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Circulating surfactant protein-B levels increase acutely in response to exercise-induced left ventricular dysfunction.

1. As a result of its enormous surface area and necessary thinness for gas exchange, the alveolocapillary barrier is vulnerable to mechanical disruption from raised pulmonary microvascular pressure (Pmv). 2. Because surfactant protein-B (SP-B) leaks into the blood stream from the alveoli in response to alveolocapillary barrier damage and exercise leads to increased Pmv, we sought to determine whether exercise results in increased plasma SP-B. Moreover, in the setting of exercise-induced left ventricular dysfunction, the consequent increase in left heart filling pressure and, therefore, P(mv) would be expected to further increase plasma SP-B levels. 3. Twenty consecutive subjects referred for treadmill exercise stress echocardiography (ESE) had venous blood sampled immediately before and after ESE for batch atrial natriuretic peptide (ANP) and SP-B assay. Echocardiographic measures of pulmonary haemodynamics (pulmonary artery flow acceleration time (pafAT) and right ventricular outflow tract velocity time integral (rVTI)) were also taken pre- and post-exercise. 4. Although circulating ANP levels increased following exercise (P < 0.001), there was no change in circulating SP-B levels in the entire cohort. 5. Ten subjects had a positive ESE for ventricular dysfunction. Although circulating ANP was increased post-exercise in both the negative and positive ESE groups (P < 0.05 and P < 0.01, respectively), circulating SP-B only increased post-exercise in the positive ESE group (P < 0.05). Echocardiographic parameters supported an increment in P(mv) in the cohort with exercise-induced left ventricular dysfunction because this group had an increase in pafAT (P < 0.05; reflecting pulmonary artery pressure) and no change in rVTI. 6. Physical exertion associated with a Bruce protocol ESE is insufficient to increase circulating SP-B, despite evidence of increased left atrial and pulmonary vascular pressure. However, in the setting of exercise-induced myocardial dysfunction, there is a detectable increase in circulating SP-B. 7. The exaggerated increase in pulmonary vascular pressure in exercise-induced myocardial dysfunction may result in increased SP-B leakage from the alveoli into the circulation by altering the integrity of the alveolocapillary barrier to protein.

Atrial Natriuretic Factor↗

The mid-term outcome of geometric endoventricular repair for the patients with ischemic left ventricular dysfunction.

OBJECTIVE: Recent studies have suggested that increased left ventricular (LV) size is a risk factor for perioperative mortality in patients with low ejection fraction (EF) undergoing coronary artery bypass surgery (CABG). We previously presented a new method of LV reconstruction, called geometric endoventricular repair (GER) as representing a physiologically effective repair. The aim of this study is to assess whether GER confers benefits compared to patients undergoing CABG alone. METHODS: Between July 1996 and July 2001, 110 patients with a low EF of less than 35% documented by radionuclide ventriculogram (RNVG) underwent CABG in Austin Hospital, Australia, and were divided into two groups. Group I consisted of 52 patients undergoing isolated CABG. Group II comprised 58 patients undergoing CABG and GER. We compared the two groups in terms of EF, NYHA class, incidence of recurrent heart failure, and mortality. RESULTS: Preoperative EF was 27.7+/-6.1% in group I and 27.4+/-5.7% in group II, respectively (NS), with significant improvement in both groups (33.8+/-13.0% in group I, 35.1+/-13.3% in group II). NYHA class was also significantly improved postoperatively (from 3.3 to 1.8 in group I, and 3.6 to 1.7 in group II). There were 15 patients (28.8%) hospitalized for heart failure in group I, postoperatively, compared to seven patients (10.9%) in group II (p=0.026). Cardiac event-free survival rate at 28 months (mean follow-up) was also significantly higher in group II (88.9% in group II vs. 70.6% in group I, p=0.05). The actuarial survival rate at 31 months (mean follow-up) was 88.2% in group I and 95.3% in group II, respectively (NS). CONCLUSIONS: LV reconstruction along with CABG for ischemic ventricular dysfunction may provide symptomatic and cardiac event free survival benefits, compared to CABG alone.

Aged↗

[Mitral valve repair in ischemic cardiomyopathy with severe left ventricular dysfunction].

