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  • Família ABC
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  • International Journal of Cardiovascular Sciences
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  • ABC Imagem Cardiovascular
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  1. Início
  2. Palavra-chave: Myocardium
IJCS
Review Article

Current Role of Myocardial Blood Flow Quantification with PET/CT in the Management of Coronary Artery Disease

Raffaele Giubbini et al. Elisa Milan

Abstract

The ability to measure myocardial blood flow (MBF) offers significant advantages in interpreting the phenomena underlying myocardial ischemia. Nuclear cardiology using hybrid positron emission tomography/computed tomography (PET/CT) systems allows accurate measurement of MBF using noninvasive techniques. Short- or very short-lived radiopharmaceuticals are now available, as well as standardized analytical models and software for clinical use. The incremental value of quantitative measurement of MBF in the pathophysiologic assessment of ischemic heart disease compared with anatomic variables or qualitative or semi-quantitative assessment by single-photon emission computed tomography (SPECT) with gamma-emitting tracers will be analyzed. The clinical role of MBF, myocardial flow reserve (MFR), and coronary flow capacity (CFC) will be clarified. However, the widespread availability of this technology is limited by the need for on-site cyclotron tracer production or the purchase of expensive radionuclide generators. The ability to obtain quantitative measurements using newer SPECT with cadmium-zinc-telluride technology and technetium-labeled tracers may offer the possibility of extending MBF measurement to most nuclear cardiology units in the near future.

  • Blood Circulation
  • Myocardium
  • Positron Emission Tomography Computed Tomography
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Creative Commons Attribution (CC BY) Creative Commons license
06/09/2024 DOI: 10.36660/ijcs.20240115
ABC
Original Article

Quantitative study of myocardial microcirculation in arterial hypertension due to progressive inhibition of NO synthesis

Leila Maria Meirelles Pereira et al. Carlos Alberto Mandarim-de-Lacerda

OBJECTIVE: To study the quantitative changes in intramyocardial blood vessels in rats in whom nitric oxide synthesis was inhibited. METHODS: Four groups of 10 rats were studied: control (C25 and C40) and L-NAME (L25 and L40). The animals L25 and L40 received L-NAME in the dosage of 50mg/kg/day for 25 and 40 days, respectively. On days 26 and 41 the animals in groups 25 and 40 were sacrificed. Analysis of the myocardium was performed using light microscopy and stereology. RESULTS: Arterial blood pressure and heart weight increased 74.5 and 57.8% after 25 days and 90.2 and 34.6% after 40 days, respectively. Comparing the L-NAME rats with the respective controls revealed that vessel volume density decreased 31.3% after 40 days, and the vessel length-density decreased 53.5% after 25 days and 25.7% after 40 days. The mean cross-sectional area of the vessels showed an important reduction of 154.6% after 25 days. The intramyocardial vessels decreased significantly in length- density in the L-NAME animals. The mean cross-sectional area of the vessels, which normally increases during heart growth between 25 and 40 days, showed a precocious increase by the 25th day in the L-NAME rats. This suggests an increase of the size of the heart, including blood vessels. CONCLUSION: The inhibition of the NO synthesis provokes rarefaction in the intramyocardial vessels that progresses with the time of administration of L-NAME.

  • Hypertension
  • Myocardium
  • nitric oxide
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Creative Commons Attribution (CC BY) Creative Commons license
08/01/2002 DOI: 10.1590/S0066-782X1999001100001

Como citar este artigo

EndNote RIS

Formato de Documento Eletrônico (Vancouver)

Giubbini R, Milan E. Current Role of Myocardial Blood Flow Quantification with PET/CT in the Management of Coronary Artery Disease. International Journal of Cardiovascular Sciences 2024;37:e20240115.

Formato de Documento Eletrônico (ABNT)

Giubbini, Raffaele; Milan, Elisa. Current Role of Myocardial Blood Flow Quantification with PET/CT in the Management of Coronary Artery Disease. International Journal of Cardiovascular Sciences, v. 37, e20240115, set. 2024.

Formato de Documento Eletrônico (APA)

Giubbini, R., & Milan, E. (2024). Current Role of Myocardial Blood Flow Quantification with PET/CT in the Management of Coronary Artery Disease. International Journal of Cardiovascular Sciences, 37, e20240115.

Formato de Documento Eletrônico (ISO)

Giubbini, Raffaele and Milan, Elisa. Current Role of Myocardial Blood Flow Quantification with PET/CT in the Management of Coronary Artery Disease. International Journal of Cardiovascular Sciences [online]. 2024, vol. 37, [citado 2026-10-14], e20240115. Disponível em: <https://journals.cardiol.br/article/current-role-of-myocardial-blood-flow-quantification-with-pet-ct-in-the-management-of-coronary-artery-disease-2/>. ISSN 2359-4802

EndNote RIS

Formato de Documento Eletrônico (Vancouver)

Pereira LMM, Mandarim-de-Lacerda CA. Quantitative study of myocardial microcirculation in arterial hypertension due to progressive inhibition of NO synthesis. Arquivos Brasileiros de Cardiologia 2002;73(5):413-8.

Formato de Documento Eletrônico (ABNT)

Pereira, Leila Maria Meirelles; Mandarim-de-Lacerda, Carlos Alberto. Quantitative study of myocardial microcirculation in arterial hypertension due to progressive inhibition of NO synthesis. Arquivos Brasileiros de Cardiologia, v. 73, n. 5, p. 413-418, jan. 2002.

Formato de Documento Eletrônico (APA)

Pereira, L. M. M., & Mandarim-de-Lacerda, C. A. (2002). Quantitative study of myocardial microcirculation in arterial hypertension due to progressive inhibition of NO synthesis. Arquivos Brasileiros de Cardiologia, 73(5), 413-418.

Formato de Documento Eletrônico (ISO)

Pereira, Leila Maria Meirelles and Mandarim-de-Lacerda, Carlos Alberto. Quantitative study of myocardial microcirculation in arterial hypertension due to progressive inhibition of NO synthesis. Arquivos Brasileiros de Cardiologia [online]. 2002, vol. 73, n. 5, [citado 2026-10-14], pp. 413-418. Disponível em: <https://journals.cardiol.br/article/quantitative-study-of-myocardial-microcirculation-in-arterial-hypertension-due-to-progressive-inhibition-of-no-synthesis-2/>. ISSN 0066-782X

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