Current Cardiology Reviews - Volume 19, Issue 2, 2023

Congenital heart disease (CHD) is the most common congenital anomaly in newborns. Current treatment for cyanotic CHD largely relies on the surgical intervention; however, significant morbidity and mortality for patients with CHD remain. Recent research to explore new avenues of treating CHD includes the utility of stem cells within the field. Stem cells have since been used to both model and potentially treat CHD. Most clinical applications to date have focused on hypoplastic left heart syndrome. Here, we examine the current role of stem cells in CHD and discuss future applications within the field.

Atrial fibrillation (AF) is the commonest arrhythmia in clinical practice and is associated with increased morbidity and mortality. Various predictive scores for new-onset AF have been proposed, but so far, none have been widely used in clinical practice. CHARGE-AF score was developed from a pooled diverse population from three large cohorts (Atherosclerosis Risk in Communities study, Cardiovascular Health Study and Framingham Heart Study). A simple 5-year predictive model includes the variables of age, race, height, weight, systolic and diastolic blood pressure, current smoking, use of antihypertensive medication, diabetes mellitus, history of myocardial infarction and heart failure. Recent studies report that the CHARGE-AF score has good discrimination for incident AF and seems to be a promising prediction model for this arrhythmia. New screening tools (smartphone apps, smartwatches) are rapidly developing for AF detection. Therefore, the wide application of the CHARGE-AF score in clinical practice and the upcoming usage of mobile health technologies and smartwatches may result in better AF prediction and adequate stroke prevention, especially in high-risk patients.

Background: Heart failure (HF) is predominately a chronic disease. There are overlaps in HF and chronic disease research and care. Chronic disease and HF research are conducted with multiple goals. The overarching goal is “optimized patient outcomes at maximum costeffectiveness”. However, observations on patients can come with many variables; thus, we see differences in clinical translation. This document discusses an argument for three important gaps common to HF and chronic disease, i.e., screening, self-management, and patient-reported outcomes (PRO), and provides a glance of how it could fit into the evidence tree. Pertinent arguments for a framework for health services and models of care are provided as a prelude to future consensus. Methodology: 1) A preliminary literature review to identify a taxonomy for cardiovascular research, and 2) a review of the published literature describing the translation of research studies into clinical practice for cardiovascular disorders. A spectrum from observational to large randomized controlled trials to post-marketing studies were identified. Discussion: A brief discussion on traditional research and differences focusing on screening, mixed methods research concepts, and chronic diseases models of care. Six steps to facilitate this: 1) Research design; 2) Research application (translation) i. routine ii. challenges; 3. Transforming research to translational level; 4. Funding and infrastructure; 5. Clinical Centres of Research Excellence (CCRE) and collaboration; 6. Governance and cost-effectiveness. Conclusion: Implementation research that aims to link research findings to improved patient outcomes in an efficient and effective way is a neglected area. Skills required to perform implementation research are complex. Ways to maximize translational impacts for chronic disease research to clinical practice are described in a HF context.

Due to the fact that atherosclerotic cardiovascular diseases (CVDs) dominate in the structure of morbidity, disability and mortality of the population, the study of the risk factors for the development of atherosclerotic CVDs, as well as the study of the underlying pathogenetic mechanisms thereof, is the most important area of scientific research in modern medicine. Understanding these aspects will allow improving the set of treatment and preventive measures and activities. One of the important risk factors for the development of atherosclerosis, which has been actively studied recently, is air pollution with fine particulate matter (PM 2.5). According to clinical and epidemiological data, the level of air pollution with PM 2.5 exceeds the normative indicators in most regions of the world and is associated with subclinical markers of atherosclerosis and mortality from atherosclerotic CVDs. The aim of this article is to systematize and discuss in detail the role of PM 2.5 in the development of atherosclerosis and myocardial damage with the consideration of epidemiological and pathogenetic aspects. Materials and Methods: This narrative review is based on the analysis of publications in the Medline, PubMed, and Embase databases. The terms "fine particles" and "PM 2.5" in combination with "pathophysiological mechanisms," "cardiovascular diseases", "atherosclerosis", "cardiac troponins", "myocardial damage" and "myocardial injury" were used to search publications. Conclusion: According to the conducted narrative review, PM 2.5 should be regarded as the significant risk factor for the development of atherosclerotic CVDs. The pro-atherogenic effect of fine particulate matter is based on several fundamental and closely interrelated pathophysiological mechanisms: endothelial dysfunction, impaired lipid metabolism, increased oxidative stress and inflammatory reactions, impaired functioning of the vegetative nervous system and increased activity of the hemostatic system. In addition, PM 2.5 causes subclinical damage to cardiac muscle cells by several mechanisms: apoptosis, oxidative stress, decreased oxygen delivery due to coronary atherosclerosis and ischemic damage of cardiomyocytes. Highly sensitive cardiac troponins are promising markers for detecting subclinical myocardial damage in people living in polluted regions.