Patients with ischemic mitral insufficiency and poor left ventricular function are high operative risks. We present 101 patients who had mitral valve repair in our department: 21 had severely reduced left ventricular function, 19 were in NYHA functional Class IV, and 2 in Class III. All had concomitant coronary artery bypass. There was no early operative mortality, but there were 2 late deaths (9.6%). At follow-up (3-36 months) all valves were functioning normally, 9 patients (43%) were in NYHA functional Class I, and 4 (19%) in Class II. Our experience shows that repair of ischemic mitral insufficiency in the presence of severe left ventricular dysfunction can be performed with good results, and is preferable to mitral valve replacement. Late follow-up showed significant symptomatic improvement.

Aged↗

Effect of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease.

To assess the effects of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease, we performed radionuclide ventriculography on eight patients with normal right ventricular ejection fraction (RVEF greater than or equal to 35%) and 14 patients with mild to moderate right ventricular dysfunction (RVEF less than 35%) at rest. All patients had chronic stable angina pectoris, and nine patients had prior myocardial infarction. Radionuclide ventriculography was performed on placebo and during clinical beta-blockade (heart rate, 50 to 60 beats per minute and less than or equal to 20% increase in heart rate over baseline during stage I treadmill exercise, Bruce protocol) with the oral, cardioselective beta-blocking agent, betaxolol. The resting RVEF (mean +/- 1 SD) was 33% +/- 7% on placebo and 34% +/- 7% during clinical beta-blockade. Mean exercise RVEF was 40% +/- 8% on placebo and 39% +/- 8% during clinical beta-blockade. These differences were not statistically significant. Resting left ventricular ejection fraction ranged from 22% to 60% (mean, 42% +/- 8%). On placebo, one of eight patients with a resting RVEF greater than or equal to 35% had a normal exercise RVEF response (greater than or equal to 5% increment) whereas nine of 14 patients with resting RVEF less than 35% had normal exercise response. The discordant relationship between baseline RVEF and exercise response on placebo became less marked during clinical beta-blockade. We conclude that beta-blockade does not produce significant deterioration of right ventricular systolic function or right ventricular reserve either in patients with normal or in those with mild to moderately impaired resting right ventricular systolic function.

Adrenergic beta-Antagonists↗

Effectiveness of implantable cardioverter-defibrillators in patients with ischemic heart disease and left ventricular dysfunction.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) have been shown in primary prevention efficacy trials to reduce mortality in patients with ischemic heart disease and left ventricular dysfunction. To investigate the generalizabilty of this mortality reduction, we examined the effectiveness of ICDs in clinical practice. METHODS: We developed a prospective multicenter cohort of 770 patients with ischemic left ventricular dysfunction (ejection fraction < or =35%) and without a history of ventricular arrhythmia, of whom 395 (52%) received ICDs. Mean +/- SD follow-up was 27 +/- 12 months. We assessed the degree to which ICDs decreased mortality risk using Cox proportional hazards analyses that controlled for clinical predictors of death, receipt of ICD (a propensity score analysis), and predictors of arrhythmic death (including electrophysiologic variables). RESULTS: Multivariate Cox analyses showed that those with ICDs had significantly lower all-cause mortality (hazard ratio [HR], 0.53; 95% confidence interval [CI], 0.33-0.86). This mortality reduction was mediated through dramatically lower arrhythmia-related mortality (HR, 0.35; 95% CI, 0.17-0.73), with no significant effect on cardiovascular nonarrhythmic (HR, 0.81; 95% CI, 0.34-1.96) and noncardiovascular (HR, 0.76; 95% CI, 0.29-2.05) mortality. No differences were found between the ICD and non-ICD groups for a composite outcome of all-cause mortality, appropriate ICD shocks, or documented symptomatic ventricular arrhythmia, which suggests that the 2 groups had similar baseline risk for life-threatening arrhythmic events (HR, 0.96; 95% CI, 0.63-1.45). CONCLUSION: In clinical practice, ICDs appear to reduce all-cause and arrhythmic rates of mortality at levels similar to those found in primary prevention trials.

Aged↗

Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after myocardial infarction. Relative efficacy of medical therapy and revascularization.

