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PubMed1998

Is heart rate variability a reliable method to assess autonomic modulation in left ventricular dysfunction and heart failure? Assessment of autonomic modulation with heart rate variability.

Autonomic dysfunction seems to be involved in the progression and prognosis of congestive heart failure. Measurement of heart rate variability (HRV) provides a noninvasive method to obtain reliable and reproducible information on autonomic modulation of heart rate, but there is a difficulty in using HRV as a quantitative estimate of autonomic dysfunction in heart failure. This study was aimed at testing the hypothesis that abnormal modulation of heart rate assessed by power spectrum analysis may be present also in asymptomatic patients with left ventricular dysfunction and progress in patients with overt symptoms of congestive heart failure. HRV was measured in three groups of subjects: Group 1: 30 patients with chronic heart failure; Group 2: 21 patients with asymptomatic left ventricular dysfunction; and Group 3: 25 healthy volunteers as control group. HRV was evaluated by autoregressive spectral analysis with 600-beat ECG samples, while subjects were quietly recumbent (BSI), in conditions of controlled breathing (15 acts/min) (RSC) and passive orthostatism after tilting (80 degrees) (TLT). Patients in group 1 showed a reduction in the standard deviation of the R-R intervals (SDRR) (p<0.0003) and in the low frequency component (LF) (p<0.0001) compared to normal subjects. Low frequency component was not detectable in 11 patients of group I (p<0.0008). On RSC and TLT, group 1 failed to show any modification in the low frequency and high frequency components (HF) under any stimulation. Group 2 showed no modification at baseline evaluation, no increase in the high frequency component on RSC and in LF during TLT compared to controls (p<0.01 and p<0.0001 respectively). At baseline, group 1 had a lower SDRR (p<0.03) and LF (p<0.0001) vs. group 2, whereas during stimulation the two groups exhibited the same behaviour. In conclusion, reduced heart rate variability is specific for both asymptomatic and symptomatic post-ischemic left ventricular dysfunction. Our results suggest that frequency domain analysis of heart rate variability during a stimulation test allows a more accurate definition of the degree of autonomic control of heart rate.

Autonomic Nervous System↗
PubMed1988

Diastolic filling in acute left ventricular dysfunction: role of the pericardium.

Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1999

Carvedilol prevents remodeling in patients with left ventricular dysfunction after acute myocardial infarction.

OBJECTIVE: The aim of the study was to assess the effects of carvedilol, a vasodilating nonselective beta-blocker, on the indexes of left ventricular remodeling after acute myocardial infarction in those with left ventricular dysfunction. METHODS AND RESULTS: Forty-nine patients with predischarge left ventricular ejection fraction <45% after acute myocardial infarction were evaluated in a double-blind, randomized, placebo-controlled, parallel group study (selected from the database of the Carvedilol Heart Attack Pilot Study: CHAPS). Patients received medication after thrombolysis and continued to do so for 6 months. Two-dimensional echocardiography was performed before discharge (7 to 10 days after admission) and at 3 months after acute myocardial infarction. Analysis of variance showed that wall thickness opposite the site of infarction decreased from (mean +/- SD) 12.3 +/- 2.1 mm to 11.0 +/- 2.4 mm with carvedilol compared with 11.6 +/- 1.9 mm to 12.2 +/- 1.9 mm with placebo (P =.01). Left ventricular mass changed from 235 +/- 74 g to 217 +/- 64 g with carvedilol compared with 227 +/- 80 g to 252 +/- 85 g with placebo ( P =.02). Carvedilol prevented alteration of sphericity index (ratio of long and short axis of left ventricle) that changed from 1.65 +/- 0.29 to 1.66 +/- 20 with carvedilol compared with 1.58 +/- 0.33 to 1.39 +/- 0.19 with placebo (P =.02); alteration was also prevented of wall thickening abnormality at infarct site, which changed from 9.2 +/- 3.1 cm2 to 9.1 +/- 3.5 cm 2 with carvedilol compared with 10.3 +/- 3.3 cm2 to 13.5 +/- 4.6 cm2 with placebo (P =.002). CONCLUSION: Carvedilol administered early after acute myocardial infarction results in attenuation of left ventricular remodeling in patients with persistent left ventricular dysfunction before discharge.

