Current Cardiology Reviews最新文献

Aortic valve insufficiency (AI) describes the pathology of blood leaking through the aortic valve to the left ventricle during diastole and is classified as mild, moderate or severe according to the volume of regurgitating blood. Intervention is required in severe AI when the patient is symptomatic or when the left ventricular function is impaired. Aortic valve replacement has been considered the gold standard for decades for these patients, but several repair techniques have recently emerged that offer exceptional stability and long-term outcomes. The appropriate method of repair is selected based on the mechanism of AI and each patient's anatomic variations. This review aims to describe different pathologies of AI based on its anatomy, along with the different surgical techniques of aortic repair and their reported results.

Catheter ablation is an effective and durable treatment option for patients with atrial fibrillation (AF). Ablation outcomes vary widely, with optimal results in patients with paroxysmal AF and diminishing results in patients with persistent or long-standing persistent AF. A number of clinical factors including obesity, hypertension, diabetes, obstructive sleep apnea, and alcohol use contribute to AF recurrence following ablation, likely through modulation of the atrial electroanatomic substrate. In this article, we review the clinical risk factors and the electro-anatomic features that contribute to AF recurrence in patients undergoing ablation for AF.

Heart rate is an important indicator of health and disease and the modulation of heart rate can help to improve cardiovascular outcomes. Besides β-blockers, Ivabradine is a wellestablished heart rate modulating drug that reduces heart rate without any hemodynamic effects. This consensus document was developed with the help of expert opinions from cardiologists across India on effective heart rate management in routine clinical practice and choosing an appropriate Ivabradine-based therapy considering the available scientific data and guideline recommendations. Based on the discussion during the meetings, increased heart rate was recognized as a significant predictor of adverse cardiovascular outcomes among patients with chronic coronary syndromes and heart failure with reduced ejection fraction making heart rate modulation important in these subsets. Ivabradine is indicated in the management of chronic coronary syndromes and heart failure with reduced ejection fraction for patients in whom heart rate targets cannot be achieved despite guideline-directed β-blocker dosing or having contraindication/intolerance to β-blockers. A prolonged release once-daily dosage of Ivabradine can be considered in patients already stabilized on Ivabradine twice-daily. Ivabradine/β-blocker fixed-dose combination can also be considered to reduce pill burden. Two consensus algorithms have been developed for further guidance on the appropriate usage of Ivabradine-based therapies. Ivabradine and β-blockers can provide more pronounced clinical improvement in most chronic coronary syndromes and heart failure with reduced ejection fraction patients with a fixed-dose combination providing an opportunity to improve adherence.

Heart failure (HF) is a global healthcare burden and a leading cause of morbidity and mortality worldwide. Type 2 diabetes mellitus (T2DM) appears to be one of the major risk factors that significantly worsen HF prognosis and increase the risk of fatal cardiovascular outcomes. Despite a great knowledge of pathophysiological mechanisms involved in HF development and progression, hospitalization rates in patients with HF and concomitant T2DM remain elevated. In this review, we discuss the complex interplay between systemic neurohumoral regulation and local cardiac mechanisms participating in myocardial remodeling and HF development in T2DM with special attention to cardiomyocyte energy metabolism, mitochondrial function and calcium metabolism, cardiomyocyte hypertrophy and death, extracellular matrix remodeling.

Introduction: Heart failure (HF) is a leading cause of death worldwide. The global prevalence of heart failure is projected to increase rapidly in the coming decades, and significant attention has turned to improving biomarker-based risk prediction of incident HF. This paper aimed to qualitatively and quantitatively evaluate the evidence associating levels of galectin-3 with the risk of incident HF.

Methods: A review of PUBMED-indexed peer-reviewed literature was performed. Nine studies met the inclusion criteria, and all nine had data eligible for conversion and pooling. A randomeffects meta-analysis was performed using hazard ratios and 95% confidence intervals from a minimally adjusted model, a further adjusted model, and from subgroups within the further-adjusted model.

Results: The minimally-adjusted model provided an HR of 1.97 (95% CI 1.74-2.23) when comparing the top quartile of log-gal-3 to the bottom quartile. The further-adjusted model provided an HR of 1.32 (95% CI 1.21-1.44) for the same comparison. The positive, significant association was conserved during sensitivity analysis.

