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PubMed2002

[Clinical evaluation of the cause of left ventricular dysfunction in type 2 diabetes without significant cardiac disease].

OBJECTIVES: The relationship between left ventricular dysfunction and hypertension or proteinuria was evaluated in type 2 diabetic patients without significant cardiac disease to investigate the cause of diabetic cardiac dysfunction. METHODS: Twenty-one patients with type 2 diabetes mellitus (mean age 63.8 +/- 7.4 years) underwent left ventriculography and Doppler echocardiography to calculate the ejection fraction and E/A ratio (E/A). RESULTS: Thirteen patients had hypertension (61.9%) and six patients had proteinuria (28.6%). The E/A was 0.82 +/- 0.21 in all patients. The E/A in patients with hypertension or proteinuria was significantly less than in those without these diseases (0.74 +/- 0.18 vs 0.97 +/- 0.18, p = 0.011; 0.65 +/- 0.10 vs 0.89 +/- 0.20, p = 0.010, respectively). The ejection fraction was 73.3 +/- 7.2% in all patients. The ejection fraction in patients with proteinuria was significantly less than in those without proteinuria (67.6 +/- 10.0% vs 75.5 +/- 4.4%, p = 0.019), but there was no significant difference in ejection fraction between patients with and without hypertension. The duration of diabetes was significantly related to the ejection fraction (r = -0.436, p = 0.048) but not to the E/A. CONCLUSIONS: In patients with type 2 diabetes without significant cardiac disease, left ventricular diastolic function may be related to both hypertension and proteinuria and left ventricular systolic function may be related to proteinuria and duration of diabetes. Therefore, in addition to hypertension, complications of nephropathy or long duration of diabetes may be related to the cause of the diabetic cardiac dysfunction.

Diabetes Mellitus, Type 2↗
PubMed1992

Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.

Coronary artery narrowing, ranging from 19% to 61%, was induced in rats and ventricular performance, myocardial damage, and myocyte hypertrophy were examined 1 mo later. Animals were separated into two groups, exhibiting ventricular dysfunction and failure, respectively. Dysfunction consisted of a 2.4-fold increase in left ventricular end diastolic pressure (LVEDP), 15% decrease in left ventricular peak systolic pressure (LVPSP), 24% reduction in developed pressure (DP), and a 16% depression in-dP/dt. Failure was defined on the basis of a 4.7-fold elevation in LVEDP, and a 26%, 47%, 45%, and 41% decrease in LVPSP, DP, +dP/dt, and -dP/dt. Moreover, in this group, right ventricular end diastolic and systolic pressures increased 5.5- and 1.2-fold. Left and right ventricular weights expanded 23% and 51% with dysfunction and 30% and 56% with failure. Left ventricular hypertrophy was characterized by ventricular dilation and wall thinning which were more severe in the failing animals. Foci of damage were found in both groups but tissue injury was more prominent in the endomyocardium and in failing rats. Finally, myocyte loss in the ventricle was 10% and 20% with dysfunction and failure whereas the corresponding enlargements of the unaffected myocytes were 34% and 53%. Thus, coronary narrowing led to abnormalities in cardiac dynamics with an increase in diastolic wall stress and extensive ventricular remodeling in spite of a moderate loss of myocytes and compensatory reactive hypertrophy of the viable cells.

Animals↗
PubMed1999

Attenuation correction improves the detection of viable myocardium by thallium-201 cardiac tomography in patients with previous myocardial infarction and left ventricular dysfunction.

