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PubMed2003

Effects of glucose-insulin-potassium infusion on chronic ischaemic left ventricular dysfunction.

BACKGROUND: Glucose-insulin-potassium (GIK) infusion improves cardiac function and outcome during acute ischaemia. OBJECTIVE: To determine whether GIK infusion benefits patients with chronic ischaemic left ventricular dysfunction, and if so whether this is related to the presence and nature of viable myocardium. METHODS: 30 patients with chronic ischaemic left ventricular dysfunction had dobutamine echocardiography and were given a four hour infusion of GIK. Segmental responses were quantified by improvement in wall motion score index (WMSI) and peak systolic velocity using tissue Doppler. Global responses were assessed by left ventricular volume and ejection fraction, measured using a three dimensional reconstruction. Myocardial perfusion was determined in 15 patients using contrast echocardiography. RESULTS: WMSI (mean (SD)) improved with dobutamine (from 1.8 (0.4) to 1.6 (0.4), p < 0.001) and with GIK (from 1.8 (0.4) to 1.7 (0.4), p < 0.001); there was a similar increment for both. Improvement in wall motion score with GIK was observed in 55% of the 62 segments classed as viable by dobutamine echocardiography, and in 5% of 162 classed as non-viable. There was an increment in peak systolic velocity after both dobutamine echocardiography (from 2.5 (1.8) to 3.2 (2.2) cm/s, p < 0.01) and GIK (from 3.0 (1.6) to 3.5 (1.7) cm/s, p < 0.001). The GIK effects were not mediated by changes in pulse, mean arterial pressure, lactate, or catecholamines, nor did they correlate with myocardial perfusion. End systolic volume improved after GIK (p = 0.03), but only in 25 patients who had viable myocardium on dobutamine echocardiography. CONCLUSIONS: In patients with viable myocardium and chronic left ventricular dysfunction, GIK improves wall motion score, myocardial velocity, and end systolic volume, independent of effects on haemodynamics or catecholamines. The response to GIK is observed in areas of normal and abnormal perfusion assessed by contrast echocardiography.

Aged↗

PubMed2004

New positive inotropic agents in the treatment of left ventricular dysfunction.

Three major classes of inotropic agents have been clinically evaluated in patients with left ventricular dysfunction: a) agents that increase the intracellular concentration of cyclic adenosine monophosphate by stimulating the beta-adrenergic receptor or inhibiting phosphodiesterase; b) drugs that increase the intracellular sodium concentration; c) the new calcium-sensitizing drugs. This review will focus on the newest drug for each of the above-mentioned classes of inotropic agents. Moreover, we present a new protocol which provides the use of levosimendan in patients with post-ischemic left ventricular dysfunction.

Cardiotonic Agents↗

PubMed1993

Reversible left ventricular dysfunction with coronary stenotic or obstructive lesions in Kawasaki disease.

BACKGROUND: Few studies have been reported on the prognosis or reversibility of ischemic myocardial lesions in Kawasaki disease. In this study, the pathophysiologic causes of reversible left ventricular dysfunction were evaluated in seven children with severe stenotic coronary lesions caused by Kawasaki disease. METHODS: The clinical process and the changes of coronary lesions in the repeated angiography were retrospectively evaluated in seven children. The ages of the seven patients (six boys and one girl) ranged from 7 to 15 years (mean, 10.4 +/- 2.6 y); the duration from the onset of Kawasaki disease to the last angiographic study ranged from 6 to 15 years (mean, 9.6 +/- 3.0 y). RESULTS: During the acute stage, an acute myocardial infarction was detected clinically in two patients, transient ST depression in two, and deep Q waves without any symptoms in the remaining three patients. In the first angiographic study (2 mo to 6 y after the onset of Kawasaki disease), significant left ventricular dysfunction was observed in the posterior or inferior wall in all patients. In the right coronary arteries, giant aneurysms (> or = 8 mm in diameter) were angiographically detected in two patients, localized stenosis (> or = 95%) in one, and recanalization in four. In a recent angiographic study, the left ventricular dysfunction had normalized in all seven patients. Recanalization was observed, even in two patients with giant aneurysms and in one with localized stenosis. Collateral circulation was detected in five patients in this study. Abnormal deep Q waves on ECG were detected in only one patient, and no abnormal findings on ECG were seen in the remaining six. Upon 201TI myocardial scintigraphy, no reduction of 201TI uptake was observed in any of the seven patients at the site of the abnormal wall motion on the first angiography. CONCLUSIONS: The regional left ventricular dysfunction in the seven patients may have been induced by severe acute ischemia due to a transient right coronary obstruction or by severe chronic ischemia due to coronary lesions. Eventually, left ventricular wall motion normalized after an improvement in the blood flow supply as a result of early recanalization and development of collateral circulation.

