1570 LETTERS

I M P O R T O F E X E R C I S E - I N D U C E D

V E N T R I C U L A R A R R H Y T H M I A IN

M A L I G N A N T V E N T R I C U L A R

A R R H Y T H M I A

Weaver et all detail an experience with sur- vivors of out-of-hospital cardiac arrest undergoing exercise testing. The landmark work by this group in defining this complex pat ient population remains unparalleled. There is a fundamental methodologic flaw, however, in these current data which limit conclusions regarding the import of exer- tionally induced ventricular ar rhythmia (VA). The exercise testing protocol did not include continuous recording of all rhythm to allow true quantification of the density or complexity of ventricular premature beats (VPB). Rather, rhythm was "monitored continuously by the oscilloscope and recorded each minute." Several years ago we addressed the issue of continuous recording of rhythm versus intermit tent sampling and found an 18% increase in coded VPB during continu- ous recordings but, more importantly, a 6- fold increase in the disclosure of complex and repetitive VPB (56 versus 9 episodes).2 Sec- ond, the indication for termination of exercise by Weaver et al was increasing VA. Thus, the prognostic weight of those forms of VPB (repetitive or salvos) now considered to carry highest risk 3 cannot be assessed in the cur- rent report.

Our experience with a similar population is considerably different. The indications for terminating exercise in our laboratory is provocation of salvos of ventricular tachy- cardia (VT). Thus, 65% of our patients with a history of malignant VA exhibit VT salvos and 91%, ventricular couplets. 4 Patients with malignant VA who continue to exhibit VT salvos during exercise despite control of ar- rhythmia during extended electrocardio- graphic recordings remain at extreme risk for sudden death or recurrence. Abolition of these forms of VPB with antiarrhythmic drugs, however, results in enhanced long- term survival. 4

Thomas B. Graboys, MD Boston, Massachusetts

1. Weaver WO, Cobb LA, Hallstrom AP. Characteristics of survivors of exertion- and none;~ertion-related cardiac arrest: value of subsequent exercise testing, Am J Cardio11982;50(Oct):671-676.

2. Antman E. Graboys TB, Lown B. Continuous monitoring for veetricalar arrhythmia during exercise tests. JAMA 1979;26:2802.

3. Bigger JT, Weld FM, Rolnitzky LM. Prevalence, char- acteristics and significance of ventricular tachycardia detected with ambulatory electrocardiographic recording in the late hospital phase of acute myocardial infarction. Am J Cardio11961;48:815-823.

4. Graboys TB, Lown B, Podrid P J, DeSilva R. Loog-term survival of patients with malignant ventricular arrhythmia treated with antiarrhythmic drugs, Am J Cardiol 1982; 50:437-443.

REPLY: We agree tha t the qualitative and quantitative assessment of complex VA during exercise testing can be enhanced by continuous monitoring during the test. Al- though we did not report the results, contin- uous recording of the electrocardiogram on magnetic tape during and after exercise was

accomplished in all but 3 of the 90 patients in our report. With continuous monitoring we detected only 5 additional (6%) patients (total 49%) with any complex VA. In 10% of patients, the physician missed repetitive forms present on the magnetic tapes. The forms of arrhythmias documented by either the physician or by the continuous recordings were not of prognostic value in subsequent determinations of survival. Therefore, in as- sessing outcome in this group of patients, only exercise-evoked angina or failure to augment systolic blood pressure were of prognostic importance. Exercise testing was most often patient-limited because of com- plaints of fatigue and not because of ar- rhythmias,

Graboy's patients and ours have both ex- perienced recurrent serious arrhythmias. We believe tha t the patients followed by our group, tha t is, survivors of out-of-hospital ventrieular fibrillation, may differ from pa- tients referred for management of recurrent symptomatic VT. Few of our patients exhibit paroxysms of symptomatic VT during fol- low-up. We do not know if sustained VT preceded the episodes of cardiac arrest in patients treated by our emergency care sys- tem; however, we suspect tha t was not usual, Sustained VT has rarely been recorded at the t ime these patients are initially assessed by the paramedical personnel, and most patients had no apparent symptoms immediately before collapse. I t is, of course, quite likely that ventricular fibrillation was preceded by a few beats of rapid VT. In survivors of out- of-hospital ventricular fibrillation, VT is relatively uncommon during exercise testing as well as 24-hour ambulatory electrocar- diographic recording. 1 o n the other hand, rates of 65 to 90% have been repeated in pa- t ients with malignant symptomatic ar- rhythmias. 2,~ The former group more com- monly stops exercise with symptoms of left ventricular dysfunction, while the latter stops because of arrhythmias. Because of the in- frequent occurrence of VT during ambula- tory monitoring (10%) and exercise testing (8%), these tests appear to be of limited use and offer guidelines to t reatment in only a few of our previously resuscitated patients.

