Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism: An experimental strain rate echocardiographic study

Josef Korinek, Peter C. Anagnostopoulos, Cristina D Pislaru, Petras P Dzeja, James B. Seward, Andre Terzic, Marek Belohlavek

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR (P <. 0001), end-systolic strain (P <. 0001), and peak SRs of myocardial early and late filling waves (P <. 0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.

Original languageEnglish (US)
Pages (from-to)1239-1244
Number of pages6
JournalJournal of the American Society of Echocardiography
Volume17
Issue number12
DOIs
StatePublished - Dec 2004

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Iodoacetamide
MB Form Creatine Kinase
Energy Metabolism
Troponin I
Creatine Kinase
Muscle Cells
Isoenzymes
Echocardiography
Sarcomeres
Energy Transfer
Contracture
Microscopy
Myocardium
Theoretical Models
Swine
Ischemia
Phosphates
Biopsy

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. CK activity in the iodoacetamide-perfused myocardium decreased to 0.5{\%} of the original value and was accompanied by a reduction in peak systolic SR (P <. 0001), end-systolic strain (P <. 0001), and peak SRs of myocardial early and late filling waves (P <. 0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.",
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T1 - Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism

T2 - An experimental strain rate echocardiographic study

AU - Korinek, Josef

AU - Anagnostopoulos, Peter C.

AU - Pislaru, Cristina D

AU - Dzeja, Petras P

AU - Seward, James B.

AU - Terzic, Andre

AU - Belohlavek, Marek

PY - 2004/12

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N2 - Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR (P <. 0001), end-systolic strain (P <. 0001), and peak SRs of myocardial early and late filling waves (P <. 0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.

AB - Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction. In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage. CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR (P <. 0001), end-systolic strain (P <. 0001), and peak SRs of myocardial early and late filling waves (P <. 0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change. Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.

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