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PubMed2002

Simultaneous angiotensin converting enzyme inhibition moderates ventricular dysfunction caused by doxorubicin.

AIMS: The purpose of this study was to determine that the administration of an angiotensin converting enzyme (ACE) inhibitor enalapril would confer protection against doxorubicin-induced experimental heart failure, and attenuate the development of left ventricular dysfunction. METHODS: Seventeen dogs were chronically instrumented with an intracoronary catheter and received doxorubicin weekly for 4 weeks. Animals were assigned to two groups: group 1: untreated heart failure; and group 2: simultaneous enalapril administration (5 mg twice a week). Hemodynamic data were obtained at week 0 and 12. Echocardiography was performed weekly. RESULTS: Survival improved with simultaneous enalapril administration (36% in group 1 vs. 100% in group 2, P=0.04). The increase in the left ventricular end-diastolic pressure was significantly reduced at week 12 (17+/-1 mmHg in group 1 vs. 9+/-1 mmHg in group 2, P=0.0042). The fall in left ventricular stroke work index was significantly prevented (52% in group 1 vs. 21% in group 2, P=0.006). The increase in right ventricular end-diastolic diameter was significantly reduced by enalapril prophylaxis. CONCLUSION: Simultaneous treatment with enalapril was beneficial in the prevention of doxorubicin-induced cardiomyopathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Left ventricular dysfunction in human immunodeficiency virus (HIV)-infected patients.

We evaluated left ventricular function by echocardiography in a prospective study that included 98 consecutive human immunodeficiency virus (HIV)-infected patients and 40 HIV-seronegative normal controls. When compared with controls, HIV patients showed increased isovolumic relaxation time (101+/-18 ms versus 71+/-10 ms; p<0.0001) and left ventricular diastolic diameters (51+/-6 mm versus 47+/-3 mm; p<0.0005), and decreased fractional shortening (31+/-6% versus 37+/-2%; p<0.0001). Diastolic dysfunction was the most frequent finding (63% of the patients). We found depressed ejection fraction in 31 (32%) patients. Only 8 (8%) patients had symptomatic congestive heart failure. Left ventricular dysfunction was not attributable to intravenous drug abuse or to therapy. It was less severe in earlier stages of the infection (fractional shortening: acquired immunodeficiency syndrome=30%+/-6%, asymptomatic HIV-seropositives 34%+/-5%; p<0.005) and in HIV-2-infected patients. Patients with opportunistic infections (all aetiologies mixed) had more frequent congestive heart failure than those without infections (16% of the patients with versus 4% of the patients without infections; p<0.05). The fact that even asymptomatic HIV-seropositives had signs of left ventricular dysfunction (fractional shortening: asymptomatic HIV-seropositives=34%+/-5%; controls=37%+/-2%; p<0.05) favours the hypothesis of the HIV being one of the causes of these abnormalities.

AIDS-Related Opportunistic Infections↗
PubMed1999

[Importance of respiration for non-invasive assessment of cardiac autonomic control in patients with ischemic left ventricular dysfunction].

UNLABELLED: Respiratory rate is an important factor influencing heart rate variability (HRV), but is usually ignored in the studies in patients with ischaemic heart disease (IHD). This factor may significantly contribute to the changes in HRV in ischaemic left ventricular impairment. We examined 186 patients with IHD (46 females, 140 males), including 54 pts with left ventricular ejection fraction < 40% and 132 pts with preserved LVEF (> or = 40%). HRV was evaluated in supine and standing position from short-term ECG (512 beats, 1 kHz, 12 bit) in time- (mean RR interval--RRI, and standard deviation of RRI-SD-RR) and frequency-domain (FFT). Power spectral density of high and low frequency (HF 0.14-0.5 and LF 0.04-0.15 Hz) was estimated and expressed as log-values. The frequency of respiration (fResp, Hz) was defined as the frequency of maximum HF power. RESULTS: Patients with LVEF < 40% had shorter RRI in supine (879 + 157 vs 942 +/- 147 ms, p < 0.05), but similar in standing. FResp was greater both in supine (0.308 +/- 0.05 vs 0.274 +/- 0.047 Hz) and in standing (0.329 +/- 0.055 vs 0.274 +/- 0.047, all p < 0.001) in low, as compared to preserved LVEF. As expected, HRV parameters were more reduced in LVEF < 40%. The differences of raw values were as follows: SD-RR 29 +/- 16 vs 34 +/- 15 i 27 +/- 13 vs 31 +/- 12 ms, both p < 0.05, HF 3.21 +/- 0.36 vs 3.33 +/- 0.32, p < 0.05 and 3.19 +/- 0.32 vs 3.21 +/- 0.29 p > 0.1, LF 3.41 +/- 0.33 vs 31.49 +/- 0.30 and 3.52 +/- 0.30 vs 3.61 +/- 0.32, p < 0.05, ANOVA). The differences were observed despite adjustment for age, sex and RRI. When fResp was added as covariate they became not significant. CONCLUSION: Patients with left ventricular dysfunction had faster rate of respiration. This finding may explain, in part, reduced HRV in these patients. The rate of respiration should be taken into account for correct interpretation of HRV analysis.

