Left Ventricular Dysfunction Group Research Articles

Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction.

Patients with congestive heart failure or left ventricular dysfunction (LVD) have a high incidence of ventricular tachyarrhythmias and sudden cardiac death. In addition to structural, metabolic and neuroendocrine changes, mechanoelectrical feedback may play a role in arrhythmogenesis in heart failure. Three groups of rabbits (n = 10 for each) were studied: chronic coronary ligation with ejection fraction (EF) > or = 0.45 or < 0.45, and sham-operated controls. Ventricular fibrillation (VF) thresholds were measured at LV pressures of 0 and 40 mm Hg during modified Langendorff perfusion. Intervals between local activations during VF (VFI) were used as an index of refractoriness. Global dispersion was expressed as coefficient of variation of VFI; local dispersion by maximum difference in VFI between adjacent sites. Median VF threshold was lower at 0 mm Hg in the lower EF group compared to controls (30 vs. 67.5 mA, P<0.05). VF threshold in control hearts was lower at 40 mm Hg than at 0 mm Hg (P<0.01), but there was no further reduction in threshold in LVD hearts at 40 mm Hg. Global dispersion of VFI did not differ significantly between groups. Local dispersion of VFI in the lower EF group was greater than in controls at 0 mm Hg in the infarct border zone (P<0.05). At 40 mm Hg, local dispersion of VFI in zones bordering and remote from the infarct were greater in both LVD groups than in controls (P<0.05). Local inhomogeneity of refractoriness is more marked in the infarct border zone, but latent abnormalities are evident in normal myocardium of rabbits with left ventricular dysfunction and are revealed by left ventricular distension.

Measurements and day-to-day variabilities of left ventricular volumes and ejection fraction by three-dimensional echocardiography and comparison with magnetic resonance imaging

The aim of this study was to assess day-to-day variability of left ventricular (LV) volume and ejection fraction (EF) calculated from 3-dimensional echocardiography (3-DE) and to compare the reproducibility of the measurement with magnetic resonance imaging. Forty-six subjects were examined including 15 normal volunteers (group A) and 31 patients with LV dysfunction (group B). Precordial 3-DE acquisition was performed at 2° rotational intervals and repeated 1 week later. Magnetic resonance imaging was performed at 0.5 T. End-diastolic and end-systolic LV volumes were derived using Simpson’s rule by manual endocardial tracing of 8 equidistant parallel LV short-axis slices with 3-DE, whereas 9-mm slices were used with magnetic resonance imaging. The mean ± SD of end-diastolic and end-systolic LV volumes (ml) and EF (%) from magnetic resonance imaging were 182 ± 75, 121 ± 76, and 39 ± 18, whereas those from 3-DE were 182 ± 76, 121 ± 77, and 39 ± 18 respectively. Day-to-day measurements of end-diastolic and end-systolic LV volumes, and EF on 3-DE were not significantly different as assessed with SEE (2.7, 1.1, and 2.4, respectively). Intra- and interobserver SEE for calculating end-diastolic and end-systolic LV volumes and EF for magnetic resonance imaging were 6.3, 4.7, and 2.1 and 13.6, 11.5, and 4.7, respectively, whereas those for 3-DE were 3.1, 4.4, and 2.2 and 6.2, 3.8, and 3.6, respectively. Day-to-day variability of LV volume and EF calculation on 3-DE were small and not significantly different for normal and dysfunctional left ventricles. Observer variabilities of 3-DE were fewer than those of magnetic resonance imaging. Therefore, 3-DE is recommended for serial assessment of LV volume and EF in normal and abnormally shaped ventricles.

Effects of epanolol, a selective beta1-blocker with intrinsic sympathomimetic activity, in patients with ischemic left ventricular dysfunction.

Recently, different beta-blockers have been shown to be effective in the treatment of chronic heart failure (CHF), but the importance of their ancillary properties is not clear. Epanolol is a selective beta1-blocker with intrinsic sympathomimetic activity, which has been shown useful in angina pectoris, but its value in patients with left ventricular (LV) dysfunction and CHF is unknown. We examined the effects of epanolol in patients with LV dysfunction (n = 8; mean LV ejection fraction, 0.33 +/- 0.08) and compared them with patients with normal LV function (n = 8; mean LV ejection fraction, 0.52 +/- 0.04). Measurement of invasive hemodynamics and neurohormones was performed at rest and during myocardial ischemia, which was induced by atrial pacing. All measurements were performed before and after epanolol. Before epanolol, pacing-induced ischemia led to a similar increase in norepinephrine and coronary sinus blood flow in both groups. After epanolol, the increase in neurohormones was more pronounced in the group with LV dysfunction (norepinephrine, 1,130 +/- 164 pg/ml for patients with LV dysfunction vs. 637 +/- 41 pg/ml for normal subjects; p < 0.05). A similar effect was observed for angiotensin II. Further, in the LV-dysfunction group, coronary sinus blood flow increased less, and coronary vascular resistance decreased less (both values, p < 0.05). Despite the fact that the increase in double product was decreased to a similar extent in both groups, ischemia was reduced only in normal LV function (p < 0.05). In ischemic LV dysfunction, neurohumoral activation after epanolol may impair adequate coronary flow response, and this may limit its antiischemic properties. Because of the small size of the study, no definitive inference on the clinical benefit of epanolol in patients with ischemic LV function can be made from this study.

Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: increased oxygen cost of contractility.

Although the use of inotropic agents to treat congestive heart failure (CHF) in patients with coronary artery disease has yielded short-term hemodynamic improvement, long-term mortality has shown less improvement. The loss of cardiac muscle as a result of infarction not only decreases the pumping ability of the heart but also leads to some dramatic changes in myocardial energetics. However, little is known about the mechanoenergetics of the heart in patients with left ventricular (LV) dysfunction after myocardial infarction. The present study was designed to compare by means of the Vo2-pressure-volume area relation (PVA, a measure of total mechanical energy) and Emax (LV contractility index), the incremental oxygen cost of contractility measured as nonmechanical energy per unit increment in contractility in patients with various kinds of LV dysfunction. We assessed Emax, Vo2, and PVA using conductance and Webster catheters under control conditions and during different rates of dobutamine infusion (3 and 6 micrograms x kg-1 x min-1) in 30 patients with coronary artery disease. Patients were divided into three groups according to LV ejection fraction (EF): 10 without LV dysfunction (EF>/= 60%), 10 with mild LV dysfunction (40% </= EF < 60%), and 10 with severe LV dysfunction (EF < 40%). Under control conditions, the Vo2-PVA relation was linear in each group. Contractile efficiency, the reciprocal of the slope of this relation, was comparable among the three groups. The oxygen cost of contractility in the severe LV dysfunction group was significantly greater than in the groups without and with mild LV dysfunction (0.022 +/- 0.014 versus 0.005 +/- 0.002 and 0.0012 +/- 0.005 mL O2 x mL x mm Hg-1 per beat, P <.05). These findings suggest that the alteration in mechanoenergetics in patients with severe LV dysfunction after myocardial infarction may result from the increased oxygen cost of excitation-contraction coupling rather than from a reduction in the efficiency of chemomechanical energy transduction.

Serial changes in left ventricular function after coronary artery bypass: Implications in viability assessment

Improvement in left ventricular (LV) performance after coronary artery bypass surgery remains the gold standard in myocardial viability assessment. The time-related changes, however, are not well known. This study examined the LV ejection fraction (EF) by gated blood pool imaging early (6 ± 4 days) and late (62 ± 24 days) after surgery in patients with normal preoperative EF (group 1, n = 12) and those with LV dysfunction (group 2, n = 15). There were no changes in the clinical status between the early and late studies, and all patients had normal sinus rhythm. Group 1 had no significant change in EF (preoperatively 62%, early postoperatively 64%, late postoperatively 63%; p = NS). In group 2, EF was 26% ± 8% preoperatively; 30% ± 10% early postoperatively; and 34% ± 8% late postoperatively ( p < 0.05). Postoperatively there was ≥5% improvement in EF in 4 patients early and 11 patients late ( p < 0.05). Patients who showed early improvement continued to do so in the late study but, additionally, 7 patients showed improvement only in the late study. Thus the timing of EF measurement after surgery is important in patients with LV dysfunction but not in patients with normal LV function. Early assessment may underestimate the prevalence and degree of recovery.

Usefulness of dipyridamole-thallium-201 perfusion scanning for distinguishing ischemic from nonischemic cardiomyopathy

To determine noninvasively the etiology of left ventricular (LV) dysfunction, 22 patients with a diagnosis of cardiomyopathy determined via cardiac catheterization and 5 normal control subjects underwent radionuclide ventriculography and intravenous dipyridamole-thallium-201 perfusion scanning. Both ischemically and nonischemically induced LV dysfunction had comparable global LV ejection fractions (24 ± 6 vs 23 ± 8%, respectively) and extent of segmental wall motion abnormalities. Right ventricular ejection fraction was significantly better in the group with an ischemic etiology of LV dysfunction (41 ± 26 vs 13 ± 10%, p < 0.005) but significant group overlap was present. However, computer-assisted analysis of dipyridamole-thallium-201 myocardial perfusion scanning demonstrated more homogeneous myocardial perfusion in idiopathic cardiomyopathy (mean perfusion defect 25 ± 11 vs 6 ± 6%, p < 0.001) and successfully predicted the correct etiology of LV dysfunction in 20 of 22 (91%) patients.