The aim of this study was to determine the influence of attenuation-corrected thallium-201 stress/redistribution/reinjection single-photon emission tomography (SPET) on the number of viable segments in patients with previous myocardial infarction and dysfunctional myocardium. Fifty-one patients with previous myocardial infarction and left ventricular dysfunction were included in the study. In all patients, 201Tl non-corrected (NC) and attenuation-corrected (AC) SPET was performed using a stress/redistribution/reinjection protocol followed by coronary angiography. A semiquantitative analysis was performed using polar maps for NC and AC stress, redistribution and reinjection short-axis and vertical long-axis (apex) slices. Severe (perfusion defect below 50%/maximal count rate: PD < 50), mild and moderate persistent defects for redistribution and reinjection were evaluated for both NC and AC studies. A total of 1581 segments were evaluated by semiquantitative segmental analysis for both NC and AC studies for each redistribution and reinjection map. In the redistribution maps, NC revealed a total of 352 segments and AC a total of 222 segments with impaired perfusion below 50% of the maximal count rate (PD < 50). The mean number of affected segments was 6.9 +/- 5.5 in the case of NC and 4.4 +/- 4.8 in the case of AC (P < 0.001). In the reinjection maps, NC revealed a total of 263 non-viable segments (PD < 50) and AC a total of 169 non-viable segments. The mean number of affected segments was 5.2 +/- 5.3 in the case of NC and 3.3 +/- 4.2 in the case of AC (P < 0.001). Recovery of function was better predicted by AC than by NC in 20% of patients in the follow-up group. Therefore, the use of attenuation correction influences the extent of viable segments by showing more viable segments in either redistribution or reinjection maps. 201Tl imaging without attenuation correction may underestimate the extent of tissue viability, which may contribute to the lower sensitivity compared to fluorine-18-fluorodeoxyglucose positron emission tomography, where attenuation correction is a routinely performed procedure.

Exercise Test↗
PubMed2000

A nonsurgical porcine model of left ventricular dysfunction. Validation of myocardial viability using dobutamine stress echocardiography and positron emission tomography.

BACKGROUND: Although several short-term animal models of stunning and hibernation have been studied extensively, it has been difficult to produce a consistent animal model of chronic hibernation. The aim of the present study was to develop a nonsurgical porcine stent model of coronary stenosis in order to investigate the relationship between chronic dysfunctional myocardium and viability using 2D-echo, dobutamine stress echo (DSE) and positron emission tomography (PET). METHODS AND RESULTS: Focal progressive coronary stenosis was induced by implantation of an oversized stent in the left anterior descending (LAD) and/or circumflex (LCX) coronary artery in a total of 115 pigs, according to various experimental protocols: copper stent in the LAD (group I, n = 5); noncoated stainless steel stent in the LAD combined with balloon overstretch (group II, n = 7); poly(organo)phosphazene-coated stent in the LAD (group III, n = 77); and poly(organo)phosphazene-coated stent in both the LAD and the LCX (group IV, n = 26). Occurrence of left ventricular dysfunction was evaluated weekly by 2D-echo. At the time of left ventricular dysfunction the presence of viable myocardium within the dysfunctional region was investigated with DSE and PET, and confirmed by histology. The degree of coronary artery stenosis was measured by quantitative coronary angiography and morphometry. Severe coronary artery stenosis in the presence of dysfunctional, but viable, myocardium was induced in groups III and IV (47% and 11% of the animals, respectively). CONCLUSIONS: The authors developed a nonsurgical porcine stent model of progressive coronary stenosis using an oversized polymer-coated stent resulting in chronically decreased myocardial function, with residual inotropic reserve and viable myocardium. This condition may arise from repetitive periods of ischemia, or from sustained hypoperfusion, or a combination of these processes eventually leading to myocardial hibernation.

Journal Article↗
PubMed1998

[Ebstein's anomaly associated with left ventricular dysfunction: a case report].

A 66-year-old man presented with Ebstein's anomaly associated with left ventricular dysfunction. He had been followed since 40 years of age for cardiomegaly and arrhythmia, and experienced episodes of orthopnea at the age of 64. He was referred to our hospital in April 1997 because of lower extremity edema. Physical examination revealed dilated external jugular vein, tenderness of the right hypocondorium, and lower extremity edema. Electrocardiography confirmed atrial fibrillation. Transthoracic echocardiography revealed bilateral atrial and ventricular dilation, and paradoxical septal movement. The apical four-chamber view demonstrated 15 mm apical displacement of the septal leaflet. Color Doppler echocardiography revealed moderate tricuspid regurgitation. Transesophageal echocardiography revealed low echoic and hypoplastic tricuspid valve. Left ventriculography showed diffuse hypokinesis, and the ejection fraction was 49%. The coronary artery was normal. Atrial septal defect was not detected. Diffuse fibrosis, which may be found in the hearts of patients with Ebstein's anomaly at autopsy may have been responsible for the left ventricular depressed systolic function in this patient.