Autonomic Nervous System↗
PubMed1997

Accuracy of currently available techniques for prediction of functional recovery after revascularization in patients with left ventricular dysfunction due to chronic coronary artery disease: comparison of pooled data.

OBJECTIVES: This study evaluated the relative merits of the most frequently used techniques for predicting improvement in regional contractile function after coronary revascularization in patients with left ventricular dysfunction due to chronic coronary artery disease. BACKGROUND: Several techniques have been proposed for predicting improvement in regional contractile function after revascularization, including thallium-201 (Tl-201) stress-redistribution-reinjection, Tl-201 rest-redistribution, fluorine-18 fluorodeoxyglucose with positron emission tomography, technetium-99m sestamibi imaging and low dose dobutamine echocardiography (LDDE). METHODS: A systematic review of all reports on prediction of functional recovery after revascularization in patients with chronic coronary artery disease (published between 1980 and March 1997) revealed 37 with sufficient details for calculating the sensitivity and specificity of each imaging modality. From the pooled data, 95% and 99% confidence intervals were also calculated. RESULTS: Sensitivity for predicting regional functional recovery after revascularization was high for all techniques. The specificity of both Tl-201 protocols was significantly lower (p < 0.05) and LDDE significantly higher (p < 0.01) than that of the other techniques. CONCLUSIONS: Pooled analysis of 37 studies showed that although all techniques accurately identify segments with improved contractile function after revascularization, the Tl-201 protocols may overestimate functional recovery. The evidence available thus far indicates that LDDE appears to have the highest predictive accuracy.

Chronic Disease↗
PubMed2004

Rapid reversal of global left ventricular dysfunction after accidental injection of 0.75 mg epinephrine in a 20-year-old patient.

We report an accidental injection of epinephrine before spinal anaesthesia in a 20-year-old patient who subsequently developed immediate myocardial ischemia and global left ventricular dysfunction (ejection fraction of 20%). Hemodynamic status dramatically improved after nitroglycerin, calcium antagonists, acetyl salicylic acid and unfractionated heparin injections. Over 24 h, patient's ejection fraction fully recovered without kinetic abnormality.

Adult↗
PubMed1994

Left ventricular dysfunction during exercise in patients with angina pectoris and angiographically normal coronary arteries (syndrome X)

Left ventricular function during exercise and recovery was investigated in patients with angina pectoris, ST segment depression during exercise and angiographically normal coronary arteries (syndrome X) using a continuous left ventricular function monitor with cadmium telluride detector (CdTe-VEST). Fourteen patients with syndrome X and 14 patients with atypical chest pain without ST segment depression during exercise and normal coronary arteries (control group) performed supine ergometric exercise after administration of 740-925 MBq of technetium-99m labelled red blood cells, and left ventricular function was monitored every 20 s using CdTe-VEST. Left ventricular ejection fraction (EF) response was impaired (< or = 5% increase from rest to peak exercise) in 11 or 14 patients with syndrome X but in none of the control patients. Resting EF was similar in the two groups (62.1% +/- 6.7% in patients with syndrome X, 61.9% +/- 6.2% in controls); however, EF increase from rest to peak exercise was lower in syndrome X (-3.1 +/- 9.5% vs 14.7% +/- 7.4%, P < 0.001). After cessation of exercise, all patients showed rapid EF increase over baseline and this EF overshoot was lower (19.3% +/- 8.3% vs 26.4% +/- 7.3%, P < 0.001) with the time to EF overshoot longer (114 +/- 43 s vs 74 +/- 43 s, P < 0.05) in patients with syndrome X. Thus, in patients with syndrome X, left ventricular dysfunction was frequently observed during exercise in spite of normal epicardial coronary arteries.