BACKGROUND: The uptake of F-18 deoxyglucose into dysfunction segments after myocardial infarction identifies metabolically active (FDG+) or inactive (FDG-) myocardium. Although patients with FDG+ segments have been found to be at risk for adverse events, the prognostic significance of viable myocardium in relation to other influences on postinfarction prognosis, including revascularization, remain ill defined. The purpose of this study was to investigate the relative prognostic significance of FDG+ tissue and to establish whether myocardial revascularization in patients with viable tissue attenuates the risk of adverse outcome. METHODS AND RESULTS: One hundred thirty-seven patients with left ventricular dysfunction and resting perfusion defects after myocardial infarction underwent positron emission tomography with both dipyridamole stress Rb-82 perfusion imaging and FDG imaging. After the exclusion of 4 patients proceeding to transplantation, 2 with uninterpretable scans and 2 lost to follow-up, 129 patients were followed clinically for 17 +/- 9 months. Four groups were defined: patients with FDG+ dysfunctional myocardium who were revascularized (n = 49) or treated medically (n = 21) and those with FDG- segments who were revascularized (n = 19) or treated medically (n = 40). The groups of patients with FDG+ or FDG- findings, with and without revascularization, did not differ with respect to known determinants of postinfarction prognosis: age, left ventricular ejection fraction, or the prevalence of multivessel disease. Nonfatal ischemic events occurred in 48% of medically treated FDG+ patients compared with 8% of revascularized patients with FDG+ tissue (P < .001) and 5% of patients with FDG- myocardium (P < .001). Thirteen patients died from cardiac causes; 11 (85%) had a left ventricular ejection fraction of < 30%, and these patients were evenly distributed between FDG+ and FDG- groups. Using Cox's proportional hazards model, only the presence of FDG+ myocardium (odds ratio, 12.9; P < .001) and the absence of revascularization (odds ratio, 5.8; P = .002) independently predicted ischemic events, while only age (P = .02) and ejection fraction (P < .001) but not the presence of viable myocardium were predictive of death. CONCLUSIONS: Residual viable myocardium after myocardial infarction may act as an unstable substrate for further events unless it is revascularized. Despite this association, age and left ventricular dysfunction remained the strongest predictors of cardiac death after myocardial infarction in these patients with a spectrum of left ventricular dysfunction.

Aged↗

Regional and global right ventricular dysfunction in asymptomatic or minimally symptomatic patients with congenitally corrected transposition.

Patients with congenitally corrected transposition are at risk of right ventricular dysfunction and failure. With this in mind, we examined 13 patients with congenitally corrected transposition, 7 not having undergone surgery, and 6 after physiological repair, comparing them with 6 healthy subjects matched for age and sex, using cardiac magnetic resonance imaging, at rest and during dobutamine stress, in order to determine regional and global right ventricular response to stress. At rest, the patients had significantly decreased overall wall motion compared to their healthy peers (7.2 +/- 0.5, versus 9.8 +/- 0.4 mm). During infusion of dobutamine, overall wall motion increased to 12.8 +/- 0.4 mm in the healthy subjects, versus 8.8 +/- 1.0 mm in patients. At the regional level, significant differences in mural motion were found between patients and controls in the anterior (9.5 +/- 1.1, versus 13.2 +/- 0.6 mm), posterior (10.2 +/- 1.6, versus 13.2 +/- 0.8 mm), and septal segments (5.0 +/- 0.8, versus 11.2 +/- 0.6 mm). At rest, overall mural thickening in patients was similar to that of controls, but significantly less in patients during stress. During dobutamine stress, patients showed significantly less regional wall thickening than controls, particularly in the septal (2.7 +/- 0.6, versus 6.0 +/- 0.4 mm, respectively) and in the anterior segments (4.2 +/- 0.6, versus 7.8 +/- 0.6 mm, respectively). Right ventricular ejection fraction strongly correlated with mural motion and thickening, both at rest and during stress. Abnormal regional function in the systemic morphologically right ventricle may occur in patients with congenitally corrected transposition, which strongly correlates with right ventricular ejection fraction. Our findings support the hypothesis that, in patients with congenitally corrected transposition, ischemia of the right ventricular myocardium contributes to the development of right ventricular dysfunction.

Adult↗

Severe right ventricular dysfunction in a neonate with aortic origin of the RPA.

