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Titolo:
Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy
Autore:
Li, ST; Tack, CJ; Fananapazir, L; Goldstein, DS;
Indirizzi:
NINCDS, Clin Neuroradiol Sect, NIH, Bethesda, MD 20892 USA NINCDS Bethesda MD USA 20892 euroradiol Sect, NIH, Bethesda, MD 20892 USA Univ Nijmegen Hosp, Dept Internal Med, NL-6500 HB Nijmegen, Netherlands Univ Nijmegen Hosp Nijmegen Netherlands NL-6500 HB Nijmegen, Netherlands NHLBI, Cardiol Branch, Bethesda, MD 20892 USA NHLBI Bethesda MD USA 20892NHLBI, Cardiol Branch, Bethesda, MD 20892 USA
Titolo Testata:
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
fascicolo: 7, volume: 35, anno: 2000,
pagine: 1867 - 1873
SICI:
0735-1097(200006)35:7<1867:MPASII>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSITRON EMISSION TOMOGRAPHY; CORONARY VASODILATOR RESERVE; BLOOD-FLOW; HUMAN-HEART; SYMPTOMATIC PATIENTS; ALPHA-TROPOMYOSIN; NEURONAL UPTAKE; N-13 AMMONIA; NOREPINEPHRINE; MUTATIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Li, ST NINCDS, Clin Neuroradiol Sect, NIH, Bldg 10,Room 6N252,10 Ctr Dr,MSC-1620,Bethesda, MD 20892 USA NINCDS Bldg 10,Room 6N252,10 Ctr Dr,MSC-1620 Bethesda MD USA 20892
Citazione:
S.T. Li et al., "Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy", J AM COL C, 35(7), 2000, pp. 1867-1873

Abstract

OBJECTIVE This study assessed left ventricular myocardial perfusion and sympathetic innervation and function in hypertrophied and nonhypertrophied myocardial regions of patients with hypertrophic cardiomyopathy (HCM). BACKGROUND Patients with HCM often have clinical findings consistent with increased cardiac sympathetic outflow. Little is known about the status of sympathetic innervation specifically in hypertrophic regions. METHODS We conducted positron emission tomographic (PET) scanning using the perfusion imaging N-13-ammonia ((NH3)-N-13) and the sympathoneuronal imaging agent 6-[F-18]agent fluorodopamine (F-18-FDA) in 8 patients with HCM and 15 normal volunteers. Positron emission tomographic data corrected for attenuation and the partial volume effect were analyzed using the region-of-interest technique. RESULTS Myocardial (NH3)-N-13-derived radioactivity was similar in hypertrophied and nonhypertrophied regions of patients with HCM and in normal volunteers. At all time points, the F-18:N-13 ratio was lower in hypertrophied than in nonhypertrophied regions of HCM patients and in the F-18-FDA-derived radioactivity over time septum of normal volunteers (p = 0.001). Trends in were normal in both hypertrophied and nonhypertrophied myocardium. CONCLUSIONS The results are consistent with decreased neuronal uptake of catecholamines in hypertrophied but not in nonhypertrophied myocardium of patients with HCM. Other aspects of cardiac sympathoneural function seem normal. Decreased neuronal uptake could reflect local relative hypoinnervation,decreased numbers of neuronal uptake sites, or metabolic limitations on cell membrane transport. By enhancing norepinephrine delivery to adrenoceptors for a given amount of sympathetic nerve traffic, decreased neuronal uptake can explain major clinical features of HCM. (J Am Coll Cardiol 2000;35:1867-73) (C) 2000 by the American College of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 10:08:47