Cardiac magnetic resonance imaging in a patient with temporary external pacemaker: a case report.

BACKGROUND: Magnetic resonance imaging (MRI) is increasingly becoming the imaging modality of choice for many clinical disorders due to superior image quality and absence of radiation. However, access to MRI remains limited for most patients with cardiac implantable electronic devices due to potential safety concerns. In line with guidelines, there is no absolute contraindication to perform MRI, but warrants careful risk-benefit assessment. CASE SUMMARY: A 59-year-old man was admitted with a 5-day history of central chest pain and few week's history of general malaise, dry cough, and breathlessness. Electrocardiogram confirmed complete atrioventricular block (CAVB). A slight increase in cardiac enzyme was noted. Coronary angiogram revealed atheromatous changes, but no obstructive coronary lesion. A temporary transvenous pacemaker was inserted. Transthoracic echocardiogram confirmed a dilated left ventricle with severely reduced left ventricular function. To facilitate diagnosis (hence prognosis), management and mobilization, investigation with cardiovascular magnetic resonance (CMR) was warranted but contraindicated by the temporary transvenous pacemaker. An active fixation pacemaker lead was therefore placed in the right ventricle via percutaneous puncture of the right subclavian vein and connected to a pulse generator, both secured to the skin with sutures and adhesive medical dressing. Appropriate device programming and close patient monitoring ensured that CMR could be performed without any adverse effects. A diagnosis of acute myocarditis was confirmed. Regular device interrogation during an extended 3-week period with temporary pacing ruled out any device failure. As there was no resolution of CAVB, the patient received a dual-chamber pacemaker. DISCUSSION: Cardiovascular magnetic resonance was feasible and safely performed on a patient with a temporary permanent external pacemaker system using a standard screw-in pacing lead and a regular pulse generator fixed to the skin. Although more studies are needed for generalizability, CMR may be used in highly selected patients with a temporary pacemaker.

Clinical experience of a new reference material for exercise capacity in exercise stress testing in Sweden.

BACKGROUND: In 2014, the Swedish Association of Clinical Physiology recommended the use of a new reference material for exercise capacity in bicycle exercise stress testing, 'the Kalmar material'. Compared to the formerly used reference material, 'the Kristianstad material', an increase in the amount of patients being classified as having decreased exercise capacity was expected, but the extent of this in clinical practice is not known. METHODS: Results of exercise capacity from 1449 bicycle exercise tests, in patients aged ≥20 years (656 women, 793 men) performed at two departments of Clinical Physiology before and after change of reference materials, were collected. Maximal workload was related to the predicted values of both reference materials. If made, recommendations for supplemental nuclear myocardial perfusion imaging study by the attending physician were noted. RESULTS: Using the new reference material, 31% of all patients were classified as having a decreased exercise capacity, compared to 17% using the formerly used reference material. The difference between the two reference materials was largest in the older age groups. In one of the departments, an increase in recommendations of supplemental myocardial perfusion studies was seen after introduction of the new reference material, whereas the opposite was seen at the other department. CONCLUSION: A large amount of patients are being classified as having decreased exercise capacity and very few as having good exercise capacity using the new reference material for exercise capacity.

Physiological variation in left atrial transverse orientation does not influence orthogonal P-wave morphology.

BACKGROUND: It has previously been demonstrated that orthogonal P-wave morphology in healthy athletes does not depend on atrial size, but the possible impact of left atrial orientation on P-wave morphology remains unknown. In this study, we investigated if left atrial transverse orientation affects P-wave morphology in different populations. METHODS: Forty-seven patients with atrial fibrillation, 21 patients with arrhythmogenic right ventricular cardiomyopathy, 67 healthy athletes, and 56 healthy volunteers were included. All underwent cardiac magnetic resonance imaging or computed tomography and the orientation of the left atrium was determined. All had 12-lead electrocardiographic recordings, which were transformed into orthogonal leads and orthogonal P-wave morphology was obtained. RESULTS: The median left atrial transverse orientation was 87 (83, 91) degrees (lower and upper quartiles) in the total study population. There was no difference in left atrial transverse orientation between individuals with different orthogonal P-wave morphologies. CONCLUSIONS: The physiological variation in left atrial orientation was small within as well as between the different populations. There was no difference in left atrial transverse orientation between subjects with type 1 and type 2 P-wave morphology, implying that in this setting the P-wave morphology was more dependent on atrial conduction than orientation.

