Current Cardiology Reviews - Volume 16, Issue 1, 2020

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme family of phospholipase A2 produced by the inflammatory cell in atherosclerotic plaque. It is transported in the circulation, attached mainly to low-density lipoprotein-cholesterol (LDL-C). It hydrolyzes glycerophospholipids particularly fatty acids at the sn-2 position and produces numerous bioactive lipids; and leads to endothelial dysfunction, atherosclerotic plaque inflammation, and development of the necrotic core in plaques. There are two kinds of phospholipase A2, namely: secretory phospholipase A2 (sPLA2) and Lp- PLA2. They are deemed as evolving predictors of cardiovascular disease (CVD) risk in hospitaland population-based studies, including healthy subjects, acute coronary syndromes (ACS) and patients with CVD. Unfortunately, Lp-PLA2 inhibitor (darapladib) and s-PLA2 inhibitor (varespladib methyl) failed to prove to lower the risk of composite CVD mortality, myocardial infarction and stroke in those with stable CVD and ACS. Herein, we describe the explanation based on the existing data why there is still a discrepancy among them. So, it highlights the opinion that phospholipase A2 is merely the inflammatory biomarkers of CVD and playing an important role in atherosclerosis. Further, there is more spacious room to prove the causation.

The article represents literature review dedicated to molecular and cellular mechanisms underlying clinical manifestations and outcomes of acute myocardial infarction. Extracellular matrix adaptive changes are described in detail as one of the most important factors contributing to healing of damaged myocardium and post-infarction cardiac remodeling. Extracellular matrix is reviewed as dynamic constantly remodeling structure that plays a pivotal role in myocardial repair. The role of matrix metalloproteinases and their tissue inhibitors in fragmentation and degradation of extracellular matrix as well as in myocardium healing is discussed. This review provides current information about fibroblasts activity, the role of growth factors, particularly transforming growth factor β and cardiotrophin-1, colony-stimulating factors, adipokines and gastrointestinal hormones, various matricellular proteins. In conclusion considering the fact that dynamic transformation of extracellular matrix after myocardial ischemic damage plays a pivotal role in myocardial infarction outcomes and prognosis, we suggest a high importance of further investigation of mechanisms underlying extracellular matrix remodeling and cell-matrix interactions in cardiovascular diseases.

Arterial hypertension is the most prevalent chronic disease in the adult population of developed countries and it constitutes a significant risk factor in the development of cardiovascular disease, contributing to the emergence of many comorbidities, among which heart failure excels, a clinical syndrome that nowadays represents a major health problem with uncountable hospitalizations and the indolent course of which progressively worsens until quality of life decreases and lastly death occurs prematurely. In the light of this growing menace, each day more efforts are invested in the field of cardiovascular pharmacology, searching for new therapeutic options that allow us to modulate the physiological systems that appear among these pathologies. Therefore, in the later years, the study of natriuretic peptides has become so relevant, which mediate beneficial effects at the cardiovascular level such as diuresis, natriuresis, and decreasing cardiac remodeling; their metabolism is mediated by neprilysin, a metalloproteinase, widely expressed in the human and capable of catalyzing many substrates. The modulation of these functions has been studied by decades, giving room to Sacubitril, the first neprilysin inhibitor, which in conjunction with an angiotensin receptor blocker has provided a high efficacy and tolerability among patients with heart failure, for whom it has already been approved and recommended. Nonetheless, in the matter of arterial hypertension, significant findings have arisen that demonstrate the potential role that it will play among the pharmacological alternatives in the upcoming years.

Background: Dyslipidemia is the main factor involved in the occurrence and progression of coronary artery disease. Objective: The research strategy is aimed at analyzing new data on the pathophysiology of dyslipidemia involvement in coronary artery disease, the modalities of atherogenic risk estimation and therapeutic advances. Methods: Scientific articles published in PubMed from January 2017 to February 2018 were searched using the terms "dyslipidemia" and "ischemic heart disease". Results: PCSK9 contributes to the increase in serum levels of low-density lipoprotein-cholesterol and lipoprotein (a). The inflammation is involved in the progression of hyperlipidemia and atherosclerosis. Hypercholesterolemia changes the global cardiac gene expression profile and is thus involved in the increase of oxidative stress, mitochondrial dysfunction, and apoptosis initiated by inflammation. Coronary artery calcifications may estimate the risk of coronary events. The cardioankle vascular index evaluates the arterial stiffness and correlates with subclinical coronary atherosclerosis. The carotid plaque score is superior to carotid intima-media thickness for risk stratification in patients with familial hypercholesterolemia and both can independently predict coronary artery disease. The lipoprotein (a) and familial hypercholesterolemia have a synergistic role in predicting the risk of early onset and severity of coronary atherosclerosis. A decrease in atherosclerotic coronary plaque progression can be achieved in patients with plasma LDL-cholesterol levels below 70 mg/dL. A highly durable RNA interference therapeutic inhibitor of PCSK9 synthesis could be a future solution. Conclusion: The prophylaxis and treatment of coronary artery disease in a dyslipidemic patient should be based on a careful assessment of cardio-vascular risk factors and individual metabolic particularities, so it may be personalized.

