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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↗
PubMed2005

Clinical course and implantable cardioverter defibrillator therapy in postinfarction women with severe left ventricular dysfunction.

BACKGROUND: There are limited data regarding implantable cardioverter defibrillator (ICD) therapy in postinfarction women with severe left ventricular dysfunction. The aim of this study was to evaluate the risk of cardiac events and effects of ICD therapy in women as compared to men enrolled in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II). METHODS AND RESULTS: Among 1,232 patients enrolled in MADIT II, there were 192 (16%) women and 1,040 (84%) men. When compared to men, women had an increased frequency of NYHA class > or =II (70 vs 63%; P = 0.067), hypertension (60% vs 52%; P = 0.047), diabetes (42% vs 34%; P = 0.027), and LBBB (25% vs 17%; P = 0.011), and less frequent CABG surgery (42% vs 60%; P < 0.001). The 2-year cumulative mortality in patients randomized to conventional therapy was not significantly different in women and men (30% and 20%, respectively; P = 0.19). Adjusting for relevant clinical covariates, the hazard ratios for ICD effectiveness were similar in women (0.57; 95% CI = 0.28-1.18; P = 0.132) and men (0.66; 95% CI = 0.48-0.91; P = 0.011). The risk of appropriate ICD therapy for VT/VF was lower in women than in men (hazard ratio = 0.60 for female vs male gender; 95% CI = 0.37-0.98; P = 0.039). CONCLUSIONS: MADIT II women had similar mortality and similar ICD effectiveness when compared to men. MADIT II women with ICDs had a lower risk of arrhythmic events with fewer episodes of ventricular tachycardia than men.

Aged↗
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↗
PubMed2004

[Right ventricular dysfunction and ischemia in pulmonary embolism].

Patients with pulmonary embolism and right ventricle dysfunction (determined with clinical, hemodynamic or echocardiographic methods) are a subgroup at high risk for complications. One of the pathogenic factors of right ventricular dysfunction in pulmonary embolism is myocardial ischemia, usually secondary to hemodynamic overload, and sometimes worsened by underlying coronary artery disease. We described a patient with pulmonary embolism and dyskinesia of the right ventricular free wall, related to chronic atherosclerotic occlusion of the right coronary artery proximal to the acute marginal branches that irrigate the free wall.

Aged↗
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↗
PubMed1993

[Symptomatic mitral valve prolapse. Left ventricular dysfunction and beneficial effect of digitalis].

PURPOSE: To study the left ventricular function by M-mode echocardiography in symptomatic patients with primary mitral valve prolapse (MVP), without significant mitral regurgitation, during the phenylephrine test, before and after digitalization. METHODS: Thirty one patients with MVP and 10 normal subjects as a control group were studied by M mode echocardiography: Percentage of systolic shortening (DD), ejection fraction (EF) and mean velocity of circumferential fibers shortening (Vcf) were measured. The echocardiographic recordings were obtained at rest and during the continuous infusion of phenylephrine (40-60 micrograms/min) in order to allow an increase of 20-30 mmHg in systolic pressure. RESULTS: At rest, cardiac size and function were normal in both groups. During phenylephrine infusion in 27 patients a decrease in DD (from 37.7 +/- 4.6 to 31.0 +/- 4.0, p < 0.001); in EF (from 0.76 +/- 0.05 to 0.66 +/- 0.6, p < 0.001); in Vcf (from 1.05 +/- 0.77 to 0.76 +/- 0.13, p < 0.001) were observed. From this group 20 patients received digoxin. After the digitalization the phenylephrine test did not cause changes in DD (from 38.3 +/- 5.0 to 39.2 +/- 3.8, NS); in EF (from 0.77 +/- 0.06 to 0.77 +/- 0.04, NS); in Vcf (from 1.05 +/- 0.19 to 0.94 +/- 0.13, NS). These patients during the submaximal exercise test, showed significant increases at the total work load (from 617 +/- 248 to 982 +/- 244 watts, p < 0.001) and cardiac efficiency (from 25.0 +/- 11.5 to 37.2 +/- 10.4, p < 0.001). On the other hand the phenylephrine infusion in the control group did not result in changes in DD, EF and Vcf. CONCLUSION: Symptomatic patients with primary MVP showed total recovering of left ventricular dysfunction with digitalization during the phenylephrine test, with improvement of cardiac efficiency.

Adolescent↗
PubMed1994

[Can irreversible ventricular dysfunction be identified in patients with heart valve disease?].

