participation in its more severe stages. Existing studies of lung function decline as a predictor of morbidity and mortality are focused upon assessing lung function decline as an independent risk factor among other known risk factors. The objective of this study was to assess lung function as a predictor of morbidity and mortality in minimally-adjusted models to provide information for prevention purposes of both lung function decline and associated morbidity and mortality outcomes. The population-based Copenhagen City Heart Study data (I976-2003) were used to investigate this objective. These data were fitting because many of the study participants were at risk for lung function decline due to high rates of smoking and the study also offered long follow-up for COPD morbidity, and mortality due to COPD, coronary heart disease, and all-causes. The first study was designed to examine the relative contributions of lung function decline and respiratory symptoms in predicting the adverse health outcomes. The first study relates to workplace respiratory disease prevention programs where spirometry testing and a respiratory symptom questionnaire are often used. The results of the first study indicated that lung function decline was associated with increased risks of COPD morbidity and mortality, that the effect was greater than for respiratory symptoms and asthma, emphasizing the potential usefulness of monitoring for lung function change over time for prevention in at-risk occupational populations. The second study investigated morbidity and mortality risks in two areas that are not well investigated: in younger individuals, and in relation to long-term patterns of lung function decline. The results indicated that increased lung function decline in individuals age 45 years or younger and the persistency of accelerated lung function decline over follow-up time were significant predictors for increased respiratory morbidity and mortality. The third study evaluated whether the combined effect of the level of lung function at baseline and subsequent rate of lung function decline could further identify high-risk groups. The results showed that the combined effect of a decreasing level of baseline forced expiratory volume in one second (FEV1b) and increasing FEV1 decline was associated with progressively greater morbidity and mortality risks. Groups with `normal' lung function but accelerated declines had significantly increased mortality risks, including never smokers and individuals 45 years or younger. The results of these three studies using an at-risk population demonstrate the potential for COPD morbidity and mortality prevention through monitoring for lung function decline in males, females, never smokers, younger individuals, and those with 'normal' lung function. 041b061a72