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Volume 16, No 3 - 2015

Volume 16, No 3 - 2015

Table of Contents

Tricuspid Regurgitation, the Forgotten Valvular Lesion—A Contemporary Review of Etiology, Prevalence, and Management Options Management Update
Tricuspid regurgitation (TR) is a common finding. Pathologic TR is an independent risk factor for mortality. TR can be classified by etiology into functional versus organic. Organic TR is caused by structural damage to the tricuspid valve (TV) by a spectrum of etiologies, including pacemaker leads and right heart biopsies, whereas functional TR is predominantly due to elevated pulmonary pressures. Atrial fibrillation and chamber enlargement, among other risk factors, are strong predictors of functional TR. Correction of elevated pulmonary pressures improves TR, and concurrent repair of severe TR at the time of left heart valve surgery improves postoperative heart failure symptoms but does not improve survival. TR repair is associated with less operative and long-term mortality than TV replacement, and demonstrates similar improvements in heart failure symptoms. Substantial residual TR remains after repair, and reoperative mortality for residual TR is considerable. Percutaneous TV replacement may offer a rescue strategy. [Rev Cardiovasc Med. 2015;16(3):171-181 doi: 10.3909/ricm0766] © 2015 MedReviews®, LLC
Targeting the Papillary Muscles in Mitral Valve Repair for Ischemic Mitral Regurgitation Treatment Update
Ischemic mitral regurgitation due to left ventricular remodeling and leaflet tethering is associated with decreased survival, and the optimal management remains unknown. Restrictive mitral annuloplasty is the current treatment of choice, but it is associated with a 15% to 30% incidence of late recurrent mitral regurgitation, which confers a poor prognosis. A pathophysiology-guided approach to surgical repair is preferable, with a goal of alleviating leaflet tethering and restoring proper subvalvular mechanics. In patients with preoperative predictors of annuloplasty failure, combining a papillary muscle repositioning technique with conventional annuloplasty repair allows for complete geometric repair of the ventriculomitral unit. [Rev Cardiovasc Med. 2015;16(3):182-188 doi: 10.3909/ricm0772] © 2015 MedReviews®, LLC
Heparin: Physiology, Pharmacology, and Clinical Application Drug Review
Heparin is stored endogenously within the secretory granules of basophils and mast cells, and is only released into the vasculature at sites of injury. At these sites, it helps maintain proper blood flow by balancing the active anticoagulant and procoagulant processes. Pharmaceutical-grade heparin is derived from animal tissue, but one form is made synthetically. Heparin is commonly used in the management of coronary artery disease, deep vein thrombosis, pulmonary embolism, and atrial fibrillation, and in the prevention of thrombosis during cardiopulmonary bypass and extracorporeal membrane oxygenation. Heparin treatment is a key component in elective percutaneous coronary intervention (PCI). It plays an important role in minimizing the risk of thrombotic events during PCI and is one of the most popular anticoagulants used. However, some studies show that higher heparin doses are associated with more frequent bleeding complications, which can increase morbidity and mortality. The optimal heparin dosing regimens are still debated, as well as their efficacy in PCI compared with that of other drugs such as bivalirudin. This review examines the physiology, pharmacology, therapeutic applications, dosing regimens, and efficacy of heparin in the setting of PCI. In addition, included is a review of data on addition of glycoprotein IIb/IIIa inhibitors to heparin and comparison of heparin monotherapy to bivalirudin in PCI. [Rev Cardiovasc Med. 2015;16(3):189-199 doi: 10.3909/ricm0778] © 2015 MedReviews®, LLC
Coronary Plaque Characteristics Affect No-Reflow During Primary Percutaneous Coronary Intervention: A Pooled Analysis of 14 Observational Studies Using Intravascular Ultrasound Disease State Review
The association between coronary plaque composition and no-reflow during percutaneous coronary intervention (PCI) is still debated. We performed a systematic literature search using MEDLINE, Embase, Cochrane, and Ovid databases for intravascular ultrasound (IVUS) studies evaluating the relationship between coronary plaque characteristics and no-reflow after PCI. Fourteen observational trials were included in the meta-analysis, including 1457 patients (237 in the no-reflow group, 1220 in the normal reflow group). Pooled analysis indicated that the no-reflow group had a significantly higher absolute volume of fibrofatty plaque (weighted mean differences [WMD], 4.94 mm3; 95% confidence interval [CI], 1.83-8.06; P = .002), external elastic membrane cross-sectional area (EEM-CSA) (WMD, 3.40 mm2; 95% CI, 2.22-4.58; P < .00001), plaque area (WMD, 4.06 mm2; 95% CI, 2.24-5.89; P < .0001), and artery remodeling index (WMD, 0.09; 95% CI, 0.06-0.13; P < .00001), and a smaller percentage of fibrous plaque (WMD, −5.89 %; 95% CI, −0.66 to −11.12; P = .03) than in the normal reflow group. There were no significant differences in the other plaque components between the two groups. This meta-analysis confirmed that high absolute volume of fibrofatty plaque, EEM-CSA, plaque area, and coronary artery remodelingindex, and a decreased percentage of fibrous plaque as detected by IVUS in culprit lesions, are linked with the development of the no-reflow phenomenon after PCI. [Rev Cardiovasc Med. 2015;16(3):200-213 doi: 10.3909/ricm0780] © 2015 MedReviews®, LLC
Flecainide-induced Torsades de Pointes: Case Report and Review of Literature
Several antiarrhythmic drugs are prone to cause QT interval prolongation and torsades de pointes (TDP). Predisposing risk factors include congenital channelopathies, severe bradycardia, drugs, and hypokalemia. Individual genetic variation and drug metabolism exaggerate susceptibility to adverse reactions. These proarrhythmic effects create a deficit in the repolarization reserve and prolong action potential duration, resulting in early afterdepolarizations, which promote a reentry circuit. Flecainide, a class IC drug, also exhibits inhibitory actions on the K1 channels, causing QT interval prolongation. We identified six cases of flecainide-induced TDP in the literature. Most patients had other predisposing factors. Bradycardia was present in all cases. Our case demonstrates two arrhythmias caused by flecainide: atrial flutter with 1:1 atrioventricular conduction and TDP. Both arrhythmias developed in the absence of hypokalemia, with the use of other drugs that prolong QT interval, or genetic predisposition. Therefore, this is purely a drug effect. This case report illustrates a rare but serious proarrhythmic property of flecainide observed particularly in women. [Rev Cardiovasc Med. 2015;16(3):214-220 doi: 10.3909/ricm0761] © 2015 MedReviews®, LLC
Anomalous Origin of the Right Coronary Artery From the Left Anterior Descending Artery With Anomalous Course Between the Great Vessels: A Case for Conservative Management With Review of the Literature
A single left coronary artery is a rare coronary anomaly. In such situations, the right coronary artery arises from the left anterior descending artery and traverses an unusual proximal course between the aorta and pulmonary trunk. There are only 10 such reported cases in the medical literature to date. After a detailed risk-to-benefit consideration, the decision was made for conservative management. In this report, we describe this rare case with a detailed review of the literature. [Rev Cardiovasc Med. 2015;16(3):221-224 doi: 10.3909/ricm0774] © 2015 MedReviews®, LLC