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PubMed2001

Relationship of current and past smoking to mortality and morbidity in patients with left ventricular dysfunction.

OBJECTIVES: The aim of this study was to evaluate the impact of smoking in patients with left ventricular dysfunction. BACKGROUND: The impact of smoking in patients with left ventricular dysfunction has not been well-studied. METHODS: We compared the incidence of death, hospitalization due to heart failure and myocardial infarction (MI) in current smokers to ex-smokers of < or =2 years and ex-smokers of >2 years duration to never-smokers among participants of the Study Of Left Ventricular Dysfunction (SOLVD) Prevention and Intervention trials. Participants all had left ventricular ejection fraction (LVEF) <35% and follow-up was over a mean of 41 months. RESULTS: Complete smoking status and outcome data were available in 6,704 subjects. There were 1,562 current smokers, 1,317 ex-smokers of < or =2 years, 2,354 ex-smokers of >2 years and 1,471 never-smokers. After adjusting for baseline differences of age, LVEF, race and etiology of heart failure, current smoking was associated with a significantly increased all-cause mortality (relative risk [RR]: 1.41, 95% confidence interval [CI]: 1.25 to 1.58, p < 0.001) compared with ex-smokers and never-smokers. The incidence of death or recurrent congestive heart failure requiring hospitalization or MI was significantly greater (RR: 1.39, 95% CI: 1.26 to 1.52, p < 0.001) in current smokers compared with ex-smokers and never-smokers. There were no significant differences in the number of deaths or hospitalizations due to heart failure between ex-smokers and never-smokers. This effect was consistent across both the SOLVD Prevention and Treatment trials. CONCLUSIONS: Current smoking is a powerful independent predictor of morbidity (recurrent heart failure and MI) and mortality in patients with left ventricular dysfunction. Quitting smoking appears to have a substantial and early effect (within two years) on decreasing morbidity and mortality in patients with left ventricular dysfunction, which is at least as large as proven drug treatments recommended in patients with left ventricular dysfunction.

Aged↗

PubMed1996

Relation of ventricular size and function to heart failure status and ventricular dysrhythmia in patients with severe left ventricular dysfunction.

Patients with severe left ventricular (LV) dysfunction may or may not have overt heart failure and ventricular dysrhythmia. To study factors behind this variability, we examined a subset of 311 patients from the Studies of Left Ventricular Dysfunction-95 with a history of moderate heart failure (treatment trial) and 216 with no failure (prevention trial), all with ejection fractions <0.35. Echocardiographic variables were compared between trials and also correlated with dysrhythmia in 258 patients, and with neurohormones in 199 patients. Compared with prevention patients, treatment patients had larger LV end-diastolic diameter, end-systolic volume, sphericity index, and ratio of early to late diastolic filling velocity by Doppler (E/A ratio), lower LV ejection fraction and atrial contribution to ventricular filling, and similar LV mass, end-diastolic volume, and estimates of systolic wall stress. With prevention and treatment patients combined, the prevalence of abnormally elevated atrial natriuretic peptide was 92% in the highest tertile of E/A ratio compared with 55% in the lower tertiles (p=0.006). Across tertiles of LV end-diastolic volume, there was an increase in the prevalence of nonsustained ventricular tachycardia (24%, 45%, and 45%; p=0.007) and premature ventricular complexes >10/hour (48%, 62%, and 80%; p<0.001). Thus, in severe LV dysfunction, ventricular filling indexes suggestive of high filling pressures, along with larger and more spherical ventricles, are particularly common in patients with overt heart failure, thus suggesting that diastolic properties and the degree of ventricular remodeling affect clinical status. Once ejection fraction is significantly reduced, the prevalence of ventricular dysrhythmia correlates with LV size rather than systolic function. This observation lends support to previous experimental findings on the role of myocardial stretch and scar in the genesis of dysrhythmia.

Aged↗

PubMed1994

Detection of left ventricular dysfunction after acute myocardial infarction: comparison of clinical, echocardiographic, and neurohormonal methods.

