Influence of abrupt pressure increments on left ventricular relaxation

ABSTRACTS

EFFECT OF CORONARY COLLATERALS ON EXERCISE PERFORMANCE. IdD: David A. Levi”, MD; Peter F. Cohn, Julian L. Berman, MD, FACC, Peter Bent Brigham Hospital, Boston, MA To evaluate the effect of well-developed collateral circulation (WDCC) on response to maximal exercise, 142 patients (pts) with angiographically proven coronary artery disease (CAD) who underwent maximal treadmill exerWDCC was considered present when the cise were studied. distal segment of a” obstructed vessel was well opacified via collateral channels and had a” average distal lumen diameter > 1.0 mm. We compared exercise duration (ED), peak Sy5t01 ic bi00d pressure-heart rate product (HRxBP), increase in R wave sum, and occurST depth and duration, Group I consisted rence of chest pain in 2 groups of pts. of 48 pts with I vessel CAD with (17) and without (31) collaterals; Group 2 consisted of 103 pts with 2 or 3 vessel CAD with complete (9) and partial (71) collateralizaNo signifition, as well as 23 pts without collaterals. cant differences were obtained in any of the variables tested except for significantly lower HRXBP (l9.4+0.7 vs. 23.3t1.4, meaniSEM)(p<.05) and ED (5.9i0.3 vs. 7.6~0.7, pc.05) in Group 2 pts with partial collateral formation. The small number of Group 2 pts totally collateralized did not differ significantly in these variables from either We conGroup I pts or Group 2 pts without collaterals. clude I) collaterals do not appear to decrease manifestations of exercise induced ischemia, nor do they improve maximal exercise tolerance or myocardial oxygen uptake; 2) pts with multivessel CAD and partial collateralization appear to have more limitation in exercise tolerance and myocardial oxygen uptake than pts with multivessel CAD who have not formed collaterals, possibly because the latter pts have less severe degrees of ischemia.

PHYSICAL CONDITIONING IN PATIENTS WITH SEVERELY DEPRESSED LEFT VENTRICULAR FUNCTION. Eric H. Corm, MD, R. Sanders Williams, MD; Andrew G. Wallace, MD; Duke University Medical Center, Durham, North Carolina. The purpose of this study was to determine if patients with severely depressed left ventricular function could demonstrate physical conditioning (PC). Ten patients were identified with documented prior myocardial infarction and a resting left ventricular ejection fraction of 427% (range 13-26% mean 20%) assessed by radionuclide angioto maingraphy. Subjects exercised (walk/jog/ergometry) tain exercise heart rates at 70-80% of their symptom limited maximum rate 3 to 5 times weekly for periods ranging from 4-21 months, mean 11 months. Performance was evaluated by treadmill testing using a modified Balke protocol. Heart rate at 50% of the initial maximal workload was used to assess (PC), and decreased from a mean of 135 2 13 to 114 * 7 beats/min with training (p x.001). Maximal treadmill time was used to assess functional capacity and increased from 7.75 min to 10.55 min, p = .05. There were no cardiovascular complications during the exercise sessions. Mortality in this group was 2/10 (both non-exercise related) which compared with a one year mortality of 35% in a group of 95 patients with coronary artery disease matched for age and ventricular function. We conclude that (1) a low ejection fraction -per se does not identify a group which is physically incapcitated, (2) these patientscan undergo supervised exercise without clinical deterioration, (3) despite extensive cardiac impairment a definite training effect can be demonstrated and functional capacity improved. Though preliminary, these data indicate that selected patients with a low ejection fraction can participate safely and benefit from a supervised conditioning program.

MONDAY, MARCH 10, 1980 AM VENTRICULAR DIASTOLIC FUNCTION 10:30- 12:oo INFLUENCE OF ASYNCHRONOUS EARLY DIASTOLIC LEFT VENTRICULAR RELAXATION ON DIASTOLIC FUNCTION Philip A. Ludbrook, M.D., F.A.C.C., Joseph D. Byrne, CPT, Washington University, St. Louis, MO. Asynchronous early diastolic segmental left ventricular (LV) relaxation (ASR) is observed commonly in patients (pts) with, and without coronary disease. To define the relationship between ASR and altered diastolic LV function, we examined early diastolic wall motion in 21 pts during catheterization, also measuring LV pressure (P) by micromanometqand simultaneous volume (V) by angiography. Diastolic relaxation was assessed by T, reflecting the rate of isovolumic LV relaxation independent of loading conditions. Normal synchronous diastolic wall motion was present in 11 pts (group I) all of whom also had normally synergic systolic contraction; ASR was seen in 10 pts (group II), 6 of whom had systolic asynergy. Ejection fraction (EF) was subnormal ( 50%) in the 6 group II pts with systolic asynergy, but was normal in the other 4 group II pts with normal contraction, EF was normal in all group I pts. Aortic; LV systolic; minimal and end diastolic pressures; peak + dP/dt; peak LV systolic pressure to end-systolic volume ratio; mean Vcf; and mean systolic LV chamber ejection rate were similar in both groups. stiffness rate constant of exponential LV P-V relation, volume normalized chamber stiffness, operational chamber stiffness at end diastole, and the slope of the LV log Plog V relation at end diastole, were also similar in each group. Conversely, T was prolonged in group II (55 + 2.3 msec) compared to values in group I (46 + 3.6), and peakdP/dt was lower in group I (1310 2 57 mm Hg/sec) than group II (1544 + 93) (p .05 for both). Thus, ASR is unrelated to systolic asynergy or ContraCtility, LV pre- and/ or afterload, or diastolic chamber stiffness, but is associated with prolongation of T, and reduction of peak dP/dt, suggesting global impairment of LV relaxation.

INFLUENCE VENTRICULAR

ABRUPT PRESSURE INCREMENTS ON LEFT RELAXATION. Marc A. Goetholr, MD, Ivo E. Kersschot, MD, Victor A. C&s, Carlo F. Hermans, Antony H. Jageneou and Dirk L. Brutsoert, MD. Department of Physiology, University of Anhverp, Antwerp, Belgium. In view of the marked load-sensitivity malian heart muscle, load-sensitivity ation

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February 1980

The American Journal of CARDIOLOGY

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