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Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: Clinical, hemodynamic, and angiographic findings
American CLINICAL
Heart
Founded
in 1925
March
1983 Volume 105, Number 3
Journal
INVESTIGATIONS
Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: Clinical, hemodynamic, and angiographic findings Surgical cure of right ventricular tachycardia (RVT) has been recently described in patients with a disease characterized by abnormal electrical “arrhythmogenic right ventricular dysplasia,” activation of the right ventricle and localized or generalized angiographic right ventricular (RV) wall motion abnormalities (WMA). In search of a selective RV cardiomyopathy complicated by chronic recurrent RVT, 38 consecutive patients (mean age 30.5 k 12 years) with RVT and no ischemic heart disease were studied clinically, noninvasively, and by cardiac catheterization including left and right ventriculography. RV volumes were as follow: end-systolic volume ranged from 23 to 103 (mean + SD, 45.8 f 20) cc/m2 and was abnormal in 14 patients (37%); end-diastolic volume ranged from 57 to 138 (90.5 +- 28) cc/m* and was abnormal in 15 patients (39%); ejection fraction (EF) ranged from 0.18 to 0.84 and was decreased in five patients (13%). Seventeen patients (45%) had abnormal RV volume, EF, and/or pressures (RVD), five (13%) of whom had abnormal LV volume, EF, and/or pressures (LVD), and 12 (32%) patients with RVD had no LVD. Twenty-one patients (55%) had no RVD, two of whom had LVD. Only two of the 17 patients had RV regional WMA, one with and one without LVD. Most patients with LVD five of seven (71%) also had RVD while 12 of 31 patients (39%) with no LVD had RVD. In conclusion, less than one half of patients with RVT had selective RV cardiomyopathy and more than one half of patients with RVT had normal RV hemodynamics and angiography. (AM HEART J 105:357, 1983.)
Raymond J. Pietras, M.D., Wilfred Lam, M.D., Robert Bauernfeind, Amjad Sheikh, M.D., Edwin Palileo, M.D., Boris Strasberg, M.D., Steven, Swiryn, M.D., and Kenneth M. Rosen, M.D. Chicago, Ill.
In 1977, we noted an association of chronic recurrent right ventricular tachycardia and absence of organic heart disease.’ The diagnosis of absence of organic heart disease was based upon clinical examination, chest x-ray, and diagnostic left heart catheterization with coronary angiography. Recently, Fontaine et a1.2s3 described a group of patients with recurrent right ventricular tachycardia, abnormal electrical From Lincoln
the Section of Cardiology, Shoal of Medicine, University
Department of Illinois
of Medicine, Abraham College of Medicine.
Supported in part by National Heart, Lung and Blood Institute tional training grant HL 07387, by research grants HL 18794 23566; and by a grant from the Banes Estate.
Instituand HL
Received accepted
3, 1981;
for publication Nov. 12, 1981.
Reprint requests: of Illinois Hospital,
Aug.
10, 1981;
revision
Raymond J. Pietras, M.D., P.O. Box 6998, Chicago,
received
Cardiology IL 60680.
Nov. Dept.,
University
M.D.,
activation of the right ventricle, and localized or generalized right ventricular angiographic wall motion abnormality. These patients have been characterized as having “arrhythmogenic right ventricular dysplasia.” Since the right ventricle was not scrutinized in our initial reported group of patients with recurrent right ventricular tachycardia, it is possible that some or all of our patient group had clinically silent “arrhythmogenic right ventricular dysplasia.” To further elucidate the pathophysiology of recurrent right ventricular tachycardia, we now report a systematic evaluation of right ventricular function and right ventricular angiographic anatomy in a large series of patients referred to us with chronic recurrent right ventricular tachycardia. Because we were looking for the presence of selective right ventricular 357
358
Pietras et al
cardiomyopathy, we have excluded patients with recurrent ventricular tachycardia complicating acute or chronic ischemic heart disease. METHODS Patients. Thirty-eight consecutive referred patients with chronic recurrent unifocal right ventricular tachycardia were evaluated clinically, hemodynamically, and angiographically. Patients with known ischemic heart diseasewith prior myocardial infarction and/or significant obstructive coronary disease were excluded from this study. Patients in whom drugs or pacing catheters might have induced ventricular tachycardia were also excluded. Characterization of ventricular tachycardia. Ventricular tachycardia was diagnosedusing standard ECG criteria-i.e., a prolonged QRS complex (38 patients), atrioventricular dissociation (37 patients), fusion complexes (24 patients), and captures (24 patients). Ventricular tachycardia was also verifed by His bundle recordings in 28 patients including all patients in whom the diagnosisof ventricular tachycardia might be uncertain. Both frequency and duration of the tachycardia were determined utilizing symptoms and ECG tracings. The term “chronic recurrent” defined a minimum of two documented episodesof ventricular tachycardia at least 1 month apart. The majority of patients far exceeded this minimal frequency of ventricular tachycardia. Patients were also classified as having paroxysmal sustained, paroxysmal nonsustainedor exercise-inducedventricular tachycardia. “Sustained” referred to protracted paroxysms which could usually be electrophysiologically induced and terminated. “Nonsustained” ventricular tachycardia was characterized by frequent short, selfterminating episodeswith many premature beats (usually identical in morphology to QRS complexesduring ventricular tachycardia) on most or all ECGs. “Exercise provoked” ventricular tachycardia referred to patients whose ventricular tachycardia could be reproducibly provoked by exertion (history) and treadmill testing. Patients were said to have right ventricular tachycardia when ventricular tachycardia wasnoted with a left bundle branch pattern on the 12-leadsurface ECG. The origin of ventricular tachycardia from the right ventricle was also supported by endocardial mapping the earliest onset of tachycardia QRS complexesfrom the right ventricle with a catheter electrode during this dysrhythmia (27 patients). Diagnostic cardiac catheterization. Intracardiac pressureswere recorded at rest from the right and left heart chambers through fluid-filled catheters using the midchest as the zero reference level. Mean right atria1 and right ventricular end-diastolic pressure >7 mm Hg, and mean pulmonary capillary wedge pressureand left ventricular end-diastolic pressure >12 mm Hg were considered abnormal. Biplane right ventricular angiography wasperformed in the posteroanterior and lateral projection with radiopaque contrast material introduced through a right ventricular
catheter (32 patients) or a right atria1 catheter (six patients) at a rate of 12 cc/set over 3 to 4 seconds. Ventricular ectopic beats and postventricular ectopic~ beatswere rejected for analysis.Right ventricular volumes were measured at, end-systole and end-diastole from biplane cineangiogramsusing a computer (Echo-C’omp, Digisonics, Houston, Texas) programmed for Simpson’s rule method of analysis where the right ventricle is assumedto be an elliptical cylinder. The measuredvolumes were corrected with the regression equation oi’ Gentzler et al.’ Right, ventricular ejection fraction was calculated from end-systolic and end-diastolic volumes and normal values usedwere thosereported by Gentzler et al. where right ventricular end-diastolic volume indexed was 81 t_ 1‘2.3cc/m’ (mean r SD), right vent,ricular endsystolic volume Indexed was 39 : 8.5 cc/m-, and right ventricular ejection fraction was 0.51 + 0.08.’ Right ven. tricular regional wall motion wasqualitatively assessed by two observers(RP and WL). Tricuspid valve prolapsewas diagnosedwhen angiography revealed a scallopedtricuspid valve bulging into the right atrium during systole. Thirty patients had 40 to 26 cc of radiopaque contrast material injected into the left ventricle at a rate of 12 cc/set and the remaining eight, patients had ievophase ventriculograms from the right-sided injection. Left ventriculograms were obtained with biplane cineangiography in 27 patients in the 30-degreeright anterior oblique and 60-degree left anterior oblique project,ions, m three patients in the posteroanterior and lateral projections, and with single plane angiography in eight patients (four in the right anterior oblique projection and four in the posteroanterior projection). I,eft ventricular end-diastolic and end-systolic, vulumes were calculated by thr arealength method. Left ventricular volumes were corrected for true volume with appropriate regressionequations. The normal values used for left \,entricular volume and ejection fraction were those reported by Kennedy et al.,” where left ventricular end-diast.olic volume indexed was 70 i 20 cc/m left venlricular end-systcblit. volume indexed was 24 ? 10 cc/nl~. and left ventricular eject.ion fraction was 0.67 -i (1.08. I,eft ventricular regional wall motion was qualitatively assessedby two ohservers (RI’ and WL). Mitral valve prolapse was diagnosed when angiographyrevealed a scallopedmitral valve bulging into the left atrium during systole. Selective coronary arteriography was performed in 22 patients using either a femoral or brachial artery approach. These arteriograms were interpreted as having no significant lesion in any vessel(by study design).There were absolutely no data in the remaining 16 patients, who had not undergone coronary angiography, suggestingischemic heart, disease.The chi-square test with the Yates correction was used to assesst,he significance of differencesbetween groups of patients. RESULTS Clinical
characteristics.