Adrenergic beta-Antagonists↗
PubMed1995

Calcium antagonists and left ventricular dysfunction.

Calcium antagonists are used in the management of a variety of cardiovascular disorders. Ischemia leads to left ventricular dysfunction, which is the clinical entity on which the calcium antagonists are expected to have their effect as a result of their anti-ischemic action. This article reviews the efficacy of calcium antagonists in several different settings of left ventricular dysfunction due to ischemia and reperfusion.

Calcium Channel Blockers↗
PubMed1995

Reversible left ventricular dysfunction associated with Guillain-Barré syndrome--an expression of catecholamine cardiotoxicity?

The patient was a 76-year-old female who had a history of Guillain-Barré syndrome 3 years previously; ST-segment elevation was noted in association with reversible left ventricular dysfunction. Left ventrioculogram and coronary angiograms were normal and ergonovine test was negative during the chronic period of Guillain-Barré syndrome. She was hospitalized again due to the recurrence of Guillain-Barré syndrome. Two days later, ST-segment elevation in leads V2 through V5 prompted us to perform cardiac catheterization, although she did not complain of any chest symptoms. A large akinetic area was found mainly around the apex on left ventriculography, despite the lack of coronary stenoses. Peak creatine kinase and C-reactive protein were 400 IU/ml and 3.5 mg/dl, respectively. Left ventricular dysfunction was normalized within one week. During the acute phase of the cardiac episode, plasma norepinephrine and epinephrine were 1340 pg/ml and 112 pg/ml, respectively. I123 metaiodobenzyl-guanidine myocardial scintigram 3 weeks after the episode showed an extensive apical defect which was improved markedly 3 months later. We think that this reversible left ventricular dysfunction was due to the synergistic toxic effect of mildly increased catecholamine and transiently damaged sympathetic nerve endings in the myocardium, presumably due to Guillain-Barré syndrome.

3-Iodobenzylguanidine↗
PubMed1993

A stable model of left ventricular dysfunction in an intact animal assessed with high fidelity pressure and cinemagnetic resonance imaging.

OBJECTIVE: Numerous models of acute and chronic left ventricular dysfunction have been used over the years. However, few can produce a rapid onset of global systolic and diastolic dysfunction that is stable and potentially reversible. The aim of this study was to develop such a model. METHODS: A model of left ventricular dysfunction was produced in six intact dogs using 1% halothane anaesthesia and pharmacological autonomic blockade with atropine (0.1 mg.kg-1) and propranolol (2 mg.kg-1). Left ventricular function was assessed by combined high fidelity pressure and cinemagnetic resonance imaging (cine-MR) during increases in afterload using infusions of angiotensin. RESULTS: Left ventricular systolic dysfunction was characterised by a diminished resting ejection fraction of 45(SD 4)% and a depressed +dP/dtmax of 1537(100) mm Hg.s-1. Diastolic dysfunction was manifested by an increased left ventricular end diastolic pressure of 16(2) mm Hg, a decreased -dP/dtmax of -1705(369) mm Hg.s-1, and a prolonged time constant of left ventricular relaxation of 42(9) ms. As left ventricular systolic pressure steadily rose with angiotensin infusion from 87(7) to 124(13) to 152(10) mm Hg (p < 0.001), left ventricular ejection fraction decreased markedly from 45(4) to 35(4) to 27(4)% (p < 0.001). Left ventricular +dP/dtmax did not change [1537(100) to 1500(110) to 1498(84) mm Hg.s-1] in spite of a significant increase in left ventricular end diastolic pressure from 16(2) to 21(5) to 29(7) mm Hg (p < 0.001) and left ventricular end diastolic volume from 59(12) to 71(14) to 78(17) ml (p < 0.001). Individual slopes of the end systolic pressure-volume relationship were also low, ranging between 2.1 and 4.4 mm Hg.s-1 (r = 0.99 to 1.00), typical of impaired contractility. CONCLUSIONS: Halothane anaesthesia in dogs pretreated with large amounts of propranolol and appropriate muscarinic cholinergic blockade produces a moderate decrease in baseline systolic and diastolic function in our intact dog model. However, left ventricular systolic function showed limited contractile reserve when challenged by physiological increases in systemic arterial pressure. Impaired systolic and diastolic function may, at least in part, be related to diminished activator calcium produced by halothane in addition to the well known negative inotropic action of beta adrenergic blockade.