Cardiologists and heart surgeons are often faced with the problem of the optimal therapeutic indication in patients with valvular heart disease presenting with severe myocardial dysfunction, as it is difficult to evaluate the degree of reversibility of a severe alteration of ventricular function in these patients. Myocardial dysfunction is often multifactorial in patients with valvular heart disease and the role of myocardial ischaemia secondary to associated coronary heart disease must not be neglected. On the other hand, the compensatory capacity of the myocardium varies from one patient to another ("constitutional" myocardial factor or related to the aetiology of the valvular heart disease?). Although the methods of investigation of myocardial function currently available are able to precisely evaluate the degree of severity of myocardial dysfunction, they are unable to accurately predict the degree of reversibility. 1. In pure mitral stenosis, severe left ventricular dysfunction is very rare; more or less rapidly, pulmonary hypertension induces slowly progressive right ventricular dysfunction which remains reversible for a long time. 2. In mitral incompetence, left ventricular systolic function is correctly evaluated by the ejection fraction (LVEF). There is a high risk of irreversible left ventricular dysfunction in operated patients with an LVEF of less than 0.40. In these patients, left ventricular function is slightly improved after mitral repair, while LVEF decreases after mitral valve replacement. The combined study of right ventricular systolic function is useful in patients with mitral disease, as this function may be insidiously altered and the presence of right heart failure, regardless of its cause, considerably increases the late postoperative mortality of mitral valve disease. 3. In aortic stenosis, left ventricular dysfunction, hypertrophy and interstitial fibrosis remain reversible for a long time. Severe alteration of LV function therefore does not exclude the possibility of very good postoperative recovery. However, this is improbable in the presence of: a very marked increase in LV mass and/or end-systolic volume, and/or inoperable associated coronary artery disease, and/or the combination of low ejection fraction, severely decreased cardiac output, and low transvalvular gradient (not increased by cautious dobutamine infusion), and/or clinical signs of complete heart failure. 4. In aortic incompetence, progressive alteration of left ventricular function, often asymptomatic, is reflected by the increased dimensions of the LV and a reduction of the fraction of ejection. The reversibility of LV dysfunction is difficult for evaluate. The long clinical course of this dysfunction is one of the most reliable predictors of irreversibility, together with a fall in the resting isotope LVEF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed1984

Improvement of left ventricular dysfunction after control of persistent tachycardia.

Five children are described who had persistent, chronic tachycardia and left ventricular dysfunction manifested by decreased left ventricular percent fractional shortening on echocardiogram (five patients) cardiomegaly on chest roentgenogram (three), ventricular or atrial hypertrophy on ECG (three), and symptoms of congestive heart failure (three). After antidysrhythmia therapy and control of the tachycardia, signs and symptoms of congestive heart failure resolved in two infants. Moreover, in each patient signs of cardiomegaly resolved on chest roentgenogram, hypertrophy resolved on ECG, and the fractional shortening improved to normal (mean 20.2% +/- 2.4% SEM before vs 36.2% +/- 2.4%, P = 0.02, after treatment). Evaluation in the child who has dilated cardiomyopathy should include assessment of heart rate and rhythm. Moreover, when persistent tachycardia is found in an asymptomatic child, evaluation of left ventricular function is indicated.

Adolescent↗
PubMed2005

The role of 5-hydroxytryptamine in the control of pulmonary vascular tone in a rabbit model of pulmonary hypertension secondary to left ventricular dysfunction.

The role of 5-hydroxytryptamine (5-HT) in a rabbit model of pulmonary hypertension (PHT) secondary to left ventricular dysfunction was investigated. Following pulmonary artery catheterisation under anaesthesia, 5-HT (1-400 microg kg(-1) i.v.) was administered before and after either 5-HT(2A) receptor antagonism with ketanserin (0.5 mg kg(-1)) or infusion of the nitric oxide synthase inhibitor, l-NAME (30 micromol min(-1)). Eight week coronary artery ligated rabbits demonstrate increased mean pulmonary arterial pressure (PAP) compared to controls (17.0+/-0.5 versus 12.0+/-0.5 mmHg, P<0.001) accompanied by right ventricular hypertrophy. 5-HT alone produced a greater pulmonary pressor response in rabbits with PHT (increase of 7.5+/-1.2, n=12 c.f. 3.5+/-0.4 mmHg in shams, n=12, P<0.01). Ketanserin had no effect on basal PAP in either PHT or control rabbits but inhibited the response to 5-HT in both groups. The response to 5-HT following l-NAME was increased in both groups and was greater in rabbits with PHT (an increase of 20.1+/-2.9, n=6 c.f. 11.4+/-1.8 mmHg, n=6, P<0.05). These results suggest that the difference shown in the in vivo pulmonary response to exogenous 5-HT is mediated largely through 5-HT(2A) receptors in this model. However, activity of endogenous 5-HT at the 5-HT(2A) receptors is not responsible for maintaining the raised basal PAP through vasoconstriction in PHT rabbits once PHT has developed.

Animals↗