1
LETTERS TO THE EDITOR WAVELESS PULMONARY CAPILLARY WEDGE observation can be useful in the diagnosis of subdivided left PRESSURE TRACING IN COR TRIATRIATUM atrium. The clinical and hemodynamic diagnosis of car triatriatum- subdivided left atrium is fairly difficult1 If no communication exists between the right and left atria, selective injection cannot be performed, and angiographic demonstration of the fibromuscular membrane that divides the left atrium may be impossible, as in the following case. M&ty&s Keltai, MD Hungarian Institute of Cardiology Budapest, Hungary Case report: An 18 year old man was admitted to this in- stitute because of severe hemoptysis. On examination a holosystolic murmur was heard and the clinical and radiologic signs for postcapillary pulmonary hypertension were found. 1. Thilenius 00, Bharaii S, Lev M: Subdivided left atrium: an expanded concept of car triatriatum sinistrum. Am J Cardiol 37:743-752. 1976 REPLY On cardiac catheterization no communication between the right and left heart chambers was demonstrated and high pulmonary arterial (100/65 mm Hg) and pulmonary capillary wedge (mean 40 mm Hg) pressures were measured. No a or IJ waves could be demonstrated in the pulmonary capillary wedge pressure tracing with use of a conventional. but well flushed no. 8F catheter-transducer system. However, on withdrawal of the catheter tip into the pulmonary artery, a fairly good quality pulmonary arterial pressure curve was registered, thus demonstrating the good frequency response of the measuring system. This procedure was repeated several times with the same result (Fig. 1). Keltai’s letter implies that the proximal high pressure left atria1 chamber of tri-atria1 hearts has only minimal pressure fluctuations, resulting in a “waveless” pulmonary wedge pressure tracing. This phenomenon can be expected only in patients who have a small obstructive communication between the proximal and distal chamber; it does not differentiate obstruction within the left atrium from obstruction of the pulmonary venous ostia. On angiocardiography, the dividing membrane in the left atria1 cavity could not be demonstrated, but the two parts of the left atrium could be distinguished by their pattern of motion. The proximal (high pressure) portion of the left atrium showed no movement, whereas the distal (low pres- sure) portion manifested a hyperkinetic movement synchro- nous with the P waves of the electrocardiogram. The diagnosis was later proved at operation. In our case the waveless pulmonary wedge pressure tracing provided support for assuming that a stenosis existed between the measuring catheter and the contracting left atrium. This There has been almost no published information on the phasic behavior of the pulmonary wedge pressure in car tri- atriaturn. Maitre et al.’ reported in their Figures 3 and 9b pulmonary capillary pressures that are indeed waveless. On the other hand, Figure 4 of Michaud et a1.,2 shows an a wave of 34 mm Hg that has an x descent of at least 5 mm Hg. We have found it generally difficult to obtain satisfactory pulmonary wedge pressure recordings in patients with pul- monary hypertension. Such tracings are frequently “wave- less,” showing only respiratory fluctuations. This waveless appearance is not caused by overdamping but indicates an unsatisfactory location of the wedged,catheter tip or possibly severe arteriolar vasoconstriction and obstruction. The in- terpretation of a nonpulsatile wedge pressure tracing as sug- gestive of car triatriatum with obstruction to flow can be maintained only in the presence of other convincing evidence for this rare cardiac malformation. FIGURE 1. Electrocardiograms and pressure tracings References Otto G. Thilenius, MD, FACC Department of Pediatrics The University of Chicago Chicago, Illinois 1. Ma’hre MJ, Gtero E, Ouerro’Jlm&mez M, et al: Cor triatriatum. Rev Esp Cardiol 25: 119-126, 1972 2. Mlchaud P, Dalloz C, Age C. etal: A propos d’un nouveau cas de COBW triatrial de I’a- dub. op&C avec succlrs. Arch Mal Cceur 63:291-300. 1970 MID VENTRICULAR OBSTRUCTIVE CARDIOMYOPATHY VERSUS VENTRICULAR ANEURYSM Rae,’ arguing that left ventricular dyskinesia is a misnomer, presents a left ventriculogram in systole and diastole showing an apparent aneurysm. I contend that the example given is not an aneurysm. Mid ventricular obstruction, as a variant of obstructive cardiomyopathy, has been discussed in a case report by Falicov et a1.2 and an abstract presented by my group3 at the 49th session of the American Heart Association. In this entity, the level of intraventricular obstruction is in the August 1977 The American Journal of CARDIOLOGY Volume 40 295

