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The close interrelationship between the heart and lungs was early recognised by medical scientists. In a paper from 1895, Alfred Lee Loomis stated that dyspnoea could be divided into four categories on an aetiological basis: laryngeal dyspnoea, bronchial dyspnoea, pulmonic dyspnoea and cardiac dyspnoea. The term cardiac dyspnoea was used if dyspnoea arose ‘from arrest in the passage of blood through the heart to the lungs’.1 Early studies using spirometry observed that patients with heart disease had lower vital capacity than ‘normal individuals’.2 Many years later, prospective analyses of population-based cohorts showed that reduced lung function also could predict the onset of cardiac diseases.3 ,4 Many studies since have shown that reduced vital capacity or FEV1 is associated with increased incidence of cardiovascular diseases among individuals from the general population.5 ,6 The relationships have been quite strong and comparable with the effects of traditional cardiovascular risk factors, such as obesity or hyperlipidaemia. The increased risk is not limited to those with the smallest lung volumes; in many studies there is a dose–response relationship over the whole distribution of FEV1 or FVC.
However, even though much research has been performed over the past decades, the underlying causal reasons for the increased cardiovascular risk remain elusive. …
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