Anomalous origin of the right pulmonary artery from the ascending aorta (AORPA) with severe right ventricular dysfunction in a neonate was completely diagnosed by echocardiography. Cardiac catheterization was performed to explore further right ventricular dysfunction, which is extremely rare at this age. Following cardiac catheterization, the patient died. We suggest that in critically ill infants with the aforementioned condition surgical repair guided by modern echocardiography must be the chosen management.

Aorta↗

Studies of Left Ventricular Dysfunction (SOLVD).

Given the increasing incidence and dismal prognosis in congestive heart failure, it is not surprising that strenuous efforts have been made to limit the morbidity and mortality that result from this syndrome. The National Institutes of Health designed and implemented the Studies of Left Ventricular Dysfunction (SOLVD) to assess the effect of therapy with enalapril, an angiotensin-converting enzyme inhibitor, on all cause mortality in a population with left ventricular dysfunction (i.e., ejection fraction at or below 35%). Important secondary objectives included the effects of this therapy on cause-specific mortality, development of heart failure, and hospitalization for congestive heart failure. Patients within each of two arms of the trial were randomized on the basis of the administration (treatment arm) or lack (prevention arm) of concomitant therapy for congestive heart failure. The trial was double blind and placebo controlled. The mean follow-up period for the combined arms was 39.2 months, during which time there was a 16% risk reduction in all-cause mortality in the treatment arm of the trial (P equals 0.008) and an 8% risk reduction in the prevention arm (P equals NS). In the prevention arm, however, there was a 12% reduction risk for cardiovascular mortality (P equals 0.12) and a 37% reduction in risk of progression to heart failure (P is less than 0.001). Thus, the results of SOLVD indicate that therapy with an angiotensin-converting enzyme inhibitor has beneficial effects on morbidity and mortality that are apparent in a broad spectrum of patients with left ventricular dysfunction.

Journal Article↗

Prediction of global left ventricular function after bypass surgery in patients with severe left ventricular dysfunction. Impact of pre-operative myocardial function, perfusion, and metabolism.

AIMS: Previous studies have compared the accuracy of various tests of viability for the prediction of recovery of regional left ventricular function; global left ventricular recovery has been less well studied, although it has important prognostic and functional ramifications. We sought to identify the relative contribution of ischaemia, regional and global contractile reserve, perfusion and metabolic function to changes in left ventricular volumes and global function after coronary artery bypass surgery in patients with severe left ventricular dysfunction. METHODS AND RESULTS: Dipyridamole stress Rb-82, fluorodeoxyglucose positron emission tomography and low and high-dose dobutamine-atropine stress echocardiography were obtained in 66 patients with left ventricular impairment. Myocardial segments were considered viable if ischaemia or either metabolic or contractile reserve were present, on positron emission tomography or dobutamine echocardiography. Resting left ventricular function was reassessed after surgery (mean 10+/-3 weeks) in the 59 patients who had not suffered a major peri-operative event; functional improvement was defined by a 5% increment of ejection fraction. Myocardial viability was found in 37 (63%) patients using positron emission tomography and in 42 (71%) patients using dobutamine echocardiography; post-operative functional improvement was noted in 28 (47%) patients. In univariate analyses, predictors of global post-operative functional recovery included: the extent of viability according to positron emission tomography [OR (odds ratio): 2.08 for each additional viable segment, 95% CI (confidence interval): 1.33-3. 25, P=0.001] or dobutamine echocardiography (OR: 2.06 for each additional viable segment, 95% CI: 1.28-3.30, P=0.003) and the increase in ejection fraction with low-dose dobutamine (OR: 1.9 for each 1% increase in ejection fraction with low dose dobutamine, 95% CI 1.39-2.61, P<0.0001). In a multivariate model which included evidence of viability by either technique, and change in ejection fraction with low-dose dobutamine echocardiography, only change in ejection fraction with low-dose dobutamine echocardiography was predictive of post-operative left ventricular functional recovery (adjusted OR: 1.81, 95% CI: 1.30-2.52, P=0.0005). CONCLUSION: Among patients with severe left ventricular dysfunction who are referred for surgical revascularization, the overall accuracies of positron emission tomography and dobutamine echocardiography for the prediction of post-operative myocardial recovery are comparable. However, the strongest predictor of overall improvement of post-operative left ventricular function is an increase of ejection fraction with a low-dose dobutamine infusion.

Aged↗

Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine.

