Publications by authors named "Marcelo Puzzi"

Background: Mortality resulting from coronary artery disease (CAD) among women is a complex issue influenced by many factors that encompass not only biological distinctions but also sociocultural, economic, and healthcare-related components. Understanding these factors is crucial to enhance healthcare provisions. Therefore, this study seeks to identify the social and clinical variables related to the risk of mortality caused by CAD in women aged 50 to 79 years old in Paraná state, Brazil, between 2010 and 2019.

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Background: Guidelines recommend that in suspected stable coronary artery disease (CAD), a clinical (non-invasive) evaluation should be performed before coronary angiography.

Objective: We assessed the efficacy of patient selection for coronary angiography in suspected stable CAD.

Methods: We prospectively selected consecutive patients without known CAD, referred to a high-volume tertiary center.

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Introduction: Abnormal ventricular repolarization has been proposed as a marker of arrhythmogenesis, and cardiovascular morbidity and mortality. However, little is known about the influence of the interval between the peak and the end of the T wave (Tp-Te) on the inducibility of sustained ventricular arrhythmias (VA) in patients with Chagas disease (CD).

Methods: Using a case-control design, chagasics undergoing electrophysiological study (EPS) in the last three years were matched by age and sex.

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Atrial fibrillation (AF), gastroesophageal reflux disease (GERD) and hiatal hernias are commonly seen in clinical practice. GERD and hiatal hernias have been proposed to be a possible cause of AF. In this paper, we will briefly review GERD, AF and hiatal hernias, consider the available literature covering the association between these diseases and provide further insight into the topic in general.

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Hyperinsulinemia in obesity has been attributed to insulin oversecretion by pancreatic beta-cells. Beta-cells are equipped with cholinergic and adrenergic receptors; whereas overall acetylcholine action is to potentiate, catecholamines' effect is to inhibit glucose-induced insulin release (GIIR) via alpha2-adrenoceptor. However, it has been shown that beta-adrenergic agonists potentiate glucose response.

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