Aged↗
PubMed1996

Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol.

BACKGROUND: Left ventricular dysfunction after myocardial infarction is associated with an increased risk of death. Other studies have suggested that a potassium-channel blocker might reduce this risk with minimal adverse effects. We investigated whether d-sotalol, a pure potassium-channel blocker with no clinically significant beta-blocking activity, could reduce all-cause mortality in these high-risk patients. METHODS: Patients with a left ventricular ejection fraction of 40% or less and either a recent (6-42 days) myocardial infarction or symptomatic heart failure with a remote (> 42 days) myocardial infarction were randomly assigned d-sotalol (100 mg increased to 200 mg twice daily, if tolerated) or matching placebo twice daily. FINDINGS: After 3121 of the planned 6400 patients had been recruited, the trial was stopped. Among 1549 patients assigned d-sotalol, there were 78 deaths (5.0%) compared with 48 deaths (3.1%) among the 1572 patients assigned placebo (relative risk 1.65 [95% CI 1.15-2.36], p = 0.006). Presumed arrhythmic deaths (relative risk 1.77 [1.15-2.74], p = 0.008) accounted for the increased mortality. The effect was greater in patients with a left ventricular ejection fraction of 31-40% than in those with lower ( <or= 30%) ejection fractions (relative risk 4.0 vs 1.2, p = 0.007). INTERPRETATION: Among the 1549 patients evaluated, administration of d-sotalol was associated with increased mortality, which was presumed primarily to be due to arrhythmias. The prophylactic use of a specific potassium-channel blocker does not reduce mortality, and may be associated with increased mortality in high-risk patients after myocardial infarction.

Administration, Oral↗
PubMed2002

Immunoglobulin G3 cardiac myosin autoantibodies correlate with left ventricular dysfunction in patients with dilated cardiomyopathy: immunoglobulin G3 and clinical correlates.

BACKGROUND: Effector functions of an aberrant immune response have been implicated in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). The immunologic determinants of myocardial dysfunction, however, remain poorly understood. This study sought to determine the relation of different immunologic responses to hemodynamic dysfunction in DCM. METHODS: Immunoglobulin (Ig) G class/subclass response ELISA (enzyme-linked immunosorbent assay) against cardiac myosin heavy chain, histologic characteristics (DALLAS criteria), immunohistochemistry, plasma interleukin-4 and plasma interferon gamma (IFN-gamma) were determined in patients (n = 76) with clinically suspected myocarditis or DCM. Patients were prospectively evaluated, both clinically and hemodynamically, on admission (baseline) and at 6-month follow-up. RESULTS: Indices of hemodynamic dysfunction (by cardiac catheterization and transthoracic echocardiography) correlated significantly with an Ig subclass response. IgG3 levels correlated with left ventricular ejection fraction (P =.02), pulmonary capillary wedge pressure (P <.0001), left ventricular end-systolic volume index (P =.002), left ventricular end-diastolic volume index (P =.033), left ventricular end-diastolic pressure (P =.04), right ventricular end-diastolic pressure (P =.039), and left ventricular end-systolic dimension and left ventricular end-diastolic dimension (P <.05). Patients positive for IgG3 (predominantly male, P =.01) had depressed left ventricular ejection fraction (< or =45%, relative risk 3.0, 95% CI 1.5-5.7, P =.005) at baseline and 6 months. Mitral-septal separation at follow-up improved in patients negative for IgG3 (P =.018), and the number of patients on conventional therapy in this group declined at 6-month follow-up (P <.05). Lymphocyte counts/high-power field; CD2, CD3, CD4, and CD8 (independent of IgG class/subclass response and left ventricular dysfunction) were significantly higher in patients positive for IFN-gamma (25%). A positive IFN-gamma response was higher in patients positive for IgG3. These patients, positive for IgG3 and IFN-gamma (10%), had significantly shorter duration of clinical symptoms: 0.17 years (0.12-2.36 y) versus 1.01 years (0.49-5.35 y, P =.04). CONCLUSION: IgG3 reactivity correlated with depressed myocardial dysfunction. This may render this subclass Ig a surrogate target for therapeutic intervention in DCM. With IFN-gamma, IgG3 may reflect a more aggressive disease.

