Heart Rate and Heart Failure: Not a Simple Relationship
Resting heart rate (HR) is increased in patients with heart failure (HF). Sustained tachycardia can cause HF. The magnitude of HR reduction in treatment trials of patients with HF is associated with a reduction in mortality. Yet, the mechanistic and causal role of HR in HF is unclear, and recent tri...
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| Veröffentlicht in: | Circulation Journal 2011, Vol.75(2), pp.229-236 |
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| creator | Heusch, Gerd |
| description | Resting heart rate (HR) is increased in patients with heart failure (HF). Sustained tachycardia can cause HF. The magnitude of HR reduction in treatment trials of patients with HF is associated with a reduction in mortality. Yet, the mechanistic and causal role of HR in HF is unclear, and recent trials with selective HR reduction have not consistently achieved benefit: the BEAUTIFUL trial in patients with coronary artery disease and left ventricular dysfunction did not achieve a significant benefit in the primary endpoint, and only the coronary outcome, not the HF outcome, was improved; in the SHIFT trial, however, patients with symptomatic heart failure had a significant benefit in the primary endpoint of cardiovascular mortality and hospitalization for worsening HF. The present review addresses the pathophysiology of tachycardia-induced HF, the force-frequency relationship, and the clinical potential of HR reduction in HF. (Circ J 2011; 75: 229-236) |
| doi_str_mv | 10.1253/circj.CJ-10-0925 |
| format | Article |
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Sustained tachycardia can cause HF. The magnitude of HR reduction in treatment trials of patients with HF is associated with a reduction in mortality. Yet, the mechanistic and causal role of HR in HF is unclear, and recent trials with selective HR reduction have not consistently achieved benefit: the BEAUTIFUL trial in patients with coronary artery disease and left ventricular dysfunction did not achieve a significant benefit in the primary endpoint, and only the coronary outcome, not the HF outcome, was improved; in the SHIFT trial, however, patients with symptomatic heart failure had a significant benefit in the primary endpoint of cardiovascular mortality and hospitalization for worsening HF. The present review addresses the pathophysiology of tachycardia-induced HF, the force-frequency relationship, and the clinical potential of HR reduction in HF. 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Sustained tachycardia can cause HF. The magnitude of HR reduction in treatment trials of patients with HF is associated with a reduction in mortality. Yet, the mechanistic and causal role of HR in HF is unclear, and recent trials with selective HR reduction have not consistently achieved benefit: the BEAUTIFUL trial in patients with coronary artery disease and left ventricular dysfunction did not achieve a significant benefit in the primary endpoint, and only the coronary outcome, not the HF outcome, was improved; in the SHIFT trial, however, patients with symptomatic heart failure had a significant benefit in the primary endpoint of cardiovascular mortality and hospitalization for worsening HF. The present review addresses the pathophysiology of tachycardia-induced HF, the force-frequency relationship, and the clinical potential of HR reduction in HF. (Circ J 2011; 75: 229-236)</description><subject>Animals</subject><subject>Atrial fibrillation</subject><subject>Benzazepines - pharmacology</subject><subject>Benzazepines - therapeutic use</subject><subject>Cardiac Pacing, Artificial - adverse effects</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Excitation-contraction coupling</subject><subject>Force-frequency relation</subject><subject>Heart failure</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - prevention & control</subject><subject>Heart Rate - drug effects</subject><subject>Humans</subject><subject>Ivabradine</subject><subject>Models, Cardiovascular</subject><subject>Multicenter Studies as Topic</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardium - pathology</subject><subject>Randomized Controlled Trials as Topic</subject><subject>Stress, Mechanical</subject><subject>Tachycardia</subject><subject>Tachycardia - complications</subject><subject>Tachycardia - drug therapy</subject><subject>Tachycardia - physiopathology</subject><subject>Tachycardia, Supraventricular - drug therapy</subject><subject>Tachycardia, Supraventricular - physiopathology</subject><subject>Treatment Outcome</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Dysfunction, Left - prevention & control</subject><subject>Vertebrates</subject><issn>1346-9843</issn><issn>1347-4820</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkDtPwzAURi0EoqWwMyDUjcnl-pXYI4oopaqEhGC2XOcGUqUP7GTg35M0pV3uS-d-wyHklsGEcSUefRn8apLNKQMKhqszMmRCplRqDuf7OaFGSzEgVzGuALgBZS7JgDOQzKQwJHczdKEev7sax26Tj_t16sqqCXhNLgpXRbw59BH5nD5_ZDO6eHt5zZ4W1Esjapqj14yhZ1LmCRfCgUNIfS5ReZUo6TFB5oCrXEgJS1WgTNEbrwVLjdGFGJGHPncXtj8Nxtquy-ixqtwGt020WraoZtq0JPSkD9sYAxZ2F8q1C7-Wge2U2L0Sm827Q6ekfbk_hDfLNebHh38HLTDtgVWs3RcegVZE6Ss8JKbK8q6ckk_AtwsWN-IPGNd0hw</recordid><startdate>2011</startdate><enddate>2011</enddate><creator>Heusch, Gerd</creator><general>The Japanese Circulation Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>2011</creationdate><title>Heart Rate and Heart Failure</title><author>Heusch, Gerd</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c493t-dec811ec144d6233a0ae07cd4e5c5654ce6e1a025d3440b5fe47ec9c8317998f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Atrial fibrillation</topic><topic>Benzazepines - pharmacology</topic><topic>Benzazepines - therapeutic use</topic><topic>Cardiac Pacing, Artificial - adverse effects</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Excitation-contraction coupling</topic><topic>Force-frequency relation</topic><topic>Heart failure</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - prevention & control</topic><topic>Heart Rate - drug effects</topic><topic>Humans</topic><topic>Ivabradine</topic><topic>Models, Cardiovascular</topic><topic>Multicenter Studies as Topic</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardium - pathology</topic><topic>Randomized Controlled Trials as Topic</topic><topic>Stress, Mechanical</topic><topic>Tachycardia</topic><topic>Tachycardia - complications</topic><topic>Tachycardia - drug therapy</topic><topic>Tachycardia - physiopathology</topic><topic>Tachycardia, Supraventricular - drug therapy</topic><topic>Tachycardia, Supraventricular - physiopathology</topic><topic>Treatment Outcome</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Dysfunction, Left - prevention & control</topic><topic>Vertebrates</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Heusch, Gerd</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Heusch, Gerd</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heart Rate and Heart Failure: Not a Simple Relationship</atitle><jtitle>Circulation Journal</jtitle><addtitle>Circ J</addtitle><date>2011</date><risdate>2011</risdate><volume>75</volume><issue>2</issue><spage>229</spage><epage>236</epage><pages>229-236</pages><issn>1346-9843</issn><eissn>1347-4820</eissn><abstract>Resting heart rate (HR) is increased in patients with heart failure (HF). 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| fulltext | fulltext |
| identifier | ISSN: 1346-9843 |
| ispartof | Circulation Journal, 2011, Vol.75(2), pp.229-236 |
| issn | 1346-9843 1347-4820 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_848318189 |
| source | J-STAGE Free; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Atrial fibrillation Benzazepines - pharmacology Benzazepines - therapeutic use Cardiac Pacing, Artificial - adverse effects Coronary Artery Disease - physiopathology Disease Models, Animal Excitation-contraction coupling Force-frequency relation Heart failure Heart Failure - drug therapy Heart Failure - etiology Heart Failure - physiopathology Heart Failure - prevention & control Heart Rate - drug effects Humans Ivabradine Models, Cardiovascular Multicenter Studies as Topic Myocardial Ischemia - physiopathology Myocardium - pathology Randomized Controlled Trials as Topic Stress, Mechanical Tachycardia Tachycardia - complications Tachycardia - drug therapy Tachycardia - physiopathology Tachycardia, Supraventricular - drug therapy Tachycardia, Supraventricular - physiopathology Treatment Outcome Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology Ventricular Dysfunction, Left - prevention & control Vertebrates |
| title | Heart Rate and Heart Failure: Not a Simple Relationship |
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