Current Cardiology Reviews - Volume 5, Issue 1, 2009

Interventional cardiology procedures result in substantial patient radiation doses due to prolonged fluoroscopy time and radiographic exposure. The procedures that are most frequently performed are coronary angiography, percutaneous coronary interventions, diagnostic electrophysiology studies and radiofrequency catheter ablation. Patient radiation dose in these procedures can be assessed either by measurements on a series of patients in real clinical practice or measurements using patient-equivalent phantoms. In this article we review the derived doses at non-pediatric patients from 72 relevant studies published during the last 22 years in international scientific literature. Published results indicate that patient radiation doses vary widely among the different interventional cardiology procedures but also among equivalent studies. Discrepancies of the derived results are patient-, procedure-, physician-, and fluoroscopic equipmentrelated. Nevertheless, interventional cardiology procedures can subject patients to considerable radiation doses. Efforts to minimize patient exposure should always be undertaken.

A series of reports in the past decade have ascribed pro-angiogenic activity to several thyroid hormone analogues, including L-thyroxine (T4), 3,5,3-triiodo-L-thyronine (T3) and diiodothyropropionic acid (DITPA). Model systems of angiogenesis have demonstrated that thyroid hormone-induced neovascularization is initiated at a cell surface receptor for the hormone on an integrin. The hormone signal is transduced within the cell by extracellular regulated kinase 1/2 (ERK1/2) into secretion of basic fibroblast growth factor (bFGF) and other vascular growth factors and consequent angiogenesis. Intact animal studies have shown that endogenous thyroid hormone supports blood vessel density in heart and brain and that thyroid hormone administration can induce angiogenesis in ischemic limbs.

Catheter ablation is an evolving treatment option in patients with atrial fibrillation. Contrast enhanced electrocardiogram-gated multi-detector computed tomography (MDCT) has rapidly evolved over the past few years into an important tool in the diagnosis of coronary atherosclerosis. There is increasing recognition that MDCT is a useful tool to evaluate non-coronary structures, such as cardiac chambers, valves, the coronary sinus and adjacent structures including pulmonary veins. In particular, MDCT is playing an increasingly important role in the evaluation of the left atrium and the pulmonary veins in patients undergoing catheter ablation for atrial fibrillation. It provides accurate and reliable identification of the pulmonary veins and anatomical relationship between the left atrium and esophagus although the mobile esophagus may limit the value of MDCT to reduce the risk of atrio-esophagus fistula. In this article, we will review the evaluation of the left atrium and pulmonary veins using MDCT in patients undergoing catheter ablation of atrial fibrillation.

Despite ample evidence that right ventricular function is a critical determinant of the clinical response to a spectrum of cardiovascular diseases, there has been only a limited analysis of the unique and distinguishing physiologic properties of the RV under normal circumstances and in response to pathologic insults. This review highlights some of these features and underscores the fact that rational therapy in RV failure should acknowledge this physiology and ought to be chamber specific.

Patients with symptomatic severe aortic stenosis (AS) benefit from aortic valve replacement surgery, but the management of patients with asymptomatic severe AS is more controversial. While cholesterol and angiotensin have been linked to AS progression, we should await the results of ongoing randomized trials before medical therapy to lower cholesterol or inhibit angiotensin can be recommended to limit disease progression. Clinical factors, echocardiographic parameters, valve morphology, exercise stress testing results, and cardiac biomarkers may be useful in identifying patients who will have early development of symptoms during follow-up and require closer monitoring. The risks associated with aortic valve replacement outweigh the benefits in the majority of patients with asymptomatic severe AS.

This review summarizes the microbiology, and antimicrobial management of mycotic aneurysm of the aorta (MAA) due to anaerobic bacteria. Anaerobic bacteria are an uncommon but important cause of MAA. Most cases of anaerobic MAA are caused anaerobic gram-negative bacilli (mostly B. fragilis group), Clostridium spp. (mostly Clostridium septicum, and Propionobacterium spp. (mostly P. acnes). Clostridial infection is frequently associated with gastrointestinal or hematologic malignancy. A review of all the reported cases is presented. Treatment of MAA involving anaerobic bacteria includes the use of antimicrobial effective against these organisms.

Cardiac Resynchronization therapy has become an important management tool in adults with heart failure and dilated cardiomyopathy. The role of CRT in children with CHF is still unclear. Evidence is slowly emerging in the pediatric cardiology literature that CRT may have an important and useful role in certain select populations with CHF. These include patients with complete heart block who develop pacing-induced cardiomyopathy, certain forms of congenital heart disease associated with systemic ventricular failure (even if the systemic ventricle is a morphologic RV) and in patients with idiopathic dilated cardiomyopathy. Studies in children supporting the use of CRT include many case reports, a few studies of CRT in post-operative patients, and one multi-center registry reporting the use of CRT in children. These papers will be summarized.

