To investigate the effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy, we studied 14 patients at catheterization with a nonimaging scintillation probe before and after serial intravenous infusions of low-, medium-, and highdose verapamil (total dose 0.17 to 0.72 mg/kg). Percent change in radionuclide stroke counts after verapamil correlated well with percent change in thermodilution stroke volume (r = .87), and changes in diastolic and systolic counts were used to assess relative changes in left ventricular volumes after verapamil. Verapamil produced dose-related increases in end-diastolic counts (19 ± 9% increase; p < .001), end-systolic counts (91 ± 54% increase; p < .001), and stroke counts (7 ± 10% increase; p < .02). This was associated with a decrease in ejection fraction (83 ± 8% control, 73 ± 10% verapamil; p < .001) and, in the 10 patients with left ventricular outflow tract gradients, a reduction in gradient (62 + 27 mm Hg control, 32 ± 35 mm Hg verapamil; p < .01). The end-systolic pressure-volume relation was shifted downward and rightward in all patients, suggesting a negative inotropic effect. In 10 patients, left ventricular pressure-volume loops were constructed with simultaneous micromanometer pressure recordings and the radionuclide time-activity curve. In five patients, verapamil shifted the diastolic pressure-volume curve downward and rightward, demonstrating improved pressure-volume relations despite the negative inotropic effect, and also increased the peak rate of rapid diastolic filling. In the other five patients, the diastolic pressure-volume relation was unaltered by verapamil, and increased end-diastolic volumes occurred at higher end-diastolic pressures; in these patients, the peak rate of left ventricular diastolic filling was not changed by verapamil. The negative inotropic effects of intravenous verapamil are potentially beneficial in patients with hypertrophic cardiomyopathy by decreasing left ventricular contractile function and increasing left ventricular volume. Verapamil also enhances left ventricular diastolic filling and improves diastolic pressure-volume relations in some patients despite its negative inotropic effect.

Human and small-animal positron emission tomography (PET) scanners with cylindrical geometry and conventional detectors exhibit a progressive reduction in radial spatial resolution with increasing radial distance from the geometric axis of the scanner. This “depth-of-interaction” (DOI) effect is sufficiently deleterious that many laboratories have devised novel schemes to reduce the magnitude of this effect and thereby yield PET images of greater quantitative accuracy. Here we examine experimentally the effects of a particular DOI correction method (dual-scintillator phoswich detectors with pulse shape discrimination) implemented in a small-animal PET scanner by comparing the same phantom and same mouse images with and without DOI correction. The results suggest that even this relatively coarse, two-level estimate of radial gamma ray interaction position significantly reduces the DOI parallax error. This study also confirms two less appreciated advantages of DOI correction: a reduction in radial distortion and radial source displacement as a source is moved toward the edge of the field of view and a resolution improvement detectable in the central field of view likely owing to improved spatial sampling.

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The hemodynamic effects of sublingual nifedipine were examined in 36 patients with hypertrophic cardiomyopathy. Twenty-one patients were initially given 20 mg 14 + 7 mm Hg; p < .01) and in patients with significant basal LVOTG (15 ± 8 to 20 + 10 mm Hg; p < .01). In 10 patients, systolic and diastolic function were studied simultaneously by a nonimaging scintillation probe. No changes in systolic or diastolic function were detected when determinations obtained at the time of the peak nifedipine effect were compared with control values recorded at similar heart rates obtained by atrial pacing. The pattern of change in the pressure-counts loops after administration of nifedipine was not consistent; in only three of 10 patients was an improvement in the diastolic pressure-volume relationship observed. These results indicate that in patients with hypertrophic cardiomyopathy sublingual nifedipine induces a marked reduction in afterload without demonstrating any beneficial effects on LVOT obstruction and diastolic function. Moreover, in patients with normal pulmonary arterial wedge pressures and/or significant LVOTGs, nifedipine seems to be detrimental because it increases filling pressures, with these changes being exaggerated in patients with more marked falls in peripheral vascular resistance.