Adult↗
PubMed2005

Transgenic overexpression of locally acting insulin-like growth factor-1 inhibits ubiquitin-mediated muscle atrophy in chronic left-ventricular dysfunction.

Metabolic abnormalities develop in various chronic diseases and lead to progressive catabolism with decrements in the skeletal musculature that result in muscle atrophy. We investigated pathways of skeletal muscle proteolysis using an experimental model of chronic left-ventricular dysfunction. Skeletal muscle atrophy developed in wild-type mice 12 weeks following myocardial infarction accompanied by an increase in total protein ubiquitination and enhanced proteasome activity, activation of Foxo transcription factors, and robust induction of the ubiquitin-protein ligase atrogin-1/MAFbx. Further studies identified skeletal muscle myosin as a specific target of ubiquitin-mediated degradation in muscle atrophy. In contrast, transgenic overexpression of a local isoform of insulin-like growth factor-1 prevented muscle atrophy and increased proteasome activity, inhibited skeletal muscle activation primarily of Foxo4, and blocked the expression of atrogin-1/MAFbx. These results suggest that skeletal muscle atrophy occurs through increased activity of the ubiquitin-proteasome pathway. The inhibition of muscle atrophy by local insulin-like growth factor-1 provides a promising therapeutic avenue for the prevention of skeletal muscle wasting in chronic heart failure and potentially other chronic diseases associated with skeletal muscle atrophy.

Animals↗
PubMed1995

Importance of a non-dominant right coronary artery occlusion presenting as sudden cardiac death with prolonged right ventricular dysfunction and malignant arrhythmias.

We report a case of a patient who presented with sudden cardiac death secondary to a subtotal occlusion of a small non-dominant right coronary system. Catheterization several weeks following the initial episode revealed persistent severe right ventricular dysfunction with moderate hemodynamic compensation. Continued unstable arrhythmogenic potential at this point led to placement of an AICD device. The case highlights the potential hazard and often complacency involved in dealing with benign appearing lesions as this one.

Arrhythmias, Cardiac↗
PubMed1996

Heart failure. A decision analytic analysis of New Zealand data using the published results of the SOLVD Treatment Trial. Studies of Left Ventricular Dysfunction.

This study sought to evaluate the changes in direct medical costs and life-years gained or lost by adding enalapril to conventional treatment (digoxin and diuretics) for heart failure (HF). The published results of the Studies of Left Ventricular Dysfunction (SOLVD) Treatment Trial, and a decision analytical model developed by the University of Pennsylvania, were used in combination with New Zealand data to undertake the evaluation. All costs were measured in 1993 New Zealand dollars ($NZ) [$NZ1 = $US0.5509, September 1993]. Potential net cost savings per patient treated over a 4-year period were $NZ652 together with an additional 2 months of life gained. If these individual potential cost savings are extended to the New Zealand population who have HF (but are at present not receiving an ACE inhibitor) then $NZ6 517 000 in discounted health sector costs could be avoided. The model was sensitive to changes in the price of enalapril, to estimates of the population with HF, the percentage of the population with HF treated with enalapril, and to hospital unit costs for nonfatal cases of HF. The study demonstrated that the addition of enalapril to the conventional treatment of HF was cost effective when compared with conventional medical therapy alone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Presence of lobeline-like sensations in exercising patients with left ventricular dysfunction.

