Current Cardiology Reviews - Volume 13, Issue 3, 2017

Background: Low-density lipoprotein cholesterol (LDL), and especially its oxidized form, renders the atherosclerotic plaque vulnerable to rupture in acute coronary syndromes (ACS). On the other hand, high-density lipoprotein (HDL) is considered an anti-atherogenic molecule. The more recent HDL-targeted drugs may prove to be superior to those used before. Indeed, delipidated HDL and HDL mimetics are efficient in increasing HDL levels, while the apoA-I upregulation with RVX-208 appears to offer a clinical benefit which is beyond the HDL related effects. HDL treatment however has not shown a significant improvement in the outcomes of patients with ACS so far, studies have therefore focused again on LDL. In addition to statins and ezetimibe, novel drugs such as PSCK9 inhibitors and apolipoprotein B inhibitors appear to be both effective and safe for patients with hyperlipidemia. Conclusion: Data suggest these could potentially improve the cardiovascular outcomes of patient with ACS. Yet, there is still research to be done, in order to confirm whether ACS patients would benefit from LDL- or HDL-targeted therapies or a combination of both.

Background: The concept of antioxidant therapies assumes high importance as oxidative stress is associated with cardiovascular aging via endothelial dysfunction. This review focuses on exploring the interaction between nrf-2 and ADMA in influencing the nitric oxide pathway and cardiovascular function. Objective: A systematic review of literature from 1990 to 2016 was conducted using Pubmed and Google Scholar. The literature suggests a strong influence of nrf-2 activation on up regulation of DDAH I which degrades ADMA, the endogenous inhibitor of nitric oxide synthase. The resulting decrease of ADMA would in turn enhance nitric oxide (NO) production. This would support endothelial function by adequate NO production and homeostasis of endothelial function. Conclusion: As NO production has many positive pleiotropic effects in the cardiovascular system, such an interaction could be utilized for designing molecular therapeutics. The targets for therapy need not be limited to activation of nrf-2. Modulation of molecules downstream such as DDAH I can be used to regulate ADMA levels. Most current literature is supported by animal studies. The concept of antioxidant therapies needs to be tested in well-defined randomized control trials. The biochemical basis of nrf-2 activation needs to be substantiated in human studies.

Background: Heart type fatty acid protein (HFABP) is a cytosolic protein released early after acute coronary syndrome (ACS) even in the absence of myocardial necrosis. Objectives: The purpose of this systematic review was to determine whether HFABP levels in patients with suspected, or confirmed ACS, improve risk stratification when added to established means of risk assessment. Methods: We searched Medline, Pubmed and Embase databases from inception to July 2015 to identify prospective studies with suspected or confirmed ACS, who had HFABP measured during the index admission with at least 1 month follow up data. A prognostic event was defined as allcause mortality or acute myocardial infarction (AMI). Results: 7 trials providing data on 6935 patients fulfilled inclusion criteria. There were considerable differences between studies and this was manifest in variation in prognostic impact of elevated HFABP(Odds ratio range 1.2-15.2 for death). All studies demonstrated that HFABP provide unadjusted prognostic information and in only one study this was negated after adjusting for covariates. A combination of both negative troponin and normal HFABP conferred a very low event rate. No study evaluated the incremental value of HFABP beyond that of standard risk scores. Only one study used a high sensitive troponin assay. Conclusion: There was marked heterogeneity in prognostic impact of HFABP in ACS between studies reflecting differences in sampling times and population risk. Prospective studies of suspected ACS with early sampling of HFABP in the era of high sensitivity troponin are necessary to determine the clinical value of HFABP. HFABP should not currently be used clinically as a prognostic marker in patients with suspected ACS.

Background: Pulmonary vein isolation (PVI) is an accepted treatment strategy for catheter ablation (CA) of paroxysmal atrial fibrillation (PAF). In this study, we aimed to assess the short, mid- and long-term outcome of PVI as a sole treatment strategy for PAF. Methods: Six bibliographic electronic databases were searched to identify all published relevant studies until December 14, 2015. Search of the scientific literature was performed for studies describing outcomes with mean follow-up > 24 months after PAF ablation. Only articles with 1, 3 or 5-year follow up were included, from the same group of investigators. Results: Of the 2398 references reviewed for eligibility, 13 articles (enrolling a total of 1774 patients) were included in the final analysis. Pooled analysis showed that the 12- and 62 -month success rate of a single CA procedure was 78% (95% CI 0.76% to 0.855) and 59% (95% CI 0.56% to 0.64%), respectively. The results did not differ by type of CA performed. Major complications mentioned in the enrolled studies were cerebrovascular event, pericardial tamponade and PV stenosis. Conclusion: There is a progressive and significant decline in freedom from AF between 1, 3 and 5- year after successful PVI in patients with PAF. Our analysis suggests that a high short-time success rate after PVI does not necessarily result in high chronic success rate.

Background: Statins have long been used for the protection against coronary artery disease (CAD). Their beneficial effect apart from cholesterol reduction lies in their pleiotropic properties. Emerging evidence from laboratory studies and clinical trials as well have pointed out the pivotal role of inflammation on the initiation and exacerbation of atherosclerosis; a major cause of CAD. Inflammation markers such as high sensitivity C-reactive protein and adhesion molecules are shown to increase in CAD patients and are used as prognostic tools. It is well known that statins can actually reduce the circulating levels of these agents slowing therefore the inflammatory process; interestingly not all types have the same outcome. Conclusion: The anti-inflammatory effect of statins on the formation of atherosclerotic plaque and the function of endothelial cells is thus of particular importance as these agents can actually ameliorate CAD prognosis.