Patients
ranged in age from
13 to 56 (mean +- SD, 30.5 t 12) years. Nineteen
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Right
VT without
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359
I. Right ventricular hemodynamic and angiographic findings
Table
RV WMA
Patient Group I-No
right ventricular
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0
ventricular
22 23 24 25 26 27 28 29
Apical ALW
+ + IW + +
Mean Standard
RV EDV (cc/m2)
R VEF
RA (mm Hg)
R VSIED (mm Hg)
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 + 0 0 0 + 0
23 36 36 29 26 28 39 29 31 36 32 38 28 40 27 40 40 40 28 38 38
65 86 63 70 68 69 93 69 61 85 57 80 70 78 63 73 72 83 69 67 al
0. 64 0.58 0.43 0.59 0.62 0.59 0.58 0.58 0.49 0.58 0.44 0.52 0.60 0.49 0.58 0.45 0.44 0.52 0.59 0.43 0.53
3 6 2 7 4 6 5 5 0 1 6 2 0 2 2 1 5 4 2 4 1
2414 33/4 2014 2616 2516 20/4 1912 2015 2214 13/3 20/6 2214 18/3 24/4 2414 1812 1915 24/6 2513 1815 1612
0 0 0 0 0 0 0 +
59* 35 57* 97: 52* 35 52' 83'
L27* 77 107* 155' 115* 98' 99* 115*
0.54 0.55 0.47 0.37* 0.55 0.64 0.47 0.28*
6 3 4 2 4 6 3 7
2816 41/a* 2816 1512 2012 16/6 19/4 2317
+ f 0 0 t 0 0 0 0
48* 51* 79’ 60* 50* 88s 103’ 58* 31 45.8 20
112* loa* 124* 119* 97* 129* 126* 138* 70 90.5 26
0.57 0.53 0.36* 0.49 0.48 0.32* 0.18* 0.58 0.56 0.50 0.10
4 I 4 0 7 9* 101 2 a* 3.9 2.6
1714 14/5 2014 14/3 26/8* 22/9' 28/10* 2414 22/S* 21.814.8 5.412.1
disease
+
30 31 32 33 34 35 36 37 38
RV ESV (cclm2j
disease
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
Group Ii-Right
TVP
0 0 0 Global 0 0 0 hypokinesis, akinesis 0 0 Global 0 hypokinesis Global Global 0 0
deviation
Abbreviations and symbols: RV WMA = right ventricular wall motion abnormality; TVP = tricuspid valve prolapse; RV ESV = right ventricular end-systolic volume indexed; RVEF = right ventricular ejection fraction; m = mean right atrial pressure; RVS/ED = right ventricular systolic/right ventricular end-diastolic pressure; ALW = anterolateral wall; IW = inferior wall; * = abnormal value.
patients (50% ) were male and 19 patients (50% ) were female. Thirty-five had symptoms related to episodes of ventricular tachycardia which included one or more of the following: palpitations (30), syncope (12), dyspnea (S), chest pain (10). Eight patients had systolic murmurs five of whom had midsystolic clicks; four others had midsystolic clicks alone. One patient had a third heart sound and another had a fourth heart sound. Only one patient
had cardiomegaly on chest x-ray examination. Excluding the occurrence of right ventricular tachycardia, the EGG was entirely normal in 24 patients and the remaining 14 patients had nonspecific ST-T wave changes; two of these had left anterior superior hemiblock, and one each had left ventricular enlargement, Q-T interval prolongation, and abnormal Q waves in leads I and aV,. Most of these abnormal clinical findings were present in the group
360
Pietras
et al.
March, American
Heart
1983 Journal
Fig. 1. Normal right ventricular biplane angiogramof patient No. 5. The frames on the left are from the lateral view and those on the right from the posteroanterior view. The two upper frames are at end-systole and the two lower frames are at end-diastole. There is uniform contraction of all regions of the ventricle and global ejection fraction is normal. The tricuspid valve is normal in appearance.
of patients subsequently designated as having right ventricular disease. As noted in our previous study, many patients (23 or 60% ) were free of clinically manifest organic heart disease utilizing history, physical examination, ECG (excluding ventricular tachycardia), chest x-ray examination, and noninvasive studies. Nine patients (24 % ) had clinically diagnosed mitral valve prolapse (precatheterization); six patients (16 % ) were considered cardiomyopathic (precatheterization) . Characteristics of ventricular tachycardia. Five patients (13 % ) had paroxysmal sustained ventricular tachycardia, 25 patients (66%) had paroxysmal nonsustained ventricular tachycardia, and eight patients (21% ) had exercise-induced ventricular tachycardia. The QRS morphology during ventricular tachycardia was left bundle branch block pattern in leads I, aV,, V1, and V,. The mean frontal plane QRS axis during ventricular tachycardia was normal in 24 patients, was right axis in eight patients, left axis in four patients, and was indeterminant in two.
Heart rate during ventricular tachycardia from 95 to 240 (164 ? 31) bpm.
ranged
Right ventricular angiographic anatomy (Table I; Figs. 1 and 2). Visual inspection of biplane right
ventricular angiography revealed normal wall motion in 32 patients (84%), regional wall motion abnormality in two patients (5%) (inferior wall hypokinesis and akinetic anterolateral wall with hypokinesis of the apex), and generalized decreased contractility in four patients (11% ). Six patients (16%) had tricuspid valve prolapse. Of these six patients, wall motion was normal in four and abnormal in two, each of whom had regional wall motion abnormalities. Right ventricular end-systolic volume ranged from 23 to 103 (45.8 +- 20) cc/m2 and was abnormal in 14 patients (37%). Right ventricular end-diastolic volume ranged from 57 to 138 (90.5 + 26) cc/m2 and was abnormal in 15 patients (39 % ). Calculated right ventricular ejection fraction ranged from 0.18 to 0.64 and was decreased in five patients (13%). To summarize, 23 patients (61% ) had no abnormality of right ventricular angiograph-
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Fig. 2. Abnormal right ventricular biplane angiogram of patient No. 29. The frames on the left are from the lateral view and those on the right from the posteroanterior view. The two upper frames are at end-systole and the two lower frames are at end-diastole. Apical hypokinesis and anterolateral wall akinesis are seen with a reduced ejection fraction. This angiogram is similar in appearance to that described by Fontaine et al.*,” as characteristic of arrhythmogenic right ventricular dysplasia. The
tricuspid valve is scalloped and bulges into the right atrium during systole, typical of tricuspid valve prolapse.
ic anatomy (excluding tricuspid valve prolapse). This includes all 21 patients in group I (no RV disease) and patients No. 23 and 38 in group II (RV disease). Fifteen patients (39%) had one or more abnormalities (excluding tricuspid valve prolapse). Right heart pressures (Table I). Right atria1 pressure ranged from 0 to 10 (3.9 f 2.6) mm Hg and was abnormal in three patients. Right ventricular systolic pressure ranged from 13 to 41 (21.9 f 5.4) mm Hg and was abnormal in one patient. Right ventricular end-diastolic pressure ranged from 2 to 10 (4.8 + 2.1) mm Hg and was abnormal in five patients. We compared right heart pressures and right ventricular angiographic findings. Of the 15 patients with one or more angiographic features abnormal, three had increased right atrial and/or right ventricular enddiastolic pressures. Two patients with normal angiographic features had elevated right atrial and right ventricular end-diastolic pressures. Two additional patients with elevated right atrial and right ventric-
ular end-diastolic pressures had normal right ventricular volumes and ejection fraction. Five of the six patients with tricuspid valve prolapse had normal right atria1 and right ventricular end-diastolic pressures. Summary
of evidence
for right
ventricular
disease.
Excluding tricuspid valve prolapse, twenty-one patients (55 % ) had normal right heart pressure and right ventricular angiographic findings and 17 patients (45% ) had abnormal right heart pressure and/or right ventricular angiographic findings. These latter patients will henceforth be called the right ventricular disease (RVD) group (Table I). Two patients with no RVD had tricuspid valve prolapse and four patients with RVD had tricuspid valve prolapse. Left
ventricular
angiographic
anatomy
(Table
II).
Visual inspection of left ventricular angiograms revealed normal wall motion in 33 patients (87%), regional wall motion abnormalities in no patients
March.
362
Pietras
Table
et al.
II. Left ventricular
American
hemodynamic
Patients
and angiographic
LV WMA
MVP
right uentricular
disease 0 0 0 0 0 0 0 0 0 0
L1’ ES\’ jcc,‘m’i
LVEDb
PC I&. I, VEb
Ccc/m-i
0
7:
0.75 0.67 0.69 0.70 0.65 0.64 0.59 0.77 0.68 0.w
56
U.:‘2
78 7"'
0.7" 0.71
48 84 71
0 68 76
0 0
86 88 56
0 .~
---.-_-----
11
0
12 13
0 0
0
14
0 0
0 0
0.70 0.76
0
0.62
15 16 17 18
0 0
0 t +
0.66 0.68
19
0
+
0.68
20
0
+
lJ.81) 0.-s*
21
Group II-Right “2
ventricular
+ Global disease 0
23
0 0
24 2<5
0 0
26 27
0
28 2.9
0 0
30
0 0
31 32
0
x1
0
+ t + t
34
:i:’ 36
37 38
Global Global Global Global 0
U
k&J
0
5
0 0 0
,’ LGP ---
/ mm Fig) _.-_--.
8 7
6 5
H ; 10
+
10 r,
10 r,
+ t
x Ii
10 ,I
0
11 12
1’ 1 ‘.I‘.
0 0 +
0
14*
0 0
x
0
9 7.6 2.3
deviation
Abbreviations and symbols: LV WMA = left ventricular volume indexed; LV EDV = left ventricular end-diastolic wedge pressure; LVEDP = left ventricular end-diastolic
(mm
0
Mean Standard
1983 Journal
findings
.-
Group I-No 1 2 :I 4 5 6 7 8 9 10
Heart
wall motion abnormality; MVP volume indexed; LVEF = left pressure: * = abnormal value.
