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PubMed1998

[Biphasic course of left ventricular dysfunction in a 22-year-old female with acute myocarditis].

HISTORY AND CLINICAL FINDINGS: Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pain. Physical examination was unremarkable. INVESTIGATIONS: Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 609 U/l, creatine kinase-MB 42 U/l, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECG. Echocardiography revealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricular function. Antimyosin scintigraphy was very abnormal. Cardiac catheterization confirmed the left ventricular dysfunction, rise of left ventricular enddiastolic pressure to 17 mm Hg, and a markedly reduced cardiac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis with marked myocytolysis and considerable lymphocytic infiltrations. Enteroviral RNA was demonstrated in the myocardium by polymerase chain reaction. TREATMENT AND COURSE: The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histologically and immunohistologically, and left ventricular function was also normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, though moderate, impairment in left ventricular function, indicating a dilated cardiomyopathy. INTERPRETATION: Even when histological and immunohistological evidence of healing of an acute viral myocarditis has been achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiological mechanism of this occurrence remains unknown.

Acute Disease↗

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↗

PubMed1991

[The effect of nifedipine and diltiazem on left ventricular function in patients with stable angina pectoris and severe left ventricular dysfunction].

In a double blind crossover five-week trial with a randomized onset in 12 patients with normal blood pressure, stable angina pectoris and more severe left ventricular dysfunction (ejection fraction less than or equal to 40%) the effect of placebo nifedipine and diltiazem on left ventricular function and tolerance of exercise was compared. The investigation was done by means of echocardiography after a load with stimulation of the heart by an oesophageal electrode. As compared with placebo, only diltiazem retarded significantly the period before development of stenocardia on stimulation of the heart. There was no significant difference between nifedipine and diltiazem as regards the effect exerted on the ejection fraction and time which elapsed after stimulation before stenocardia developed. The authors observed an unequal response of patients to the administration of nifedipine and diltiazem (some patients had less favourable findings, although they were not subjectively aware of this deterioration). Therefore these drugs must be administered to patients with angina pectoris and more severe left ventricular dysfunction with care and only if other drugs (nitrates or angiotensin convertase inhibitors) do not eliminate ischaemia and pain.

Adult↗

PubMed1993

Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors.

BACKGROUND: Left ventricular enlargement and the development of chronic heart failure are potent predictors of survival in patients after myocardial infarction. Prospective studies relating progressive ventricular enlargement in individual patients to global and regional cardiac dysfunction and the onset of late chronic heart failure are not available. It was the aim of this study to define the relation between left ventricular dilatation and global and regional cardiac dysfunction and to identify early predictors of enlargement and chronic heart failure in patients after myocardial infarction. METHODS AND RESULTS: Left ventricular volumes, regional area shrinkage fraction in 18 predefined sectors (gated single photon emission computed tomography), global ejection fraction, and hemodynamics at rest and during exercise (supine bicycle, 50 W, 4 minutes, Swan-Ganz catheter) were assessed prospectively 4 days, 4 weeks, 6 months, and 1.5 and 3 years after first myocardial infarction. Seventy patients were assigned to groups with progressive, limited, or no dilatation. Patients without dilatation (n = 38) maintained normal volumes and hemodynamics until 3 years. With limited dilatation (n = 18), left ventricular volume increased up to 4 weeks after infarction and stabilized thereafter; depressed stroke volume was restored 4 weeks after infarction and then remained stable at rest. Wedge pressure during exercise, however, progressively increased. With progressive dilatation (n = 14), depressed cardiac and stroke indexes were also restored by 4 weeks but progressively deteriorated thereafter. Area shrinkage fraction as an estimate of regional left ventricular function in normokinetic sectors at 4 days gradually deteriorated during 3 years, but hypokinetic and dyskinetic sectors remained unchanged. Global ejection fraction fell after 1.5 years, whereas right atrial pressure, wedge pressure, and systemic vascular resistance increased. By multivariate analysis, ejection fraction and stroke index at 4 days, ventriculographic infarct size, infarct location, and Thrombolysis in Myocardial Infarction trial grade of infarct artery perfusion were significant predictors of progressive ventricular enlargement and chronic dysfunction. CONCLUSIONS: Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.

