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PubMed2006

Prosthesis-patient mismatch after aortic valve replacement predominantly affects patients with preexisting left ventricular dysfunction: effect on survival, freedom from heart failure, and left ventricular mass regression.

OBJECTIVE: The effect of prosthesis-patient mismatch on clinical outcome and left ventricular mass regression after aortic valve replacement remains controversial. Data on whether the clinical effect of prosthesis-patient mismatch depends on left ventricular function at the time of aortic valve replacement are lacking. This study examined the long-term clinical and echocardiographic effects of prosthesis-patient mismatch in patients with and without left ventricular systolic dysfunction at the time of aortic valve replacement. METHODS: Preoperative and serial postoperative echocardiograms were performed in 805 adults who underwent aortic valve replacement between 1990 and 2003 and who were subsequently followed up in a dedicated valve clinic (follow-up, mean +/- SD, 5.5 +/- 3.5 years; maximum, 14.2 years). Preoperative left ventricular function was defined as normal (ejection fraction > or =50%) in 548 patients and impaired (ejection fraction <50%) in 257 patients. RESULTS: Patients with impaired preoperative left ventricular function and prosthesis-patient mismatch (indexed effective orifice area < or =0.85 cm2/m2) had a decreased overall late survival (hazard ratio, 2.8; P = .03), decreased freedom from heart failure symptoms or heart failure death (odds ratio of 5.1 at 3 years after aortic valve replacement; P = .009), and diminished left ventricular mass regression compared with patients with impaired preoperative left ventricular function and no prosthesis-patient mismatch. These effects of prosthesis-patient mismatch were not observed in patients with normal preoperative left ventricular function. CONCLUSIONS: Prosthesis-patient mismatch at an indexed effective orifice area of 0.85 cm2/m2 or less after aortic valve replacement primarily affects patients with impaired preoperative left ventricular function and results in decreased survival, lower freedom from heart failure, and incomplete left ventricular mass regression. Patients with impaired left ventricular function represent a critical population in whom prosthesis-patient mismatch should be avoided at the time of aortic valve replacement.

Aged↗
PubMed1994

Angiotensin as local modulating factor in ventricular dysfunction and failure due to coronary artery disease.

Congestive heart failure is the end product of a progressive series of events resulting from acute myocardial damage. Circulatory neurohormonal systems are activated during the acute phase of left ventricular dysfunction resulting from initial myocardial damage and again in the latter phase of decompensated heart failure. However, these neurohormonal mechanisms return to normal during the compensated stage of heart failure. Recent studies have suggested that autocrine/paracrine modulators of cardiovascular function are activated in the preclinical phase preceding the development of overt heart failure. The renin-angiotensin system in particular has been shown to modulate many of the chronic processes involved in the pathophysiology of cardiovascular disorders. Recent studies suggest that locally generated angiotensin II may contribute to the secondary structural changes seen in cardiovascular disorders, such as cardiac hypertrophy and remodelling, coronary artery disease, and atherosclerosis. Thus, inhibition of angiotensin formation with angiotensin converting enzyme (ACE) inhibitors, particularly at the tissue level, may provide valuable cardioprotective effects. Additional evidence points to the efficacy of ACE inhibitors in preventing the progression of asymptomatic left ventricular dysfunction to overt heart failure.

Angiotensin II↗
PubMed2006

Takotsubo-like left ventricular dysfunction in an HIV-infected patient.

Takotsubo cardiomyopathy (in Japanese language "takotsubo" is a fishing pot with a round bottom and a neck that is used for trapping octopuses) is a new syndrome, which is characterized by transient left ventricular dysfunction and by a typical left ventriculogram showing transient extensive akinesis of the apical and mid portions of the left ventricle with hypercontraction of the basal segment, from which this disease takes its name. Since 1990 sporadic cases of takotsubo cardiomyopathy were reported by Japanese authors, and only a few European reports are available. We report a case of takotsubo-like left ventricular dysfunction in an human immunodeficiency virus (HIV)-infected caucasian patient.

Adrenergic beta-Antagonists↗
PubMed1998

EndothelinB receptors in rabbit pulmonary resistance arteries: effect of left ventricular dysfunction.