Atrial remodelling is less pronounced in female endurance-trained athletes compared with that in male athletes.

OBJECTIVES: Little data exists on atrial adaptation to training in women. Furthermore, data on right atrial (RA) volumes is lacking for both male and female athletes. The objective of this study was therefore to investigate atrial volumes in male and female athletes. DESIGN: A total of 75 athletes (33 women) and 53 controls (21 women) underwent cardiovascular magnetic resonance imaging. Left atrial (LA) and RA volumes were measured by manual delineation. The atrial appendage was included in the volumes, and pulmonary veins were excluded. RESULTS: Atrial volumes were larger in athletes compared with those in controls (males: LA 116 ± 19 ml versus 93 ± 19 ml, RA 166 ± 32 ml versus 133 ± 23 ml, p < 0.0001, females: LA 90 ± 15 ml versus 83 ± 17 ml, p < 0.05, RA 119 ± 24 ml versus 108 ± 18 ml, p = 0.07). When normalized for body surface area, atrial volumes remained larger in athletes. However, when normalized for total heart volume (THV) there were no differences between groups except for LA volumes in females where controls had higher LA/THV compared with those in athletes (p < 0.05). CONCLUSION: Atrial volumes were significantly larger in athletes. Atrial volumes normalized for THV did not differ between athletes and controls indicating a balanced enlargement. There was only a small difference between female controls and female athletes, suggesting that atrial adjustment to training is more modest in women.

Cardiac output and cardiac index measured with cardiovascular magnetic resonance in healthy subjects, elite athletes and patients with congestive heart failure.

BACKGROUND: Cardiovascular Magnetic Resonance (CMR) enables non-invasive quantification of cardiac output (CO) and thereby cardiac index (CI, CO indexed to body surface area). The aim of this study was to establish if CI decreases with age and compare the values to CI for athletes and for patients with congestive heart failure (CHF). METHODS: CI was measured in 144 healthy volunteers (39 ± 16 years, range 21-81 years, 68 females), in 60 athletes (29 ± 6 years, 30 females) and in 157 CHF patients with ejection fraction (EF) below 40% (60 ± 13 years, 33 females). CI was calculated using aortic flow by velocity-encoded CMR and is presented as mean ± SD. Flow was validated in vitro using a flow phantom and in 25 subjects with aorta and pulmonary flow measurements. RESULTS: There was a slight decrease of CI with age in healthy subjects (8 ml/min/m² per year, r² = 0.07, p = 0.001). CI in males (3.2 ± 0.5 l/min/m²) and females (3.1 ± 0.4 l/min/m²) did not differ (p = 0.64). The mean ± SD of CI in healthy subjects in the age range of 20-29 was 3.3 ± 0.4 l/min/m², in 30-39 years 3.3 ± 0.5 l/min/m², in 40-49 years 3.1 ± 0.5 l/min/m², 50-59 years 3.0 ± 0.4 l/min/m² and >60 years 3.0 ± 0.4 l/min/m². There was no difference in CI between athletes and age-controlled healthy subjects but HR was lower and indexed SV higher in athletes. CI in CHF patients (2.3 ± 0.6 l/min/m²) was lower compared to the healthy population (p < 0.001). There was a weak correlation between CI and EF in CHF patients (r² = 0.07, p < 0.001) but CI did not differ between patients with NYHA-classes I-II compared to III-IV (n = 97, p = 0.16) or patients with or without hospitalization in the previous year (n = 100, p = 0.72). In vitro phantom validation showed low bias (-0.8 ± 19.8 ml/s) and in vivo validation in 25 subjects also showed low bias (0.26 ± 0.61 l/min, QP/QS 1.04 ± 0.09) between pulmonary and aortic flow. CONCLUSIONS: CI decreases in healthy subjects with age but does not differ between males and females. We found no difference in CI between athletes and healthy subjects at rest but CI was lower in patients with congestive heart failure. The presented values can be used as reference values for flow velocity mapping CMR.

Peak oxygen uptake in relation to total heart volume discriminates heart failure patients from healthy volunteers and athletes.