Adult↗
PubMed2000

Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction.

BACKGROUND: The role of echocardiographic right ventricular (RV) dysfunction in predicting clinical outcome in clinically stable patients with pulmonary embolism (PE) is undefined. In this study, we assessed the prevalence and clinical outcome of normotensive patients with RV dysfunction among a broad spectrum of PE patients. METHODS AND RESULTS: This prospective clinical outcome study included cohort of 209 consecutive patients (age, 65+/-15 years) with documented PE. Acute RV dysfunction was diagnosed in the presence of >/=1 of the following: RV dilatation (without hypertrophy), paradox septal systolic motion, and Doppler evidence of pulmonary hypertension. Four groups were identified: 28 patients presenting with shock or cardiac arrest (13%), 19 hypotensive patients without shock (9%), 65 normotensive patients with echocardiographic RV dysfunction (31%), and 97 normotensive patients without RV dysfunction (47%). Among normotensive patients with RV dysfunction, 6 (10%) developed PE-related shock after admission: 3 of these patients died, and 3 were successfully treated with thrombolytic agents. In comparison, none of the 97 normotensive patients without RV dysfunction developed shock or died as a result of PE. CONCLUSIONS: A significant proportion (31%) of normotensive patients with acute PE presents with RV dysfunction; these patients with latent hemodynamic impairment have a 10% rate of PE-related shock and 5% in-hospital mortality and may require aggressive therapeutic strategies. Conversely, normotensive patients without echocardiographic RV dysfunction have a benign short-term prognosis. Thus, early detection of echocardiographic RV dysfunction is of major importance in the risk stratification of normotensive patients with acute PE.

Acute Disease↗
PubMed1997

An ovine model of acute myocardial infarction and chronic left ventricular dysfunction.

In order to develop and validate an ovine model of myocardial infarction with subsequent impairement of left ventricular function, 15 instrumented sheep underwent selective microembolization of the left coronary arteries with 0.5 mL 90 microns polystyrene beads. Hemodynamics and plasma hormones were measured preembolization (baseline) and then at hours 2, 4, 6, and 12 and days 1, 2, 3, 5 and 7 postembolization. Of the 15 sheep studied, 2 (13%) died on the day of embolization from arrhythmias. In the remaining sheep, left ventricular systolic pressure and stroke work (both P < 0.001) were reduced promptly and remained below basal levels. Mean arterial pressure (P < 0.001) increased initially, then decreased to below basal levels by hour 6. Heart rate (P < 0.001) and left atrial pressure (P < 0.05) were increased while cardiac output was decreased (P < 0.05). Left ventricular ejection fraction at day 7 was reduced (38.8 +/- 3.5 vs 46.0 +/- 3.9% preembolization; P < 0.05). The cardiac enzymes creatine kinase (P < 0.001) and troponin-T (P < 0.001) were increased following microembolization and returned to basal levels by days 2 and 5 respectively. Plasma atrial and brain natriuretic peptides (both P < 0.001) and plasma renin activity (P < 0.005) were all increased following embolization. This ovine model mimics the hemodynamic and neurohumoral features of acute myocardial infarction, resulting in left ventricular dysfunction, and should prove suitable for the study of interventions in a number of these conditions.

