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PubMed1995

Prognostic significance of right ventricular dysfunction in patients with acute inferior myocardial infarction and right ventricular involvement.

Little is known about the influence of right ventricular (RV) dysfunction on prognosis of patients with acute inferior myocardial infarction (IMI) and RV involvement. Therefore, 99 consecutive patients (mean age 56.6 +/- 3.4 years) with RV involvement during acute IMI were followed for a 12-month period to clarify the influence of acute RV dysfunction on short- and long-term survivals. Forty-one patients with IMI evolved with severe arterial hypotension due to RV dysfunction, while 58 patients had no hemodynamic impairment due to RV involvement. Basal hemodynamic data (mean +/- SD) for patients with RV dysfunction were blood pressure (BP) 92/59 +/- 22/20 mmHg, systemic vascular resistance (SVR) 2314 +/- 252 dynes.s.cm-5, and cardiac index (CI) 1.3 +/- 0.3 l/min/m2. Patients without RV dysfunction demonstrated BP 113/74 +/- 20/16 mmHg (p < or = 0.05), SVR 1324 +/- 354 dynes.s.cm-5 (p < or = 0.01), and CI 2.6 +/- 0.5 l/min/m2 (p < or = 0.05). Angiographic differences noted were that hemodynamically compromised patients showed lower RV ejection fractions (0.27 +/- 0.08) than patients without hemodynamic disturbance [0.41 +/- 0.11 (p < or = 0.05)]; however, left ventricular ejection fractions were 0.48 +/- 0.10 and 0.52 +/- 0.12, respectively. Short- and long-term mortality rates were assessed during the follow-up period. Patients with hemodynamic impairment due to RV infarction had a higher mortality rate for the first month and for 11 subsequent months post MI than patients without hemodynamic impairment, that is 24.4 vs. 6.9 and 14.6 (p <or = 0.05) vs. 3.4 (p < or = 0.05), respect ively.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗
PubMed1994

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

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

Angiotensin II↗
PubMed1998

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

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

Animals↗
PubMedDate not supplied

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

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

Aged↗
PubMed2000

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

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

Adult↗
PubMed1998

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

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

Aged↗
PubMed1988

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

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

Adult↗
PubMed1993

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

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

Cardiac Catheterization↗
PubMed1987

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

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

Aged↗
PubMed2001

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

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

Animals↗
PubMed1985

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

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

Adult↗
PubMed1993

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

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

Adolescent↗
PubMed2000

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

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

1-Deoxynojirimycin↗
PubMedDate not supplied

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

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

Adult↗
PubMed1998

[Pulmonary uptake of thallium-201 at rest and diastolic function in patients with ischemic cardiopathy and left ventricular dysfunction].

An elevated thallium-201 lung uptake after stress is currently considered a marker of severe coronary artery involvement and related to adverse prognosis. The meaning of this scintigraphic finding on rest thallium-201 images is yet poorly investigated. We compared the thallium-201 lung uptake and the left ventricular diastolic function from mitral Doppler in 24 patients (64 +/- 10 years) with ischemic heart disease and severe left ventricular dysfunction (ejection fraction 28 +/- 10%). All patients underwent a 3-view planar rest-redistribution thallium-201 and 2D-echo studies within 6 days, while clinically stable. The amount of thallium-201 lung uptake was quantified as the ratio (L/H) between the activity in a left lung region of interest (L) and that observed in the left ventricle (H). From mitral Doppler, early (E) and late (A) filling velocities, the E/A ratio and the deceleration time of early filling (DecT) were calculated. An elevated L/H (> or = 0.54) was observed in 9 patients (37%). They showed a lower ejection fraction (20 +/- 4% vs 33 +/- 10% in patients with normal L/H; p < 0.01) and a higher wall motion score index (2.5 +/- 0.4 vs 2.1 +/- 0.4, p < 0.05). A significant inverse linear relation was observed between L/H and the left ventricular ejection fraction (r = -0.70); no significant relation was observed between L/H and left ventricular end-diastolic volumes or wall motion score index. A significant linear relation was also observed between L/H and E/A (r = 0.74; p < 0.001) as well as L/H and DecT (r = -0.61; p < 0.001); an even stronger, inverse, relation was found between L/H and A (r = -0.81; p < 0.001). An abnormal L/H identified 80% of patients with a restrictive filling pattern (specificity 93% and accuracy 88%, respectively). In conclusion, in stable patients with ischemic heart disease and ventricular dysfunction, L/H on rest thallium-201 images is closely correlated with Doppler indexes of left ventricular diastolic filling dynamic; an abnormal L/H is highly predictive of a restrictive filling pattern.

