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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EMichael Zile, MD, Medical University of South Carolina, discussed the HTN-HF continuum, focusing on matrix mettalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Research conducted at his own institution measured plasma profiles of MMPs and TIMPs in HF patients and age-matched healthy people. \u201cWe know that inflammatory cytokines induce MMP expression in vitro,\u201d Dr. Zile said. The South Carolina investigators detected MMP\/TIMP ratios elevated as high as 16-fold in hypertensive patients with HF.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003Eheart failure\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Ehypertension\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EMMPs and TIMPs: An Aspect of Pathophysiology\u003C\/h2\u003E\n         \u003Cp id=\u0022p-2\u0022\u003EMichael Zile, MD, Medical University of South Carolina, discussed the HTN-HF continuum, focusing on matrix mettalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Research conducted at his own institution measured plasma profiles of MMPs and TIMPs in HF patients and age-matched healthy people. \u201cWe know that inflammatory cytokines induce MMP expression in vitro,\u201d Dr. Zile said. The South Carolina investigators detected MMP\/TIMP ratios elevated as high as 16-fold in hypertensive patients with HF.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EWhether routine measurement of MMP\/TIMP ratios might someday serve as a biomarker or a diagnostic tool in HF remains unclear. But \u201ccytokine activity was linked to changes in MMP levels,\u201d Dr. Zile said, \u201cand it\u0027s evident that MMP proliferation is related to the ventricular non-compliance that can ultimately degrade to florid HF.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EThe Framingham Perspective\u003C\/h2\u003E\n         \u003Cp id=\u0022p-4\u0022\u003E\u201cWe wanted to identify risk factors that contributed to\u2014and connected\u2014HTN and HF,\u201d said Dan Levy, MD, Director, Framingham Heart Study. Study participants included original Framingham Heart Study and Framingham Offspring Study participants between 40 and 89 years of age who had no HF.\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EOver a 14-year follow-up investigators found that 91% of patients who ultimately developed HF had a history of HTN, according to Dr. Levy. \u201cThe risk of developing HF after HTN as compared with normotensive individuals was about 2-fold in men and 3-fold in women.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EPost-MI Progression\u003C\/h2\u003E\n         \u003Cp id=\u0022p-6\u0022\u003E\u201cWhen any of us has a heart attack we bring all our baggage with us,\u201d said Marc A. Pfeffer, MD, PhD, Harvard Medical School. Hypertension, diabetes, obesity\u2014whatever the risk factor, \u201cwe carry it with us into the MI and beyond.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003E\u201cThe most sensible recommendation any doctor can offer is: Don\u0027t have the MI to begin with,\u201d Dr. Pfeffer said. \u201cOr, if you\u0027re going to have one, make it the smallest infarct possible.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EDr. Pfeffer noted compelling emerging evidence for genetic factors that dictate how any given individual heart handles the stress of infarction. \u201cSome of us appear to have better intrinsic repair capacity than others. But until we know a great deal more about the genomics of CV disease, no one can afford to ignore risk factor modification.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EBarry Greenberg, MD, Director, Heart Failure\/Cardiac Transplantation Unit, University of California, observed that \u201cthe road from an MI to HF is metabolically treacherous. Post-MI patients are very likely to remodel and go on to HF. Neurohormonal activation is a major factor in this pathway.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EDr. Greenberg recommended neurohormonal blocking agents (e.g., ARBs, ACEIs). \u201cIs it possible to attenuate the pathological changes that follow in the wake of MI? The answer is a resounding yes.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EValvular Disease: From Recognition to HF\u003C\/h2\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EBlase Carabello, MD, Professor, Baylor College of Medicine, offered a crisply delineated approach to valvular heart disease (VHD) and HF: VHD is a mechanical problem that demands a mechanical solution. \u201cIt\u0027s a given that any valve disease that creates increased load on the heart might eventually go on to HF,\u201d Dr. Carabello said.\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003E\u201cAny symptoms at all in a person with VHD is a turn for the worse,\u201d said Dr. Carabello. \u201cWe need to remember the \u2018melanoma metaphor\u2019\u2014we never say that a person has \u2018just has a little melanoma\u2019. We should approach VHD the same way. The earliest symptoms mark the time to consider surgery in appropriate patients who can tolerate it.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2006 MD Conference Express\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/6\/1\/27.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzlxyp\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}