Achados tomográficos incidentais de calcificações coronarianas: um estudo de prevalência na região sul do Brasil / Incidental tomographic findings of coronary artery calcifications: a prevalence study in southern Brazil

Fundamento: As calcificações de artérias coronárias (CAC) mostram-se como fator preditivo de doenças cardiovasculares (DCV). A tomografia computadorizada (TC) de tórax com protocolo de aquisição de baixa dose apresenta acurácia na identificação de CAC e propicia achados incidentais dessas calcificações, que são comumente negligenciados. Este estudo analisará a prevalência de achados incidentais de calcificação em artérias coronárias em indivíduos não cardiopatas submetidos à TC de tórax. Métodos: Estudo transversal consecutivo de caráter analítico e descritivo. Foram incluídos indivíduos de ambos os sexos que realizaram TC de tórax por encaminhamento, acima de 18 anos e não cardiopatas. A coleta de dados foi realizada por meio de prontuários e ficha de anamnese auto aplicada. As variáveis referentes às CAC e à extensão do comprometimento foram obtidas a partir da reavaliação das imagens de TC de tórax disponíveis no sistema da instituição. Os exames foram anonimizados e avaliados por dois médicos radiologistas experientes. Considerou-se como estatisticamente significativo p≤0,05. Resultados: Foram analisados 397 exames. Encontrou-se prevalência de calcificações em 176 (44%) dos casos. A existência dessas calcificações coronárias está relacionada à idade (p<0,001). As calcificações possuem relação com o sexo (p = 0,03) com maior razão de chance de desenvolvimento em homens (odds ratio [OR] = 1,55). O tabagismo (p<0,001), o sedentarismo (p<0,001), a hipertensão arterial sistêmica (p<0,001), o diabetes mellitus (p = 0,04) e as dislipidemias (p<0,001) mostraram associação positiva. Conclusão: A prevalência de achados incidentais de CAC foi de 44%; variam em maior número entre leve e grave; maior razão de chance no sexo masculino e aumento da prevalência com a idade. Portanto, a TC de tórax mostra-se um efetivo método para avaliar as CAC, e juntamente com a história clínica do paciente pode ser utilizada para medir os fatores de risco para doenças cardiovasculares e intervir no desfecho do quadro.(AU)

Introduction: Coronary artery calcifications (CAC) are shown to be a predictive factor of cardiovascular diseases. Computed tomography (CT) of the chest with a low-dose acquisition protocol is accurate in identifying CAC and provides incidental findings of these calcifications, which are commonly overlooked. This study will analyze the prevalence of incidental findings of calcification in coronary arteries in non-cardiac individuals undergoing chest CT. Methods: Consecutive cross-sectional study of an analytical and descriptive nature. Individuals of both genders who underwent chest CT by referral, over 18 years of age and without heart disease were included. Data collection was carried out using medical records and a self-applied anamnesis form. The variables referring to the CAC and the extension of the impairment were obtained from the reassessment of the chest CT images available in the institution's system. The exams were anonymized and evaluated by two experienced radiologists. P≤0.05 was considered statistically significant. Results: 397 exams were analyzed. A prevalence of calcifications was found in 176 (44%) of the cases. The existence of these coronary calcifications is related to age (p<0.001). Calcifications are related to gender (p = 0.03) with a higher odds ratio of development in men (odds ratio [OR] = 1.55). Smoking (p<0.001), sedentary lifestyle (p<0.001), systemic arterial hypertension (p<0.001), Diabetes Mellitus (p = 0.04), and dyslipidemia (p<0.001) showed a positive association. Conclusion: The prevalence of incidental CAC findings was 44%; vary in greater numbers between mild and severe; higher odds ratio in males and increased prevalence with age. Therefore, chest CT proves to be an effective method to assess CAC, and together with the patient's clinical history, it can be used to measure risk factors for CVD and intervene in the outcome of the condition.(AU)

