Current Cardiology Reviews - Volume 15, Issue 2, 2019

Percutaneous mitral valve repair is emerging as a reasonable alternative especially in those with an unfavorable surgical risk profile in the repair of mitral regurgitation. At this time, our understanding of the effects of underlying renal dysfunction on outcomes with percutaneous mitral valve repair and the effects of this procedure itself on renal function is evolving, as more data emerges in this field. The current evidence suggests that the correction of mitral regurgitation via percutaneous mitral valve repair is associated with some degree of improvement in cardiac function, hemodynamics and renal function. The improvement in renal function was more significant for those with greater renal dysfunction at baseline. The presence of Chronic Kidney Disease (CKD) in turn has been associated with poor long-term outcomes including increased mortality and hospitalization among patients who undergo percutaneous mitral valve repair. This was true regardless of the degree of improvement in GFR post repair advanced CKD. The adverse impact of CKD on long-term outcomes was consistent across all studies and was more prominent in those with GFR<30 mL/min/1.73 m². It is clear that from these contrasting evidences of improved renal function post mitral valve repair but poor long-term outcomes including increased mortality in patients with CKD, that proper patient selection for percutaneous mitral valve repair is key. There is a need to have better-standardized criteria for patients who should qualify to have percutaneous mitral valve replacement with Mitraclip. In this new era of percutaneous mitral valve repair, much work needs to be done to optimize long-term patient outcomes.

Introduction: Congestive Heart Failure (CHF) is a disorder in which the heart is unable to supply enough blood for body tissues. Since heart is an adaptable organ, it overcomes this condition by going under remodeling process. Considering cardiac myocytes are capable of proliferation after MI, stimulation of neovascularization as well as their regeneration might serve as a novel target in cardiac remodeling prevention and CHF treatment. Granulocyte Colony-Stimulating Factor (G-CSF), is a hematopoietic cytokine that promotes proliferation and differentiation of neutrophils and is involved in cardiac repair after MI. So far, this is the first review to focus on GCSF as a novel treatment for heart failure. Methods: We conducted a search of some databases such as PubMed for articles and reviews published between 2003 and 2017, with different keywords including “G-CSF”, “congestive heart failure”, “new therapies for CHF”, “filgrastim”, “in vivo study”. Results: GCSF exerts its beneficial effects on cardiac repair through either stem cell mobilization or direct angiogenesis promotion. All of which are capable of promoting cardiac cell repair. Conclusion: GCSF is a promising target in CHF-therapy by means of cardiac repair and remodeling prevention through multiple mechanisms, which are effective enough to be used in clinical practice.

Vascular calcification is a pathologic phenomenon consisting of calcium phosphate crystal deposition in the vascular walls. Vascular calcification has been found to be a risk factor for cardiovascular diseases, due to its correlation with cardiovascular events and mortality, and it has been associated with aging, diabetes, and chronic kidney disease. Studies of vascular calcification have focused on phosphate homeostasis, primarily on the important role of hyperphosphatemia. Moreover, vascular calcification has been associated with loss of plasma pyrophosphate, one of the main inhibitors of calcification, thus indicating the importance of the phosphate/pyrophosphate ratio. Extracellular pyrophosphate can be synthesized from extracellular ATP by ecto-nucleotide pyrophosphatase/ phosphodiesterase, whereas pyrophosphate is hydrolyzed to phosphate by tissuenonspecific alkaline phosphatase, contributing to the formation of hydroxyapatite crystals. Over the last decade, vascular calcification has been the subject of numerous reviews and studies, which have revealed new agents and activities that may aid in explaining the complex physiology of this condition. This review summarizes current knowledge about alkaline phosphatase and its role in the process of vascular calcification as a key regulator of the phosphate/pyrophosphate ratio.

Background: Acute Kidney Injury as a complication of cardiac catheterization is associated with increased length of hospital stay and mortality. In recent years, the use of the radial artery for cardiac catheterization is increasing in frequency. Objective: The objective of this concise review was to evaluate the method of cardiac access site and its impact on Acute Kidney Injury following cardiac catheterization. Methods: After a thorough search on Medline, Google Scholar and PubMed, we included all the literature relevant to Acute kidney injury following transradial and transfemoral cardiac catheterization. Results: While acute kidney injury was caused due to a variety of reasons, it was important to consider each case on an individual basis. We found a trend towards increased use of transradial approach in patients at high risk of developing kidney injury. However, limitations such as operator experience, anatomical challenges and so on do exist with this approach. Conclusion: Transradial access offers several advantages to a patient at high risk of acute kidney injury undergoing cardiac catheterization. Further large studies are needed to establish this trend in the years ahead.