Anesthesia↗
PubMed1990

Systemic and regional hemodynamic effects of alpha-adrenoceptor blockade in chronic left ventricular dysfunction in the conscious dog.

In seven dogs with long-standing left ventricular dysfunction induced 16 weeks earlier by repetitive transmyocardial direct current (DC) shock, the acute hemodynamic effect of the alpha 1-adrenoceptor antagonist urapidil was studied. Left ventricular end-diastolic pressure (LVEDP) was significantly increased from preshock levels at the time of study and cardiac output was reduced. Plasma norepinephrine was significantly increased from control levels and was not altered by urapidil infusion. The mean arterial pressure fell in response to alpha 1-blockade from 111 to 85 mm Hg, the LVEDP fell from 16 to 9 mm Hg, and cardiac output increased from 2.90 to 3.70 L/min (all p less than 0.01). Regional blood flows measured by microsphere injection revealed an increase in blood flow to skeletal muscle, which had not been significantly decreased by the left ventricular dysfunction in this model, and further decreases in splanchnic flow, which was already depressed compared with that in normal dogs. Therefore acute alpha-adrenoceptor blockade improves central hemodynamics in experimental heart failure but does not normalize the resting blood flow maldistribution in this model.

Adrenergic alpha-Antagonists↗
PubMed2004

Effects of eplerenone, a selective aldosterone blocker, on the progression of left ventricular dysfunction and remodeling in rats with dilated cardiomyopathy.

Aldosterone blockade reduces morbidity and mortality in patients with heart failure. We studied the effects of eplerenone, a novel aldosterone blocker, on the progression of left ventricular dysfunction and remodeling in rats with dilated cardiomyopathy after autoimmune myocarditis. Twenty-eight days after immunization, the surviving Lewis rats were randomized to 1 month's oral treatment with low-dose eplerenone (group L), high-dose eplerenone (group H) or vehicle (group V). Five of 15 (33%) rats in group V and 3 of 15 (20%) rats in group L died during the course of treatment. High-dose eplerenone significantly reduced cardiomyocyte hypertrophy, heart weight and heart weight to body weight ratio. Eplerenone improved left ventricular function in a dose-dependent manner. Central venous pressure and left ventricular end-diastolic pressure were lower, and +/-dP/dt and fractional shortening were higher in group H than group V. Eplerenone also attenuated myocardial fibrosis and reduced left ventricular mRNA expressions of TGF-beta(1) and collagen-III. Our results indicate that treatment with eplerenone improved left ventricular dysfunction and attenuated left ventricular remodeling in rats with heart failure.

Animals↗
PubMed2000

Comparison between blood and crystalloid cardioplegia in patients with left ventricular dysfunction undergoing coronary surgery.

This study was done to compare the protective effect of blood and crystalloid cardioplegia in patients with left ventricular dysfunction undergoing coronary artery bypass grafting (CABG). Sixty consecutive patients with left ventricular ejection fraction < 35% scheduled for CABG with the use of cardiopulmonary bypass without additional procedures were randomly divided into two groups. In the first group we used cold blood cardioplegia, in the second group cold crystalloid cardioplegia, both delivered only ortogradely. We measured hemodynamic data in early hours after operation, enzyme release and we collected other clinical data which could be influenced by perioperative myocardial protection. There was no death in either group. We also didn't find any significant difference in incidence of perioperative myocardial infarction, arrhythmias and use of intraaortic balloon pumping between both groups. In an early hours after operation in the group with blood cardioplegia we found significantly better hemodynamic data (LVSWI, RVSWI) and significantly lower enzyme release. We conclude, that cold blood cardioplegia shows superior perioperative myocardial protection resulting in earlier restoration of myocardial function. This difference could be important in patients with high degree of left ventricular dysfunction.

