Myocardial perfusion, oxidative metabolism, and free fatty acid uptake in patients with hypertrophic cardiomyopathy attributable to the Asp 175Asn mutation in the α-tropomyosin gene: A positron emission tomography study

[1]  M. Laakso,et al.  Cine MR imaging of myocardial contractile impairment in patients with hypertrophic cardiomyopathy attributable to Asp175Asn mutation in the alpha-tropomyosin gene. , 2005, Radiology.

[2]  M. Laakso,et al.  Genetics of hypertrophic cardiomyopathy in eastern Finland: few founder mutations with benign or intermediary phenotypes , 2004, Annals of medicine.

[3]  Lionel H. Opie,et al.  Heart Physiology: From Cell to Circulation , 2003 .

[4]  A. Blamire,et al.  Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy. , 2003, Journal of the American College of Cardiology.

[5]  H. Watkins,et al.  Hypertrophic cardiomyopathy:a paradigm for myocardial energy depletion. , 2003, Trends in genetics : TIG.

[6]  M. Laakso,et al.  Cardiac adrenergic activity is associated with left ventricular hypertrophy in genetically homogeneous subjects with hypertrophic cardiomyopathy. , 2003, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[7]  J. Seidman,et al.  Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly , 2002, Circulation.

[8]  D. Fatkin,et al.  Molecular mechanisms of inherited cardiomyopathies. , 2002, Physiological reviews.

[9]  A. Marian,et al.  The molecular genetic basis for hypertrophic cardiomyopathy. , 2001, Journal of molecular and cellular cardiology.

[10]  A. Marian Pathogenesis of diverse clinical and pathological phenotypes in hypertrophic cardiomyopathy , 2000, The Lancet.

[11]  U Ruotsalainen,et al.  Myocardial oxygen consumption is unchanged but efficiency is reduced in patients with essential hypertension and left ventricular hypertrophy. , 1999, Circulation.

[12]  H. Watkins,et al.  Properties of mutant contractile proteins that cause hypertrophic cardiomyopathy. , 1999, Cardiovascular Research.

[13]  G. Boivin,et al.  Mouse model of a familial hypertrophic cardiomyopathy mutation in alpha-tropomyosin manifests cardiac dysfunction. , 1999, Circulation research.

[14]  S. Nekolla,et al.  Oxidative metabolism of the transplanted human heart assessed by positron emission tomography using C-11 acetate. , 1999, The American journal of cardiology.

[15]  H. Watkins,et al.  Functional analyses of troponin T mutations that cause hypertrophic cardiomyopathy: insights into disease pathogenesis and troponin function. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[16]  M. Laakso,et al.  The cardiac beta-myosin heavy chain gene is not the predominant gene for hypertrophic cardiomyopathy in the Finnish population. , 1998, Journal of the American College of Cardiology.

[17]  Stephan G. Nekolla,et al.  Reproducibility of polar map generation and assessment of defect severity and extent assessment in myocardial perfusion imaging using positron emission tomography , 1998, European Journal of Nuclear Medicine.

[18]  Y. Magata,et al.  Impairment of BMIPP uptake precedes abnormalities in oxygen and glucose metabolism in hypertrophic cardiomyopathy. , 1998, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[19]  M. Senda,et al.  Mechanical efficiency in hypertrophic cardiomyopathy assessed by positron emission tomography with carbon 11 acetate. , 1997, American heart journal.

[20]  M. Senda,et al.  Myocardial blood flow and metabolism in patients with hypertrophic cardiomyopathy--a study with carbon-11 acetate and positron emission tomography. , 1997, Japanese circulation journal.

[21]  Y. Yonekura,et al.  Myocardial metabolic changes in hypertrophic cardiomyopathy. , 1996, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[22]  M. Christe,et al.  Altered glucose and fatty acid oxidation in hearts of the spontaneously hypertensive rat. , 1994, Journal of molecular and cellular cardiology.

[23]  V. Dilsizian,et al.  Regional systolic function, myocardial blood flow and glucose uptake at rest in hypertrophic cardiomyopathy. , 1993, The American journal of cardiology.

[24]  O. Ratib,et al.  Regional Myocardial Blood Flow and Glucose Utilization in Symptomatic Patients With Hypertrophic Cardiomyopathy , 1993, Circulation.

[25]  A. Lammertsma,et al.  Use of the left ventricular time-activity curve as a noninvasive input function in dynamic oxygen-15-water positron emission tomography. , 1992, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[26]  T. DeGrado Synthesis of 14 (R,S)‐[18F]fluoro‐6‐thia‐heptadecanoic acid (FTHA) , 1991 .

[27]  M. Phelps,et al.  Regional myocardial blood flow and metabolism at rest in mildly symptomatic patients with hypertrophic cardiomyopathy. , 1989, Journal of the American College of Cardiology.

[28]  N. Reichek,et al.  Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. , 1986, The American journal of cardiology.

[29]  C. Patlak,et al.  Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data. Generalizations , 1985, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[30]  C S Patlak,et al.  Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data , 1983, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[31]  V. Pike,et al.  Preparation of [1-11C]acetate--an agent for the study of myocardial metabolism by positron emission tomography. , 1982, The International journal of applied radiation and isotopes.

[32]  A. DeMaria,et al.  Recommendations Regarding Quantitation in M-Mode Echocardiography: Results of a Survey of Echocardiographic Measurements , 1978, Circulation.

[33]  T. Laitinen,et al.  Inducibility of life-threatening ventricular arrhythmias is related to maximum left ventricular thickness and clinical markers of sudden cardiac death in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the alpha-tropomyosin gene. , 2004, Journal of molecular and cellular cardiology.

[34]  A. Komatani,et al.  Heterogeneous myocardial distribution of iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) in patients with hypertrophic cardiomyopathy , 2004, European Journal of Nuclear Medicine.

[35]  Esko Vanninen,et al.  First-pass MR imaging in the assessment of perfusion impairment in patients with hypertrophic cardiomyopathy and the Asp175Asn mutation of the alpha-tropomyosin gene. , 2003, Radiology.

[36]  K. Fukuchi,et al.  Clinical analysis of myocardial perfusion and metabolism in patients with hypertrophic cardiomyopathy by single photon emission tomography and positron emission tomography. , 2001, Journal of cardiology.

[37]  A. Lammertsma,et al.  Myocardial blood flow: comparison of oxygen-15-water bolus injection, slow infusion and oxygen-15-carbon dioxide slow inhalation. , 1995, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.