Aged↗
PubMed1990

[Can ventricular dysfunction be prevented or delayed in course?].

Left ventricular dysfunction is asymptomatic or paucisymptomatic for a long time. It would be beneficial if progression to the symptomatic stages could be prevented. This is only possible when the abnormal conditions of cardiac load or perfusion which cause the myocardial disease, can be corrected. The treatment of hypertension or valvular disease is an example of this approach. Another approach is to reduce the perverse effects of the neurohormonal adaptations to cardiac failure. The treatment of chronic myocardial infarction by angiotensin converting enzyme inhibitors is an example of this approach.

Animals↗
PubMed2000

Effect of exercise training on heart rate variability in patients with new-onset left ventricular dysfunction after myocardial infarction.

BACKGROUND: Cardiac rehabilitation with exercise training alters sympathovagal control of heart rate variability (HRV) toward parasympathetic dominance in patients after acute myocardial infarction (MI). However, its effects on HRV in patients after MI with new-onset left ventricular dysfunction are yet unknown. We aimed to investigate the effects of 8 weeks of supervised, high-intensity exercise training on time- and frequency-domain measures of HRV in this selected patient population. METHODS AND RESULTS: Twenty-five men with an acute MI and a low ejection fraction were randomly assigned to enter or not to enter a training program in a regional rehabilitation center. HRV was evaluated before and after 1 and 2 months of training and at 12 months. Maximal exercise testing with respiratory gas exchange was performed at baseline and after training. Resting heart rate decreased (P <. 01) and the percentage of R-R intervals differing >50 ms from the preceding one (pNN50) increased (P <.05) after training. The standard deviation of R-R intervals (SDRR) tended to increase, but frequency-domain indexes remained unchanged. There was a significant decrease in SDRR (P <.05) and high-frequency power (P <.01) at 12 months in untrained patients. Exercise time increased by 38% and maximal oxygen uptake increased by 29% in the training group (P <. 01). CONCLUSIONS: Despite beneficial effects on clinical variables, exercise training did not markedly alter HRV indexes. A significant decrease in SDRR and high-frequency power in the control group suggests an ongoing process of sympathovagal imbalance in favor of sympathetic dominance in untrained patients after MI with new-onset left ventricular dysfunction.

Aged↗
PubMed1996

Is severe left ventricular dysfunction a contraindication to participation in an exercise rehabilitation programme?

OBJECTIVE: To evaluate the effects of an exercise training programme on patients with chronic left ventricular dysfunction. DESIGN: Intervention, before and after the trial. SETTING: Johannesburg Cardiac Rehabilitation Centre, a phase III community-based cardiac rehabilitation facility. PATIENTS: A consecutive sample of 28 patients who were recovering from acute myocardial infarction and who had a left ventricular ejection fraction of 30% or less. Twenty two patients completed the exercise training programme. INTERVENTION: A medically supervised exercise training programme of 6 months' duration. Type of exercise: walking, jogging or cycling. Intensity: 65-85% of the patient's maximal heart rate achieved during treadmill testing. DURATION: 30-45 minutes. Frequency: 3 times a week. Patients who attended fewer than 60% of all prescribed sessions were considered drop-outs. MAIN OUTCOME MEASURES: Haemodynamic, left ventricular function and effort tolerance parameters before and after training. RESULTS: Patients who completed the exercise training programme showed a significant improvement in maximal exercise capacity and a significant reduction in their cardiovascular demands during submaximal exercise. Peak oxygen consumption was increased by 12% after training (19.4 +/- 3 v. 21.8 +/- 4.8 ml/kg/min; P < 0.05) and exercise time to exhaustion by 33% (527 +/- 171 v. 700 +/- 186 seconds; P < 0.001). The double product at the same submaximal workload was significantly reduced (214 +/- 52 v. 194 +/- 44 beats/min x mmHg x 10(2); P < 0.05). These benefits were achieved without any adverse effects on resting (25.4 +/- 5 v. 28.5 +/- 7.9%; P < 0.05) or exercise (27.3 +/- 7.7 v. 29.9 +/- 9.5%; P > 0.05) left ventricular ejection fraction. CONCLUSIONS: Our results show that patients with chronic left ventricular dysfunction can benefit from an exercise training programme and that those benefits can be achieved without risk of further deterioration in left ventricular function. Physical training constitutes another therapeutic option which could be added to the comprehensive management of these patients.

Adult↗