Ventricular tachycardia in the posthospital phase of myocardial infarction

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ABSTRACTS

VENTRICULAR TACHYCARDIA IN THE POSTHOSPITAL PHASE OF MYO- LIMITATIONS OF INFREQUENT HOLTER MONITORING IN ASSESSING CARDIAL INFARCTION ANTIARRHYTHMIC EFFICACY

Kelley Anderson, M.D., John DeCamilla, B.S., and Arthur J. Moss, M.D., F.A.C.C., University of Rochester Medical Cen- ter, Rochester, New York.

Joel Morganroth, MO, FACC; Leonard N. Horowitz, MD; Mark E. Josephson, MD, FACC; Eric L. Michelson, MD, University of Pennsylvania, Philadelphia, Pa.

The clinical significance of ventricular tachycardia (VT) recorded during ambulatory monitoring in postcoronary pa- tients was determined from an ongoing prospective study. Six-hour Holter ECG recordings were performed every four months during follow-up periods (4-48 mo) in 915 patients ~66 years of age who survived the hospital phase of myo- cardial infarction. Over 5000 ECG recordings in this pop- ulation revealed 199 episodes of VT in 66 patients. Most patients (74%) had only one episode of VT, and in 47% of the patients the longest run of VT consisted of 3 ventri- cular premature beats in a row. A double set of control patients (n=132) was assembled by matching each VT patient according to sex, admission date and VT recording date. The VT and control patients were similar in almost all clinical characteristics. However, VT patients had more rapid heart rates and more evidence of ventricular irrita- bility (~~0.01) than their matched controls. The mortal- ity rate was 16% (11/66) in the VT group and 8% (11/132) in the control group (p=O.O56). The risk ratio was 2.35 (95% confidence interval 0.82 to 6.77). Life table analy- sis of the survival of VT and control patients revealed a 48 mo VT survival of 75% compared to 87% in the control group. Among those who died, the age, sex, cause of death, suddenness of death and mechanism of death were similar in the VT and control patients. Within the VT group, those who died had more severe underlying heart disease than the survivors. The findings suggest that VT in the posthospi- tal phase of myocardial infarction has less ominous impli- cations than previously assumed.

Variations in frequency of ventricular (VPD) and atria1 (APD) premature depolarizations were evaluated by three consecutive 24 hr Holter (H) recordings using the Avion- ics P-channel 445 recorder and 660A scanner at 120X real time (with a 7% error rate compared to real time analy- sis). 15 patients (pts)(mean age 56 + 10 yrs) with various cardiac disorders with VPD frequency of 37-l,379/hr underwent 20 study periods, and 8 pts (58 + 12 yrs) with APD frequency of 63-694/hr underwent 9 study periods. VPDs varied from +578 to -73% and APDs -96 to +748% over 3 days. Mean ectopic frequencies were subjected to a 4 and 5 factor nested analysis of variance to determine the source of variation. 50% of the VPD variation was due to differences between hourly rates whereas the largest APD variation was due to day to day variations. For signifi- cant change in ectopic frequency to exceed spontaneous variation, the following % decrement in ectopic frequency (depending on the protocol used) is necessary:

Post-Inter Control (H) Vention (H)_ VPDs API&

Protocol One: 8 hr One: 8 hr -90% -99% Design: One: 24 hr One: 24 hr -83% -98%

Three: 24 hr Seven: 24 hr -58% -85% Seven: 24 hr Seven: 24 hr -49% -78%

Thus, to determine the efficacy of an antiarrhythmic agent using specific research or clinical protocols, the decrease in ectopic frequency must exceed the values given in the table before that change in frequency can be considered statistically significant,

EVIDENCE FOR DOMINANCE OF THE LEFT STELLATE GANGLION IN THE LONG Q-T SYNDROME Richard S. Crampton, MD, FACC, 158 Medical Center, University of Virginia, Charlottesville, Virginia 22901.