(O%), and generalized decrease in contractility in five patients (13%). Eight patients (21%) had angiographic mitral valve prolapse. Of these eight, wall motion was normal in all. Left ventricular end-systolic volume ranged from 14 to 67 (26 k 12.5) cc/m2 and was abnormal in five patients (13 % ). Left ventricular end-diastolic volume ranged from 48 to 111 (73.8 + 16) cc/m2 and was abnormal in four patients (11% ). Calculated left ventricular ejection fraction ranged from 0.40 to 0.77 and was decreased in five patients (13%). One patient with
= mitral ventricular
15 * X.6 2.x
valve prolapse: LV ESV = left ventricular end-systolic ejection fraction: PCW = mean pulmonary capillary
abnormal left ventricular volume and ejection fraction also had a small ventricular septal defect with an aneurysm of the membranous interventricular septum. To summarize, 33 patients (87 % ) had no abnormalities of left ventricular angiographic anatomy (excluding mitral valve prolapse). Five patients (13%) had one or more abnormalities (excluding mitral valve prolapse). Left ventricular pressures (Table II). Pulmonary capillary wedge pressure ranged from 3 to 12 (7.6 + 2.3) mm Hg and was normal in all patients. Left ventric-
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ular end-diastolic pressure ranged from 4 to 15 (8.6 + 2.8) mm Hg and was abnormal in two patients. One patient had significant left ventricular outflow tract obstruction provoked by the administration of isoproterenol. We compared left heart pressure and left ventricular angiographic findings. Of the five patients with abnormal left ventricular volumes and/or ejection fraction, only one had increased left ventricular end-diastolic pressure and pulmonary capillary wedge pressure. One additional patient with an increased left ventricular enddiastolic pressure had both normal left ventricular volume and ejection fraction. The eight patients with mitral valve prolapse had normal resting pressures, one of whom had provocable left ventricular outflow obstruction with the administration of isoproterenol. Summary of left ventricular disease. Excluding mitral valve prolapse, 31 patients (82 % ) had normal left heart pressure and left ventricular angiographic findings and seven patients (18 % ) had abnormal left heart pressures and/or angiographic findings. These latter patients will henceforth be called the left ventricular disease (LVD) group. Seven patients with no LVD had mitral valve prolapse and one patient with LVD had mitral valve prolapse. Correlation of RVD and LVD. We evaluated whether right ventricular involvement in the RVD group was selective-i.e., involving the right ventricle alone or whether both the right ventricle and left ventricle were affected. Of 21 patients with no RVD, two had LVD (9% ). In contrast to 17 patients with RVD, five had LVD (29%). Thus 12 patients (32%) had RVD alone and five patients (13 % ) had both RVD and LVD (NS). However, when examined in another way, we noted that five of seven (71%) with LVD had RVD. In contrast, 12 of 31 (39%) without LVD had RVD (NS). The relationship of mitral valve prolapse and tricuspid valve prolapse was also examined. Of six patients with tricuspid valve prolapse, three (50%) had mitral valve prolapse, and of 32 patients with no tricuspid valve prolapse, five (16 % ) had mitral valve prolapse (NS). Follow-up. Of the 38 patients, two have been lost to follow-up, 34 (89 % ) are alive followed for 3 to 59 (24.5 f 17.4) months, and two (5%) are dead (No. 23 and 34), both dying suddenly. These two patients who died were among the youngest in the present series (both age 13 years). One had isolated RVD (although LVD was also found on postmortem examinationg), and one had both obvious RVD and LVD. Eighteen patients (53%) are on no antiarrhythmic therapy and 16 (47%) are on antiarrhythmic drug medication.
Right VT without
coronary disease
363
DISCUSSION RV vs LV origin of VT. In 1971, we began to classify patients with chronic recurrent ventricular tachycardia, based upon QRS morphology during ventricular tachycardia. A QRS morphology of right bundle branch block was felt to be consistent with ventricular tachycardia arising from the left ventricle. In contrast, a QRS morphology of left bundle branch block was felt to be consistent with ventricular tachycardia originating from the right ventricle. In 1977, we reported’ our experience based upon the above classification. We specifically reported 27 patients with chronic recurrent ventricular tachycardia. Twelve were felt to have recurrent right ventricular tachycardia and 15 were felt to have recurrent left ventricular tachycardia. Evaluation at that time included history, physical examination, chest x-ray examination, ECG during sinus rhythm, and left heart catheterization with coronary arteriography. We noted that most right ventricular tachycardia patients had no apparent organic heart disease, while all the patients with left ventricular tachycardia had heart disease. The reason for association of right ventricular tachycardia and absence of organic heart disease was obscure. Origin of VT in CAD. Since our report in 1977, there has been some clarification regarding the ECG prediction of site of origin of ventricular tachycardia. In patients with recurrent paroxysmal ventricular tachycardia complicating chronic ischemic heart disease (usually with ventricular aneurysm), endocardial mapping (catheter electrodes) and epicardial mapping have demonstrated that ventricular tachycardia usually arises from the periphery of left ventricular aneurysms.“‘,” In the setting of chronic ischemic heart disease, ventricular tachycardia thus usually appears to arise from the septal, paraseptal, or free left ventricle, whether or not the pattern of ventricular tachycardia is that of right bundle branch block or left bundle branch block. Origin of VT in non-CAD. In the absence of ischemic heart disease, the electrocardiographically predicted site of origin (based upon the QRS morphology) still appears to be relatively accurate in predicting the site of origin of ventricular tachycardia.2,“~1z-20 In the present series of patients without ischemic heart disease, all tachycardias that were mapped appeared to arise from within the right ventricle. It is possible that some of the tachycardias might have arisen from the left septum, with initial right ventricular breakthrough. Relation of RVT to RV disease. As mentioned above, in our 1977 series the absence of organic heart disease was based primarily upon scrutiny of the left
364
Pietras et al.
ventricle and coronary arteries. Specifically, right ventricular angiography had not been performed. In the present series of cases the right ventricle was carefully scrutinized. Right ventricular angiography was performed because this was an obvious step in the evaluation of patients with right ventricular tachycardia (RVT). In addition, we became cognizant of recent French reports linking right ventricular tachycardia with specific pathologic findings in the right ventricle. Uhl’s anomaly. In 1968, Froment et al.“’ noted an association of Uhl’s anomaly and right ventricular tachycardia. Uhl’s anomaly is characterized by fibrous and fatty replacement of all or part of the right ventricle. Additional cases associating right ventricular tachycardia with Uhl’s anomaly were reported by Fontaine’s group.2’“.‘” Fontaine et al. reported a few patients with recurrent ventricular tachycardia in which electrophysiologic study, as well as epicardial mapping, demonstrated an origin of ventricular tachycardia from the right ventricle. In these patients pathologic findings demonstrated the presence of Uhl’s anomaly. Arrhythmogenic RV dysplasia. Fontaine’s laboratory subsequently reported a disease entity possibly related to Uhl’s anomaly, which also results in right ventricular tachycardia. 2,3.LZ This disease process was called “arrhythmogenic right ventricular dysplasia.” This entity is characterized by the presence of local or generalized right ventricular wall motion abnormalities, delayed potentials arising from the right ventricle, and recurrent right ventricular tachycardia which is electrophysiologically inducible. Surgical ablation of zones of apparent reentry responsible for right ventricular tachycardia in these patients has apparently been successful in curing the dysrhythmia. Little attention has been paid to the presence or absence of left ventricular disease in previously reported patients with right ventricular tachycardia complicating Uhl’s anomaly or with arrhythmogenic right ventricular dysplasia.“” Present study of RVT without CAD. We can now attempt to reconcile our findings with the previous reports in the literature. In the present series we report results of right and left ventricular angiography in 38 consecutive referred patients with chronic recurrent unifocal right ventricular tachycardia, without ischemic heart disease and/or prior myocardial infarction. In most of the present series of cases there was no clinical evidence of manifest organic heart disease. Utilizing biplane right ventriculography, 55% of the present series of patients had no demonstrable right ventricular disease (excluding
tricuspid valve prolapse); in 45%, we found objective evidence of right ventricular disease. In most of the patient this consisted of a slight to moderate increase in right ventricular volumes, without apparent regional or generalized abnormality of right ventricular contractility. Riplane left ventricular angiography revealed left ventricular dysfunction in relatively few patients (with and without RVD). Delayed right ventricular activation was not. seen on surface ECG or on intracavitary recordings. Do our patients have arrhythmogenic right ventricular dysplasia? This is a difficult question to answer in view of the lack of specific criteria for making this diagnosis. Arrhythomogenic right ventricular dysplasia could be proposed as a diagnosis in the 45% of patients with abnormalities of right ventricular function. In most of these patients with evidence of right ventricular disease we did not find evidence of left ventricular disease, so that the right ventricular involvement could be called selective. In some of the patients with right ventricular disease there was additional obvious left ventricular disease, so that right ventricular cardiomyopathic findings were not selective but reflective of a biventricular disease process. In the absence of pathologic data (endocardial biopsy was not performed in the present group of patients), one cannot be sure whether right ventricular dysplasia was responsible for ventricular tachycardia in the patients with (or without) right ventricular disease. Our present policy is to currently label patients with idiopathic right ventricular tachycardia as having no cardiomyopathy, selective right ventricular cardiomyopathy, selective left. ventricular cardiomyopathy, or biventricular cardiomyopathy, based upon catheterization. The finding of tricuspid valve prolapse in some of our patients deserves comment. We recognize the difficulty in making this angiographic diagnosis. In some of our patients tricuspid valve prolapse coexisted with mitral valve prolapse. With our current level of knowledge it is impossible to delineate a cause-and-effect relationship between tricuspid valve prolapse and right ventricular tachycardia in our patients with both of these conditions. It is worthwhile to speculate as to why the present group of patients, usually without clinically apparent heart disease, is afflicted with right ventricular tachycardia. Our present experience suggests that most patients without ischemic heart disease who have electrocardiographically diagnosed right ventricular tachycardia, do not have obvious organic
Volume Number
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Right VT without coronary disease 365
heart disease. This is somewhat surprising in that if ventricular tachycardia in the absence of heart disease reflected a random process, then left ventricular tachycardia should be more common, since the bulk of the ventricles is at least by weight, left ventricular. What is it that makes the right ventricle a site of ventricular tachycardia in patients without apparent disease ? The right ventricle is a more anatomically complex chamber than the left ventricle, at least in terms of geometry. The right ventricle has an unusually shaped cavity with an infundibulum and highly trabeculated endocardium frequently including a moderator band. Perhaps the more complex anatomy predisposes in some way to occurrence of ventricular tachycardia. In addition, it is possible that the right ventricle is prone to selective degenerative processes such as Uhl’s anomaly and arrhythmogenic right ventricular dysplasia, as proposed by the French. It is also possible, that congenital abnormality of the conduction system within the right ventricle or the right ventricle itself plays a role in the genesis of right ventricular tachycardia in patients without ischemic heart disease.g Clinical significance of right ventricular tachycardia without ischemic heart disease. The clinical signifi-
cance of diagnosing recurrent right ventricular tachycardia in the absence of ischemic heart disease is not totally known. The majority of the present series of patients have done well within a relatively short period of follow-up. There is no clear-cut difference in the present group of patients in regard to clinical findings, symptoms, pattern of ventricular tachycardia, and the presence or absence of objective evidence of right ventricular disease. Only two of the present series of patients have died, both suddenly. These were among the youngest of the patients in the present series, one having obvious left ventricular disease with right ventricular disease, and the other having right ventricular disease (with left ventricular disease diagnosed at postmortem examination). The presence of left ventricular disease in these two patients might well have played a role in their fatal clinical course. We will continue to follow the present group of patients to further define the life history of chronic recurrent right ventricular tachycardia with and without demonstrable right ventricular disease. Endocardial biopsy would appear to be indicated in this group of patients, so that histologic correlates of abnormal right ventricular angiographic anatomy might be found. We gratefully acknowledge the technical Schlag and Jonas Juska and the secretarial Jefferson in the preparation of this paper.
