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Partial atrioventricular canal defect in elderly patients (age ≥ 60 years )
ABSTRACTS
PARTIAL ATRIOVENTRI~ULAR (AGE x30 YEARS)
CANAL DEFECT IN ELDERLY PATIENTS
John i?. Hynes, MD; Abdul J. Tajik, MD, FACC; James B. Seward, MD, FACC; Dwight C. McGoon, MD, FACC. Mayo . Clinic. Rochester, MN. Survival of patients (pts) with partial atrioventricular canal (PAVC) into the seventh decade of life is rare (9 reported cases in the literature). The clinical profile and surgical experience of PAVC in this age group are unknown. We therefore report our experience in 6 elderly pts (4 women, 2 men) with a mean age of 68 yr (3 pts >70 yr). All pts were symptomatic: Class II--2 pts, Class III--l, and Class IV--3. Electrocardiograms showed characteristic left axis deviation and right bundle-branch block in 5 pts, atria1 fibrillation in 3, and intermittent complete heart block (CHB) in 1. Chest roentgenograms showed cardiomegaly and enlarged pulmonary arteries in all. Diagnosis was confirmed by 2-dimensional echocardiography, cardiac catheterization, or both. Left ventriculography showed severe mitral regurgitation in 2 pts. Operation was performed in 4 pts; 2 pts declined operation. There were no operative deaths or cases of CHB. Surgical repair included patch closure of the primum defect--4 pts, suturing of the cleft mitral leaflet--3 pts, and mitral valve replacement--l pt with severe mitral regurgitation. All pts had significant symptomatic improvement (mean follow-up, 46 mo). Of the 2 nonoperative pts, 1 (age 73) died of noncardiac cause, and 1 (age 78) is presently functional Class III. Conclusions: (1) This first reported series of elderly pts with PAVC includes the 2 oldest known survivors--age 78 (nonoperative) and age 79 (6 yr after operation). (2) Our surgical experience, based on small numbers, nevertheless suggests that operation can be performed at low risk with gratifying symptomatic improvement. Therefore, surgical repair in symptomatic elderly pts with PAVC is justified.
VALUE OF LEAD V R IN ACUTE INFERIOR WALL INFARCTION TO IDENTIFY RIGHT VENTRICULAR INVOLVEMENT AND RISK OF DEVELOPMENT OF AV NODAL BLOCK. Simon H. Braat, MD, Pedro Brugada, MD, Chris de Zwaan, MD, Joseph M. Coenegracht, MD and Hein J.J. Wellens, MD, FACC. Dept. of Cardiology and Nuclear Medicine, University of Limburg, Annadal Hospital, Maastricht, The Netherlands. In 52 consecutive patients (pts.) with an acute inferior wall myocardial infarction, the right precordial lead, V4R, was also recorded on admission and every 8 hours for the next 3 days. All pts. were continiously monitored for at least 3 days to detect rhythm and conduction disturExact infarct localisation was done by performing c pyrophosphate scintigraphy (TPS). Results: 1. 22 Pts. (42%) showed right ventricular involvement in the TPS. 86% Of these pts: had ST-elevation in V,R 1 '1 = lmm on admission. 2. 14 Pts. (27%) developed conduction disturbances in the AV node. IO Of these pts. had ST-elevation 2 lnanin V4R. 3. The duration of ST-elevations in V4R was shorter than 10 hours in 65%. Conclusions: In 86% of pts. with an acute inferior wall infarction right ventricular involvement was detected by ST-segment elevation 1 lmm in lead V4R. In 50% of pts. with ST-elevation 2 Imm in lead V4R AV nodal conduction disturbances.developed. In contrast this occurred only in 15% of pts. without this electrocardiographic finding. The duration of ST-elevation in V R > lmm is shortlived stressing the necessity of $arlTV4R recording in pts. with an acute inferior wall infarctlon. 999
March 1982
The American Journal of CARDIOLOGY