OBJECTIVE: The SAVE study showed that captopril improves mortality in patients with left ventricular dysfunction after myocardial infarction and that this benefit occurred even in patients with no clinically overt heart failure. On the basis of this, it seems important to identify correctly which patients have left ventricular dysfunction after a myocardial infarction. The objective was to compare various methods of identifying patients with left ventricular dysfunction (left ventricular ejection fraction, LVEF, < or = 40%) after acute myocardial infarction. The methods compared were echocardiography (quantitative and qualitative visual assessment), clinical evaluation (subjective assessment and three clinical score methods), and measurement of plasma concentrations of cardiac natriuretic peptide hormones (atrial and brain natriuretic peptides, ANP and BNP). DESIGN: Cross sectional study of left ventricular function in patients two to eight days after acute myocardial infarction. SETTING: Coronary care unit of a teaching hospital. PATIENTS: 75 survivors of a recent myocardial infarction aged 40 to 88 with no history of cardiac failure and without cardiogenic shock at the time of entry to the study. MAIN OUTCOME MEASURES: Sensitivities and specificities of the various methods of detecting left ventricular dysfunction were calculated by comparing them with a cross sectional echocardiographic algorithm for LVEF. RESULTS: Clinical impression was poor at identifying LVEF < 40% (sensitivity 46%). Clinical scoring improved this figure somewhat (modified Peel index sensitivity 64%). Qualitative visual assessment echocardiography was a more sensitive method (sensitivity 82%) for detecting LVEF < 40%. Plasma BNP concentration was also a sensitive measure for detecting left ventricular dysfunction (sensitivity 84%) but plasma ANP concentration was much poorer (sensitivity 64%). CONCLUSION: Left ventricular dysfunction is easily and reliably detected by echocardiographic measurement of LVEF and also by a quick qualitative echocardiographic assessment but is likely to be missed by clinical assessment alone. High concentrations of plasma BNP maybe another useful indicator of left ventricular dysfunction, particularly in hospitals where not all patients can be screened by echocardiography or radionuclide ventriculography after myocardial infarction.

Adult↗

PubMed1993

Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction.

Early identification of patients with symptomless left-ventricular dysfunction and early pharmacologic intervention may have an impact on the outlook of patients with heart failure. Atrial natriuretic peptide (ANP) is a cardiac hormone that is released as a C-terminal (C-ANP) and an N-terminal peptide (N-ANP). Since N-ANP has reduced clearance rates compared with C-ANP, N-ANP circulates at higher concentrations. Based on the known increased concentration of C-ANP in symptomatic congestive heart failure, our study was designed to evaluate prospectively N-ANP profile and left-ventricular function in subjects with symptomless and symptomatic heart failure, and the role of plasma N-ANP as a marker for early identification of patients with heart failure. 180 patients who were referred for rest and exercise radionuclide angiography for evaluation of left-ventricular function were studied. Blood was taken for measurement of C-ANP and N-ANP before angiography. Patients were grouped according to New York Heart Association (NYHA) heart failure classification and left-ventricular function. Mean (SD) plasma N-ANP concentration in patients with symptomless left-ventricular dysfunction (NYHA class I, n = 70) was 243 (256) pmol/L (range 27-922 pmol/L), and was higher (p < 0.001) than in 25 control subjects (28 pmol/L). A plasma N-ANP concentration above 54 pmol/L (mean +/- 1.96SD of the control group) had a sensitivity of 90% and a specificity of 92% for detection of patients with symptomless left-ventricular dysfunction. We have shown that plasma N-ANP concentrations are significantly increased in patients with symptomless left-ventricular dysfunction and that this peptide can serve as a marker for diagnosis of such patients.

Adult↗

PubMed1988

Differential ventricular ischemic injury: an experimental model of right ventricular failure with a variable degree of left ventricular dysfunction.

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.

Adenine Nucleotides↗

PubMed1996

Left ventricular dysfunction after heart transplantation: incidence and role of enhanced immunosuppression.

