Current Cardiology Reviews - Volume 11, Issue 3, 2015

Atrial flutter (AFL) is a common arrhythmia which may decrease cardiac output and may cause embolic events. Direct current (DC) cardioversion, medical cardioversion and radiofrequency (RF) ablation are therapeutic options, but over all RF ablation therapy has the longest event free period. Although development of AFL after myocardial infarction is quite common it may spontaneously recover or results in atrial fibrillation. Herein we report a patient with medical and electrical cardioversion resistant AFL which developed in the early post-myocardial infarction period causing hemodynamic instability, who was successfully treated with RF catheter ablation.

Atrial fibrillation (AF) continues to impose a significant burden upon healthcare resources. A sustained increase in the ageing population and better survival from conditions such as ischaemic heart disease have ensured that both the incidence and prevalence of AF continue to increase significantly. AF can lead to complications such as embolism and heart failure and these acting in concert with its associated co-morbidities portend increased mortality risk. Whilst some studies suggest that the mortality risk from AF is due to the “bad company it keeps” i.e. the associated co-morbidities rather than AF itself; undoubtedly some of the mortality is also due to the side-effects of various therapeutic strategies (anti-arrhythmic drugs, bleeding side-effects due to anti-coagulants or invasive procedures). Despite several treatment advances including newer anti-arrhythmic drugs and developments in catheter ablation, anti-coagulation remains the only effective means to reduce the mortality due to AF. Warfarin has been used as the oral anticoagulant in the treatment of AF for many years but suffers from disadvantages such as unpredictable INR levels, bleeding risks and need for haematological monitoring. This has therefore spurred a renewed interest in research and clinical studies directed towards developing safer and more efficacious anti-coagulants. We shall review in this article the epidemiological features of AF-related mortality from several studies as well as the cardiovascular and non-cardiac mortality mechanisms. We shall also elucidate why a rhythm control strategy has appeared to be counter-productive and attempt to predict the likely future impact of novel anti-coagulants upon mortality reduction in AF.

Currently a quarter of all patients treated with percutanous coronary intervention (PCI) are aged >75 years, with this proportion steadily growing. This subset of patients have a number of unique characteristics, such as a greater number of cardiovascular risk factors and frequently a larger burden of coronary artery disease, when compared to younger patients, therefore potentially deriving increased benefit from revascularization. Nonetheless this population are also more likely to experience procedural complications, secondary to age-related physiological alterations, increased frailty and increased prevalence of other co-morbidities. This article reviews the various aspects and data available to clinicians pertaining to and guiding revascularization in the elderly, including the use of adjuvant pharmacotherapy, specific considerations when considering age-related physiology, and revascularization in acute coronary syndromes.

Fractional flow reserve (FFR) is a physiological index of the severity of a stenosis in an epicardial coronary artery, based on the pressure differential across the stenosis. Clinicians are increasingly relying on this method because it is independent of baseline flow, relatively simple, and cost effective. The accurate measurement of FFR is predicated on maximal hyperemia being achieved by pharmacological dilation of the downstream resistance vessels (arterioles). When the stenosis causes FFR to be impaired by > 20%, it is considered to be significant and to justify revascularization. A diminished hyperemic response due to microvascular dysfunction can lead to a false normal FFR value, and a misguided clinical decision. The blunted vasodilation could be the result of defects in the signaling pathways modulated (activated or inhibited) by the drug. This might involve a downregulation or reduced number of vascular receptors, endothelial impairment, or an increased activity of an opposing vasoconstricting mechanism, such as the coronary sympathetic nerves or endothelin. There are data to suggest that microvascular dysfunction is more prevalent in post-menopausal women, perhaps due to reduced estrogen levels. The current review discusses the historical background and physiological basis for FFR, its advantages and limitations, and the phenomenon of microvascular dysfunction and its impact on FFR measurements. The question of whether it is warranted to apply gender-specific guidelines in interpreting FFR measurements is addressed.

With the advent of transcatheter aortic valve implantation (TAVI) techniques, a renewed interest has developed in sutureless aortic valve concepts in the last decade. The main feature of sutureless aortic valve implantation is the speed of insertion, thus making implantation easier for the surgeon. As a result, cross clamp times and myocardial ischemia may be reduced. The combined procedures (CABG with AVR in particular) can be done with a short cross clamp time. Perceval valve also provides an increased effective orifice area as compared with a stented bioprosthesis. Sutureless implantation of the Perceval valve is not only associated with shorter cross-clamp and cardiopulmonary bypass times but improved clinical outcomes too. This review covers the sutureless aortic valves and their evolution, with elaborate details on Perceval S valve in particular (which is the most widely used sutureless valve around the globe).

