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PubMed1981

Improved long-term survival following myocardial revascularization in patients with severe left ventricular dysfunction.

The natural history of patients with coronary artery disease associated with poor left ventricular (LV) function is dismal. This report analyzes the efficacy of myocardial revascularization in this subset of patients with coronary artery disease manifesting severe LV dysfunction on the basis of LV angiography, LV ejection fraction (LVEF), and left ventricular end-diastolic pressure (LVEDP). For the 2 1/2 year period ending November, 1977, 59 consecutive patients with coronary artery disease complicated by severe LV dysfunction underwent aorta-coronary bypass at the University of Western Ontario. All patients had angina refractory to medical therapy. Objective criteria for compromised LV function included the presence of three or more dysfunctional (hypokinetic of akinetic) segments on biplane LV angiography. Eighty-three percent (49/59) of patients had triple-vessel coronary artery disease. The mean LVEF for the series was 0.28 and the mean LVEDP was 18 mm Hg. The duration of follow-up was 24 to 60 months (mean 37 months), with follow-up survival data available on 100% of patients. The hospital mortality was 1.7% (1/59), and there were nine late deaths. The 5 year actuarial survival rate (+/- SEM) was 80% +/- 6%. Of the 44 long-term survivors available for direct assessment, 98% (43/44) report improvement with respect to angina and 66% (29/44) are totally asymptomatic. Eighty percent (28/35) of the long-term survivors under the age of 65 years are currently employed. These results indicate that myocardial revascularization can be performed in patients with severe ischemic LV dysfunction at very low risk and, further, that operation results in a dramatic improvement in survival expectations compared with optimal medical therapy.

Aged↗
PubMed2000

[Transient left ventricular dysfunction is still present one hour after exercise stress test: evaluation by gated SPECT with 99mTc-labeled perfusion agent].

It has been reported that quantitative gated SPECT (QGS) has revealed post-stress dysfunction of the left ventricle (LV) 30 minutes after a stress test. The purpose of this study was to determine whether post-stress dysfunction of LV is still present one hour after an exercise stress test. The subjects comprised 152 patients (124 males and 28 females, mean age 59 +/- 10 years). Exercise stress myocardial scintigraphy was performed using a one-day, stress and rest protocol. 99mTc labeled myocardial perfusion tracer, tetrofosmin, 370 MBq was injected at the end-point of a supine ergometer stress test for stress imaging. ECG gated SPECT was carried out 1 hour after injection. Three hours later, 740 MBq to 1100 MBq of 99mTc labeled myocardial perfusion tracer was injected for rest imaging. ECG gated SPECT was again performed 1 hour after injection. We divided the subjects into four groups according to the severity score of defects on the stress image and the presence or absence of fill-in; normal (NOR, n = 59), myocardial infarct (MI, n = 65), small ischemia (S-IS, n = 13) and large ischemia (L-IS, n = 15). Post-stress dysfunction is defined according to two criteria: 1) rest LVEF--post-stress LVEF > or = 5% and 2) post-stress ESV--rest ESV > or = 5 ml. The frequency of post-stress dysfunction was 3.4%, 9.1%, 23.1% and 40% in NOR, MI, S-IS and L-IS, respectively. Post-stress LV dysfunction was found to be more frequent in the large ischemia group. In conclusion, post-stress dysfunction was present 1 hour after the stress test and was more frequent in the large ischemia group.

Aged↗
PubMed2004

[Ischemic heart disease and left ventricular dysfunction: the role of trimetazidine].

In patients with ischemic heart disease, contractility of dysfunctional myocardium may improve through metabolic modulation. Trimetazidine is the first of a new class of cytoprotective agents with antianginal properties. There is recent evidence that trimetazidine reduces fatty acid beta-oxidation and stimulates glucose oxidation by selective inhibition of 3-ketoacyl coenzyme A thiolase. In experimentally-induced myocardial ischemia, trimetazidine increases glucose oxidation by 210%, and this effect is associated with a 37% increase of pyruvate dehydrogenase. The increased rate of glucose oxidation reduces hydrogen ions and lactate accumulation, translating into improved myocardial contractility. In a recent randomized longitudinal placebo-controlled study in humans with ischemic cardiomyopathy, trimetazidine improved the contractile response of dysfunctional myocardium at doses of 20 mg tid for 8 weeks. This effect was associated with enhanced functional capacity and a higher ischemic threshold. The lack of effects on heart rate and blood pressure offers potential advantage in conditions of bradycardia and arterial hypotension. These important benefits need to be confirmed in larger longitudinal trials.

