Coronary Microvascular Rarefaction and Myocardial Fibrosis in Heart Failure With Preserved Ejection Fraction

BACKGROUND—Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosi...

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Published in	Circulation (New York, N.Y.) Vol. 131; no. 6; pp. 550 - 559
Main Authors	Mohammed, Selma F., Hussain, Saad, Mirzoyev, Sultan A., Edwards, William D., Maleszewski, Joseph J., Redfield, Margaret M.
Format	Journal Article
Language	English
Published	United States by the American College of Cardiology Foundation and the American Heart Association, Inc 10.02.2015
Subjects	Aged Aged, 80 and over Algorithms Autopsy Cardiomegaly - epidemiology Cardiomegaly - pathology Cause of Death Comorbidity Coronary Artery Disease - epidemiology Coronary Artery Disease - pathology Coronary Vessels - pathology Diabetes Mellitus - epidemiology Echocardiography Electrocardiography Endomyocardial Fibrosis - epidemiology Endomyocardial Fibrosis - pathology Endomyocardial Fibrosis - physiopathology Female Heart - anatomy & histology Heart Failure - diagnosis Heart Failure - epidemiology Heart Failure - pathology Heart Failure - physiopathology Humans Immunohistochemistry Male Microvessels - pathology Myocardium - pathology Myocytes, Cardiac - pathology Organ Size Postmortem Changes Reference Values Stroke Volume heart failure, diastolic endothelium pathology hypertrophy fibrosis autopsy microvessels
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Abstract	BACKGROUND—Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology. METHODS AND RESULTS—We identified HFpEF patients (n=124) and age-appropriate control subjects (noncardiac death, no heart failure diagnosis; n=104) who underwent autopsy. Heart weight and CAD severity were obtained from the autopsy reports. With the use of whole-field digital microscopy and automated analysis algorithms in full-thickness left ventricular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantified. Subjects with HFpEF had heavier hearts (median, 538 g; 169% of age-, sex-, and body size–expected heart weight versus 335 g; 112% in controls), more severe CAD (65% with ≥1 vessel with >50% diameter stenosis in HFpEF versus 13% in controls), more left ventricular fibrosis (median % area fibrosis, 9.6 versus 7.1) and lower MVD (median 961 versus 1316 vessels/mm) than control (P<0.0001 for all). Myocardial fibrosis increased with decreasing MVD in controls (r=–0.28, P=0.004) and HFpEF (r=–0.26, P=0.004). Adjusting for MVD attenuated the group differences in fibrosis. Heart weight, fibrosis, and MVD were similar in HFpEF patients with CAD versus without CAD. CONCLUSIONS—In this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls. Each of these findings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impairment characteristic of HFpEF.
AbstractList	Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology. We identified HFpEF patients (n=124) and age-appropriate control subjects (noncardiac death, no heart failure diagnosis; n=104) who underwent autopsy. Heart weight and CAD severity were obtained from the autopsy reports. With the use of whole-field digital microscopy and automated analysis algorithms in full-thickness left ventricular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantified. Subjects with HFpEF had heavier hearts (median, 538 g; 169% of age-, sex-, and body size-expected heart weight versus 335 g; 112% in controls), more severe CAD (65% with ≥1 vessel with >50% diameter stenosis in HFpEF versus 13% in controls), more left ventricular fibrosis (median % area fibrosis, 9.6 versus 7.1) and lower MVD (median 961 versus 1316 vessels/mm(2)) than control (P<0.0001 for all). Myocardial fibrosis increased with decreasing MVD in controls (r=-0.28, P=0.004) and HFpEF (r=-0.26, P=0.004). Adjusting for MVD attenuated the group differences in fibrosis. Heart weight, fibrosis, and MVD were similar in HFpEF patients with CAD versus without CAD. In this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls. Each of these findings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impairment characteristic of HFpEF. Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology.BACKGROUNDCharacterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology.We identified HFpEF patients (n=124) and age-appropriate control subjects (noncardiac death, no heart failure diagnosis; n=104) who underwent autopsy. Heart weight and CAD severity were obtained from the autopsy reports. With the use of whole-field digital microscopy and automated analysis algorithms in full-thickness left ventricular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantified. Subjects with HFpEF had heavier hearts (median, 538 g; 169% of age-, sex-, and body size-expected heart weight versus 335 g; 112% in controls), more severe CAD (65% with ≥1 vessel with >50% diameter stenosis in HFpEF versus 13% in controls), more left ventricular fibrosis (median % area fibrosis, 9.6 versus 7.1) and lower MVD (median 961 versus 1316 vessels/mm(2)) than control (P<0.0001 for all). Myocardial fibrosis increased with decreasing MVD in controls (r=-0.28, P=0.004) and HFpEF (r=-0.26, P=0.004). Adjusting for MVD attenuated the group differences in fibrosis. Heart weight, fibrosis, and MVD were similar in HFpEF patients with CAD versus without CAD.METHODS AND RESULTSWe identified HFpEF patients (n=124) and age-appropriate control subjects (noncardiac death, no heart failure diagnosis; n=104) who underwent autopsy. Heart weight and CAD severity were obtained from the autopsy reports. With the use of whole-field digital