Macroautophagy (hereafter termed autophagy) is a highly evolutionarily conserved pathway that degrades intracellular components such as damaged organelles in lysosome. Autophagy occurs at low basal levels in virtually all types of cells, which is required for the maintenance of cellular homeostasis. Beclin 1 protein, encoded by the beclin 1 gene, plays a central role in the regulation of autophagy. Beclin 1 primarily functions as a scaffolding protein assembling Beclin 1 interactome to regulate Class III PI3K/VPS34 activity, which in turn, tightly controls autophagy at multiple stages. In addition to autophagy, Beclin 1 participates in the regulation of other biological processes such as endocytosis, apoptosis and phagocytosis. Fine-tuning of Beclin 1 protein levels, intracellular localization and the assembly of its interactome is pivotal for the proper execution of these biological functions. Deregulation of Beclin 1 contributes to the pathogenesis of a variety of human diseases. In this review, we summarize biology of Beclin 1 and its role in human pathology, with an emphasis on heart disease.

This is a comprehensive narrative review of the literature on the current science and evidence of population-level differences in risk factors for heart disease among different racial and ethnic population in the United States (U.S.). It begins by discussing the importance of population-level risk assessment of heart disease in light of the growth rate of specific minority populations in the U.S. It describes the population-level dynamics for racial and ethnic minorities: a higher overall prevalence of risk factors for coronary artery disease that are unrecognized and therefore not treated, which increases their likelihood of experiencing adverse outcome and, therefore, potentially higher morbidity and mortality. It discusses the rate of Acute Coronary Syndrome (ACS) in minority communities. Minority patients with ACS are at greater risk of myocardial infarction (MI), rehospitalization, and death from ACS. They also are less likely than non-minority patients to receive potentially beneficial treatments such as angiography or percutaneous coronary intervention. This paper looks at the data surrounding the increased rate of heart disease in racial and ethnic minorities, where the risk is related to the prevalence of comorbidities with hypertension or diabetes mellitus, which, in combination with environmental factors, may largely explain CHF disparity. The conclusion is that it is essential that healthcare providers understand these various communities, including nuances in disease presentation, risk factors, and treatment among different racial and ethnic groups. Awareness of these communities’ attributes, as well as differences in incidence, risk factor burdens, prognosis and treatment are necessary to mitigate racial and ethnic disparities in heart disease.

Nowadays, the worldwide number of left ventricular assist devices (LVADs) being implanted per year is higher than the number of cardiac transplantations. The rapid developments in the field of mechanical support are characterized by continuous miniaturization and enhanced performance of the pumps, providing increased device durability and a prolonged survival of the patients. The miniaturization process enabled minimally-invasive implantation methods, which are associated with generally benefitting the overall outcome of patients. Therefore, these new implantation strategies are considered the novel state of the art in LVAD surgery. In this paper we provide a comprehensive review on the existing literature on minimally-invasive techniques with an emphasis on the different implantation approaches and their individual surgical challenges.

For decades, it has been recognized that men have a higher age-adjusted risk of ischemic cardiovascular (CVD) events compared to women, thus generating hypotheses that sex steroids contribute to CVD risk. Potential mechanisms include genomic and non-genomic effects of sex steroids as well as mediation through classic CVD risk factors and obesity. However, results from randomized studies suggest that sex steroid supplementation in men and women do not result in improved CVD outcomes and may increase CVD risk. In contrast, prospective observations from endogenous sex steroid studies, i.e. among participants not using sex steroids, have suggested the opposite relationship. We reviewed the findings of prospective observational studies in men (17 studies) and women (8 studies) that examined endogenous sex steroids and CVD risk. These studies suggested a lack of association or that lower levels of testosterone or dihydrotestosterone are associated with higher CVD risk in both men and women. Higher, rather than lower, estradiol levels were associated with higher CVD risk in women. There were several significant gaps in the literature. First, it is unclear whether more sensitive measures of sex steroid levels might detect significant differences. Second, there are few prospective studies in women. Similarly, no studies report outcomes for high-risk groups such as African-Americans and Hispanics. Finally, few studies report upon ischemic coronary disease as opposed to ischemic stroke separately, although relationships between sex steroids and CVD may vary by vascular bed. Future investigations need to examine high risk groups and to distinguish between subtypes of CVD.

Patients with advanced chronic kidney disease (CKD), including those treated with dialysis, are at high risk for the development of cardiovascular disease (CVD). CVD accounts for 45-50% of deaths among dialysis patients. Therapy of acute and chronic coronary heart disease (CHD) that is effective in the general population is frequently less effective in patients with advanced CKD. Drug therapy in such patients may require dose modification in some cases. Oral anti-platelet drugs are less effective in those with advanced CKD than in persons with normal or near normal renal function. The intravenous antiplatelet drugs eptifibatide and tirofiban both require dose reductions in patients with advanced CKD. Enoxaparin requires dose reduction in early stage CKD and is contraindicated in hemodialysis patients. Unfractionated heparin and warfarin maybe used without dose adjustment in CKD patients. Atenolol, acetbutolol and nadolol may require dose adjustments in CKD. Metoprolol and carvedilol do not. Calcium channel blockers and nitrates do not require dose adjustment, whereas ranolazine does. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers may safely be used in CKD patients with close observation for hyperkalemia. The safety of spironolactone in such patients is questionable. Statins are less effective in reducing cardiovascular complication in CKD patients and their initiation is not recommended in dialysis patients. Coronary artery bypass grafting is associated with higher shortterm mortality, but better long-term morbidity and mortality than percutaneous coronary interventions in patients with advanced CKD with non-ST segment ACS and chronic CHD.