Animals↗
PubMed1996

Mechanisms of right ventricular dysfunction after pulmonary resection.

BACKGROUND: Significant right ventricular (RV) dysfunction as measured by increased end-diastolic volume and reduced ejection fraction has been documented in the postoperative period after pulmonary resection. We hypothesized that changes in RV contractile state or afterload may contribute to this RV pump dysfunction. METHODS: In part one of the study, RV preload was altered on postoperative day 2 (n = 6) by rapid infusion of Hespan to a total of 250, 500, and 1,000 mL. The relationship between RV stroke work and end-diastolic volume was plotted using linear regression. This preload recruitable stroke work relation had been previously validated as a load-insensitive index of RV contractility. The slopes of the preoperative relation (n = 35) and postoperative relation were compared. In part two of the study, RV afterload was reduced by continuous infusion of prostaglandin E1 (n = 6) through postoperative day 2 and RV pump function was assessed. RESULTS: Comparison of the slopes of the preload recruitable stroke work relation plotted preoperatively and on postoperative day 2 revealed no significant difference, indicating no change in RV contractile state. Infusion of prostaglandin E1 in the postoperative period (n = 6) significantly reduced pulmonary vascular resistance (3.67 +/- 0.19 versus baseline 5.72 +/- 0.19 dyne . s . cm-5/ m2; p < 0.05). However, RV ejection fraction remained significantly reduced (0.34 +/- 0.01 versus baseline 0.42 +/- 0.01; p < 0.05) and end-diastolic volume significantly increased (105 +/- 5 versus baseline 93 +/- 2 mL/m2; p < 0.05). Heart rate was increased compared with baseline throughout the postoperative period. CONCLUSIONS: The present study suggests that RV dysfunction after pulmonary resection is not caused by primary alterations in contractility or immediate changes in afterload. Better control of heart rate with minimal effect on inotropy may enhance RV pump function.

Alprostadil↗
PubMed2001

Biphasic and monophasic transthoracic defibrillation in pigs with acute left ventricular dysfunction.

OBJECTIVE: Our purpose was to compare biphasic versus monophasic shock success for VF termination in a porcine model of acute left ventricular (LV) dysfunction. BACKGROUND: For the termination of ventricular fibrillation (VF), transthoracic biphasic waveform shocks achieve higher success rates than monophasic shocks. However, the effectiveness of biphasic versus monophasic defibrillation in a setting of left ventricular dysfunction has not been reported. METHODS: In 23 open-chest adult swine (15-25 kg), LV dysfunction [> or =25% decline in cardiac output (CO)] was induced by continuous inhalation of halothane (1-1.75%). Each pig randomly received transthoracic biphasic and monophasic shocks at three energy levels (30, 50 and 100 J) in two conditions: baseline and LV dysfunction. Halothane effect on left ventricular size and contraction was measured by echocardiography in three additional swine. RESULTS: With halothane, pigs demonstrated a decline in CO (baseline 4.16+/-0.19, halothane 2.72+/-0.19 l/min, P<0.01), mean arterial pressure (baseline 107.2+/-3.5, halothane 80.1+/-3.4 mmHg, P<0.01) and increased left ventricular end-diastolic pressure (baseline 6.4+/-0.9, halothane 12.7+/-0.8 mmHg, P<0.01). LV diameters increased and fractional shortening fell. During baseline, biphasic shocks achieved significantly greater success (termination of VF) compared to monophasic waveforms (100 J: biphasic 83.3+/-9.5 versus monophasic 38.9+/-9.5%, P<0.01; 50 J: biphasic 67.1+/-8.8 versus monophasic 11.8+/-5.7%, P<0.01; 30 J: biphasic: 31.9+/-6.4 versus monophasic 0+/-0%, P<0.01). The superiority of the biphasic waveform to terminate VF was retained during LV dysfunction at all energy levels (100 J: biphasic 78.3+/-7.3 versus monophasic 37.5+/-8.1%, P<0.01; 50 J: biphasic 65.5+/-11.5 versus monophasic 11.7+/-5.9%, P<0.01; 30 J: biphasic: 40.6+/-8.0 versus monophasic 3.1+/-3.1%, P<0.01). Within both waveforms, there were no significant differences in percent shock success at any energy level comparing baseline with LV dysfunction. CONCLUSION: In this porcine model of acute LV dysfunction, biphasic waveform shocks were not only superior to monophasic waveform shocks for termination of VF during baseline, but retained superiority to monophasic waveform shocks when LV dysfunction was present.

