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PubMed1990

Unrecognized left ventricular dysfunction in an apparently healthy cocaine abuse population.

To determine the frequency and severity of clinically unrecognized left ventricular (LV) dysfunction related to cocaine use, 84 asymptomatic cocaine abusers underwent cardiac evaluation which included chest x-ray, electrocardiography (ECG), and radionuclide angiography after a two-week abstinence from cocaine use. LV dysfunction was discovered in 6/84 (7%). Regional wall motion abnormalities suggesting a localized myocardial abnormality were found in 2, whereas an ejection fraction less than 50% suggesting a more global process was noted in 4. An abnormal chest x-ray was found in only 1 subject and none had abnormal ECGs. In each of these cases, repeated and protracted use of cocaine was documented and the suggestion of cardiac dysfunction was supported by at least one other independent abnormal finding. In these 6 cases, the dysfunction was clinically unrecognized and unsuspected after routine evaluation. The significance of subclinical LV dysfunction in this population has not been determined and requires long-term study.

Adult↗
PubMed2005

Left ventricular dysfunction in subjects with mild secondary hyperparathyroidism detected with pulsed wave tissue Doppler echocardiography.

AIMS: To assess left ventricular function by conventional and pulsed wave tissue Doppler (PWTD) echocardiography in subjects with mild secondary hyperparathyroidism, and to evaluate whether PWTD would be more sensitive than conventional echocardiography in detecting subtle changes in LV systolic and diastolic function. METHODS: In the fifth Tromsø study (2001) serum PTH and calcium were measured in 7,954 subjects. One hundred subjects with secondary hyperparathyroidism (SHPT; serum PTH >6.40 pmol/l and serum calcium <2.40 mmol/l) and 106 control subjects with normal PTH and calcium levels and with no history of cardiovascular disease were examined at the follow-up 6-12 months later. RESULTS: Conventional transthoracic echocardiography and PWTD of mitral annulus were successfully performed in 83 cases and 88 controls. At follow-up mean serum PTH values were 6.0 +/- 2.2 versus 3.2 +/- 1.3 pmol/l (p < 0.05) and mean calcium 2.28 +/- 0.10 versus 2.33 +/- 0.08 mmol/l (p < 0.05) in cases and controls, respectively. Unpaired t test and multiple linear regression analyses were used. No significant differences in conventional echocardiographic parameters were found. However, PWTD showed reduced systolic velocity in septal, lateral and anterior mitral annulus (p < 0.05) and also reduced early diastolic velocity in septal and anterior mitral annulus (p < 0.05). CONCLUSION: Subjects with mild SHPT have impaired left ventricular long axis function as evaluated by PWTD compared to conventional echocardiography. PWTD seems to be a more sensitive tool in detecting minor changes in left ventricular function and the new modality should routinely be included in studies evaluating left ventricular function, especially the long axis function.

Aged↗
PubMed1995

Assessment of myocardial viability in chronic left ventricular dysfunction.

Differentiation of infarcted from viable myocardium is of critical clinical importance in patients with severely impaired left ventricular function. While positron emission tomography is considered the "gold-standard" modality for detection of viable myocardium, expense has limited its more widespread use. Therefore, many centers employ surrogate tests for metabolic viability. In several recent studies, low-dose dobutamine echocardiography has been useful in predicting recovery of poorly contractile myocardium. Myocardial contrast echocardiography is a promising new technique which may predict viability by defining areas of preserved microvascular integrity. The clinical role of these diagnostic modalities in the setting of depressed ventricular function is as yet uncertain. Clarification of the utility of these tests should allow more judicious selection of patients who would derive the greatest survival benefit from revascularization procedures.

Chronic Disease↗
PubMed2006

Enalapril attenuates downregulation of Angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat.

The early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfarction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.

Angiotensin I↗
PubMed1983

Effect of combined nitroglycerin and dobutamine infusion in left ventricular dysfunction.