Aged↗

PubMed1991

[The long-term results of aortocoronary bypass surgery in patients with a severe preoperative left ventricular dysfunction].

We analyze retrospectively the short- and long-term results of coronary artery bypass surgery in 50 patients with severe left ventricular dysfunction operated in a period of 11 years. Sixty-six percent of patients had unstable angina and 12% of total presented angina post-acute postmyocardial infarction. Thirty-eight percent of patients were in preoperative functional class III-IV of NYHA. Three-vessel disease was present in 70% of the patients, two-vessel in 30%, and the main trunk was affected in 12% of the global. Hospital mortality was 4% (2/50) due to low cardiac output syndrome. Follow-up was available in all the survivors and ranged 6 months-11 years (mean: 4.8 +/- 3.1). During follow-up, 13 patients died, but in only six was due to cardiac cause. The 35 patients followed were in functional class I-II of NYHA. Eighty-eight percent of the patients were angina free at follow-up. Actuarial analysis, after exclusion of 3 patients who died of causes no directly related to the heart, showed an intrahospital survival rates of 96%; at first year was 92, at 3rd was 78%, and 5th year survival rates were 75%. In conclusion, patients with symptomatic angina and preoperative severe left ventricular dysfunction, coronary artery bypass graft has a low hospital mortality, is effective in improving angina and heart failure, and the long-term survival is acceptable.

Actuarial Analysis↗

PubMed1993

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↗

PubMed1999

Effect of the angiotensin-converting enzyme inhibitor trandolapril on mortality and morbidity in diabetic patients with left ventricular dysfunction after acute myocardial infarction. Trace Study Group.

OBJECTIVES: This study evaluated the efficacy of long-term treatment with the angiotensin-converting enzyme (ACE) inhibitor trandolapril in diabetic patients with left ventricular dysfunction after acute myocardial infarction (AMI). BACKGROUND: Patients with diabetes mellitus have a high mortality following AMI, probably due to a high risk of congestive heart failure and reinfarction. Because ACE inhibition effectively reduces progression of heart failure, it could be particularly beneficial in diabetic patients after AMI. METHODS: The study is a retrospective analysis using data from the Trandolapril Cardiac Evaluation (TRACE) study, which was a randomized, double-blind, placebo-controlled trial of trandolapril in 1,749 patients with AMI and ejection fraction < or =35%. The mean follow-up time was 26 months. RESULTS: A history of diabetes was found in 237 (14%) of the 1,749 patients. Treatment with trandolapril resulted in a relative risk (RR) of death from any cause for the diabetic group of 0.64 (95% confidence interval 0.45 to 0.91) versus 0.82 (0.69 to 0.97) for the nondiabetic group. In the diabetic group, trandolapril reduced the risk of progression to severe heart failure markedly (RR, 0.38 [0.21 to 0.67]), and no significant reduction of this end point was found in the nondiabetic group. CONCLUSIONS: The ACE inhibition after myocardial infarction complicated by left ventricular dysfunction appears to be of considerable importance in patients with diabetes mellitus by saving lives and substantially reducing the risk of progression to severe heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

[The CAPITOL study (Captopril Post Infarction Tolerance). A trial of progressive titration of captopril after myocardial infarct with left ventricular dysfunction].