Clinical Trials as Topic↗
PubMed2002

Hypoxia induces aortic hypertrophic growth, left ventricular dysfunction, and sympathetic hyperinnervation of peripheral arteries in the chick embryo.

BACKGROUND: Low birth weight is associated with an increased incidence of cardiovascular diseases, including hypertension, later in life. This suggests that antenatal insults program for fetal adaptations of the circulatory system. In the present study, we evaluated the effects of mild hypoxia on cardiac function, blood pressure control, and arterial structure and function in near-term chick embryos. METHODS AND RESULTS: Chick embryos were incubated under normoxic (21% O2) or hypoxic (15% O2) conditions and evaluated at incubation day 19 by use of histological techniques, isolated heart preparations, and in vivo measurements of sympathetic arterial tone and systemic hemodynamics. Chronic hypoxia caused a 33% increase in mortality and an 11% reduction in body weight in surviving embryos. The lumen of the ascending aorta in hypoxic embryos was 23% smaller. Left ventricular systolic pressure was 22% lower, and heart weight/body weight ratio was 14% higher. In resistance arteries of hypoxic embryos, in vivo baseline tone was 23% higher, norepinephrine sensitivity was similar, and norepinephrine release from sympathetic nerves increased 2-fold, indicating sympathetic hyperinnervation. Mean arterial pressure and heart rate were similar under resting conditions, but chronically hypoxic embryos failed to maintain blood pressure during acute stress. CONCLUSIONS: This study indicates that mild hypoxia during embryonic development induces alterations in cardiac and vascular function and structure and affects hemodynamic regulation. These findings reveal that antenatal insults have profound effects on the control and design of the circulatory system that are already established at birth and may program for hypertension and heart failure at a later age.

Animals↗
PubMed1999

Long-term hemodynamic responses to vasodilator therapy in patients with severe left ventricular dysfunction.

Maximal oral vasodilator therapy resulted in long-term reduction of initially elevated pulmonary vascular resistance in 10 of 13 patients with severe heart failure who tolerated inotrope-supported uptitration of afterload reduction. Eleven patients were unable to tolerate vasodilator therapy and required inotropic support for successful cardiac transplantation.

Analysis of Variance↗
PubMed1995

Severe reversible global and regional ventricular dysfunction associated with high-dose interleukin-2 immunotherapy.

Cardiac toxicity and hemodynamic alterations are frequently associated with high-dose interleukin-2 (IL-2) immunotherapy in cancer patients. Serious cardiac events including myocardial infarction, ischemia, and noninfectious myocarditis have been observed. We document two cases of unusually severe but reversible cardiac abnormalities related to IL-2 therapy: one patient with a profound form of global myocardial hypocontractility and a second patient with regional aneurysmal and dyskinetic changes of the left ventricle. These cases exhibit unique features not previously described in IL-2-treated patients. The possible pathophysiologic mechanisms underlying these global and regional forms of cardiomyopathy, including the production of secondary-messenger molecules such as nitric oxide and myocardial stunning, are discussed. Both patients remain disease free of their cancer (> 3 years since completing therapy), are without residual cardiac dysfunction or recurrent related symptoms, and have not experienced any additional cardiac events. The report demonstrates the complexity of the cardiac toxicities associated with IL-2-based immunotherapy and recognizes a need for treating physicians to be familiar with their management.

Carcinoma, Renal Cell↗
PubMed2003

Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction.