Adolescent↗

PubMed2003

Enalapril reduces the incidence of diabetes in patients with chronic heart failure: insight from the Studies Of Left Ventricular Dysfunction (SOLVD).

BACKGROUND: Diabetes mellitus is a predictor of morbidity and mortality in patients with heart failure. The effect of angiotensin-converting enzyme (ACE) inhibitors on the prevention of diabetes in patients with left ventricular dysfunction is unknown. The aim of this retrospective study was to assess the effect of the ACE inhibitor enalapril on the incidence of diabetes in the group of patients from the Montreal Heart Institute enrolled in the Studies of Left Ventricular Dysfunction (SOLVD). METHODS AND RESULTS: Clinical charts were evaluated for fasting plasma glucose (FPG) levels by blinded reviewers. A diagnosis of diabetes was made when a FPG > or =126 mg/dL (7 mmol/L) was found at 2 visits (follow-up, 2.9+/-1.0 years). Of the 391 patients enrolled at the Montreal Heart Institute, 291 were not diabetic (FPG <126 mg/dL without a history of diabetes), 153 of these were on enalapril and 138 were on placebo. Baseline characteristics were similar in the 2 groups. Forty patients developed diabetes during follow-up, 9 (5.9%) in the enalapril group and 31 (22.4%) in the placebo group (P<0.0001). By multivariate analysis, enalapril remained the most powerful predictor for risk reduction of developing diabetes (hazard ratio, 0.22; 95% confidence intervals, 0.10 to 0.46; P<0.0001). The effect of enalapril was striking in the subgroup of patients with impaired FPG (110 mg/dL [6.1 mmol/L] < or =FPG <126 mg/dL) at baseline: 1 patient (3.3%) in the enalapril group versus 12 (48.0%) in the placebo group developed diabetes (P<0.0001). CONCLUSIONS: Enalapril significantly reduces the incidence of diabetes in patients with left ventricular dysfunction, especially those with impaired FPG.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2000

[Chronic ischemic left ventricular dysfunction: myocardial hibernation?].

Hibernating myocardium is a term which covers chronic ischaemic left ventricular dysfunction which is potentially reversible after revascularisation. Hibernating myocardium is classically associated with chronic hypoperfusion responsible for hypocontraction and cellular degeneration. This "classical" conception has been questioned as some workers emphasise that the reduction in coronary reserve responsible for repeated episodes of ischaemia and stunning could be the main causes of myocardial dysfunction. Position emission tomography (PET), and, most of all, myocardial scintigraphy and dobutamine echocardiography are the most commonly used techniques for detecting hibernating myocardium. Their sensitivity is good but the specificity and positive predictive value of dobutamine echocardiography seems to be better than the isotopic techniques. Structural abnormalities of hibernating myocardium and the delay, which is often long, between revascularisation and improvement, may explain some of the discordances between these techniques. Irrespective of the term used, hibernation or chronic ischaemic left ventricular dysfunction with myocardial viability, the reported data is in favour of coronary revascularisation with improved long-term quality of life and reduced mortality in patients with positive viability tests.

Cardiotonic Agents↗

PubMed1986

Relation between left ventricular diastolic function and exercise tolerance in patients with left ventricular dysfunction.

Previous studies show no correlation between resting systolic left ventricular performance assessed as the ejection fraction and exercise tolerance. This study examined the relation between left ventricular diastolic performance and exercise tolerance in 63 patients with left ventricular dysfunction (ejection fraction less than 50%) due to known or suspected coronary artery disease. The 51 men and 12 women, aged 54 +/- 8 years (mean +/- standard deviation), underwent symptom-limited upright exercise testing on a bicycle ergometer. The exercise end-points were angina (n:5), dyspnea (n:16), and fatigue (n:42). The patients were divided into three groups: group 1 (n:28) with normal exercise tolerance (9.5 +/- 2.4 minutes), group 2 (n:18) with mild exercise intolerance (5.8 +/- 0.5 minutes), and group 3 (n:17) had severe exercise intolerance (3.7 +/- 0.9 minutes). The three groups did not differ in age, ejection fraction, end-diastolic volume, exercise end-point, exercise heart rate, and left ventricular peak filling rate at rest. The exercise peak filling rate was, however, significantly higher in group 1 (p = 0.03). Stepwise multivariate discriminant analysis of important variables identified the exercise peak filling rate as the only predictor of exercise tolerance (F = 6.0). Thus, variation in exercise peak filling rate may in part explain the variability of exercise tolerance in patients with left ventricular dysfunction; patients with preserved exercise capacity have higher exercise peak filling rate than those with exercise intolerance.