The influence of left (L) and right (R) stellate ganglion block (SGB) and stimulation (S) and drug treatment upon Q-Tc (Bazett), Q-T and T altemans (ALT) and ventricular ectopy (VE) was assessed in 6 patients with Romano-Ward syndrome with Q-Tc mean (range) .61(.52-.71) sec. Five had ventricular tachycardia and 4 fibrillation. For SGB with lidocaine and for SGS (technic of GM Vincent et al, Am J Cardiol 33:174, 1974) with 1.5 maec rectangular DC pulses (9-10 Hz, 0.5-3OV), the Q-Tc of 10 consecutive sinus beats before, during and after intervention was com- pared (t test) for directional change (Table). P ranged from 1.0001 to <.05 for significant decrease (4) or in- crease (t) and >.6 for no change (-1. The 12 lead ECG (3 simultaneous) was recorded at 50 mmlsec, 0.5 mV/cm.

LSGB RSGB LSGS RSGS Q-Tc u+,t1 14 t2.+1 &2,tl Q-T&T ALTERNANS +2 t2 t2 -c

V ECTOPY +2 ?l t1 -b

Propranolol and phenytoin, alone or together, abolished ALT in 5 of 6 and KCL and Mg SO4 in 1 of 1. These agents and bretylium suppressed VR. Procainamide and quinidine worsened ALT and VE in 2 of 2. In aummary, the shortening of Q-Tc and suppression of ALT and VE by LSG block and by antisympathetic drugs and the elongation of Q-Tc and pro- duction of ALT and VE by LSG stimulation and RSG block mi- litate for asynrmetric cardiac innervation with LSG domin- ance as the major cause of syncope. VE and sudden death in long Q-T syndrome. Moreover, the rationale (PJ Schwartz et al, Am J Cardiol 37:1034. 1976) for excision of the LSG for refractory ventricular tachydysrhythmias in the long Q-T syndrome is supported by these observations.

DOES CORONARY REVASCULARIZATION REDUCE THE PREVALENCE OF VENTRICULAR ECTOPIC ACTIVITY? Thomas 8. Graboys, MD; Bernard Lown, MD, FACC; John J. Collins, MD, FACC; Lawrence H. Cohn, MD, FACC, Harvard School of Public Health and Peter Bent Brigham Hospital, Boston, Mass.

If ventricular ectopic activity (VEA) in patients with coronary heart disease relates to myocardial ischemia, then improved vascularization should reduce the preva- lence of arrhythmia. This question was examined in 58 patients (PTS)(50 male, 8 female; mean age 51, range 25- 74) who were subjected to 24 hour ambulatory monitoring (MON) two days before and at least one week after coro- nary bypass graft surgery (CABG). Twenty-eight of these PTS underwent a third MON at 3 months post CABG. VEA was classified as follows: Grade 1 (5 1 VPB/min); Grade 2 (2 30 VPBs/hr); Grade 3 (multiform);-Grade 4 (couplets, 4A or ventricular tachycardia, VT, 4B). Detailed below are the results of monitoring at 1 week (HON 2) and at 3 months (MON 3) as compared to pre-CABG MON:

VEA

MON 2 MON 3

Increased De;r$ecl)(%) ;; [;,fe;;

4 (14:3) 10 (35.7)

Eleven (39.2%) of the 28 PTS monitored at 3 months demon- strated advanced grades (4A,4B) of VEA, 5 of whom first developed VT post CABG persisting during MON 3. Nine of the 28 PTS monitored at 3 months who had been free of VEA prior to CABG persistently demonstrated VEA post CABG. Among 37 of 58 PTS (63.7%) in the immediate post CABG period and 18 of 28 PTS (64.2%) monitored at 3 months the same or an increased grade of VEA could be demonstrated. Hence coronary revascularization does not have a salutary effect upon VEA.

Falvurn ip28 Thehnarlcan Jaurnal ol CARDIDLDDY Volume 41 A01