OBJECTIVES: We sought to assess myocardial perfusion and metabolism in patients with peculiar transient asynergy, which consisted of basal normokinesia and apical akinesia of the left ventricle (LV) at the same time. BACKGROUND: This asynergy has been widely called "tako-tsubo-like LV dysfunction" in Japan, but little is known about its pathophysiology. METHODS: We performed rest tallium-201 ((201)Tl) and iodine-123-beta-methyl-p-iodophenyl penta-decanoic acid ((123)I-BMIPP) dual-isotope myocardial single-photon emission computed tomography (SPECT) in 14 patients with tako-tsubo-like LV dysfunction. The LV was divided into 17 segments, and each segment was graded with scores between normal uptake (0) and defect (4). We also measured the Thrombolysis in Myocardial Infarction trial (TIMI) frame count in 28 patients and 20 control subjects. RESULTS: Early SPECT (5 +/- 3 days) revealed that the total defect score value with BMIPP was significantly higher than reduced uptake with (201)Tl (p < 0.01). Reduced uptake of BMIPP was observed in parallel with an apical akinetic region and usually involved uptake of (201)Tl. This discrepancy improved gradually during the follow-up period (29 +/- 6 days) (p = 0.36). Compared with control subjects, patients had a TIMI frame count that was significantly higher in all coronary arteries immediately after onset. This higher TIMI frame count decreased but was sustained even after resolution of tako-tsubo-like LV dysfunction. CONCLUSIONS: Our data suggest that myocardial fatty acid metabolism is more severely impaired than myocardial perfusion, in parallel with an apical akinetic region during the early phase, and that impaired multivessel coronary microcirculation is involved, at least in part, in tako-tsubo-like LV dysfunction.

Aged↗
PubMed2003

[Value of Doppler indices of diastolic left ventricular dysfunction in acute cardiac insufficiency].

OBJECTIVE: To examine the prevalence of diastolic dysfunction by Doppler study in acute cardiac failure. CONTEXT: A recent study showed that diastolic dysfunction is constant in stable cardiac failure with preserved systolic function and suggested that its measurement was not necessary for the diagnosis of diastolic cardiac failure, but the prevalence of diastolic dysfunction in acute cardiac failure is not known. METHOD: The mitral and pulmonary venous profiles, the propagation velocity Vp of colour filling flow, and the lateral velocity Ea of the mitral ring in DTI were studied at the time of treatment initiation in 28 patients in sinus rhythm and in acute cardiac failure (11 NYHA IV and 17 with pulmonary oedema), of whom 18 had an ejection fraction greater than 50%. RESULTS: Diastolic dysfunction was present in the combined study of mitral and pulmonary profiles in 95% and 100% respectively of patients in cardiac failure with preserved systolic function and altered systolic function, and Vp < 45 and/or Ea < 8 cm/s was observed in 55% and 100% respectively of these patients. At respective pathological threshold values of 1.5 and 10, the combined indices E/Vp and E/Ea were concordant with the evaluation of filling pressures in 83% of patients with preserved systolic function and 100% of the systolic cardiac failure cases. CONCLUSION: Diastolic dysfunction is almost constant in acute cardiac failure independently of the ejection fraction value. However, normal values of Ea and Vp do not exclude the diagnosis of diastolic cardiac insufficiency in the acute situation.

Acute Disease↗
PubMed2006

Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction.

OBJECT: Neurogenic stunned myocardium in aneurysmal subarachnoid hemorrhage (SAH) is associated with a wide spectrum of reversible left ventricular wall motion abnormalities and includes a subset of patients with a pattern of apical akinesia and concomitant sparing of basal segments called "tako-tsubo cardiomyopathy". METHODS: After obtaining institutional review board approval, the authors retrospectively identified among all patients admitted to the Mayo Clinic's Neurological Intensive Care Unit between January 1990 and January 2005 those with aneurysmal SAH who had met the echocardiographic criteria for tako-tsubo cardiomyopathy. Among 24 patients with SAH-induced reversible cardiac dysfunction, the authors identified eight with SAH-induced tako-tsubo cardiomyopathy. All eight patients were women with a mean age of 55.5 years (range 38.6-71.1). Seven patients presented with a poor-grade SAH, reflected by a Hunt and Hess grade of III or IV. Four patients underwent aneurysm clip application, and four underwent endovascular coil occlusion. The initial mean ejection fraction (EF) was 38% (range 25-55%), and the mean EF at recovery was 55% (range 40-68%). Cerebral vasospasm developed in six patients, but cerebral infarction developed in only three patients. CONCLUSIONS: The authors describe the largest cohort with aneurysmal SAH-induced tako-tsubo cardiomyopathy. In the SAH population, tako-tsubo cardiomyopathy predominates in postmenopausal women and is often associated with pulmonary edema, prolonged intubation, and cerebral vasospasm. Additional studies are warranted to understand the complex mechanism involved in tako-tsubo cardiomyopathy and its intriguing relationship to neurogenic stunned myocardium.

Adult↗
PubMed1998

Effect of left ventricular sphericity on the evolution of ventricular dysfunction in rats with diffuse isoproterenol-induced myocardial necrosis.

