ABSTRACTS

NIFEDIPINE in HYPERTROPHIC CARDIOMYOPATHY: TUESDAY, APRIL 27, 1982 HAEMODYNAMIC and METABOLIC EFFECTS AM

Kieran Daly MRCPI, G.Bergman MXCP, M.Monaghan M.Sc., P.J.Richardson MRCP, C.Jackson MRCP, D.E.Jewitt FRCP Cardiac Dept., King's College Hospital, London, SE5

The role of calcium channel blocking agents in hypertrophic cardiomyopathy has not been established. We have examined the haemodynamic and metabolic effects of Nifedipine (N), 2Omgs sublingually, in 10 patients at rest and during incremental atria1 pacing. In addition, the effect of the drug on the rate of LV dimension changes were assessed from the digitised echocardiogram. All pts had characteristic angiographic echocardiographic and histological features of hypertrophic cardiomyopathy. 4 had resting LV intracavity gradients (range 50 - 95 mmHg).

At rest after N, mean arterial pressure fell (84 to 79 mmHg p<O.O5) with an increase in stroke volume (63 to 72 mls). Total peripheral resistance (1632 to l;!O dyne.sec cm') and LV dp/dt max (1655 to 1495 mmHg set ) also fell. There was no change in LV filling pressure. Similar effects were seen during atria1 pacing. Coronary blood flow increased both at rest and on atria1 pacing. Evidence of improved diastolic function after N was See” on echocardiography (peak rate of LV dimension increase 12.9 to 17 cmfsec). No significant change in LV gradients was seen. Importantly, in 5 pts (3 with LV gradients) myocardial ischaemia as evidenced by lactate production was reversed following N (lactate extraction ratio -13.6% to 10.5%). In 4 pts symptom limited atria1 pacing time was prolonged after N from 243 to 406 sacs.

Within this group of patients we have demonstrated symptomatic, haemodynamic and metabolic benefit following N. However the heterogeneous response suggests that pts should be individually assessed for potential benefit.

ELEVATED LEFT VENTRICULAR FILLING PRESSURE AS A CAUSE OF ANGINA IN PATIENTS WITH NORMAL CORONARY ARTERIES Charles A. Bush MD, FACC; William Fanning MD; Albert J. Kolibash MD: Carl V. Leier MD: Ohio State Universitv Hospitals, &lumbus, OH ’ Of 2875 patients studied consecutively in the cardiac catheterization laboratories with coronary angiography for diagnosis of angina1 chest pain, 125 were found to have normal coronary angiograms, normal LV ejection fraction (>0.60)and no other cardiac pathology. The patients were divided into Group I, 50 patients with resting LV end-diastolic pressure (EDP)c12 mm Hg and post angiographic LVEPDL 22 mm Hg and Group II, 75 patients with LVEDP>12 mm Hg and/or post angiographic LVEDP>22mm Hg. There were no differences in historical features, physical examination, electrocardiograms, or exercise tolerance between the two groups. Nine of 30 Group II patients experienced chest pain and 7 developed ST segment depression with treadmill exercise while "one of the Group I patients had these findings (p<O.Ol). None of the 50 Group I patients developed chest pain during catheterization study while 33 Group II patients developed their usual chest pain always associated with a rise in LVEDP to greater than 24 mm Hg (p< 0.001). The 33 Group II patients who developed chest pain had a higher post angiographic LVEDP (30fl mm Hg) than the 42 who did not get chest pain (2621 mm Hg) (p<O.QOl). All Group II patients with chest pain experienced total relief of chest pain and drop in LVEDP to 12 mm Hg or less with nitroglycerin. Hence, elevated LV filling pressures have been demonstrated to be associated with the precipitation of angina1 chest pain in patients with angiographically normal coronary arteries. Such patients appear to have isolated diastolic dysfunction the mechan- ism of which is undefined. Chest pain and elevated filling pressures both are responsive to nitroglycerin.