Aged↗
PubMed1996

Medium-term effects of beta-blockade on left ventricular mechanics: a double-blind, placebo-controlled comparison of nebivolol and atenolol in patients with ischemic left ventricular dysfunction.

The aim of this study was to compare the effects on left ventricular function and exercise tolerance of a selective beta-antagonist (atenolol) with those of another selective beta 1-antagonist with vasodilator properties (nebivolol) in patients with ischemic left ventricular dysfunction but no overt congestive heart failure. Beta blockers are widely used in ischemic heart disease, but their effects on left ventricular mechanics and exercise tolerance are poorly defined in the subgroup of patients with significant systolic dysfunction but without clinical evidence of ischemia or congestive heart failure. Angiographic and symptom-limited exercise data were obtained at baseline and after an 8-10-week double-blind treatment with placebo (n = 10), 50 mg atenolol daily (n = 10), or 2.5 mg (n = 10) or 5 mg (n = 10) nebivolol daily. When compared to placebo, both atenolol and nebivolol reduced resting heart rate and improved left ventricular ejection fraction (from 33.9 to 39.2% with atenolol and from 36.5 to 40.8% with nebivolol, both P < .05) while lowering mean systolic wall stress. Only nebivolol, however, produced a parallel downward shift of the pressure-volume relationship during early diastolic filling and improved the early peak filling rate when compared to placebo (+ 10%, P < .05). When compared to baseline, maximal exercise duration increased by 7 and 13 seconds with placebo and atenolol, respectively (both NS vs baseline), and increased by 44 seconds with nebivolol (P = .0077 vs baseline). Both atenolol and nebivolol decreased maximal exercise heart rate; the reduction was more pronounced with atenolol. Prolonged beta 1-adrenoceptor blockade leads to a significant increase in left ventricular ejection fraction in patients with ischemic left ventricular dysfunction. The dissociation between the changes in resting left ventricular function and the changes in exercise duration suggests that in this clinical setting, the changes in systolic function may have less impact on functional capacity than an improvement in diastolic distensibility during the rapid filling phase.

Adrenergic beta-Antagonists↗
PubMed1998

[Pulmonary hypertension in patients with left ventricular dysfunction studied with contrast-enhanced Doppler echocardiography: relations with diastolic parameters and prognostic implications].

In patients with left ventricular dysfunction, the prognostic value of both pulmonary hypertension and mitral flow patterns has been recognized. However, the effect of the association of different degrees of pulmonary hypertension on prognosis and the corresponding left ventricular diastolic dysfunction is not clear. Accordingly, we considered the impact on survival of a categorization based on the relationship between pulmonary artery pressure and left ventricular diastolic dysfunction, as assessed by mitral and pulmonary venous flow analyses. Transthoracic Doppler echocardiography was carried out in 92 patients with ejection fraction < 45%, pulmonary artery systolic pressure > 25 mmHg and sinus rhythm. Tricuspid regurgitant velocity and Doppler parameters derived from transmitral and pulmonary venous flows were evaluated. In the case of inadequate baseline tracings, weak or poor Doppler signals were enhanced by intravenous injection of a galactose-based contrast agent (Levovist 8 ml suspension at a concentration of 400 mg/ml). To select those whose pulmonary hypertension was either proportional or unproportional to left side filling pressures, patients were divided as follows: Group 1 (n = 69) with low discrepancies and Group 2 (n = 23) with marked discrepancies between Doppler estimates of pulmonary artery systolic pressure and left side filling abnormalities. The patients of each group were also classified according to their mitral flow pattern: abnormal relaxation, pseudonormal and restrictive. Mean pulmonary artery systolic pressure was 49 +/- 16 mmHg in the total population, 43 +/- 11 mmHg in Group 1 and 68 +/- 14 mmHg in Group 2 (p < 0.0001). Several mitral and pulmonary venous flow variables significantly correlated with pulmonary artery systolic pressure in the total population and in the study groups. The best correlations were observed in Group 1 as regards the ratio of reverse-to-forward atrial wave duration (r = 0.83), E wave deceleration rate (r = 0.81), E wave deceleration time (r = -0.81) and the systolic fraction of pulmonary venous flow peak velocities (r = -0.75). In Group 1, the lower heart failure-free survival rate at 10 months was observed in patients with restrictive pattern (68%) as opposed to those with pseudonormal (94%) and abnormal relaxation patterns (97%). The overall heart failure-free survival rate in Group 2 was 86%. In conclusion, the classification according to the relationship between pulmonary hypertension and the alterations of left chamber filling may contribute to the prognostic stratification of patients with left ventricular dysfunction. The patients with pulmonary hypertension proportional to the increase in left chamber filling pressures and restrictive pattern exhibited the worst prognosis.