The immediate therapy of severe left ventricular (LV) failure after acute myocardial infarction (AMI) frequently requires simultaneous preload reduction, pump output augmentation, and maintenance of systemic blood pressure. Therefore the effects of intravenous nitroglycerin (NG) and dobutamine (DB) were evaluated in 12 patients with severe LV failure following AMI. Nitroglycerin achieved salutary lowering of abnormally elevated LV filling pressure (23 to 14 mm Hg, p less than 0.001) while DB markedly augmented LV pump function (cardiac index rose from 1.7 to 2.5 L/min/m2, p less than 0.005). Notably, the combined infusion of NG + DB simultaneously decreased preload (LV filling pressure 23 to 14 mm Hg, p less than 0.001) and markedly enhanced LV pump performance (cardiac index increased from 1.7 to 2.4 L/min/m2, p less than 0.001). Minor decline in mean systemic blood pressure with NG (72 to 66 mm Hg, p less than 0.05) was rapidly reversed by DB addition (69 mm Hg, p greater than 0.05). Both agents were well tolerated without clinical or ECG evidence of myocardial ischemia or dysrhythmias. Thus the principally venodilator effects of NG minimize systemic hypotension while salutary augmentation of cardiac function in AMI with LV failure is achieved by NG + DB.

Catecholamines↗
PubMed2002

Apoptosis and oncosis in the early progression of left ventricular dysfunction in the cardiomyopathic hamster.

The genetic defect in the cardiomyopathic (CM) hamster is a mutation in the glycoprotein-sarcoglycan (a component of the dystrophin-glycoprotein complex). Apoptosis has been identified in skeletal muscle of dystrophin-deficient mice, and therefore the role of myocardial apoptosis in relation to oncosis in causing myocardial necrosis was assessed at the onset of left ventricular (LV) dysfunction in CM hamsters. LV size and function were evaluated in normal and CM hamsters (CHF147 line) by echocardiography at 1, 2, 3, and 5 months (mo) of age. The decrease of LV fractional shortening was found to be most marked (45%) between 1 and 2 mo of age. Apop totic nuclei were identified at each time point using in situ end-labeling of DNA strand breaks (TUNEL), together with immunolabeling of myocytes; DNA fragmentation (laddering) and nuclear morphology were also assessed. Myocyte oncotic necrosis was assessed at 2 mo by Evans blue dye (EBD), wheat germ agglutinin, hematoxylin/eosin staining, and electron microscopy. Apoptotic nuclei were not detected in age-matched normal hamsters. In the CM hamsters apoptotic myocyte nuclei comprised an average of 0.041% of myocyte nuclei between 1 and 5 mo, an increase at 2 mo (to 0.076%) was not significant, and DNA laddering was not detected. The number of myocyte nuclei per unit area decreased by 32% between 1 and 2 mo, and in 2 mo old CM hamsters myocardial staining with EBD was positive in 9.82% of the myocardial cross sectional areas examined, most of which was consistent with sarcolemmal rupture and oncosis with inflammatory cell infiltration. It is concluded that myocyte oncosis provides the major mechanism for the decreased number of myocyte nuclei and the early decrease of cardiac function between 1 and 2 mo of age in the CM hamster, with only a small contribution of myocyte apoptosis.

Animals↗
PubMed2006

Usefulness of clinical, electrocardiographic, and echocardiographic parameters to detect cardiac asynchrony in patients with left ventricular dysfunction secondary to ischemic or nonischemic heart disease.

