Changes induced in left ventricular (LV) hemodynamics by isometric exercise were analyzed in 43 patients: 30 with coronary heart disease (CAD), four with noncoronary heart disease, nine normal. Volumes were angiographically determined and correlated with left ventricular end-diastolic pressure (LVEDP) both at rest and during the fifth minute of 30% sustained handgrip (HNG). All normals and eight with CAD improved LV function during HNG. LVEDP decreased or remained constant, end-diastolic volume (EDV) decreased, end-systolic volume (ESV) decreased, as ejection fraction (EF) remained constant. None of these eight CAD cases altered their regional LV contraction pattern during HNG. Twenty-five patients, 21 CAD and four nonCAD, showed diminished LV function during HNG. LVEDP increased, EDV decreased, ESV increased, as EF declined. In these 21 CAD patients, at least one major coronary vessel was narrowed 70% or more and, with but two exceptions, was not supported by adequate collaterals. In 18, new asynergic zones developed in previously normally contracting areas or pre-existing asynergic zones extended during HNG.

A B S T R A C T High speed oscilloscopic recordings (4000 mm/sec) of left ventricular pressure (micromanometer) and its first derivative were used to calculate contractile element velocity (Vce) during the isovolumic period of auxotonic beats in anesthetized dogs. At 0.5-2.0 msec intervals of isovolumic systole, Vce was derived as (dP/dt)/kP, where k = 24 cm-'. Plots of Vce and P yielded inverse curves from peak Vce to aortic valve opening pressure which averaged 27 msec in controls, and 11 msec during norepinephrine administration. Extrapolated Vmax, in muscle lengths/second, averaged 3.6 (controls), 3.6 (volume load), and 6.6 (norepinephrine). In each experimental state, Vmax was also determined from force-velocity relations of isovolumic beats (abrupt aortic occlusion) analyzed at 10 msec intervals from conventional pressure recordings.Vmax by both methods correlated well (r = 0.88). While good correlations were also noted between Vmax and maximum dP/dt, (max dP/dt)/integrated isovolumic pressure, (max dP/dt)/peak isovolumic pressure, and (max dP/dt)/kP, only the last two of these successfully distinguished changes between volume load and inotropic stimulation. Thus, assuming an unchanged series elasticity, the contractile state of the auxotonic ventricle may be determined utilizing a single high-fidelity catheter system and high speed recordings of isovolumic pressure. INTRODUCTIONThe contractile state of the myocardium can be characterized by the instantaneous relationship between developed force and contractile element velocity, provided that information regarding muscle length and time are

Spectacular transient increases in serum alkaline phosphatase were observed in five infants in the absence of demonstrable pathology.

A B S T R A C T The mechanical behavior of isolated cat, rat, and dog ventricular muscle was examined during hypoxia and after reoxygenation. During hypoxia, an early abbreviation of tension duration was followed by a decline in the rate of tension development. After reoxygenation, a marked, early prolongation of tension development and relaxation time was invariably observed with little, if any, increase in peak tension. As recovery progressed, the duration of contraction gradually shortened as tension returned to control levels. This phenomenon was also observed in the intact dog heart after release of a coronary artery ligature. Isometric tension gauges sewn to ischemic portions of the left ventricle demonstrated that after reinstitution of coronary flow, segment tension duration "outlasts" the duration of left ventricular pressure development and is associated with ventricular irritability. Epicardial electrograms showed shortening of the QT interval within the ischemic segment with prolongation of the QT interval after release of the coronary ligature. Prolongation of tension development during recovery from hypoxia was not observed in experiments with rat skeletal muscle. These observations identify localized mechanical abnormalities during recovery from myocardial ischemia which may be important in the syndrome of acute coronary heart disease. INTRODUCTIONThe effects of hypoxia on the performance of heart muscle have been studied extensively both in vitro and in the intact organism. Little attention, however, has been given to the mechanical behavior of heart muscle during recovery from hypoxia. The present study describes an unusual alteration in the time course of tension developThis work was presented in part at the Eastern Section Meeting, American Federation for Clinical Research, Boston, Mass., December, 1968.

Simultaneous, high-fidelity pressure recordings were obtained from the left and right ventricles of anesthetized dogs. Abrupt elevation of left ventricular pressure produced an immediate rise in right ventricular systolic pressure, while mechanical asynchrony of the two ventricles, induced by endocardial pacing of either ventricle, identified discrete pressure transients in the right ventricular pressure pulse which occurred coincident with peak left ventricular dP/dt. During normal conduction, peak right ventricular dP/dt regularly occurred after pulmonic valve opening and simultaneously with peak left ventricular dP/dt. Thus, the rising portion of the right ventricular pressure pulse is an impure signal, influenced directly by the amplitude and timing of left ventricular isovolumic pressure. These observations suggest that right ventricular pumping function is aided by an in series left ventricle.