Aged↗
PubMed2000

Neurohormones in an ovine model of compensated postinfarction left ventricular dysfunction.

Clinical heart failure, often the result of myocardial infarction, may be preceded by a period of compensated left ventricular impairment. There is substantial need for an experimental model that reflects this human condition. In sheep, coronary artery ligation produced consistent left ventricular anteroapical myocardial infarctions resulting in chronic (5 wk), stable hemodynamic changes compared with sham controls, including reductions in ejection fraction (51 +/- 2 vs. 30 +/- 5%, P < 0.001), cardiac output (6.3 +/- 0.2 vs. 5.1 +/- 0.2 l/min, P < 0.01), and arterial pressure (93 +/- 2 vs. 79 +/- 3 mmHg, P < 0.001), and increases in cardiac preload (left atrial pressure, 3.3 +/- 0.1 vs. 8.3 +/- 1.3 mmHg, P < 0.001). These changes were associated with acute and sustained increases in plasma concentrations of atrial natriuretic peptide (ANP; 5 wk, 11 +/- 2 vs. 27 +/- 5 pmol/l, P < 0.001), brain natriuretic peptide (BNP; 3 +/- 0.2 vs. 11 +/- 2 pmol/l, P < 0.001), and amino-terminal pro-brain natriuretic peptide (NT-BNP; 17 +/- 3 vs. 42 +/- 12 pmol/l, P < 0.001). Significant correlations were observed between plasma levels of the natriuretic peptides (ANP, day 7 to week 5 samples; BNP and NT-BNP, day 1 to week 5 samples) and changes in left ventricular volumes and ejection fraction. In contrast, renin activity, aldosterone, catecholamines, and endothelin were not chronically elevated postinfarction and were not related to indexes of ventricular function. Coronary artery ligation in sheep produces the pathological, hemodynamic, and neurohormonal characteristics of compensated left ventricular impairment secondary to myocardial infarction. Plasma concentrations of the cardiac natriuretic peptides are sensitive markers of left ventricular dysfunction. This is a reproducible model that reflects the clinical condition and should prove suitable for investigating the pathophysiology of, and experimental therapies in, early left ventricular dysfunction.

Aldosterone↗
PubMedDate not supplied

Prognostic value of tomographic rest-redistribution thallium 201 imaging in medically treated patients with coronary artery disease and left ventricular dysfunction.