BACKGROUND: The purpose of this study was to examine the incidence, natural history, and outcome of left ventricular dysfunction in 102 consecutive heart transplant recipients. Left ventricular dysfunction (defined as a decline in the echocardiographic ejection fraction to < 0.45) occurred in 16 of 102 transplant recipients (16%) at a mean of 9.7 +/- 8.6 (standard deviation) months after transplantation. METHODS: Diagnostic evaluation included right heart catheterization and endomyocardial biopsy in all patients and coronary angiography in 13 patients. RESULTS: Four patients were found to have moderate cellular rejection (International Society for Heart and Lung Transplantation grade 2 or higher) and were treated with enhanced immunosuppression. Two patients had angiographically apparent coronary allograft vasculopathy; both died of electromechanical dissociation within 4 months. The remaining ten patients had no or mild cellular rejection (International Society for Heart and Lung Transplantation grade 0 or 1). Therapy in these ten patients included corticosteroids (n = 8). OKT3 (n = 5), and plasmapheresis (n = 2). Three patients died within 2 months of diagnosis, two from undetected severe coronary allograft vasculopathy and one from unrecognized constrictive pericarditis. The echocardiographic ejection fraction improved in the surviving patients after enhanced immunosuppressive therapy (0.33 to 0.53, p < 0.005). With the benefit of long-term clinical follow-up and autopsy data, the origins of left ventricular dysfunction in the 16 patients included moderate cellular rejection (n = 4), vascular rejection (n = 1), coronary allograft vasculopathy (n = 3), intercurrent cytomegalovirus infection (n = 1), constrictive pericarditis (n = 1), and either mild or no evident rejection (n = 6). Survival of the 16 patients with left ventricular dysfunction was similar to that of the 86 patients without left ventricular dysfunction. CONCLUSIONS: The cause of left ventricular dysfunction after heart transplantation includes cellular rejection, vascular rejection, coronary allograft vasculopathy, cytomegalovirus infection, constrictive pericarditis, and unexplained mechanisms. Given the improvement in left ventricular function observed after empiric therapy with enhanced immunosuppression in patients with left ventricular dysfunction, immune-mediated phenomena may play an important pathogenic role.

Biopsy↗

PubMedDate not supplied

Myocardial blood flow at rest and contractile reserve in patients with chronic coronary artery disease and left ventricular dysfunction.

BACKGROUND: The mechanisms that determine chronic left ventricular dysfunction in coronary artery disease (in particular, critical reductions in coronary artery blood flow leading to hibernating myocardium) may affect the ability of the myocardium to respond to inotropic stimulation with dobutamine. This study was designed to investigate the relationship between resting myocardial blood flow and contractile reserve in patients with coronary artery disease and chronic left ventricular dysfunction. METHODS AND RESULTS: Twenty-three patients (21 men and 2 women; age 61 +/- 9 years) underwent transesophageal echocardiography during infusion of dobutamine (2.5 microg/kg to 40 microg/kg per minute) and positron emission tomography (PET) with 150-water (9 patients) or 13N-ammonia (14 patients). Systolic wall thickening at each dose of dobutamine and resting myocardial blood flow were quantitatively analyzed in 8 anatomically matched regions at mid-ventricular level. Myocardial regions with preserved contraction had higher blood flow compared with regions with basal dyssynergy (0.99 +/- 0.3 vs 0.65 +/- 0.3 mL/min/gm; P < .0001). Among myocardial regions with preserved resting contraction, no relation was observed between blood flow and the response to dobutamine (r = 0.06). In contrast, among myocardial regions with diminished resting contraction, a significant correlation was observed between resting blood flow and contractile reserve (r = 0.53; P < .0001). The maximum increase in percent systolic wall thickening with dobutamine was 32.8% +/- 14% in regions with normal blood flow, 21.5% +/- 17% in regions with mildly to moderately reduced blood flow, and 10.7% +/- 10% in regions with severely reduced blood flow (P < .0001). CONCLUSIONS: These findings emphasize the importance of resting myocardial blood flow for the preservation of contractile reserve in patients with coronary artery disease and left ventricular dysfunction. Because a positive inotropic response to dobutamine is more likely to occur in dyssynergic regions with preserved rather than reduced myocardial blood flow, regional perfusion may determine in which circumstances dobutamine echocardiography contributes to the assessment of myocardial viability.

Chronic Disease↗

PubMed1988

Treatment of life-threatening ventricular tachycardia with encainide hydrochloride in patients with left ventricular dysfunction. The Encainide-Ventricular Tachycardia Study Group.

