As an initial management strategy in patients with stable coronary artery disease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy. (ClinicalTrials.gov number, NCT00007657 [ClinicalTrials.gov].).

Most patients with non-Q-wave myocardial infarction do not benefit from routine, early invasive management consisting of coronary angiography and revascularization. A conservative, ischemia-guided initial approach is both safe and effective.

Serial changes in left ventricular (LV) size and function during the adaptation to chronic pressure overload and the transition to pump failure were studied in 16 conscious dogs (aortic bands placed at 8 weeks of age). Echocardiographic data at baseline and at 3, 6, 9, and 12 months after banding revealed a progressive increase in LV mass in all dogs. In six dogs with LV pump failure, there was a progressive decline in circumferential fiber shortening (29+±4% at 12 months); this was significantly less than that seen in five littermate controls (38+±3%, p<0.05). The average LV to body weight ratio in this group was 9.8±2.7 g/kg. In 10 dogs without pump failure (compensated LVH group), shortening exceeded that seen in the controls (43 ±4%, p<0.05); the LV to body weight ratio was 7.7±1.0 g/kg. At 12 months (cardiac catheterization), the LV end-diastolic pressure was higher in the failure (25±+15 mm Hg) than in the compensated group (8±5 mm Hg, p <0.05); mean systolic stress was also higher in the failure group (313 ±67 g/cm2) than in the compensated group (202 ±53 g/cm2, p <0.05). The transmural distribution of myocardial blood flow was measured (at 12 months) with the radioactive microsphere technique; flow data were then related to an index of demand (a stress-time index). There was preferential blood flow to the subendocardial layers in the control (endo/epi= 1.28) and compensated hearts (endo/epi= 1.10), but in the failure group there was a relative decrease in subendocardial flow (endo/epi=0.92). However, the absolute values for subendocardial flow in the normal, compensated, and failure groups were 77±54, 125 ±48, and 113±64 ml/min/100 g; the stress-time indexes in the subendocardial shell were 38+11, 74±19, and 93 +34 g sec 102/cm2/min. Despite what appears to be a marginal balance between blood flow and the stress time index in the failure group, the myocardial high energy phosphates were not depleted and the inoptropic state was not depressed. In this model of LV hypertrophy, the observed differences in fiber shortening can be explained on the basis of the inverse afterloadshortening relation; pump failure was due to an inadequate LV hypertrophy with afterload excess. Pump failure due to afterload excess was associated with adequate subendocardial blood flow at rest; during exercise or other hemodynamic stress, however, these hearts are likely to be especially vulnerable to ischemia and its consequences. (Circulation 1989;79:872-883

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic hearts and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +-0.7 vs 3.1 0.8 sec (p < .02) at the endocardium, 2.3 -+ 0.4 vs 1.6 + 0.4 sec '(p < .02) at the midwall (conventional method), and 2.1 ± 0.3 vs 1.4 + 0.3 sec -' (p < .01 ) at the midwall (modified method). Chamber filling and fiber lengthening rates are depressed in patients with concentric LVH. Conventional measurements overestimate "true" fiber velocities more in those with LVH than in normal subjects; thus, the modified midwall method offers a theoretical advantage, especially in studies in which data from normal and hypertrophic hearts are compared. Circulation 71, No. 2, 266-272, 1985. INCREASED chamber stiffness in patients with left ventricular pressure overload hypertrophy has been largely attributed to increased myocardial mass; however, it is generally accepted that increased intrinsic myocardial stiffness and/or abnormal myocardial re-

The hemodynamic determinants of the time constant of left ventricular (LV) isovolumic pressure (P) decline were studied in 32 anesthetized dogs. The time constant, tau (an index of LV relaxation), was determined from the best exponential fit of the equation P = Poe-t/r, to LVP measured at 5-ms intervals during isovolumic relaxation; Po = LVP at maximum negative dP/dt and t = time. At a constant heart rate of 120 beats/min, tau was determined during steady-state increases in preload (volume expansion), increases in afterload (methoxamine infusion), reductions in afterload (nitroprusside infusion), and in variably afterloaded beats at a constant preload (single-beat interventions). tau was directly related to LV systolic pressure and length during the alterations in LV loading conditions, but tau was not closely related to the extent of fiber shortening. During isoproterenol infusion, relaxation was more rapid (tau), and following the administration of propranolol, relaxation was prolonged (tau). While data from the variably afterloaded contractions indicate the presence of systolic load-dependent LV relaxation velocity, the steady-state studies do not exclude the possibility that altered contractility through reflex or other mechanisms contributes to the observed changes in tau.