The endothelin (ET) receptor that mediates vasoconstriction of the isolated rabbit pulmonary resistance artery was characterized using selective ET receptor agonists and antagonists. We also examined changes in ET-induced vasoconstriction brought about by left ventricular dysfunction using the rabbit coronary ligation model. The rank order of potency for contraction was sarafotoxin S6c (S6c) > ET-1 = ET-3, which is characteristic of an ETB-like receptor. The combined ETA/ETB receptor antagonist SB209670 (1 microM) antagonized responses to ET-1 and S6c with estimated pKb values of 6.8 +/- 0.2 and 7.8 +/- 0.2, respectively. BQ788 (1 microM) antagonized responses to S6c and ET-3 (but not ET-1) with estimated pKb values of 7.1 +/- 0.2 and 6.6 +/- 0.1, respectively. The ETA receptor antagonist FR139317 (1 microM), either alone or in combination with BQ788, did not inhibit responses to ET-1. The profile of the ET-1 response was not altered by left ventricular dysfunction. In control rabbits, the inhibitor of nitric oxide synthase N omega-nitro-L-arginine methyl ester (100 microM) had no significant effect on the potency of either ET-1 or S6c. In the coronary-ligated rabbits, however, it significantly increased the potency (10-15-fold) of both ET-1 and S6c. These results suggest that the ET receptor that mediates contraction in rabbit pulmonary resistance arteries has the characteristics of an ETB-like receptor. The responses to ET-1 are not altered by LVD but may be modified by increased release of nitric oxide.

Animals↗
PubMedDate not supplied

The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults.

OBJECTIVE: To evaluate the effect of echocardiographically determined left ventricular hypertrophy (LVH) on survival in comparison with number of stenosed vessels and left ventricular systolic dysfunction. DESIGN: Cohort study based on a consecutive sample from a hospital registry, with a mean follow-up of 5 years. SETTING: An inner-city public hospital in Chicago, Ill. PATIENTS: The study included 1089 consecutive black patients who underwent both coronary angiography and M-mode echocardiography as part of a diagnostic evaluation. RESULTS: Nonstenosed coronary arteries, single-vessel disease, and multivessel disease were found in 48%, 16%, and 36% of patients, respectively; LVH (left ventricular mass index > 131 g/m2 in men and > 100 g/m2 in women) was detected in 50% of patients. Hypertrophy without coexistent obstructive coronary disease was associated with a lower survival rate than that observed for single-vessel disease and was similar to multivessel disease. When LVH, number of diseases vessels, and left ventricular dysfunction were subjected to multivariate analysis, hypertrophy conferred a relative risk (RR) of 2.4 (95% confidence interval [CI], 1.7 to 3.2). By comparison, the presence of a single stenosed vessel did not increase the risk of death. Multivessel disease and ejection fraction less than 45% were associated with an RR of 1.6 (95% CI, 1.1 to 2.2) and 2.0 (95% CI, 1.4 to 2.7), respectively. Calculation of the attributable risk fraction demonstrated that for every 100 deaths in this cohort, LVH independently accounted for 37. The corresponding attributable risk fractions were 1%, 22%, and 9% for single-vessel disease, multivessel disease, and ventricular dysfunction, respectively. CONCLUSIONS: Left ventricular hypertrophy was associated with a greater RR and attributable risk than the traditional measures of coronary disease severity. The high prevalence and powerful risk of LVH make an important contribution to the adverse survival rates among black patients with heart disease and may account for much of the black-white differential.

Aged↗
PubMed2000

Evaluation of global and regional left ventricular function obtained by quantitative gated SPECT using 99mTc-tetrofosmin for left ventricular dysfunction.

OBJECTIVE: The quantitative gated SPECT (QGS) software is able to calculate LV volumes and visualize LV wall motion and perfusion throughout the cardiac cycle using an automatic edge detection algorithm of the left ventricle. We evaluated the reliability of global and regional LV function assessment derived from QGS by comparing it with the results from left ventriculo-cineangiography (LVG). PATIENTS: In 20 patients with left ventricular dysfunction who underwent ECG gated 99mTc-tetrofosmin SPECT, the end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (LVEF) were calculated. The QGS-assessed regional wall motion was determined using the cinematic display. RESULTS: QGS-derived EDV, ESV and LVEF correlated well with those by LVG (p<0.001 for each). There was a good correlation between wall motion score (WMS) derived from the QGS and the LVG (r=0.40, p<0.05). In some patients with extensive myocardial infarction, there was a discrepancy in the regional wall motion results between QGS and LVG. CONCLUSIONS: The ECG-gated SPECT using QGS is useful to evaluate global and regional LV functions in left ventricular dysfunction.

Adult↗
PubMed1998

Marked elevation of brain natriuretic peptide levels in pericardial fluid is closely associated with left ventricular dysfunction.