WEDNESDAY, APRIL 28, 1982 AM CONGENITAL HEART DISEASE: POSTOPERATIVE UP AND DYSRHYmMlAS 10:30- 12:oo
FOLLOW-
SUDDEN DEATH AFTER CORRECTION OF TETPALOGY OF FALLOT: A CLINICAL PATHOLOGICAL STUDY. John Deanfield, MB, William McKenna, MD, Siew Yen Ho, MPhil, Katherine Hallidie-Smith, MB, FACC, Robert Anderson, MD, Sally Allwork, PhD, Royal Postgraduate Medical School and Cardiothoracic Institute, London. During longterm (mean 10 yrs) follow-up after correction of tetralogy of Fall&, 6 of 196 patients died suddenly and unexpectedly. Their age at operation and at death was 8-16 yrs (mean 12) and 12-25 yrs (mean 18) respectively. None had functional limitation but one had rapid palpitation, and 2 syncope; of these one had documented ventricular tachycardia and the other frequent ventricular extra fiystoles. All had right bundle branch block but none left axis deviation. Autopsy was performed in 3. The ventricular septal (IVS) defect was perimembranous (2) and musculo-infundibular (1). These defects were closed and the right ventricular outflow tract (RVGT) resection was adequate. Serial sections of 10~ thickness were cut from tissue blocks of: the proximal IV.9 including the AV node, penetrating bundle and proximal bundle branches; the distal IVS; left and right ventricular wall; right ventriculotomy site; and the RVOT. Histology showed fibrous tissue replacement at the ventriculotomy site in all. Severe fibrosis was also found in the RVOT (1) and on the crest and right side of the IVS (1). In all:the AV node, penetrating bundle, proximal bundle branches and left bundle were normal and well clear of sutures; the right bundle branch however crossed the suture line on the right side of the IVS. This suggests that sudden death was not due to AV block. The clinical presentation and marked RV fibrosis support ventricular arrhythmia as the cause of sudden death in these patients.
SUSTAINED VENTRICULAR TACHYCARDIA FOLLOWING REPAIR OF TETRALOGY OF FALLOT: NE# ELECTROPHYSIOLOGIC FINDINGS John 0. Kuqler, MD, Paul K. Mooring, MD, FACC, William W. Pinsky, MD, FACC, John P. Cheatham, MD, Phil J. Hofschire, MD, FACC, Pediatric Cardiology, llniversity of NE, Omaha. Ventricular (V) dysrhythnia originating from the RV outflow tract is a presumed cause of sudden death in ots following repair of tetralogy of Fallot (TF). Phenytoin (PH) has been reported to control PVCs in these pts and thus has been used to prevent sudden death. Contrary to this data, we have had 4 pts undergo electrophysiological studies (EPS) at postop cath and 3 had induced sustained V tachycardia (T) originating from the RV septum. Also, VT was later induced after PH (oral loading) but not after propranolol (PR) (0.1-0.2 ma/kg/IV). The EPS included bursts of V pacing at high rates, single and double V stimuli. Five electrode catheters were used. Pts 1 and 2 had no PVCs on Holter (H) and no symptoms. Pt 3 had chest pain unassociated with 30 total PVCs on 24 hr H. None had PVCs durina exercise (El. PTAGE SEXD;( R,,(mmHg)‘vT: Serum level: VT: Serum level: 1 14 M TF* R&T; PH(;;s/ml) “$4’0 PR (~~~1) 2 3 14 16 F TF+ 85/10 ::;;2 272 286 :Y 250 285 :6' Abbreviations: Dx, diagnosis; *also postop pulmonary valve, tricuspid valve replacement; talso postop Rastelli conduit In pt 1, lidocaine, procainamide, quinidine each failed to prevent VT. We conclude that this VT differs from previously described VT in pts following TF repair by: l)refractorinessto PH; 2) lack of 100% association of pacing induced VT with PVC or VT on H&E; 3) lack of 100% association with high RV pressure; 4)siteof origin in RVseptus rather than RV outflow tract thus possibly related in these pts to ventricular septal defect patch.