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.

Background: Hypertension is a chronic, multifactorial clinical condition characterized by sustained high blood pressure levels. It is often associated with functional-structural alterations of target organs, which include heart, brain, kidneys, and vasculature. Objective: This study highlights the recent correlation between the immune system and hypertension and its repercussions on target-organ damage. Methods: The descriptors used for the search of the study were "hypertension", "immunity", and "target organs". The methodology of the study followed the main recommendations of the PRISMA statement. Results: The damage to the vasculature arises mainly from the migration of T cells and monocytes that become pro-inflammatory in the adventitia, releasing TNF-α, IFN-γ, and IL-17, which induce endothelial damage and hinder vascular relaxation. In the renal context, the inflammatory process associated with hypertension culminates in renal invasion by leukocytes, which contribute to the injury of this organ by mechanisms of intense sympathetic stimulation, activation of the reninangiotensin system, sodium retention, and aggravation of oxidative stress. In the cardiac context, hypertension increases the expression of pro-inflammatory elements, such as B, T, and NK cells, in addition to the secretion of IFN-γ, IL-17, IL-23, and TNF-α from angiotensin II, reactive oxygen species, and aldosterone. This pro-inflammatory action is also involved in brain damage through SphK1. In view of the above, the participation of the immune system in hypertension-induced injuries seems to be unequivocal. Conclusion: Therefore, understanding the multifactorial mechanisms related to hypertension will certainly allow for more efficient interventions in this condition, preventing target organ damage.

Introduction: Peripartum cardiomyopathy (PPCM) is a rare but potentially lifethreatening disease, defined as idiopathic cardiomyopathy occurring towards the end of pregnancy or in the months following delivery, abortion or miscarriage. We aim to raise awareness of this condition and give an overview of current knowledge as well as an insight and comparison of clinical trials focusing on randomized controlled trials. Material and Methods: Systematic literature searches were conducted using PubMed up to December 2021. Studies published involving clinical trials and interventions in women with PPCM after 1970 were selected. Results: Randomized controlled trials have shown that the addition of Bromocriptine to standardized heart failure therapy improves outcome in terms of recovery of Left Ventricular Ejection Fraction (LVEF), symptoms and death. Bromocriptine 2.5 mg twice daily for two weeks followed by 2.5 mg once daily for six weeks had the best trend and outcome. The addition of Levosimendan to standardized heart failure therapy had no effect, whereas the addition of Selenium improved heart failure symptoms but did not reduce risk in terms of unrecovered LVEF or death. One prospective study showed potential usage of TNF-alfa inhibitors, but was never tried in a randomized clinical trial. Conclusion: PPCM is a rare and potentially fatal disease. New insights on pathophysiology, genetics and clinical studies, particularly randomized controlled trials, have shown that the addition of Bromocriptine has a beneficial effect in terms of improved LVEF and death. However, some clinical studies have shown promising results using anti-inflammatory pharmacological agents with an improvement in LVEF. We suggest that targeting an anti-inflammatory route may prove beneficial in patients with PPCM. However, further research is highly warranted.