Background: Enigmas often lead to hypotheses and speculations. For this reason, especially for the sake of the reader’s motivation, we opted for the plain discussion of some cardiology enigmas. Objective: The present text was aimed to discuss speculatively some cardiology enigmas. Method: Text was freely designed in the context of coronary artery and heart valve diseases. Results: The results were presented as the combination enigma/hypothesis. 1) The absence of arteriosclerosis in intramyocardial coronary arteries/ endothelium-myocardial interaction (crosstalk); 2) The unique and always confirmed superior evolution of the internal thoracic artery as coronary graft/ higher NO basal release 3) The prophylactic left internal thoracic artery graft in mildlystenosed coronary lesions/need of more accurate functional imaging techniques; 4) The high incidence of perioperative atrial fibrillation in patients with coronary artery disease/atrial ischemia associated to left circumflex coronary lesions; 5) The handling of disease-free saphenous vein grafts at the time of reoperation/biological serendipity with graft vein segments; 6) The possible aortic stenosis protection against coronary artery disease/ endothelium-myocardium interaction (crosstalk) improving NO release. Conclusion: The discussed topics associated with their respective speculative hypothesis remain as enigmas, but would become motivations for investigations

Background: Cardiovascular diseases (CVD) still represent the leading cause of mortality worldwide, despite the remarkable advances in interventional cardiology, cardiac surgery, and modern pharmacotherapy, particularly in the setting of acute myocardial infarction (AMI), chronic ischemic heart failure (HF), cardiomyopathy (CM), and the associated left ventricular (LV) dysfunction. A significant loss of cardiomyocytes that underlies all of these conditions was previously considered irreversible. However, current evidence indicates that the human heart has some potential for repair, and over the past decade, many research studies have been exploring the use of stem cells (SCs) to facilitate restoration of myocardium. Consequently, the safety, feasibility, and effectiveness of SC therapy have been reported in many randomized clinical trials (RCTs), using different lineages of adult SCs. Nevertheless, the clinical benefits of SC therapy are not yet well established. In the near future, understanding of the complex interrelations between SCs, paracrine factors, genetic or epigenetic predispositions, and myocardial microenvironment, in the context of an individual patient, will be crucial for translation of this knowledge into practical development of successful, long-term regenerative SC therapeutic applications, in a growing population of patients suffering from previous myocardial infarction (MI) leading to chronic ischemic cardiomyopathy. Conclusion: This overview highlights the therapeutic potential of adult SCs in terms of their possible regenerative capacity, safety, and clinical outcomes, in patients with AMI, and/or subsequent HF (due to chronic ischemic cardiomyopathy). This review was based upon PubMed database search for trials on SC therapy, in patients with AMI and HF, and the main timeframe was set from 2006 to 2016.

Background: Contemporary management of coronary disease focuses on the treatment of stenoses in the major epicardial vessels. However, myocardial blood flow is known to be contingent on a range of factors in addition to the patency of the epicardial vessels. These include anatomical and physiological factors such as the extent of myocardium supplied by the vessel, systemic blood pressure, the natural variation in vascular tone in response to physiological needs which allows for coronary autoregulation and pathological factors such as the presence of downstream obstruction to flow due to disease of the small coronary vessels or myocardium. The assessment of clinical effectiveness and adequacy of coronary revascularisation requires the ability to comprehensively and accurately assess and measure myocardial perfusion. Conclusion: In this article, we review the current methods of evaluating coronary blood flow and myocardial perfusion in the cardiac catheterisation laboratory.

Background: The “hepatic factor,” a molecule or group of molecules present in the hepatic venous blood, essential for the prevention of the development of pulmonary arteriovenous malformations (PAVMs) and right-to-left shunting has been a conceptual enigma in the understanding of many related conditions. Methods: Patients with various forms of liver diseases including acute hepatic failure, and others with normal hepatic function like hereditary hemorrhagic telangiectasia (HHT), inflammatory and parasitic disorders, cardiogenic hepatopulmonary syndrome (cHPS) and skin disorders like Dyskeratosis congenita are all known to cause PAVMs. Over a period of the last two decades our understanding of the pathogenesis of PAVMs has changed, but the mechanisms are still not clearly understood. The presence of PAVMs once considered a contraindication for liver transplantation is now a cure for PAVMs in patients with HPS. Results: In this article the molecular mechanisms and the underlying pathogenesis of PAVMs are discussed and the role of microRNA (miRNA) in its pathogenesis is favorably argued. Identifying and preventing or treating the underlying mechanisms will significantly influence the management of a large group of patients who at present cannot be effectively treated with a very poor prognosis. Progressive polycythemia, desaturation, stroke, and infection are serious complications of PAVMs. Conclusion: The clinical data and current understanding leads to the possible role of miRNA, which inhibits Vascular Endothelial Growth Factor (VEGF) synthesis as a pathogenic mechanism for the development of PAVMs.