microscopy and automated analysis algorithms in full-thickness left ventricular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantified. Subjects with HFpEF had heavier hearts (median, 538 g; 169% of age-, sex-, and body size-expected heart weight versus 335 g; 112% in controls), more severe CAD (65% with ≥1 vessel with >50% diameter stenosis in HFpEF versus 13% in controls), more left ventricular fibrosis (median % area fibrosis, 9.6 versus 7.1) and lower MVD (median 961 versus 1316 vessels/mm(2)) than control (P<0.0001 for all). Myocardial fibrosis increased with decreasing MVD in controls (r=-0.28, P=0.004) and HFpEF (r=-0.26, P=0.004). Adjusting for MVD attenuated the group differences in fibrosis. Heart weight, fibrosis, and MVD were similar in HFpEF patients with CAD versus without CAD.In this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls. Each of these findings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impairment characteristic of HFpEF.CONCLUSIONSIn this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls. Each of these findings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impairment characteristic of HFpEF. BACKGROUND—Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology. METHODS AND RESULTS—We identified HFpEF patients (n=124) and age-appropriate control subjects (noncardiac death, no heart failure diagnosis; n=104) who underwent autopsy. Heart weight and CAD severity were obtained from the autopsy reports. With the use of whole-field digital microscopy and automated analysis algorithms in full-thickness left ventricular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantified. Subjects with HFpEF had heavier hearts (median, 538 g; 169% of age-, sex-, and body size–expected heart weight versus 335 g; 112% in controls), more severe CAD (65% with ≥1 vessel with >50% diameter stenosis in HFpEF versus 13% in controls), more left ventricular fibrosis (median % area fibrosis, 9.6 versus 7.1) and lower MVD (median 961 versus 1316 vessels/mm) than control (P<0.0001 for all). Myocardial fibrosis increased with decreasing MVD in controls (r=–0.28, P=0.004) and HFpEF (r=–0.26, P=0.004). Adjusting for MVD attenuated the group differences in fibrosis. Heart weight, fibrosis, and MVD were similar in HFpEF patients with CAD versus without CAD. CONCLUSIONS—In this study, patients with HFpEF had more cardiac hypertrophy, epicardial CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls. Each of these findings may contribute to the left ventricular diastolic dysfunction and cardiac reserve function impairment characteristic of HFpEF.
Author	Edwards, William D. Mirzoyev, Sultan A. Maleszewski, Joseph J. Hussain, Saad Mohammed, Selma F. Redfield, Margaret M.
AuthorAffiliation	From the Division of Cardiovascular Diseases (S.F.M., S.H., M.M.R.), Mayo Graduate School (S.F.M.), Mayo Medical School (S.A.M.), and Division of Anatomic Pathology (W.D.E., J.J.M.), Mayo Clinic, Rochester, MN
AuthorAffiliation_xml	– name: From the Division of Cardiovascular Diseases (S.F.M., S.H., M.M.R.), Mayo Graduate School (S.F.M.), Mayo Medical School (S.A.M.), and Division of Anatomic Pathology (W.D.E., J.J.M.), Mayo Clinic, Rochester, MN – name: 4 Division of Anatomic Pathology, Mayo Clinic, Rochester, MN – name: 3 Mayo Medical School, Mayo Clinic, Rochester, MN – name: 1 Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN – name: 2 Mayo Graduate School, Mayo Clinic, Rochester, MN
Author_xml	– sequence: 1 givenname: Selma surname: Mohammed middlename: F. fullname: Mohammed, Selma F. organization: From the Division of Cardiovascular Diseases (S.F.M., S.H., M.M.R.), Mayo Graduate School (S.F.M.), Mayo Medical School (S.A.M.), and Division of Anatomic Pathology (W.D.E., J.J.M.), Mayo Clinic, Rochester, MN – sequence: 2 givenname: Saad surname: Hussain fullname: Hussain, Saad – sequence: 3 givenname: Sultan surname: Mirzoyev middlename: A. fullname: Mirzoyev, Sultan A. – sequence: 4 givenname: William surname: Edwards middlename: D. fullname: Edwards, William D. – sequence: 5 givenname: Joseph surname: Maleszewski middlename: J. fullname: Maleszewski, Joseph J. – sequence: 6 givenname: Margaret surname: Redfield middlename: M. fullname: Redfield, Margaret M.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/25552356$$D View this record in MEDLINE/PubMed
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Snippet	BACKGROUND—Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited... Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of...
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SubjectTerms	Aged Aged, 80 and over Algorithms Autopsy Cardiomegaly - epidemiology Cardiomegaly - pathology Cause of Death Comorbidity Coronary Artery Disease - epidemiology Coronary Artery Disease - pathology Coronary Vessels - pathology Diabetes Mellitus - epidemiology Echocardiography Electrocardiography Endomyocardial Fibrosis - epidemiology Endomyocardial Fibrosis - pathology Endomyocardial Fibrosis - physiopathology Female Heart - anatomy & histology Heart Failure - diagnosis Heart Failure - epidemiology Heart Failure - pathology Heart Failure - physiopathology Humans Immunohistochemistry Male Microvessels - pathology Myocardium - pathology Myocytes, Cardiac - pathology Organ Size Postmortem Changes Reference Values Stroke Volume
Title	Coronary Microvascular Rarefaction and Myocardial Fibrosis in Heart Failure With Preserved Ejection Fraction
URI	https://www.ncbi.nlm.nih.gov/pubmed/25552356 https://www.proquest.com/docview/1654699861 https://pubmed.ncbi.nlm.nih.gov/PMC4324362
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