Encainide, a newly released class IC antiarrhythmic agent, was studied in 193 patients with ventricular tachycardia (VT) and depressed left ventricular ejection fraction or important arrhythmia-related symptoms. Therapy was evaluated by 24-hour continuous Holter monitoring if patients had nonsustained VT or by electrophysiologic testing if they had sustained VT. Holter monitoring was used in 99 patients and electrophysiologic testing in 94 patients. At baseline the mean age, percent men, percent with coronary artery disease and mean ejection fraction in the 2 groups was 62 versus 58 years, 76 versus 72%, 62 versus 89%, and 27 versus 30%, respectively. In the Holter monitoring group, 71 of 99 (72%) responded with a significant reduction in VT (35% received 25 mg 3 times day, 47% received 35 mg 3 times a day, 14% received 50 mg 3 times a day and 4% received 50 mg 4 times a day). Adverse cardiac effects in these patients included a 7% incidence of serious proarrhythmic events that were probably related to encainide and a 2% incidence of sick sinus syndrome. In this group no patient developed congestive heart failure that was clearly attributed to encainide. Using electrophysiologic testing, 14 of 94 (15%) had sustained VT rendered noninducible, whereas 18 of 94 (19%) additional patients had partial electrophysiologic response defined as a more tolerable, slower VT. Overall, 32 of 94 (34%) were believed to be effectively treated in this group and were treated with encainide long-term. In the population evaluated by electrophysiologic testing, serious proarrhythmic events occurred in 15 of 94 (16%) and 3% had sinus pauses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1999

Demasking of subclinical left ventricular dysfunction in anemic children.

OBJECTIVE: To study subclinical left ventricular dysfunction in anemic children. SETTING: Hospital. SUBJECTS: The study population consisted of 52 cases of anemia (16 mild, 14 moderate, 22 severe) and 20 normal age and height matched children aged between 7-12 years. METHODS: These children were subjected to Echocardiography on Ascuson XP model using 3.5 MHz Transducer during rest and immediately after maximum tolerated exercise on Quniton Model Q-5000 treadmill using modified Naughton protocol. Left ventricular end diastolic dimensions, left ventricular systolic dimension, fractional shortening, left ventricular end diastolic volume, systolic volume, stroke volume and ejection fraction were studied on M-mode echocardiography, and E/A ratio on doppler mode. RESULTS: Significant differences were observed in resting heart rate, gain in heart rate at peak exercise compared to basal values and double product, total exercise duration and metabolic equivalents at peak exercise in controls and anemic subjects. Left ventricular dysfunction was present in all severely anemic subjects after maximum tolerated exercise on treadmill. The only evidence of left ventricular diastolic dysfunction was in form of decreased left ventricular end diastolic volume after exercise in moderate and severely anemic subjects. CONCLUSIONS: Exercise is helpful in demasking subtle left ventricular dysfunctions in anemic subjects that are not detected during rest.

Anemia↗

PubMed1994

Right ventricular dysfunction after major pulmonary resection.

Right ventricular performance was assessed by thermodilution in 20 patients at rest and during exercise before and after lobectomy or pneumonectomy. The right ventricular ejection fraction was significantly decreased on the first postoperative day (0.36 +/- 0.34), the second postoperative day (0.34 +/- 0.04), and the third postoperative week (0.37 +/- 0.06) relative to the preoperative right ventricular ejection fraction value (0.43 +/- 0.07, p < 0.05). The right ventricular end-diastolic volume index was significantly increased by the second postoperative day (130 +/- 24 ml/m2) compared with the preoperative value (112 +/- 20 ml/m2). A significant decrease in the right ventricular stroke volume index was observed after operation, with a significant increase in heart rate considered necessary to maintain cardiac output. Pulmonary arterial pressure, the pulmonary vascular resistance index, and central venous pressure were unaltered over time. Indices of left ventricular function (that is, cardiac index, arterial pressure, and pulmonary arterial wedge pressure) were also preserved throughout the postoperative period. To explain the right ventricular dysfunction, ergometric exercise values were compared and the heart rate, pulmonary arterial pressure, central venous pressure, pulmonary vascular resistance index, and right ventricular end-diastolic volume index were all higher and the right ventricular ejection fraction lower during exercise after the operation. However, indices of left ventricular function remained unchanged. Significant elevations in pulmonary arterial pressure and the pulmonary vascular resistance index only during exercise occurred. These findings indicate that changes in right ventricular function at rest compensate for the increase in right ventricular volume, but adequate compensation does not occur during exercise, with a resultant increase in pulmonary arterial pressure and the pulmonary vascular resistance index. This suggests that a change in afterload may be the main determinant of the deterioration in right ventricular pump performance during exercise. We speculate that the main cause of right ventricular dysfunction after major pulmonary resection might be the changes in right ventricular afterload. The right ventricle may play an important role serving as a "reservoir" for afterload.