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in humans and animals. However, this ventricular failure is poorly characterized, and the ultrastructural consequences of supraventricular tachycardia are unknown. We serially examined right and left ventricular function, endomyocardial ultrastructure, and creatine kinase activity in eight pigs at base line and again at 1, 2, and 3 wk following rapid atrial pacing. Left and right ventricular ejection fractions fell significantly from base line after 1 wk of chronic tachycardia. Three weeks of chronic pacing resulted in further deterioration in ejection fractions. Significant biventricular chamber dilatation developed and was associated with a reduction in end-diastolic wall thickness after 2 wk of tachycardia. Mitochondrial injury and diminished mitochondrial cytochrome oxidase staining of subendocardial myocytes were observed after 2 wk of tachycardia. Endomyocardial creatine kinase activity fell from control levels following 2 wk of pacing. Postmortem examination revealed a reduction in left ventricular wall thickness compared with 14 control animals. Fibrosis occurred along the subendocardial layer in paced animals, and glycogen content was also reduced. In summary, chronic supraventricular tachycardia resulted in severe biventricular pump dysfunction and chamber dilatation that were associated with ultrastructural alterations and reduced enzyme activity of the subendocardial myocytes. These ultrastructural and metabolic changes may be potential mechanisms responsible for the ventricular dysfunction and dilatation observed in this model.

Animals↗

Adverse effects of enalapril in the Studies of Left Ventricular Dysfunction (SOLVD). SOLVD Investigators.

In the Studies of Left Ventricular Dysfunction (LVD), enalapril or placebo was administered in a double-blind fashion to 6797 participants with ejection fraction < or = 0.35. During 40 months' average follow-up, 28.1% of participants randomized to enalapril reported side effects compared with 16.0% in the placebo group (p < 0.0001). Enalapril use was associated with a higher rate of symptoms related to hypotension (14.8% vs 7.1%, p < 0.0001), azotemia (3.8% vs 1.6%, p < 0.0001), cough (5.0% vs 2.0%, p < 0.0001), fatigue (5.8% vs 3.5%, p < 0.0001), hyperkalemia (1.2% vs 0.4%, p = 0.0002), and angioedema (0.4% vs 0.1%, p < 0.05). Side effects resulted in discontinuation of blinded therapy in 15.2% of the enalapril group compared with 8.6% in the placebo group (p < 0.0001). Thus enalapril is well tolerated by patients with LVD; however, hypotension, azotemia, cough, fatigue, and other side effects result in discontinuation of therapy in a significant minority of patients.

Aged↗

Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction.

OBJECTIVE: Angiotensin-converting enzyme inhibitors are an effective therapy for all stages of heart failure due to reduced systolic left ventricular function. Because sufficient data on intravenous angiotensin-converting enzyme inhibitors following coronary artery bypass surgery complicated by postoperative left ventricular dysfunction are unavailable, the efficacy and safety of intravenously administered enalaprilat were evaluated. DESIGN: A placebo-controlled, randomized, double-blind protocol. SETTING: Postoperative intensive care unit at the German Heart Institute Berlin. PATIENTS: Forty patients with a left ventricular ejection fraction <35% following coronary artery bypass surgery on the second postoperative day or after weaning from intra-aortic balloon counterpulsation. INTERVENTIONS: A loading dose of enalaprilat 0.625 mg infused over 1 hr was followed by 5 mg/24 hrs administered continuously for up to 72 hrs. MEASUREMENTS AND MAIN RESULTS: Systemic and pulmonary hemodynamic variables, blood gases, hormonal variables, renal function, and electrolytes were measured before and repeatedly during therapy. Acute effects were as follows: At 1 hr, enalaprilat increased the cardiac index (p <.001), stroke volume index (p <.001), and right ventricular stroke work index (p <.03) compared with placebo, whereas mean arterial pressure (p <.008) and both systemic (p <.001) and pulmonary (p <.02) vascular resistance decreased. Continuous effects were as follows: Over 72 hrs, enalaprilat decreased diastolic pulmonary artery pressure (p <.019), pulmonary artery occlusion pressure (p <.02), and central venous pressure (p <.02). The cardiac and stroke volume indexes were consistently higher in the enalaprilat group, whereas systemic and pulmonary vascular resistances were lower. The arterial blood-pressure lowering effect was blunted and heart rate remained unchanged. Mixed venous oxygenation (p <.02) was higher and arterial oxygenation was not modified. Finally, enalaprilat increased creatinine clearance (p <.002) and decreased creatinine (p <.02) and urea (p <.03). CONCLUSIONS: Intravenous enalaprilat safely and effectively improves cardiac and renal function following coronary artery bypass surgery complicated by postoperative left ventricular dysfunction.