BACKGROUND: An early sign of heart failure (HF) is a decreased cardiac reserve or inability to adequately increase cardiac output during exercise. Under normal circumstances maximal cardiac output is closely related to peak oxygen uptake (VO2peak) which has previously been shown to be closely related to total heart volume (THV). Thus, the aim of this study was to derive a VO2peak/THV ratio and to test the hypothesis that this ratio can be used to distinguish patients with HF from healthy volunteers and endurance athletes. Thirty-one patients with HF of different etiologies were retrospectively included and 131 control subjects (60 healthy volunteers and 71 athletes) were prospectively enrolled. Peak oxygen uptake was determined by maximal exercise test and THV was determined by cardiovascular magnetic resonance. The VO2peak/THV ratio was then derived and tested. RESULTS: Peak oxygen uptake was strongly correlated to THV (r2 = 0.74, p < 0.001) in the control subjects, but not for the patients (r2 = 0.0002, p = 0.95). The VO2peak/THV ratio differed significantly between control subjects and patients, even in patients with normal ejection fraction and after normalizing for hemoglobin levels (p < 0.001). In a multivariate analysis the VO2peak/THV ratio was the only independent predictor of presence of HF (p < 0.001). CONCLUSIONS: The VO2peak/THV ratio can be used to distinguish patients with clinically diagnosed HF from healthy volunteers and athletes, even in patients with preserved systolic left ventricular function and after normalizing for hemoglobin levels.

Impaired glucose-stimulated insulin secretion in the GK rat is associated with abnormalities in islet nitric oxide production.

We investigated implications of nitric oxide (NO) derived from islet neuronal constitutive NO synthase (ncNOS) and inducible NOS (iNOS) on insulin secretory mechanisms in the mildly diabetic GK rat. Islets from GK rats and Wistar controls were analysed for ncNOS and iNOS by HPLC, immunoblotting and immunocytochemistry in relation to insulin secretion stimulated by glucose or l-arginine in vitro and in vivo. No obvious difference in ncNOS fluorescence in GK vs control islets was seen but freshly isolated GK islets displayed a marked iNOS expression and activity. After incubation at low glucose GK islets showed an abnormal increase in both iNOS and ncNOS activities. At high glucose the impaired glucose-stimulated insulin release was associated with an increased iNOS expression and activity and NOS inhibition dose-dependently amplified insulin secretion in both GK and control islets. This effect by NOS inhibition was also evident in depolarized islets at low glucose, where forskolin had a further amplifying effect in GK but not in control islets. NOS inhibition increased basal insulin release in perfused GK pancreata and amplified insulin release after glucose stimulation in both GK and control pancreata, almost abrogating the nadir separating first and second phase in controls. A defective insulin response to l-arginine was seen in GK rats in vitro and in vivo, being partially restored by NOS inhibition. The results suggest that increased islet NOS activities might contribute to the defective insulin response to glucose and l-arginine in the GK rat. Excessive iNOS expression and activity might be deleterious for the beta-cells over time.

Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy.

Previous studies using echocardiography in healthy subjects have reported conflicting data regarding the percentage of the stroke volume (SV) of the left ventricle (LV) resulting from longitudinal and radial function, respectively. Therefore, the aim was to quantify the percentage of SV explained by longitudinal atrioventricular plane displacement (AVPD) in controls, athletes, and patients with decreased LV function due to dilated cardiomyopathy (DCM). Twelve healthy subjects, 12 elite triathletes, and 12 patients with DCM and ejection fraction below 30% were examined by cine magnetic resonance imaging. AVPD and SV were measured in long- and short-axis images, respectively. The percentage of the SV explained by longitudinal function (SV(AVPD%)) was calculated as the mean epicardial area of the largest short-axis slices in end diastole multiplied by the AVPD and divided by the SV. SV was higher in athletes [140 +/- 4 ml (mean +/- SE), P = 0.009] and lower in patients (72 +/- 7 ml, P < 0.001) when compared with controls (116 +/- 6 ml). AVPD was similar in athletes (17 +/- 1 mm, P = 0.45) and lower in patients (7 +/- 1 mm, P < 0.001) when compared with controls (16 +/- 0 mm). SV(AVPD%) was similar both in athletes (57 +/- 2%, P = 0.51) and in patients (67 +/- 4%, P = 0.24) when compared with controls (60 +/- 2%). In conclusion, longitudinal AVPD is the primary contributor to LV pumping and accounts for approximately 60% of the SV. Although AVPD is less than half in patients with DCM when compared with controls and athletes, the contribution of AVPD to LV function is maintained, which can be explained by the larger short-axis area in DCM.

