Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship
The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval su...
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| Veröffentlicht in: | International Heart Journal 2016, Vol.57(3), pp.317-322 |
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| creator | Watanabe, Tohru Kashimura, Takeshi Kodama, Makoto Tanaka, Komei Fujiki, Shinya Hayashi, Yuka Obata, Hiroaki Hanawa, Haruo Minamino, Tohru |
| description | The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner. In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated. Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001). Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR. |
| doi_str_mv | 10.1536/ihj.15-374 |
| format | Article |
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In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner. In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated. Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001). Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.</description><identifier>ISSN: 1349-2365</identifier><identifier>EISSN: 1349-3299</identifier><identifier>DOI: 10.1536/ihj.15-374</identifier><identifier>PMID: 27181036</identifier><language>eng</language><publisher>Japan: International Heart Journal Association</publisher><subject>Calcium ; Calcium - metabolism ; Cardiac Pacing, Artificial - adverse effects ; Cardiac Pacing, Artificial - methods ; Cardiomyopathy, Dilated - complications ; Cardiomyopathy, Dilated - physiopathology ; Electrophysiologic Techniques, Cardiac - methods ; Female ; Heart contractility ; Heart Failure, Systolic - diagnosis ; Heart Failure, Systolic - etiology ; Heart Failure, Systolic - physiopathology ; Heart Failure, Systolic - therapy ; Heart Rate ; Humans ; Male ; Middle Aged ; Myocardial Contraction ; Refractoriness ; Refractory Period, Electrophysiological ; Stroke Volume ; Systolic heart failure ; Ventricular Dysfunction, Left - diagnosis ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Dysfunction, Left - therapy</subject><ispartof>International Heart Journal, 2016, Vol.57(3), pp.317-322</ispartof><rights>2016 by the International Heart Journal Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c477t-ab266c3237a1eb469a00cf5baa7c5addc6ff78feac1dd8bd3bc87f45ad2edb6b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1881,4022,27922,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27181036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Watanabe, Tohru</creatorcontrib><creatorcontrib>Kashimura, Takeshi</creatorcontrib><creatorcontrib>Kodama, Makoto</creatorcontrib><creatorcontrib>Tanaka, Komei</creatorcontrib><creatorcontrib>Fujiki, Shinya</creatorcontrib><creatorcontrib>Hayashi, Yuka</creatorcontrib><creatorcontrib>Obata, Hiroaki</creatorcontrib><creatorcontrib>Hanawa, Haruo</creatorcontrib><creatorcontrib>Minamino, Tohru</creatorcontrib><title>Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship</title><title>International Heart Journal</title><addtitle>Int. Heart J.</addtitle><description>The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner. In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated. Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001). Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.</description><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Cardiac Pacing, Artificial - adverse effects</subject><subject>Cardiac Pacing, Artificial - methods</subject><subject>Cardiomyopathy, Dilated - complications</subject><subject>Cardiomyopathy, Dilated - physiopathology</subject><subject>Electrophysiologic Techniques, Cardiac - methods</subject><subject>Female</subject><subject>Heart contractility</subject><subject>Heart Failure, Systolic - diagnosis</subject><subject>Heart Failure, Systolic - etiology</subject><subject>Heart Failure, Systolic - physiopathology</subject><subject>Heart Failure, Systolic - therapy</subject><subject>Heart Rate</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Contraction</subject><subject>Refractoriness</subject><subject>Refractory Period, Electrophysiological</subject><subject>Stroke Volume</subject><subject>Systolic heart failure</subject><subject>Ventricular Dysfunction, Left - diagnosis</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Dysfunction, Left - therapy</subject><issn>1349-2365</issn><issn>1349-3299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kNFOwjAUhhujEURvfADTa5Ppum7rdqdBJiQkGkVvl7PujJWMMdtigk9vcchN-7fnO__FR8g18-9YxON7Va9c8LgIT8iQ8TD1eJCmp4cc8DgakAtjVr4fssgX52QQCJYwn8dD8pOBalS7pHOsLP3E1molGzR0Ct9IoaWTtoZWYklfN8Z671attw1YtWndh3W46h9PaDplkS5qVJrO1h0o7ZayjZZIM41fW2zljr5hv2xq1V2Sswoag1eHe0Q-ssliPPXmL8-z8ePck6EQ1oMiiGPJAy6AYRHGKfi-rKICQMgIylLGVSWSCkGyskyKkhcyEVXoRgGWRVzwEbnte6XeGKOxyjut1qB3OfPzvcDcCXQhdwIdfNPD3bZYY3lE_4054KEHVsbCEo8AaLsX99cViZzvj77zOJI16Bxb_gseC4c6</recordid><startdate>2016</startdate><enddate>2016</enddate><creator>Watanabe, Tohru</creator><creator>Kashimura, Takeshi</creator><creator>Kodama, Makoto</creator><creator>Tanaka, Komei</creator><creator>Fujiki, Shinya</creator><creator>Hayashi, Yuka</creator><creator>Obata, Hiroaki</creator><creator>Hanawa, Haruo</creator><creator>Minamino, Tohru</creator><general>International Heart Journal Association</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></search><sort><creationdate>2016</creationdate><title>Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship</title><author>Watanabe, Tohru ; Kashimura, Takeshi ; Kodama, Makoto ; Tanaka, Komei ; Fujiki, Shinya ; Hayashi, Yuka ; Obata, Hiroaki ; Hanawa, Haruo ; Minamino, Tohru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-ab266c3237a1eb469a00cf5baa7c5addc6ff78feac1dd8bd3bc87f45ad2edb6b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>Cardiac Pacing, Artificial - adverse effects</topic><topic>Cardiac Pacing, Artificial - methods</topic><topic>Cardiomyopathy, Dilated - complications</topic><topic>Cardiomyopathy, Dilated - physiopathology</topic><topic>Electrophysiologic Techniques, Cardiac - methods</topic><topic>Female</topic><topic>Heart contractility</topic><topic>Heart Failure, Systolic - diagnosis</topic><topic>Heart Failure, Systolic - etiology</topic><topic>Heart Failure, Systolic - physiopathology</topic><topic>Heart Failure, Systolic - therapy</topic><topic>Heart Rate</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Contraction</topic><topic>Refractoriness</topic><topic>Refractory Period, Electrophysiological</topic><topic>Stroke Volume</topic><topic>Systolic heart failure</topic><topic>Ventricular Dysfunction, Left - diagnosis</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Dysfunction, Left - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Watanabe, Tohru</creatorcontrib><creatorcontrib>Kashimura, Takeshi</creatorcontrib><creatorcontrib>Kodama, Makoto</creatorcontrib><creatorcontrib>Tanaka, Komei</creatorcontrib><creatorcontrib>Fujiki, Shinya</creatorcontrib><creatorcontrib>Hayashi, Yuka</creatorcontrib><creatorcontrib>Obata, Hiroaki</creatorcontrib><creatorcontrib>Hanawa, Haruo</creatorcontrib><creatorcontrib>Minamino, Tohru</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>International Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Watanabe, Tohru</au><au>Kashimura, Takeshi</au><au>Kodama, Makoto</au><au>Tanaka, Komei</au><au>Fujiki, Shinya</au><au>Hayashi, Yuka</au><au>Obata, Hiroaki</au><au>Hanawa, Haruo</au><au>Minamino, Tohru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship</atitle><jtitle>International Heart Journal</jtitle><addtitle>Int. Heart J.</addtitle><date>2016</date><risdate>2016</risdate><volume>57</volume><issue>3</issue><spage>317</spage><epage>322</epage><pages>317-322</pages><issn>1349-2365</issn><eissn>1349-3299</eissn><abstract>The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner. In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated. Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001). Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.</abstract><cop>Japan</cop><pub>International Heart Journal Association</pub><pmid>27181036</pmid><doi>10.1536/ihj.15-374</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Calcium Calcium - metabolism Cardiac Pacing, Artificial - adverse effects Cardiac Pacing, Artificial - methods Cardiomyopathy, Dilated - complications Cardiomyopathy, Dilated - physiopathology Electrophysiologic Techniques, Cardiac - methods Female Heart contractility Heart Failure, Systolic - diagnosis Heart Failure, Systolic - etiology Heart Failure, Systolic - physiopathology Heart Failure, Systolic - therapy Heart Rate Humans Male Middle Aged Myocardial Contraction Refractoriness Refractory Period, Electrophysiological Stroke Volume Systolic heart failure Ventricular Dysfunction, Left - diagnosis Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology Ventricular Dysfunction, Left - therapy |
| title | Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship |
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