Underuse of Anticoagulants in Atrial Fibrillation

READERS’ COMMENTS Underuse of Anticoagulants in Atrial Fibrillation The excellent review “Characterization of the Proportion of Untreated and Antiplatelet Therapy Treated Patients With Atrial Fibrillation”1 merits additional clinical commentary. This study adds further fuel to the continuing debate over the underuse of anticoagulation for atrial fibrillation (AF), as did the previous reports of Ogilvie et al2 and Brophy et al.3 The issue actually involves the use of the vitamin K antagonist warfarin as the basis for successful therapy in a usually highly diseased patient population hosting a multitude of co-morbidities. Having been involved in anticoagulation for ⬎4 decades enables one to be in a somewhat unique position for additional commentary and to play the position of devil’s advocate with the intent of diminishing the implications these reviews place upon practicing physicians, whether cardiologists or generalists.4,5 I am certain that it is not the guidelines that come into question when a clinician is faced with choosing anticoagulation therapy for each patient, nor the accepted contraindications to such therapy, which are generally well known and mainly irrefutable. The aforementioned studies choose to implicate practicing clinicians as being greatly responsible and at fault for the statistical results indicating anticoagulation underuse in AF in up to 50% of eligible patients. I support and applaud these studies, but there is no study even remotely definitive enough to allow us to accept a mathematical conclusion by the application of incomplete data and using further statistical analyses in attempts to confirm the conclusion. It is highly doubtful that the studies thus far presented as a criticism of underuse of anticoagulation take into account the “hidden” logistics behind this statistical underuse. The reasons extend beyond cost, travel, fear, frailty, traumas, severe debility, and the usual medical limitations and contraindications. Reasons unaccounted for in these studies include dementia with no backup assistance, the plain and simple inability of a patient to grasp and follow orders and

instructions, and poor memory without dementia. There are also patients who cannot hear and are unable to respond to instructions given by telephone or in faceto-face encounters. They cannot be relied on to manage an anticoagulation program at home or the office. There are significant logistics involved in formulating an anticoagulation protocol for an individual patient, notwithstanding an indeterminate number of patients and families who refuse anticoagulation despite explanations of the risk/benefit ratio. Homebound patients are increasing in number and pose their own unique characteristics. When the aforementioned adversities are settled, the final logistic path of underuse embodies those patients who have “no veins” (inadequate access) for venipuncture. Reasons given are age in some patients, obesity, inherent anatomic variants (deep and small veins), and the loss of suitable veins due to previous severe illnesses during which the veins have been overused and subsequently become occluded, causing all involved to relinquish the attempts at venipuncture. Physicians are then forced to choose antiplatelet therapy as a less effective alternative, still having some degree of success on an ill-defined basis. One can select clopidogrel plus low-dose entericcoated aspirin or extended-release dipyridamole/aspirin plus low-dose entericcoated aspirin. The gloomy horizon is beginning to clear with the advent of oral direct thrombin inhibitors and factor Xa inhibitors. The scorecard is likely to improve in subsequent analyses. Basil M. RuDusky, MD Wilkes-Barre, Pennsylvania 2 August 2011

1. Ogilvie IM, Weiner SA, Cowell W, Lip GY. Characterization of the proportion of untreated and antiplatelet therapy treated patients with atrial fibrillation. Am J Cardiol 2011;108:151– 161. 2. Ogilvie IM, Newton N, Weiner SA, Cowell W, Lip GY. Underuse of oral anticoagulants in atrial fibrillation: a systematic review. Am J Med 2010;123:638 – 645. 3. Brophy MT, Snyder KE, Gaehde S, Ives C, Gagnon D, Fiore LD. Anticoagulant use for atrial fibrillation in the elderly. J Am Geriatr Soc 2004;52:1151–1156.

Am J Cardiol 2011;108:1686 –1688 0002-9149/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved.

4. RuDusky BM. More on anticoagulation in older people. J Am Geriatr Soc 2005;53:547– 548. 5. RuDusky BM. Underuse of anticoagulation for atrial fibrillation in older adults—revisited. J Am Geriatr Soc 2011;59:774 –775. doi:10.1016/j.amjcard.2011.08.017

Rotational Mechanics of the Left Ventricle in Amyloid Light Chain Amyloidosis In their extensive state-of-art report on the echocardiographic evaluation of systolic and diastolic function in patient with cardiac amyloidosis, Liu et al1 dedicated much space to tissue Doppler imaging, strain rate imagining, and 2-dimensional speckle-tracking imagining but made no mention of a particular behavior of left ventricular (LV) motion defined as twisting and untwisting. It consists of LV torsional deformation around the longitudinal axis, originating from the dynamic interaction between the systolic clockwise rotation of the base and the counterclockwise rotation of the apex, followed by untwisting during diastole. Porciani et al2 recently published a comprehensively 2-dimensional strain evaluation of patients with amyloid light chain amyloidosis. They demonstrated that LV longitudinal strain was reduced in patients with echocardiographic evidence of cardiac amyloidosis. Moreover, they demonstrated that LV twisting and untwisting motions are increased in patients with amyloid light chain systemic amyloidosis and no evidence of cardiac involvement, while these motions are reduced in patients with evident amyloidosis cardiac involvement. This finding suggests that early in the disease, the impaired LV relaxation induces a compensatory mechanism that fails in more advanced stages of the disease, when twisting and untwisting rates are reduced. Moreover, the investigators demonstrated that the LV untwisting rate peak time was delayed in patients with and those without echocardiographic evidence of cardiac amyloidosis, irrespective of LV mass. Cappelli et al3 extended these observations, comparing patients with amyloidosis and normal LV mass to those with essential arterial hypertension and normal LV mass. Despite similar values of twisting and untwisting rates, patient with systemic amyloidosis and norwww.ajconline.org