Adult↗

PubMed1994

Identification and revascularization of hibernating myocardium in angina-free patients with left ventricular dysfunction.

We examined 17 angina-free patients with left ventricular dysfunction, referred for surgical decision-making, who presented with no or few signs and symptoms of myocardial ischemia according to treadmill stress test. On cardiac catheterization they were affected by severe multi-vessel coronary artery disease; the mean left end-diastolic pressure of this population was 26.3 +/- 5.5 mm Hg (mean +/- SD) and their mean ejection fraction was 27.6 +/- 4.9% (mean +/- SD). They all were investigated for the presence of viable myocardium by the combined assessment of cardiac perfusion and metabolism using single photon emission tomography with [99mTc] labelled hexakis-2-methoxy-isobutyl-isonitrile [99mTc]MIBI/SPET) and positron emission tomography with [18F]-2-fluoro-2-deoxy-D-glucose ([18F]FDG/PET), respectively. Patients were considered for coronary surgery when [18F]FDG was detectable in at least two cardiac segments with wall motion abnormalities and perfusion defects. Nine patients were operated on, six were medically treated and two were scheduled for heart transplantation. We recorded no in-hospital mortality. At a mean follow-up of 28.4 +/- 9.8 (mean +/- SD) months all surgical patients were alive and their NYHA functional classes have improved, except in one case. Among the patients refused for bypass surgery, three are in stable conditions, three have worsened clinical statuses and two died while waiting for heart transplantation. In conclusion, for patients with bypassable coronaries, left ventricular dysfunction and lack of angina, successful coronary revascularization may be predicted by the presence of viable myocardium demonstrated with positron emission tomography.

Adult↗

PubMed1994

Molecular and physiological alterations in murine ventricular dysfunction.

The present study reports the development and characterization of a murine model of right ventricular dysfunction following graded constriction in the pulmonary artery via microsurgical approaches. To analyze in vivo ventricular function, a technique of x-ray contrast microangiography was developed to allow the quantitative analysis of ventricular volumes and of ejection fraction in normal and pressure-overloaded right ventricle. Severe, chronic pulmonary arterial banding for 14 days resulted in right ventricular dilatation and dysfunction, associated with right atrial enlargement, and angiographic evidence of tricuspid regurgitation. These effects were dependent on the extent of hemodynamic overload, since more moderate pulmonary arterial constriction resulted in hypertrophy with maintenance of right ventricular function. With severe pulmonary artery constriction, the murine right ventricle displays a failing heart phenotype including chamber dilation with reduced function that resembles right ventricular dysfunction in man during chronic pulmonary arterial hypertension. Northern and immunoblot analyses demonstrate a marked down-regulation of phospholamban mRNA and its corresponding protein with both levels of constriction, while a less pronounced but significant depression of sarcoplasmic reticulum Ca(2+)-ATPase protein was observed with severe overload, suggesting that this pattern is an early genetic marker of ventricular dysfunction. By coupling mouse genetics with this murine model and the ability to assess cardiac function in vivo, one should be able to test the role of the down-regulation of phospholamban and other defined alterations in the cardiac muscle gene program in the onset of the failing heart phenotype.

Adenosine Triphosphatases↗

PubMed2006

Daily dialyses decrease plasma levels of brain natriuretic peptide (BNP), a biomarker of left ventricular dysfunction.