BACKGROUND: Previous studies in heart failure have suggested that increased left ventricular (LV) sphericity is a precursor to hemodynamic deterioration, although these studies have predominantly used models with segmental damage due to coronary vessel occlusion and have only made baseline assessments of LV function. The purpose of this study was to examine the relationship between LV geometry and hemodynamic compromise through time in heart failure due to graded, diffuse myocardial injury with a patent coronary circulation. METHODS AND RESULTS: Rats received two injections of either 0, 85, 170, or 340 mg/kg isoproterenol. At 2, 6, and 16 weeks after injection, baseline hemodynamics, peak pressure-generating (aortic occlusion) and flow-generating (Tyrode's volume loading) capacities, and ventricular pressure-volume curves, dimensions, and histological scoring were measured. Increased LV sphericity preceded deterioration in baseline cardiac output, although it was the most powerful correlate of the dose-dependent decreases in peak cardiac output and ejection fraction. Time-dependent increases in pressure-generating capacity at a given volume were also due to compensatory increases in LV sphericity. The extent of right ventricular damage was also a strong correlate of peak flow-generating capacity. CONCLUSIONS: This study demonstrates that isoproterenol-induced myocardial necrosis resulted in progressive hemodynamic dysfunction of the left ventricle which most closely correlated with alterations in LV geometry. Although increases in LV sphericity preceded decrements in baseline function, techniques that assessed peak LV function demonstrated that increased LV sphericity was directly correlated with decreased peak flow-generating capacity, underscoring the clinical importance of these geometric alterations.

Adrenergic beta-Agonists↗
PubMed2000

'Tako-Tsubo' transient ventricular dysfunction: a case report.

During admission for investigation of dysphagia, an 82-year-old woman suddenly complained of dyspnea, which was followed by cardiogenic shock. Her symptoms, electrocardiogram, echocardiogram and laboratory data were compatible with an extensive acute anterior myocardial infarction. Emergency cardiac catheterization showed no atheromatous narrowing in any coronary artery. However, the contractions of the left and right ventricles were diffusely and severely impaired, except for some hyperkinesis of the basal area. The asynergy, as well as the abnormalities on the ECG, improved almost to normal by the 35th hospital day. An endomyocardial biopsy from the right ventricle during the acute phase showed atypical myocardial damage with proliferation of fine collagen fibers and small round-cell infiltration including polymorphologic leukocytes. This type of transient cardiac disorder has recently been described in Japan, and is called 'Tako-tsubo cardiomyopathy' because of the characteristic appearance of the left ventricular asynergy. In the present case, ventricular asynergy was not limited to the left ventricle, but was also present in the right ventricle.

Aged↗
PubMed1998

Significance of rest technetium-99m sestamibi imaging for the prediction of improvement of left ventricular dysfunction after Q wave myocardial infarction: importance of infarct location adjusted thresholds.

OBJECTIVE: The value of rest technetium-99m (Tc-99m) sestamibi scintigraphy under oral nitrate medication to predict myocardial viability was examined in patients with chronic infarcts. BACKGROUND: The value of rest Tc-99m sestamibi to predict viability in infarct regions has not been fully established because significant underestimation of viability, especially in the inferior myocardial wall, has been reported. METHODS: Forty patients with Q wave myocardial infarction underwent Tc-99m sestamibi single-photon emission computed tomography under nitrate medication before revascularization of the infarct-related artery. Wall motion was quantified from paired angiograms before and 4 months after revascularization. Tracer uptake was quantified in the central infarct region identified on the angiogram. RESULTS: The average Tc-99m sestamibi uptake in the central infarct region of patients with anterior infarcts and improvement of left ventricular function was significantly higher (68+/-12%, mean+/-SD) than in patients without improvement of function (40+/-14%, p < 0.02). The average Tc-99m sestamibi uptake in the central infarct region of patients with improvement of function and inferior infarcts was significantly lower (43+/-7%) than in patients with anterior infarcts (68+/-12%, p < 0.003), but was significantly higher than in patients with inferior infarction and no improvement of function (31+/-7%, p < 0.02). Using an infarct location adjusted optimal threshold (50% for anterior infarcts, 35% for inferior infarcts), Tc-99m sestamibi had a positive predictive value of 90% and a negative predictive value of 91% for improvement of left ventricular function. CONCLUSION: Quantitative rest Tc-99m sestamibi scintigraphy after oral nitrates reliably predicts improvement of left ventricular function after revascularization if infarct location adjusted thresholds are used.