Aged↗

PubMed1996

Role of basal release of nitric oxide in the presence of acute left ventricular dysfunction: comparative study with normal condition.

The basal release of nitric oxide (NO) plays an important role in the regulation of vascular circulation in the presence of acute left ventricular dysfunction. It is not clear, however, whether the role is as important in the presence of acute left ventricular dysfunction as it is in the normal condition. In addition, the effects of flow rate on the role of basal NO have not been clarified in the presence of acute left ventricular dysfunction. This in vivo study was attempted to compare the contribution of the basal release of NO to the regulation of vascular circulation and the effects of a mechanically reduced basal flow rate on the contribution of basally released NO between the normal condition and acute left ventricular dysfunction. In eight anesthetized dogs, the responses of femoral artery blood flow to NG-monomethyl-L-arginine (L-NMMA, 10(-5)M) were observed with and without a reduction in basal flow. The same observation was performed after the production of acute left ventricular dysfunction by coronary microembolization. Without the reduction in basal flow, the L-NMMA-induced decrease in femoral artery flow was significantly larger in acute left ventricular dysfunction than in the normal condition (-40 +/- 12% vs-17 +/- 6%, P < .01). Under the reduction in basal flow, there was no significant change in flow during the infusion of L-NMMA in the normal condition and only a small decrease in acute left ventricular dysfunction. There was no significant difference in the L-NMMA-induced changes in flow between these conditions. The contribution of basally released NO to the regulation of vascular circulation is larger in the presence of acute left ventricular dysfunction than in the normal condition; however, the role of basal NO is reduced with a decrease in basal flow rate.

Acetylcholine↗

PubMed1988

Death after acute myocardial infarction: interrelation between left ventricular dysfunction, arrhythmias and ischemia.

Patients who survive an acute myocardial infarction face an increased risk of sudden death for approximately 6 months after hospital discharge; their prognosis is determined by the severity of their coronary arteriosclerosis and the degree of left ventricular dysfunction. Frequent ventricular premature complexes and evidence of ischemia either spontaneously or on treadmill are also markers for early morbidity and mortality in patients who are discharged from the hospital after acute myocardial infarction. The degree of left ventricular dysfunction is the strongest predictor of mortality; patients who have both left ventricular dysfunction, frequent premature ventricular beats and evidence of ischemia are at the highest risk of mortality after hospital discharge. It appears likely that all 3 of these risk factors interact and that therapy to reduce morbidity and mortality after myocardial infarction should aim at the amelioration of each of these risk factors. A model for the interaction of these risk factors is proposed and an approach to treatment for patients at high risk of mortality after hospital discharge after myocardial infarction is suggested.

Arrhythmias, Cardiac↗

PubMed1994

Left ventricular dysfunction due to stunning and hibernation in patients.

Left ventricular dysfunction is in most cases the consequence of myocardial ischemia. It may occur transiently during an attack of angina and usually it is reversible. It may persist over hours or even days in patients after an episode of ischemia followed by reperfusion, leading to the so-called condition of stunning. In patients with persistent limitation of coronary flow, left ventricular dysfunction may be present over months and years, or indefinitely in subjects with fibrosis, scar formation, and remodeling after myocardial infarction. However, chronic left ventricular dysfunction does not mean permanent or irreversible cell damage. Hypoperfused myocytes can remain viable but akinetic. This type of dysfunction has been called hibernating myocardium. The dysfunction due to hibernation can be partially or completely restored to normal by reperfusion. It is, therefore, important to clinically recognize a hibernating myocardium. In the present article we evaluate stunning and hibernation with respect to clinical decision making and, when possible, we refer to our ongoing clinical experience.

Humans↗

PubMed2000

Late arrhythmia in adults with the mustard procedure for transposition of great arteries: a surrogate marker for right ventricular dysfunction?

