alcohol septal ablation ( asa ) is becoming a popular treatment choice for symptomatic patients with hypertrophic obstructive cardiomyopathy ( hocm ) and resting left ventricular outflow tract obstruction gradient ( lvotg ) above 50  mmhg.the recurrence of symptomatic lvotg is approximately 10 percent in the first 2 years after asa [ 1 , 2 ] . current hypotheses to explain this recurrence include possible incomplete remodeling of the septum due to imprecise location of the iatrogenic lesion , a small infarct size because of suboptimal ethanol tissue concentration and an underestimation of existent surgical pathology such as massive calcification of the mitral ring [ 24 ] . to the best of our knowledge , late recurrence of symptoms due to  migration  of obstruction to midcavity level following asa has not been described in the literature . therapeutic options for symptomatic patients with high residual lvotg after asa include surgery , repeat asa , permanent pacing , and medical therapy . it is reasonable to speculate that permanent pacing has a synergistic effect on lvotg after asa and could be attempted before deciding on a repeat asa or surgical myectomy .   here we present our experience with permanent pacing in three patients with hocm who had recurrence of symptoms and lvg after initially successful alcohol septal ablation . sixty - one patients with hocm who remained symptomatic despite medical treatment underwent alcohol septal ablation at our institution between october 2004 and october 2007 . only patients with typical systolic anterior motion ( sam ) and our technique is described in a separate article and does not differ considerably from the one described in the literature . one milliliter of 95% ethanol per cm of septum thickness was injected through an otw balloon catheter after positive pressure reduction test . if equivocal results were observed , echo contrast was injected through an inflated balloon to delineate the part of the septum supplied by the septal branch . long - term success was defined as resting lvotg less than 20  mmhg and/or 50% reduction of resting and provoked lvotg matched by relief of the symptoms . success was achieved in 53 patients ( 87% ) who were followed for a median of 21 months ( 335 ) . no mortality was observed at 30 days , 2 patients died at 9 and 18 months , and the causes of death were sudden cardiac death and terminal heart failure . recurrence of lvg and symptoms were observed in 10 patients during the follow - up period . six patients were successfully treated with repeat asa because of echo findings of sam recurrence and three patients received permanent right ventricular pacing . we focus on three patients who share a similar clinical scenario : late relapse of symptoms due to dynamic obstruction at midcavity level following asa despite remodeling and thinning of the basal septum . all patients underwent initial asa at our institution due to effort - limiting angina refractory to beta blockers . all three had a similar underlying lv morphology with echocardiography revealing thickening of the whole septum , typical sam leading to outflow tract obstruction , and eccentric mitral regurgitation . the septal thickness at anterior mitral leaflet contact was 21 , 24 , and 20  mm , respectively for , patients 1 , 2 , and 3 . six months after asa the result was judged as excellent based on the disappearance of symptoms and virtual abolishment of lvotg at rest echo . thinning and akinesia of the basal septum was evident as a proof of well - placed scar ( figure 1 ) . patient n1 was a 54-year - old man who presented with syncope 26 months after asa and echocardiography at rest showed left ventricular systolic gradient of 42  mmhg at midcavity level and no sam . at the index procedure , 2.2  ml of alcohol were injected in the 1st septal perforator artery with complete resolution of the lvotg and reduction of the mitral regurgitation grade . similarly , patients n2 ( a 42-year - old woman ) and n3 ( a 61-year - old man ) presented 7 and 23 months after successful asa with recurrence of effort angina . invasive assessment of all three patients revealed intracavitary pressure gradient at the level of the papillary muscles with formation of a distal akinetic chamber ( figure 2 ) . in all three patients , echocardiography demonstrated marked scarring of the basal septum as expected late after asa ( septum thickness 16 , 18 , and 15  mm , resp . , for patients 1 , 2 , and 3 ) and relatively hypokinetic apex with systolic kissing of the midsegments of lv . after failure to control symptoms with beta blockers , we decided to proceed with permanent pacemaker implantation .   