Aged↗
PubMed1998

Ischemia and left ventricular dysfunction: a reciprocal relation?

There is convincing evidence that (prolonged) episodes of myocardial ischemia lead to impairment of left ventricular (LV) function and ultimately to chronic congestive heart failure (CHF), but whether the opposite is also true has not been well established. We studied this issue in two groups of CHF patients with positron emission tomography (PET) by using [13N]ammonia (13NH3) as a tracer. In the first protocol we compared 12 patients with idiopathic dilated cardiomyopathy (who have normal coronary arteries) with 12 healthy controls. In the second protocol we studied a group of 24 patients with documented coronary artery disease (CAD). In this protocol, we compared patients with normal LV function to those with LV dysfunction and CHF. In patients with cardiomyopathy, myocardial blood flow at rest was normal but flow reserve (after dipyridamole infusion) was significantly impaired (1.7 +/- 0.08) compared with normal subjects (2.7 +/- 0.04; p <0.05). Furthermore, by examining [18F]fluorodeoxyglucose (18FDG) uptake, a perfusion-metabolism mismatch was observed in 24 +/- 6% of the myocardium in patients with cardiomyopathy as opposed to 0% of normals (p <0.05). In patients with CAD, myocardial blood flow reserve (measured in non-stenotic arteries to non-infarcted area) was impaired in CHF patients (1.7 +/- 0.06) compared to those with normal LV function (2.3 +/- 0.05; p <0.05). In both groups of CHF patients, the impairment of blood flow reserve showed a significant correlation with the severity of CHF. In conclusion, myocardial blood flow reserve is impaired in patients with CHF in proportion to the degree of CHF. Metabolic studies with 18FDG further show that, in patients with idiopathic dilated cardiomyopathy and CHF, flow-metabolism mismatch is present in a substantial part of the myocardium, suggesting a pathogenetic role for ischemia.

Adult↗
PubMed2007

Disturbed glucose metabolism is associated with left ventricular dysfunction using tissue Doppler imaging in patients with myocardial infarction.

AIMS: To investigate the association between glucose abnormalities and left ventricular (LV) function assessed by tissue Doppler imaging (TDI) in patients with previous history of myocardial infarction and without known diabetes mellitus. PATIENTS AND METHODS: In a cross-sectional study, 123 patients, aged 31-80 years, with a history of previous myocardial infarction and without known diabetes mellitus were examined with TDI echocardiography. A standard oral glucose test (OGTT) with 75 g of glucose was performed. RESULTS: Two-hour plasma glucose were significantly and negatively associated with TDI parameters such as LV ejection time; early diastolic filling velocity (E'-v); ratio of the early to late diastolic filling velocity (E'/A') and positively associated with regional myocardial performance index (MPI) (P<0.05). Left ventricular ejection time and MPI were significantly higher; E'/A' and E'-v were significantly lower in patients with disturbed glucose metabolism compared with patients with normal glucose tolerance (P<0.01). These differences remain significant also when the patients with DM were excluded. CONCLUSIONS: The present study demonstrates that disturbed glucose metabolism is associated with more pronounced LV dysfunction using TDI in patients with myocardial infarction. These abnormalities in LV function were more common not only in subjects with diabetes, but also in patients with prediabetic condition, impaired glucose intolerance.

Adult↗
PubMedDate not supplied

Treatment of high-risk African American patients: left ventricular dysfunction, heart failure, renal disease, and postmyocardial infarction.

African Americans experience more mortality and morbidity from hypertension-related complications than other racial groups. Although angiotensin-converting enzyme (ACE) inhibitors have clearly been shown to reduce mortality and morbidity in hypertensive white patients with heart failure, renal dysfunction, stroke, and acute myocardial infarction, African American patients have been underrepresented in these trials. The lack of direct evidence of the benefit of ACE inhibitors in these individuals and the suggestion that ACE inhibitors are less efficacious in this group has resulted in a reluctance to use ACE inhibitors in African Americans. However, retrospective analyses in black patients with heart failure and a recent randomized clinical trial in African Americans with renal dysfunction suggest that a regimen based on ACE inhibitors is efficacious in this racial group. Although diuretics remain first-line therapy, data now suggest that ACE inhibitors provide additional benefit and should be considered for use in patients with high-risk complications regardless of race.