OBJECTIVES: The purpose of this study was to investigate whether atrial and brain natriuretic peptides (ANP and BNP, respectively) represent autocrine/paracrine factors and are accumulated in pericardial fluid. BACKGROUND: ANP and BNP, systemic hormones produced by the heart, have elevated circulating levels in patients with heart failure. Recent evidence suggests that the heart itself is one of the target organs for these peptides. METHODS: With an immunoreactive radiometric assay, we measured the concentrations of these peptides in plasma and pericardial fluid simultaneously in 28 patients during coronary artery bypass graft surgery. RESULTS: The pericardial levels of BNP were markedly elevated in patients with impaired left ventricular function. We investigated the correlation of ANP and BNP levels in plasma or pericardial fluid with left ventricular hemodynamic variables. None of the hemodynamic variables correlated with ANP levels in plasma or pericardial fluid. Both plasma and pericardial fluid levels of BNP were significantly related to left ventricular end-diastolic and systolic volume indexes (LVEDVI and LVESVI, respectively). In addition, BNP pericardial fluid levels had closer relations with LVEDVI (r = 0.679, p < 0.0001) and LVESVI (r = 0.686, p < 0.0001) than did BNP plasma levels (LVEDVI: r = 0.567, p = 0.0017; LVESVI: r = 0.607, p = 0.0010). BNP levels in pericardial fluid but not in plasma correlated with left ventricular end-diastolic pressure (r = 0.495, p = 0.0074). CONCLUSIONS: BNP levels in pericardial fluid served as more sensitive and accurate indicators of left ventricular dysfunction than did BNP levels in plasma. Thus, BNP may be secreted from the heart into the pericardial space in response to left ventricular dysfunction, and it may have a pathophysiologic role in heart failure as an autocrine/paracrine factor.

Aged↗
PubMed1988

Left ventricular dysfunction in excess of the size of infarction: a possible management strategy.

In this report we describe two patients whose left ventricular dysfunction was far in excess of infarct size as evidenced by ECG changes and the magnitude of creatine kinase release. Both patients demonstrated redistribution in myocardial beds remote from the infarct zone on delayed rest thallium 201 images and both had multivessel disease evident on coronary angiography. Both patients experienced relief of symptoms and improvement in regional and global left ventricular function after revascularization surgery. The possible mechanisms of left ventricular dysfunction in myocardial beds remote from the zone of infarction are discussed.

Adult↗
PubMed1993

Regional remodeling and nonuniform changes in diastolic function in patients with left ventricular dysfunction: modification by long-term enalapril treatment. The SOLVD Investigators.

OBJECTIVES: The purpose of the present study was to assess the process of late regional remodeling and the changes in regional diastolic function at the base and apex of the left ventricle in patients with chronic systolic dysfunction. BACKGROUND: Remodeling has been suggested to play an important role in the progression of left ventricular dysfunction and heart failure. However, the regional difference in the process of late remodeling and its relation to diastolic function remain unclear. METHODS: In 32 patients with previous myocardial infarction and left ventricular ejection fraction < or = 35%, left ventricular hemodynamic and angiographic data were studied before and 1 year after randomization to conventional therapy with placebo (n = 12) or enalapril, 10 mg twice daily (n = 20). Left ventricular regional wall dynamics were analyzed in the basal and apical regions by the area method. RESULTS: In the placebo group, left ventricular end-diastolic and end-systolic regional areas increased significantly over time at the base but were unchanged at the apex. At the base, the diastolic left ventricular pressure-regional area relation shifted rightward and the regional stiffness constant decreased (6.9 +/- 4.3 to 5.0 +/- 3.1 x 10(-3) mm-2, p < 0.05), indicating an increase in regional distensibility. At the apex, however, the diastolic pressure-regional area relation shifted upward slightly, and the regional stiffness constant increased from 11.5 +/- 4.4 to 14.4 +/- 5.6 x 10(-3) mm-2 (p = 0.08). The regional peak filling rate was maintained at the base but decreased at the apex (1,014 +/- 436 to 762 +/- 306 mm2/s, p < 0.05); further, the changes in regional peak filling rate during follow-up were inversely related to the changes in the regional stiffness constant (r = -0.78, p < 0.001) at the apex. In contrast, in the enalapril group, end-diastolic and end-systolic regional areas significantly decreased over time both at the base and at the apex. Diastolic pressure-regional area relations shifted leftward, but the regional stiffness constant and regional peak filling rate did not change significantly either at the base or at the apex. CONCLUSIONS: These findings suggest that in patients with severe systolic left ventricular dysfunction, there was a regional difference in the process of late remodeling between the base and apex of the left ventricle, which was associated with nonuniform changes in regional diastolic function in the placebo group. The data also suggest that the nonuniform progression of regional remodeling and diastolic dysfunction was prevented by long-term enalapril treatment.