The objective of CAPITOL (Captopril Post Infarction Tolerance) multicentre open trial was to study the tolerance of a protocol of titration of Captopril in patients with recent myocardial infarction complicated by left ventricular dysfunction. Five hundred and four patients, with a mean age of 62 +/- 12 years, were included during the hospital period in the 74 participating intensive care units, 9 +/- 6 days after myocardial infarction (ejection fraction 34 +/- 6%). After a 6.25 mg test dose of Captopril, the dosage was progressively increased to the target dose of 150 mg at the end of the first month. Of the 504 patients included, 343 finished the trial and 161 stopped the trial prematurely. At the end of the hospital period, 73% received 75 mg/day: at the first follow-up visit (27 +/- 16 days after inclusion), 59% had attained 150 mg/day, this proportion increasing to 71% at the end of the trial (79 +/- 33 days after inclusion). There was no significant change in blood pressure for the whole study population. However, the systolic blood pressure of the patients receiving 150 mg/day of Captopril at the end of the trial was slightly higher than that observed at the end of the hospital period (126 +/- 17 mmHg and 116 +/- 17 mmHg respectively, p = 0.006). Severe Intercurrent events were observed in 89 patients: 24 deaths, 7 recurrent infarctions, 58 hospital admissions (21 for cardiac failure, 15 for recurrence of angina, 11 aorto-coronary bypass operations, 7 coronary angioplasties, 2 cerebro-vascular accidents, 2 systemic emboli). Of the benign complications, hypotension was observed in 25% of patients, nearly half of which occurred during the hospital admission. The drugs prescribed in association with Captopril were Aspirin (78%), betablockers (57%), nitrate derivatives (42%) and diuretics (27%). Multivariate analysis showed 3 factors associated with good tolerance of the 150 mg dosage of Captopril: Killip Class I or II on admission, an ejection fraction > 30% and an initial systolic blood pressure > 100 mmHg. In conclusion, in this trial of dose titration, 3 out of 4 patients with myocardial infarction and left ventricular dysfunction, tolerated the 150 mg/day dosage of Captopril. Patients in the trial could also be treated with drugs recommended after myocardial infarction, in particular the betablockers. Arch Mal Coeur 1999: 92: 395-403.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Combined assessment of left ventricular function and rest-redistribution regional myocardial thallium-201 activity for prognostic evaluation of patients with chronic coronary artery disease and left ventricular dysfunction.

BACKGROUND: This study evaluated the prognostic value of combined assessment of left ventricular (LV) function and regional myocardial thallium activity in patients with nonrecent myocardial infarction and LV dysfunction. METHODS AND RESULTS: Eighty-two patients with previous myocardial infarction (>8 weeks) and echocardiographic evidence of LV dysfunction underwent thallium-201 rest-redistribution tomography and cardiac catheterization. During the follow-up period (mean 25 months) there were 18 cardiac events (14 deaths and 4 nonfatal myocardial infarctions). Multivariate Cox regression analysis on clinical, angiographic, and thallium variables showed that the number of echocardiographic dysfunctional segments with preserved thallium uptake (> or =50% of peak activity; chi-square 11.03; p<0.005) and age (chi-square 8.12, p<0.01) were predictive of poor outcome. At incremental analysis, combined echocardiographic and thallium data provided significant additional information to clinical, thallium, and LV functional data, increasing global chi-square value from 22.4 to 31.5 (p< 0.01). Similarly, combined data gave additional information after considering clinical, echocardiographic, and LV functional data, increasing global chi-square from 17.8 to 22.3 (p <0.05). Differently, the number of diseased vessels at coronary angiography did not add further prognostic information. CONCLUSIONS: In patients with previous myocardial infarction and chronic LV dysfunction, the combination of echocardiographic and thallium rest-redistribution imaging data gives prognostic information incremental to those of clinical and LV functional data and to those of each technique considered separately.

Cardiac Catheterization↗

PubMed2002

Reversible left ventricular dysfunction simulating a myocardial infarction after pericardiectomy.

A 39 year old man with postoperative constrictive pericarditis after pericardiectomy developed major left ventricular systolic dysfunction with an anterior wall infarct pattern on ECG but no regional wall motion abnormalities by echocardiography or serum enzymatic evidence of a myocardial infarction. The left ventricular dysfunction resolved over two weeks with supportive treatment. It is postulated that this patient's transient left ventricular dysfunction and ECG changes were caused by myocardial inflammation and oedema induced by operative trauma during pericardiectomy.

