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Volume 15, No 1 - 2014

Volume 15, No 1 - 2014

Table of Contents

Use of Microsomal Triglyceride Transfer Protein Inhibitors in Patients With Homozygous Familial Hypercholesterolemia: Translating Clinical Trial Experience Into Clinical Practice Treatment Update
Homozygous familial hypercholesterolemia (HoFH) is associated with severe hypercholesterolemia and premature cardiovascular morbidity and mortality. The most frequent cause of HoFH is loss of function mutations in the gene for the low-density lipoprotein receptor, resulting in reduced clearance of low-density lipoprotein (LDL) cholesterol from the circulation. Patients with HoFH have attenuated responsiveness to lipid-lowering therapies such as statins, cholesterol absorption inhibition, and bile acid-binding resins because of impaired LDL receptor expression. Lomitapide is a novel microsomal triglyceride transfer protein inhibitor that does not depend on the ability to upregulate LDL receptors on the surface of hepatocytes. Lomitapide reduces production of apolipoprotein B-containing lipoproteins, significantly reduces serum levels of LDL cholesterol, and is approved for use in patients with HoFH in the United States and the European Union. [Rev Cardiovasc Med. 2014;15(1):1-10 doi: 10.3909/ricm0702] © 2014 MedReviews®, LLC
Acute and Chronic Cardiovascular Effects of Hyperkalemia: New Insights Into Prevention and Clinical Management Management Update
The plasma pool of potassium is a partial reflection of the overall body, transient cellular shifts, and potassium elimination regulated by the kidneys. Potassium concentrations elevating above the upper limit of normal (> 5.0 mEq/L) have become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad applications of drugs that modulate potassium excretion by either reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, beta-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). In addition, acute kidney injury, critical illness, crush injuries, and massive red blood cell transfusions can result in hyperkalemia. Progressively more severe elevations in potassium are responsible for abnormalities in cardiac depolarization and repolarization and contractility. Untreated severe hyperkalemia results in sudden cardiac death. Traditional management steps have included reducing dietary potassium and discontinuing potassium supplements; withdrawal of exacerbating drugs; acute treatment with intravenous calcium gluconate, insulin, and glucose; nebulized albuterol; correction of acidosis with sodium bicarbonate for short-term shifts out of the plasma pool; and, finally, gastrointestinal ion exchange with oral sodium polystyrene sulfonate in sorbitol, which is mainly used in the hospital and is poorly tolerated due to gastrointestinal adverse effects. This review explores hyperkalemia as a complication in cardiovascular patients and highlights new acute, chronic, and preventative oral therapies (patiromer calcium, cross-linked polyelectrolyte, ZS-9) that could potentially create a greater margin of safety for vulnerable patients with combined heart and kidney disease. [Rev Cardiovasc Med. 2014;15(1):11-23 doi:10.3909/ricm0727] © 2014 MedReviews®, LLC
Reassessing the Importance of Complete Versus Incomplete Coronary Revascularization Management Review
Coronary revascularization may be performed for relief of anginal symptoms or, in specific patient subgroups, to reduce the incidence of myocardial infarction and mortality. Achieving complete revascularization of all significantly obstructed coronary segments has been an established goal of coronary bypass graft surgery (CABG) and more recent data demonstrate a salutary effect of complete revascularization following percutaneous coronary intervention (PCI) on long-term clinical outcomes as well. Incomplete coronary revascularization is associated with increased mortality following both CABG and PCI, as well as with an increased incidence of myocardial infarction, repeat revascularization, and major adverse cardiovascular or cerebrovascular events following PCI. The relationship between completeness of revascularization and late adverse clinical outcomes is both qualitative and quantitative as reflected by the residual SYNTAX score (angiographic lesion complexity) following PCI. Thus, complete revascularization has evolved as an important objective for either CABG or PCI and the ability to achieve complete revascularization should enter into the decision algorithm for choice of revascularization modality. [Rev Cardiovasc Med. 2014;15(1):24-30 doi: 10.3909/ricm0714] © 2014 MedReviews®, LLC
Emerging Treatment Options for Refractory Angina Pectoris: Ranolazine, Shock Wave Treatment, and Cell-Based Therapies Treatment Update
