ABSTRACTS

EXERCISE-ECG IN PATIENTS WITH ACUTE mOCARDIBL INFARCTION BEFORE DISCHARGE FROM TRE CCU J,STYPEREI:,;uQ, H,IBSEN,MD, E,KJOLLER,MD, A,PE- TERSEN,MD,:SPXNH&GEN COURl'Y HOSPITAL, GLOSTRUP, DX4I&iRK

Since beginning of 1972 exercise-ecg has been used as a routine for all patients with acute myocdrdi;il infarction/&dI/ prior to discharge from the CCU.Exercise-ecg was performed on 209 p4tients,average 18 days after the onset of AML Technique:Bicycle ergometer,stepwise increase of work load by 300kpm/min. every sixth minute. ECG in 3 precordial and 3 extremity leads, and heart rate were recorded continuously,and blood pressure measured every minute.The patients were encouraged to continue work until the limit of their physical ability.The reason for stoc- ping exercise was in 121 patients fatigue,in 24 angina pectoris,in 26 dyspnoea,in 10 arrhythmias in 9 pronounced ST-elevation or depression,and in 19 various physical inabilities.The exercise loads varied from 300kpm/min.through 1 minute to gOOkpm/min.through 6 minutes.Serious compli- cations were never observed.ST-T deviations,indi- eating myocardial ischemia,were observed in 117 patients at rest?and in further 32 during exer- ciae.Heart rate increased from an aver-e of 80 to 129 beats/min.Systolic blood pressure from an average of 126 to 170 mmHg and the product: HRxSBP from 10,250 to 22,300 on the average. The exercise-ecg is an objective measurement of patients physical and response in terms of HR and BP-It provided a better basis for advising the patient regarding return to work.It also had a tremendous psychological importcutce on the overall rehabilitation program.

RIGHT VENTRICULAR FUNCTION IN PRESSURE AND VOLUME

OVERLOAD Richard Sutton MRCP; National Heart Hospital, London, England

Study of Right Ventricular (RV) behaviour in congenital heart diseose has been made using catheter-tip-micromanometers in the

right and left heart to yield pressure and its first derivative and

systolic time intervals. 12 patients (ages 12-35, bundle branch

block excluded) were divided into physiological groups: RV

pressure overload without pulmonary hypertension (PHT), 2 Fallot, 1 pulmonary valve stenosis; RV pressure overload with PHT, 2 Eisenmenger ventricular septal defect o/SD); RV volume overload

without PtiT, 2 atria1 septal defect (ASD), 1 VSD; RV volume over-

load with PHT, 2 ASD; 2 normals. RV volume overload without

PHT and normals behave identically. Left ventricular dp/di maximum (max.)occurs before RV dp/dt mox. and both these events occur after pulmonary valve opening. RV dp/dt max.

LV dp/dt max.> In RV pressure overlood with PHT RV dp/dt max.

occurs before LVdp/dt max. and before pulmonary valve opening. The RV pre-ejection period (PEP) is prolonged. RV dp/dt max>

LV dp/dt max. In RV pressure overload without PHT RV dp/dr

max. occurs with or before LV dp/dt max. but not before pulmonary valve opening. RV PEP is not prolonged. RV dp/dr max .> LV dp/dt max. In RV volume overload with PHT RV dp/dt max. occurs before LV dp/‘dt max. but not before pulmonary valve

opening . RV PEP is prolonged. RV dp/dt max.> LV dp/dt max. Thus, when RV pressure overioad is due to chronic elevation of the pulmonary resistance the RV behaves in these respects like an LV;

when RV pressure overload is due to RV outflow obstruction or

when RV pressure and volume overloads are combined the RV shows some features of LV behaviour but the two groups are separable. Changes in RV behaviour are not seen when the ventricle is only volume loaded.

INABILITY OF HYPOTHERMIA TO PREVENT ANOXIC DAMAGE TO NYOCARDIAL PROTEIN SYNTHESIS Heinrich Taegtmeyer, MD; Alan G. Ferguson, MS; and Michael Lesch, MD, FACC, Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115.

Anoxia causes irreversible damage to myocardial protein synthesis while hypothermia causes reversible inhibi- tion of the same process.

The effect of anoxia and additive hypothermia on resi- dual myocardial protein synthesis (&W'S) was evaluated using 14C-L-phenylalanine (14C-phe) incorporation into total protein of isolated rabbit right ventricular papillary muscles (RVPM) in vitro. RVPM were incubated at 37OC and at 25OC in buffer under anoxia (95% N2, 5% CO2) for two to four hours and then reox genated (95% 02, 5% ~02) at 37OC for two hours with 1x ._ L phe in the media for the final hour of incubation.

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activity was expressed as mean d/m per mg total protein and as percent incorporation of paired oxygenated con- trol RVPMs at 37'C.

14C-phe incorporation in 12 paired muscles incubated for two hours was 38% of control (3,267 VS. 8,581 d/m control) following anoxia and 49% of control (4,166 d/m) following anoxia at 25'C (PcO.05). Similar re- sults were obtained after four hours of anoxic and hypothermic intervention with 15 mM glucose present in the media.

It is concluded that depression of RMPS after two and four hours of anoxia was lessened but not prevented by hypothermic temperatures. Likewise the protective effect of high glucose concentration in the media on RMPS was not significantly enhanced by hypothermia.

PULMONARY HYPERTENSION WITH DIAZOXIDE AND MINOXIDIL Robert C. Tarazi, MD, FACC; Fabio Maqrini, MD; Harriet P. Dustan, MD, FACC; Emmanuel L. Bravo, MD; John Garvey, MD, Research Division, Cleveland Clinic Foundation, Cleveland, Ohio.

Vasodilators are patent antihypertensive agents; recently however pulmonary hypertension was found to occur with their use despite the reduction in systemic pressure (BP). Because of its importance in regard to cardiac competence and possible long-term effects on pulmonary vessels, stud- ies were done during both acute (diazoxide) and long-term (minoxidil) therapy in 18 patients with different degrees and types of hypertension. Diazoxide in 8 patients low- ered BE' and systemic resistance, increased cardiac output (CO) but raised pulmonary artery pressure by 26.4% (pd.01 with non-significant changes in pulmonary vascular resis- tance (PVRJ or wedge pressure. Minoxidil use (9 patients) reduced BP in all (-39/-32 nun Hg, ~4.01) but was assoc- iated with definite pulmonary hypertension (PAP>30/15 mm Hg) In six. In two this appeared to reflect cardiac decom- pensation. In four, however, it was related to increased CO; two of them were treated with propanolol which lower- ed both CO and PAP. One of the four developed progressive Increase over 6 months in PAP (46/20 mm Hq) and PVR (2.7 units) with maintained good BP control (165/92), and no sfgns of cardiac decompensation. Thus vasodilator drugs may have different effects on the systemic and pulmonary circulation, and the resultant pulmonary hypertension may be of critical importance during treatment in some hypertensive patients.

172 January 1975 The American Journal of CARDIOLOGY Volume 35