assistance assistance
of Donna of Frances
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19.
20.
RJ, Mautner R, Denes P, Wu D, Dhingra R, Towne W, Rosen KM: Chronic recurrent right and left ventricular tachycardia: Comparison of clinical, hemodynamic and angiographic findings. Am J Cardiol 40:32, 1977. Fontaine G, Guiraudon G, Frank R: Mechanism of ventricular tachycardia with and without associated chronic myocardial ischemia. In Narula OS. editor: Cardiac arrhythmias. Baltimore, 1979, The Williams & Wilkins Co, p 516. Fontaine G, Guiraudon G, Frank R, Vedel J, Grosgogeat Y, Cabrol C: Modern concepts of ventricular tachycardia. Eur J Cardiol 8:565, 1978. Gentzler RD, Briselli MF, Gault JH: Angiographic estimation of right ventricular volume in man. Circulation 50:324, 1974. Wynne J, Green LH, Mann T, Levin D, Grossman W: Estimation of left ventricular volumes in man from biplane cineangiograms filmed in oblique projections. Am J Cardiol 411726, 1978. Kennedy JW, Baxley WA, Figley MM, Dodge HT, Blackman JR: Quantitative angiocardiography. I. The normal left ventricle in man. Circulation 34:272, 1966. Sandler ^ H, .Dodge . HT: The use of single plane angiocardio. grams for the calculation of left ventricular volume in man. AM HEART J 75:325, 1968. Dodge HT: Determination of left ventricular volume and mass. Radio1 Clin North Am 9:459, 1971. Bharati S, Bauernfeind R, Scheinman M, Massie B, Cheitlin M, Denes P, Wu D, Lev M, Rosen KM: Congenital abnormalities of the conduction system in two patients with tachyarrhythmias. Circulation 59:593, 1979. Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA, Moore EN: Recurrent sustained ventricular tachycardia. 2. Endocardial mapping. Circulation 57:440, 1978. Horowitz LN. Josephson ME, Harken AH: Epicardial and endocardial activation during sustained ventricualr tachycardia in man. Circulation 61:1227, 1980. Vetter VL, Josephson ME, Horowitz LN: Idiopathic recurrent sustained ventricular tachycardia in children and adolescents. Am J Cardiol 47:315, 1981. Horowitz LN, Vetter VL, Harken AH, Josephson ME: Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of Fallot. Am J Cardiol 46:446, 1980. Gallagher H, Anderson RW, Kasell J, Rice JR, Pritchett ELC, Gault JM, Harrison L, Wallace AG: Cryoablation of drug-resistant ventricular tachycardia in a patient with a variant of scleroderma. Circulation 57:190, 1978. Palileo E, Ashley W, Lam W, Bauernfeind R, Swiryn S, Wyndham C, Rosen KM: Exercise provocable right ventricular outflow tract tachycardia (abstr). Circulation 62 (suppl 111):267, 1980. Vedel J, Frank R, Fontaine G, Drobinski G, Guiraudon G, Brocheriou C, Grosgogeat Y: Tachycardies ventriculaires recidivantes et ventricule droit naovrace de l’adulte. Arch Ma1 Coeur 71:973, 1978. Fontaine G, Guiraudon G, Frank R, Gerbaux A, Cousteau JP, Barillon A, Gay J, Cabrol C, Facquet J: La cartographic epicardique et le traitement chirugical par simple ventriculotomie de certaines tachycardies ventriculaires rebelles par reentree. Arch Ma1 Coeur 68:113, 1975. Spurrell RAJ, Yates AK, Thorburn CW, et al: Surgical treatment of ventricular tachycardia after epicardial mapping studies. Br Heart J 37:115, 1975. Kastor JA, Horowitz LN, Harken AH, Josephson ME: Clinical electrophysiology of ventricular tachycardia. N Engl J Med 304:1004, 1981. Fontaine G, Guiraudon G, Frank R, Vedel J, Coutte R, Dragodanne C: Epicardial mapping and surgical treatment in 6 cases of resistant ventricular tachycardia not related to
Pietras et al. coronary artery disease. In Wellens HJJ, Lie KI, Lanse Md. editors: ‘I’he conduction system of’ the heart. Leiden, 1976. Stenfert Kroese BV, p 54.5. 21. Froment R, Perrin A, Loire R, Dalloz CL: Ventricule droit papyrace du jeune adulte par dystrophie congenitale. Arch Ma1 Coeur 61:477, 1968.
Yt!. Frank R. Fontaine G, Vedel .I. Mialet, G, Sol C, Gunaudon (,. Grosgogeat ‘IT, I’:lect,rocardiologie de quatre cas de dysplasir ventriculsiw drflite arythmogrne. Arch Ma1 f’treitr 71:96:i, 1978. 3. Bharati S. Felt1 A. Rosen K, Katus AA, l,e\ M: Right ventricular t;rcbvcardia in a vase c!I llhl‘s disease. iin press1
Effect of alpha-adrenergic receptor stimulation on ventricular electrical properties in the normal canine heart We examined the effects of alpha-adrenergic stimulation on ventricular excitability, refractoriness, and vulnerability to fibrillation.’ Methoxamine or phenylephrine was infused in five dogs each before and after aortic arch and carotid sinus baroreceptor denervation, in doses which increased mean arterial blood pressure by 20 to 30 mm Hg. Methoxamine or phenylephrine caused an increase in the ventricular fibrillation threshold (VFT) (from 27% to 41%) and in the repetitive extrasystole threshold (RET) (from 28% to 39%). This effect was abolished by baroreceptor denervation. Neither drug altered mid-diastolic threshold or effective refractory period duration either before or after denervation. We conclude that alpha-receptor activation exerts no direct effect on ventricular excitability or refractoriness in the normal intact heart. (AM HEART J 105366, 1983.)
Peter R. Kowey, M.D.,* Boston,
Richard
L. Verrier, Ph.D., and Bernard
Mass.
Considerable evidence implicates the sympathetic nervous system in modulating electrical properties of the heart.‘-‘j The importance of beta-adrenergic receptor stimulation in the enhancement of myocardial electrical instability has been documented.‘.’ The role of the alpha-adrenergic receptor, and in particular, the effect of alpha-receptor stimulation on myocardial electrical properties, has not been adequately examined. Prior investigations have
From the Cardiovascular Laboratories, Department of Nutrition, Harvard School of Public Health; and the Cardiovascular Division, Department of Medicine of the Brigham and Women’s Hospital, Harvard Medical School. Supported in part by Grants HL-06104 and HL-07776 from the National Heart, Lung and Blood Institute, National Institutes of Health, United States Public Health Service, Bethesda, Md. Received for publication Aug. 10, 1981; revision received Nov. 20, 1981; accepted Nov. 24, 1981. Heprint requests: Bernard Lawn, M.D., Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115. *Present address: Cardiology Division, Medical College of Pennsylvania, Philadelphia. Pa.
“CC
Lown, M.D.
evaluated the effects of selected alpha-adrenergic stimulant drugs on effective and absolute refractory periods ,8,g or have been performed in isolated tissue preparations. lo. lL In an earlier study from this laboratory, phenylephrine was shown to raise the threshold current required for precipitating ventricular fibrillation (VF).12 The elevation of the VF threshold was abolished with baroreceptor denervation or with prevention of hypertension by measured exsanguination. This suggested that phenylephrine exerted an indirect effect on myocardial vulnerability. The objective of the present study was to examine the action of two alpha-adrenergic stimulants on four electrophysiologic variables: effective refractory period (ERP), the mid-diastolic threshold (MDT), the threshold current for inducing ventricular fibrillation (VFT), and the threshold current for eliciting a repetitive extrasystole (RET). The investigations were carried out in animals with aortic arch and carotid sinus baroreceptor denervation in order to eliminate the confounding neural effects of systemic hypertension.