OBJECTIVES: Specific evaluation using echocardiographic Doppler is superior to the measurement of the QRS complex to detect cardiac asynchrony. Nevertheless, no clinical, electrocardiographic, or echocardiographic parameters have been evaluated to obtain an accurate and easy-to-use marker of cardiac asynchrony in patients with depressed left ventricular (LV) ejection fraction. Our aim was to determine whether there is any marker of cardiac asynchrony in patients with LV systolic dysfunction that allows us to obviate the performance of a specific echocardiographic study before cardiac resynchronization therapy. METHODS: In all, 316 consecutive patients with LV ejection fraction less than 40% were enrolled. Interventricular asynchrony was defined as an interventricular mechanical delay longer than 40 milliseconds. Intraventricular asynchrony was defined as the difference between time from Q wave to LV ejection end and the time from Q wave to the end of the systolic wave of the most delayed basal segment by Doppler tissue imaging greater than 50 milliseconds. RESULTS: In all, 177 (56%) had ischemic and 139 (44%) had nonischemic heart disease. The logistic regression analysis showed that only the presence of left bundle branch block was an independent predictor of interventricular asynchrony despite the cause of the underlying disease (odds ratio and 95% confidence interval 7.2 [3.9-13.4], P < .001; 5.99 [2.7-13.2], P < .001; and 8.75 [3.2-23.8], P < .001 for the total population, ischemic and nonischemic groups, respectively). Nevertheless, none of the studied parameters was found as a predictor of intraventricular asynchrony. CONCLUSIONS: The presence of left bundle branch block is a marker of interventricular asynchrony in patients with ventricular dysfunction despite the cause of the underlying cardiac disease. Nevertheless, intraventricular cardiac asynchrony cannot be detected using conventional parameters. A specific echocardiographic evaluation before cardiac resynchronization therapy must be performed in all these patients. Our aim was to determine whether there is any marker of cardiac asynchrony in patients with left ventricular systolic dysfunction that allows us to obviate the performance of a specific echocardiographic study before cardiac resynchronization therapy. Our results showed that only the presence of left bundle branch block was an independent predictor of interventricular asynchrony despite the cause of the underlying disease but none of the studied parameters was found as a predictor of intraventricular asynchrony.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Relation of myocardial perfusion at rest and during pharmacologic stress to the PET patterns of tissue viability in patients with severe left ventricular dysfunction.

BACKGROUND: Stress perfusion imaging can assess effectively the amount of jeopardized myocardium, but its use for identifying underperfused but viable myocardium has yielded variable results. We evaluated the relation between measurements of myocardial perfusion at rest and during pharmacologic stress and the patterns of tissue viability as determined by positron emission tomographic (PET) imaging. METHODS AND RESULTS: We studied 33 patients with coronary artery disease and left ventricular (LV) dysfunction (LV ejection fraction, 30%+/-8%). PET imaging was used to evaluate regional myocardial perfusion at rest and during pharmacologic stress with [13N]-ammonia as a flow tracer, and to delineate patterns of tissue viability (i.e., perfusion-metabolism mismatch or match) using [18F]-deoxyglucose (FDG). We analyzed 429 myocardial regions, of which 229 were dysfunctional at rest. Of these, 30 had normal perfusion and 199 were hypoperfused. A severe resting defect (deficit >40% below normal) predicted lack of significant tissue viability; 31 of 35 regions (89%) had a PET match pattern denoting transmural fibrosis. Although regions with mild or moderate resting defects (deficit <40% below normal) showed evidence of metabolic activity, perfusion measurements alone failed to identify regions with PET mismatch (reflecting hibernating myocardium). Reversible stress defects were observed with slightly higher frequency in regions with a PET mismatch (10 of 37) than in those with a PET match (36 of 162) pattern of viability. A reversible stress defect was a specific (78%) marker, but was a relatively insensitive marker (27%) of viable myocardium as defined by the PET mismatch pattern. CONCLUSIONS: In patients with LV dysfunction, the severity of regional contractile abnormalities correlates with the severity of flow deficit at rest. Severe reductions in resting blood flow in these dysfunctional regions identify predominantly nonviable myocardium that is unlikely to have improved function after revascularization. Although dysfunctional myocardium with mild to moderate flow reductions contains variable amounts of viable tissue (as assessed by FDG uptake), flow measurements alone do not distinguish between regions with PET mismatch (potentially reversible dysfunction) and PET match (irreversible dysfunction). The presence of an irreversible defect on stress imaging is a relatively specific (78%) marker of PET match, whereas a reversible stress defect is a rather insensitive (27%) marker of viability, as defined by the PET mismatch pattern.

Aged↗
PubMed2004

Effects of pranidipine, a novel calcium channel antagonist, on the progression of left ventricular dysfunction and remodeling in rats with heart failure.