Since there is evidence that lobeline-induced sensations, associated with discomfort in the mouth, throat and chest arise by stimulating juxtapulmonary or J receptors, we were interested in investigating if similar sensations are felt by patients with left ventricular dysfunction (LVD) in whom a natural stimulation of these receptors would occur by transient interstitial oedema or during augmentation of the stimulus, by increased pulmonary blood flow during exercise. Threshold doses of lobeline produced three or more respiratory sensations simultaneously in 9 out of 10 patients, which was greater than the response of the controls (P < 0.01). With mild exercise, a greater number of patients (7) than controls (1) reported feeling two or more sensations (P < 0.01); in fact half the controls did not express a respiratory sensation with equivalent exercise (P < 0.05). The predominant lobeline-like sensations reported by patients with exercise were a feeling of heat or burning and pressure in the throat or chest (P < 0.05). The presence of cough in three patients and in none of the controls was noteworthy. The mean latency with which sensations appeared during exercise in patients (4.4 +/- 0.3 min) was almost half that in controls (7.4 +/- 0.2 min) (P < 0.005). Since, respiratory sensations in response to lobeline and exercise were intensified in patients compared to controls and since both lobeline and exercise-induced sensations were similar (P < 0.05), we speculate that a common origin exists. Despite important caveats, that we discuss, in our view these respiratory sensations and cough arise from stimulation of J receptors.

Adult↗
PubMed2006

Early revascularization and ACC/AHA guideline-compliant medical management improve left ventricular function and short-term prognosis in patients presenting with acute myocardial infarction and severe left ventricular dysfunction.

BACKGROUND: Myocardial infarction (MI) complicated by severe left ventricular (LV) dysfunction is associated with significant morbidity and mortality. The natural history of this population with contemporary revascularization and guideline-based medical therapies is poorly defined. We sought to determine the impact of contemporary treatment strategies on LV function and prognosis in patients with MI and severe LV dysfunction. METHODS: Consecutive MI patients were prospectively followed as part of an ongoing internal database. The current report comprises 75 patients with first MI and severe LV systolic dysfunction (EF less than or equal to 3%). Initial demographic and clinical data were collected during hospitalization and at 1-, 3- and 6-month follow up. RESULTS: Patients were 71% male, 36% diabetic and 51% had prior coronary disease with a mean (+/- SD) age of 65 +/- 14 years. The average hospital stay was 5.7 days for ST-elevation (CPK range 424 to 5,250) and 2.4 days for non-ST-elevation MI (CPK range 175 to 705). Revascularization in-hospital was performed in 87% of patients (62 percutaneous, 3 surgical). At hospital discharge, treatment included beta-blockers (84%), ACE-inhibitors (73%), statins (81%), aspirin (88%) and clopidogrel (84%). Mean (+/- SD) LVEF was 25.7 +/- 5.9% in hospital, 36.6 +/- 11.8% by 1 to 3 months (p < 0.01), and 37.6 +/- 9.3% at 6 months (p < 0.01). By 1 to 3 months, 63% had improved LVEF, 24% were unchanged and 14% were worse. One patient died in the hospital and 3 died by 6-month follow up (mortality 5.3%). CONCLUSION: A strategy of early revascularization combined with guideline-based medical management favorably impacts LV function and short-term prognosis in MI patients with severe LV systolic dysfunction. With contemporary treatment strategies, the majority (> 60%) of patients demonstrate improvement in LVEF and mortality is low (5.3%).

Aged↗
PubMed1996

Effects of dobutamine and enoximone on transmitral and pulmonary venous flow characteristics in patients with left ventricular dysfunction after coronary artery bypass grafting.

