Prognosis of congestive heart failure in patients aged ≥62 years with unoperated severe valvular aortic stenosis

quency energy until accessory pathway loss, suggesting that this accessory pathway may have been slightly removed from the ablation catheter, thus resulting in a suboptimal ablation temperature. Although one might suspect our patients with an early recurrence and delayed cure would be at risk of subsequent recurrence of accessory pathway function, the absence of accessory pathway function on the follow-up electrophysiologic study as well as their complete lack of symptoms for 9 to 15 months of additional follow-up strongly suggests that they are cured of their accessory pathways. Our patients are therefore different from those of Leitch et aJ8 who reported a group of 4 patients undergoing seemingly unsuccessful ablation who had delayed loss of preexcitation 3 to 5 days after ablation, but subsequently regained accessory pathway function 3 to 5 months later. The explanation these investigators advanced was that their patients’ accessory pathways were located in the rim of tissue edema and intlammation surrounding the area of complete necrosis so that accessory pathway conduction disappeared between the third to fifth days (when the local edema and inflammation would be expected to be at its peak) and then recurred as further healing took place during the next several weeks. The fact that .our patients did show immediate loss of accessory pathway function would suggest their pathways were closer to the center of the radiofrequency lesion than those of Leitch et al, and this may account for their eventually being completely cured.

Whatever the exact mechanism of our patients’ response, our observation implies that patients exhibiting early recurrence after apparently successful radiofrequency catheter ablation should be observed for at least several days to 1 week or more to rule out a potential delayed cure before proceeding with repeat ablationparticularly if the recurrence begins within the iirst 12 hours and the recurrent preexcitation is intermittent. 1. Calkins H, Sousa J, El-Atassi R, Rosenheck S, de Buitleir M, Kou WH, Kadish AH, Langberg JJ, Morady F. Diagnosis and cure of the Wolff-Parkinson-W syndrome or paroxysmal supraventricular tachycxdias during a single electrophysiologic test. N Engl J Med 1991;324:1612-1618. 2. Jackman WM, Xtiang W, Friday KJ, Roman CA, Moulton KP, Beckman KJ, McClelland JH, Twidale N, Ha&t Z, Prior MI, Margolis PD, &lame JD, Overholt ED, Lazzara R. Catheter ablation of accessory ahioventricula pathways (Wolff-Parkinson-W syndrome) by radiofrequency current. N Engl .l Med 1991;324:1605-1611, 3. Scheimnan MM, for the NASPE Ad Hoc Committee on Catheter Ablation. Catheter ablation for cardiac arrhythmias, personnel, and facilities. PACE 1992;15:711-721. 4. Langbag JJ, Calkins H, Kim Y, Sousa J, El-Atassi R, Leon A, Borganelli M, Kalbfleisch SJ, Morady F. Recurrence of conduction in accessory atrioventricular connections after initially successful radiofrequency catheter ablation. J Am CoN Cardid 1992;69:1588-1592. 5. Twiddle N, Wang X, Beckman KJ, McClelland JH, Moulton KP, Prior MI, Ha&t HA, Lazzara R, Jackman WM. Factors associated with recurrence of accessory pathway conduction after radiofrequency catheter ablation. PACE 1991; 142042%2048. 6. Langberg JJ, Calkim H, El-Atassi R, Borganelli M, Leon A, Kalbfleisch SJ, Morady F. Temperature monitoring during radiofrequency catheter ablation of accessoty pathways. Circulation 1992;86:146%1474. 7. Chen X, Borggrefe M, Hiidricks G, Haverkamp W, Karbenn LJ, Shenasa M, Breithardt G. Radiofrequency ablation of accessory pathways: characteristics of transiently and permanently effective pulses. PACE 199&15:1122-l 130. 8. Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Does delayed loss of preexcitation after unsuccessful radiofrequency catheter ablation of accessory pathways result in permanent cure? Am J Cardiol 1992;70:83&832.