Heart
Founded
in 1925
March
1983 Volume 105, Number 3
Journal
INVESTIGATIONS
Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: Clinical, hemodynamic, and angiographic findings Surgical cure of right ventricular tachycardia (RVT) has been recently described in patients with a disease characterized by abnormal electrical “arrhythmogenic right ventricular dysplasia,” activation of the right ventricle and localized or generalized angiographic right ventricular (RV) wall motion abnormalities (WMA). In search of a selective RV cardiomyopathy complicated by chronic recurrent RVT, 38 consecutive patients (mean age 30.5 k 12 years) with RVT and no ischemic heart disease were studied clinically, noninvasively, and by cardiac catheterization including left and right ventriculography. RV volumes were as follow: end-systolic volume ranged from 23 to 103 (mean + SD, 45.8 f 20) cc/m2 and was abnormal in 14 patients (37%); end-diastolic volume ranged from 57 to 138 (90.5 +- 28) cc/m* and was abnormal in 15 patients (39%); ejection fraction (EF) ranged from 0.18 to 0.84 and was decreased in five patients (13%). Seventeen patients (45%) had abnormal RV volume, EF, and/or pressures (RVD), five (13%) of whom had abnormal LV volume, EF, and/or pressures (LVD), and 12 (32%) patients with RVD had no LVD. Twenty-one patients (55%) had no RVD, two of whom had LVD. Only two of the 17 patients had RV regional WMA, one with and one without LVD. Most patients with LVD five of seven (71%) also had RVD while 12 of 31 patients (39%) with no LVD had RVD. In conclusion, less than one half of patients with RVT had selective RV cardiomyopathy and more than one half of patients with RVT had normal RV hemodynamics and angiography. (AM HEART J 105:357, 1983.)
Raymond J. Pietras, M.D., Wilfred Lam, M.D., Robert Bauernfeind, Amjad Sheikh, M.D., Edwin Palileo, M.D., Boris Strasberg, M.D., Steven, Swiryn, M.D., and Kenneth M. Rosen, M.D. Chicago, Ill.
In 1977, we noted an association of chronic recurrent right ventricular tachycardia and absence of organic heart disease.’ The diagnosis of absence of organic heart disease was based upon clinical examination, chest x-ray, and diagnostic left heart catheterization with coronary angiography. Recently, Fontaine et a1.2s3 described a group of patients with recurrent right ventricular tachycardia, abnormal electrical From Lincoln
the Section of Cardiology, Shoal of Medicine, University
Department of Illinois
of Medicine, Abraham College of Medicine.
Supported in part by National Heart, Lung and Blood Institute tional training grant HL 07387, by research grants HL 18794 23566; and by a grant from the Banes Estate.
Instituand HL
Received accepted
3, 1981;
for publication Nov. 12, 1981.
Reprint requests: of Illinois Hospital,
Aug.
10, 1981;
revision
Raymond J. Pietras, M.D., P.O. Box 6998, Chicago,
received
Cardiology IL 60680.
Nov. Dept.,
University
M.D.,
activation of the right ventricle, and localized or generalized right ventricular angiographic wall motion abnormality. These patients have been characterized as having “arrhythmogenic right ventricular dysplasia.” Since the right ventricle was not scrutinized in our initial reported group of patients with recurrent right ventricular tachycardia, it is possible that some or all of our patient group had clinically silent “arrhythmogenic right ventricular dysplasia.” To further elucidate the pathophysiology of recurrent right ventricular tachycardia, we now report a systematic evaluation of right ventricular function and right ventricular angiographic anatomy in a large series of patients referred to us with chronic recurrent right ventricular tachycardia. Because we were looking for the presence of selective right ventricular 357
358
Pietras et al
cardiomyopathy, we have excluded patients with recurrent ventricular tachycardia complicating acute or chronic ischemic heart disease. METHODS Patients. Thirty-eight consecutive referred patients with chronic recurrent unifocal right ventricular tachycardia were evaluated clinically, hemodynamically, and angiographically. Patients with known ischemic heart diseasewith prior myocardial infarction and/or significant obstructive coronary disease were excluded from this study. Patients in whom drugs or pacing catheters might have induced ventricular tachycardia were also excluded. Characterization of ventricular tachycardia. Ventricular tachycardia was diagnosedusing standard ECG criteria-i.e., a prolonged QRS complex (38 patients), atrioventricular dissociation (37 patients), fusion complexes (24 patients), and captures (24 patients). Ventricular tachycardia was also verifed by His bundle recordings in 28 patients including all patients in whom the diagnosisof ventricular tachycardia might be uncertain. Both frequency and duration of the tachycardia were determined utilizing symptoms and ECG tracings. The term “chronic recurrent” defined a minimum of two documented episodesof ventricular tachycardia at least 1 month apart. The majority of patients far exceeded this minimal frequency of ventricular tachycardia. Patients were also classified as having paroxysmal sustained, paroxysmal nonsustainedor exercise-inducedventricular tachycardia. “Sustained” referred to protracted paroxysms which could usually be electrophysiologically induced and terminated. “Nonsustained” ventricular tachycardia was characterized by frequent short, selfterminating episodeswith many premature beats (usually identical in morphology to QRS complexesduring ventricular tachycardia) on most or all ECGs. “Exercise provoked” ventricular tachycardia referred to patients whose ventricular tachycardia could be reproducibly provoked by exertion (history) and treadmill testing. Patients were said to have right ventricular tachycardia when ventricular tachycardia wasnoted with a left bundle branch pattern on the 12-leadsurface ECG. The origin of ventricular tachycardia from the right ventricle was also supported by endocardial mapping the earliest onset of tachycardia QRS complexesfrom the right ventricle with a catheter electrode during this dysrhythmia (27 patients). Diagnostic cardiac catheterization. Intracardiac pressureswere recorded at rest from the right and left heart chambers through fluid-filled catheters using the midchest as the zero reference level. Mean right atria1 and right ventricular end-diastolic pressure >7 mm Hg, and mean pulmonary capillary wedge pressureand left ventricular end-diastolic pressure >12 mm Hg were considered abnormal. Biplane right ventricular angiography wasperformed in the posteroanterior and lateral projection with radiopaque contrast material introduced through a right ventricular
catheter (32 patients) or a right atria1 catheter (six patients) at a rate of 12 cc/set over 3 to 4 seconds. Ventricular ectopic beats and postventricular ectopic~ beatswere rejected for analysis.Right ventricular volumes were measured at, end-systole and end-diastole from biplane cineangiogramsusing a computer (Echo-C’omp, Digisonics, Houston, Texas) programmed for Simpson’s rule method of analysis where the right ventricle is assumedto be an elliptical cylinder. The measuredvolumes were corrected with the regression equation oi’ Gentzler et al.’ Right, ventricular ejection fraction was calculated from end-systolic and end-diastolic volumes and normal values usedwere thosereported by Gentzler et al. where right ventricular end-diastolic volume indexed was 81 t_ 1‘2.3cc/m’ (mean r SD), right vent,ricular endsystolic volume Indexed was 39 : 8.5 cc/m-, and right ventricular ejection fraction was 0.51 + 0.08.’ Right ven. tricular regional wall motion wasqualitatively assessed by two observers(RP and WL). Tricuspid valve prolapsewas diagnosedwhen angiography revealed a scallopedtricuspid valve bulging into the right atrium during systole. Thirty patients had 40 to 26 cc of radiopaque contrast material injected into the left ventricle at a rate of 12 cc/set and the remaining eight, patients had ievophase ventriculograms from the right-sided injection. Left ventriculograms were obtained with biplane cineangiography in 27 patients in the 30-degreeright anterior oblique and 60-degree left anterior oblique project,ions, m three patients in the posteroanterior and lateral projections, and with single plane angiography in eight patients (four in the right anterior oblique projection and four in the posteroanterior projection). I,eft ventricular end-diastolic and end-systolic, vulumes were calculated by thr arealength method. Left ventricular volumes were corrected for true volume with appropriate regressionequations. The normal values used for left \,entricular volume and ejection fraction were those reported by Kennedy et al.,” where left ventricular end-diast.olic volume indexed was 70 i 20 cc/m left venlricular end-systcblit. volume indexed was 24 ? 10 cc/nl~. and left ventricular eject.ion fraction was 0.67 -i (1.08. I,eft ventricular regional wall motion was qualitatively assessedby two ohservers (RI’ and WL). Mitral valve prolapse was diagnosed when angiographyrevealed a scallopedmitral valve bulging into the left atrium during systole. Selective coronary arteriography was performed in 22 patients using either a femoral or brachial artery approach. These arteriograms were interpreted as having no significant lesion in any vessel(by study design).There were absolutely no data in the remaining 16 patients, who had not undergone coronary angiography, suggestingischemic heart, disease.The chi-square test with the Yates correction was used to assesst,he significance of differencesbetween groups of patients. RESULTS Clinical
characteristics.