The cardioprotective properties of pranidipine were studied in a rat model of heart failure after autoimmune myocarditis. Twenty-eight days after immunization the surviving rats were divided into three groups and received oral treatment of 0.03 mg/kg/day (group 0.03) or 0.3 mg/kg/day (group 0.3) of pranidipine or vehicle (group V) for 1 month. High-dose pranidipine (group 0.3) improved the survival rate, and significantly reduced heart weight, heart weight to body weight ratio, myocardial fibrosis, central venous pressure and left ventricular end-diastolic pressure than low-dose pranidipine (group 0.03) and group V. Pranidipine at high dose also decreased the left ventricular systolic and diastolic dimensions, and increased fractional shortening compared with group V. The increase in level of TGF-beta1 and collagen-III mRNA were suppressed by pranidipine in a dose-dependent manner. Our results indicated that pranidipine has cardioprotective effects on heart failure, and that the beneficial effect can be partly explained by attenuation of fibrotic response through suppression of TGF-beta1 and collagen-III mRNA expression, and regression of myocyte hypertrophy.

Animals↗
PubMed1995

A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group.

BACKGROUND: Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces mortality among survivors of acute myocardial infarction, but whether to use ACE inhibitors in all patients or only in selected patients is uncertain. METHODS: We screened 6676 consecutive patients with 7001 myocardial infarctions confirmed by enzyme studies. A total of 2606 patients had echocardiographic evidence of left ventricular systolic dysfunction (ejection fraction, < or = 35 percent). On days 3 to 7 after infarction, 1749 patients were randomly assigned to receive oral trandolapril (876 patients) or placebo (873 patients). The duration of follow-up was 24 to 50 months. RESULTS: During the study period, 304 patients (34.7 percent) in the trandolapril group died, as compared with 369 (42.3 percent) in the placebo group (P = 0.001). The relative risk of death in the trandolapril group, as compared with the placebo group, was 0.78 (95 percent confidence interval, 0.67 to 0.91). Trandolapril also reduced the risk of death from cardiovascular causes (relative risk, 0.75; 95 percent confidence interval, 0.63 to 0.89; P = 0.001) and sudden death (relative risk, 0.76; 95 percent confidence interval, 0.59 to 0.98; P = 0.03). Progression to severe heart failure was less frequent in the trandolapril group (relative risk, 0.71; 95 percent confidence interval, 0.56 to 0.89; P = 0.003). In contrast, the risk of recurrent myocardial infarction (fatal or nonfatal) was not significantly reduced (relative risk, 0.86; 95 percent confidence interval, 0.66 to 1.13; P = 0.29). CONCLUSIONS: Long-term treatment with trandolapril in patients with reduced left ventricular function soon after myocardial infarction significantly reduced the risk of overall mortality, mortality from cardiovascular causes, sudden death, and the development of severe heart failure. That mortality was reduced in a randomized study enrolling 25 percent of consecutive patients screened should encourage the selective use of ACE inhibition after myocardial infarction.

Adult↗
PubMed2001

[Effect of postinfarct left ventricular dysfunction on late occurrence of mitral regurgitation--two year experience].

The aim of this study was to evaluate factors that might influence on the occurrence of mitral regurgitation (MR) in patients (pts) following myocardial infarction (MI) after fibrinolysis--two year experience. The study group comprised 118 pts: 40 women and 78 men (mean age: 58 +/- 9 years) following MI, who underwent Doppler echocardiography which revealed no MR 3 weeks after the MI. The second echocardiographic examination was performed after 2 years. We evaluated the following parameters: presence and stage of MR, left ventricular end-diastolic diameter (LVDD), left atrial diameter (LA), end-diastolic volume (EDV), wall motion score index (WMSI), asynergic area (AA) and ejection fraction (EF). Results after 2 years were as follows: 43 pts (36%) presented without MR, 45 (38%) MR I degree, 27 (23%) MR II degree, 3 (3%) MR III degree. Echocardiographic parameter comparison after 2 years demonstrated the following changes: LVDD increase from 5.0 +/- 0.5 cm to 5.3 +/- 4.6 cm (p < 0.005), LA increase from 3.7 +/- 0.4 cm to 4.3 +/- 0.4 cm (p < 0.00001), EDV increase from 130 +/- 29 ml to 147 +/- 39 ml (p < 0.005), WMSI increase from 1.37 +/- 0.23 to 1.45 +/- 0.21 (p < 0.05), AA increase from 23.5 +/- 10.1% to 27.8 +/- 7.9% (p < 0.005) and significant EF decrease 50.4 +/- 7.9% to 46.9 +/- 7.1% (p < 0.005). These results demonstrate that the occurrence of MR 2 years after the MI is caused by left ventricular remodelling, as well as segmental and global function deterioration.