Volume 49
PARTIAL ATRIOVENTRI~ULAR (AGE x30 YEARS)
CANAL DEFECT IN ELDERLY PATIENTS
John i?. Hynes, MD; Abdul J. Tajik, MD, FACC; James B. Seward, MD, FACC; Dwight C. McGoon, MD, FACC. Mayo . Clinic. Rochester, MN. Survival of patients (pts) with partial atrioventricular canal (PAVC) into the seventh decade of life is rare (9 reported cases in the literature). The clinical profile and surgical experience of PAVC in this age group are unknown. We therefore report our experience in 6 elderly pts (4 women, 2 men) with a mean age of 68 yr (3 pts >70 yr). All pts were symptomatic: Class II--2 pts, Class III--l, and Class IV--3. Electrocardiograms showed characteristic left axis deviation and right bundle-branch block in 5 pts, atria1 fibrillation in 3, and intermittent complete heart block (CHB) in 1. Chest roentgenograms showed cardiomegaly and enlarged pulmonary arteries in all. Diagnosis was confirmed by 2-dimensional echocardiography, cardiac catheterization, or both. Left ventriculography showed severe mitral regurgitation in 2 pts. Operation was performed in 4 pts; 2 pts declined operation. There were no operative deaths or cases of CHB. Surgical repair included patch closure of the primum defect--4 pts, suturing of the cleft mitral leaflet--3 pts, and mitral valve replacement--l pt with severe mitral regurgitation. All pts had significant symptomatic improvement (mean follow-up, 46 mo). Of the 2 nonoperative pts, 1 (age 73) died of noncardiac cause, and 1 (age 78) is presently functional Class III. Conclusions: (1) This first reported series of elderly pts with PAVC includes the 2 oldest known survivors--age 78 (nonoperative) and age 79 (6 yr after operation). (2) Our surgical experience, based on small numbers, nevertheless suggests that operation can be performed at low risk with gratifying symptomatic improvement. Therefore, surgical repair in symptomatic elderly pts with PAVC is justified.
VALUE OF LEAD V R IN ACUTE INFERIOR WALL INFARCTION TO IDENTIFY RIGHT VENTRICULAR INVOLVEMENT AND RISK OF DEVELOPMENT OF AV NODAL BLOCK. Simon H. Braat, MD, Pedro Brugada, MD, Chris de Zwaan, MD, Joseph M. Coenegracht, MD and Hein J.J. Wellens, MD, FACC. Dept. of Cardiology and Nuclear Medicine, University of Limburg, Annadal Hospital, Maastricht, The Netherlands. In 52 consecutive patients (pts.) with an acute inferior wall myocardial infarction, the right precordial lead, V4R, was also recorded on admission and every 8 hours for the next 3 days. All pts. were continiously monitored for at least 3 days to detect rhythm and conduction disturExact infarct localisation was done by performing c pyrophosphate scintigraphy (TPS). Results: 1. 22 Pts. (42%) showed right ventricular involvement in the TPS. 86% Of these pts: had ST-elevation in V,R 1 '1 = lmm on admission. 2. 14 Pts. (27%) developed conduction disturbances in the AV node. IO Of these pts. had ST-elevation 2 lnanin V4R. 3. The duration of ST-elevations in V4R was shorter than 10 hours in 65%. Conclusions: In 86% of pts. with an acute inferior wall infarction right ventricular involvement was detected by ST-segment elevation 1 lmm in lead V4R. In 50% of pts. with ST-elevation 2 Imm in lead V4R AV nodal conduction disturbances.developed. In contrast this occurred only in 15% of pts. without this electrocardiographic finding. The duration of ST-elevation in V R > lmm is shortlived stressing the necessity of $arlTV4R recording in pts. with an acute inferior wall infarctlon. 999
March 1982
The American Journal of CARDIOLOGY
WEDNESDAY, APRIL 28, 1982 AM CONGENITAL HEART DISEASE: POSTOPERATIVE UP AND DYSRHYmMlAS 10:30- 12:oo