Patients
ranged in age from
13 to 56 (mean +- SD, 30.5 t 12) years. Nineteen
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105
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Right
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359
I. Right ventricular hemodynamic and angiographic findings
Table
RV WMA
Patient Group I-No
right ventricular
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0
ventricular
22 23 24 25 26 27 28 29
Apical ALW
+ + IW + +
Mean Standard
RV EDV (cc/m2)
R VEF
RA (mm Hg)
R VSIED (mm Hg)
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 + 0 0 0 + 0
23 36 36 29 26 28 39 29 31 36 32 38 28 40 27 40 40 40 28 38 38
65 86 63 70 68 69 93 69 61 85 57 80 70 78 63 73 72 83 69 67 al
0. 64 0.58 0.43 0.59 0.62 0.59 0.58 0.58 0.49 0.58 0.44 0.52 0.60 0.49 0.58 0.45 0.44 0.52 0.59 0.43 0.53
3 6 2 7 4 6 5 5 0 1 6 2 0 2 2 1 5 4 2 4 1
2414 33/4 2014 2616 2516 20/4 1912 2015 2214 13/3 20/6 2214 18/3 24/4 2414 1812 1915 24/6 2513 1815 1612
0 0 0 0 0 0 0 +
59* 35 57* 97: 52* 35 52' 83'
L27* 77 107* 155' 115* 98' 99* 115*
0.54 0.55 0.47 0.37* 0.55 0.64 0.47 0.28*
6 3 4 2 4 6 3 7
2816 41/a* 2816 1512 2012 16/6 19/4 2317
+ f 0 0 t 0 0 0 0
48* 51* 79’ 60* 50* 88s 103’ 58* 31 45.8 20
112* loa* 124* 119* 97* 129* 126* 138* 70 90.5 26
0.57 0.53 0.36* 0.49 0.48 0.32* 0.18* 0.58 0.56 0.50 0.10
4 I 4 0 7 9* 101 2 a* 3.9 2.6
1714 14/5 2014 14/3 26/8* 22/9' 28/10* 2414 22/S* 21.814.8 5.412.1
disease
+
30 31 32 33 34 35 36 37 38
RV ESV (cclm2j
disease
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
Group Ii-Right
TVP
0 0 0 Global 0 0 0 hypokinesis, akinesis 0 0 Global 0 hypokinesis Global Global 0 0
deviation
Abbreviations and symbols: RV WMA = right ventricular wall motion abnormality; TVP = tricuspid valve prolapse; RV ESV = right ventricular end-systolic volume indexed; RVEF = right ventricular ejection fraction; m = mean right atrial pressure; RVS/ED = right ventricular systolic/right ventricular end-diastolic pressure; ALW = anterolateral wall; IW = inferior wall; * = abnormal value.
patients (50% ) were male and 19 patients (50% ) were female. Thirty-five had symptoms related to episodes of ventricular tachycardia which included one or more of the following: palpitations (30), syncope (12), dyspnea (S), chest pain (10). Eight patients had systolic murmurs five of whom had midsystolic clicks; four others had midsystolic clicks alone. One patient had a third heart sound and another had a fourth heart sound. Only one patient
had cardiomegaly on chest x-ray examination. Excluding the occurrence of right ventricular tachycardia, the EGG was entirely normal in 24 patients and the remaining 14 patients had nonspecific ST-T wave changes; two of these had left anterior superior hemiblock, and one each had left ventricular enlargement, Q-T interval prolongation, and abnormal Q waves in leads I and aV,. Most of these abnormal clinical findings were present in the group
360
Pietras
et al.
March, American
Heart
1983 Journal
Fig. 1. Normal right ventricular biplane angiogramof patient No. 5. The frames on the left are from the lateral view and those on the right from the posteroanterior view. The two upper frames are at end-systole and the two lower frames are at end-diastole. There is uniform contraction of all regions of the ventricle and global ejection fraction is normal. The tricuspid valve is normal in appearance.
of patients subsequently designated as having right ventricular disease. As noted in our previous study, many patients (23 or 60% ) were free of clinically manifest organic heart disease utilizing history, physical examination, ECG (excluding ventricular tachycardia), chest x-ray examination, and noninvasive studies. Nine patients (24 % ) had clinically diagnosed mitral valve prolapse (precatheterization); six patients (16 % ) were considered cardiomyopathic (precatheterization) . Characteristics of ventricular tachycardia. Five patients (13 % ) had paroxysmal sustained ventricular tachycardia, 25 patients (66%) had paroxysmal nonsustained ventricular tachycardia, and eight patients (21% ) had exercise-induced ventricular tachycardia. The QRS morphology during ventricular tachycardia was left bundle branch block pattern in leads I, aV,, V1, and V,. The mean frontal plane QRS axis during ventricular tachycardia was normal in 24 patients, was right axis in eight patients, left axis in four patients, and was indeterminant in two.
Heart rate during ventricular tachycardia from 95 to 240 (164 ? 31) bpm.
ranged
Right ventricular angiographic anatomy (Table I; Figs. 1 and 2). Visual inspection of biplane right
ventricular angiography revealed normal wall motion in 32 patients (84%), regional wall motion abnormality in two patients (5%) (inferior wall hypokinesis and akinetic anterolateral wall with hypokinesis of the apex), and generalized decreased contractility in four patients (11% ). Six patients (16%) had tricuspid valve prolapse. Of these six patients, wall motion was normal in four and abnormal in two, each of whom had regional wall motion abnormalities. Right ventricular end-systolic volume ranged from 23 to 103 (45.8 +- 20) cc/m2 and was abnormal in 14 patients (37%). Right ventricular end-diastolic volume ranged from 57 to 138 (90.5 + 26) cc/m2 and was abnormal in 15 patients (39 % ). Calculated right ventricular ejection fraction ranged from 0.18 to 0.64 and was decreased in five patients (13%). To summarize, 23 patients (61% ) had no abnormality of right ventricular angiograph-
Volume
105
Number
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Right
VT without
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361
Fig. 2. Abnormal right ventricular biplane angiogram of patient No. 29. The frames on the left are from the lateral view and those on the right from the posteroanterior view. The two upper frames are at end-systole and the two lower frames are at end-diastole. Apical hypokinesis and anterolateral wall akinesis are seen with a reduced ejection fraction. This angiogram is similar in appearance to that described by Fontaine et al.*,” as characteristic of arrhythmogenic right ventricular dysplasia. The
tricuspid valve is scalloped and bulges into the right atrium during systole, typical of tricuspid valve prolapse.
ic anatomy (excluding tricuspid valve prolapse). This includes all 21 patients in group I (no RV disease) and patients No. 23 and 38 in group II (RV disease). Fifteen patients (39%) had one or more abnormalities (excluding tricuspid valve prolapse). Right heart pressures (Table I). Right atria1 pressure ranged from 0 to 10 (3.9 f 2.6) mm Hg and was abnormal in three patients. Right ventricular systolic pressure ranged from 13 to 41 (21.9 f 5.4) mm Hg and was abnormal in one patient. Right ventricular end-diastolic pressure ranged from 2 to 10 (4.8 + 2.1) mm Hg and was abnormal in five patients. We compared right heart pressures and right ventricular angiographic findings. Of the 15 patients with one or more angiographic features abnormal, three had increased right atrial and/or right ventricular enddiastolic pressures. Two patients with normal angiographic features had elevated right atrial and right ventricular end-diastolic pressures. Two additional patients with elevated right atrial and right ventric-
ular end-diastolic pressures had normal right ventricular volumes and ejection fraction. Five of the six patients with tricuspid valve prolapse had normal right atria1 and right ventricular end-diastolic pressures. Summary
of evidence
for right
ventricular
disease.
Excluding tricuspid valve prolapse, twenty-one patients (55 % ) had normal right heart pressure and right ventricular angiographic findings and 17 patients (45% ) had abnormal right heart pressure and/or right ventricular angiographic findings. These latter patients will henceforth be called the right ventricular disease (RVD) group (Table I). Two patients with no RVD had tricuspid valve prolapse and four patients with RVD had tricuspid valve prolapse. Left
ventricular
angiographic
anatomy
(Table
II).
Visual inspection of left ventricular angiograms revealed normal wall motion in 33 patients (87%), regional wall motion abnormalities in no patients
March.
362
Pietras
Table
et al.
II. Left ventricular
American
hemodynamic
Patients
and angiographic
LV WMA
MVP
right uentricular
disease 0 0 0 0 0 0 0 0 0 0
L1’ ES\’ jcc,‘m’i
LVEDb
PC I&. I, VEb
Ccc/m-i
0
7:
0.75 0.67 0.69 0.70 0.65 0.64 0.59 0.77 0.68 0.w
56
U.:‘2
78 7"'
0.7" 0.71
48 84 71
0 68 76
0 0
86 88 56
0 .~
---.-_-----
11
0
12 13
0 0
0
14
0 0
0 0
0.70 0.76
0
0.62
15 16 17 18
0 0
0 t +
0.66 0.68
19
0
+
0.68
20
0
+
lJ.81) 0.-s*
21
Group II-Right “2
ventricular
+ Global disease 0
23
0 0
24 2<5
0 0
26 27
0
28 2.9
0 0
30
0 0
31 32
0
x1
0
+ t + t
34
:i:’ 36
37 38
Global Global Global Global 0
U
k&J
0
5
0 0 0
,’ LGP ---
/ mm Fig) _.-_--.
8 7
6 5
H ; 10
+
10 r,
10 r,
+ t
x Ii
10 ,I
0
11 12
1’ 1 ‘.I‘.
0 0 +
0
14*
0 0
x
0
9 7.6 2.3
deviation
Abbreviations and symbols: LV WMA = left ventricular volume indexed; LV EDV = left ventricular end-diastolic wedge pressure; LVEDP = left ventricular end-diastolic
(mm
0
Mean Standard
1983 Journal
findings
.-
Group I-No 1 2 :I 4 5 6 7 8 9 10
Heart
wall motion abnormality; MVP volume indexed; LVEF = left pressure: * = abnormal value.