Cardiac Catheterization↗
PubMed2006

Transient left ventricular dysfunction (tako-tsubo phenomenon): Findings and potential pathophysiological mechanisms.

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) is characterized by transient left ventricular apical ballooning associated with symptoms, electrocardiographic changes and minimal cardiac enzyme release in the absence of coronary artery disease. Initially described in Japan, TTP occurs worldwide, predominantly in women and frequently after emotional or physical stress. Symptoms include anginal chest pain, dyspnea and syncope. Electrocardiographic ST elevations may be present only for several hours, and are followed by negative T waves that persist for months. Arterial hypertension is found in up to 76% of TTP patients, hyperlipidemia in up to 57% and diabetes mellitus in up to 12%. Potential pathophysiological mechanisms for TTP include catecholamine-induced myocardial stunning or hyperkinesis of the basal left ventricular segments, coronary vasospasm, plaque rupture, myocarditis and genetic factors. TTP patients should be monitored similarly to myocardial infarction patients because organ failure, cardiogenic shock, ventricular fibrillation or rupture may occur. Beta-blockers are indicated, whereas catecholamines and nitrates should be avoided. The long-term prognosis is unknown.

Chest Pain↗
PubMed1987

Comparison of the acute hemodynamic response to intravenous nisoldipine (Bay k 5552) and intravenous nifedipine for left ventricular dysfunction secondary to myocardial infarction.

Dihydropyridine calcium blocking drugs exert potentially dangerous negative inotropic action in selected patients with severe left ventricular dysfunction. In 10 patients peripheral and central hemodynamic effects of nisoldipine were intraindividually compared with nifedipine using a sequential crossover protocol. The drugs were titrated to a similar steady-state reduction of mean arterial pressure by 15 +/- 3% and 15 +/- 2% and systemic vascular resistance by 25 +/- 5% and 17 +/- 2%, respectively. The equi-effective dosage was 0.17 +/- 0.06 microgram/min/kg for nisoldipine and 0.58 +/- 0.1 microgram/min/kg for nifedipine. In contrast to nifedipine, administration of nisoldipine was associated with increases in cardiac index of 0.45 +/- 0.33 liters/min/m2 (p less than 0.05), stroke volume index of 3.91 +/- 3.0 ml/m2 (p less than 0.05) and left ventricular ejection fraction of 4.6 +/- 2.8% (p less than 0.05). Mean pulmonary capillary wedge pressure decreased with nisoldipine from 11.8 +/- 3.4 to 8.0 +/- 3.4 mm Hg (p less than 0.005) and mean pulmonary arterial pressure from 20.4 +/- 4.06 to 16.1 +/- 3.2 mm Hg (p less than 0.005); these variables were unaffected by nifedipine. Thus, intraindividual comparison revealed no cardiodepressive action of nisoldipine, whereas with nifedipine the conceptually beneficial effect of afterload reduction appears to be offset by intrinsic negative inotropic action. Due to higher vasospecificity and more effective unloading, nisoldipine appears to be superior to nifedipine in patients with left ventricular dysfunction secondary to ischemic heart disease.

Aged↗
PubMed2001

Metabolic and structural abnormalities in dogs with early left ventricular dysfunction induced by incessant tachycardia.

OBJECTIVE: To assess morphologic and metabolic abnormalities in dogs with early left ventricular dysfunction (ELVD) induced by rapid right ventricular pacing (RRVP). ANIMALS: 7 Beagles. PROCEDURE: Plasma carnitine concentrations were measured before and after development of ELVD induced by RRVP. At the same times, transvenous endomyocardial biopsy was performed, and specimens were submitted for determination of myocardial carnitine concentrations and histologic, morphometric, and ultrastructural examination. RESULTS: In 4 dogs in which baseline plasma total carnitine concentration was normal, RRVP induced a decrease in myocardial total and free carnitine concentrations and an increase in myocardial esterified carnitine concentration. In 3 dogs in which baseline plasma total carnitine concentration was low, plasma and myocardial carnitine concentrations were unchanged after pacing. Structural changes associated with pacing included perinuclear vacuolization in 3 dogs. Morphometric analyses indicated there was a decrease in myofiber cross-sectional diameter and area following pacing. Electron microscopy revealed changes in myofibrils and mitochondria following pacing. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that moderate to severe alterations in myocyte cytoarchitecture are present in dogs with ELVD induced by RRVP and that in dogs with normal plasma carnitine concentrations, myocardial carnitine deficiency may be a biochemical marker of ELVD. Results also indicated that transvenous endomyocardial biopsy can be used to evaluate biochemical and structural myocardial changes in dogs with cardiac disease.

