Effect of clofibrate on progression of coronary disease: A prospective, angiographic study in man

ABSTRACTS

EFFECT OF CLOFIBRATE ON PROGRESSION OF CORONARY DISEASE: A PROSPECTIVE, ANGIOGRAPHIC STUDY IN MAN Keith Cohn, MD, FACC; Manly Langston, MD, Pacific Medical Center, San Francisco, California

HEMODYNAMIC STUDIES OF SEQUENCED AND NON-SEQUENCED EXTERNAL COUNERPULSATION Lawrence s. Cohen, MD, FACC; Rene Langou, MD; Steven Wolfson, MD, FACC; Dean Porterfield, BS; Jere H. Mitchell, MD, FACC, Yale IJ. Sch. of Med., New Haven, Ct.

Lowering blood lipids has been invoked as a means of conIn this prospective trolling fiture coronary events. study, the effect of a lipid-reducing agent clofibrate (CL, 2g daily) on extent of coronary artery (CA) disease Forty pts, 31 having aortocoronary bywas investigated. pass, 7 having Vineberg operations, 11 having neither, were placed double-blind in placebo (PL, 24 pts) and CL (16 pts) groups, and restudied by selective coronary An additional 24 pts dropped angiography one year later. Each from the study, due to adverse drug reactions in 6. pt's right, left, anterior descending, and circumflex CAs (with their branches) were separately rated according to degree of obstruction. The CL group showed a significantly greater fall in triglyceride than PL group (-13.7% vs +2.3%; P=.45). 1n the CL group, :t9 of 64 CAs (29.6%) showed progressive coronary narrowing, not significantly different from the PL group (24 of 96 CAs, 25%, narrowed; ~=.26). No significant differences between drug groups emerged,when the data were corrected for degree of fall of blood lipids, initial lipoprotein type, or effect in bypassed vs nonbypassed vessels (P always ).2). Regression of CA disease was not. seen. We conclude that CL did not significantly influence the rate of progression of coronary artery disease in a one-year period.

External counterpulsation, using sequential (S) inflation of pressurized leg cuffs (first distally and then proximally), "as compared to simultaneous nonSix patients sequenced (NS), inflation of the cuffs. were studied during diagnostic cardiac catheterization, four with documented coronary artery disease, two with normal coronary vessels. Central aortic (Ao) and left ventricular pressures (mm.Hg.), and cardiac output (CO) in L/min., were measured in the control (C), non-sequenced, another control Non-sequenced and sequenced were and sequenced states. each compared to their own control measurements. HR Syst. Diast. Mean co Peak AO. Diast.Ao. Ao. Ao. 72+2 4.85.6 c 69ti 118+5 8053 9024 108+5" 5.0+.4 NS 692 11578 732 9425 72:3 4.82.4 C 6873 11676 SO894 963 5.5+_.5"" 11 1+5 -:; S 6773 11377 7354 ->,:;r+, < 0~005 ‘:'p < 07boo5 The rise in CO with non-sequenced pulsation "as not The rise in CO with sequenced significant (p< 0.4). pulsation "as significant (p ~0.005). Peak diastolic augmentation and left ventricular end-diastolic pressure "as equivalent in both modes of counterpulsation. Sequential counterpulsation leads to a greater increase in CO than does non-sequenced, presumably through more efficient augmentation of venous return.

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DETECTION

AND SIZING OF M-YOCARDIAL INFARC-

TION WITH TECHNETIUM-99m-TETRACYCLINE AND ELECTROPHYSIOLOGIC TECHNIQUES Guillermo A. Cook, MD; B. Leonard Holman, MD; Nelson Westmoreland, PhD; John V. Temte, MD, PhD; Franklin Zweiman, MD; Bernard Lawn, MD, FACC, Harvard School of Public Health, Boston, Mass.

OCCLUSION.

and

injury.

January

Electrophysiologic data were correlated with Technetium-99m-Tetracycline (33mTc-TC) concentration and histopathology. Suction electrode recordings of monophasic action potentials (MAP's) and epicardial electrocardiography (EE) were used to map the location and site of myocardial infarction (MI). MI was produced in 18 mongrel dogs by external occlusion (EO) (11 animals) or embolization (EB) (7 animals). 99mTc-TC was injected IV 24 hr (EO) and 40 hr (EB) post-occlusion and studied 24 hr (EO) and 8 hr (EB) later. In normal areas the EE showed Rs complexes with inverted T waves. The MAP's had a normal configuration with an amplitude of 52 + 6 mA. In infarcted areas EE showed QS, Qr, or 2-3 mm ST segment elevation. MAP's showed either an isoelectric line, an electrogram, or decreased amplitude (11 mA ? 5) with increased ratio of phase 0 to phase 2 amplitudes and a "hump" or prolongation of phase 3 repolarization. There was excellent correlation between MAP, EE, and 99mTc-TC concentration for sizing and locating the MI in 17/18 dogs. In 1 dog the 99mTc-TC concentrated in a small area of myocardium (1%) while electrophysiological studies were normal. In tissue samples taken from an area that appeared from 93mTc-TC and electrophysiological mapping to be infarcted, the electron microscopic examination also revealed an infarct. Microscopic examination showed small cellular areas of damage in two hearts that appeared normal by electro hysiological and isotopic studies. MAP's, EE, and ! '"Tc-TC mapping accurately size and localize areas of MI.

1974

The American

Journal

of CARDIOLOGY

Volume

33

131