{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T20:13:32Z","timestamp":1789935212453,"version":"4.0.1"},"reference-count":48,"publisher":"ASME International","issue":"9","content-domain":{"domain":["asmedigitalcollection.asme.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,9,1]]},"abstract":"<jats:p>Patients who survive a myocardial infarction (MI) are at high risk for ventricular dilation and heart failure. While infarct size is an important determinant of post-MI remodeling, different patients with the same size infarct often display different levels of left ventricular (LV) dilation. The acute physiologic response to MI involves reflex compensation, whereby increases in heart rate (HR), arterial resistance, venoconstriction, and contractility of the surviving myocardium act to maintain mean arterial pressure (MAP). We hypothesized that variability in reflex compensation might underlie some of the reported variability in post-MI remodeling, a hypothesis that is difficult to test using experimental data alone because some reflex responses are difficult or impossible to measure directly. We, therefore, employed a computational model to estimate the balance of compensatory mechanisms from experimentally reported hemodynamic data. We found a strikingly wide range of compensatory reflex profiles in response to MI in dogs and verified that pharmacologic blockade of sympathetic and parasympathetic reflexes nearly abolished this variability. Then, using a previously published model of postinfarction remodeling, we showed that observed variability in compensation translated to variability in predicted LV dilation consistent with published data. Treatment with a vasodilator shifted the compensatory response away from arterial and venous vasoconstriction and toward increased HR and myocardial contractility. Importantly, this shift reduced predicted dilation, a prediction that matched prior experimental studies. Thus, postinfarction reflex compensation could represent both a source of individual variability in the extent of LV remodeling and a target for therapies aimed at reducing that remodeling.<\/jats:p>","DOI":"10.1115\/1.4043867","type":"journal-article","created":{"date-parts":[[2019,5,29]],"date-time":"2019-05-29T20:31:56Z","timestamp":1559161916000},"update-policy":"https:\/\/doi.org\/10.1115\/crossmarkpolicy-asme","source":"Crossref","is-referenced-by-count":22,"title":["The Impact of Hemodynamic Reflex Compensation Following Myocardial Infarction on Subsequent Ventricular Remodeling"],"prefix":"10.1115","volume":"141","author":[{"given":"Colleen M.","family":"Witzenburg","sequence":"first","affiliation":[{"name":"Biomedical Engineering, University of Wisconsin, Madison, WI 53706; Mechanical Engineering, University of Wisconsin, Madison, WI 53706; Cardiovascular Research Center, University of Wisconsin, Madison, WI 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey W.","family":"Holmes","sequence":"additional","affiliation":[{"name":"Biomedical Engineering, Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908; Medicine, Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908; Center for Engineering in Medicine, University of Virginia, Charlottesville, VA 22908"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"33","published-online":{"date-parts":[[2019,8,2]]},"reference":[{"issue":"12","key":"2019100602485016400_bib1","doi-asserted-by":"publisher","first-page":"E67","DOI":"10.1161\/CIR.0000000000000558","article-title":"Heart Disease and Stroke Statistics\u20142018 Update: A Report From the American Heart Association","volume":"137","year":"2018","journal-title":"Circulation"},{"issue":"3","key":"2019100602485016400_bib2","doi-asserted-by":"publisher","first-page":"201","DOI":"10.1016\/j.jchf.2017.09.015","article-title":"Post-Myocardial Infarction Heart Failure","volume":"6","year":"2018","journal-title":"JACC Heart Failure"},{"issue":"24","key":"2019100602485016400_bib3","doi-asserted-by":"publisher","first-page":"2577","DOI":"10.1161\/CIRCULATIONAHA.113.003668","article-title":"National Trends in Heart Failure Hospitalization After Acute Myocardial Infarction for Medicare Beneficiaries 1998-2010","volume":"128","year":"2013","journal-title":"Circulation"},{"issue":"1","key":"2019100602485016400_bib4","doi-asserted-by":"publisher","first-page":"30","DOI":"10.1038\/nrcardio.2016.163","article-title":"Neurohormonal Activation in Heart Failure With Reduced Ejection Fraction","volume":"14","year":"2017","journal-title":"Nat. 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