Acute Disease↗
PubMed1998

Pulmonary responses to 5-hydroxytryptamine and endothelin-1 in a rabbit model of left ventricular dysfunction.

OBJECTIVE: To determine whether pulmonary hypertension developed in a coronary artery-ligated rabbit model of left ventricular dysfunction (LVD) and to examine the effects of i.v. 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) on pulmonary arterial pressure (PAP). METHODS: Eight weeks after experimental coronary artery ligation or sham operation, ejection fractions were assessed by echocardiography. The rabbits were later anaesthetised and pulmonary arterial pressure was measured via a catheter inserted into the pulmonary artery via the right external jugular vein. 5-HT (1-400 micrograms/kg) and ET-1 (0.001-4 nmol/kg) were administered i.v. RESULTS: Ejection fraction was significantly decreased from 76.6 +/- 1.4% in sham-operated to 42.2 +/- 1.3% in coronary artery-ligated rabbits (n = 9 in each group; P < 0.001), consistent with LVD. Baseline mean pulmonary arterial pressure was significantly increased in the coronary artery-ligated group compared to the shams, (16.5 +/- 0.5 vs. 11.5 +/- 0.8 mmHg; P < 0.001). A significant degree of right ventricular hypertrophy was found in the coronary artery-ligated rabbits (0.70 +/- 0.04 g/kg final body weight (f.b.wt.), n = 8 cf. 0.48 +/- 0.02 g/kg f.b.wt. in sham-operated controls, n = 8; P < 0.001). There was a significant increase in the percentage of muscularised pulmonary vessels adjacent to alveolar ducts and alveoli < 60 microns i.d. in the LVD rabbits compared with their sham-operated controls (8.5 +/- 0.4 cf. 20 +/- 0.5%; P < 0.0005). 5-HT produced a greater response in the coronary artery-ligated rabbits (a maximum increase of 8.7 +/- 1.0 mmHg in mean pulmonary artery pressure vs. 4.6 +/- 1.5 mmHg for sham-operated controls; P < 0.05). ET-1 did not have any effect on pulmonary arterial pressure in either group. CONCLUSION: In the rabbit, LVD secondary to coronary artery ligation, causes right ventricular hypertrophy, pulmonary vascular remodelling, and an increased PAP consistent with the onset of pulmonary hypertension (PHT). The greater PAP response to i.v. 5-HT in the PHT group supports the hypothesis that this substance could be involved in the development of PHT. A role for ET-1 cannot be excluded, despite its lack of effect on PAP when intravenously administered in either group.

Animals↗
PubMed2002

GH-independent cardiotropic activities of hexarelin in patients with severe left ventricular dysfunction due to dilated and ischemic cardiomyopathy.