Background: A systematic review was performed to deliver a critical view of clinical and research practice on hypertrophic cardiomyopathy (HCM) in Saudi Arabia. Scopus, PubMed, and Google Scholar databases were searched for original articles reporting clinical and/or imaging findings among HCM patients in Saudi Arabia. Of 559 records identified, 3 studies and 1 abstract were included, involving 169 patients. Methods: The mean age ranged between 40and 56 years, up to 93.3% were males. A family history of HCM was reported in one study (5%), and sudden cardiac death was investigated in two studies (9% and 13%). Dyspnea was the most frequent symptom (60-68.7%) reported, followed by chest pain (12.5%-73.3%). Results: Regarding complications, atrial fibrillation was reported among 0-25% of the patients, mitral regurgitations among 13.3-50%, and ventricular tachycardia among 5-12.5%. Imaging parameters were inadequately documented and suggested a high prevalence of left atrial enlargement, SVI + RV5 > 35 mm, blocks, and asymmetric septal hypertrophy. Conclusion: The ejection fraction was reported by two studies with a mean±SD of 68±13% and 77.2±8.07%. The researchers stress the paucity, low quality, and disparity in time of original studies about HCM in Saudi Arabia and recommend conducting national multicenter studies, with appropriate design, notably using screening-based recruitment methods.

Coronavirus Disease 2019 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has become a worldwide pandemic. Since 2019, the virus has mutated into multiple variants that have made it harder to eradicate and have increased the rate of infection. This virus can affect the structure and the function of the heart and can lead to cardiovascular symptoms that can have long-lasting effects despite recovery from COVID-19. These symptoms include chest pain, palpitations, fatigue, shortness of breath, rapid heartbeat, arrhythmias, cough and hypotension. These symptoms may persist due to myocardial injury, cardiac inflammation or systemic damage that may have been caused during infection. If these symptoms persist, the patient should visit their cardiologist for diagnosis and treatment plan for any type of cardiovascular disease that may have developed Post-COVID 19.

Background: Takotsubo cardiomyopathy is characterized by transient regional ventricular abnormalities in the absence of coronary artery disease and is reported as a complication of COVID-19. Case Presentation: It can have a diverse clinical presentation, occasionally resembling an acute coronary syndrome, and progress to acute heart failure and cardiogenic shock, adversely affecting patients' prognosis. A high index of suspicion and a thorough diagnostic approach supported by ancillary studies like echocardiography and coronary angiography is key for an accurate diagnosis and correct medical treatment. Herein, we report a patient with severe COVID-19 who developed Takotsubo cardiomyopathy. Conclusion: We also present a detailed literature review regarding the relationship between COVID-19 and Takotsubo cardiomyopathy.

Background: Quadricuspid pulmonary valve (QPV) is a rare congenital anomaly. Simple QPV had been mainly diagnosed at the time of autopsy before 2000, and the frequency rates of QPV are approximately 0.02%–0.41%. QPV was initially diagnosed using transthoracic echocardiography (TTE) after 2000 and with contrast computed tomography (CT) or cardiac magnetic resonance imaging (CMR) after 2009. Obtaining the cross-sectional view of the pulmonary valve using TTE is difficult. We aimed to review the papers regarding the incidence, embryology, diagnosis, associated congenital heart anomalies, and prognosis in patients with QPV, and furthermore to compare with those in patients with quadricuspid aortic valve (QAV). Case Presentation: We diagnosed QPV with mild stenosis in a 12-month-old infant. With a slight angulation of the transducer superiorly from the left high parasternal short-axis view, a short-axis view of QPV was obtained. Results: In QPV cases diagnosed at autopsy, Hurwitz’s type-b with three equal cusps and one smaller cusp is dominant, whereas Hurwitz’s type-a with four equal cusps is dominant in clinically diagnosed cases. Congenital heart anomaly and valvular stenosis are more frequent in patients with QPV than in patients with QAV. Coronary artery anomalies and infectious endocarditis are more frequent in patients with QAV than in patients with QPV. The incidence of PR is more common in type-a QPV than in type-b QPV. There is no difference between type-a QAV and type-b QAV with respect to the incidence of aortic regurgitation (AR). It is assumed that QPV is a risk factor for a Ross operation. However, QPVs have been used as autografts in certain patients. Conclusion: Between QPV and QAV, various differences were found in frequency rates, diagnostic methods, valve morphology, valve function, associated congenital heart diseases, and frequencies of infectious endocarditis.