Brain natriuretic peptide or B-type natriuretic peptide (BNP) is a sensitive marker of heart disease. Plasma levels of BNP increase in left ventricular failure and determination of plasma BNP has become a useful tool in the diagnosis of heart failure. Hemodialysis (HD) patients may have elevated plasma levels of BNP, particularly predialysis, that correlate with echocardiographic signs of left ventricular dysfunction. High BNP levels are also a strong predictor of mortality in both nonrenal and HD patients. We studied plasma BNP levels in patients who changed from conventional thrice-weekly dialysis to daily dialysis 6 times a week while maintaining a total weekly time on dialysis of 12 hr. Twelve HD patients, mean age 55 years, had 4 hr of conventional thrice-weekly treatment for 4 weeks. Predialysis and postdialysis blood samples were obtained at the last dialysis. Patients were then dialyzed for 2 hr, 6 times weekly, for 4 weeks (daily dialysis). Again, predialysis and postdialysis blood samples were collected at the last HD. Brain natriuretic peptide plasma concentrations were determined by immunoradiometric assay. Predialysis BNP levels decreased from 194+/-51 ng/L (68+/-19 pmol/L; mean+SE) during thrice-weekly HD to 113+/-45 ng/L (41+/-18 pmol/L; p = 0.001) after 4 weeks on daily dialysis. With thrice-weekly HD, predialysis BNP levels were higher than postdialysis levels: 120+/-26 ng/L (39+/-8 pmol/L; p = 0.059). With daily dialysis, predialysis BNP levels did not differ significantly from postdialysis levels. Elevated predialysis plasma levels of BNP, considered sensitive and early markers of left ventricular dysfunction, decreased when patients were changed from conventional thrice-weekly HD to daily dialysis maintaining total hours of dialysis per week constant. Given the accumulated evidence that BNP is a biomarker of left ventricular dysfunction and can be used for risk stratification and guidance in pharmacotherapy of heart failure, daily dialysis appears to lead to less cardiac distress.

Adult↗

PubMed2001

Early neurohormonal effects of trandolapril in patients with left ventricular dysfunction and a recent acute myocardial infarction: a double-blind, randomized, placebo-controlled multicentre study.

Angiotensin-converting enzyme inhibitors improve long-term survival in patients with left ventricular dysfunction after a myocardial infarction, but their mechanism of action is not entirely clear. The neurohormonal effects may be important in this respect, as well as an early hemodynamic unloading induced by these drugs. The primary objective was to assess the effect of trandolapril on plasma levels of atrial natriuretic peptide. A secondary objective was to assess the effects of trandolapril on selected neurohormones, vasoactive peptides and enzymes, which may be important in the development of left ventricular remodeling and heart failure following an acute myocardial infarction. A total of 119 patients with an acute myocardial infarction and a wall motion index < or =1.2 (16-segment echocardiographic model) were randomized to double blind treatment with trandolapril or placebo within 3-7 days after the onset of infarction. Blind treatment was discontinued 21 days after the index infarction. Venous blood samples were collected at rest, before randomization and on the day after treatment was discontinued. At the end of the study, there were no differences in plasma levels of atrial natriuretic peptide between the two treatment groups. Angiotensin-converting enzyme activity was suppressed and plasma renin activity was higher in the trandolapril group. No differences in plasma levels of N-terminal pro-atrial natriuretic peptide, brain natriuretic peptide, aldosterone, noradrenaline, adrenaline, vasopressin, big endothelin-1 and neuropeptide Y were found between the two treatment groups. There were positive correlations between several markers of neurohormonal activation at baseline and variables expressing left ventricular dysfunction and clinical heart failure. Neurohormonal activation is related to left ventricular dysfunction. The effects of 2-3 weeks of angiotensin-converting enzyme inhibition on neurohormonal activation does not predict the already established beneficial long-term effects after myocardial infarction. Thus, early modulation of circulatory neurohormone levels may not be a major mechanism for the efficacy of angiotensin-converting enzyme inhibitors in these patients. Selected plasma hormone markers may still be used to identify patients who might get the greatest benefit from treatment.

Aged↗

PubMed1999

Dosing of ACE inhibitors in left ventricular dysfunction: does current clinical dosing provide optimal benefit?

