Nuclear Exercise Stress Test Research Articles

Predictive value of a fragmented QRS complex in diagnosing patients with myocardial ischemia.

BackgroundA fragmented QRS complex (fQRS) is caused by conduction abnormalities of the ventricle secondary to myocardial ischemia and/or scar in patients with myocardial infarction. However, the implications of the fQRS in the development of coronary artery disease with myocardial ischemia in those without a scar remain unknown.MethodsWe studied electrocardiograms (ECGs) obtained from 150 patients (60.5 ± 8.5 years, 102 men) with myocardial ischemia, which was confirmed by performing both, a nuclear exercise stress test and coronary angiography. We also studied ECGs obtained from 601 patients (58.5 ± 10.0 years, 315 men) who showed a negative nuclear exercise stress test (control group). Patients in whom the nuclear exercise stress test showed a myocardial scar were excluded.ResultsAn fQRS was more commonly observed in patients with myocardial ischemia (n = 48, 32.0%) than in the control group (n = 133, 22.1%) (P = 0.011). The sensitivity, specificity, positive, and negative predictive values of fQRS in diagnosing myocardial ischemia were 32.0, 77.9, 26.5, and 82.1%, respectively. The fQRS (odds ratio 1.580, 95% confidence interval 1.020‐2.446, P = 0.040) was an independent predictor of myocardial ischemia after adjusting for age, sex, current smoking habits, ST‐T changes on ECG, as well as histories of hypertension, diabetes, and dyslipidemia. Moreover, the fQRS showed an incremental prognostic value over conventional risk factors (χ 2 = 5, P = 0.032) and over a combination of conventional factors and ST‐T changes (χ 2 = 9, P = 0.014).ConclusionsThe fQRS is a moderately sensitive and independent predictor of myocardial ischemia.

A study of myocardial perfusion in patients with panic disorder and low risk coronary artery disease after 35% CO2 challenge

BackgroundWe have previously reported that 35% CO2 challenge induced myocardial ischemia in 81% of coronary artery disease (CAD) patients with comorbid panic disorder (PD) and previous positive nuclear exercise stress tests. However, it is yet unclear whether this is the case among CAD patients with PD and normal nuclear exercise stress test results. We hypothesized that a potent mental stressor such as a panic challenge among CAD patients with PD would also induce ischemia in patients with normal exercise stress tests. MethodsForty-one coronary artery disease patients with normal nuclear exercise stress tests (21 patients with PD and 20 without PD) were submitted to a well-established panic challenge test (with 1 vital capacity inhalation of a gas mixture containing 35% CO2 and 65% O2) and injected with Tc-99m-tetrofosmin (Myoview), upon inhalation. Single photon emission computed tomography imaging was used to assess per-panic challenge reversible myocardial ischemia and HR, BP, and a 12 lead ECG was continuously measured during the procedure. ResultsFifty-eight percent of panic disorder patients (12/21) had a panic attack during the panic challenge vs 15% (3/20) of controls (p=0.005). Only 10% of patients in each group displayed myocardial ischemia per panic challenge. ConclusionsThese findings suggest that panic attacks among panic disorder patients with lower-risk coronary artery disease may not confer a risk for myocardial ischemia.

ST-segment elevation in the recovery phase of nuclear exercise stress test with 99mTc-sestamibi in a patient with critical RCA stenosis and subtle systolic dysfunction in speckle tracking imaging

An asymptomatic Caucasian male patient underwent coronary artery disease diagnostics. Standard exercise treadmill test was inconclusive, and Holter ECG study didn't show any significant abnormalities. Considering the high risk of ischemic heart disease nuclear exercise stress test was performed,which revealed ST-segment elevation in the recovery phase of the treadmill exercise test. Single photon emission computed tomography (SPECT/CT) showed myocardial perfusion abnormalities in the inferior and lateral walls of the left ventricle. Furthermore,speckle tracking imaging showed subtle left ventricle dysfunction. Finally critical stenosis in the second segment of right coronary artery was diagnosed in coronary angiography.

ST-segment elevation in the recovery phase of nuclear exercise stress test with 99mTc-sestamibi in a patient with critical RCA stenosis and subtle systolic dysfunction in speckle tracking imaging

Although lymphomas are generally considered as tumors of lymph nodes about 25-40% arise at extranodal sites. We report a case of a 60 years old female who developed a right breast B-diffuse large cell non-Hodgkin lymphoma in 2005 treated by chemo/radio-therapy which relapsed at the same breast in 2007 and at the other breast in 2010. The patient underwent both radiologic and nuclear medicine studies.

