Format

Send to

Choose Destination
Herz. 2019 Jun 11. doi: 10.1007/s00059-019-4816-5. [Epub ahead of print]

Left heart function in COPD : Impact of lung deflation.

Author information

1
Bereich Atemwegsforschung, Fraunhofer-Institut für Toxikologie und Experimentelle Medizin ITEM, Feodor-Lynen-Straße 15, 30625, Hannover, Germany.
2
Klinik für Kardiologie und Angiologie, Medizinische Hochschule Hannover, Hannover, Germany.
3
Klinik für Pneumologie, Medizinische Hochschule Hannover, Hannover, Germany.
4
Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Deutsches Zentrum für Lungenforschung, Hannover, Germany.
5
Bereich Atemwegsforschung, Fraunhofer-Institut für Toxikologie und Experimentelle Medizin ITEM, Feodor-Lynen-Straße 15, 30625, Hannover, Germany. jens.hohlfeld@item.fraunhofer.de.
6
Klinik für Pneumologie, Medizinische Hochschule Hannover, Hannover, Germany. jens.hohlfeld@item.fraunhofer.de.
7
Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Deutsches Zentrum für Lungenforschung, Hannover, Germany. jens.hohlfeld@item.fraunhofer.de.

Abstract

Chronic obstructive pulmonary disease (COPD) primarily affects the lungs; however, cardiovascular conditions are among the most common extrapulmonary comorbidities. Besides shared risk factors such as cigarette smoking, pathophysiological connections between the lung and the heart have been identified as mediators of reduced cardiac output. Recent research has focused on hyperinflation of the lung as a pulmonary cause for heart dysfunction. Hyperinflation is a typical lung abnormality seen in COPD; it is characterized by increased residual volume, intrathoracic gas volume, and total lung capacity while vital capacity is decreased. The degree of hyperinflation with airway obstruction is inversely related to left ventricular filling, stroke volume, and cardiac output. The underlying mechanisms are assumed to be compression of the pulmonary veins and thus reduced preload of the left heart as well as decreased pulmonary microvascular blood flow due to compression of the pulmonary vasculature. Treatment with a dual bronchodilator antagonizes this detrimental lung-heart unbalance effectively: Pulmonary blood flow, left ventricular end-diastolic volume, and stroke volume increase in COPD patients without cardiac abnormalities. Similar effects, yet less pronounced, were reported with single bronchodilator therapy. Future work needs to investigate whether these promising findings can be reproduced in COPD patients with cardiovascular diseases.

KEYWORDS:

Bronchodilator effect; Cardiovascular disease; Hyperinflation; Left ventricular function; Pulmonary disease, chronic obstructive

PMID:
31187193
DOI:
10.1007/s00059-019-4816-5

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center