OBJECTIVES: To assess the effects of dobutamine and enoximone on transmitral (TMF) and pulmonary venous flow (PVF) characteristics. DESIGN: Prospective and randomized. SETTING: A university hospital intensive care unit. PARTICIPANTS: Thirty patients with moderate left ventricular dysfunction after coronary artery bypass grafting (CABG). INTERVENTIONS: Patients received either dobutamine, 10 micrograms/kg/min, or enoximone, 20 micrograms/kg/min, for the treatment of a low cardiac index (CI) (< 2.2 L/min/m2). MEASUREMENTS AND MAIN RESULTS: Both drugs significantly (p < 0.05) increased CI from 1.91 +/- 0.17 (dobutamine) and 1.97 +/- 0.17 (enoximone) at baseline to 2.86 +/- 0.70 and 2.84 +/- 0.39 L/min/m2, respectively. Compared with the enoximone (enox)-treated group, the administration of dobutamine (dob) resulted in significantly (p < 0.05) greater increases in mean arterial pressure (dob: 18 +/- 9% v enox: -2 +/- 7%), heart rate (dob: 24 +/- 13% v enox: 3 +/- 5%) and pulmonary artery pressure (dob: 5 +/- 10% v enox: -4 +/- 9%). In contrast, the increase in stroke volume index was significantly less in the dobutamine-treated group (dob: 22 +/- 27% v enox: 41 +/- 21%). The TMF indices, peak E, and peak A wave increased significantly (p < 0.05) after both dobutamine (baseline: 37.3 +/- 6.7 and 41.1 +/- 9.3; max dose: 42.4 +/- 4.3 and 49.0 +/- 10.2 cm/s) and enoximone (baseline: 36.2 +/- 7.5 and 44.2 +/- 10.9; max dose: 40.5 +/- 5.0 and 49.4 +/- 12.1 cm/s) without significantly altering the E/A ratio. Only dobutamine significantly (p < 0.05) decreased isovolumic relaxation time from 109 +/- 24 to 94 +/- 21 ms. There was no significant change in isovolumic relaxation time between the dobutamine (-12% +/- 17%)- and the enoximone (-4% +/- 21%)- treated group. PVF recordings demonstrated a significant increase in time velocity integrals of the S wave with both dobutamine (12.2 +/- 3.1 v 13.7 +/- 3.2 cm) and enoximone (11.0 +/- 3.0 v 12.2 +/- 3.2 cm). No changes in the systolic fraction of the PVF were noted. CONCLUSIONS: There were no major differences in parameters reflecting diastolic function between the dobutamine- and the enoximone-treated groups.

Adult↗
PubMed1995

Surgical therapy of chronic heart failure and severe ventricular dysfunction.

Even with multiple medical advancements, heart failure patients still have a dismal prognosis. Technologic improvements in coronary artery bypass graft (CABG) surgery have led to the use of high-risk myocardial revascularization for the treatment of patients with heart failure and severe ventricular dysfunction. This article describes advances in cardiac surgery and their impact on the treatment of heart failure. Postoperative management of the heart failure patient is also discussed. Because patient selection is important in achieving positive surgical outcomes, the role of prospective severity risk score is also addressed.

Heart Failure↗
PubMed2002

The relevance of subgroup-specific treatment effects: the Studies Of Left Ventricular Dysfunction (SOLVD) revisited.

BACKGROUND: The overall effect sizes estimated from randomized clinical trials may not apply similarly to all patients. Univariate subgroup analyses are often used to help determine the generalizability of a trial's results, but may themselves be misleading. We reanalyzed the Studies of Left Ventricular Dysfunction (SOLVD) to determine whether the treatment effect depended on the patients' baseline prognosis, defined on the basis of multiple clinical variables. METHODS: The SOLVD prevention (4228 patients) and the SOLVD treatment (2569 patients) trials were randomized, double-blind trials that studied the effect of enalapril in patients with reduced left-ventricular function or congestive heart failure. We combined both SOLVD populations and compared the results of a univariate analysis to a multivariate approach in which 3 patient subgroups were defined according to baseline risks for the combined end point of death or hospitalization for heart failure. RESULTS: Enalapril treatment resulted in 24% fewer events. The strongest predictors of an event were ejection fraction, New York Heart Association classification and age, antiplatelet agents, history of diabetes mellitus, treatment with digoxin or diuretics, and race. Only ejection fraction produced a significant treatment interaction (P =.004). Consistent with the original SOLVD reports, this interaction was also demonstrable when ejection fraction was scaled into tertiles and examined on its own (P =.012). However, there was no interaction present when patients were divided into tertiles of multifactorial baseline risk. CONCLUSIONS: We confirmed the treatment effect of enalapril, the impact of left-ventricular systolic function, and the negative prognostic importance of diabetes mellitus in this population. Although ejection fraction led to a subgroup-treatment interaction in the main SOLVD publications, a multifactorial approach to prognostic grouping abolished the interaction. These findings highlight the limitations of univariate subgroup analyses and illustrate that multivariate risk group analysis may be a complementary method for assessing the generalizability of the overall treatment effects observed in randomized trials.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Right ventricular dysfunction in congenitally corrected transposition of the great arteries.

