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e thank Dr. Falk for his interest in our study (1) and for directings to these earlier published data on the association between drivingnd ventricular arrhythmias. As Dr. Falk points out, the majority ofhe arrhythmias in the prior studies seemed to be stress-induced2–4), and most occurred in patients with active ischemia (4).lthough the majority of implantable cardioverter-defibrillator (ICD)atients in the TOVA (Triggers Of Ventricular Arrhythmias) studyopulation had a history of coronary artery disease (n � 802; 73.6%),nly 12% of participants reported experiencing any angina at baseline.herefore, as Dr. Falk surmised, the number of patients with active

schemia in this ICD population is quite low. Therefore, it isotentially possible that a higher rate of ventricular arrhythmias mighte observed in patients with active ischemia. Unfortunately, the smallumber of patients with active ischemia in our study limited ourbility to perform this important subgroup analysis. It is also ofnterest that the majority of the rhythm disturbances in these earliertudies occurred during the driving episode (2–4) itself as opposed tohose in our study, which occurred after (1), suggesting that interme-iary mechanisms, such as exposure to air pollution, might play areater role in the precipitation of ventricular arrhythmias associatedith driving in more recent times. We agree about the enduring valuef historic studies, and to paraphrase another famous quotation,History is the present. That’s why every generation writes it anew.”

Christine M. Albert, MD, MPHurray A. Mittleman, MD, MPH

Brigham and Women’s Hospital Center for Arrhythmiareventionivision of Preventive Medicine and Cardiovascular Division

00 Commonwealth Avenue Eastoston, Massachusetts 02215-mail: calbert@partners.org

doi:10.1016/j.jacc.2008.03.053

EFERENCES

. Albert CM, Rosenthal L, Calkins H, et al. Driving and implantablecardioverter-defibrillator shocks for ventricular arrhythmias: resultsfrom the TOVA study. J Am Coll Cardiol 2007;50:2233–40.

. Littler WA, Honour AJ, Sleight P. Direct arterial pressure andelectrocardiogram during motorcar driving. BMJ 1973;2:273–7.

. Taggart P, Gibbons D. Motor-car driving and heart rate. Br Med J1967;1:411–2.

. Taggart P, Gibbons D, Somerville W. Some effects of motorcar drivingon normal and abnormal heart rate. BMJ 1969;4:130–4.

he Timing of Thrombolysisor Strokes Complicatingardiac Catheterization

e read with great interest the article by Khatri et al. (1)escribing the first systematic study of cerebrovascular accidentsomplicating cardiac catheterization.

In one of the largest single-center series of strokes complicatingardiac catheterization (2), we report how immediate on-table an-

iography was the key strategy to successful treatment in most r

atients. Four patients were treated with intra-arterial thrombolysis, 1y mechanical reperfusion, and the last with prolonged intravenousnfusion of abciximab. In the 2 patients in whom a neuroimagingtrategy was adopted before intervention, inferior outcomes werebserved. In particular, the only hemorrhagic transformation followedy death was observed in 1 of the 2 patients in whom a thrombolyticgent was administered more than 180 min after the event with theelay to allow brain magnetic resonance imaging.

Clearly with such small numbers, definitive demonstration of theuperiority of immediate intervention over a neuroimaging strategy isot possible; however, we feel that “an expedited cerebral CT oragnetic resonance imaging scan to evaluate for possible intracerebral

emorrhage” as advocated by Lyden (3) may not be the best option inhis setting. In strokes occurring in the general population, delay inhrombolysis is an important predictor of hemorrhagic transforma-ion, and strokes complicating cardiac catheterization are unlikely toepresent an exception to this rule. To this regard it is interesting toote that in the report by Khatri et al. (1) the median delay in

ntra-arterial lysis was 240 min, whereas only a 90-min delay occurredefore intravenous therapy. It would be interesting to know in whichroup the 3 asymptomatic hemorrhages occurred.

We suggest that immediate on-table angiography might be aood time-saving and brain-saving point to include in the catheteraboratory Code Stroke protocol.

Federico De Marco, MDelen Routledge, MD, MRCPhierry Lefèvre, MD, FESC

Institut Cardiovasculaire Paris SudAvenue du Noyer Lambert

1300 Massyrance-mail: federico.demarco@gmail.com

doi:10.1016/j.jacc.2008.03.057

EFERENCES

. Khatri P, Taylor RA, Palumbo V, et al., Treatment of Acute StrokeAfter Cardiac Catheterization (TASCC) Study Group. The safety andefficacy of thrombolysis for strokes after cardiac catheterization. J AmColl Cardiol 2008;51:906–11.