Prognosis of Congestive Heart Failure in Patients Aged 262 Years with Unoperated Severe Valvular Aortic Stenosis Wilbert S. Aronow, MD, Chul Ahn, PhD, ltzhak Kronzon, MD, and Michael Nanna, MD oss and Braunwaldl reported that the average surR vival rate after the onset of congestive heart failure (CL-IF) in patients with severe aortic stenosis (AS) was

vascular congestion present on the chest roentgenogram interpreted by both an experienced radiologist and the senior author. 1.5 to 2 years. We reported that left ventricular (LV) M-mode and 2-dimensional echocardiograms, and ejection fraction was the most important prognostic vari- continuous-wave Doppler recordings for determining able for mortality in elderly patients with CHF associ- LV ejection fraction and the severity of AS were obated with coronary artery disease.2 We report the results tained as previously described.2-4 The peak transvalvufrom a prospective study of elderly patients with CHF lar gradient was determined by using the simpl@ed associated with unoperated severe valvular AS, correlat- Bernoulli equation: AP = 4V2 (where AP = peak presing normal and abnormal LV ejection fraction with car- sure gradient in mm Hg; and V = peak transvalvular diac and total mortality. flow velocity in mls). The peak pressure gradient across In a prospective study, CHF was diagnosed in 48 el- the aortic valve was 30 mm Hg if the peak aortic flow derly patients with severe valvular AS who refused aor- velocity was 23.6 mls. Aortic valve area was calculattic valve replacement or balloon aortic valvuloplasty. ed, when feasible, by the continuity equation using CHF was diagnosed if the following 2 criteria werefulpulsed Doppler echocardiography to evaluate LV outfilled: (I) pulmonary basilar vales heard by 2 physi- flow tract flow velocity, continuous-wave Doppler echocarcians, including the senior author; and (2) pulmonary diography to evaluate transvalvular flow velocity, and the 2-dimensional parasternal long-axis view to measure LV outflow tract area.5 Severe AS was diagnosed From the Hebrew Hospital Home, 801 Co-op City Boulevard, Bronx, New York 10475; the Department of Geriatrics and Adult Developtf the aortic valve area was ~0.7 cm2, or in the absence ment, Mount Sinai School of Medicine, New York, New York, the of a measured aortic valve area, tf the peak pressure Department of Biostatistics, City of Hope National Medical Center, gradient across the aortic valve was 250 mm Hg. Duarte, California; and the Department of Medicine, New York UniLV volumes at end-diastole and end-systole were versity School of Medicine, New York, New York. Manuscript received March 8,1993; revised manuscript received and accepted May 20,1993. calculated by planimetry from the digitized 2-dimen846

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TABLE I Baseline Characteristics of Patients Heart Failure Associated with Severe Valvular and Normal Versus Abnormal Left Ventricular Fraction

Variable Age (years) Women (%) Atrial fibrillation (%) Mean LV ejection fraction (%I Mean follow-up (mos)

with Congestive Aortic Stenosis (LV) Ejection

TABLE RI Regression Model

Abnormal LV Ejection Fraction (n = 18)

84 '-+ 8(66-97) 25(83%) 13(43%) 62 2 5(51-75)

83 rt 7(62-91) 13 (72%) 9(50%) 38t9C19-49)

0.0001

13 f 9 (Z-24)

0.062

11 (2-36)

Death and Their Cox Regression

p Value

NS NS NS

Variable Sex LV ejection fraction Age Atrial fibrillation

Regression Coefficient

Standard Error

p Value

0.157 -0.041

0.391

0.684

1.170

(0.543-2.520)

0.015

0.006

0.960

(0.932-0.988)

0.014 ,0.186

0.023 0.305

0.525 0.543

1.015 1.204

(0.970-1.061) (0.662-2.190)

Normal LV Ejection Fraction (n = 30)

Abnormal LV Ejection Fraction (n = 18)

p Value

25 (83) 27 (90)

17 (94) 18 (100)

NS* NS”

L-a ‘- 1-.

Confidence Limits

Abnormal LV Ejection Fraction - - - - - Normal LV Ejection Fraction I____

‘- > .

I

*Calculated by Fisher’s exact test.

Relative Risk

LV = left ventricular; Sex = 0 if male, and 1 if female.

TABLE II lncidences of Cardiac and Total Death in Patients with Congestive Heart Failure Associated with Severe Valvular Aortic Stenosis and Normal Versus Abnormal Left Ventricular (LV) Ejection Fraction

_ Cardiac death (%) Total death (%)

Variables for Total in the Multivariate

95%

Normal LV Ejection Fraction (n = 30)