Adult↗

PubMed2004

Effect of physical exercise training on health-related quality of life and exercise tolerance in patients with left ventricular dysfunction.

OBJECTIVES: The improvement of exercise tolerance and quality of life (QOL) are essential in the treatment of patients with heart failure. The influence of physical exercise training on QOL was investigated in patients with left ventricular dysfunction. METHODS: Health-related QOL was evaluated using the Medical Outcomes Study Short-Form 36 Health Status Survey (SF-36) before and 3 months after individualized exercise training determined by cardiopulmonary exercise testing in 65 patients. The 44 patients who could carry out more than two-thirds of the prescribed exercise were classified into two groups: Group A (11 patients)with left ventricular ejection fraction < 40% and Group B (33 patients) with left ventricular ejection fraction > or = 40%. The remaining 21 patients served as the control group. RESULTS: The mean value of SF-36 improved significantly with exercise training only in Group A (50.8 +/- 25.3 to 62.1 +/- 22.2, p < 0.05). Group A also had an increase in peak Vo2 (18.9 +/- 3.5 to 21.4 +/- 3.6 ml/min/kg, p < 0.005) and a decrease in brain natriuretic peptide. The 24 patients (9 in Group A, 15 in Group B) with improved SF-36 values after the exercise training showed a negative correlation between the change of the mental component summary and the peak Vo2 (r = - 0.606, p < 0.05). CONCLUSIONS: Exercise training improves both the QOL, especially the mental component, and the exercise tolerance in patients with left ventricular dysfunction.

Adult↗

PubMed1992

Regional left ventricular wall thickening. Relation to regional uptake of 18fluorodeoxyglucose and 201Tl in patients with chronic coronary artery disease and left ventricular dysfunction.

BACKGROUND: In previous studies comparing regional 201Tl (201Tl) and 18fluorodeoxyglucose (FDG) activity in patients with chronic coronary artery disease and left ventricular dysfunction, we hypothesized that regions with mild-to-moderate reduction in FDG activity and regions with mild-to-moderate irreversible 201Tl defects after 3- to 4-hour redistribution represent viable myocardium. In the present study, regional FDG and 201Tl activities were compared with regional systolic wall thickening by gated magnetic resonance imaging (MRI) to confirm the presence of viable myocardium in these territories. METHODS AND RESULTS: Twenty-five patients with chronic stable coronary artery disease and left ventricular dysfunction (ejection fraction, 28 +/- 10) underwent exercise 201Tl tomographic imaging (SPECT), using a reinjection protocol, positron emission tomography (PET) with FDG and H2(15)O, and gated MRI. Matched SPECT, PET, and MRI tomograms were analyzed. From the PET data, 105 regions had matched reduction in FDG and blood flow, of which 69 regions had moderately reduced FDG uptake (50-79% uptake relative to a normal reference region) and 36 had severely reduced FDG uptake (less than 50% of normal activity). Regions with moderately reduced as compared with severely reduced FDG activity had greater end-diastolic wall thickness (9.4 +/- 2.6 versus 8.0 +/- 3.7 mm; p less than 0.05) and regional systolic wall thickening (1.7 +/- 2.7 versus -0.7 +/- 2.1 mm; p less than 0.01). From the SPECT data, 169 irreversible 201Tl defects after 3-4 hour redistribution were identified, of which 70 were mild (greater than 65 to less than 85% of maximal 201Tl activity), 52 were moderate (50-65% of maximal activity), and 47 were severe (less than 50% of maximal activity). Regional systolic wall thickening was greater in regions with normal 201Tl uptake (3.3 +/- 2.3 mm) as compared with all other regions. Regions showing only mild or moderate irreversible defects at redistribution, however, showed wall thickening (2.4 +/- 2.4 and 2.2 +/- 2.5 mm, respectively), which was similar to that observed in regions with reversible 201Tl defects (2.1 +/- 2.2 mm). Only regions with severe irreversible defects at redistribution showed absence of thickening (-0.1 +/- 2.9 mm, p less than 0.01 versus all other groups). After 201Tl reinjection, 12 of 47 (26%) regions with severe irreversible defects showed enhanced 201Tl uptake. The impairment in regional systolic wall thickening was not significantly different between 201Tl defects with and without enhanced 201Tl uptake after reinjection. FDG activity, however, was present in all 12 regions (100%) with enhanced 201Tl uptake after reinjection as compared with only five of 35 (14%) that were unchanged after reinjection (p less than 0.01). CONCLUSIONS: Therefore, preserved wall thickness and systolic wall thickening in regions with moderate reduction in blood flow and FDG activity, and in irreversible 201Tl defects that are only mild-to-moderate, provide additional evidence that such regions represent viable myocardium. Moreover, the finding of metabolic activity and 201Tl uptake in regions with reduced blood flow and absent wall thickening provides clinical evidence of hibernating myocardium in humans.