The management of patients with shock is extremely challenging because of the myriad of possible clinical presentations in cardiogenic shock, septic shock and hypovolemic shock and the limitations of contemporary therapeutic options. The treatment of shock includes the administration of endogenous catecholamines (epinephrine, norepinephrine, and dopamine) as well as various vasopressor agents that have shown efficacy in the treatment of the various types of shock. In addition to the endogenous catecholamines, dobutamine, isoproterenol, phenylephrine, and milrinone have served as the mainstays of shock therapy for several decades. Recently, experimental studies have suggested that newer agents such as vasopressin, selepressin, calcium-sensitizing agents like levosimendan, cardiac-specific myosin activators like omecamtiv mecarbil (OM), istaroxime, and natriuretic peptides like nesiritide can enhance shock therapy, especially when shock presents a more complex clinical picture than normal. However, their ability to improve clinical outcomes remains to be proven. It is the purpose of this review to describe the mechanism of action, dosage requirements, advantages and disadvantages, and specific indications and contraindications for the use of each of these catecholamines and vasopressors, as well as to elucidate the most important clinical trials that serve as the basis of contemporary shock therapy.

Background: Observational studies in Asia show that dietary intake of soy isoflavones had a significant inverse association with coronary heart disease (CHD). A recent randomized controlled trial (RCT) of soy isoflavones on atherosclerosis in the US, however, failed to show their benefit. The discrepancy may be due to the much lower prevalence of S-equol producers in Westerners: Only 20-30% of Westerners produce S-equol in contrast to 50-70% in Asians. S-equol is a metabolite of dietary soy isoflavone daidzein by gut microbiome and possesses the most antiatherogenic properties among all isoflavones. Several short-duration RCTs documented that soy isoflavones improves arterial stiffness. Accumulating evidence shows that both atherosclerosis and arterial stiffness are positively associated with cognitive decline/dementia. Therefore, potentially, soy isoflavones, especially S-equol, are protective against cognitive decline/dementia. Methods/Results: This narrative review of clinical and epidemiological studies provides an overview of the health benefits of soy isoflavones and introduces S-equol. Second, we review recent evidence on the association of soy isoflavones and S-equol with CHD, atherosclerosis, and arterial stiffness as well as the association of atherosclerosis and arterial stiffness with cognitive decline/ dementia. Third, we highlight recent studies that report the association of soy isoflavones and S-equol with cognitive decline/dementia. Lastly, we discuss the future directions of clinical and epidemiological research on the relationship of S-equol and CHD and dementia. Conclusions: Evidence from observational studies and short-term RCTs suggests that S-equol is anti-atherogenic and improves arterial stiffness and may prevent CHD and cognitive impairment/ dementia. Well-designed long-term (≥ 2years) RCTs should be pursued.

Atrial fibrillation is the most common sustained cardiac arrhythmia. The scope and impact of atrial fibrillation are wide; it can affect cardiac function, functional status, and quality of life, and it confers a stroke risk. There are sex differences in atrial fibrillation across the scope of the disease process, from epidemiology and causative mechanisms to management and outcomes. The approach to management of atrial fibrillation differs between women and men, and there are sex differences in response to medical therapy and catheter ablation. There are many gaps in our knowledge of the gender differences in atrial fibrillation, and many opportunities for future research.

Several studies have focused on the deleterious consequences of Right Ventricular Apical (RVA) pacing on Left Ventricular (LV) function, mediated by pacing-induced ventricular dyssynchrony. Therapeutic strategies to reduce the detrimental consequences of RVA pacing have been proposed, that includes upgrading of RVA pacing to Cardiac Resynchronization Therapy (CRT), alternative Right Ventricular (RV) pacing sites, minimal ventricular pacing strategies, as well as atrial-based pacing. In developing countries, single chamber RV pacing still constitutes a majority of cases of permanent pacing, and assessment of the optimal RV pacing site is of paramount importance. In chronically-paced patients, it is crucial to maintain as close and normal LV physiological function as possible, by minimizing ventricular dyssynchrony, reducing the chances for heart failure and other complications to develop. This review provides an analysis of the deleterious immediate and long-term consequences of RVA pacing, and the most recent available evidence regarding improvements in pacing options and strategies to optimize LV diastolic and systolic function. Furthermore, the place of advanced echocardiography in the identification of patients with pacing-induced LV dysfunction, the potential role of a new predictor of LV dysfunction in RV-paced subjects, and the long- term outcomes of patients with RV septal pacing will be explored.