A challenge of modern cardiovascular medicine is to find new, effective treatments for patients with refractory angina pectoris, a clinical condition characterized by severe angina despite optimal medical therapy. These patients are not candidates for surgical or percutaneous revascularization. Herein we review the most up-to-date information regarding the modern approach to the patient with refractory angina pectoris, from conventional medical management to new medications and shock wave therapy, focusing on the use of endothelial precursor cells (EPCs) in the treatment of this condition. Clinical limitations of the efficiency of conventional approaches justify the search for new therapeutic options. Regenerative medicine is considered the next step in the evolution of organ replacement therapy. It is driven largely by the same health needs as transplantation and replacement therapies, but it aims further than traditional approaches, such as cell-based therapy. Increasing knowledge of the role of circulating cells derived from bone marrow (EPCs) on cardiovascular homeostasis in physiologic and pathologic conditions has prompted the clinical use of these cells to relieve ischemia. The current state of therapeutic angiogenesis still leaves many questions unanswered. It is of paramount importance that the treatment is delivered safely. Direct intramyocardial and intracoronary administration has demonstrated acceptable safety profiles in early trials, and may represent a major advance over surgical thoracotomy. The combined efforts of bench and clinical researchers will ultimately answer the question of whether cell therapy is a suitable strategy for treatment of patients with refractory angina. [Rev Cardiovasc Med. 2014;15(1):31-37 doi:10.3909/ricm0672] © 2014 MedReviews®, LLC
Prevention and Treatment of No-Reflow Phenomenon by Targeting the Coronary Microcirculation Management Update
The coronary no-reflow phenomenon refers to the post–percutaneous coronary intervention (PCI) state in which, despite successful revascularization of the epicardial conduit coronary arteries, substantial regions of the myocardium do not receive adequate perfusion. In most cases, the underlying mechanism can be attributed to alterations in the microvascular circulation caused by factors intrinsic or extrinsic to the coronary microcirculation. Because the no-reflow phenomenon is associated with poor clinical outcomes, it is of great importantance to identify and apply effective strategies for reducing post-PCI morbidity and mortality. Successful prevention strategies aim to ad dress increased vasoreactivity, intravascular platelet aggregation, microvascular inflammation, and down-stream plaque particle embolization. This review provides an updated overview on the pathomechanism of no-reflow and the current available prevention strategies from the perspective of coronary microcirculation. Although large randomized clinical trials have not yet identified any effective treatment, studying the coronary microcirculation may reveal new therapeutic targets for successful amelioration of the adverse clinical consequences from no-reflow phenomenon. [Rev Cardiovasc Med. 2014;15(1):38-51 doi:10.3909/ricm0699] © 2014 MedReviews®, LLC
L-carnitine for the Treatment of Acute Myocardial Infarction Treatment Review
Although the therapeutic strategies available for treating acute myocardial infarction (AMI) have evolved dramatically in recent decades, coronary artery disease remains the leading cause of death in our society, and the rates of recurrent myocardial infarction and mortality are still unacceptably high. Therefore, exploration of alternative therapeutic strategies for AMI is of utmost importance. One such strategy is to target metabolic pathways via L-carnitine supplementation. L-carnitine is a physiologically essential metabolic cofactor that has been shown to provide a plethora of benefits when administered after AMI. L-carnitine has been shown to lessen infarct size, to reduce ventricular arrhythmias, left ventricular dilation, and heart failure incidence, as well as improve survival. These benefits may, in part, be related to its ability to boost glucose oxidation in is chemic tissues, while moderating increases in fatty acyl-coenzyme A levels that can impair mitochondrial efficiency and promote oxidative stress and inflammation. This article summarizes the evidence pertinent to the therapeutic use of L-carnitine for AMI. [Rev Cardiovasc Med. 2014;15(1):52-62 doi:10.3909/ricm0710] © 2014 MedReviews®, LLC
Notes From the American College of Cardiology Board of Governors Meeting
[Rev Cardiovasc Med. 2014;15(1):63-64 doi: 10.3909/ricm151CAACC] © 2014 MedReviews®, LLC
Left Main Coronary Artery Perforation During Percutaneous Coronary Intervention in a Patient With Noninfectious Aortitis
Noninfectious aortitis is increasingly recognized as an important cause of aortic aneurysms and dissection. Coronary involvement in noninfectious aortitis has been reported in several case reports and is marked by a high mortality. Here, we describe the case of a 72-year-old patient suffering from aortitis with involvement of the left main coronary artery trunk, who underwent percutaneous coronary intervention (PCI), which was complicated by left coronary artery perforation. Active inflammatory disease of the vessel wall may cause excessive tissue frailty and therefore has to be considered as a risk factor for perforation during PCI. [Rev Cardiovasc Med. 2014;15(1):66-70 doi:10.3909/ricm0708] © 2014 MedReviews®, LLC
Evaluation of Long-term Cardiovascular Effects Thoracic Irradiation
[Rev Cardiovasc Med. 2014;15(1):71-73 doi 10.3909/ricm0711] © 2014 MedReviews®, LLC
Nonischemic Dilated Cardiomyopathy Electrophysiology
[Rev Cardiovasc Med. 2014;15(1):73 doi: 10.3909/ricm0711] © 2014 MedReviews®, LLC