Adult↗

PubMed2000

Augmented response in plasma brain natriuretic peptide to dynamic exercise in patients with left ventricular dysfunction and congestive heart failure.

OBJECTIVES: We have previously demonstrated that patients with symptomatic congestive heart failure (CHF), but not with asymptomatic left ventricular dysfunction (LVD), have augmented plasma atrial natriuretic peptide (ANP) response to exercise. Plasma brain natriuretic peptide (BNP) response to exercise is less extensively studied. The aim of this study was to determine whether responses of plasma BNP during exercise normalized for exercise workload are altered in patients with LVD and CHF. SUBJECTS AND METHODS: Twenty-nine patients with LVD, 32 patients with CHF (NYHA classes II-III) and 27 age-matched control subjects were studied. Ventilatory, plasma ANP and BNP responses were assessed during symptom-limited cardiopulmonary exercise testing. Plasma natriuretic peptide levels were measured at rest and immediately after peak exercise. The increment in plasma BNP was divided by the increment in oxygen uptake (VO2) from rest to peak exercise, and this ratio [BNP exercise ratio: (peak BNP - rest BNP)/(peak VO2 - rest VO2)] was compared amongst the three groups. RESULTS: Peak VO2 (Control, LVD and CHF: 28.2 +/- 1.7, 21.1 +/- 1.8, 16.2 +/- 0.6 ml, min(-1) kg(-1), respectively), anaerobic threshold and peak workload became smaller as heart failure worsened. Resting and peak plasma ANP levels were significantly higher only in CHF, whilst resting and peak plasma BNP levels displayed a significant and continuous increase from normal subjects to LVD and CHF. The ANP exercise ratio (1.25 +/- 0.36, 2.61 +/- 0.57, 7.72 +/- 1.65, ANOVA P = 0.0002) was significantly higher only in patients with CHF, whilst the BNP exercise ratio (0.35 +/- 0.10, 2.60 +/- 0.69, 4.98 +/- 0.97, ANOVA P = 0.0001) was significantly higher in patients with LVD and became progressively higher in patients with CHF. CONCLUSIONS: These data showed that the BNP exercise ratio, an exercise plasma BNP response normalized with exercise workload, was augmented in patients with LVD, and became progressively higher in CHF, suggesting that an augmented exercise BNP ratio exists early in the course of developing CHF.

Anaerobic Threshold↗

PubMed2006

Critical level of cerebral oxygenation during exercise in patients with left ventricular dysfunction.

