Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications
Systolic and diastolic myocardial dysfunction has been demonstrated to be associated with an activation of the circulating and local renin-angiotensin-aldosterone system (RAAS), and with a subsequent inappropriately increased production of reactive oxygen species (ROS). While, at low concentrations,...
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| Published in: | European heart journal Vol. 36; no. 38; pp. 2555 - 2564 |
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| Main Authors: | , , , , |
| Format: | Journal Article |
| Language: | English |
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England
07.10.2015
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| ISSN: | 1522-9645 |
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| Abstract | Systolic and diastolic myocardial dysfunction has been demonstrated to be associated with an activation of the circulating and local renin-angiotensin-aldosterone system (RAAS), and with a subsequent inappropriately increased production of reactive oxygen species (ROS). While, at low concentrations, ROS modulate important physiological functions through changes in cellular signalling and gene expression, overproduction of ROS may adversely alter cardiac mechanics, leading to further worsening of systolic and diastolic function. In addition, vascular endothelial dysfunction due to uncoupling of the nitric oxide synthase, activation of vascular and phagocytic membrane oxidases or mitochondrial oxidative stress may lead to increased vascular stiffness, further compromising cardiac performance in afterload-dependent hearts. In the present review, we address the potential role of ROS in the pathophysiology of myocardial and vascular dysfunction in heart failure (HF) and their therapeutic targeting. We discuss possible mechanisms underlying the failure of antioxidant vitamins in improving patients' prognosis, the impact of angiotensin-converting enzyme inhibitors or AT1 receptor blockers on oxidative stress, and the mechanism of the benefit of combination of hydralazine/isosorbide dinitrate. Further, we provide evidence supporting the existence of differences in the pathophysiology of HF with preserved vs. reduced ejection fraction and whether targeting mitochondrial ROS might be a particularly interesting therapeutic option for patients with preserved ejection fraction. |
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| AbstractList | Systolic and diastolic myocardial dysfunction has been demonstrated to be associated with an activation of the circulating and local renin-angiotensin-aldosterone system (RAAS), and with a subsequent inappropriately increased production of reactive oxygen species (ROS). While, at low concentrations, ROS modulate important physiological functions through changes in cellular signalling and gene expression, overproduction of ROS may adversely alter cardiac mechanics, leading to further worsening of systolic and diastolic function. In addition, vascular endothelial dysfunction due to uncoupling of the nitric oxide synthase, activation of vascular and phagocytic membrane oxidases or mitochondrial oxidative stress may lead to increased vascular stiffness, further compromising cardiac performance in afterload-dependent hearts. In the present review, we address the potential role of ROS in the pathophysiology of myocardial and vascular dysfunction in heart failure (HF) and their therapeutic targeting. We discuss possible mechanisms underlying the failure of antioxidant vitamins in improving patients' prognosis, the impact of angiotensin-converting enzyme inhibitors or AT1 receptor blockers on oxidative stress, and the mechanism of the benefit of combination of hydralazine/isosorbide dinitrate. Further, we provide evidence supporting the existence of differences in the pathophysiology of HF with preserved vs. reduced ejection fraction and whether targeting mitochondrial ROS might be a particularly interesting therapeutic option for patients with preserved ejection fraction. |
| Author | Münzel, Thomas Keaney, Jr, John F Gori, Tommaso Daiber, Andreas Maack, Christoph |
| Author_xml | – sequence: 1 givenname: Thomas surname: Münzel fullname: Münzel, Thomas email: tmuenzel@uni-mainz.de organization: 2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany tmuenzel@uni-mainz.de – sequence: 2 givenname: Tommaso surname: Gori fullname: Gori, Tommaso organization: 2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany – sequence: 3 givenname: John F surname: Keaney, Jr fullname: Keaney, Jr, John F organization: University of Massachusetts Medical School, Worcester, MA, USA – sequence: 4 givenname: Christoph surname: Maack fullname: Maack, Christoph organization: Klinik für Innere Medizin III Universitätsklinikum des Saarlandes, Homburg/Saar, Germany – sequence: 5 givenname: Andreas surname: Daiber fullname: Daiber, Andreas organization: 2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26142467$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Angiotensin-Converting Enzyme Inhibitors - therapeutic use Antioxidants - therapeutic use Cardiovascular System - enzymology Cardiovascular System - metabolism Drug Therapy, Combination Exercise Therapy - methods Heart Failure, Diastolic - etiology Heart Failure, Systolic - enzymology Heart Failure, Systolic - etiology Humans Hydralazine - therapeutic use Mitochondria - metabolism NADPH Oxidases - physiology Nitrates - therapeutic use Nitric Oxide - deficiency Nitric Oxide Synthase - physiology Oxidative Stress - physiology Phosphodiesterase Inhibitors - therapeutic use Reactive Oxygen Species - chemistry Reactive Oxygen Species - metabolism Stroke Volume - physiology Vitamins - therapeutic use Xanthine Oxidase - physiology |
| Title | Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications |
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