SYSTEMIC HYPERTENSION: VEN7RKWLAR FlJNCTtON AND HYPERTROPHY-REGRESSION OF HYPERTROPHY 10:30- 12:oo NORMAL LEFT VENTRICULAR FUNCTIONAL RESPONSES TO UPRIGHT BICYCLE EXERCISE IN HYPERTENSION Michael W. Cleman, MD; Charles K. Francis, MD, FACC; Harvey J. Bereer. MD: Ross A. Davies. MD: Robert W. Giles; MD; Henry-R. Black, MD; Ruben'A. Vito, MD, FACC; Barry L. Zaret, MD, FACC, Yale University, New Haven, CT.

The left ventricular (LV) functional response to exercise (EX) in hypertension has not been completely elucidated. LV ejection fraction (EF) and wall motion were evaluated using first-pass radionuclide angiocardiography at rest and during maximal upright bicycle EX in 28 hypertensive patients (pts) (mean age, 43 yrs; range 20-68 yrs). All pts were hypertensive when studied, systolic blood pres- sure (BP) 140 mmHg and/or diastolic 590 mmHg. None had clinical or ECG evidence of other cardiac diseases. LV hypertrophy (H) was present by ECG in 15128 pts. 8128 were on no antihypertensive drugs; 14/28 were on propran- 0101 (Prop) (mean dose, 320 mg/day); 6/28 were on diur- etics only. In 27128 pts, the LV functional response to EX was normal (25% absolute increase in LVEF). LV wall motion was normal at rest and with EX. Resting LVEF (mean-$E) was 65+2% (range, 49-83%) and LVEF augmented by 11+1X with EX. The EF response to EX was comparable in pt< with and without LVH (q+_2 vs 13+2X, p NS). In pts receiving Prop, the augmentation in LVEF with EX was of similar magnitude to that observed in the remaining pts (1252 vs 1%2X, p NS). Heart rate increased less with EX in pts on Prop than in the others (43+4 vs 71+4 bpm, p <O.OOl), while the increments in systolic BP were com- parable (46+6 vs 64+7 mmHg, p NS). There was no signifi- cant difference in duration of EX or maximum workload in those receiving Prop compared to others. Thus, global and regional LV functional responses to up- right bicycle EX are normal in hypertensive pts including those with LVH or receiving Prop.

DETECTION OF EAPLY IEE'I VENTRICULAR DYSFUNCTION IN PATIENTS WITH HYPEPTENSION WITH NONINVASIVE METHODS. Dimitrios Mantzouratos, M.D.; Harisios Boudoulas, M.D., F.A.C.C.; Young H. Sohn, M.D.: Arnold M. Weissler, M.D., F.A.C.C., Wayne State university School of Medicine, Detroit, MI.

Patients (pts) with arterial hypertension (HPT) may have left ventricular hypertrcphy (LWI) but normal LV systolic performance. This study was undertaken to define the earliest manifestation of LV systolic dysfunction in pts with HPT. One hundred ninety five pts with chronic HPT were canpared to 41 angiographically prove" normals (nl). LV mass was calculated fran the M-wde echocardiogram (Echo). Pts were divided into 3 groups (Gr) with LV mass up to 2 (n=138), 2-4 (n=48) and > 4 (n=19), SD above mean nl. The ratio of the pre-ejection period to the left ven- tricular ejection time (PEP/LVET, nl < .42), the % short- ening of the echo internal diameter (%AD, nl > 30.5) and the velocity of circumferential fiber shortening (VCF, nl > 1) were used as indices of LV systolic performance. Data are show".* < 0.05 canpared to nl.

LV Mass PEP/LVET %AD VCF NL 232 + 64 1.2 + .13 GI 292 5 36*

.34 + .04 35.9 2 2.7

.39 + .07* 36.4 + 6.3 1.32+ .25 GII 417 T 3ci* .47 T .13* 31.9 ; 6.9’ 1.17 5 .20 GIII 563 T 58* .59 5 .15’ 25.1 7 6.8’ 1.05 T .30’ LV end diastolic diameter was normal T< 55 mm) in ail three Grs. Thus, in pts with HPT, PEP/LVET is the first measure to show difference fras nl and baccetes abnormal early. The %AD and Vcf remains within normal limits even with high degree of LVH. It is concluded that in LVH secondary to HPT the systolic time interval abnormalities evidence abnormality in systolic contraction prior to extent and rate of contraction. Only with advanced hyper- trophy are changes in %AD and Vcf evident.

950 March 1992 The American Journal of CARDIOLOGY Volume 49