(O%), and generalized decrease in contractility in five patients (13%). Eight patients (21%) had angiographic mitral valve prolapse. Of these eight, wall motion was normal in all. Left ventricular end-systolic volume ranged from 14 to 67 (26 k 12.5) cc/m2 and was abnormal in five patients (13 % ). Left ventricular end-diastolic volume ranged from 48 to 111 (73.8 + 16) cc/m2 and was abnormal in four patients (11% ). Calculated left ventricular ejection fraction ranged from 0.40 to 0.77 and was decreased in five patients (13%). One patient with
= mitral ventricular
15 * X.6 2.x
valve prolapse: LV ESV = left ventricular end-systolic ejection fraction: PCW = mean pulmonary capillary
abnormal left ventricular volume and ejection fraction also had a small ventricular septal defect with an aneurysm of the membranous interventricular septum. To summarize, 33 patients (87 % ) had no abnormalities of left ventricular angiographic anatomy (excluding mitral valve prolapse). Five patients (13%) had one or more abnormalities (excluding mitral valve prolapse). Left ventricular pressures (Table II). Pulmonary capillary wedge pressure ranged from 3 to 12 (7.6 + 2.3) mm Hg and was normal in all patients. Left ventric-
Volume
105
Number
3
ular end-diastolic pressure ranged from 4 to 15 (8.6 + 2.8) mm Hg and was abnormal in two patients. One patient had significant left ventricular outflow tract obstruction provoked by the administration of isoproterenol. We compared left heart pressure and left ventricular angiographic findings. Of the five patients with abnormal left ventricular volumes and/or ejection fraction, only one had increased left ventricular end-diastolic pressure and pulmonary capillary wedge pressure. One additional patient with an increased left ventricular enddiastolic pressure had both normal left ventricular volume and ejection fraction. The eight patients with mitral valve prolapse had normal resting pressures, one of whom had provocable left ventricular outflow obstruction with the administration of isoproterenol. Summary of left ventricular disease. Excluding mitral valve prolapse, 31 patients (82 % ) had normal left heart pressure and left ventricular angiographic findings and seven patients (18 % ) had abnormal left heart pressures and/or angiographic findings. These latter patients will henceforth be called the left ventricular disease (LVD) group. Seven patients with no LVD had mitral valve prolapse and one patient with LVD had mitral valve prolapse. Correlation of RVD and LVD. We evaluated whether right ventricular involvement in the RVD group was selective-i.e., involving the right ventricle alone or whether both the right ventricle and left ventricle were affected. Of 21 patients with no RVD, two had LVD (9% ). In contrast to 17 patients with RVD, five had LVD (29%). Thus 12 patients (32%) had RVD alone and five patients (13 % ) had both RVD and LVD (NS). However, when examined in another way, we noted that five of seven (71%) with LVD had RVD. In contrast, 12 of 31 (39%) without LVD had RVD (NS). The relationship of mitral valve prolapse and tricuspid valve prolapse was also examined. Of six patients with tricuspid valve prolapse, three (50%) had mitral valve prolapse, and of 32 patients with no tricuspid valve prolapse, five (16 % ) had mitral valve prolapse (NS). Follow-up. Of the 38 patients, two have been lost to follow-up, 34 (89 % ) are alive followed for 3 to 59 (24.5 f 17.4) months, and two (5%) are dead (No. 23 and 34), both dying suddenly. These two patients who died were among the youngest in the present series (both age 13 years). One had isolated RVD (although LVD was also found on postmortem examinationg), and one had both obvious RVD and LVD. Eighteen patients (53%) are on no antiarrhythmic therapy and 16 (47%) are on antiarrhythmic drug medication.
Right VT without
coronary disease
363
DISCUSSION RV vs LV origin of VT. In 1971, we began to classify patients with chronic recurrent ventricular tachycardia, based upon QRS morphology during ventricular tachycardia. A QRS morphology of right bundle branch block was felt to be consistent with ventricular tachycardia arising from the left ventricle. In contrast, a QRS morphology of left bundle branch block was felt to be consistent with ventricular tachycardia originating from the right ventricle. In 1977, we reported’ our experience based upon the above classification. We specifically reported 27 patients with chronic recurrent ventricular tachycardia. Twelve were felt to have recurrent right ventricular tachycardia and 15 were felt to have recurrent left ventricular tachycardia. Evaluation at that time included history, physical examination, chest x-ray examination, ECG during sinus rhythm, and left heart catheterization with coronary arteriography. We noted that most right ventricular tachycardia patients had no apparent organic heart disease, while all the patients with left ventricular tachycardia had heart disease. The reason for association of right ventricular tachycardia and absence of organic heart disease was obscure. Origin of VT in CAD. Since our report in 1977, there has been some clarification regarding the ECG prediction of site of origin of ventricular tachycardia. In patients with recurrent paroxysmal ventricular tachycardia complicating chronic ischemic heart disease (usually with ventricular aneurysm), endocardial mapping (catheter electrodes) and epicardial mapping have demonstrated that ventricular tachycardia usually arises from the periphery of left ventricular aneurysms.“‘,” In the setting of chronic ischemic heart disease, ventricular tachycardia thus usually appears to arise from the septal, paraseptal, or free left ventricle, whether or not the pattern of ventricular tachycardia is that of right bundle branch block or left bundle branch block. Origin of VT in non-CAD. In the absence of ischemic heart disease, the electrocardiographically predicted site of origin (based upon the QRS morphology) still appears to be relatively accurate in predicting the site of origin of ventricular tachycardia.2,“~1z-20 In the present series of patients without ischemic heart disease, all tachycardias that were mapped appeared to arise from within the right ventricle. It is possible that some of the tachycardias might have arisen from the left septum, with initial right ventricular breakthrough. Relation of RVT to RV disease. As mentioned above, in our 1977 series the absence of organic heart disease was based primarily upon scrutiny of the left
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ventricle and coronary arteries. Specifically, right ventricular angiography had not been performed. In the present series of cases the right ventricle was carefully scrutinized. Right ventricular angiography was performed because this was an obvious step in the evaluation of patients with right ventricular tachycardia (RVT). In addition, we became cognizant of recent French reports linking right ventricular tachycardia with specific pathologic findings in the right ventricle. Uhl’s anomaly. In 1968, Froment et al.“’ noted an association of Uhl’s anomaly and right ventricular tachycardia. Uhl’s anomaly is characterized by fibrous and fatty replacement of all or part of the right ventricle. Additional cases associating right ventricular tachycardia with Uhl’s anomaly were reported by Fontaine’s group.2’“.‘” Fontaine et al. reported a few patients with recurrent ventricular tachycardia in which electrophysiologic study, as well as epicardial mapping, demonstrated an origin of ventricular tachycardia from the right ventricle. In these patients pathologic findings demonstrated the presence of Uhl’s anomaly. Arrhythmogenic RV dysplasia. Fontaine’s laboratory subsequently reported a disease entity possibly related to Uhl’s anomaly, which also results in right ventricular tachycardia. 2,3.LZ This disease process was called “arrhythmogenic right ventricular dysplasia.” This entity is characterized by the presence of local or generalized right ventricular wall motion abnormalities, delayed potentials arising from the right ventricle, and recurrent right ventricular tachycardia which is electrophysiologically inducible. Surgical ablation of zones of apparent reentry responsible for right ventricular tachycardia in these patients has apparently been successful in curing the dysrhythmia. Little attention has been paid to the presence or absence of left ventricular disease in previously reported patients with right ventricular tachycardia complicating Uhl’s anomaly or with arrhythmogenic right ventricular dysplasia.“” Present study of RVT without CAD. We can now attempt to reconcile our findings with the previous reports in the literature. In the present series we report results of right and left ventricular angiography in 38 consecutive referred patients with chronic recurrent unifocal right ventricular tachycardia, without ischemic heart disease and/or prior myocardial infarction. In most of the present series of cases there was no clinical evidence of manifest organic heart disease. Utilizing biplane right ventriculography, 55% of the present series of patients had no demonstrable right ventricular disease (excluding
tricuspid valve prolapse); in 45%, we found objective evidence of right ventricular disease. In most of the patient this consisted of a slight to moderate increase in right ventricular volumes, without apparent regional or generalized abnormality of right ventricular contractility. Riplane left ventricular angiography revealed left ventricular dysfunction in relatively few patients (with and without RVD). Delayed right ventricular activation was not. seen on surface ECG or on intracavitary recordings. Do our patients have arrhythmogenic right ventricular dysplasia? This is a difficult question to answer in view of the lack of specific criteria for making this diagnosis. Arrhythomogenic right ventricular dysplasia could be proposed as a diagnosis in the 45% of patients with abnormalities of right ventricular function. In most of these patients with evidence of right ventricular disease we did not find evidence of left ventricular disease, so that the right ventricular involvement could be called selective. In some of the patients with right ventricular disease there was additional obvious left ventricular disease, so that right ventricular cardiomyopathic findings were not selective but reflective of a biventricular disease process. In the absence of pathologic data (endocardial biopsy was not performed in the present group of patients), one cannot be sure whether right ventricular dysplasia was responsible for ventricular tachycardia in the patients with (or without) right ventricular disease. Our present policy is to currently label patients with idiopathic right ventricular tachycardia as having no cardiomyopathy, selective right ventricular cardiomyopathy, selective left. ventricular cardiomyopathy, or biventricular cardiomyopathy, based upon catheterization. The finding of tricuspid valve prolapse in some of our patients deserves comment. We recognize the difficulty in making this angiographic diagnosis. In some of our patients tricuspid valve prolapse coexisted with mitral valve prolapse. With our current level of knowledge it is impossible to delineate a cause-and-effect relationship between tricuspid valve prolapse and right ventricular tachycardia in our patients with both of these conditions. It is worthwhile to speculate as to why the present group of patients, usually without clinically apparent heart disease, is afflicted with right ventricular tachycardia. Our present experience suggests that most patients without ischemic heart disease who have electrocardiographically diagnosed right ventricular tachycardia, do not have obvious organic
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heart disease. This is somewhat surprising in that if ventricular tachycardia in the absence of heart disease reflected a random process, then left ventricular tachycardia should be more common, since the bulk of the ventricles is at least by weight, left ventricular. What is it that makes the right ventricle a site of ventricular tachycardia in patients without apparent disease ? The right ventricle is a more anatomically complex chamber than the left ventricle, at least in terms of geometry. The right ventricle has an unusually shaped cavity with an infundibulum and highly trabeculated endocardium frequently including a moderator band. Perhaps the more complex anatomy predisposes in some way to occurrence of ventricular tachycardia. In addition, it is possible that the right ventricle is prone to selective degenerative processes such as Uhl’s anomaly and arrhythmogenic right ventricular dysplasia, as proposed by the French. It is also possible, that congenital abnormality of the conduction system within the right ventricle or the right ventricle itself plays a role in the genesis of right ventricular tachycardia in patients without ischemic heart disease.g Clinical significance of right ventricular tachycardia without ischemic heart disease. The clinical signifi-
cance of diagnosing recurrent right ventricular tachycardia in the absence of ischemic heart disease is not totally known. The majority of the present series of patients have done well within a relatively short period of follow-up. There is no clear-cut difference in the present group of patients in regard to clinical findings, symptoms, pattern of ventricular tachycardia, and the presence or absence of objective evidence of right ventricular disease. Only two of the present series of patients have died, both suddenly. These were among the youngest of the patients in the present series, one having obvious left ventricular disease with right ventricular disease, and the other having right ventricular disease (with left ventricular disease diagnosed at postmortem examination). The presence of left ventricular disease in these two patients might well have played a role in their fatal clinical course. We will continue to follow the present group of patients to further define the life history of chronic recurrent right ventricular tachycardia with and without demonstrable right ventricular disease. Endocardial biopsy would appear to be indicated in this group of patients, so that histologic correlates of abnormal right ventricular angiographic anatomy might be found. We gratefully acknowledge the technical Schlag and Jonas Juska and the secretarial Jefferson in the preparation of this paper.
