Takotsubo cardiomyopathy and microvascular dysfunction: Another diagnostic criteria or predisposing factor?

Abstract

Objective To investigate potential associations of the PlA1/A2 polymorphism of the platelet glycoprotein IIIa (GPIIIa) gene with susceptibility to, and clinical expression of, giant cell arteritis (GCA). Methods One hundred forty patients with biopsy‐proven GCA who were residents of Reggio Emilia, Italy, and 241 population‐based healthy controls from the same geographic area were genotyped for the PlA1/A2 polymorphism of the platelet GPIIIa gene by molecular methods. The patients were divided into subgroups according to the presence or absence of polymyalgia rheumatica and cranial ischemic complications. The distribution of the PlA1/A2 genotype was investigated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results The distribution of the PlA1/A2 genotype differed significantly between GCA patients with and those without visual loss caused by anterior ischemic optic neuritis (P = 0.016, corrected P [Pcorr] = 0.048). The PlA2 allele was found significantly more frequently in GCA patients with anterior ischemic optic neuritis than in those without anterior ischemic optic neuritis (P = 0.023, Pcorr = 0.046, OR 2.4 [95% CI 1.2–4.8]). Homozygosity for the PlA2 allele was significantly more frequent among GCA patients with anterior ischemic optic neuritis than among those without (P = 0.019, Pcorr = 0.038, OR 7.1 [95% CI 1.64–30.6]). Cranial ischemic complications occurred in 8 of 19 patients (42.1%) receiving antiplatelet therapy, compared with 22 of 118 patients (18.6%) not receiving such therapy (P = 0.03, OR 3.2 [95% CI 1.1–8.8]). Conclusion Our findings show that A2/A2 homozygosity is associated with an increased risk of visual loss due to anterior ischemic optic neuritis in GCA patients. Antiplatelet therapy, however, was not effective in reducing the risk of ischemic events in this population of GCA patients.

Takotsubo Cardiomyopathy following a L2–L5 Laminectomy and Fusion In Situ with Bone Morphogenic Protein

“…Relative estrogen deficiency in postmenopausal women, resulting in some endothelial dysfunction, may be one of the key predisposing factors linking them to TC [8]. Other predisposing factors include pheochromocytoma, thyroid storm, anaphylaxis, exogenous epinephrine administration, stroke, sepsis, Addison's disease, Guillain-Barre syndrome, and illicit drug use and withdrawal [9–24].…”