AIM: To investigate acute cardiotropic activities of hexarelin in patients with severe left ventricular dysfunction due to ischemic (iCMP) and dilated cardiomyopathy (dCMP). METHODS AND RESULTS: We studied the effect of intravenous hexarelin administration on growth hormone (GH) levels and left ventricular ejection fraction (LVEF) evaluated by radionuclide angiography in eight patients with dCMP (age 53.0+/-2.8, LVEF 16.7+/-2.1%) and five patients with iCMP (age 52.0+/-2.8 years, LVEF 22.6+/-2.1). Results were compared with a group of seven normal subjects (age 37.4+/-3.4 years, LVEF 64.0+/-1.5%) and seven patients with severe growth-hormone deficiency (GHD; age 42.0+/-4.4 years, LVEF 50.0+/-1.9%) previously studied with the same methodology. In dCMP and iCMP patients hexarelin induced a similar significant (P<0.05) increase in GH levels. In iCMP patients hexarelin induced a LVEF increase (peak LVEF 26.2+/-2.5%, P<0.05) as observed in normals and GHD, while in dCMP LVEF was unchanged (peak LVEF 17.7+/-1.7, P=NS). In all groups other hemodynamic parameters were unchanged. CONCLUSIONS: Acute hexarelin administration increases LVEF in iCMP patients (as in normals and GHD) but not in dCMP patients in spite of a similar GH releasing effect and basal LVEF. A possible explanation of the positive inotropic effect of hexarelin in iCMP could be a direct stimulation on viable myocardium or myocardial contractile reserve.

Adult↗
PubMed2003

Spectrum of left ventricular dysfunction in potential pediatric heart transplant donors.

BACKGROUND: Although myocardial dysfunction severe enough to preclude harvest for transplantation has been reported in approximately 20% of potential adult organ donors, the incidence of myocardial dysfunction in the pediatric population has not been studied systematically. Therefore, the purpose of this study was to determine the spectrum of myocardial dysfunction in potential pediatric heart transplant donors. METHODS: We reviewed the pediatric cardiology database at Primary Children's Medical Center to identify all children who had screening echocardiograms for potential organ donation. We reviewed charts for patient age and size, cause of brain death, and type of pharmacologic support. Echocardiograms were reviewed retrospectively for left ventricular systolic function (shortening or ejection fraction), wall motion abnormalities, diastolic function (mitral E/A ratio), Tei index, and mitral regurgitation. RESULTS: We identified 23 potential donors (age, 6.7 +/- 4.4 years; range, 5 days to 15 years). All patients were receiving pharmacologic support. We found systolic left ventricular dysfunction, defined as an ejection fraction <50% or a shortening fraction <28%, in 57% (13/23) of the patients. We found mitral regurgitation in 85% (11/13) of the patients with systolic dysfunction and in zero of 10 with normal ejection phase indices. Diastolic dysfunction (mitral E/A reversal) was found in 45% (6/13) of those with systolic dysfunction and in 60% (6/10) of patients with normal systolic ejection phase indices. The Tei index was abnormal in 8 of 13 patients with left ventricular systolic dysfunction (range, 0.5-1.4), and was normal in the 6 patients with isolated diastolic dysfunction. One patient, who was electrocuted, had regional wall motion abnormalities. Of the 23 potential donors, 19 (87%) had evidence of systolic or diastolic dysfunction. A total of 13 hearts (3 with normal systolic function, 4 with systolic dysfunction, and 6 with isolated diastolic dysfunction) were harvested for transplantation. CONCLUSIONS: Left ventricular systolic and diastolic dysfunctions are common findings in potential pediatric organ donors. Despite this, previous studies have shown that some of these hearts can be transplanted successfully. We speculate that some of the abnormalities occur as a physiologic consequence of brain death and, thus, may be reversible after transplantation. To avoid wasting a valuable, limited resource, further study is needed to identify the donors suitable for pediatric heart transplantation.

Adolescent↗
PubMed2001

Prediction of long-term outcomes by signal-averaged electrocardiography in patients with unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction.

BACKGROUND: An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. METHODS AND RESULTS: A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P=0.0001), cardiac death (37% versus 25%, P=0.0001), and total mortality (43% versus 35%, P=0.0001) were significantly higher. The combination of EF <30% and abnormal SAECG identified a particularly high-risk subset that constituted 21% of the total population. Thirty-six percent and 44% of patients with this combination succumbed to arrhythmic and cardiac death, respectively. CONCLUSIONS: SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.

Coronary Disease↗
PubMed1996

Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: a report from the Studies of Left Ventricular Dysfunction (SOLVD).