Animals↗
PubMed2003

Evaluation of outcome and cost-effectiveness using an FDG PET-guided approach to management of patients with coronary disease and severe left ventricular dysfunction (PARR-2): rationale, design, and methods.

Patients with severe ventricular dysfunction and coronary disease have high morbidity and mortality. They may benefit from revascularization but have significant perioperative morbidity and mortality. Positron emission tomography (PET) imaging with F-18-fluorodeoxyglucose (FDG) can detect viable myocardium that may recover from revascularization in such patients. It is unclear whether use of FDG PET in this population improves outcome or is cost-effective. The principal aim of this study is to determine whether FDG PET-guided therapy improves clinical outcome compared to standard care. Secondary objectives are to determine whether FDG PET-guided therapy improves left ventricular (LV) function, improves quality of life, and provides a cost benefit versus standard care. Included in this multicenter randomized controlled trial are patients with coronary artery disease and severe LV dysfunction who are referred for revascularization, heart failure, or cardiac transplantation or in whom FDG PET is potentially useful. Consenting subjects will be randomized to therapy directed by FDG PET or standard care. The primary outcome is the composite cardiovascular endpoint of cardiac death, myocardial infarction, transplantation, or rehospitalization for unstable angina or heart failure. Secondary outcomes include health-related quality of life, costs, mortality, cardiovascular events, and LV function. Assuming two-sided alpha=0.05, power=80%, a sample size of 206 patients per group is required to detect a 15% absolute difference in the primary outcome between PET-directed therapy compared to standard care. Analyses will be conducted on an intention-to-treat basis. To our knowledge, this is the first large trial to evaluate whether FDG PET-directed therapy is effective and provides a cost benefit in patients with severe LV dysfunction. If so, thousands of such patients can be risk-stratified to select who is likely to benefit from revascularization.

Cost-Benefit Analysis↗
PubMed2004

Furosemide and the progression of left ventricular dysfunction in experimental heart failure.

OBJECTIVES: We tested the hypothesis that furosemide accelerates the progression of left ventricular systolic dysfunction in a tachycardia-induced porcine model of heart failure. BACKGROUND: Furosemide activates the renin-angiotensin-aldosterone system in patients with congestive heart failure (CHF). Such activation may contribute to CHF progression, but prospective data are lacking. METHODS: Thirty-two Yorkshire pigs were randomized to furosemide (1 mg/kg intramuscularly daily, mean 16.1 +/- 0.9 mg) or placebo. Thereafter, a pacing model of heart failure was utilized to produce systolic dysfunction in both sets of animals (fractional shortening <0.16 by echocardiogram). The goal was to determine if furosemide would accelerate the progression of left ventricular dysfunction in the "treated" group. After sacrifice, sodium-calcium exchanger currents and their responsiveness to isoproterenol were measured during voltage clamp. All investigators were blinded to treatment assignment. RESULTS: Furosemide shortened the time to left ventricular dysfunction (35.1 +/- 5.1 days in placebo versus 21.4 +/- 3.2 days for furosemide animals; p = 0.038, log-rank test). By day 14, aldosterone levels were significantly higher in furosemide animals (43.0 +/- 11.8 ng/dl vs. 17.6 +/- 4.5 ng/dl; p < 0.05). Serum sodium was reduced (133.0 +/- 0.9 mmol/l furosemide vs. 135.7 +/- 0.8 mmol/l placebo; p < 0.05), but no difference in norepinephrine, potassium, magnesium, creatinine, or urea nitrogen was present. Basal sodium-calcium exchanger currents were significantly increased and isoproterenol responsiveness depressed by furosemide. CONCLUSIONS: Tachycardic pigs given furosemide had significant acceleration of both contractile and metabolic features of CHF, including left ventricular systolic dysfunction, elevated serum aldosterone levels, and altered calcium handling in a controlled experimental model of heart failure.