Adult↗

Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction.

OBJECTIVES: Using a model of arrhythmias associated with ischemic left ventricular (LV) dysfunction, this study investigated autonomic and electrophysiologic mechanisms associated with sudden cardiac death (SCD) in chronic heart failure (HF). BACKGROUND: Left ventricular dysfunction from ischemic heart disease is associated with many instances of SCD. Electrophysiologic and autonomic derangements occur in HF, but their contribution to SCD risk is poorly understood. METHODS: Sudden death risk was assessed in 15 dogs with a healed anterior myocardial infarction (MI) during submaximal exercise and brief acute circumflex ischemia. Left ventricular dysfunction was then induced by repetitive circumflex microembolization until LV ejection fraction reached 35%. Before embolization, six dogs were susceptible to SCD, and nine were resistant. RESULTS: Baroreflex sensitivity was lower in susceptible dogs (10 ms/mm Hg +/- 4 ms/mm Hg vs. 20 ms/mm Hg +/- 11 ms/mm Hg, p = 0.04). QT intervals from susceptible dogs were longer after MI (246 ms +/- 26 ms susceptible vs. 231 ms +/- 20 ms resistant, p < 0.001) and prolonged within eight weeks after LV dysfunction was established (from 246 ms +/- 26 ms to 274 ms +/- 56 ms, +11%, p < 0.01). Heart rate in susceptible dogs increased during transient ischemia (+20%) and with progressive LV dysfunction (102 beats/min +/- 28 beats/min baseline to 154 beats/min +/- 7 beats/min LV dysfunction, p = 0.003). All susceptible dogs had spontaneous sustained ventricular tachycardia culminating in SCD. In contrast, QT intervals in resistant dogs prolonged after 24 +/- 6 weeks (from 231 ms +/- 20 ms to 238 ms +/- 15 ms, p < 0.05), and heart rates were unchanged. Only one resistant dog died suddenly with LV dysfunction. CONCLUSIONS: Depressed vagal and elevated sympathetic control of heart rate coupled with abnormal repolarization are associated with high SCD risk when post-MI LV dysfunction develops.

Animals↗

Cardiac depression by intravenous disopyramide in patients with left ventricular dysfunction.

The hemodynamic effects of disopyramide phosphate were studied in nine patients with left ventricular dysfunction. After control measurements, administration of a 2 mg/kg bolus of disopyramide phosphate over 5 or 15 minutes was followed by a 20 minute 0.4 mg/kg/hour infusion and a 15 minute recovery period. Response to the 5 and 15 minute bolus injection was similar. Maximum hemodynamic effects occurred immediately after the bolus was given; there were decrements in systolic pressure (142 to 124 mm Hg)(p less than 0.005), cardiac index (2.5 to 1.8 liters/min/m2)(p less than 0.001) and stroke index (29.4 to 20.6 ml/beat/m2)(p less than 0.001), and increases in right atrial pressure (9 to 12 mm Hg)(p less than 0.005) and total peripheral resistance (21.2 to 25.7 U)(p less than 0.005). Two studies had to be terminated after the bolus was given due to profound hemodynamic deterioration. In the remainder, the systolic pressure returned to control by the end of the infusion, whereas the mean arterial pressure increasd significantly (92 to 96 mm Hg)(p less than 0.01). Little further change in mean arterial pressure, cardiac and stroke index, and total peripheral resistance occurred during the recovery period. These data indicated that intravenous disopyramide phosphate is a potent cardiac depressant when given over 5 to 15 minutes to patients with left ventricular dysfunction. It is concluded that disopyramide should not be administered to such patients unless conventional therapy fails. In such circumstances it should be used with extreme caution and careful monitoring.

Aged↗

Does the extended use of arterial grafts compromise the myocardial recovery after coronary artery bypass grafting in left ventricular dysfunction?