OBJECTIVE: To examine the relation between ventricular dysfunction and late clinical arrhythmia in adults who underwent the Mustard procedure for transposition of the great arteries. DESIGN: Observational study based on periodic outpatient assessment of biventricular function. SETTING: Tertiary referral centre. INTERVENTIONS: Analysis of data from 12 lead ECGs, echocardiography, exercise radionuclide ventriculography, and magnetic resonance imaging. MAIN OUTCOME MEASURES: Clinical outcome and late onset clinical arrhythmia during follow up. ECG and ventricular function indices obtained before arrhythmia onset were used for analysis. RESULTS: 51 patients (mean (SD) age 25.7 (5.0) years) fulfilled entry criteria at a mean of 23.4 (4.0) years after the Mustard procedure. Late arrhythmia occurred in 11 (22%): sustained atrial flutter/fibrillation in 10, ventricular tachycardia in one. Compared with patients who remained arrhythmia free, patients with arrhythmia had longer QRS (129 (26) v 112 (16) ms, p = 0.01), greater QT dispersion (107 (28) v 51 (24) ms, p < 0.001), and increased ratio of right to left ventricular end diastolic diameter (2.4 (0.9) v 1.7 (0.7), p = 0.02), but no difference in wall thickness. Systemic ejection fraction was also reduced in the arrhythmia subgroup (at rest: 34.1 (13)% v 47 (16)%, p = 0.04; during exercise: 37.8 (12)% v 52 (17)%, p = 0.03). QRS duration correlated with right ventricular end diastolic diameter (r = 0.59, p < 0.001), suggesting a possible mechano-electric relation after the Mustard procedure. QT dispersion was the only predictor of clinical arrhythmia in multivariate analysis. CONCLUSIONS: Impaired ventricular function in adults with the Mustard procedure for transposition of the great arteries relates to clinical arrhythmia. Late atrial flutter/fibrillation may be a surrogate marker for ventricular dysfunction, and these patients may also be at risk of ventricular tachycardia.

Adult↗

PubMed1995

Right ventricular dysfunction in low output syndrome after cardiac operations: assessment by transesophageal echocardiography.

BACKGROUND: Low output syndrome after cardiac operations is associated with high morbidity and mortality rates. The contribution of right ventricular dysfunction to this syndrome has not been fully characterized. The purpose of this study was to evaluate the utility of transesophageal echocardiography to identify the frequency and the in-hospital mortality from right ventricular dysfunction in patients with this syndrome. METHODS: Seventy-five consecutive patients undergoing transesophageal echocardiography for low output syndrome early after cardiac operations were evaluated. The findings from transesophageal echocardiography were correlated with the type of surgical procedure, cross-clamp time, right heart hemodynamics, and coronary angiography. RESULTS: Right ventricular systolic dysfunction occurred in 36 patients (42%); in 17 patients it was isolated and in 19 patients it occurred in combination with left ventricular dysfunction. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or with prolonged ischemic time during cardiopulmonary bypass. Hemodynamic data were not useful to distinguish the group with postoperative right ventricular dysfunction. Patients with right ventricular dysfunction had a high (44%) in-hospital mortality rate. CONCLUSIONS: Right ventricular dysfunction occurs frequently in patients with low output syndrome after cardiac operations and is associated with a high in-hospital mortality rate. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication.

Adult↗

PubMed1993

Ventricular arrhythmias in rehabilitated and nonrehabilitated post-myocardial infarction patients with left ventricular dysfunction.

The incidence of ventricular arrhythmias in rehabilitated post-myocardial infarction (MI) patients with left ventricular dysfunction included in a long-term rehabilitation program was assessed and compared with that in similar patients who were not in such a program. Thirty-eight post-MI patients (2 to 19 years after the acute event) with ejection fraction < 40% were investigated by 48-hour Holter monitoring. They were divided into the following 3 groups: group I, 11 patients who underwent arm training for 60 months; group II, 11 patients who underwent calisthenics for 36 months; and group III, 16 patients who were not in any rehabilitation program; the age of the patients was 61 +/- 7, 61 +/- 6 and 61 +/- 9 years, respectively, (p = not significant). Ejection fraction at rest was 31 +/- 9 for group I, 29 +/- 7 for group II, and 29 +/- 7 for group III (p = not significant). There were no significant differences concerning the location of MI, and antiarrhythmic treatment received by patients from all groups. At the conclusion of 48-hour Holter monitoring, 2 blood samples were obtained for assessment of norepinephrine (at rest and after postural change). Quality of life was determined by a detailed questionnaire, including questions concerning social activity, life satisfaction and sexual function. After 36 and 60 months, an improvement in hemodynamic condition of patients in group I was noted. Quality of life was higher in the rehabilitated patients, with enhanced emotional stability, satisfaction with work and social life, and a high percentage of return to work (82 vs 40%).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed1994