In the present review, we discuss the role of clinical dosing of angiotensin converting enzyme (ACE) inhibitors in the treatment of left ventricular dysfunction. Although the precise mechanism of action of ACE inhibitors is still unresolved, the clinical efficacy of ACE inhibitors in the treatment of left ventricular dysfunction is well established. However, it is unclear whether the doses used in clinical trials translate directly into daily practice. Several reasons may cause differences between clinical practice and controlled trials: (1) clinical trials used higher doses than in normal practice; (2) some patients may be relatively 'resistant' to ACE inhibition; and/or (3) ACE activity increases during ACE inhibitor therapy and may provide escape mechanisms when the drug regimen is not strictly adhered to. Therefore, it is of interest that recent trials suggest that only the higher doses of ACE inhibition are clinically efficacious. In conclusion, it is suggested that optimal benefit from treatment with an ACE inhibitor in patients with left ventricular dysfunction requires sufficient and frequent dosing of the ACE inhibitor, e.g., enalapril 10 mg twice daily or captopril 25 mg three times daily.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1996

[Relationship between exercise induced ischemia and left ventricular dysfunction; simultaneous assessment of perfusion and function images with 99mTc-tetrofosmin myocardial scintigraphy].

The purpose of this study was to evaluate the relationship between exercise induced ischemia and left ventricular dysfunction, ergometer exercise 99mTc-tetrofosmin myocardial scintigraphy was performed using one day protocol (exercise/rest). Subjects consisted of 68 patients without previous myocardial infarction; without coronary artery disease (CAD) (n = 36) and with CAD (n = 32). Perfusion and function images were evaluated simultaneously. Perfusion image was taken by single photon emission tomography (SPECT). Quantitative analysis was performed with normal data-base. The area of abnormal perfusion, less than normal lower limits, was named as extent score (ES). Left ventricular ejection fraction (LVEF) was measured by first-pass study. According to ES on stress image, 32 patients with CAD were divided into 3 groups; ES < 10% (n = 15), ES = 10-20% (n = 7) and ES > 20% (n = 10). LVEF at rest among 4 groups were not different. LVEF at peak exercise was 61.7+/ -5.3% in CAD (-), 59.0 +/- 5.8% in ES < 10%, 57.4 +/- 6.6% in ES = 10-20% and 47.4 +/- 10.5% in ES > 20%. LVEF in ES > 20% at peak exercise was lowest significantly. Thus, simultaneous perfusion and function images were evaluated for the relationship between exercise induced ischemia and left ventricular dysfunction. If extent score on stress image was more than 20% of left ventricle, significant left ventricular dysfunction was observed.

Aged↗

PubMed1996

Comparison of dobutamine echocardiography and positron emission tomography in patients with chronic ischemic left ventricular dysfunction.

OBJECTIVES: The aim of this study was to correlate dobutamine-induced contractile reserve as detected by echocardiography with findings on positron emission tomography in patients with chronic ischemic left ventricular dysfunction. BACKGROUND: Contractile reserve induced by low dose dobutamine infusion has been proposed as a marker of myocardial viability. METHODS: Sixty patients with stable coronary artery disease and left ventricular dysfunction (mean ejection fraction [+/- SD] 29 +/- 10%) underwent transthoracic echocardiography with dobutamine infusion (up to 10 micrograms/kg body weight per min) and positron emission tomography with nitrogen-13 ammonia and fluorine-18 (F-18) fluorodeoxyglucose as a perfusion and a metabolic tracer, respectively. Regional wall motion, perfusion and metabolism were analyzed semiquantitatively by using a 16-segment model. Segments with F-18 fluorodeoxyglucose uptake > 50% were considered viable on positron emission tomography. RESULTS: After dobutamine infusion, hemodynamic variables changed significantly, and myocardial ischemia was evident in 17 patients. All 60 patients had dysfunctional myocardium considered viable on positron emission tomography (8 +/- 4 segments/patient), whereas 52 patients had dysfunctional myocardium with contractile enhancement by dobutamine echocardiography (4 +/- 2 segments/patient, p = 0.01). The extent of dysfunctional myocardium with contractile reserve appeared to correlate less closely with the total extent of viable dysfunctional myocardium identified by positron emission tomography than with the number of such segments associated with a pattern of perfusion-metabolism mismatch. CONCLUSIONS: In patients with chronic ischemic left ventricular dysfunction, echocardiography can be used to identify enhancement in the contractile function of viable dysfunctional myocardium after infusion of low dose dobutamine. In this study, the presence and extent of such enhancement were relatively less than the values obtained from positron emission tomography.

Coronary Disease↗

PubMed1993

Resting thallium-201 scintigraphy for identifying viable myocardium in a patient with severe left ventricular dysfunction.

