Nonobstructive left ventricular ejection pressure gradients in man.

Simultaneous intraventricular pressure gradients and ejection flow patterns were measured by a multisensor catheter in 6 patients with normal left ventricular function and no valve abnormalities, at rest and in exercise. Peak measured intraventricular pressure gradients were attained very early in ejection, amounted to 6.7 +/- 1.9 (SD) mm Hg at rest, and were intensified to 13.0 +/- 2.3 mm Hg during submaximal supine bicycle exercise. The augmentation of the gradients during exercise was associated with a pronounced accentuation of the flow acceleration and flow at the instant of peak gradient. A peak flow, the intraventricular gradients amounted to 5.4 +/- 1.7 mm Hg at rest and 10.0 +/- 1.8 mm Hg during submaximal exercise. The exercise-induced enhancement of the measured intraventricular pressure difference at the time of peak flow was underlain by an accentuation of the peak flow itself. A semiempirical fluid dynamic model for ejection was applied to the pressure gradient and simultaneous outflow rate and acceleration data to identify the contributions by local and convective acceleration effects to the instantaneous intraventricular gradient values. The peak intraventricular pressure gradient, which is attained very early in ejection, is mostly accounted for by local acceleration effects (85 +/- 5% of the total). Conversely, at peak flow only convective acceleration effects are responsible for the measured pressure gradient. Thus, when inertial effects are augmented, as in exercise and other hyperdynamic states, the intrinsic component of the total left ventricular systolic load can be substantial, even with no outflow tract or valve abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Anomalous origin of the right coronary artery from the main pulmonary artery: incidental finding in a case of dilated cardiomyopathy.

We have described a 25-year-old man with an idiopathic dilated biventricular cardiomyopathy and end-stage glomerulonephritis due to IgA nephropathy, who was found incidentally at angiographic examination to have an anomalous right coronary artery arising from the main pulmonary artery.

The effects of intraventricular gradients on left ventricular ejection dynamics.

The generation of abnormal gradients between the apical cavity and the subaortic valvular region of the left ventricle in patients with hypertrophic cardiomyopathy (HCM) has traditionally been equated to a dynamic obstruction to left ventricular outflow. To examine this concept in more detail, left ventricular ejection dynamics were studied during cardiac catheterization in 30 patients with HCM and 29 patients with no evidence of cardiovascular disease. Using multisensor catheterization techniques, ascending aortic flow velocity and micromanometer left ventricular and aortic pressures were simultaneously recorded during rest (n = 47). Dynamic left ventricular emptying was also analyzed with frame-by-frame angiography (n = 46). The temporal distribution of left ventricular outflow was independently derived from both flow velocity and angiographic techniques. The HCM patients were subdivided into three groups: I, intraventricular gradients at rest (n = 9); II, intraventricular gradients only with provocation (n = 12); III, no intraventricular gradients despite provocation (n = 9). Expressed as a precentage of the available systolic ejection period (%SEP), the time required for ejection of the total stroke volume was (mean +/- 1 S.D.): Group I, 69 +/- 17% (flow), 64 +/- 6% (angio); Group II, 63 +/- 14% (flow), 65 +/- 6% (angio); Group III, 61 +/- 16% (flow), 62 +/- 4% (angio); control group, 90 +/- 5% (flow) 86 +/- 10% (angio). No significant difference was observed between any of the three HCM subgroups, but, compared with the control group, ejection was completed much earlier in systole independent of the presence or absence of intraventricular gradients. The presence of coexisting mitral regurgitation in 12 of the HCM patients did not alter these results. This study demonstrates that 'outflow obstruction', as traditionally defined by the presence of an abnormal intraventricular pressure gradient and systolic anterior motion of the mitral valve, does not impede left ventricular outflow in HCM. In a pure fluid dynamic sense, we believe that outflow obstruction does not exist in this disease entity.

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.

Serum myoglobin determination: laboratory and clinical evaluation.

Quality assurance examination of a commercially available radioimmunoassay kit for determination of serum myoglobin level conformed the measurement to be accurate, precise, and reproducible under all assay performance variables. Initial clinical evaluation in patients admitted to the Coronary Care Unit revealed comparable diagnostic parameters and earlier detection when compared with the present standard indicator of myocardial necrosis, creatine phosphokinase MB isoenzyme. Interpretation that an elevated myoglobin reflects acute myocardial infarction should be made only in the appropriate clinical context.