Nitric oxide inhibits, and carbon monoxide activates, islet acid alpha-glucoside hydrolase activities in parallel with glucose-stimulated insulin secretion.

We have studied the influence of nitric oxide (NO) and carbon monoxide (CO), putative messenger molecules in the brain as well as in the islets of Langerhans, on glucose-stimulated insulin secretion and on the activities of the acid alpha-glucoside hydrolases, enzymes which we previously have shown to be implicated in the insulin release process. We have shown here that exogenous NO gas inhibits, while CO gas amplifies glucose-stimulated insulin secretion in intact mouse islets concomitant with a marked inhibition (NO) and a marked activation (CO) of the activities of the lysosomal/vacuolar enzymes acid glucan-1,4-alpha-glucosidase and acid alpha-glucosidase (acid alpha-glucoside hydrolases). Furthermore, CO dose-dependently potentiated glucose-stimulated insulin secretion in the range 0.1-1000 microM. In intact islets, the heme oxygenase substrate hemin markedly amplified glucose-stimulated insulin release, an effect which was accompanied by an increased activity of the acid alpha-glucoside hydrolases. These effects were partially suppressed by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one. Hemin also inhibited inducible NO synthase (iNOS)-derived NO production probably through a direct effect of CO on the NOS enzyme. Further, exogenous CO raised the content of both cGMP and cAMP in parallel with a marked amplification of glucose-stimulated insulin release, while exogenous NO suppressed insulin release and cAMP, leaving cGMP unaffected. Emiglitate, a selective inhibitor of alpha-glucoside hydrolase activities, was able to markedly inhibit the stimulatory effect of exogenous CO on both glucose-stimulated insulin secretion and the activityof acid glucan-1,4-alpha-glucosidase and acid alpha-glucosidase, while no appreciable effect on the activities of other lysosomal enzyme activities measured was found. We propose that CO and NO, both produced in significant quantities in the islets of Langerhans, have interacting regulatory roles on glucose-stimulated insulin secretion. This regulation is, at least in part, transduced through the activity of cGMP and the lysosomal/vacuolar system and the associated acid alpha-glucoside hydrolases, but probably also through a direct effect on the cAMP system.

Defective glucose-stimulated insulin release in the diabetic Goto-Kakizaki (GK) rat coincides with reduced activity of the islet carbon monoxide signaling pathway.

The Goto-Kakizaki (GK) rat displays a markedly reduced insulin response to glucose, a defect that is thought to be coupled to an impaired glucose signaling in the beta-cell. We have examined whether carbon monoxide (CO), derived from beta-cell heme oxygenase (HO), might be involved in the secretory dysfunction. Immunocytochemical labeling of constitutive HO (HO-2) showed no overt difference in fluorescence pattern in islets from GK vs. Wistar controls. However, isolated islets from GK rats displayed a markedly impaired HO activity measured as CO production (-50%), and immunoblotting revealed an approximately 50% reduction of HO-2 protein expression compared with Wistar controls. Furthermore, there was a prominent expression of inducible HO (HO-1) in GK islets. Incubation of isolated islets showed that the glucose-stimulated CO production and the glucose-stimulated insulin response were considerably reduced in GK islets compared with Wistar islets. Addition of the HO activator hemin or gaseous CO to the incubation media brought about a similar amplification of glucose-stimulated insulin release in GK and Wistar islets, suggesting that distal steps in the HO-CO signaling pathway were not appreciably affected. We conclude that the defective insulin response to glucose in the GK rat can be explained, at least in part, by a marked impairment of the glucose-HO-CO signaling pathway as manifested by a prominent decrease in glucose stimulation of islet CO production and a reduced expression of HO-2. A possible role of HO-1 expression as a compensatory mechanism in the GK islets is presently unclear.