The role of stress cardiac MRI imaging in patients with complete left bundle branch block

Background Left bundle branch block (LBBB) is a condition associated with increased mortality and poor prognosis, depending on the underlying etiology. Identification of the etiology and appropriate risk stratification of patients with LBBB is a challenge, despite the availability of various testing modalities. Nuclear exercise stress testing can show artificial perfusion defects in the interventricular septum. The artifacts are reduced but not completely excluded by use of vasodilator stress agents. In this study, we retrospectively reviewed the stress cardiac magnetic resonance (CMR) findings in patients with LBBB. Methods We retrospectively reviewed 49 consecutive patients with complete LBBB who underwent stress CMR. Of these 49 patients, 23 also underwent concurrent coronary angiography, 20 underwent nuclear stress test and 8 underwent all the three tests. The reference standard for flow limiting coronary artery disease (CAD) was coronary artery stenosis greater than 50% on coronary angiogram. Results Stress CMR correctly identified all patients (n=13) with more than 50% coronary artery stenosis and all patients (n=7) without significant coronary artery stenosis. Overall, the sensitivity, specificity, positive predictive value and negative predictive value of CMR in diagnosing flow limiting CAD were 100%, 70%, 81% and 100% respectively. In patients who underwent both stress CMR and nuclear stress test (n=20), stress CMR showed late gadolinium enhancement (LGE) in the coronary artery distribution in thirteen patients (n=13 of 20), consistent with fibrosis due to myocardial infarction. Where as nuclear stress test showed fixed defect in a coronary artery distribution in only six patients (n=6 of 20). Stress CMR also demonstrated other etiologies like hypertrophic cardiomyopathy, cardiac iron overload and idiopathic dilated cardiomyopathy. Conclusions Stress CMR imaging has high sensitivity and negative predictive value in the identification of CAD, in patients with complete LBBB. It can also assess infiltrative cardiomyopathies. Stress CMR appears to provide a better comprehensive assessment than nuclear scintigraphy in patients with LBBB. Funding None.

The Impact of Anxiety Disorders on Assessment of Myocardial Ischemia and Exercise Stress Test Performance

To evaluate the sensitivity of electrocardiogram (ECG) versus single photon emission computed tomography (SPECT) assessments of ischemia in patients with anxiety disorders (AD) and the extent to which patients exhibit poorer exercise performance, compared with patients without AD. Patients referred for nuclear exercise stress testing (N = 2271) underwent a structured psychiatric interview (PRIME-MD) to assess for AD. Exercise performance parameters were assessed during ECG treadmill testing, after which patients underwent SPECT imaging. Analyses revealed that patients with AD exhibited lower peak exercise systolic blood pressure and rate pressure product than patients without AD. When major depressive disorder was included as an additional covariate, the previous results became trends. Results also indicated a lower rate of electrically positive ecg tests and a higher rate of false-negative diagnoses of myocardial ischemia according to ecg among patients with AD. Including major depressive disorder as a covariate rendered the effects of ad nonsignificant. There was no evidence of reduced exercise performance in patients with AD. Findings suggest that AD may be associated with mild impairments in cardiovascular exercise reactivity and may also alter the detection of myocardial ischemia using ecg assessments in patients referred for exercise stress testing. However, the influence of AD appears to be moderated by comorbid depression. Results suggest that exercise test performance and detection of ischemia may be influenced by mood and/or anxiety disorders and that greater efforts should be made to include routine mood and/or anxiety disorder screening as part of exercise stress testing protocols.