Adrenergic beta-Agonists↗
PubMed1985

Left ventricular dysfunction after non-cardiac surgical procedures in patients with ischemic heart disease.

In order to demonstrate the presence of postischemic ventricular dysfunction after non-cardiac surgical procedures, myocardial perfusion scintigraphy with thallium 201 and radionuclide ventriculography were performed before and 24 h after intervention in 20 patients suffering from angina pectoris. A long-term ECG recording was used in all patients to detect peroperative myocardial ischemia. In 14 of the 20 patients studied, both ventriculography and thallium scintigraphy were unchanged at the postoperative study. Comparison of pre- and postoperative radionuclide data revealed an increased deficit in one patient, both increased deficit and decreased ejection fraction in four others and a decreased ejection fraction in one other. In these five last patients, continuous ECG recording demonstrated the occurrence of peroperative ST segment depression. These results underline the part played by prolonged peroperative episodes of myocardial ischemia in the occurrence of postoperative left ventricular dysfunction.

Adult↗
PubMed1993

Spectrum of right heart involvement in patients with ventricular tachycardia unrelated to coronary artery disease or left ventricular dysfunction.

We studied 41 patients with clinically symptomatic ventricular tachycardia in the absence of coronary artery disease or left ventricular dysfunction to define the extent of right and left heart derangement and their relation to electrophysiologic and clinical data. Individual echocardiographic measurements as well as global assessment scores of the right and left heart demonstrated a wide spectrum of right heart echocardiographic abnormalities. There was much less variation in the left heart, with the majority of patients being close to normal. There was an association between the right heart score, the clinical presentation of arrhythmia, the response to programmed electrical stimulation, and the recurrence of arrhythmia (p < 0.05). Thus echocardiographic findings demonstrate the whole spectrum of right heart involvement in patients with apparent idiopathic ventricular tachycardia and can give insight into clinical history, arrhythmia inducibility, and prognosis.

Adolescent↗
PubMed2000

N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction.

We examined whether pharmacological inhibition of glycogenolysis by N-methyl-1-deoxynojirimycin (MOR-14), a new compound which reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase activity of the glycogen-debranching enzyme, can protect the heart against postischemic left ventricular dysfunction. The hearts of male Sprague-Dawley rats were excised, and perfused on a Langendorff apparatus with Krebs-Henseleit solution with a gas mixture of 95% O2 and 5% CO2. The hearts were paced at 320 beats/min except during the ischemia. Left ventricular developed pressure (LVDP, mmHg), +/-dP/dt (mmHg/s), and coronary flow (ml/min) were continuously monitored. All hearts were perfused for a total of 120 min including a 30-min preischemic period followed by a 30-min episode of global ischemia and 60 min reperfusion. with or without 0.5 or 2 mM of MOR-14 during the 30-min preischemic period or the first 30 min of reperfusion. In another series of experiments, the myocardial content of glycogen and lactate was measured during the 30-min episode of ischemia in groups treated with and without 2mM of MOR-14. Preischemic but not postischemic treatment with MOR-14 significantly improved LVDP and +/-dP/dt without altering coronary flow during reperfusion in a dose-dependent manner. MOR-14 significantly preserved the glycogen content and significantly attenuated the lactate accumulation during the 30-min episode of ischemia. Preischemic treatment with MOR-14 is protective against postischemic left ventricular dysfunction through the inhibition of glycogenolysis in the isolated rat heart.

1-Deoxynojirimycin↗
PubMedDate not supplied

Possibilities of predicting results after surgical correction of ischemic mitral regurgitation on the basis of the degree of left ventricular dysfunction.

Results of surgical treatment for ischemic mitral regurgitation were retrospectively analyzed in 209 patients. All patients underwent myocardial revascularisation as well as mitral valve surgery. Preoperative myocardial infarction was registered in 75% of cases. These patients had different degrees of left ventricular dysfunction. Postoperative 30-day mortality was 4.3% for the whole group but higher in patients with lower ejection fraction. Looking at preoperative values of ejection fraction (EF), long term follow-up of 75 months, there is a statistically significant differences in survival rate (p < 0.05), freedom from cardiac decompensation (p < 0.05), and other complications (p < 0.001), but only comparing two subgroups of patients, those with preoperatively ejection fraction lower and higher than 20%. Early postoperative, and especially long term results, are better in patients with higher ejection fraction. According to our experience, it is possible to predict the results after surgery for ischemic mitral regurgitation, depending on the degree of preoperative left ventricular dysfunction.

Adult↗