19 f

Prognostic Coefficients

‘- , ----I

-. ‘- *._ 0

I 6

I 12

I 18 Months

24

30

1 36

Log-Rank: Jo= 0.010

sional echocardiographic frames using Simpson’s rule. LV ejection fraction was calculated as: (LV end-diastolic - end-systolic volume)/LV end-diastolic volume X 100%. An abnormal LV ejection fraction was ~50%.~ Patients were followed for incidences of cardiac and total death. Follow-up was from the time LV ejection fraction was obtained until the time of death or the cutof date for analysis of the data. Group comparisons were obtained using the t test for continuous variables (Table I), and either the chi-square or Fisher-S exact test for categoric variables (Tables I and II) between patients with normal versus abnormal LV ejection fraction. Survival curves of patients with normal versus abnormal LV ejection fraction were estimated using the Kaplan-Meier product-limit estimator and tested for homogeneity with the log-rank test (Figure 1). The relation between prognostic variables measured at baseline and time to death was examined using the multivariate Cox regression model (Table III). Table I shows the baseline data for patients with normal versus abnormal LV ejection fraction. Table II shows the incidences of cardiac and total death for patients with normal versus abnormal LV ejection ft-action. Table III lists 4 prognostic variables for total mortality and their regression coeficients in the Cox regression model. In Table III, LV ejection fraction was exa.mined by using the actual LV ejection fraction. There was a 1.22-fold higher death rate for a decrement of 5% of LV ejection paction and a 1.51-fold higher rate for a decrement of 10% of LV ejection fraction after controlling other prognostic variables. If the presence of a normal versus abnormal LV ejection fraction was used for Table III, LV ejection fraction was still the only signiJicant independent predictor of total mortali-

FIGURE 1. KaplarrMeier survival derly patients with unoperated sis and normal versus abnormal fraction.

curvee for total death in eleevere valvular aortic stene left ventricular (LV) ejection

ty (p = 0.016; relative risk 2.307; 95% confidence limits 1.1734.544; after controlling other prognostic variables). Patients with an abnormal LV ejection fraction had a 2.3-fold higher mortality rate than did those with a normal LV ejection fraction after controlling other prognostic variables. Kaplan-Meier survival curves for total death are shown in Figure 1. The log-rank test shows that patients with abnormal LV ejection fraction have a sign@cantly higher mortality rate than do those with normal LV ejection fraction (p = 0.010). Ross and Braunwald’ reported that the average survival rate after the onset of CHF in patients with severe valvular AS was 1.5 to 2 years. Figure 1 shows that elderly patients with CHF associated with severe valvular AS who refuse aortic valve replacement or balloon aortic valvuloplasty have a very poor prognosis, in accordance with the data reported by Ross and Braunwald. Normal LV ejection fraction occurred in 30 of 48 patients (62%) with CHF due to severe valvular AS. The data also show that LV ejection fraction is an independent predictor of mortality in these patients. At a mean 19-month follow-up (range 2 to 36), 90% of 30 patients with CHF associated with unoperated severe valvular AS and normal LV ejection fraction were dead. At a mean 13-month follow-up (range 2 to 24) 100% of 18 patients with CHF associated with unoperated severe valvular AS and abnormal LV ejection fraction were dead. BRIEF REPORTS

847

1. Ross J Jr, Braunwald E. Aortic stenosis. Circulation

1968;36(suppl V):V-61-V-

tion n~nmmrs. Am J Cardiol 1987;60:399-401. 4. Aronow WS, Kronzon I. Prevalence and severity of valwlar

67.

2. Aronow WS, Ahn C, Kronzon I. Prognosis of congestive heti failure in elderly patients with normal versus abnormal left venhiculax systolic function associated with coronq artery disease. Am J Cardiol 1990;66:1257-1259. 3. Aronow WS, Kronzon I. Correlation of prevalence and severity of valvnlar aortic stenosis determined by continuous-wave Doppler echocardiography with physical signs of aortic stenosis in patients aged 62 to 100 years with aortic systolic ejec-

aortic stenosis determined by Doppler echocaxliography and its association with echocardiographic and electrocardiographic left ventricular hypertrophy and physical signs of aortic stenosis in elderly patients. Am J Cardiol 1991;67:77&777. 5. Teirstein P, Yeager M, Yock PG, Popp RL. Doppler echocardiographic measurements of aortic valve area in AS: a noninvasive application of the Gorlin formula. J Am Coil Car&l 1986;7:1059-1065.

