Sustancias de contraste para estudios radiográficos en cardiología intervencionista

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Abstract

Las sustancias de contraste (SC) radiográficas utilizadas en Cardiología se clasifican en: 1. Iónicas de osmolalidad muy alta (OMA); 2. No iónicas de osmolalidad no muy alta (ONMA); 3. Iónicas de ONMA; 4. No iónicas Isosmolares. Todas las SC de OMA son iónicas, monómeras y triyodadas: un anillo de benceno con 3 átomos de yodo. Las iónicas de ONMA son dímeras y hexayodadas: dos anillos de benceno y 6 átomos de yodo. Las no iónicas de ONMA son monómeras y triyodadas y las isosmolares dímeras y hexayodadas. Generalmente, las SC son más viscosas que la sangre sobre todo las dímeras. Todas son capaces de producir reacciones adversas incluyendo la muerte aunque son menos frecuentes con las de ONMA y con las Isosmolares, pero de uso limitado por su alto precio. No existe consenso acerca de la mejor SC ya que hay discrepancia en los ensayos clínicos aleatorizados.

Translated abstract

The radiographic contrast agents (CA) used in cardiology are classified into: 1. Very high osmolality ionic contrast agents (VHO); 2. Not very high osmolality nonionic contrast agents (NVHO); 3. NVHO ionic contrast agents; 4. Isoosmolar nonionic contrast agents. All the VHO contrast agents are ionic, monomeric and triiodinated: a ring of benzene with 3 iodine atoms. The NVHO ionic contrast agents are dimeric and hexoiodinated: 2 rings of benzene and 6 iodine atoms. The NVHO nonionic contrast agents are monomeric and triiodinated and the isosmolar contrast agents are dimeric and hexaiodinated. Generally, the CA are more viscuous than blood, mainly the dimeric ones. All of them may cause adverse reactions, including death, although they are less frequent with NVHO CA, but their use is limited because of its high price. There is no consensus about the best CA, since there are discrepancies in the randomized clinical trials.

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Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine.

Martin Tepel, Marcus Van Der Giet, Carola Schwarzfeld … (2000)

Radiographic contrast agents can cause a reduction in renal function that may be due to reactive oxygen species. Whether the reduction can be prevented by the administration of antioxidants is unknown. We prospectively studied 83 patients with chronic renal insufficiency (mean [+/-SD] serum creatinine concentration, 2.4+/-1.3 mg per deciliter [216+/-116 micromol per liter]) who were undergoing computed tomography with a nonionic, low-osmolality contrast agent. Patients were randomly assigned either to receive the antioxidant acetylcysteine (600 mg orally twice daily) and 0.45 percent saline intravenously, before and after administration of the contrast agent, or to receive placebo and saline. Ten of the 83 patients (12 percent) had an increase of at least 0.5 mg per deciliter (44 micromol per liter) in the serum creatinine concentration 48 hours after administration of the contrast agent: 1 of the 41 patients in the acetylcysteine group (2 percent) and 9 of the 42 patients in the control group (21 percent; P=0.01; relative risk, 0.1; 95 percent confidence interval, 0.02 to 0.9). In the acetylcysteine group, the mean serum creatinine concentration decreased significantly (P<0.001), from 2.5+/-1.3 to 2.1+/-1.3 mg per deciliter (220+/-118 to 186+/-112 micromol per liter) 48 hours after the administration of the contrast medium, whereas in the control group, the mean serum creatinine concentration increased nonsignificantly (P=0.18), from 2.4+/-1.3 to 2.6+/-1.5 mg per deciliter (212+/-114 to 226+/-133 micromol per liter) (P<0.001 for the comparison between groups). Prophylactic oral administration of the antioxidant acetylcysteine, along with hydration, prevents the reduction in renal function induced by contrast agents in patients with chronic renal insufficiency.

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Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity.

K-T Wei, S Kaul, P J H Poi … (2001)

During maximal hyperemia, capillaries provide the greatest resistance to flow. A major determinant of capillary resistance is viscosity. We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion. Maximal hyperemia was induced in 9 dogs using adenosine. Serum triglyceride levels were increased by incremental doses of Intralipid. A good correlation was noted between serum triglyceride levels and blood viscosity (r=0.82). Neither total coronary blood volume nor myocardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion. Myocardial vascular resistance (MVR) increased with increasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64). The decrease in hyperemic MBF was associated with a decrease in blood velocity (r=-0.56). These findings were confirmed with direct intravital microscopic observations in the mice cremaster muscle. Increasing lipid levels in a fully dilated normal coronary bed causes no change in large or small vessel dimensions. Instead, the increase in blood viscosity causes capillary resistance to rise, which attenuates hyperemic CBF. Therefore, the abnormal CBF reserve associated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function.