Recognizing patients with coronary artery disease in whom severe left ventricular dysfunction is attributed to a chronic decrease in myocardial blood flow without infarction is often difficult but important because such patients may benefit from surgical revascularization. Herein we describe a patient with severe left ventricular dysfunction who had appreciable resting wall motion abnormalities; tomographic thallium-201 myocardial scintigraphy performed while the patient was resting identified viable myocardium. Subsequent revascularization improved regional and global left ventricular function considerably.

Aged↗

PubMed1998

Relative usefulness of measures of heart rate variability and neuroendocrine activity as indicators of autonomic nervous abnormality in patients with left ventricular dysfunction.

The aim of the study was to assess the relationship between changes in heart rate variability (HRV) and parameters of neuroendocrine activation in patients with various levels of left ventricular dysfunction. Measurements of HRV, plasma norepinephrine (PNE), and plasma atrial natriuretic peptide (ANP) were performed in 17 age- and gender-matched control subjects (group C) and in 39 patients with ischemic heart disease or cardiomyopathy who were subdivided into 3 equal groups according to their left ventricular ejection fraction: group N (normal); group M (mildly impaired); and group S (severely impaired). Spectral analysis of HRV (from 10-min electrocardiograms) was analyzed by the method of coarse-graining spectral analysis. PNE and ANP were significantly elevated in group S only (p<0.05). Log low-frequency power and log total power for group M were significantly lower than for group N (p<0.05). Log high-frequency power was significantly lower for group M than for group C (p<0.05). Thus, assessment of changes in HRV, which were observed earlier in the progress of left ventricular dysfunction than changes in neuroendocrine factors, may be a useful non-invasive method for the early detection of autonomic abnormality in patients with left ventricular dysfunction.

Aged↗

PubMed1991

Studies of left ventricular dysfunction following myocardial infarction.

Early treatment of patients with myocardial infarction and left ventricular dysfunction was performed in 90 patients aiming at influencing left ventricular remodelling. After twelve months of treatment with 25 mg captopril t.i.d. left ventricular ejection fraction was improved by 10% in comparison to a treatment with 40 mg of frusemide or placebo (p = 0.001). Late treatment of the patients not treated with captopril resulted in partial reversal of left ventricular dilatation, while withdrawal of captopril therapy in stable patients with ejection fractions over 30% and without clinical signs of congestive heart failure did not result in deterioration of left ventricular function. These results give a sound rationale for the earlier use of ACE-inhibitors in the treatment of congestive heart failure and left ventricular dysfunction.

Captopril↗

PubMed2005

Accuracy of B-type natriuretic peptide levels in the diagnosis of left ventricular dysfunction and heart failure: a systematic review.

OBJECTIVES: To evaluate the accuracy of B-type natriuretic peptide levels (BNP) in the diagnosis of heart failure and left ventricular dysfunction. DATA SOURCES: Electronic search in Medline, Embase, Cochrane Library and Medion database, and hand search of reference lists. REVIEW METHODS: We have included published studies on the accuracy of BNP which had both sufficient information to construct the 2x2 diagnostic cross table and an appropriate spectrum of patients. RESULTS: Fifty five studies (16,730 patients) were analyzed. The main determinants of diagnostic accuracy were the reference standard analyzed (clinical heart failure versus left ventricular dysfunction), and the methodological quality of the study. BNP levels were highly accurate for the diagnosis of clinical heart failure (diagnostic OR=41; 95% CI 23-74). The negative likelihood ratios were homogeneous, and useful for excluding the existence of heart failure (pooled negative likelihood ratio=0.11; 95% CI 0.08-0.16). The studies focused on the identification of left ventricular dysfunction were heterogeneous, with indications of publication bias, and showed less overall diagnostic accuracy than studies focused on heart failure. CONCLUSIONS: BNP levels are useful for ruling out heart failure. The accuracy of BNP for identifying patients with systolic dysfunction is more limited.

Cardiac Output, Low↗

PubMed1991

Ventricular dysfunction does occur during liver transplantation.

Ventricular dysfunction, then, does indeed occur during liver transplantation, particularly at the time of reperfusion. Pulmonary embolism contributes to right ventricular and right atrial encroachment on left-heart filling, and paradoxical embolism may occur. Pericardial effusions, tricuspid regurgitation, hypothermia, and the release of substances, particularly potassium from the donor liver, may further contribute to compromises in ventricular function. Proper monitoring and appropriate treatment, however, lead to successful operative outcomes in most cases.

Heart Arrest↗