in two patients permanent ddd mode pacemakers were implanted with passive fixation electrodes positioned at rv apex and right atrial appendage . in one patient ( n1 ) the rv electrode was implanted aiming at the pig - tail catheter positioned at lv apex . ventricular pacing of 99 percent was achieved in all patients ( pv interval of 160  msec for ddd pacemakers ) . all three patients had echo at rest and after a stress test at the 6-month followup the resting lvgs measured by doppler echocardiography before asa , at symptom recurrence and at 6 months after pacing are shown in table 1 . all three patients were able to achieve 5 mets on a modified bruce protocol at 6-month followup , and echo detected no lvotg ( defined as velocity > 2  m / s a ) at rest and after exercise . functional class significantly improved from nyha iii prior to treatment to nyha ii after - pacing . despite promising early results , permanent pacing is falling out of favor as a first - line therapy for drug - resistant hocm due to its lower success rate demonstrated in randomized studies as compared to myectomy and asa [ 6 , 7 ] . a possible explanation is the inability to achieve full reverse excitation of the septum in a significant proportion of the patients due to short intrinsic av interval or technical factors such as the inability to place the electrode at the true rv apex . even if some patients do respond to asa in terms of long - lasting symptom relief , the factors leading to asa failure are also far from clear . on the basis of studies that followed patients with mri after asa , it can be extrapolated that in a significant number of ablated patients the localization of the infarct is away from the zone of contact between the anterior mitral leaflet and the septum . other investigators suggest on the basis of postmortem histology that , for unknown reasons , even a properly located lesion can lead to patchy instead of dense fibrosis with only mild septum thinning . in both cases , in contrast to other investigators , we have observed several cases of recurrence of lvotg and symptoms well after the first year of followup . this might be related to the selection of patients or to a technical factor although we have not found major differences between our technique and the one already published in the literature . in the proportion of our patients , distal displacement of the level of obstruction due to remodeling of to the best of our knowledge , no such case has been previously described in the literature . choice of treatment after asa failure appears to depend on the underlying mechanism , with drug therapy rarely effective in our experience . the small number of cases of asa failures makes it highly unlikely that a comparative study of different treatment modalities can be conducted . repeat asa appears to be a logical choice if there is relapse of lvotg , sam and no evidence of effective remodeling of the septum . due to the lack of reliable criteria for selection of responders , current guidelines recommend pacing in hocm only in case of coexistent bradycardia / conduction disease or indications for icd placement [ 2 , 8 ] . there is also agreement that patients with preexisting bundle branch block who are candidates for asa or surgery should receive a pacemaker if the risk of procedure - related av block is high . in our institution , we consider pacing as a first - line treatment for midcavity obstruction because it is relatively non - invasive and at least 1 publication suggests that it is efficacious . overall , we have found permanent pacing to be a good solution even when midcavity obstruction manifested late after asa . we found a specific pattern of progression of hocm after successful asa . in our experience permanent rv pacing appears to be a safe and effective treatment option with no major drawbacks . it could be proposed as a niche treatment for patients with recurrence of lvg at midventricular level after asa .
treatment of symptom recurrence after initially successful alcohol septal ablation ( asa ) in hypertrophic obstructive cardiomyopathy ( hocm ) when accompanied by relapse of intracavitary left ventricular pressure gradient ( lvg ) is guided by the underlying mechanism . 
 we describe our experience with permanent pacing in three patients with relapse of both lvg and symptoms 7 to 12 months after successful asa . 
 even though pressure gradient recurrence was observed at midventricular level , we were able to achieve symptomatic improvement and lvg reduction after right ventricular apex pacing in all three cases . 
 the effect on symptoms was long lasting 
 the 6-month followup echo - stress tests confirmed good exercise capacity and lack of provocable lvg . 
 we found pacing to be a safe and effective treatment option in this clinical scenario . 
 based on our overall observations , we propose pacing as a niche treatment for patients with recurrence of lvg at midventricular level after asa .