Atrial and brain natriuretic peptides (ANP and BNP, respectively) are cardiac hormones, secretions of which are markedly upregulated during cardiac failure, making their plasma levels clinically useful diagnostic markers. ANP and BNP exert potent diuretic, natriuretic and vasorelaxant effects, which are mediated via their common receptor, guanylyl cyclase (GC)-A (also called natriuretic peptide receptor (NPR)-A). Mice deficient for GC-A are mildly hypertensive and show marked cardiac hypertrophy and fibrosis that is disproportionately severe, given their modestly higher blood pressure. Indeed, the cardiac hypertrophy seen in these mice is enhanced in a blood pressure-independent manner and is suppressed by cardiomyocyte-specific overexpression of GC-A. These results suggest that the actions of a local cardiac ANP/BNP-GC-A system are essential for maintenance of normal cardiac architecture. In addition, GC-A was shown to exert its cardioprotective effects by inhibiting angiotensin II-induced hypertrophic signaling, and recent evidence suggests that regulator of G protein signaling (RGS) subtype 4 is involved in the GC-A-mediated inhibition of Gαq-coupled hypertrophic signal transduction. Furthermore, several different groups have reported that functional mutations in the promoter region of the human GC-A gene are associated with essential hypertension and ventricular hypertrophy. These findings suggest that endogenous GC-A protects the heart from pathological hypertrophic stimuli, and that humans who express only low levels of GC-A are genetically predisposed to cardiac remodeling and hypertension.

The use of cardiac imaging modalities has grown steadily, and cardiac nuclear studies constitute a large part of this number. Nuclear Cardiology is often mistakenly considered a synonym of myocardial perfusion imaging (MPI), but has broader applications, including metabolic imaging, innervation imaging, among other technologies. MPI has been a powerful diagnostic and prognostic tool in the assessment of patients for known or suspected CAD for decades, and is now increasingly used for the evaluation of the anti-ischemic effects of various therapies, according to changes in left ventricular perfusion defect size defined by sequential MPI. Neuronal dysfunction identified with iodine-123- metaiodobenzylguanidine may give information on prognosis in different disease conditions, such as after myocardial infarction, in diabetes and dilated cardiomyopathy. Molecular imaging may identify the predominant cellular population in the atherosclerotic plaque and help predict the likelihood of clinical events. Therefore, although its usefulness is well established, Nuclear Cardiology remains a moving science, whose roles keep in pace with evolving clinical needs and expectations.

Sudden cardiac death (SCD) is a serious public health problem; the annual incidence of out-of-hospital cardiac arrest in North America is approximately 166,200. Identifying patients at risk is a difficult proposition. At the present time, left ventricular ejection fraction (LVEF) remains the single most important marker for risk stratification. According to current guidelines, most patients with LVEF <35% could benefit from prophylactic ICD implantation, particularly in the setting of symptomatic heart failure. Current risk stratification strategies fail to identify patients at risk of SCD in larger population groups encompassing a greater number of potential SCD victims. However, the best approach to identifying patients and the value of various risk stratification tools is not entirely clear. The goal of this review is to discuss the problem of SCD and the value of the different risk stratification markers and their potential clinical use either alone or in combination with other risk stratification markers.

It is known that long lasting changes in cell volume are incompatible with cellular functions. In the present review, I discussed the role of cell volume on gene expression and protein synthesis as well as the importance of the renin angiotensin system on the regulation of cell volume in the failing heart. Moreover, the relationship between mechanical stretch, cell volume and the renin angiotensin system as well some translational studies are also described and their relevance to the prevention or reduction of cardiac damage during myocardial ischemia is emphasized.

Homelessness [and poverty] is rapidly escalating across North America and is associated with dire implications for public health and our health care systems. Both are compelling states of existence affecting all ages, ethnicities and both genders. Homelessness frequently evolves through a complex interaction of factors that are both internal and external to the individual themselves. Once homeless, equitable access to both preventative and remedial health care is lacking and is associated with a higher than average burden of cardiovascular disease [CVD] risk factors, morbidity and mortality and is accompanied by disproportionately high health care costs. The emergence of limited, small scale programs aimed at addressing the unique health and social needs of the homeless is encouraging. However, there has been inadequate commitment at the National, State or Provincial and local levels to implement policies and dedicate funding and resources to the expansion of such “individual level” interventions into comprehensive programs that deliver sustainable, integrated prevention and services, especially with regard to CVD. The long-term solutions that address the links between homelessness and CVD lie in preventing homelessness and reversing the trends in our health care system that create disparities for lower socioeconomic status [SES] and homeless individuals.