Black or African American↗
PubMed2003

Expression of lectin-like oxidized low-density lipoprotein receptors during ischemia-reperfusion and its role in determination of apoptosis and left ventricular dysfunction.

OBJECTIVES: The goal of this study was to determine the role of lectin-like oxidized low-density lipoprotein receptors (LOX-1), a recently identified oxidized low-density lipoprotein (ox-LDL) receptor, in ischemia-reperfusion injury to the heart. BACKGROUND: Reactive oxygen species (ROS) released during ischemia-reperfusion oxidize low-density lipoproteins; LOX-1 is upregulated by ox-LDL and ROS, and is involved in cell injury. METHODS: Anesthetized rats were subjected to left coronary artery ligation for 60 min (n = 10, ischemia group), or ischemia followed by 60 min of reperfusion (n = 30, ischemia-reperfusion group). Rats in the latter group were treated with saline, the LOX-1 blocking antibody JXT21 (10 mg/kg), or nonspecific anti-goat immunoglobulin G (IgG) (10 mg/kg). Ten other rats underwent thoracotomy without coronary ligation (sham control). RESULTS: Ischemia-reperfusion was associated with an increase in LOX-1 expression, lipid peroxidation and apoptosis, a large infarct area, and a decrease in left ventricular function (all, p < 0.01 vs. sham control and ischemia alone groups). Treatment of rats with LOX-1 antibody prevented ischemia-reperfusion-induced upregulation of LOX-1. Importantly, the LOX-1 antibody reduced apoptosis by 48%, lipid peroxidation by 39%, and myocardial infarct size by 45%, and improved left ventricular function (first derivative of pressure measured over time: -47% to -18%, p < 0.01). Nonspecific IgG had no effect. CONCLUSIONS: Lectin-like oxidized low-density lipoprotein receptors are upregulated during myocardial ischemia-reperfusion, and appear to be associated with apoptosis, necrosis, and left ventricular functional deterioration.

Animals↗
PubMed2005

Revascularization in severe left ventricular dysfunction: the role of viability testing.

Revascularization is a treatment option for moderate-to-severe ischemic cardiomyopathy. Limitations of the current literature, lack of completed randomized trials, and higher periprocedural risks create significant uncertainty about the optimal treatment strategy. This review focuses on the available literature describing the effect of revascularization on outcome and the role of noninvasive viability testing. It attempts to identify a subset of patients likely to benefit from therapy.

Algorithms↗
PubMed2005

Comparison of mental stress-induced myocardial ischemia in coronary artery disease patients with versus without left ventricular dysfunction.

To examine the susceptibility to myocardial ischemia with mental stress in patients who have coronary artery disease and normal left ventricular (LV) function versus those who have impaired LV function, we examined 58 patients who had coronary artery disease, including 22 who had normal LV function (ejection fraction >/=50%), 16 who had mild to moderate LV dysfunction (ejection fraction 30% to 50%), and 20 who had severe LV dysfunction (ejection fraction </=30%) and underwent bicycle and mental stress testing with myocardial perfusion scintigraphy on consecutive days in random order. Ischemia was assessed based on summed difference scores in regional rest versus stress myocardial perfusion and defined as a summed difference score >3. At comparable double products across the 3 groups, ischemia was induced with mental stress more frequently in patients who had severe LV dysfunction (50%) than in those who had normal LV function (9%; p <0.01). The frequency of exercise-induced ischemia was different only between those who had mild/moderate LV dysfunction and those who had normal LV function (56% vs 18%, respectively, p <0.05). The pattern of mental stress versus exercise ischemia differed between groups (p <0.02): there was a higher prevalence of mental stress ischemia versus exercise ischemia in patients who had severe LV dysfunction (p = 0.06), a marginally higher prevalence of exercise versus mental stress ischemia in those who had moderate LV dysfunction (p = 0.07), and no difference in mental stress versus exercise ischemia in those who had normal LV function. Thus, at comparable double products during mental stress and similar extent of coronary artery disease, ischemia with mental stress was induced more frequently in patients who had severe LV dysfunction than in those who had normal LV function. These data suggest that mental stress ischemia may be of particular clinical importance in patients who have coronary artery disease and LV dysfunction.

Analysis of Variance↗