OBJECTIVE: To assess the prognostic factors of myocardial recovery expected after coronary bypass surgery and the impact of surgical technique used, a prospective non-randomized study including a 1-year postoperative evaluation of left ventricular function was performed in patients with left ventricular dysfunction (left ventricular ejection fraction (LVEF) < 0.40). METHODS: From 1993 to 1996, 110 patients (mean age 61+/-11 years) were included in the study. The mean LVEF was 31+/-6%. All patients had preoperative radionuclide investigations based on the combination of stress/reinjection thallium single photon emission computed tomography (SPECT) and planar evaluation of LVEF; 88% of patients had reversible ischemic thallium defects. Two surgical technique were used: 53 patients received the left internal mammary artery with associated sequential vein graft, and 57 patients received only arterial grafts, internal mammary and gastroepiploic arteries. The mean number of distal anastomoses was 3.2+/-0.8 and 54% of patients had complete revascularization. At 1 year, all survivors had clinical evaluation and the same radionuclide investigations. RESULTS: The early mortality was 2.7%. At 1 year, 100 patients were surviving; on average, NYHA class decreased 1.9+/-0.8 to 1.4+/-0.6 (P < 0.01) and CCS class from 2.8+/-0.6 to 1+/-0.3 (P < 0.01). The mean LVEF increase from 31+/-9 to 34+/-10% (P < 0.01) and the mean LV end-diastolic volume decreased from 317+/-112 to 285+/-108 ml (n.s.). The postoperative improvement in LV function was higher in patients in NYHA class 3 or 4 before surgery (P < 0.05), when associated sequential vein graft had been used (P < 0.01), and in patients with low preoperative LVEF (P < 0.01). The postoperative LVEF improvement observed was significantly correlated with the improvement in left ventricular end-diastolic (LVED) volume and the improvement in redistribution/reinjection thallium uptake. Multivariate analysis showed that the surgical technique used and the preoperative LVEF were independent prognostic factors of the postoperative myocardial function recovery, with a significant positive impact of the vein use. CONCLUSION: This study confirms the excellent clinical results of coronary artery bypass grafting (CABG) in patients with coronary artery disease and LV dysfunction; improvement in LV function can be documented objectively and is correlated with reperfusion of hibernating myocardium. However, the extended use of arterial grafts does not allow to achieve the significant myocardial recovery observed with the use of one internal mammary artery (IMA) and associated sequential vein graft; it seems to be related to the preoperative selection of patients, but a direct negative impact of arterial grafts was documented and leads to be cautious in patients with severe LV dysfunction.

Abdominal Muscles↗

Impact of valvular regurgitation and ventricular dysfunction on long-term survival in patients with chest pain.

Doppler echocardiography is often used in evaluating patients with chest pain, but information on prognostic value of this testing and data to help guide selective use are limited. We prospectively studied 448 patients admitted from the emergency department for acute chest pain to assess the utility of qualitative echocardiographic data in predicting long-term survival and the incremental value of this information over routine clinical and electrocardiographic data. Doppler echocardiograms, recorded an average of 21 hours after presentation, were analyzed independently by 2 echocardiographers for global left and right ventricular function and valvular disease. Regional function was assessed by wall motion index. Data on long-term survival were collected with an average follow-up of 35.0 +/- 12.1 months. In univariate Cox regression analysis, left ventricular function and size, wall motion index, right ventricular function, and aortic, mitral, and tricuspid insufficiency were significant predictors of total and cardiovascular mortality. In multivariate analysis, moderate or severe left ventricular dysfunction (mortality rate ratio 3.2, 95% confidence intervals 1.8 to 5.8] and more than mild valvular regurgitation (mortality rate ratio 2.0, 95% confidence interval 1.1 to 3.6) were independent predictors of mortality in a model adjusted for clinical and electrocardiographic data. These factors were more common in patients aged >60 years, in those with prior acute myocardial infarction or angina, and in those with rales on physical examination. In the absence of these clinical characteristics, only 8 of 124 patients (7%) had moderate or severe left ventricular dysfunction or valvular regurgitation. In patients with moderate or severe regurgitation, a murmur was noted on the admission physical examination in 41 of 69 cases (59%). We conclude that echocardiographic evidence of moderate or severe left ventricular dysfunction or valvular regurgitation identifies a high-risk group for overall and cardiovascular mortality in patients with chest pain, and this evidence may not be detected clinically.

Adult↗