BACKGROUND: In a recent study the indexes of cerebral oxygenation decreased during maximal exercise in nearly half of all patients with left ventricular dysfunction. Whether these levels decrease severely enough to influence mental status or level of consciousness was evaluated in the present study. METHODS AND RESULTS: Forty-two patients with idiopathic dilated cardiomyopathy (IDC) and 29 healthy subjects underwent a symptom-limited maximal exercise test. The cerebral oxyhemoglobin (O(2)Hb) and tissue oxygenation index (TOI) were continuously monitored using near-infrared spectroscopy. The changes in O(2)Hb and TOI were also measured in 7 subjects: 2 who experienced episodes of reduced consciousness caused by sudden decreases in blood pressure during exercise recovery and 5 who exhibited sustained ventricular tachycardia during an electrophysiological study. The change in cerebral O(2)Hb during exercise in patients with IDC averaged 0.38+/-3.39 micromol/L, significantly lower than in the normal subjects (4.30+/-4.47 micromol/L, p<0.0001). The cerebral O(2)Hb decreased during exercise in 18 of 42 patients with IDC. The change in cerebral TOI in the IDC patients during exercise was significantly less than that in the normal subjects (-2.0+/-4.7 vs 2.1+/-5.8%, p=0.002). The mean decreases in cerebral O(2)Hb and TOI were -5.34 micromol/L and -9.7%, respectively, in the patients with reduced consciousness during exercise recovery, and -2.52 micromol/L and -16.5%, respectively, in those with ventricular tachycardia. CONCLUSION: The indexes of cerebral oxygenation may drop severely enough during maximal exercise in some patients with severe IDC that consciousness is affected.

Aged↗

PubMed2004

Early and midterm outcome after off-pump coronary artery bypass grafting in patients with left ventricular dysfunction.

BACKGROUND: The purpose of this study was to define the early outcome and the potential for midterm survival in patients with left ventricular dysfunction (LVD) who undergo off-pump coronary artery bypass (OPCAB) and to compare these results with those of conventional coronary artery bypass grafting (CABG). METHODS: Medical records of patients with LVD (n = 732) between January 1998 and March 2002 were retrospectively reviewed. There were 523 patients with moderate LVD (ejection fraction, 30%-50%; 463 CABG versus 60 OPCAB) and 209 patients with severe LVD (ejection fraction, < 30%; 136 CABG versus 73 OPCAB). Midterm survival data (mean follow-up, 2.3 years) were obtained from the National Death Index. Groups were compared by multivariate Cox proportional hazard models, and Kaplan-Meier curves were plotted. RESULTS: CABG patients had lower European System for Cardiac Operative Risk Evaluation values (5.3 versus 7.2 and 8.0 versus 9.6 in moderate and severe LVD subgroups, respectively; P < .001). There were no differences (OPCAB versus CABG) in 30-day mortality (3.3% versus 1.9%, moderate LVD group, P = .366; 6.8% versus 4.4%, severe LVD group, P = .521), length of stay (9.3 versus 8.6 days, moderate LVD group, P = .683; 11.9 versus 11.8 days, severe LVD group, P = .423), and postoperative complications (13.3% versus 11.0%, moderate LVD group, P = 0.663; 16.4% versus 20.6%, severe LVD group, P = .581). Successful coronary bypass in patients with severe LVD was associated with 68.2% and 66.2% actuarial 48-month survival rates for the CABG and OPCAB patients, respectively (P = .336), and these rates rose to 86.0% and 82.9% in patients with moderate LVD (P = .121). When CABG patients with moderate LVD were considered the reference group, the adjusted hazard ratio of OPCAB patients with moderate LVD for midterm mortality was 1.32 (95% confidence interval, 0.61-2.87; P = .481). CABG and OPCAB patients with severe LVD had the same adjusted hazard ratio of 1.86, and this figure was statistically significant compared with the value for the reference group (P = .011 and P = .039, respectively). CONCLUSIONS: Patients with LVD can derive midterm benefit from coronary bypass. OPCAB in higher-risk patients had early and midterm outcomes similar to those of CABG.

Aged↗

PubMed1984

Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest.

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.

Adult↗

PubMed2006

Total arterial revascularisation in left ventricular dysfunction.

The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel discase and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery (right internal mammary artery 40.8%, radial artery 33.5%, other 7.8%). The perioperative mortality was 2.2%, myocardial infarction 1.7% and stroke 0.6%. Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.

Adult↗