. De Marco F, Fernandez-Diaz JA, Lefèvre T, et al. Management ofcerebrovascular accidents during cardiac catheterization: immediatecerebral angiography versus early neuroimaging strategy. CatheterCardiovasc Interv 2007;70:560–8.

. Lyden PD. Code stroke in the cath lab. J Am Coll Cardiol 2008;51:912.

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e thank Drs. De Marco, Routledge, and Lefèvre for theirnterest in our work (1). They raise the important question ofhether to take the time to do an imaging study before adminis-

ering cerebral reperfusion therapy in the setting of stroke afterardiac catheterization. They have proposed immediate acutetroke treatment, transitioning directly from cardiovascular toerebral angiography for intra-arterial therapy, for strokes afterardiac catheterization on the table. However, the limited reportsn this topic are likely subject to a publication bias towardavorable clinical outcomes.

Even if an embolism is identified on an immediate cerebralngiogram, the possibility of an acute hemorrhagic infarction

emains a concern, particularly in the setting of antithrombotics

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318 Correspondence JACC Vol. 52, No. 4, 2008July 22, 2008:315–8

nd anticoagulants. Studies discriminating stroke subtypes haveeported hemorrhagic strokes in 24% (2) and 46.5% (3) of cases.

While we agree that, in most circumstances, the added delay ofagnetic resonance imaging (MRI) is not warranted, a computed

omography (CT) scan can and should be accomplished in noonger than 15 min. Typically, this time could be used foroncurrent stroke team evaluation and participation.

Among our 12 recombinant tissue plasminogen activator cases,was treated without acute imaging, 1 received MRI, and 10

eceived CT scans. Among the 54 cases not treated acutely, 6eceived MRI and 48 received CT scans.

The 3 asymptomatic intracranial hemorrhages reported in ourtudy occurred with intra-arterial thrombolysis initiation at 54,65, and 305 min. While longer times to treatment initiation maye associated with higher rates of symptomatic hemorrhage, theelationship of time and asymptomatic hemorrhage has not beenstablished (4). In fact, mild radiological subtypes of intracranialemorrhage may actually mark early reperfusion and good clinicalutcome, compared with cases without hemorrhage (5). Neverthe-ess, we agree that time to treatment is a critical determinant ofood clinical outcome after stroke.

In summary, we favor an immediate CT scan of the head beforetroke reperfusion therapy in the setting of stroke after cardiacatheterization. It should result in minimal loss of time if concur-ent with stroke team activation and evaluation and will providemportant diagnostic and therapeutic information.

Pooja Khatri, MDcott E. Kasner, MDaniel Kolansky, MD

University of Cincinnatiepartment of Neurology

60 Stetson Streetuite 2308.O. Box 670525incinnati, Ohio 45267-mail: pooja.khatri@uc.edu

doi:10.1016/j.jacc.2008.04.022

EFERENCES

. Khatri P, Taylor RA, Palumbo V, et al., Treatment of Acute StrokeAfter Cardiac Catheterization (TASCC) Study Group. The safety andefficacy of thrombolysis for strokes after cardiac catheterization. J AmColl Cardiol 2008;51:906–11.

. Dukkipati S, O’Neill WW, Harjai KJ, et al. Characteristics of cerebro-vascular accidents after percutaneous coronary interventions. J Am CollCardiol 2004;43:1161–7.

. Fuchs S, Stabile E, Kinnaird TD, et al. Stroke complicating percuta-neous coronary interventions: incidence, predictors, and prognosticimplications. Circulation 2002;106:86–91.

. Khatri P, Wechsler LR, Broderick JP. ICH associated with revascular-ization therapies. Stroke 2007;38:431–40.

. Molina CA, Alvarez-Sabin J, Montaner J, et al. Thrombolysis-relatedhemorrhagic infarction: a marker of early reperfusion, reduced infarctsize, and improved outcome in patients with proximal middle cerebralartery occlusion. Stroke 2002;33:1551–6.

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greatly sympathize with Dr. De Marco and colleagues; we allish there would be a way to avoid the need for a brain image after

troke. The reality for us all is that, in 2008, there is no reliable wayo sort out a hemorrhage from an ischemic stroke. I concur that thedds favor an ischemic etiology in cath lab strokes, but by noeans is the cath lab patient immunized against hemorrhage.iven that thrombolytic therapy would be a disaster in a patientith hemorrhage, it is difficult for me to see any way to avoid auick computed tomography scan to ascertain that the patient didot bleed.

Patrick Lyden, MD, FAAN, FAHA

University of California San Diegotroke Center00 West Arbor Drivean Diego, California 92103

doi:10.1016/j.jacc.2008.04.026