Conclusion: There is a significant positive association between circulating galectin-3 and the risk of incident heart failure. Given the complex mechanistic relationship between galectin-3 and cardiovascular pathophysiology, further investigation is recommended for the possible implementation of galectin-3 into clinical risk prediction models.

The acute coronary syndrome is one of the commonest life-threatening illnesses. It encompasses the clinical spectrum of acute myocardial ischemia and includes unstable angina and acute myocardial infarction both with and without ST segment elevation. The acute coronary syndrome can be attributed to a significant hemodynamic insult that leads to atherosclerosis of the epicardial coronary arteries. The main causative risk factors, such as obesity, smoking, and alcohol intake, increase the burden of acute coronary syndrome. Owing to an increase in the utilization of antioxidants, the antioxidant capacity decreases concerning the scavenging of lipid peroxides. Moreover, the thyroid hormones are important regulators of the expression of cardiac genes, and many of the cardiac manifestations of thyroid dysfunction are associated with alterations in triiodothyronine- mediated gene expression. Cardiovascular signs and symptoms of thyroid disease are among the most acute clinically relevant findings that occur in combination with both hypothyroidism and hyperthyroidism. By understanding the cellular mechanism of the action of thyroid hormones on the heart and cardiovascular system, it is possible to explain rhythm disturbances and alterations in cardiac output, blood pressure, cardiac contractility, and vascular resistance that result from thyroid dysfunction. Oxidative stress is thereby induced, together with a decrease in antioxidant capacity for overcoming oxidative stress, which leads to endothelial dysfunction, subsequent atherosclerosis, and, ultimately, acute myocardial infarction. The implications for the identification of the effects of thyroid disease on acute myocardial infarction include the observation that restoration of normal thyroid function repeatedly reverses abnormalities in cardiovascular hemodynamics.

Chimeric antigen receptor (CAR) T-cell therapy has shown remarkable efficacy in treating highly refractory and relapsing hematological malignancies in pediatric and adult patients. However, this promising therapy is limited by severe and potentially life-threatening toxicities. Cytokine release syndrome (CRS) is the most commonly observed of these toxicities. The cardiovascular manifestations of CRS include tachycardia, hypotension, left ventricular dysfunction, arrhythmias, troponin elevation, cardiogenic shock, and pulmonary edema. Recent data suggest that cardiotoxicities may be transient and reversible in younger patients with few cardiac comorbidities; however, cardiotoxicities may be fatal in older patients with significant cardiac risk factors. The literature remains sparse regarding long-term cardiotoxicities associated with CAR-T cell therapy. Furthermore, consensus guidelines for monitoring and prevention of cardiotoxicities remain illdefined. Therefore, this review will detail the cardiovascular toxicities of CAR T-cell therapy seen in clinical trials and observational studies, summarize treatment approaches for CRS, outline the currently adopted surveillance protocols for CAR T-cell associated cardiotoxicity, and explore the future directions of research in this rapidly emerging field.

Tricuspid regurgitation is a cardiac valvular anomaly that consists of the return of blood to the right atrium during systole due to incomplete valve closure. This structure can be visualized on ultrasound between 11 and 14 weeks of gestation in most cases. Despite being a common finding, even in healthy fetuses, the presence of tricuspid regurgitation may be associated with chromosomal and structural abnormalities. The evaluation of tricuspid flow and the presence of regurgitation on first-trimester ultrasound has shown promising results regarding its role in the early detection of aneuploidies, congenital heart defects, and other adverse perinatal outcomes. This review article aims to demonstrate the importance of tricuspid regurgitation as a secondary marker, and consequently, significant benefits of its early detection when added to the combined first-trimester screening. Its value will be discussed, namely its sensitivity and specificity, alone and together with other current markers in the fetal assessment performed in the first-trimester ultrasound.

Introduction: COVID-19 is often seen presenting with a myriad of signs and symptoms of multiorgan dysfunction including arterial dissection.

Methods: Various theories have been proposed such as endothelial dysfunction triggered by hyperinflammatory response that results in rupture of atherosclerotic plaque and subsequent dissection.

Results: However, the exact incidence is unknown and only case reports and case series have been published till date.

Conclusion: Here we carried out a systematic analysis of published case reports/series related to dissection of the aorta, coronary, cerebral, vertebral, cervical, renal, and splanchnic arteries.