Although both groups of patients share many common characteristics, differences in ambient arrhythmias, in the syndromes as- sociated with arrhythmias, and perhaps also in the arrhythmias immediately preceding VF all suggest tha t one should be cautious in lumping the syndromes of symptomatic VT and out-of-hospital ventr icular fibrilla- t i o n - t r e a t m e n t strategies and efficacy may differ for the groups.

W. Douglas Weaver, MD Leonard A. Cobb, MO

Alfred P. Hallstrom, PhO Seattle, Washington

1. Weaver WD, Cobb LA, Hallstrom AP. Ambulatory ar- rhythmias in resuscitated victims of cardiac arrest. Circulation 1982;66:212.

2. Graboys TB, Lown B, Podrid PJ, DeSilva R. Long-term survival of patients with malignant venkicular arrhythmia treated with antiarrhythmic drugs. Am J Cardiol 1982; 50:437-443.

3. Graboys "riB, Lampert S, Lown B. Yield of ventricular arrhythmia during exercise testing in patients with prior cardiac arrest. Circulation 1982;Supp111:11-27.

A P I C A L H Y P E R T R O P H I C

C A R D I O M Y O P A T H Y

We read with interest the article by Maron et al, 1 and wish to point out certain additional differences between their cases and the Jap- anese form of apical hypertrophic cardio- myopathy (HC). 2-4 The latter is found pre- dominantly in males and the prognosis seems to be better than in the usual HC. In addition to the mentioned differences in the degree of T-wave negativity, the QRS axis lies betwee n 0 ° and +9003 ,3 Septal Q waves are often lacking, as found in 83% of Yamaguchi's pa- t ients and in the 2 cases reported outside Japan. s,4 Neither QRS axis nor septal Q waves was commented on by the authors. 1 Spatial vectorcardiograms in our case and in those reported from Japan disclosed a QRS 10o p oriented to the left and inferiorly with characteristically elongated T-loops oriented to the right and posteriorly. 2,3 Are these ad- ditional electrocardiographic and vector- cardiographic findings available for com- parison? The spade-like angiographic ap- pearance is very different from tha t seen in Maron's cases, and we suggest tha t the term "apical hyper t rophic cardiomyopathy" should be reserved for the Japanese form 2-4 which shows marked concentric apical hy- pertrophy rather than the apical distribution of septal hypertrophy with mid-ventricular constrictionJ

Edward G. Abinafler, FRCPI Haifa, Israel

1. Maron BJ, Sonow RO, Seshagiri TN, Roberts WC, Ep- stein SE. Hypertrophic cardiomyopathy with ventricular septal hypertrophy localized to apical region of left ventricle (apical hypertrophic cardiomyopathy). Am J Cardio11982;49(June): 1838-1848.

2; Yamaguahi M, Ishlmura T, Nishiyama S, Nagasaki F, Nakanishi S, Takatsu F, Nishijo T, Umeda T, Machii K. Hypertrophic nonobstructive cardiomyopathy with giant negative T waves (apical hypertrophy): ventriculographic and echocardiographic features in 30 patients. Am J Cardio11979;44:401-412.

3. Ablnader EG, Rauchlleisch S, Naschitz J. Hypertrophic apical cardiomyopathy: a subtype of hypertrophic car- diomyopathy. Isr J Med Sci 1982;18:1005-1009.

4. Stelngo L, Dansky R, Pockock WA, Barlow JB. Apical hypertrophic nonobstructive cardiomyopathy. Am Head J 1982;104:635-637.

REPLY: Abinader raises an important con- sideration related to the morphology and nomenclature of HC. The application of 2- dimensional echocardiography to the study of patients with HC has demonstrated that a diverse spectrum of patterns of left ven- tricular (LV) hypertrophy may occur. 1,2 One pattern is characterized by disproportionate hypertrophy in the LV apical region (see References I to 4 in Abinader's letter). This morphologic form of HC appears quite com- mon in Japan (see Reference 2 in Abinader's letter), where it is associated with a distinc- tive electrocardiographic pat tern ("giant T-wave inversion") and a "spade-like" LV angiographic appearance. In our report, we described a subgroup of patients with HC who had a distribution of LV hypertrophy which was Similar (but perhaps not identical) to tha t described by the Japanese investiga- tors. Our patients also differed somewhat with regard to the LV angiographic appear- ance and electrocardiographic pattern.