Although right ventricular (RV) dysfunction is an important complication in subjects with congenitally corrected transposition of the great arteries, its pathogenesis is poorly understood. We assessed the role of RV myocardial perfusion and found perfusion defects at rest in all 20 patients, involving 4.6 +/- 2.3 of a total of 12 segments; the extent of the resting perfusion defects correlated inversely with the RV ejection fraction.

Adolescent↗
PubMedDate not supplied

Left ventricular dysfunction and duration of mechanical ventilatory support in the chronically critically ill: a survival analysis.

OBJECTIVE: The purpose of this study was to determine whether there was a greater risk for prolonged duration of mechanical ventilatory support (MVS) for those who demonstrated left ventricular dysfunction (LVD) compared to those without evidence of LVD when controlling for nutritional and general health status and spontaneous breathing pattern. DESIGN: A secondary analysis was used on data obtained in a retrospective survey of patient records. SETTING: Five adult critical care units at an academic medical center in the Midwest. SUBJECTS: Twenty-seven chronically critically ill adults requiring MVS who later successfully weaned from MVS. OUTCOME MEASURE: Duration of MVS. INSTRUMENTATION: LVD was determined with use of a criterion-based checklist. Serum albumin level as determined by the hospital's clinical laboratory served as the indicator of nutritional and general health status. The rapid shallow breathing index was used to describe the spontaneous breathing pattern. RESULTS: Adjusted survival function estimates were obtained on fitting a Cox proportional hazards model. When adjusting for the known covariates, serum albumin level and rapid shallow breathing index, the duration of MVS was significantly longer for those who demonstrated LVD when compared to those without evidence of LVD [X2Wald(1) = 4.72, p < 0.05]. CONCLUSIONS: The findings of this secondary analysis lend support to the fact that when controlling for serum albumin level and rapid shallow breathing index, LVD is related to the duration of MVS in patients who successfully wean.

Aged↗
PubMed2006

The effect of acute hypertension on left ventricular diastolic pressures in a canine model of left ventricular dysfunction with a preserved ejection fraction and elevated left ventricular filling pressures.

BACKGROUND: Decompensated heart failure with preserved left ventricular (LV) ejection fraction (EF) is often accompanied by hypertensive episodes. We hypothesized that acute increase in arterial pressure results in elevated early and late diastolic LV pressures as a result of further impaired LV relaxation. METHODS: To test this hypothesis, we used a chronic canine model of LV systolic dysfunction with preserved LV function (LVDPEF) (EF > 50%) and elevated LV end-diastolic pressure using coronary microsphere embolization. At baseline and with LVDPEF, each dog was paced 10 beats above their baseline heart rate and high-fidelity LV pressures, echocardiographic LV volumes, and transmitral Doppler were obtained before and after methoxamine pressure loading. RESULTS: With normal LV function, LV pressures at peak negative dP/dt (+18 mm Hg, P < .05) and at LV pressure minimum (+3.6 mm Hg, P < .01) increased. Both tau (P < .05) and LV end-diastolic pressure increased (5 +/- 3 vs 13 +/- 4 mm Hg, P < .01). EF was unchanged, although LV end-diastolic volume increased (P < .01). Pressure loading with LVDPEF resulted in a timing delay (P < .05) and a greater increase in LV pressures at peak negative dP/dt (+45 mm Hg) and LV minimal pressure (+7.5 mm Hg) as compared with normal LV function (P < .01). LV end-diastolic pressure increased (9 +/- 2-23 +/- 5 mm Hg, P < .001), diastolic filling period shortened (288 +/- 51-204 +/- 54 milliseconds, P < .01), and tau increased (P < .001). EF declined from 54 +/- 9% to 43 +/- 9% (P < .05) and LV size increased (P < .01). CONCLUSIONS: Pressure loading with normal LV function and with LVDPEF results in increased LV diastolic pressures, which are further exaggerated with LVDPEF as a result of prolonged relaxation and shortened diastolic filling.

Acute Disease↗