assistance assistance
of Donna of Frances
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RJ, Mautner R, Denes P, Wu D, Dhingra R, Towne W, Rosen KM: Chronic recurrent right and left ventricular tachycardia: Comparison of clinical, hemodynamic and angiographic findings. Am J Cardiol 40:32, 1977. Fontaine G, Guiraudon G, Frank R: Mechanism of ventricular tachycardia with and without associated chronic myocardial ischemia. In Narula OS. editor: Cardiac arrhythmias. Baltimore, 1979, The Williams & Wilkins Co, p 516. Fontaine G, Guiraudon G, Frank R, Vedel J, Grosgogeat Y, Cabrol C: Modern concepts of ventricular tachycardia. Eur J Cardiol 8:565, 1978. Gentzler RD, Briselli MF, Gault JH: Angiographic estimation of right ventricular volume in man. Circulation 50:324, 1974. Wynne J, Green LH, Mann T, Levin D, Grossman W: Estimation of left ventricular volumes in man from biplane cineangiograms filmed in oblique projections. Am J Cardiol 411726, 1978. Kennedy JW, Baxley WA, Figley MM, Dodge HT, Blackman JR: Quantitative angiocardiography. I. The normal left ventricle in man. Circulation 34:272, 1966. Sandler ^ H, .Dodge . HT: The use of single plane angiocardio. grams for the calculation of left ventricular volume in man. AM HEART J 75:325, 1968. Dodge HT: Determination of left ventricular volume and mass. Radio1 Clin North Am 9:459, 1971. Bharati S, Bauernfeind R, Scheinman M, Massie B, Cheitlin M, Denes P, Wu D, Lev M, Rosen KM: Congenital abnormalities of the conduction system in two patients with tachyarrhythmias. Circulation 59:593, 1979. Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA, Moore EN: Recurrent sustained ventricular tachycardia. 2. Endocardial mapping. Circulation 57:440, 1978. Horowitz LN. Josephson ME, Harken AH: Epicardial and endocardial activation during sustained ventricualr tachycardia in man. Circulation 61:1227, 1980. Vetter VL, Josephson ME, Horowitz LN: Idiopathic recurrent sustained ventricular tachycardia in children and adolescents. Am J Cardiol 47:315, 1981. Horowitz LN, Vetter VL, Harken AH, Josephson ME: Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of Fallot. Am J Cardiol 46:446, 1980. Gallagher H, Anderson RW, Kasell J, Rice JR, Pritchett ELC, Gault JM, Harrison L, Wallace AG: Cryoablation of drug-resistant ventricular tachycardia in a patient with a variant of scleroderma. Circulation 57:190, 1978. Palileo E, Ashley W, Lam W, Bauernfeind R, Swiryn S, Wyndham C, Rosen KM: Exercise provocable right ventricular outflow tract tachycardia (abstr). Circulation 62 (suppl 111):267, 1980. Vedel J, Frank R, Fontaine G, Drobinski G, Guiraudon G, Brocheriou C, Grosgogeat Y: Tachycardies ventriculaires recidivantes et ventricule droit naovrace de l’adulte. Arch Ma1 Coeur 71:973, 1978. Fontaine G, Guiraudon G, Frank R, Gerbaux A, Cousteau JP, Barillon A, Gay J, Cabrol C, Facquet J: La cartographic epicardique et le traitement chirugical par simple ventriculotomie de certaines tachycardies ventriculaires rebelles par reentree. Arch Ma1 Coeur 68:113, 1975. Spurrell RAJ, Yates AK, Thorburn CW, et al: Surgical treatment of ventricular tachycardia after epicardial mapping studies. Br Heart J 37:115, 1975. Kastor JA, Horowitz LN, Harken AH, Josephson ME: Clinical electrophysiology of ventricular tachycardia. N Engl J Med 304:1004, 1981. Fontaine G, Guiraudon G, Frank R, Vedel J, Coutte R, Dragodanne C: Epicardial mapping and surgical treatment in 6 cases of resistant ventricular tachycardia not related to
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Yt!. Frank R. Fontaine G, Vedel .I. Mialet, G, Sol C, Gunaudon (,. Grosgogeat ‘IT, I’:lect,rocardiologie de quatre cas de dysplasir ventriculsiw drflite arythmogrne. Arch Ma1 f’treitr 71:96:i, 1978. 3. Bharati S. Felt1 A. Rosen K, Katus AA, l,e\ M: Right ventricular t;rcbvcardia in a vase c!I llhl‘s disease. iin press1
Effect of alpha-adrenergic receptor stimulation on ventricular electrical properties in the normal canine heart We examined the effects of alpha-adrenergic stimulation on ventricular excitability, refractoriness, and vulnerability to fibrillation.’ Methoxamine or phenylephrine was infused in five dogs each before and after aortic arch and carotid sinus baroreceptor denervation, in doses which increased mean arterial blood pressure by 20 to 30 mm Hg. Methoxamine or phenylephrine caused an increase in the ventricular fibrillation threshold (VFT) (from 27% to 41%) and in the repetitive extrasystole threshold (RET) (from 28% to 39%). This effect was abolished by baroreceptor denervation. Neither drug altered mid-diastolic threshold or effective refractory period duration either before or after denervation. We conclude that alpha-receptor activation exerts no direct effect on ventricular excitability or refractoriness in the normal intact heart. (AM HEART J 105366, 1983.)
Peter R. Kowey, M.D.,* Boston,
Richard
L. Verrier, Ph.D., and Bernard
Mass.
Considerable evidence implicates the sympathetic nervous system in modulating electrical properties of the heart.‘-‘j The importance of beta-adrenergic receptor stimulation in the enhancement of myocardial electrical instability has been documented.‘.’ The role of the alpha-adrenergic receptor, and in particular, the effect of alpha-receptor stimulation on myocardial electrical properties, has not been adequately examined. Prior investigations have
From the Cardiovascular Laboratories, Department of Nutrition, Harvard School of Public Health; and the Cardiovascular Division, Department of Medicine of the Brigham and Women’s Hospital, Harvard Medical School. Supported in part by Grants HL-06104 and HL-07776 from the National Heart, Lung and Blood Institute, National Institutes of Health, United States Public Health Service, Bethesda, Md. Received for publication Aug. 10, 1981; revision received Nov. 20, 1981; accepted Nov. 24, 1981. Heprint requests: Bernard Lawn, M.D., Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115. *Present address: Cardiology Division, Medical College of Pennsylvania, Philadelphia. Pa.
“CC
Lown, M.D.
evaluated the effects of selected alpha-adrenergic stimulant drugs on effective and absolute refractory periods ,8,g or have been performed in isolated tissue preparations. lo. lL In an earlier study from this laboratory, phenylephrine was shown to raise the threshold current required for precipitating ventricular fibrillation (VF).12 The elevation of the VF threshold was abolished with baroreceptor denervation or with prevention of hypertension by measured exsanguination. This suggested that phenylephrine exerted an indirect effect on myocardial vulnerability. The objective of the present study was to examine the action of two alpha-adrenergic stimulants on four electrophysiologic variables: effective refractory period (ERP), the mid-diastolic threshold (MDT), the threshold current for inducing ventricular fibrillation (VFT), and the threshold current for eliciting a repetitive extrasystole (RET). The investigations were carried out in animals with aortic arch and carotid sinus baroreceptor denervation in order to eliminate the confounding neural effects of systemic hypertension.