Adult↗
PubMed1991

Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction.

1. The haemodynamic effects of adenosine 5'-monophosphate (AMP) and sodium nitroprusside (SNP) were compared in anaesthetized dogs following the induction of acute left ventricular (LV) dysfunction. 2. LV dysfunction was induced by the intracoronary administration of glass microbeads until left ventricular end diastolic pressure (LVEDP) was increased from 5 to 15 mmHg. This was associated with a decrease in LV dP/dt and cardiac index (CI) of 30% and 27%, respectively, and an increase in systemic vascular resistance index (SVRI) of 37%. 3. Graded doses of AMP (100 to 1000 micrograms kg-1 min-1) or SNP (1 to 10 micrograms kg-1 min-1) reduced SVRI and increased CI in a dose-related manner. Heart rate was not altered by either agent. At doses that caused similar reductions in SVRI, CI was increased more by AMP than by SNP. 4. The mechanisms responsible for the greater elevation of CI by AMP relative to SNP may be related to its more selective arterial vasodilator activity. SNP reduced cardiac preload that limited the expected increase in CI. 5. The haemodynamic profile of AMP suggests that it may be useful in the pharmacological management of acute cardiac failure, either when used alone or in combination with positive inotropic agents and/or selective venodilators.

Adenosine Monophosphate↗
PubMed1999

Beneficial effects of heart rate reduction on cardiac mechanics and energetics in patients with left ventricular dysfunction.

It has been shown recently that the force-frequency relationship is blunted in experimental heart failure models. Furthermore, tachycardia is thought to have adverse effects on the diseased heart for several reasons, one of which is an increase in myocardial oxygen consumption. Inversely, the oxygen-saving effects of bradycardia may be beneficial for the treatment of heart failure. The aim of this study was to elucidate how heart rate (HR) modulates cardiac mechanics and energetics in patients with left ventricular (LV) dysfunction. LV pressure-volume data and myocardial oxygen consumption (MVO2) was assessed using conductance and coronary sinus thermodilution catheters in 14 patients with moderate LV dysfunction (mean ejection fraction 34%) under 3 conditions: (a) basal, (b) HR increased by 20% using atrial pacing, and (c) HR decreased by 16% using a specific bradycardic agent, zatebradine (7.5 mg p.o.). Atrial pacing decreased external work (EW) (from 0.39 to 0.31 J beat(-1) m(-2), p<0.05) at a comparable MVO2 per beat with a marginal increase in LV contractility index (Ees) (from 2.34 to 2.76 mm Hg ml(-1) m(-2), p = 0.08), resulting in a decrease in mechanical efficiency (EW/MVO2) (from 25.9 to 22.1%, p<0.05). In contrast, zatebradine did not decrease Ees (from 2.34 to 2.24 mm Hg ml(-1) m(-2), NS), but increased EW (from 0.39 to 0.42 J beat(-1) m(-2), p<0.05 vs. basal level) without a change in MVO2 per beat, resulting in improved mechanical efficiency (from 25.9 to 29.7%, p<0.05 vs. basal level). These results suggest that mild bradycardia is energetically advantageous and does not decrease myocardial contractility and performance, whereas pacing-induced tachycardia worsens cardiac mechanics and energetics in patients with LV dysfunction. Thus, the oxygen-saving effect of bradycardia may be beneficial for the treatment of heart failure.