This article is intended to provide guidance and clinical considerations for physicians managing patients suffering from supine hypertension with orthostatic hypotension, referred to as “SH-OH”. We review the normal physiologic response to orthostasis, focusing on the appropriate changes to autonomic output in this state. Autonomic failure is discussed with a generalized overview of the disease and examination of specific syndromes that help shed light on the pathophysiology of SH-OH. The goal of this review is to provide a better framework for clinical evaluation of these patients, review treatment options, and ultimately work toward achieving a better quality of life for patients afflicted with this disease.

Heart failure with reduced ejection fraction (HFrEF) is defined as the presence of typical symptoms of heart failure (HF) and a left ventricular ejection fraction ≤ 40%. HFrEF patients constitute approximately 50% of all patients with clinical HF. Despite breakthrough discoveries and advances in the pharmacologic management of HF, HFrEF patients continue to pose a significant economic burden due to a progressive disease characterized by recurrent hospitalizations and need for advanced therapy. Although there are effective, guideline-directed medical therapies for patients with HFrEF, a significant proportion of these patients are either not on appropriate medications’ combination or on optimal tolerable medications’ doses. Since the morbidity and mortality benefits of some of the pharmacologic therapies are dose-dependent, optimal medical therapy is required to impact the burden of disease, quality of life, prognosis, and to curb health care expenditure. In this review, we summarize landmark trials that have impacted the management of HF and we review contemporary pharmacologic management of patients with HFrEF. We also provide insight on general considerations in the management of HFrEF in specific populations. We searched PubMed, Scopus, Medline and Cochrane library for relevant articles published until April 2019 using the following key words “heart failure”, “management”, “treatment”, “device therapy”, “reduced ejection fraction”, “guidelines”, “guideline directed medical therapy”, “trials” either by itself or in combination. We also utilized the cardiology trials portal to identify trials related to heart failure. We reviewed guidelines, full articles, review articles and clinical trials and focused on the pharmacologic management of HFrEF.

Exercise is a major challenge for cardiovascular apparatus since it recruits chronotropic, inotropic, pre-load, and afterload reserves. Regular physical training induces several physiological adaptations leading to an increase in both cardiac volume and mass. It appears that several genderrelated physiological and morphological differences exist in the cardiovascular adjustments and adaptations to dynamic exercise in humans. In this respect, gender may be important in determining these adjustments and adaptations to dynamic exercise due to genetic, endocrine, and body composition differences between sexes. Females seem to have a reduced vasoconstriction and a lower vascular resistance in comparison to males, especially after exercise. Significant differences exist also in the cardiovascular adaptations to physical training, with trained women showing smaller cardiac volume and wall thickness compared with male athletes. In this review, we summarize these differences.

Background: Aortopulmonary window is an uncommon congenital heart disease, with untreated cases not surviving beyond childhood. However, very rarely it can present in adult patients with features of pulmonary hypertension. Clinically these patients cannot be differentiated from other more common conditions with left to right shunt. Transthoracic echocardiography if performed meticulously, can depict the defect in aortopulmonary septum. Results: We report a case of large unrepaired aortopulmonary window in a 23 years old patient, diagnosed on transthoracic echocardiography.

Background: Advanced heart failure has extremely high mortality without advanced therapies (left ventricular assist device (LVAD) implantation or cardiac transplant). LVAD patients with bioprosthetic aortic valve are more prone to leaflet fusion resulting in valvular stenosis and regurgitation. Case Presentation: We present a 46-year-old patient who had LV systolic function recovery while on LVAD. However, he had a severely stenotic aortic valve bioprosthesis with leaflet fusion that had to be replaced before deactivating his LVAD. Due to high surgical risk, we performed valve-invalve Trans-Catheter Aortic Valve Replacement (TAVR) with an Evolut self-expanding valve, however, the patient had significant aortic regurgitation secondary to deployment above the bioprosthetic valve ring. We successfully deployed a second Evolut Self-expanding valve inside the ring with excellent results. This was followed by a successful LVAD deactivation next day. His LV systolic function continued to recover and he had no heart failure symptoms at 3 month follow up. In the right settings, TAVR in recovered LVAD patients with aortic stenosis as a bridge to LVAD deactivation is a viable option, especially for patients who fall in the high-risk group. Conclusion: To the best of our knowledge, this is the first reported case of a valve-in-valve TAVR followed by successful LVAD deactivation in the setting of recovered LV systolic function.