Clinical Medicine Insights. Cardiology最新文献

Introduction: Cardiothyreosis corresponds to the cellular effects of free thyroid hormones on the vascular wall and the myocardium. We aim to describe the clinical, para-clinical and therapeutic aspects of cardiothyreosis and to detail prognostic factors.

Methods: We conducted a descriptive retrospective study at the Endocrinology-Diabetology Department of the Hedi Chaker University Hospital in Sfax-Tunisia. We collected medical records of 100 patients with cardiothyreosis between January 1999 and December 2019. We included patients with cardiothyreosis who underwent adequate cardiac evaluation. We excluded patients with cardiac abnormalities related to conditions other than hyperthyroidism, patients who died and patients without cardiothyreosis.

Results: We included 100 adult patients (43 men and 57 women). The mean age was 49.3 ±12.9 years (20-79 years). The diagnosis of cardiothyreosis was concomitant with that of hyperthyroidism in 72% of cases. Weight loss and palpitations were the two most frequently reported signs in 91% of cases each. Hypertension was systolic in 15 patients. The average heart rate was 103.1 beats/min (52-182 bpm). The mean TSH and FT4 levels were 0.042 μIU/ml and 59.6 pmol/l, respectively. Rhythm disorders and heart failure were the most common cardiac complications with 81 and 56 cases, respectively. Cardiac ultrasound showed dilatation of the left atrium in 28.3% of patients. Pulmonary arterial hypertension was present in 43% of cases. 57 patients had been treated with benzylthiouracil at a mean dose of 157.45 mg/day. Radical treatment with radioactive iodine was indicated in 81 patients. The evolution of cardiothyreosis was favourable in 58 patients.

Conclusion: Cardiothyreosis is a serious complication of hyperthyroidism. Future prospective studies will be of great help to better characterise and manage cardiothyreosis.

Regional right ventricular dysfunction with akinesia of the mid-free wall with normal apical motion known as McConnell's sign is an under-reported echocardiographic finding in the setting of pulmonary embolism. We conducted a literature review and systematic analysis, while describing 2 cases of pulmonary embolism with findings of reverse McConnell's sign.

Tuberculosis is a common cause of pericarditis worldwide and has been associated with pericardial masses. Non-tuberculous mycobacteria are uncommonly associated with cardiac disease, having primarily been described in cases of endocarditis. Here we describe a case of an immunocompetent patient with Mycobacterium paragordonae infection causing pericarditis with a large effusion containing pericardial masses. The patient presented with chest pain, hypoxia and biochemical evidence of inflammation (CRP 216.1 mg/L). This report illustrates a rare case of pericarditis with pericardial masses associated with non-tuberculous mycobacteria and the first example of pericarditis associated with M. paragordonae.

For several decades, atherosclerosis has attracted the attention of researchers around the world. Even being a major cause of serious cardiovascular disease and events, atherosclerosis is still not fully understood. Despite the fact that the main players in the pathogenesis of atherosclerosis are well known, many mechanisms of their implementation and interactions remain unknown. The same can be said about the risk factors for atherosclerosis. Many of them are known, but exactly how they work remains to be seen. The main objective of this review is to summarize the latest data on sex as a biological variable in atherosclerosis in humans and animals; to determine what we do not still know about how sex affects the process of growth and complications of atherosclerosis. In this review, we summarized data on sex differences at 3 atherosclerotic aspects: inflammation, vascular remodeling, and plaque morphology. With all overviewed data, we came to the conclusion on the atheroprotective role of female sex.

Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood.

Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS.

Conclusions: OS (primarily from excess reactive oxygen species) and inflammation are present along the entire ASCVD pathophysiologic continuum. An expanded list of clinical and social ASCVD risk factors (including hypertension, obesity, diabetes, kidney disease, inflammatory diseases, substance use, poor nutrition, psychosocial stress, air pollution, race, and genetic ancestry) influence ASCVD largely through increased OS. Many risk factors exert a positive feedback mechanism to increase OS. One genetic risk factor, haptoglobin (Hp) genotype, is associated with higher ASCVD risk in diabetes and hypothesized to do the same in those with insulin resistance due to the Hp 2-2 genotype increasing OS.

Implications: Understanding the biological mechanisms of OS informs how these ASCVD risk factors relate to each other and compound ASCVD risk. Individualized ASCVD risk estimation should include a comprehensive, holistic perspective of risk factors to better address the clinical, social, and genetic influences of OS. Preventing and reducing OS is key to preventing ASCVD development or progression.