{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T12:46:52Z","timestamp":1767962812898,"version":"3.49.0"},"reference-count":19,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"23","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1999,12,7]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            \u2014Myocyte apoptosis is seen in ischemic heart disease, but whether it can occur after reversible ischemia or independent of necrosis and replacement fibrosis is unknown.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            \u2014Pigs were instrumented with a stenosis of the left anterior descending coronary artery to chronically reduce coronary flow reserve over a period of 3 months. At this time, there was viable dysfunctional myocardium having the physiological features of hibernating myocardium. Resting subendocardial perfusion was reduced to 0.65\u00b10.08 (mean\u00b1SEM) mL \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            in hibernating myocardium of instrumented pigs compared with 0.98\u00b10.14 mL \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            in myocardium of sham-operated pigs (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). There was a critical limitation in subendocardial flow during vasodilation to 0.78\u00b10.20 mL \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            in instrumented pigs versus 3.24\u00b10.50 mL \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            in sham-operated pigs (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001). Histology revealed a regional reduction in myocyte nuclear density to 995\u00b1100 nuclei\/mm\n            <jats:sup>2<\/jats:sup>\n            in hibernating myocardium from the instrumented group versus 1534\u00b165 nuclei\/mm\n            <jats:sup>2<\/jats:sup>\n            in myocardium from the sham-operated group (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), regional myocyte hypertrophy (myocyte volume per nucleus, 14 183\u00b12594 in the instrumented group versus 9130\u00b11301 \u03bcm\n            <jats:sup>3<\/jats:sup>\n            in the sham group;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), and minimal increases in connective tissue (5.8\u00b10.9% in the instrumented group versus 3.0\u00b10.2% in the sham group,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Necrosis was not identified, but apoptosis was increased from 30\u00b19 myocytes per 10\n            <jats:sup>6<\/jats:sup>\n            myocyte nuclei in myocardium from the sham group to 220\u00b177 myocytes per 10\n            <jats:sup>6<\/jats:sup>\n            myocyte nuclei in hibernating myocardium (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014These findings indicate that reversible ischemia in an area of chronically reduced coronary flow reserve induces regional myocyte loss via an apoptotic mechanism. This may contribute to the progression of chronic coronary disease to heart failure and explain the lack of complete functional recovery after revascularization in hibernating myocardium.\n          <\/jats:p>","DOI":"10.1161\/01.cir.100.23.2380","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:42:29Z","timestamp":1339461749000},"page":"2380-2386","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":98,"title":["Profound Apoptosis-Mediated Regional Myocyte Loss and Compensatory Hypertrophy in Pigs With Hibernating Myocardium"],"prefix":"10.1161","volume":"100","author":[{"given":"Hajin","family":"Lim","sequence":"first","affiliation":[{"name":"From the Veterans Affairs Western New York Healthcare System and the Departments of Medicine, Anatomy, Physiology, and Biophysics at the State University of New York at Buffalo School of Medicine and Biomedical Sciences."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James A.","family":"Fallavollita","sequence":"additional","affiliation":[{"name":"From the Veterans Affairs Western New York Healthcare System and the Departments of Medicine, Anatomy, Physiology, and Biophysics at the State University of New York at Buffalo School of Medicine and Biomedical Sciences."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert","family":"Hard","sequence":"additional","affiliation":[{"name":"From the Veterans Affairs Western New York Healthcare System and the Departments of Medicine, Anatomy, Physiology, and Biophysics at the State University of New York at Buffalo School of Medicine and Biomedical Sciences."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher W.","family":"Kerr","sequence":"additional","affiliation":[{"name":"From the Veterans Affairs Western New York Healthcare System and the Departments of Medicine, Anatomy, Physiology, and Biophysics at the State University of New York at Buffalo School of Medicine and Biomedical Sciences."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"Jr","given":"John M.","family":"Canty","sequence":"additional","affiliation":[{"name":"From the Veterans Affairs Western New York Healthcare System and the Departments of Medicine, Anatomy, Physiology, and Biophysics at the State University of New York at Buffalo School of Medicine and Biomedical Sciences."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"633","volume":"40","year":"1979","unstructured":"Reimer KA, Jennings RB. The \u201cwavefront phenomenon\u201d of myocardial ischemic cell death, II: transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest. 1979;40:633\u2013644.","journal-title":"Lab Invest"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117504"},{"key":"e_1_3_2_3_2","first-page":"86","volume":"74","year":"1996","unstructured":"Kajstura J, Cheng W, Reiss K, Clark WA, Sonnenblick EH, Krajewski S, Reed JC, Olivetti G, Anversa P. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. Lab Invest. 1996;74:86\u2013107.","journal-title":"Lab Invest"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118683"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.96.9.2920"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006887803970"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.89.1.8281642"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199704173361603"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.95.7.1900"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1007\/s003950050066"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.85.4.1555279"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.92.12.3436"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.90.2.8044942"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(97)00309-4"},{"key":"e_1_3_2_15_2","unstructured":"Lim H Fallavollita JA Canty JM Jr. Myocyte apoptosis and downregulation of SR gene expression are inversely related to coronary flow reserve and are early events in the evolution of ischemic LV dysfunction. Circulation. 1998;98(suppl I):I-762. Abstract."},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1139\/o90-160"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118280"},{"key":"e_1_3_2_18_2","first-page":"141","volume":"148","year":"1996","unstructured":"Sharov VG, Sabbah HN, Shimoyama H, Goussev AV, Lesch M, Goldstein S. Evidence of cardiocyte apoptosis in myocardium of dogs with chronic heart failure. Am J Pathol. 1996;148:141\u2013149.","journal-title":"Am J Pathol"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.98.14.1422"}],"container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/01.CIR.100.23.2380","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T13:01:22Z","timestamp":1715518882000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.100.23.2380"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1999,12,7]]},"references-count":19,"journal-issue":{"issue":"23","published-print":{"date-parts":[[1999,12,7]]}},"alternative-id":["10.1161\/01.CIR.100.23.2380"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.100.23.2380","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1999,12,7]]},"assertion":[{"value":"1999-05-20","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"1999-07-12","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"1999-12-07","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}