Red wine consumption, coronary calcification, and long-term clinical evolution

Coronary artery calcification (CAC) is associated with atherosclerotic complications. However, elevated CAC may not always imply a worse prognosis. Herein, we report the clinical evolution of long-term red wine (RW) drinkers in relation to CAC. We followed 200 healthy male habitual RW drinkers and compared them to 154 abstainers for a period of 5.5 years. The initial evaluation included coronary computed tomography angiography (CTA), clinical, demographics, and laboratory data. CAC was quantified by the Agatston score. The follow-up process was conducted by telephone calls and/or hospital record review. The composite end-point of total death, acute myocardial infarction (AMI), or coronary revascularization (or major adverse cardiac event - MACE) was assessed. The RW drinkers ingested 28.9±15 g of alcohol/day for 23.4±12.3 years. They had higher high-density lipoprotein and low-density lipoprotein, but lower C-reactive protein than abstainers. Age, total cholesterol, triglycerides, glucose, and liver enzymes were similar. History of diabetes was lower among drinkers, but other risk factors were similar. However, drinkers had higher CAC than abstainers; the mean value was 131.5±362 in drinkers vs 40.5±320 in abstainers (P<0.001). The median and interquartile range were 15 (0.0-131.5) in RW drinkers and 1 (0.0-40.5) in abstainers (P=0.003). During the follow-up, MACE was significantly lower in drinkers than in abstainers, despite their higher CAC. The difference was driven mainly by AMI (0 vs 6; P<0.03). Greater CAC values in this setting did not predict worse prognosis. A possible underlying mechanism is lesion calcification, which leads to plaque stabilization and less clinical events.

Vascular calcification in atherosclerosis: potential roles of macrophages and non-coding micro-RNAs / Calcificación vascular en aterosclerosis: posibles funciones de macrófagos y micro-ARNs no codificantes

Coronary heart disease, a leading cause of death in western societies, is caused by the presence of atherosclerotic plaques in the coronary arteries. Calcification is a frequent complication of atherosclerotic plaques, and often a contributing factor to their instability and rupture. Endothelial cells, smooth muscle cells and plaque macrophages, all contribute to the calcification process, which is reminiscent of that underlying bone formation. In particular, the role of macrophages in calcification has long been recognized, but whether or not distinct macrophage subsets ­v.g., M1 or inflammatory, and M2 or antinflammatory have specific functions in osteogenic signaling within the context of plaque calcification remains poorly understood. Over the past few years, accumulated evidence has revealed novel roles of non-coding micro-RNAs (miRs) in atherorelevant functions of macrophages and in mechanisms linked to macrophage divergence into different subtypes. In this article we discuss some salient findings on potential roles of miRs in vascular calcification, with focus on those miRs that have also been associated to macrophage differentiation, and speculate on their potential relation to M1 and M2 macrophages in the context of calcification of atherosclerotic plaques. (AU)

La enfermedad cardíaca coronaria, principal causa de muerte en occidente, es causada por la presencia de placas ateroscleróticas en las arterias coronarias. La presencia de depósitos de calcificación es una complicación frecuente de la placa, y puede contribuir a la inestabilidad y ruptura de la misma. El proceso de calcificación de la placa es similar al que ocurre en hueso, y contribuyen al mismo, mecanismos dependientes de células endoteliales, células musculares lisas y macrófagos, células que están presentes en todas las etapas de desarrollo de la placa aterosclerótica. El rol de los macrófagos en la calcificación de la placa se conoce desde hace tiempo, pero la contribución de los distintos tipos de macrófagos ­por ejemplo, M1 o tipo inflamatorio, y M2 o tipo antiinflamatorio a mecanismos de señalización osteogénica en dicho contexto aún no se conoce. Recientemente varios trabajos experimentales han revelado la existencia de nuevos roles de micro-ARNs no codificantes (miRs) en varias funciones de los macrófagos que son de relevancia en el proceso aterogénico, como así también en mecanismos relacionados a la diferenciación de macrófagos en subtipos específicos. En este artículo discutimos algunos de los hallazgos más importantes sobre posibles nuevos roles de miRs en calcificación vascular, poniendo énfasis en aquellos miRs que han sido también asociados a la diferenciación de macrófagos, y especulamos acerca de su posible relación con macrófagos M1 y M2 en el contexto de la calcificación de la placa aterosclerótica. (AU)

Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis

Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (controls) or a 0.5% cholesterol (chol) diet+104 IU/day vitamin D2 (vitD) for 12 weeks, and assigned to treatment with water (vehicle, n=20), 0.12 mmol·kg-1·day-1 LA (n=11) or 0.1 mmol·kg-1·day-1 tempol (n=15). Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.