BACKGROUND: Previous studies show that rest-redistribution thallium imaging is useful in the assessment of myocardial viability. The impact of such studies on patient outcome is not well defined. This study examined the prognostic value of tomographic rest-redistribution 201T1 imaging in 81 medically treated patients with coronary artery disease and left ventricular dysfunction. METHODS AND RESULTS: Rest-redistribution single-photon emission computed tomographic images were obtained and analyzed quantitatively. The segmental thallium uptake (20 segments per patient) was interpreted as normal, reversible defect, mild to moderate fixed defect, or severe fixed defect. The thallium images were abnormal in 80 patients, with no redistribution (no ischemia) in 43 patients and redistribution (ischemia) in 38 patients. The left ventricular ejection fraction was 27% +/- 8% in patients with no redistribution and 26% +/- 7% in patients with redistribution (difference not significant). In patients with no ischemia, there were 7 +/- 5 severe fixed defects and 5 +/- 4 mild to moderate fixed defects per patient. In patients with ischemia there were 7 +/- 4 reversible defects, 3 +/- 3 mild to moderate fixed defects, and 5 +/- 4 severe fixed defects per patient. The number of any abnormal segments was 11 +/- 5 in patients with no ischemia and 14 +/- 4 in patients with ischemia (p = 0.03). During a mean follow-up of 31 +/- 24 months, there were 11 cardiac deaths in patients with no ischemia (26%) and 22 in patients with ischemia (58%); the survival rate was worse in patients with than without ischemia (p < 0.05). Multivariate Cox survival analysis on important clinical, angiographic, and thallium variables showed that the presence of redistribution was an independent predictor of death (x2 = 5; p = 0.03). CONCLUSIONS: Patients with left ventricular dysfunction and redistribution on rest thallium imaging, a marker of hibernating myocardium, have a higher mortality rate with medical therapy than do patients with a comparable degree of left ventricular dysfunction but with fixed defects only. Thus observations similar to those made with positron emission tomography can be made in a much more straightforward, simple, and probably cost-effective manner with single-photon emission computed tomography.

Aged↗
PubMed1994

Atrial natriuretic peptide response is blunted in patients with acute myocardial infarction and mild left ventricular dysfunction.

Neurohumoral parameters in 45 asymptomatic patients with acute myocardial infarction were measured. In patients with mild left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mm Hg), atrial natriuretic peptide levels differed significantly from those in patients with normal left ventricular function (127 +/- 74 pg/ml vs. 79 +/- 71 pg/ml; p < 0.001). After stimulus an increase in atrial natriuretic peptide levels (79 +/- 71 to 118 +/- 86 pg/ml; p < 0.001) was found only in patients with normal hemodynamic parameters. These data show that in patients with left ventricular dysfunction, the atrial natriuretic system is activated; however, atrial natriuretic peptide response to stimulus is present only in patients with normal hemodynamics.

Adult↗
PubMed2004

[Transient ventricular dysfunction after emotional stress].

We describe a patient who developed severe ventricular dysfunction and cardiogenic shock after intense emotional stress. Her subsequent course was favorable, with complete recovery of left ventricular systolic function. The coronary arteries were normal and no specific etiologic agent was demonstrated. Her clinical picture was compatible with transient left ventricular apical ballooning. [I123]metaiodobenzyl guanidine cardiac scintigraphy showed a marked decrease in cardiac sympathetic nerve activity. We discuss the pathophysiologic mechanisms of this syndrome.

Aged↗
PubMed2001

Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction.