Platelet reactivity in diabetic patients subjected to acute exercise stress test

Previous studies have reported ambiguous results regarding the effect of acute exercise on platelet reactivity in healthy and cardiac patients. We aimed to assess platelet reactivity among diabetic patients before and immediately after an acute exercise stress test. Patients (controls: mean age 53.1 ± 12.1 years; four males; body mass index 27.0 ± 5.7 kg/m(2); HbA(1c) 6.0 ± 1.1%, n = 8) and diabetic patients (52.9 ± 11.3; six males; body mass index 30.7 ± 2.2 kg/m(2); HbA(1c) 7.8 ± 1.7%, n = 8) referred for diagnostic nuclear exercise stress test were recruited. Blood samples obtained at rest and immediately post-exercise were stimulated with adenosine diphosphate (ADP), collagen and arachidonic acid. Expression of CD41 (pan-platelet marker) and CD62p (platelet stimulation marker) were measured by flow cytometry. Aspirin responsiveness was measured using VerifyNow. Although peak systolic blood pressure was significantly higher in the diabetics compared with nondiabetics (186.3 ± 25.4 vs. 157.1 ± 19.1, respectively, P = .028), peak exercise heart rate was similar (156.5 ± 8.3 vs. 155.5 ± 12.1 for diabetics and nondiabetics, respectively). No differences were observed between groups for aspirin resistance. Platelet stimulation with ADP exhibited significantly lower CD62p-positive cell population (%) in the diabetic patients both prior to and following the exercise stress test (P = .03). In addition, although not significant, platelet stimulation was higher post-exercise in the diabetic patients (6.3 ± 4.7% vs. 12.0 ± 5.6%, for pre- and post-exercise, respectively, P = .2) with no difference in controls (9.2 ± 5.5% vs. 8.9 ± 5.9%). Platelet stimulation in diabetic patients is blunted and might be explained by the prolonged exposure of platelets to multiple diabetic risk factors.

The Role of Mood Disorders in Exercise-Induced Cardiovascular Reactivity

Increased cardiovascular (CV) reactivity has been associated with worse CV prognosis. Though mood disorders (MDs) have been associated with increased CV reactivity during behavioral stressors, the extent to which MDs and their interaction with coronary heart disease (CHD) influences exercise-induced CV reactivity has not been evaluated. Five hundred twenty-six patients underwent nuclear exercise stress testing. Cardiovascular parameters were assessed at rest, every 2 minutes during exercise, and at peak exercise. MDs were measured using a structured psychiatric interview, the Primary Care Evaluation of Mental Disorders, and CHD was defined as having a history of myocardial infarction, revascularization, heart failure, and/or cerebrovascular event. CHD patients exhibited lower peak exercise heart rate (F = 9.40, p = .002) compared with patients without CHD. Submaximal data showed that patients with CHD had a slower rate of increase of heart rate (F = 4.29, p = .04) and diastolic blood pressure (F = 3.27, p = .04). There was an interaction of CHD and MDs, indicating that in patients with CHD, the rate of submaximal increase in systolic blood pressure (F = 3.08, p = .047) and rate-pressure product (F = 5.13, p = .006) was greater in patients with a MD compared with those without a MD. These differences were not observed in patients with no CHD. No other main or interaction effects of MDs and CHD were observed. Though MDs alone do not seem to be associated with higher levels of stress CV reactivity, their combination with CHD leads to increased submaximal exercise-induced CV reactivity. Prospective studies are needed to explore the causal relationship between these variables.

Myocardial Perfusion Study of Panic Attacks in Patients With Coronary Artery Disease

Panic disorder (PD) and panic-like anxiety have been associated with an increased risk of cardiovascular death. No study has specifically examined the association between panic attacks and ischemia in patients who have coronary artery disease (CAD). We hypothesized that panic attacks would induce myocardial perfusion defects in patients who have CAD and PD. Sixty-five patients who had CAD and positive results with nuclear exercise stress testing (35 with PD and 30 without PD served as controls) underwent a well-established panic challenge test (1 vital capacity inhalation of a gas mixture containing 35% carbon dioxide and 65% oxygen) and were injected with technetium-99m sestamibi at inhalation. Single-photon emission computed tomography was used to assess per-panic challenge perfusion defects, and heart rate, blood pressure, and 12-lead electrocardiogram were continuously measured during the procedure. Patients were not withdrawn from their cardiac medications. Patients who had PD were significantly younger than the controls; otherwise groups did not differ with respect to gender, cardiac medications, nuclear exercise test results, and baseline heart rate and blood pressure. Seventy-four percent of patients (26 of 35) who had PD had a panic attack at inhalation versus 6.7% of controls (2 of 30, p <0.001). As hypothesized, patients who had PD and demonstrated a panic attack were more likely to develop a reversible myocardial perfusion defect than were controls who did not have an attack (80.9% vs 46.4% p = 0.009). Thus, despite being on their cardiac medications, panic attacks preferentially induced significant perfusion defects in patients who had CAD and PD. In conclusion, panic attacks in patients who have CAD appear to be bad for the heart.