This investigation was undertaken to assess left ventricular-arterial coupling relations in the normal human heart under varying loading conditions and inotropic states and thereby to establish whether the working point of the normal human heart is at optimal output or mechanical efficiency under basal hemodynamic conditions. In 22 patients with an atypical chest pain syndrome who had normal coronary arteriograms, left ventricular (LV) pressures, volumes, ejection fractions, and masses at cardiac catheterization, we acquired radionuclide angiograms in duplicate simultaneously with micromanometer LV pressures. These values were derived under control conditions and during methoxamine and nitroprusside infusions with heart rate held constant by right atrial pacing. Seven other patients underwent the same protocol but, in addition, we acquired these parameters during a steady-state, intravenous infusion of dobutamine (5 micrograms/kg/min). The interaction of LV chamber elastance (Ees) and effective arterial elastance (Ea) revealed that the normal human heart was operating at an Ees/Ea ratio of 1.62, a stroke work of 76 +/- 31 gm-m, and a mechanical efficiency (stroke work to pressure-volume area ratio [SW/PVA]) of 0.65 +/- 0.10. With an increase in LV load, the Ees/Ea ratio approached 1 (p < 0.01), LV stroke work increased (p < 0.01), and mechanical efficiency declined (p < 0.01). In contrast, during vasodilation, the Ees/Ea ratio increased to slightly above 2.0 (p < 0.01), LV stroke work decreased (p < 0.001), and mechanical efficiency improved (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
An analysis of left ventricular chamber elastance provides data to support the concepts that 1) contractile function is impaired in some patients with long-term mitral regurgitation and a normal ejection fraction, 2) impaired contractile function may not be irreversible in all of these patients, and 3) an earlier consideration of mitral valve surgery may be warranted to preserve contractile function in these patients.
To evaluate the potential occurrence of right ventricular infarction, 53 patients with acute inferior transmural myocardial infarction were studied within 36 hours of symptoms by right heart catheterization, equilibrium radionuclide angiography and two-dimensional echocardiography. Technetium-99m pyrophosphate myocardial scintigraphy was performed 3 days after the onset of symptoms. The hemodynamic standard for right ventricular infarction was defined as both a right atrial pressure of 10 mm Hg or more and a right atrial/pulmonary artery wedge pressure ratio of 0.8 or more. Eight (15%) of the 53 patients had hemodynamic measurements at rest characteristic of right ventricular infarction, and 6 (11%) additional patients met these criteria after volume loading (p less than 0.05). Nineteen (37%) of the 51 patients who had radionuclide angiography had right ventricular dysfunction manifested by both a reduced right ventricular ejection fraction (less than 40%) and right ventricular regional wall motion abnormalities (akinesia or dyskinesia). An abnormal radionuclide angiogram was observed in 12 of 13 patients with hemodynamic measurements indicating right ventricular infarction. In 12 patients with an abnormal radionuclide angiographic study, right ventricular ejection fraction improved 6 to 12 weeks after infarction (27 +/- 7 to 36 +/- 9%, p less than 0.01). Twenty-two (49%) of the 45 patients with adequate two-dimensional echocardiograms had a right ventricular regional wall motion abnormality. An abnormal two-dimensional echocardiogram was seen in 9 of 11 patients with hemodynamic measurements characteristic of right ventricular infarction. Technetium-99m pyrophosphate scintigraphy was positive for right ventricular infarction in 3 of 12 patients who had hemodynamic measurements indicating right ventricular infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with penetrating artery disease or cryptogenic stroke have a significantly lower frequency of asymptomatic CAD than patients with large-artery cerebrovascular disease. Large-artery cerebrovascular disease, smoking, veteran status, and possibly left ventricular hypertrophy may be useful features for identifying patients with transient ischemic attack or stroke who are at highest risk of harboring asymptomatic CAD.
This investigation was designed to determine whether the rate of isovolumic left ventricular pressure decline is affected by load in man. Fourteen patients were instrumented with micromanometer left ventricular and right atrial pacing catheters to maintain a constant heart rate during control conditions and infusion of methoxamine or nitroprusside. The isovolumic relaxation period was defined as the time from peak (-)dP/dt to 5 mm Hg above left ventricular end-diastolic pressure of the following beat. The rate of isovolumic relaxation was calculated as time constants (Tau) from the linear regression of natural log pressure vs time (Tln) and instantaneous (-)dP/dt vs pressure (TD), which includes a variable asymptote (PB). The mean heart rates and average (+)dP/dt values normalized at 40 mm Hg development pressure (DP40) did not differ significantly, despite 33% and 43% increases in left ventricular peak and end-diastolic pressures during the infusion of methoxamine (p less than .001 and p less than .01, respectively) and 24% and 29% decreases during the infusion of nitroprusside (p less than .001 and p less than .01, respectively). The average Tln and TD values were not significantly affected by these alterations in load. In two patients, an inverse linear relationship was demonstrated between decreases in Tau and increases in contractile state produced by an infusion of dobutamine, as shown by correlation of Tln and TD with (+)dP/dt/DP40 (r = -.88 and -.83, respectively). We conclude that the time constants of left ventricular isovolumic relaxation are unaffected by modest alterations in loading conditions in man when heart rate is maintained constant.(ABSTRACT TRUNCATED AT 250 WORDS)
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