BACKGROUND: Right heart failure after cardiopulmonary bypass can result in severe hemodynamic compromise with high mortality, but the underlying mechanisms remain poorly understood. After ischemia-induced right ventricular failure, alterations in the interventricular septal position decrease left ventricular compliance and limit filling but may also distort left ventricular geometry and compromise contractility and relaxation. This study investigated the effect of acute isolated right ventricular ischemia on biventricular performance and interaction and the response of subsequent right ventricular unloading by use of a modified Glenn shunt. METHODS: In 8 pigs isolated right ventricular ischemic failure was induced by means of selective coronary ligation. A modified Glenn circuit was then established by a superior vena cava-pulmonary artery connection. Ventricular performance was determined by conductance catheter-derived right ventricular pressure-volume loops and left ventricular pressure-segment length loops. Hemodynamic data at baseline, after right ventricular ischemia, and after institution of the Glenn circuit were obtained during inflow occlusion, and the load-independent contractile indices were derived. RESULTS: Right ventricular free-wall ischemia resulted in acute right ventricular dilation (118 +/- 81 mL vs 169 +/- 70 mL, P =.0008) and impairment of left ventricular contractility indicated by the reduced end-systolic pressure-volume relation slope (50.0 +/- 19 mm Hg/mm vs 18.9 +/- 8 mm Hg/mm, P =.002) and preload recruitable stroke work index slope (69.6 +/- 26 erg x cm(-3) x 10(3) vs 39.7 +/- 13 erg x cm(-3) x 10(3), P =.003). In addition, left ventricular relaxation (tau) was significantly prolonged (33.3 +/- 10 ms vs 53.0 +/- 16 ms, P =.012). Right ventricular unloading with the Glenn shunt reduced right ventricular dilation and significantly improved left ventricular contraction, end-systolic pressure-volume relation slope (18.9 +/- 8 mm Hg/mm vs 35.8 +/- 18 mm Hg/mm, P =.002), preload recruitable stroke work index slope (39.7 +/- 26 erg x cm(-3) x 10(3) vs 63.0 +/- 22 erg x cm(-3) x 10(3), P =.003), and diastolic performance (tau 53.0 +/- 16 ms vs 43.5 +/- 13 ms, P =.001). CONCLUSIONS: Right ventricular ischemia-induced dilation resulted in acute impairment of left ventricular contractility and relaxation. A modified Glenn shunt attenuated the left ventricular dysfunction by limiting right ventricular dilation and restoring left ventricular cavity geometry.

Animals↗
PubMed2001

[Efficacy of additional Dor approach to coronary bypass grafting in severe left ventricular dysfunction with large akinetic area].

Between January 1994 and August 1999, we experienced 16 cases of coronary artery bypass grafting (CABG) in severe left ventricular dysfunction with left ventricular ejection fraction (LVEF) < or = 40%. Four had additional endoventricular patch plasty in large postinfarction akinetic scars, the so-called Dor approach, to CABG (group D). Eleven had only CABG, or CABG and mitral annuloplasty (group C). One had linear repair after the resection of the left ventricular aneurysm. One died of sustained low output syndrome 5 months after the operation in group C. Fractioning shortening and left ventricular diastolic diameter were not changed after the operation in group C. On the other hand, in group D, there were no complications after the operation, LVEF was significantly improved from 31.5 +/- 4.9% to 62.5 +/- 5.9% (p < 0.01) and the left ventricular end-diastolic volume index was reduced from 118 +/- 23 ml/m2 to 74 +/- 12 ml/m2 (p < 0.01). The Dor approach is considered to be a safe and effective additional procedure to CABG in severe patients with a large akinetic antero-septal segment.

Aged↗
PubMed1998

[Significance of alcohol abstinence in alcoholic cardiomyopathy with moderate left ventricular dysfunction].

PURPOSE: To evaluate the role of a 12 month alcohol abstinence period in patients with moderate left ventricular dysfunction treated with anticongestive therapy. METHODS: Prospective observational study with 20 patients with alcoholic cardiomyopathy (ACM), 9 (45%) in functional class (FC) II and 11 (55%) in FC III, 16 (80%) men, mostly black (55%), from 35 to 56 (x = 45) years old, heavy alcohol users (> 80 g ethanol for 51 to 112 (x = 88) months. At the beginning, all agreed to participate with psychotherapy and clinical evaluation. After 12 months, they were divided in G-I, formed by those who remained abstemious and G-II of non-abstemious. RESULTS: After 12 months, among the 11 (55%) who remained in psychotherapy, 8 were in G-I, among those who did not 9 (45%), only 2 (22.22%) remained abstemious (G-I). At the end of the evaluation period, both groups had the same number of patients. Comparing them, we observed: a) lower mean systolic and diastolic left ventricular diameters in G-I; b) more hospitalizations in G-II (3); c) more patients with stable or better clinical evaluation in G-I. CONCLUSION: Despite the initial will, only 50% reached abstinence. When it was reached, patients had a better evolution in left ventricular systolic diameter and abstinence should always be tried even in the presence of moderate left ventricular dysfunction.

Adult↗