FOLLOW-
SUDDEN DEATH AFTER CORRECTION OF TETPALOGY OF FALLOT: A CLINICAL PATHOLOGICAL STUDY. John Deanfield, MB, William McKenna, MD, Siew Yen Ho, MPhil, Katherine Hallidie-Smith, MB, FACC, Robert Anderson, MD, Sally Allwork, PhD, Royal Postgraduate Medical School and Cardiothoracic Institute, London. During longterm (mean 10 yrs) follow-up after correction of tetralogy of Fall&, 6 of 196 patients died suddenly and unexpectedly. Their age at operation and at death was 8-16 yrs (mean 12) and 12-25 yrs (mean 18) respectively. None had functional limitation but one had rapid palpitation, and 2 syncope; of these one had documented ventricular tachycardia and the other frequent ventricular extra fiystoles. All had right bundle branch block but none left axis deviation. Autopsy was performed in 3. The ventricular septal (IVS) defect was perimembranous (2) and musculo-infundibular (1). These defects were closed and the right ventricular outflow tract (RVGT) resection was adequate. Serial sections of 10~ thickness were cut from tissue blocks of: the proximal IV.9 including the AV node, penetrating bundle and proximal bundle branches; the distal IVS; left and right ventricular wall; right ventriculotomy site; and the RVOT. Histology showed fibrous tissue replacement at the ventriculotomy site in all. Severe fibrosis was also found in the RVOT (1) and on the crest and right side of the IVS (1). In all:the AV node, penetrating bundle, proximal bundle branches and left bundle were normal and well clear of sutures; the right bundle branch however crossed the suture line on the right side of the IVS. This suggests that sudden death was not due to AV block. The clinical presentation and marked RV fibrosis support ventricular arrhythmia as the cause of sudden death in these patients.
SUSTAINED VENTRICULAR TACHYCARDIA FOLLOWING REPAIR OF TETRALOGY OF FALLOT: NE# ELECTROPHYSIOLOGIC FINDINGS John 0. Kuqler, MD, Paul K. Mooring, MD, FACC, William W. Pinsky, MD, FACC, John P. Cheatham, MD, Phil J. Hofschire, MD, FACC, Pediatric Cardiology, llniversity of NE, Omaha. Ventricular (V) dysrhythnia originating from the RV outflow tract is a presumed cause of sudden death in ots following repair of tetralogy of Fallot (TF). Phenytoin (PH) has been reported to control PVCs in these pts and thus has been used to prevent sudden death. Contrary to this data, we have had 4 pts undergo electrophysiological studies (EPS) at postop cath and 3 had induced sustained V tachycardia (T) originating from the RV septum. Also, VT was later induced after PH (oral loading) but not after propranolol (PR) (0.1-0.2 ma/kg/IV). The EPS included bursts of V pacing at high rates, single and double V stimuli. Five electrode catheters were used. Pts 1 and 2 had no PVCs on Holter (H) and no symptoms. Pt 3 had chest pain unassociated with 30 total PVCs on 24 hr H. None had PVCs durina exercise (El. PTAGE SEXD;( R,,(mmHg)‘vT: Serum level: VT: Serum level: 1 14 M TF* R&T; PH(;;s/ml) “$4’0 PR (~~~1) 2 3 14 16 F TF+ 85/10 ::;;2 272 286 :Y 250 285 :6' Abbreviations: Dx, diagnosis; *also postop pulmonary valve, tricuspid valve replacement; talso postop Rastelli conduit In pt 1, lidocaine, procainamide, quinidine each failed to prevent VT. We conclude that this VT differs from previously described VT in pts following TF repair by: l)refractorinessto PH; 2) lack of 100% association of pacing induced VT with PVC or VT on H&E; 3) lack of 100% association with high RV pressure; 4)siteof origin in RVseptus rather than RV outflow tract thus possibly related in these pts to ventricular septal defect patch.
Volume 49