Butane-induced acute global myocardial ischemia without coronary artery pathology

ABSTRACT The case report describes a case of acute myocardial ischemia precipitated by propane butane inhalation. The dependency of this substance around the world is still moderate but is increasing due to the easy availability of the substance and the facility with which the effects can be concealed. The toxicity of the substance is significant; affecting the heart, the brain and the liver. The most common outcome is sudden death. In this article, we describe a survivor after an episode of acute poisoning and his interesting cardiac pathology.

Reduced Platelet miR-223 Induction in Kawasaki Disease Leads to Severe Coronary Artery Pathology Through a miR-223/PDGFRβ Vascular Smooth Muscle Cell Axis

Rationale: Kawasaki disease (KD) is an acute vasculitis of early childhood that can result in permanent coronary artery structural damage. The cause for this arterial vulnerability in up to 15% of patients with KD is unknown. Vascular smooth muscle cell dedifferentiation play a key role in the pathophysiology of medial damage and aneurysm formation, recognized arterial pathology in KD. Platelet hyperreactivity is also a hallmark of KD. We recently demonstrated that uptake of platelets and platelet-derived miRNAs influences vascular smooth muscle cell phenotype in vivo. Objective: We set out to explore whether platelet/vascular smooth muscle cell (VSMC) interactions contribute to coronary pathology in KD. Methods and Results: We prospectively recruited and studied 242 patients with KD, 75 of whom had documented coronary artery pathology. Genome-wide miRNA sequencing and droplet digital PCR demonstrated that patient with KD platelets have significant induction of miR-223 compared with healthy controls (HCs). Platelet-derived miR-223 has recently been shown to promote vascular smooth muscle quiescence and resolution of wound healing after vessel injury. Paradoxically, patients with KD with the most severe coronary pathology (giant coronary artery aneurysms) exhibited a lack of miR-223 induction. Hyperactive platelets isolated from patients with KD are readily taken up by VSMCs, delivering functional miR-223 into the VSMCs promoting VSMC differentiation via downregulation of PDGFRβ (platelet-derived growth factor receptor β). The lack of miR-223 induction in patients with severe coronary pathology leads to persistent VSMC dedifferentiation. In a mouse model of KD ( Lactobacillus casei cell wall extract injection), miR-223 knockout mice exhibited increased medial thickening, loss of contractile VSMCs in the media, and fragmentation of medial elastic fibers compared with WT mice, which demonstrated significant miR-223 induction upon Lactobacillus casei cell wall extract challenge. The excessive arterial damage in the miR-223 knockout could be rescued by adoptive transfer of platelet, administration of miR-223 mimics, or the PDGFRβ inhibitor imatinib mesylate. Interestingly, miR-223 levels progressively increase with age, with the lowest levels found in <5-year-old. This provides a basis for coronary pathology susceptibility in this very young cohort. Conclusions: Platelet-derived miR-223 (through PDGFRβ inhibition) promotes VSMC differentiation and resolution of KD induced vascular injury. Lack of miR-223 induction leads to severe coronary pathology characterized by VSMC dedifferentiation and medial damage. Detection of platelet-derived miR-223 in patients with KD (at the time of diagnosis) may identify patients at greatest risk of coronary artery pathology. Moreover, targeting platelet miR-223 or VSMC PDGFRβ represents potential therapeutic strategies to alleviate coronary pathology in KD. Graphic Abstract: A graphic abstract is available for this article.

Biomarker levels, left ventricular dysfunction, and severity of coronary pathology in elderly patients with coronary heart disease

Aim. To assess the levels of selected biomarkers and the type of left ventricular (LV) dysfunction in geriatric patients, in regard to their age, gender, and the severity of coronary artery pathology. Material and methods. In total, 135 geriatric patients with coronary heart disease (CHD) were examined. The diagnostic algorithm was based on the results of coagulogram, blood biochemistry, measurement of C-reactive protein (CRP) levels, treadmill test, echocardiography (EchoCG), coronary angiography (CA), and LV ventriculography (LVG). Results. Decreased hematocrit levels (p<0,05), increased levels of urea (p<0,05) and creatinine (p<0,05), reduced LV ejection fraction (p<0,05), increased end-diastolic volume (p<0,05), as well as restrictive type of LV dysfunction, were among age-dependent determinants of angina progression in elderly patients. The major determinant of ischemia severity was multi-vessel coronary pathology, manifested in higher angina classes, reduced exercise capacity (p<0,05), and impaired local LV contractility (p<0,05). Conclusion. To objectively assess the severity of clinical course of CHD in elderly patients, the following data should be taken into account: hematocrit and CRP levels, increased levels of creatinine and urea, and the results of EchoCG, CA, and LVG.