OBJECTIVES: This study sought to assess proinflammatory cytokine levels in patients in the studies of left ventricular dysfunction trial (SOLVD) in relation to both their New York Heart Association functional classification and their neurohormonal status before randomization. BACKGROUND: Elevated levels of tumor necrosis factor-alpha have been identified in 30% to 40% of patients with heart failure. However, it is unclear which subsets of patients with heart failure elaborate tumor necrosis factor-alpha. It is also unclear what the mechanism for the increased expression of proinflammatory cytokines is. METHODS: Tumor necrosis factor-alpha and interleukin-6 levels were analyzed by enzymes-linked immunoassay using randomly selected plasma samples from patients in functional classes I to III who were enrolled in neurohormonal substudies of the SOLVD trial; age-matched healthy subjects served as the control group. RESULTS: Plasma levels of tumor necrosis factor-alpha (p < 0.001) were elevated in patients in functional classes I to III ([mean +/- SD] 1.95 +/- 0.54, 2.63 +/- 0.48, 6.4 +/- 1.9 pg/ml, respectively) compared with age-matched control subjects (0.75 +/- 0.05 pg/ml) and were progressively elevated in relation to decreasing functional status of the patient. Plasma levels of interleukin-6 (p < 0.001) were elevated in patients in functional classes I to III (3.3 +/- 0.55, 6.2 +/- 1.1, 5.22 +/- 0.9 pg/ml, respectively) compared with age-matched control subjects (1.8 +/- 0.5 pg/ml and were progressively elevated in relation to decreasing functional status of the patient. Cox proportional-hazards analysis showed that there was a trend toward significance between plasma tumor necrosis factor-alpha (p < 0.07) and survival, whereas there was no significant relation for plasma interleukin-6 (p < 0.72). Except for atrial natriuretic factor, which correlated weakly (r = 0.23, p = 0.04) with circulating tumor necrosis factor-alpha levels, there was no significance correlation between neurohormonal and proinflammatory cytokine levels. CONCLUSIONS: Circulating levels of proinflammatory cytokines increase in patients as their functional heart failure classification deteriorates. Moreover, activation of the neurohumoral axis is unlikely to completely explain the elaboration of proinflammatory cytokines in heart failure.

Aged↗
PubMed1993

Nisoldipine in severe ischaemic left ventricular dysfunction.

The use of calcium antagonists in patients with severe dysfunction is controversial because agents like verapamil, diltiazem and nifedipine have been shown to worsen or precipitate congestive heart failure. However, successive improvements in our understanding of the clinical pharmacology of these drugs, of their pharmacokinetics and of their action on several neuro-humoral regulatory mechanisms have led to a continuous improvement of the molecules available. Promising results have been obtained with nisoldipine in patients with ischaemic left ventricular dysfunction (improved exercise tolerance, improved diastolic filling probably related to a relative improvement of chronically ischaemic areas) and other studies are exploring the effects of the combination of nisoldipine with an ACE-inhibitor. Soon, these trials should tell us if there is a real clinical benefit in the use of this agent not only to improve symptoms but also to slow down progression of the ventricular dysfunction.

Coronary Circulation↗
PubMed1998

Goldberger's triad in dilated cardiomyopathy--can it predict the severity of left ventricular dysfunction?

Goldberger's triad is a specific, but relatively insensitive, electrocardiographic sign for dilated cardiomyopathy. To study the correlation between the presence of this sign and the severity of left ventricular dysfunction, the electrocardiograms and echocardiographically-determined left ventricular parameters of 17 patients (mean age 59.3 +/- 11.8 years) with dilated cardiomyopathy were examined. Five of the patients had Goldberger's triad. We found that the mean left atrial diameter, the mean left ventricular internal diameters (both end-systolic and end-diastolic) and the mean left ventricular ejection fraction of the group of patients with Goldberger's triad did not differ significantly from the group without. Coronary angiography revealed occult coronary artery disease in 5 of 12 patients. A larger, prospective study is required to verify our finding.

Cardiomyopathy, Dilated↗