Frequency of development of acute global left ventricular dysfunction in human immunodeficiency virus infection.

OBJECTIVES: This study evaluated prospectively the frequency, clinical outcome and pathologic findings of acute global left ventricular dysfunction in human immunodeficiency virus (HIV) infection during the various stages of the disease. BACKGROUND: Acute global left ventricular dysfunction in the course of HIV infection is still a poorly defined clinical entity, and little is known about the outcome after the acute onset. METHODS: Between January 1988 and June 1992, 136 HIV-positive (HIV+) patients without clinical, electrocardiographic or echocardiographic evidence of cardiovascular dysfunction on admission were prospectively studied with serial echocardiograms. Patients were assigned to three groups: 1) anti-HIV+ asymptomatic (17 patients, 12.5%); 2) acquired immunodeficiency syndrome (AIDS)-related complex (26 patients, 19.1%); 3) AIDS (93 patients, 68.4%). RESULTS: During a mean follow-up period of 415 +/- 220 days, seven patients, all in the AIDS subgroup, developed clinical and echocardiographic findings of acute global left ventricular dysfunction; of these, six (85%) died of congestive heart failure. Mean survival time from symptom onset was 41 +/- 13 days. Necropsy findings in five patients revealed acute lymphocytic myocarditis in three, cryptococcal myocarditis in one and interstitial edema and fibrosis in one. In only one patient was left ventricular dysfunction reversible with treatment. CONCLUSIONS: Although infrequent, acute global left ventricular dysfunction is not rare in the course of HIV infection. It seems to occur exclusively during the AIDS stage. Acute global left ventricular dysfunction is often fatal but may be reversible and is mainly associated with the pathologic findings of acute myocarditis.

AIDS-Related Complex↗

PubMed1998

Absence of a deleterious effect of calcium channel blockers in patients with left ventricular dysfunction after myocardial infarction: The SAVE Study Experience. SAVE Investigators. Survival and Ventricular Enlargement.

BACKGROUND: As a result of randomized controlled trials with calcium channel blockers after myocardial infarction, concern has developed that these agents are associated with an increased risk of cardiovascular events, particularly in the presence of left ventricular dysfunction. METHODS: To test the hypothesis that calcium channel blockers increase cardiovascular events in such patients, the incidence of all-cause mortality, cardiovascular death, severe heart failure, and recurrent infarction was examined in 940 patients taking calcium channel blockers and 1180 not taking them 24 hours before randomization to placebo or captopril in the Survival and Ventricular Enlargement (SAVE) Trial. All patients had an ejection fraction < or =40%. Relative risks for calcium channel blocker users versus nonusers and the 95% confidence intervals were computed with univariate and multivariate Cox regressions. Adjustments were made for differences in baseline covariates. RESULTS: For all causes of mortality, the relative risk for calcium channel blocker users versus nonusers was 0.96, with the 95% confidence interval of 0.78 to 1.17. In the SAVE placebo and captopril groups, the relative risks for the development of severe heart failure among the calcium channel block users versus nonusers were 0.95 and 1.23, with the 95% confidence interval of 0.72 to 1.25 and 0.88 to 1.71, respectively. A similar neutral result held for patients with and without a history of hypertension. Furthermore, calcium channel blockers did not alter the benefit of the angiotensin converting enzyme inhibitor, captopril. CONCLUSIONS: This analysis of the nonrandomized clinical use of calcium channel blockers in the postmyocardial infarction population with left ventricular dysfunction did not identify either a clinical deterioration or improvement with respect to subsequent cardiovascular events.

Adult↗