Benzazepines↗
PubMed1995

Results of revascularization in patients with severe left ventricular dysfunction.

BACKGROUND: In patients with coronary artery disease and poor ventricular function (ejection fraction, < 20%), bypass grafting remains a surgical challenge. This study evaluates experience with isolated revascularization in such patients. METHODS AND RESULTS: In 79 consecutive patients (69 men, 10 women; average age, 59 +/- 9 years), preoperative ejection fraction was 18 +/- 5%. Indications for surgery were congestive heart failure (CHF) in 5 of 79 patients (6%), CHF and angina in 19 (24%), angina in 41 (52%), ventricular arrhythmias (VAs) in 8 (10%), and critical anatomy in 6 (8%). Some patients had prior VAs (23 of 79; 29%) or mitral regurgitation (18; 23%) and required emergent surgery (25; 32%). At surgery, temperature mapping ensured adequate distribution of antegrade cold cardioplegia, with 3.6 +/- 0.7 grafts per patient, including left internal mammary artery graft in 60 of 79 (76%) and endarterectomy in 14 (18%). Hospital mortality was 3.8%. Perioperative support included intra-aortic balloon pump in 18 of 79 (23%) and drugs for VAs in 28 (35%). Morbidity included myocardial infarction in 2 of 79 (2.5%) and stroke in 2 (2.5%). During follow-up, there were 19 late deaths. Actuarial survival was 94%, 82%, and 68% at 1, 2, and 5 years, respectively, and was similar in patients with severe angina, CHF, mitral regurgitation, or VAs. Freedom from sudden death was 100%, 98%, and 91% at 1, 2, and 5 years, respectively. Among survivors, angina improved in 84% and heart failure improved in 26%. CONCLUSIONS: These data support bypass graft surgery in patients with severe LV dysfunction. With careful cardioplegic techniques, hospital mortality was low (3.8%). Long-term survival is encouraging, with good relief of symptoms in most patients. Perioperative VAs are frequent but respond to medical treatment, with only 23% of patients discharged on antiarrhythmic drugs. Five-year freedom from sudden death is 91%, with only 3 late sudden deaths in this series.

Actuarial Analysis↗
PubMedDate not supplied

Clinical characteristics and referral pattern of patients with left ventricular dysfunction and significant coronary artery disease undergoing radionuclide imaging.

BACKGROUND: Many observational studies that predict patient outcomes have examined the use of myocardial perfusion imaging results. However, a referral pattern for radionuclide testing could bias these analyses and should be determined. These patients may also differ with regard to the extent of coronary artery disease (CAD). All of these differences must be incorporated into proper outcomes examinations. We sought to identify the nuclear perfusion imaging referral pattern for patients with left ventricular (LV) dysfunction and significant CAD. METHODS AND RESULTS: Patients with LV dysfunction and CAD (n = 2951) meeting our inclusion criteria were compared by receipt or absence of radionuclide perfusion testing within 6 months before or after angiography. Pearson chi2 and Kruskal-Wallis analyses were used to examine differences in baseline characteristics and catheterization results, whereas logistic regression modeling was applied to predict nuclear imaging referral before and after catheterization. Precatheterization nuclear cohort patients were more likely to be minority patients (odds ratio [OR], 1.34; P =.0083) with previous cardiac revascularization (OR, 2.27; P =.0001), Charlson comorbidity index greater than 1 (OR, 1.146; P =.0091), and heart failure symptoms (OR, 1.62; P =.0001) than those without imaging. They were less likely to have a myocardial infarction (OR, 0.464; P =.0001). After catheterization, the nuclear patients were more likely to have had congestive heart failure (OR, 1.452; P =.0019), a myocardial infarction (OR, 1.353; P =.0371), an ejection fraction lower than 30% (OR, 1.058; P =.0002), and prior revascularization (OR, 1.880; P =.0001). In addition, they had fewer diseased vessels (OR, 0.731; P =.0001). CONCLUSIONS: Bias exists in nuclear referral for patients with LV dysfunction and significant CAD and must be considered when interpreting observational studies on this topic.

Aged↗