Prevalence and Clinical Significance of Mild Paraprosthetic Ring Leaks and Left Atrial Spontaneous Echo Contrast Detected on Transesophageal Echocardiography Three Months After Isolated Mitral Valve Replacement with a Mechanical Prosthesis Daniel Skudicky, MD, John Skoularigis, MD, Mohammed R. Essop, MD, Christian Rothlisberger, MD, and Pinhas Sareli, MD ransesophageal echocardiography (TEE) is a valuable T tool in the assessment of mitral valve prostheses. It

allows examination of the left atrium from its posterior wall avoiding the acoustic shadowing by the prosthesis. Both transvalvular regurgitation and spontaneous echo contrast have been more frequently detected by this method than with the transthoracic approach.‘” Although both clinically “silent” paraprosthetic leaks3 and left atrial spontaneous echo contrast have been reported in normally functioning mitral valve prostheses, the prevalence and clinical importance of these findings is unknown. This study assesses the incidence of mild paravalvular leaks and left atrial spontaneous echo contrast on routine TEE 3 months after mitral valve replacement in patients in whom the prosthetic valve was considered to function normally on clinical examination and transthoracic echocardiography. Between April 1991 and September 1992, 41 consecutive patients who underwent valve replacement for the first time were evaluated 3 months after surgery. A full clinical examination followed by transthoracic color Doppler echocardiography using a commercially available system (Hewlett Packard Sonos 500 or 1000) with either a 2.5 or 3.5 MHz transducer were per$onned in all patients. In 2 patients a moderate mitral ring leak was detected on transthoracic echocardiography, and they were excluded porn this study. The remaining 39 patients (28 women and 11 men; mean age 31.2 years [range 10 to 671) constitute the study population. All patients were in New York Heart Associationfunctional class I (n = 34) or II (n = 5); 24 patients were in sinus rhythm and 15 had atria1 jibrillation. Prosthetic valves implanted were St. Jude Medical (n = 23), Carbomedics (n = 12), and Medtronic-Hall (n = 4). All patients were treated with low-level war$arin anticoagulation (mean international normalized ratio at 3 months = 2.07 f 0.6 [range 1.1 to 3.91) and dipyridamole 300 mg/day. TEE with color flow mapping was per$ormed using a 5 MHz transducer attached to a commercially availFrom the Department of Cardiology, Baragwanath Hospital, l?O. Bertsham 2013, Johannesburg, and the University of the Witswatersrand, Johannesburg, South Africa. Manuscript received January 19, 1993; revised manuscript received April 27, 1993, and accepted April 28.

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THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 72

able imaging system (Hewlett-Packard Sonos 1000). A monoplane transducer was used in the3rst 12 patients and a biplane in the subsequent 27. All examinations were pe$ormed by the same operator (D.S.) and recorded on video tape for later analysis. The mitral valve prosthesis was scanned in dtzerent angles and using TEE and transgastric views. Each examination was petiormed with the use of the shallowest depth and narrowest sector angle capable of encompassing the entire mitral regurgitant jet area in order to maximize the frame rate. Gain was adjusted at the maximal level possible without introducing signals in areas of no flow or onto tissue from adjoining chambers. M-mode echocardiography of the regurgitant jet was performed directing the cursor line parallel and through the origin of the jets. The area of the regurgitant jets was measured by planimetry in the basal I-chamber view using the frame that showed the maximal extent of the jets. Two features of normal intraprosthetic regurgitation were noted: (1) In bileaflet prostheses multiple jets were noted when the jidl sur$ace of the valve was examined, and with dtxerent patterns depending on the imaging phme. The best defined pattern was obtained at 0” in a plane parallel to the leaflet axis in which 2 converging jets originating from the pivots points were observed. In addition a small central jet and a variable number of small peripheral jets were also noted in some cases. (2) In Medtronic-Hall prostheses a different pattern was observed. A dominant central jet was always present and depending on the imaging plane none or 1 to 3 small peripheral jets were also detected. In both bileaflet and tilting disc valves M-mode echocardiography of these intraprosthetic regurgitant jets showed 2 d$erent components including an early systolic regurgitant flow followed by a holosystolic jet (Figure 1). This was ob-. served in the central as well as in the peripheral jets. Regurgitant jets were defined as being paravalvular when they had a pattern signi$cantly different from the ones previously described: (1) a large dominant peripheral jet with a bigger area than the converging jets in bileaflet prostheses or the central jet in Medtronic-Hall valves; and (2) when the M-mode echocardiogram of that jet showed only a holosystolic regurgitant jet not preceded by the closure volume component (Figure 2). The presence of spontaneous echo contrast and throm-

OCTOBER 1,1993